Friday, July 21, 2017








      Genetically Modified Humans & Viruses Investigated

                          The Eugenics Investigation


                                     Editor: Michael James Ross
                                     Published: July 21, 2017
                                     Website: Http://MonsantoInvestigation.com



Chapter 1: Updated news
Chapter 2: Medical technology
Chapter 3: Regenomics
Chapter 4: Nanotechnology & Biotechnology
Chapter 5: Vaccines
Chapter 6: Autism
Chapter 7: Genome mining & editing
Chapter 8: Bioweapons
Chapter 9: Genetic disorders and diseases




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Chapter 1: Updated news


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Chapter 2: Medical technology


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The following article will detail information on the ethical standards of genetically modified organisms and bacteria. This information on biotechnology and nanotechnology will showcase many of the good purposes, including many bad purposes for this technology.

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Patients regrow muscles with pig bladder tissue

April 30, 2014


http://www.cbsnews.com/news/patients-regrow-muscles-with-pig-bladder-tissue/


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Onion cells used to create artificial muscles

 May 7, 2015


 Artificial muscles could one day revolutionize fields such as robotics, prosthetics and nanotechnology. So far, we've seen examples made from materials like electroactive elastomers, crumpled graphene, and vanadium dioxide. The problem is, most artificial muscles can only expand in one direction, or contract in the other. Now, however, scientists from National Taiwan University have gotten around that limitation using gold-plated onion cells.


 http://www.gizmag.com/onion-cells-artificial-muscles/37407/


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Scientists discover cause of and potential treatment for muscle weakness and loss due to aging

September 8, 2015

 As we grow older, we lose strength and muscle mass. However, the cause of age-related muscle weakness and atrophy has remained a mystery.


 Scientists at the University of Iowa have discovered the first example of a protein that causes muscle weakness and loss during aging. The protein, ATF4, is a transcription factor that alters gene expression in skeletal muscle, causing reduction of muscle protein synthesis, strength, and mass. The UI study also identifies two natural compounds, one found in apples and one found in green tomatoes, which reduce ATF4 activity in aged skeletal muscle. The findings, which were published online Sept. 3 in the Journal of Biological Chemistry, could lead to new therapies for age-related muscle weakness and atrophy.


http://medicalxpress.com/news/2015-09-scientists-potential-treatment-muscle-weakness.html

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Carbon Nanotube Artificial Muscles for Extreme Temperatures

March 20, 2009

 Researchers at the UT Dallas Alan G. MacDiarmid NanoTech Institute have demonstrated a fundamentally new type of artificial muscle, which can operate at extreme temperatures where no other artificial muscle can be used -- from below the temperature of liquid nitrogen (-196° C) to above the melting point of iron (1538° C).

 http://phys.org/news/2009-03-carbon-nanotube-artificial-muscles-extreme.html#nRlv


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Microbots could create electrically activated muscles

 Nov 11, 2014

 http://www.techtimes.com/articles/19979/20141111/microbots-could-create-electrically-activated-muscles.htm

Micro-muscles could be used to propel miniature robots through veins, acting as tiny muscles, controlled by electrical stimulation. Robots smaller than a grain of sand could link together, carrying out operations neither tiny robots alone, nor larger devices, could accomplish.


Micro-robots could be used for medical treatments, as well as in manufacturing.

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Organs-on-chips at the frontiers of drug discovery

 20 March 2015


http://www.nature.com/nrd/journal/v14/n4/full/nrd4539.html

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Human-on-a-chip

Researchers are working towards building a multi-channel 3D microfluidic cell culture system that compartmentalizes microenvironments in which 3D cellular aggregates are cultured to mimic multiple organs in the body.[23] Most organ-on-a-chip models today only culture one cell type, so even though they may be valid models for studying whole organ functions, the systemic effect of a drug on the human body is not verified.


http://en.wikipedia.org/wiki/Organ-on-a-chip

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Artificial organ


 http://en.wikipedia.org/wiki/Artificial_organ

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Engineering bioartificial tracheal tissue using hybrid fibroblast-mesenchymal stem cell cultures in collagen hydrogels


http://icvts.oxfordjournals.org/content/12/2/156.full


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Scientists growing livers, kidneys, ears in labs amidst organ shortage

 June 17, 2013


 http://www.cbsnews.com/news/scientists-growing-livers-kidneys-ears-in-labs-amidst-organ-shortage/


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Custom Organs, Printed to Order

 18 Mar 2015

http://www.pbs.org/wgbh/nova/next/body/3d-printed-organs/

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Cells and Biomaterials for Intervertebral Disc Regeneration


https://books.google.com/books?id=8KEZb5NXZj8C&pg=PA2&lpg=PA2&dq=fastest+tissue+regeneration+technologies&source=bl&ots=7v0piUsXqL&sig=kduH9xaw4zrlmoA6rSYFoVRuyC8&hl=en&sa=X&ei=gpQ5Vb-MHYLZtQX5Lw&ved=0CDIQ6AEwBTgK#v=onepage&q=fastest%20tissue%20regeneration%20technologies&f=false


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New discovery gives hope that nerves could be repaired after spinal cord injury

April, 2014

 http://www.sciencedaily.com/releases/2014/04/140401102122.htm

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Prototype 'nanoneedles' generate new blood vessels in mice

Mar 30, 2015

 http://phys.org/news/2015-03-prototype-nanoneedles-blood-vessels-mice.html?utm_source=menu&utm_medium=link&utm_campaign=item-menu

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Juvenile plasticity returned to adult mice brains


May 20, 2015


 By enabling the rigid brains of adult mice to return to the high levels of plasticity found in juvenile brains, scientists are opening new pathways to the treatment of brain injuries such as stroke. Back in 2013, researchers from Yale University reported the discovery of a molecular switch that achieved this result, and now scientists at the University of California, Irvine, have managed to make an old brain young again using a different approach.


 http://www.gizmag.com/juvenile-brain-plasticity-restored-adult-mice-brains/37592/


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Magnetic nanoparticles could stop blood clot-caused strokes


February 23, 2015


 http://www.sciencedaily.com/releases/2015/02/150223122427.htm


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Enzyme could make any type of donated blood safe for anyone to receive


May 1, 2015


 http://www.gizmag.com/blood-antigen-enzyme/37289/



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Stem cell stroke therapy shows promise after first human trial

August 8, 2014


A pilot study undertaken by researchers from Imperial College Healthcare NHS Trust and Imperial College London has shown promise in rapid treatment of serious strokes. The study, the first of its kind published in the UK, treated patients using stem cells from bone marrow.


http://www.gizmag.com/stroke-treatment-stem-cell-bone-marrow/33258/

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Tiny cellular bubbles enable delivery of Parkinson's drugs straight to the brain


May 5, 2015


 http://www.gizmag.com/medical/

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Breakthrough in cell conversion could help with Parkinson's treatment

  December 7, 2015

http://www.gizmag.com/cell-conversion-breakthrough-parkinsons-disease/40784/


A team of University at Buffalo researchers has identified a key obstacle in the cell conversion process, the manipulation of which allows for much easier transitions between cell types. The breakthrough has big implications for the treatment of Parkinson's disease, with scientists able to create functional neurons to replace those damaged by the condition.

Parkinson's disease is a degenerative disorder that involves the loss of dopamine neurons in the brain, having a significant impact on the patient's motor skills. The new study has seen researchers attack the problem head on, attempting to find an efficient method of producing new dopamine neurons, which could then be transplanted into the patient's brain to help tackle the disease.


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Drug Discovery for Parkinson's Disease: Researchers Grow Neurons in 3-D

 June 25, 2015


 http://scicasts.com/bio-it/1869-lab-technology/9563-drug-discovery-for-parkinson-s-disease-researchers-grow-neurons-in-3-d/

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Gene editing study reveals possible 'Achilles heel' of sickle cell disease

September 16, 2015

 Researchers from Dana-Farber/Boston Children's Cancer and Blood Disorders Center have found that changes to a small stretch of DNA may circumvent the genetic defect behind sickle cell disease (SCD). The discovery, published in the journal Nature, creates a path for developing gene editing approaches for treating SCD and other hemoglobin disorders, such as thalassemia.

http://medicalxpress.com/news/2015-09-gene-reveals-achilles-heel-sickle.html

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Microscale 'transformer' robots are joining forces to break through blocked arteries

Jun 27, 2015

http://phys.org/news/2015-06-microscale-robots-blocked-arteries.html?utm_source=menu&utm_medium=link&utm_campaign=item-menu


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Cardiac cells and gold nanofibers join forces to heal damaged hearts

 July 25, 2013


 http://www.gizmag.com/heart-patch-gold-nanofibers/28465/


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 Sticky gel helps stem cells heal rat hearts

September 24, 2015

A sticky, protein-rich gel created by Johns Hopkins researchers appears to help stem cells stay on or in rat hearts and restore their metabolism after transplantation, improving cardiac function after simulated heart attacks, according to results of a new study.

http://medicalxpress.com/news/2015-09-sticky-gel-stem-cells-rat.html

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Micro-bubbles may help prevent heart attacks and strokes

 December 18, 2012

 Heart attack and stroke-causing plaque deposits in the arteries are typically preceded by an inflammation of the arteries in those same areas. Therefore, if doctors could be aware of those inflamed regions before plaque deposits formed and problems such as chest pains arose, a lot of hardship could potentially be avoided. Well, that soon may be possible, thanks to some tiny bubbles.

http://www.gizmag.com/microbubbles-artery-inflammation/25497/?li_source=LI&li_medium=default-widget

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Bioengineered heart tissue can be stuck together like Velcro

 August 31, 2015

A new system for growing heart tissue in the lab may make future heart, liver, and lung repair much easier. University of Toronto scientists have developed asymmetrical honeycomb-shaped 2D meshes of protein scaffolding that stick together like Velcro and imitate the environments in which tissue and muscle cells grow in the body.

http://www.gizmag.com/bioengineered-heart-tissue-velcro/39173/

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Drug-delivering nano "drones" to help prevent heart attacks

 March 2, 2015

Scientists have developed targeted, biodegradable nano "drones" to deliver anti-inflammatory drugs that heal and stabilize arterial plaque in mice. Their work could pave the way for more effective prevention of heart attack and stroke in humans caused by atherosclerosis, in which artery walls thicken and suffer reduced plasticity due to an accumulation of white blood cells

The study, conducted by researchers from Colombia University Medical Center (CUMC), Brigham and Women’s Hospital (BWH) and Harvard Medical School (HMS), showed for the first time that it is possible to treat inflammation and repair plaques via highly targeted nanoparticles. It is also the first example of using targeted nanomedicine to reduce atherosclerosis in animals.

Essentially, the nanoparticles are injected into the bloodstream where they find their way to the arterial plaque, stick to them and release the healing peptides. Their small size – they are 1,000 times smaller than the tip of a single strand of human hair – and "sticky" surfaces enable them to accumulate and be retained within the plaques to facilitate healing and remodeling to block plaque rupture and thrombosis.

http://www.gizmag.com/nano-drones-healing-drug-heart-attacks/36342/

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Nanoparticle 'wrapper' delivers chemical that stops fatty buildup in rodent arteries

 June 23rd, 2015

 http://phys.org/news/2015-06-nanoparticle-wrapper-chemical-fatty-buildup.html?utm_source=menu&utm_medium=link&utm_campaign=item-menu

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Non-surgical procedure repairs severed nerves in minutes

 February 07, 2012

http://www.gizmag.com/ut-fast-nerve-regeneration/21345/

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Brain-computer connection helps paralyzed man walk

Researchers hope the system will lead to an implantable system that allows paralyzed people to regain use of their limbs.

      Sept. 24, 2015

http://www.upi.com/Health_News/2015/09/24/Brain-computer-connection-helps-paralyzed-man-walk/9311443096650

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Electronic memory may bring bionic brain one step closer


 May 12, 2015


 Using a matrix of nano-sized memristors, researchers working at the Royal Melbourne Institute of Technology (RMIT) and the University of California, Santa Barbara claim to have constructed the world’s first electronic memory cell that effectively mimics the analog process of the human brain. By storing memories as multiple threads of varying information, rather than a collection of ones and zeroes, scientists believe that this device may prove to be the first step towards creating a completely artificial, bionic brain.


 http://www.gizmag.com/electronic-memristor-memory-mimics-brain/37454/

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 Researchers use disordered matter for computation, evolving breakthrough nanoparticle Boolean logic network


September 25, 2015

Natural computers, such as evolved brains and cellular automata, express sophisticated interconnected networks and exhibit massive parallelism. They also adapt to exploit local physical properties such as capacitative crosstalk between circuits. By contrast, synthetic computers channel activity according to established design rules and do not adapt to take advantage of their surroundings. Thus, researchers are interested in using matter itself for computation.
 Scientists have speculated about the ability to evolve designless nanoscale networks of inanimate matter with the same robust capacities as natural computers, but have not yet realized the concept. Now, a group of researchers reports in Nature Nanotechnology a disordered nanomaterials system that was artificially evolved by optimizing the values of control voltages according to a genetic algorithm.

Using interconnected metal nanoparticles, which act as nonlinear single-electron transistors, the researchers were able to exploit the system's emergent network properties to create a universal, reconfigurable Boolean gate. The authors note that their system meets the requirements for a cellular neural network—universality, compactness, robustness and evolvability. Their approach works around the device-to-device variations that are becoming increasingly difficult to align as semiconductors approach the nanoscale, and which result in uncertainties in performance.

 http://phys.org/news/2015-09-disordered-evolving-breakthrough-nanoparticle-boolean.html#jCp

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Researchers create first neural-network chip built just with memristors

May 07, 2015

A team of researchers working at the University of California (and one from Stony Brook University) has for the first time created a neural-network chip that was built using just memristors. In their paper published in the journal Nature, the team describes how they built their chip and what capabilities it has.

Memristors may sound like something from a sci-fi movie, but they actually exist—they are electronic analog memory devices that are modeled on human neurons and synapses. Human consciousness, some believe, is in reality, nothing more than an advanced form of memory retention and processing, and it is analog, as opposed to computers, which of course are digital. The idea for memristors was first dreamed up by University of California professor Leon Chua back in 1971, but it was not until a team working at Hewlett-Packard in 2008, first built one. Since then, a lot of research has gone into studying the technology, but until now, no one had ever built a neural-network chip based exclusively on them.

 http://phys.org/news/2015-05-neural-network-chip-built-memristors.html#jCp


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Scientists build a neural network using plastic memristors

January 29, 2016

A collaborative of Russian and Italian scientists has created a neural network based on polymeric memristors, devices that can potentially be used to build fundamentally new computers. According to the researchers, these developments have applications in systems for machine vision, hearing, and other sensory organs, and also intelligent control systems for various devices, including autonomous robots.

http://phys.org/news/2016-01-scientists-neural-network-plastic-memristors.html


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Injectable electronics holds promise for basic neuroscience, treatment of neuro-degenerative diseases


 June 8th, 2015

 It's a notion that might be pulled from the pages of science-fiction novel - electronic devices that can be injected directly into the brain, or other body parts, and treat everything from neurodegenerative disorders to paralysis.


Read more at: http://phys.org/news/2015-06-electronics-basic-neuroscience-treatment-neuro-degenerative.html#jCp

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 Liquid crystals show potential for detection of neuro-degenerative disease


September 23, 2015

Liquid crystals are familiar to most of us as the somewhat humdrum stuff used to make computer displays and TVs. Even for scientists, it has not been easy to find other ways of using them.


Now a group of researchers at the University of Chicago's Institute for Molecular Engineering (IME) is putting liquid crystals to work in a completely unexpected realm: as detectors for the protein fibers implicated in the development of neuro-degenerative diseases such as Alzheimer's. Their novel approach promises an easier, less costly way to detect these fibers and to do so at a much earlier stage of their formation than has been possible before—the stage when they are thought to be the most toxic.

"It is extremely important that one develop techniques that allow us to detect the formation of these so-called amyloid fibrils when they're first starting to grow," said Juan de Pablo, whose group did the new work. "We have developed a system that allows us to detect them in a simple and inexpensive manner. And the sensitivity appears to be extremely high."

 http://phys.org/news/2015-09-liquid-crystals-potential-neuro-degenerative-disease.html#jCp

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 Defects in liquid crystals offer new approaches to molecular design of materials

September 24, 2015

http://phys.org/news/2015-09-defects-liquid-crystals-approaches-molecular.html

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Transparent optogenetic brain implants: Yet another amazing use for graphene


 October 21, 2014

 http://www.extremetech.com/extreme/192510-transparent-optogenetic-brain-implants-yet-another-amazing-use-for-graphene

Transparency is the key to many technologies. Thin conductive films, like those made from ITO (indium tin oxide) for example, can carry currents or create electric fields critical for displays or solar panels without blocking all the light. The most powerful brain implants being built today have exactly this same requirement. Namely, they need to record fast electric signals with conductive arrays while permitting light to pass out through them for high-resolution imaging — and just to take it up a notch — let light pass in to permit optogenetic control directly under the implant for the icing on the cake.

Unfortunately, ITO is generally too stiff and too brittle for brain implants. Even if it could be made flexible, the high temperatures required to process it are incompatible with many of the materials (like parylene) that are used in the implants. Furthermore the transparency bandwidth of ITO is insufficient to fully exploit the wide spectrum of new UV and IR capable optogenetic proteins that have researchers fairly excited. The solution, now emerging from multiple labs throughout the universe is to build flexible, transparent electrode arrays from graphene. Two studies in the latest issue of Nature Communications, one from the University of Wisconsin-Madison and the other from Penn, describe how to build these devices.

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How close are we to Elon Musk's brain-computer interface? (Video)

 April 12, 2017


Eb Fetz, a researcher here at the Center for Sensorimotor Neural Engineering (CSNE), is one of the earliest pioneers to connect machines to minds. In 1969, before there were even personal computers, he showed that monkeys can amplify their brain signals to control a needle that moved on a dial.

Much of the recent work on BCIs aims to improve the quality of life of people who are paralyzed or have severe motor disabilities. You may have seen some recent accomplishments in the news: University of Pittsburgh researchers use signals recorded inside the brain to control a robotic arm. Stanford researchers can extract the movement intentions of paralyzed patients from their brain signals, allowing them to use a tablet wirelessly.


http://www.cnn.com/2017/04/12/health/brain-computer-interface-partner/


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Scientists Prove That Telepathic Communication Is Within Reach
An international research team develops a way to say “hello” with your mind

http://www.smithsonianmag.com/innovation/scientists-prove-that-telepathic-communication-is-within-reach-180952868/?no-ist



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Building a Telepathic Army

 2012

The U.S. Army wants to train soldiers to communicate just by thinking.

http://discovermagazine.com/2012/brain/3-the-thought-helmet


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Brain implant

Concerns and ethical considerations

See also: Neuroethics

Who are good candidates to receive neural implants? What are the good uses of neural implants and what are the bad uses? Whilst deep brain stimulation is increasingly becoming routine for patients with Parkinson's disease, there may be some behavioural side effects. Reports in the literature describe the possibility of apathy, hallucinations, compulsive gambling, hypersexuality, cognitive dysfunction, and depression. However, these may be temporary and related to correct placement and calibration of the stimulator and so are potentially reversible.[40]

Some transhumanists, such as Raymond Kurzweil and Kevin Warwick, see brain implants as part of a next step for humans in progress and evolution, whereas others, especially bioconservatives, view them as unnatural, with humankind losing essential human qualities. It raises controversy similar to other forms of human enhancement. For instance, it is argued that implants would technically change people into cybernetic organisms (cyborgs). It's also expected that all research will comply to the Declaration of Helsinki. Yet further, the usual legal duties apply such as information to the person wearing implants and that the implants are voluntary, with (very) few exceptions.

Other concerns involve vulnerabilities of neural implants to cybercrime or intrusive surveillance as neural implants could be hacked, misused or misdesigned.[41]

Sadja states that "one's private thoughts are important to protect" and doesn't considers it a good idea to just charge the government or any company to protect them. Walter Glannon, a neuroethicist of the University of Calgary notes that "there is a risk of the microchips being hacked by third parties" and that "this could interfere with the user's intention to perform actions, violate privacy by extracting information from the chip".



 https://en.wikipedia.org/wiki/Brain_implant



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New wave in tech: hacking the brain (Update)

January 8, 2016

The next frontier for the tech sector is the human brain.

A new breed of neuro-hacker is finding ways to capture and manipulate brainwaves to improve health, with potential to help the severely handicapped.

A number of the innovations were on display at the Consumer Electronics Show in Las Vegas, where computer scientists and biomedical experts showcased ways to tap into and use brain signals.

The "mind control" headband unveiled by startup BrainCo effectively hacks into brain signals with a range of possible applications—from helping to improve attention spans, to detecting disease, controlling smart home appliances or even a prosthetic device.

The device "translates your brainwaves into electronic signals," said the Boston-based firm's Zenchuan Lei.

At CES, BrainCo demonstrated how a person could use the headband to manipulate a prosthetic hand—a potential life-changer for those paralyzed or missing limbs.

"These signals can be used to control objects like a prosthetic hand," Lei said. "You can turn the lights on or off just by focusing on that."

The device designed by scientists from Harvard and the Massachusetts Institute of Technology employs "neuro feedback," a means of allowing people to control their brain waves for various purposes. It is expected to be sold later this year for less than $150.

http://phys.org/news/2016-01-tech-hacking-brain.html

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Draper's Genetically Modified Cyborg DragonflEye Takes Flight

 June 1, 2017

In January, we wrote about a cybernetic micro air vehicle under development at Draper called DragonflEye. DragonflEye consists of a living, slightly modified dragonfly that carries a small backpack of electronics. The backpack interfaces directly with the dragonfly’s nervous system to control it, and uses tiny solar panels to harvest enough energy to power itself without the need for batteries.

http://spectrum.ieee.org/automaton/robotics/drones/drapers-genetically-modified-cyborg-dragonfleye-takes-flight

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More efficient memory-management scheme could help enable chips with thousands of cores

September 10, 2015

In a modern, multicore chip, every core—or processor—has its own small memory cache, where it stores frequently used data. But the chip also has a larger, shared cache, which all the cores can access.

If one core tries to update data in the shared cache, other cores working on the same data need to know. So the shared cache keeps a directory of which cores have copies of which data.

That directory takes up a significant chunk of memory: In a 64-core chip, it might be 12 percent of the shared cache. And that percentage will only increase with the core count. Envisioned chips with 128, 256, or even 1,000 cores will need a more efficient way of maintaining cache coherence.

http://phys.org/news/2015-09-efficient-memory-management-scheme-enable-chips.html

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Organic ion transistor blocks pain signals from reaching the brain


 May 11, 2015

 A new type of medical device could one day put the minds of chronic pain sufferers at ease by distributing the body's own natural pain relief signals at just the right time. Developed at Linköping University in Sweden, the tiny "ion pump" is made from organic electronics and could be implanted in patients, serving to cut off pain signals in the spinal chord before they make their way to the brain.

http://www.gizmag.com/organic-ion-transistor-pain-brain/37434/

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Artificial memories: French scientists implant false memories in brains of sleeping mice

March 10, 2015

 http://www.smh.com.au/technology/sci-tech/artificial-memories-french-scientists-implant-false-memories-in-brains-of-sleeping-mice-20150310-1402wz.html


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Photoswitch therapy restores vision to blind lab animals

December 9, 2014

A new genetic therapy that helped blind mice and dogs respond to light stimulus could restore sight to people who suffer from diseases such as retinitis pigmentosa (a gradual loss of vision from periphery inwards). The therapy uses chemicals known as photoswitches, which change shape when hit with light, to open the channels that activate retinal cells. Treated mice can distinguish between steady and flashing light, while dogs with late-stage retinal degeneration also regain some sensitivity to light.


http://www.gizmag.com/photoswitch-therapy-restores-vision-retinitis-pigmentosa/35139/?li_source=LI&li_medium=default-widget

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Researchers find 'lost' memories using light


 Memories that have been "lost" as a result of amnesia can be recalled by activating brain cells with light.

In a paper published today in the journal Science, researchers at MIT reveal that they were able to reactivate memories that could not otherwise be retrieved, using a technology known as optogenetics.

 http://medicalxpress.com/news/2015-05-lost-memories.html

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Protein shown to slow progress of Alzheimer’s and multiple sclerosis

March 2, 2015

http://www.gizmag.com/protein-fights-alzheimers-multiple-sclerosis/36366/

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New Alzheimer’s treatment fully restores memory function

Of the mice that received the treatment, 75 percent got their memory function back.


http://www.sciencealert.com/new-alzheimer-s-treatment-fully-restores-memory-function

Australian researchers have come up with a non-invasive ultrasound technology that clears the brain of neurotoxic amyloid plaques - structures that are responsible for memory loss and a decline in cognitive function in Alzheimer’s patients.

If a person has Alzheimer’s disease, it’s usually the result of a build-up of two types of lesions - amyloid plaques, and neurofibrillary tangles. Amyloid plaques sit between the neurons and end up as dense clusters of beta-amyloid molecules, a sticky type of protein that clumps together and forms plaques.

Neurofibrillary tangles are found inside the neurons of the brain, and they’re caused by defective tau proteins that clump up into a thick, insoluble mass. This causes tiny filaments called microtubules to get all twisted, which disrupts the transportation of essential materials such as nutrients and organelles along them, just like when you twist up the vacuum cleaner tube.

As we don’t have any kind of vaccine or preventative measure for Alzheimer’s - a disease that affects 343,000 people in Australia, and 50 million worldwide - it’s been a race to figure out how best to treat it, starting with how to clear the build-up of defective beta-amyloid and tau proteins from a patient’s brain. Now a team from the Queensland Brain Institute (QBI) at the University of Queensland have come up with a pretty promising solution for removing the former.

Publishing in Science Translational Medicine, the team describes the technique as using a particular type of ultrasound called a focused therapeutic ultrasound, which non-invasively beams sound waves into the brain tissue. By oscillating super-fast, these sound waves are able to gently open up the blood-brain barrier, which is a layer that protects the brain against bacteria, and stimulate the brain’s microglial cells to activate. Microglila cells are basically waste-removal cells, so they’re able to clear out the toxic beta-amyloid clumps that are responsible for the worst symptoms of Alzheimer’s.

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Study shows how Alzheimer's disease destroys brain cell connections early on

November 27, 2015


A research team led by scientists from the University of New South Wales (UNSW) in Australia has studied the mechanism by which connections in the brain are destroyed in the early stages of Alzheimer's disease. The findings represent another angle of attack in the ongoing battle to find a cure for the widespread degenerative condition.


http://www.gizmag.com/unsw-alzheimers-disease-synapse-destruction/40629/


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 Increased activity in older brains may point to new avenues for treating memory loss


September 22, 2015


Northwestern Medicine scientists have examined activity in a little-studied part of the brain associated with memory and found for the first time the reason that neurons there become more active in old age, findings that may suggest a new target for future therapies to combat memory loss in aging and Alzheimer's disease.


Researchers in Alaska have found the earliest known evidence that Ice Age humans in North America used salmon as a food source, according to a new paper published this week in the Proceedings of the National Academy of Sciences.


http://medicalxpress.com/news/2015-09-older-brains-avenues-memory-loss.html

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Repairing the brain: Two genes unlock potential for treatment of schizophrenia

September 18, 2015

Research led by scientists from Duke-NUS Graduate Medical School Singapore (Duke-NUS) has linked the abnormal behaviour of two genes (BDNF and DTNBP1) to the underlying cause of schizophrenia. These findings have provided a new target for schizophrenia treatment.


http://medicalxpress.com/news/2015-09-brain-genes-potential-treatment-schizophrenia.html

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Stem cell-derived 'organoids' help predict neural toxicity


September 21, 2015

A new system developed by scientists at the Morgridge Institute for Research and the University of Wisconsin-Madison may provide a faster, cheaper and more biologically relevant way to screen drugs and chemicals that could harm the developing brain.


http://medicalxpress.com/news/2015-09-stem-cell-derived-organoids-neural-toxicity.html

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Reflections on using Deep Brain Stimulation (DBS) to treat neuropsychiatric disorders

 May 25, 2015


 Deep brain stimulation (DBS) has been used to treat diverse neuropsychiatric disorders, ranging from Parkinson’s Disease to OCD.


 One of my most fascinating experiences as a doctoral student of neuroscience began with an early morning trip to the university hospital. Upon arrival, my laboratory colleagues and I met with one of the clinical neurologists, who introduced us to a patient suffering from advanced Parkinson's Disease. Medications were no longer working effectively, and the patient's motor symptoms were severe and debilitating. The day that we arrived, the patient was to have electrodes implanted deep into the brain circuitry that was misbehaving in his disease, the first step in a revolutionary therapeutic approach known as deep brain stimulation (DBS).


 http://medicalxpress.com/news/2015-05-deep-brain-dbs-neuropsychiatric-disorders.html#ajTabs



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Researchers genetically engineer Salmonella to eat brain tumors

 01.11.17

 Salmonella has earned its bad reputation. It is responsible for more than a million cases of food poisoning every year, of which nearly 400 people die. But a team of researchers from Duke University have recently engineered the bacteria to not attack the human gastrointestinal tract, but rather the most aggressive form of brain cancer known to man.

 https://www.engadget.com/2017/01/11/genetically-engineered-salmonella-eats-brain-tumors/


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Herpes virus genetically engineered to destroy skin cancer cells

 May 27, 2015

http://newatlas.com/herpes-virus-skin-cancer-treatment/37714/

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Cancer-fighting viruses win approval

 October 25, 2015

US regulators clear a viral melanoma therapy, paving the way for a promising field with a chequered past.

An engineered herpesvirus that provokes an immune response against cancer has become the first treatment of its kind to be approved for use in the United States, paving the way for a long-awaited class of therapies. On 27 October, the US Food and Drug Administration (FDA) approved a genetically engineered virus called talimogene laherparepvec (T-VEC) to treat advanced melanoma. Four days earlier, advisers to the European Medicines Agency had endorsed the drug.

 http://www.nature.com/news/cancer-fighting-viruses-win-approval-1.18651

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Here's What '60 Minutes' Didn't Tell You About The 'Miracle' Glioblastoma Treatment

 Mar 2015

 Last night, newsmagazine 60 Minutes devoted not one but two segments to an early-stage trial at Duke University of a cancer therapy that some patients are calling a “miracle.” It’s a genetically modified form of the polio virus, injected directly into the brains of patients with glioblastoma, a particularly deadly type of brain tumor. Eleven of the 22 patients treated so far died, but the other 11 have seen their tumors shrink. Three featured in the story are cancer-free.

 https://www.forbes.com/sites/arleneweintraub/2015/03/30/heres-what-60-minutes-didnt-tell-you-about-the-miracle-glioblastoma-treatment/#894b66741e24

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Chapter 3: Regenomics


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Breakthrough Device Heals Organs With A Single Touch

The technology works by converting normal skin cells into vascular cells, which helps heal wounds

Medical Xpress - August 7, 2017

https://www.infowars.com/breakthrough-device-heals-organs-with-a-single-touch/
--------------



 We now have the technology to regrow limbs and skin for people that need skin grafts, such as skin grafts for burn victims. Others claim that the use of artificial skin, including artificial limbs and body parts, will lead way to the production of body parts for half human and half machine types, or also known as cyborgs. These types of artificial body parts, combined with organic computing, is what some would refer to a real-life type of technology, to create genetically modified humans or cyborgs.


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Humans Could Regenerate Tissue Like Newts By Switching Off a Single Gene

 Posted March 16, 2010

Scientists have long been stymied by human regenerative healing -- that is, wholesale regrowth of, say, a severed limb -- an ability inherent in some species but lost on humans. But new research suggests the ability to regenerate isn't based on something newts and flatworms have that we don't; rather, it's something we do have that's keeping us from regenerating tissues. Researchers think a gene called p21 may control regenerative healing, and that by switching it off, humans could perform our own regeneration.


The new research suggests that the potential to heal without scarring -- or possibly even to regrow a limb, albeit in a limited manner -- may lie dormant in human cells, kept in check by the p21 gene. A group of lab mice engineered to lack p21 were able to regenerate surgically removed tissue to the point that no evidence of the surgery remained. Holes punched in their ears -- a standard procedure for tagging lab animals -- also healed perfectly, leaving behind no traces of scar tissue or previous damage.


Essentially, switching off the p21 gene allows adult cells to behave like pluripotent stem cells, reorienting themselves into whatever kind of tissue they need to be. But naturally there is a give-and-take; p21 is closely intertwined with another gene, p53, a cell-division regulator that, if allowed to run amok, can lead to many types of cancers. The p21 gene acts as a safety valve for p53, stopping cell division in the case of DNA damage. So switching off p21 can allow cells to engage in regenerative healing, but the risks of doing so include rampant cell division (read: cancer).



http://www.popsci.com/science/article/2010-03/humans-could-regenerate-tissue-newts-switchin-single-gene


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Regenomics

Regenomics represents the merger of two fields of scientific endeavor: Regenerative medicine and genomics. New technologies to reprogram aged somatic cells back to pluripotency and to restore telomere length are currently used in research in regenerative medicine, though FDA-approved cellular therapies using reprogrammed cells are currently not available in the United States. The culture and banking of somatic cells also allows the parallel sequencing of their nuclear DNA to provide individuals with potentially valuable information for guiding them in lifestyle choices, but also one day, potentially in preventative strategies where cell types are made in advance for high risk categories of disease, i.e. preparing cardiac progenitor cells for individuals at high risk for heart disease.


http://en.wikipedia.org/wiki/Regenomics


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Scientists come a step closer to "regrowing" limbs


June 3, 2015



 http://www.gizmag.com/decellularization-rat-limb-transplant/37857/

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3D Bioprinting and Nanotechnology in Tissue Engineering and Regenerative


 ( Challenges and future development of 3d bioprinting )



 https://books.google.com/books?id=ud6cBAAAQBAJ&pg=PA68&lpg=PA68&dq=fastest+tissue+regeneration+technologies&source=bl&ots=YY2KsChdcC&sig=BdMJMolEex5iDuynj3AR946qZl0&hl=en&sa=X&ei=gpQ5Vb-MHYLZtQX5Lw&ved=0CDcQ6AEwBjgK#v=onepage&q&f=false


---------------------------------------


3D-printed prosthetic limbs: the next revolution in medicine

 Feb 19, 2017


 https://www.theguardian.com/technology/2017/feb/19/3d-printed-prosthetic-limbs-revolution-in-medicine


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BioBots bioprinter to complement cutting-edge research

May 07, 2015


A high-resolution desktop 3D bioprinter that builds functional 3D living tissue was shown recently at TechCrunch Disrupt in New York. The machine is significant as a less expensive way for researchers to build 3D functional structures of living tissue. BioBots is the name of the company behind the printer.


Read more at: http://phys.org/news/2015-05-biobots-bioprinter-complement-cutting-edge.html#jCp



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Team unlocks the mysteries of wound healing


March 13, 2015



http://medicalxpress.com/news/2015-03-team-mysteries-wound.html


Researchers at the University of Arizona have discovered what causes and regulates collective cell migration, one of the most universal but least understood biological processes in all living organisms.


---------------------------


New model, new choices for wound healing using electrical fields

Jun 05, 2015


 http://phys.org/news/2015-06-choices-wound-electrical-fields.html#nRlv


 Scientists at the University of Cincinnati are working on ways to wirelessly stimulate the body's own electrical fields to improve self-healing.



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Elastic, wound-healing hydrogel activated by light

 July 5, 2015


 http://www.gizmag.com/elastic-wound-hydrogel-light/38312/?li_source=LI&li_medium=default-widget


 Hydrogels have huge potential in the field of biomedicine, but aren't without their shortcomings in their existing form. These tiny polypeptide chains are championed for their many possible applications. Indeed, in the last few years alone we've seen advances that suggest they could find use in generating new heart tissue, fighting off superbugs and the controlled release of anti-inflammatory drugs. But researchers have now developed a hydrogel that mimics the elasticity of human tissue and can be activated by exposure to light, claiming it could offer safer means of repairing wounded tissue.



-------------------------


New hydrogel aids skin regeneration to improve wound healing

December 18, 2015


 Healing chronic skin wounds can be difficult, particularly when they span large areas, or when healing is complicated by health problems such as a lack of mobility. A team of researchers from the University of California, Los Angeles (UCLA) has worked to improve the process, creating a more effective method of regeneration through use of a new material that creates a porous scaffold, allowing wounds to heal more effectively.


http://www.gizmag.com/ucla-maps-porous-hydrogel/40977/?li_source=LI&li_medium=default-widget


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Breakthrough graphene production could trigger revolution in artificial skin development


Jun 25, 2015


 A pioneering new technique to produce high-quality, low cost graphene could pave the way for the development of the first truly flexible 'electronic skin', that could be used in robots.


http://phys.org/news/2015-06-breakthrough-graphene-production-trigger-revolution.html#jCp



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New artificial skin can detect pressure and heat simultaneously

November 2, 2015



 A team of researchers with Ulsan National Institute of Science and Technology and Dong-A University, both in South Korea, has developed an artificial skin that can detect both pressure and heat with a high degree of sensitivity, at the same time. In their paper published in the journal Science Advances, the team describes how they created the skin, what they found in testing it and the other types of things it can sense.


http://techxplore.com/news/2015-11-artificial-skin-pressure-simultaneously.html


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Engineers create artificial skin that can send pressure sensation to brain cell

October 15, 2015

 Stanford engineers have created a plastic "skin" that can detect how hard it is being pressed and generate an electric signal to deliver this sensory input directly to a living brain cell.

http://phys.org/news/2015-10-artificial-skin-pressure-sensation-brain.html


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Hybrid material that responds to heat and light presents future potential for 4D-printed adaptive devices


December 14, 2015


Combining photo-responsive fibers with thermo-responsive gels, researchers at the University of Pittsburgh's Swanson School of Engineering and Clemson University have modeled a new hybrid material that could reconfigure itself multiple times into different shapes when exposed to light and heat, allowing for the creation of devices that not only adapt to their environment, but also display distinctly different behavior in the presence of different stimuli.


http://phys.org/news/2015-12-hybrid-material-future-potential-4d-printed.html


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Stretchable, biocompatible hydrogels with complex patterning for tissue engineering

Jun 02, 2015


Researchers have developed a new way of making tough—but soft and wet—biocompatible materials, called "hydrogels," into complex and intricately patterned shapes. The process might lead to injectable materials for delivering drugs or cells into the body; scaffolds for regenerating load-bearing tissues; or tough but flexible actuators for future robots, the researchers say.

http://phys.org/news/2015-06-stretchable-biocompatible-hydrogels-complex-patterning.html?utm_source=menu&utm_medium=link&utm_campaign=item-menu


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Electrospinning technology in tissue regeneration.


Electrospinning is one of the most versatile and effective tools to produce nanostructured fibers in the biomedical science fields. The nanofibrous structure with diameters from tens to hundreds of nanometers largely mimics the native extracellular matrix (ECM) of many tissues. Thus far, a range of compositions including polymers and ceramics and their composites/hybrids have been successfully applied for generating electrospun nanofibers. Different processing tools in electrospinning set-ups and assemblies are currently developed to tune the morphology and properties of nanofibers. Herein, we demonstrate the electrospinning process and the electrospun biomaterials for specific use in tissue regeneration with some examples, involving different material combinations and fiber morphologies.


http://www.ncbi.nlm.nih.gov/pubmed/22042677


-------------------------------


Tissue engineering of replacement skin: the crossroads of biomaterials, wound healing, embryonic development, stem cells and regeneration

  2006 Dec 5


 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2373411/


--------------------------------


Journal of Biomedical Nanotechnology


Bioactive Mesoporous Silicas as Controlled Delivery Systems: Application in Bone Tissue Regeneration


http://www.ingentaconnect.com/content/asp/jbn/2008/00000004/00000001/art00001


----------------------------


New calcium phosphate foam could help repair damage due to osteoporoses

December 23, 2015


 A team of researchers affiliated with several institutions in France has developed a type of injectable foam that may serve as a means for treating osteoporoses and other bone degenerative diseases. The team has published a paper in the journal Acta Biomaterialia describing how they came up with the foam, how it works and the uses to which it might be put.


 http://phys.org/news/2015-12-calcium-phosphate-foam-due-osteoporoses.html?utm_source=menu&utm_medium=link&utm_campaign=item-menu



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A novel approach to periodontal tissue regeneration with mesenchymal stem cells and platelet-rich plasma using tissue engineering technology: A clinical case report.

http://europepmc.org/abstract/med/16939018


-------------------------------


A material to close deep wounds and promote skin regrowth
Researchers are developing a collagen-based tissue template to aid in skin repair.

June 20, 2011


 http://articles.latimes.com/2011/jun/20/health/la-he-artificial-skin-20110620

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Mighty Mouse Holds Secret for Regrowing Skin

September 26, 2012


http://www.livescience.com/23478-mouse-regeneration-skin-regrow.html



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Scientists sequence genome of worm that can regrow body parts, seeking stem cell insights


September 21, 2015

Tourists spending a recuperative holiday on the Italian coast may be envious of the regenerative abilities of locally found flatworm Macrostomum lignano. Named for its discovery near the Italian beach town of Lignano Sabbiadoro, this tiny worm can regenerate almost its whole body following an injury, and researchers have long been trying to understand how it's able to pull off this trick.


http://medicalxpress.com/news/2015-09-scientists-sequence-genome-worm-regrow.html


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Squid sucker teeth could advance human technology

July 3, 2014

There seems to be no end to the proposed human technologies based on attributes of the squid. The animals' beaks have inspired a material that could be used for medical implants, their muscles may lead us to color-changing clothing, the chitosan in their "pens" has been used to create a proton-conducting transistor, and their movements served as the inspiration for a soft-bodied robot. Now, it turns out that the teeth inside the suckers on their tentacles might be the basis for materials that could be used in fields such as reconstructive surgery.


http://www.gizmag.com/squid-sucker-teeth/32817/?li_source=LI&li_medium=default-widget


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Tissue engineering


 http://en.wikipedia.org/wiki/Tissue_engineering

Tissue engineering is the use of a combination of cells, engineering and materials methods, and suitable biochemical and physicochemical factors to improve or replace biological functions. While it was once categorized as a sub-field of biomaterials, having grown in scope and importance it can be considered as a field in its own right.
Examples

    Bioartificial windpipe : The first procedure of regenerative medicine of an implantation of a "bioartificial" organ.
    In vitro meat: Edible artificial animal muscle tissue cultured in vitro.
    Bioartificial liver device: several research efforts have produced hepatic assist devices utilizing living hepatocytes.
    Artificial pancreas: research involves using islet cells to produce and regulate insulin, particularly in cases of diabetes.
    Artificial bladders: Anthony Atala (Wake Forest University) has successfully implanted artificially grown bladders into seven out of approximately 20 human test subjects as part of a long-term experiment.
    Cartilage: lab-grown tissue was successfully used to repair knee cartilage.
    Scaffold-free cartilage: Cartilage generated without the use of exogenous scaffold material. In this methodology, all material in the construct is cellular or material produced directly by the cells themselves.
    Doris Taylor's heart in a jar
    Tissue-engineered airway
    Tissue-engineered vessels
    Artificial skin constructed from human skin cells embedded in a hydrogel, such as in the case of bioprinted constructs for battlefield burn repairs.
    Artificial bone marrow
    Artificial bone

    Bioartificial windpipe : The first procedure of regenerative medicine of an implantation of a "bioartificial" organ.
    In vitro meat: Edible artificial animal muscle tissue cultured in vitro.
    Bioartificial liver device: several research efforts have produced hepatic assist devices utilizing living hepatocytes.
    Artificial pancreas: research involves using islet cells to produce and regulate insulin, particularly in cases of diabetes.
    Artificial bladders: Anthony Atala (Wake Forest University) has successfully implanted artificially grown bladders into seven out of approximately 20 human test subjects as part of a long-term experiment.
    Cartilage: lab-grown tissue was successfully used to repair knee cartilage.
    Scaffold-free cartilage: Cartilage generated without the use of exogenous scaffold material. In this methodology, all material in the construct is cellular or material produced directly by the cells themselves.
    Doris Taylor's heart in a jar
    Tissue-engineered airway
    Tissue-engineered vessels
    Artificial skin constructed from human skin cells embedded in a hydrogel, such as in the case of bioprinted constructs for battlefield burn repairs.
    Artificial bone marrow
    Artificial bone

Laser-assisted BioPrinting (LaBP)


    In a 2012 study, Koch et al. focused on whether Laser-assisted BioPrinting (LaBP) can be used to build multicellular 3D patterns in natural matrix, and whether the generated constructs are functioning and forming tissue. LaBP arranges small volumes of living cell suspensions in set high-resolution patterns. The investigation was successful, the researchers foresee that "generated tissue constructs might be used for in vivo testing by implanting them into animal models" (14). As of this study, only human skin tissue has been synthesized, though researchers project that "by integrating further cell types (e.g. melanocytes, Schwann cells, hair follicle cells) into the printed cell construct, the behavior of these cells in a 3D in vitro microenvironment similar to their natural one can be analyzed", useful for drug discovery and toxicology studies.

Self-assembly

Self-assembly may play an important role here, both from the perspective of encapsulating cells and proteins, as well as creating scaffolds on the right physical scale for engineered tissue constructs and cellular ingrowth. The micromasonry is a prime technology to get cells grown in a lab to assemble into three-dimensional shapes. To break down tissue into single-cell building blocks, researchers have to dissolve the extracellular mortar that normally binds them together. But once that glue is removed, it's quite difficult to get cells to reassemble into the complex structures that make up our natural tissues. While cells aren't easily stackable, building blocks are. So the micromasonry starts with the encapsulation of living cells in polymer cubes. From there, the blocks self-assemble in any shape using templates.



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Chapter 4: Nanotechnology & Biotechnology

-------------------



-------------------



Synthesized Nanoparticles Act As Artificial Viruses for Gene Therapy

04/09/2015

 Researchers of the Nanobiology Unit from the Universitat Autònoma de Barcelona (UAB) Institute of Biotechnology and Biomedicine, led by Antonio Villaverde, managed to create artificial viruses, protein complexes with the ability of self-assembling and forming nanoparticles which are capable of surrounding DNA fragments, penetrating the cells and reaching the nucleus in a very efficient manner, where they then release the therapeutic DNA fragments. The achievement represents an alternative with no biological risk to the use of viruses in gene therapy.


 http://www.cemag.us/news/2015/04/synthesized-nanoparticles-act-artificial-viruses-gene-therapy


----------------------


With new technology for cell construction, we must be cautious of certain groups that could abuse synthesized viruses, including genetic bacteria for the wrong purposes.


-------------------------


New microscope technique could speed identification of deadly bacteria

 June 8th, 2015


A new way of rapidly identifying bacteria, which requires a slight modification to a simple microscope, may change the way doctors approach treatment for patients who develop potentially deadly infections and may also help the food industry screen against contamination with harmful pathogens, according to researchers at the Korea Advanced Institute of Science and Technology (KAIST) in Daejeon, South Korea.

http://phys.org/news/2015-06-microscope-technique-identification-deadly-bacteria.html#jCp


 ------------------------------------------



 PROTACs: A New Type of Drug That Can Target All Disease-Causing Proteins


 June 11, 2015

 http://scitechdaily.com/protacs-a-new-type-of-drug-that-can-target-all-disease-causing-proteins/

A newly published study from Yale University details the discovery of a new type of drug, called Proteolysis Targeting Chimeras (PROTACs), which can target all disease-causing proteins.

Current drugs block the actions of only about a quarter of known disease-causing proteins, but Yale University researchers have developed a technology capable of not just inhibiting, but destroying every protein it targets.

The new type of drug, called Proteolysis Targeting Chimeras (PROTACs), also can continue to destroy mutant proteins in mouse tumors, according to a new study published June 10 in the journal Nature Chemical Biology.

“This new drug modality culminates a decade of work in the field by my lab,” said Craig Crews, the Lewis B. Cullman Professor of Molecular, Cellular, and Developmental Biology and senior author of the paper, which was done in collaboration with scientists from GlaxoSmithKline and Arvinas, LLC.

Almost all current drugs are small molecules designed to fit into the folds of disease-causing proteins and inhibit their function. High doses are often needed to ensure that protein function is blocked sufficiently to produce therapeutic results, which in turn can produce harmful side effects.

In contrast, PROTACs engage the cells’ own protein degradation machinery to destroy targeted proteins by tagging them for removal and can do so multiple times, meaning it can work at lower doses, the authors say. This suggests this new type of drug has not only the potential to target proteins that are not currently “pharmaceutically vulnerable” but could do so safely, Crews said.

“This is a game-changer for drug development,” Crews said.

--------------------

The future of medicine could be found in this tiny crystal ball

February 4, 2016

 A Drexel University materials scientist has discovered a way to grow a crystal ball in a lab. Not the kind that soothsayers use to predict the future, but a microscopic version that could be used to encapsulate medication in a way that would allow it to deliver its curative payload more effectively inside the body.


http://phys.org/news/2016-02-future-medicine-tiny-crystal-ball.html?utm_source=menu&utm_medium=link&utm_campaign=item-menu


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Subsurface discovery sprouts a new branch on the tree of life


June 23, 2015


 http://phys.org/news/2015-06-subsurface-discovery-tree-life.html#jCp


Bacteria are enigmatic by nature, minuscule but staggeringly—sometimes alarmingly—ubiquitous. As critical drivers of everything from global biogeochemical cycles to million dollar industries, they are the little cogs that keep our planet going. They even control our brains!

The study of bacteria is hindered because the vast majority of them cannot be cultured or grown in the lab. With the 1977 advent of a molecular technique that enabled culture-independent surveys, microbiologists thought they had a handle on the breadth of microbial diversity on earth.

They were wrong.


Last week a study published in Nature pulled the veil on a branch of the bacterial tree of life that has evaded detection for nearly a century and a half. The study, led by Christopher Brown, who is a PhD candidate in microbial biology at the University of California in Berkeley, used cutting edge genome sequencing and savvy bioinformatics techniques to make this remarkable discovery.

It all started at an abandoned uranium milling site on the banks of the Colorado River in a town called Rifle. This location, contaminated with toxic byproducts of uranium milling, has been a test ground for researchers experimenting on how microbes can be harnessed to bioremediate or clean the environment.

Previously, researchers found that when naturally occurring microbes were supplied with a food source—the simple carbon compound acetate—a fortuitous biochemical reaction ensued. When stimulated to grow, a certain group of bacteria utilized the soluble uranium present in the soil and converted it to an insoluble form. Once insoluble, the uranium would be less apt to flow through groundwater and into the adjacent Colorado River.

Researchers posit microscopic processes like this could be capitalized upon at other contaminated sites to prevent the spread of toxins to drinking water.

Current research at the Rifle site aims to delve into the ecology of the small but mighty members of this microbial community. In this most recent study, Brown and colleagues went about this by pumping groundwater through a series of filters to capture cells—some of the tiniest free living organisms ever documented.

DNA from these microbial communities was extracted en masse, sequenced into millions of short snippets, then put back together like a jigsaw puzzle—a one so big it necessitated a powerful supercomputer to finish. In the end, this process yielded nearly 800 complete or near-complete microbial genomes.

Even considering the strength of modern high throughput sequencing technology, the recovery of 800 genomes is impressive—especially considering the very first bacterial genome was completed just 20 years ago and required a prodigious entourage of researchers.

Especially surprising about these genomes recovered by Brown and colleagues is that when they tried to place them on the Tree of Life amongst other known bacteria, they didn't fit.

In these ultra small organisms, the marker genes typically used in the previously mentioned culture-independent identification experiment were riddled with extra stretches of DNA called insertion sequences.

"We were really surprised to find how diverse these groups are within the bacterial domain, and just how consistently different the organisms within this radiation are from the rest of bacteria," Brown said in a statement.

These bacteria cannot be grown in lab cultures. To further complicate things, it is predicted that between 50-100 percent of bacteria in some of the groups they discovered would be completely missed using the standard molecular techniques.

Currently the tree of life is divided into three kingdoms. Bacteria and Archaea are two branches, each composed solely of unicellular organisms. The third kingdom is Eukarya, which encompasses all multicellular life forms and some unicellular microbes as well.

The finding of this paper "represents a substantial modification of the tree of life," corresponding author Jill Banfield said in a statement. "These new major features on the tree of life mean that it probably won't be the simple three-domain view we have now," Banfield said.

These novel bacteria at the Rifle site provide a tantalizing glimpse into microscopic worlds yet to be discovered in other locales. Like the communities at Rifle, other undiscovered bacterial groups could be an untapped resource for beneficial environmental applications.

"People have seen these bacteria in surveys of many different environments all over the planet" Brown said. The next step is to find them.

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Newfound groups of bacteria are mixing up the tree of life

Jun 15, 2015

 http://news.berkeley.edu/2015/06/15/newfound-groups-of-bacteria-are-mixing-up-the-tree-of-life/

--------------------

Making Drugs Out of Dirt Is Really Hard

 January 26, 2015

http://motherboard.vice.com/read/making-drugs-from-dirt-is-really-hard

 If you’re looking for new medicines, a good place to search is in the dirt. Many of the molecules that have made human life simpler—like those used i?n antibiotics—have been found by simply analyzing the ground, where microorganisms work relentlessly to synthesize precious, possibly curative stuff.

The good news is that there are very likely still some useful products buried in the world’s dirt. The less good news is that coming across them is very hard.

A team of biologists of Rockefeller University in New York recently launched the website Drug?s from Dirt. The site is a clarion call for people around the world to grab a shovel and send samples of soil to the folks at the university, who will scour them for interesting elements. The same team also published a pa?per this month in which they underline how recent analyses “suggest the existence of an enormous untapped reservoir of natural-product-encoding biosynthetic gene clusters in the environment.”

I got in touch with Sea?n Brady, one of the authors of the paper and head of the university’s Laboratory of Genetically Encoded Small Molecules, to ask him what the deal was with dirt and drugs.


-------------------------


Assessing the biosimilarity of protein drugs: New study shows method's precision

February 5, 2016

 A first-ever interlaboratory study of four versions of a therapeutic protein drug—all manufactured from living cells—reports that an established analytical tool akin to magnetic resonance imaging reliably assessed the atomic structures of the biologically similar products, yielding the equivalent of a fingerprint for each.

The findings, described today in Nature Biotechnology, demonstrate that the method—known as two-dimensional nuclear magnetic resonance spectroscopy, or 2D-NMR—"can be a robust and powerful complementary technique for companies and regulators" when assessing these biosimilars, said Robert Brinson, a research chemist at the National Institute of Standards and Technology (NIST). This type of assessment is part of a set of comparisons required to determine whether a follow-on biological product is highly similar to an existing product, so that there is no "clinically meaningful" difference between the two.

"Other analytical methods provide useful information, but 2D-NMR is one of the few approaches that can yield complete assignment of three-dimensional structure across the entire molecule in solution at atomic-level resolution," Brinson explains. "Our study indicates that 2D-NMR data can yield a precise and unique 'fingerprint' of structural information in a biological product," he said.

 http://phys.org/news/2016-02-biosimilarity-protein-drugs-method-precision.html?utm_source=menu&utm_medium=link&utm_campaign=item-menu

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Researchers may have discovered fountain of youth by reversing aging in human cells

May 27, 2015

http://www.gizmag.com/reversal-of-aging-human-cell-lines/37721/

Researchers in Japan have found that human aging may be able to be delayed or even reversed, at least at the most basic level of human cell lines. In the process, the scientists from the University of Tsukuba also found that regulation of two genes is related to how we age.

The new findings challenge one of the current popular theories of aging, that lays the blame for humans' inevitable downhill slide with mutations that accumulate in our mitochondrial DNA over time. Mitochondrion are sometimes likened to a cellular "furnace" that produces energy through cellular respiration. Damage to the mitochondrial DNA results in changes or mutations in the DNA sequence that build up and are associated with familiar signs of aging like hair loss, osteoporosis and, of course, reduced lifespan.

So goes the theory, at least. But the Tsukuba researchers suggest that something else may be going on within our cells. Their research indicates that the issue may not be that mitochondrial DNA become damaged, but rather that genes get turned "off" or "on" over time. Most intriguing, the team led by Professor Jun-Ichi Hayashi was able to flip the switches on a few genes back to their youthful position, effectively reversing the aging process.

The researchers came to this conclusion by comparing the function level of the mitochondria in fibroblast cell lines from children under 12 years of age to those of elderly people between 80 and 97. As expected, the older cells had reduced cellular respiration, but the older cells did not show more DNA damage than those from children. This discovery led the team to propose that the reduced cellular function is tied to epigenetic regulation, changes that alter the physical structure of DNA without affecting the DNA sequence itself, causing genes to be turned on or off. Unlike mutations that damage that sequence, as in the other, aforementioned theory of aging, epigenetic changes could possibly be reversed by genetically reprogramming cells to an embryonic stem cell-like state, effectively turning back the clock on aging.

For a broad comparison, imagine that a power surge hits your home's electrical system. If not properly wired, irreversible damage or even fire may result. However, imagine another home in which the same surge trips a switch in this home's circuit breaker box. Simply flipping that breaker back to the "on" position should make it operate as good as new. In essence, the Tsukuba team is proposing that our DNA may not become fried with age as previously thought, but rather simply requires someone to access its genetic breaker box to reverse aging.

To test the theory, the researchers found two genes associated with mitochondrial function and essentially experimented with turning them on or off. In doing so, they were able to create defects or restore cellular respiration. These two genes regulate glycine, an amino acid, production in mitochondria, and in one of the more promising findings, a 97-year-old cell line saw its cellular respiration restored after the addition of glycine for 10 days.

The researchers' findings were published this month in the journal Scientific Reports.

Whether or not this process could be a potential fountain of youth for humans and not just human fibroblast cell lines still remains to be seen, with much more testing required. However, if the theory holds, glycine supplements could one day become a powerful tool for life extension.


-------------


 A barrier against brain stem cell aging


September 17, 2015


Neural stem cells generate new neurons throughout life in the mammalian brain. However, with advancing age the potential for regeneration in the brain dramatically declines. Scientists of the University of Zurich now identified a novel mechanism of how neural stem cells stay relatively free of aging-induced damage. A diffusion barrier regulates the sorting of damaged proteins during cell division.


 http://phys.org/news/2015-09-barrier-brain-stem-cell-aging.html#jCp


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Researchers discover surprisingly wide variation across species in genetic systems that influence aging


May 28th, 2015


http://phys.org/news/2015-05-surprisingly-wide-variation-species-genetic.html


A new Iowa State University study focusing on insulin signaling uncovered surprising genetic diversity across reptiles, birds and mammals.

The research sets the stage for an improved understanding of metabolism, growth and aging and may have implications for medicine and human health, said Anne Bronikowski, an associate professor of ecology, evolution and organismal biology and a lead author of the study.

Insulin signaling is a critical biological process that governs the rate at which cells grow and divide and ultimately regulates aging. Scientists previously assumed the process remained much the same throughout the animal kingdom. But the new research shows that the genetic pathways in reptiles evolved to include protein forms not observed in mammals, a finding that suggestions these proteins carry out new or additional functions in reptiles.

The researchers looked at a molecular network known as the insulin/insulin-like signaling and target of rapamycin network (IIS/TOR). Because the IIS/TOR network regulates critical aspects of animal biology, scientists have long speculated that the network would work more or less the same in most animal species.

Bronikowski and Fred Janzen, a professor of ecology, evolution and organismal biology, completed the study along with former and current members of their labs. The research team compared the genomes of mammals and birds with 17 reptile species. The team found an abundance of variation in the hormones and receptors of the network, which bucks the conventional wisdom and indicates that hormones delivered through insulin likely undertake additional functions in reptiles.

"The study provides a critical step toward understanding how the IIS/TOR network may regulate variation in metabolism, modes of reproduction and rates of aging," Bronikowski said. "It highlights genetic variants that occur in nature that may be useful in a human health context. It therefore lays the groundwork for future research to identify natural genetic variants that may work together to alter the function of this network, which may lend insight into metabolic and aging diseases and treatments."

Previous studies of insulin signaling have focused on species commonly used as laboratory models, such as mice, fruit flies and nematodes. The new study compared 66 species, including 17 reptile species for which the research group had to generate transcriptome data – or the set of all RNA molecules in a particular genome – because the data didn't exist previously. The team was able to sequence the reptile data with the help of support from the ISU Center for Integrated Animal Genomics.

The wide range of variation discovered by the study may suggest that the insulin signaling network could be targeted by new medical therapies to treat conditions associated with aging, Bronikowski said.

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"Avatar" project aims for human immortality by 2045

 July 25, 2012

 http://www.gizmag.com/avatar-project-2045/23454/

Russian media magnate Dmitry Itskov is heading "Avatar," a tremendously ambitious and far-reaching multidisciplinary research project that aims to achieve immortality in humans within the next three decades. He plans to do it by housing human brains in progressively more disembodied vehicles, first transplanting them into robots and then, by the year 2045, by reverse-engineering the human brain and effectively "downloading" human consciousness onto a computer chip.

Fact or fiction?

When speculating on seemingly unobtainable goals such as this, one must be careful not to believe that improbable technological advances automatically become more likely simply by looking further away in the future. This is the cognitive trap that, for instance, has seen many leading IT experts predict the development of a human-level artificial intelligence at roughly twenty years in the future for at least the past five decades

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Can We Reprogram Our DNA and Heal Ourselves With Frequency, Vibration & Energy?

 March 5, 2014

http://www.wakingtimes.com/2014/03/05/reprogram-dna-heal-ourselves-frequency-vibration-energy/


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Novel UV-mediated mode of DNA repair

December 22, 2015

 UV light damages DNA. But LMU researchers now show that it can also mediate non-enzymatic repair of one type of damage, albeit in a specific context. This effect may have played vital role in early evolution of living systems.The ultraviolet fraction of sunlight triggers photochemical reactions in the DNA molecules that make up the hereditary material in our cells. These reactions can result in alterations in the DNA structure which lead to mutations that may cause cell death or promote tumorigenesis. LMU researchers led by Professor Thomas Carell, who holds the Chair of Bioorganic Chemistry, and Wolfgang Zinth, Professor of Biomolecular Optics, have now shown that the DNA itself can repair one of the most common types of UV-mediated damage by a non-enzymatic mechanism which is itself dependent on UV. The new findings appear in the Journal of the American Chemical Society.

Cells possess a variety of complex, enzyme-based mechanisms which are used for the repair of damaged DNA, and this year's Nobel Prize in Chemistry was awarded to three researchers for work on the elucidation of these mechanisms. The team led by Zinth and Carell, have now discovered the first instance of a sequence-dependent repair mechanism which does not require the participation of enzymes at all.

http://phys.org/news/2015-12-uv-mediated-mode-dna.html


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Scientists Prove DNA Can Be Reprogrammed by Words and Frequencies

 Aug 2, 2012

 THE HUMAN DNA IS A BIOLOGICAL INTERNET and superior in many aspects to the artificial one. Russian scientific research directly or indirectly explains phenomena such as clairvoyance, intuition, spontaneous and remote acts of healing, self healing, affirmation techniques, unusual light/auras around people (namely spiritual masters), mind’s influence on weather patterns and much more. In addition, there is evidence for a whole new type of medicine in which DNA can be influenced and reprogrammed by words and frequencies WITHOUT cutting out and replacing single genes.


 http://wakeup-world.com/2011/07/12/scientist-prove-dna-can-be-reprogrammed-by-words-frequencies/


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Scientists Can Now Pull the DNA of Ancient Humans Out of Cave Dirt

 Apr 27, 2017


The technique will allow researchers to study Neanderthals and other prehistoric people without relying on fossils.


 https://www.theatlantic.com/science/archive/2017/04/ancient-dna-sediment-neanderthal-denisovan/524433/


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Engineers invent process to accelerate protein evolution

December 7, 2015

 All living things require proteins, members of a vast family of molecules that nature "makes to order" according to the blueprints in DNA.

Through the natural process of evolution, DNA mutations generate new or more effective proteins. Humans have found so many alternative uses for these molecules - as foods, industrial enzymes, anti-cancer drugs - that scientists are eager to better understand how to engineer protein variants designed for specific uses.

Now Stanford engineers have invented a technique to dramatically accelerate protein evolution for this purpose. This technology, described in Nature Chemical Biology, allows researchers to test millions of variants of a given protein, choose the best for some task and determine the DNA sequence that creates this variant.

"Evolution, the survival of the fittest, takes place over a span of thousands of years, but we can now direct proteins to evolve in hours or days," said Jennifer Cochran, a professor of bioengineering who co-authored the paper with Thomas Baer, director of the Stanford Photonics Research Center.

 http://phys.org/news/2015-12-protein-evolution.html

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Chapter 5: Vaccines


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Whistleblower Tells All About Forced Vaccination


 (Oct 16, 2015)


https://www.youtube.com/watch?v=cRSc2-wRlrQ


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The Vaccine Whistleblower The Main Stream Media Does Not Want You To Know About 


(  April 3rd, 2016 )


https://www.youtube.com/watch?v=EBNnR9b4F_s


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Explosive: The real reason Holistic Doctors are being killed and vanishing!


( Jul 23, 2015 )


https://www.youtube.com/watch?v=cALgIHETMDU


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Anti-vaccine doctor behind ‘dangerous’ autism therapy found dead. Family cries foul.

 June 29, 2015

https://www.washingtonpost.com/news/morning-mix/wp/2015/06/29/anti-vaccine-doctor-behind-dangerous-autism-therapy-found-dead-family-cries-foul/


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Nagalase: Friend and Foe?

What is Nagalase?

Nagalase is a protein made by all cancer cells and viruses (HIV, hepatitis B, hepatitis C, influenza, herpes, Epstein-Barr virus, and others). Its formal, official chemical name is alpha-N-acetylgalactosaminidase, but this is such a tongue-twisting mouthful of a moniker that we usually just call it “Nagalase.” (Sometimes, when I want to impress friends with my brilliance, I’ll say the entire word real fast: “alpha-N-acetylgalactosaminidase.” I have found that it’s important to practice beforehand if one doesn’t want to embarrass oneself.)

Why is Nagalase important?

    Nagalase causes immunodeficiency. Nagalase blocks production of GcMAF, thus preventing the immune system from doing its job. Without an active immune system, cancer and viral infections can grow unchecked.
    As an extremely sensitive marker for all cancers, Nagalase provides a powerful system for early detection.
    Serial Nagalase testing provides a reliable and accurate method for tracking the results of any therapeutic regimen for cancer, AIDS, or other chronic viral infection.

Nagalase proves that cancer cells break all the rules

Normal healthy cells cooperate with one another in a concerted effort to further the good of all. Cancer cells refuse to play ball. Their disdainful attitude toward the rest of our cellular community is appalling. For example, these cellular scofflaws ignore clear messages to stop growing and spreading and encroaching on their neighbor’s space. How would you like it if your neighbor moved his fence over into your backyard?

Of all the rules cancer cells break, none is more alarming than the production of Nagalase, the evil enzyme that completely hog-ties the immune system army’s ability to stop cancer cells.

Virus particles also make Nagalase. Their goal is the same as that of the cancer cells: survival by incapacitating their number one enemy: the immune system.

Nagalase precision

Like a stealth bomber, the Nagalase enzyme synthesized in and released from a cancer cell or a virus particle pinpoints the GcMAF production facilities on the surface of your T and B lymphocytes and then wipes them out with an incredibly precise bomb. How precise? Let me put it this way: Nagalase locates and attacks one specific two-electron bond located at, and only at, the 420th amino acid position on a huge protein molecule (DBP), one of tens of thousands of proteins, each containing millions of electrons. This is like selectively taking out a park bench in a major city from six thousand miles away. More astonishing, if that is possible, Nagalase never misses its target. There is no collateral damage.


As you already know, GcMAF is a cell-signaling glycoprotein that talks to macrophages, enabling them to rapidly find, attack, and kill viruses and cancer cells. By activating macrophages, GcMAF triggers a cascade that activates the entire immune system. Blockage of GcMAF production by Nagalase brings all this wonderful anti-cancer and anti-viral immune activity to a screeching halt, allowing cancer and infections to spread.


Nagalase testing: former mass murderer now works for the good guys

It’s easy to be a little schizy about Nagalase. On the one hand, this nasty protein’s behavior toward us has been reprehensible and disastrous. Working in cahoots with cancer and HIV—not shy about getting into bed with our mortal enemies—Nagalase can rightfully claim direct responsibility for billions of human deaths. And it would just as soon add you to the list, so we don’t have to be shy about placing Nagalase in the “genocidal murderer” column.

With the advent of Nagalase testing, however, this bad actor now will be harnessed to a useful purpose. By providing us with precise and reliable advance information about enemy operations, Nagalase blood level testing becomes a “Deep Throat” double agent for cancer. He helps us by giving us an early warning sign.


http://gcmaf.timsmithmd.com/book/chapter/52


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Is This the Real Story of What Happened Regarding Nagalase?

February 25, 2016

During several months of 2015, numerous physicians, who were researching the causes of autism and successfully healing autistics, suddenly met with untimely deaths, or what’s been referred to as “suicided.” Who knows what really happened; all we know is that those physicians no longer are on Planet Earth.


 http://www.activistpost.com/2016/02/is-this-the-real-story-of-what-happened-regarding-nagalase.html

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Doctors Who Discovered Cancer Enzymes In Vaccines All Found Murdered

 Feb 20, 2016

Not long ago, Neon Nettle reported on the epidemic of doctors being murdered, most of which were in Florida, U.S. The scientists all shared a common trait, they had all discovered that nagalase enzyme protein was being added to vaccines which were then administrated to humans.Nagalese is what prevents vitamin D from being produced in the body, which is the body’s main defence to naturally kill cancer cells.

According to Thebigriddle.com: Nagalase is a protein that’s also created by all cancer cells. This protein is also found in very high concentrations in autistic children. And they’re PUTTING it in our vaccines!!

This prevents the body from utilizing the Vitamin D necessary to fight cancer and prevent autism. Nagalese disables the immune system. It’s also known to cause Type 2 Diabetes. So basically…they weren’t killing these doctors because they had found the cure to cancer or were successfully treating autism… they’re killing them because these Dr’s had been researching and had the evidence that the vaccines they’re injecting our precious children with are CAUSING our current cancer and autism crisis!!

And that it’s obviously being done knowingly and on purpose! The Dr’s they killed in FL had been collaborating and were getting ready to go public with the information.

Two doctors, Bradstreet and Gonzalez, were planning on publishing their findings, which centered around nagalase and GcMAF, a definite “smoking gun” if they would have been able to pull the trigger on their alleged findings regarding nagalase in vaccines.

Dr Ted Broer of HealthMasters.com tells the story, as he knows it, in two exceptionally remarkable videos below, which I think everyone who is undecided about vaccines and vaccinations ought to listen to carefully, as Dr Broer explains some of what happens to infants, in the way of reactions after vaccinations, is explained plus why it, “the encephalitic scream,” [1,2] happens biochemically. Pediatricians and family doctors say that’s “normal” and to let baby cry it out! See what you think!

 http://cancerremedies.net/doctors-who-discovered-cancer-enzymes-in-vaccines-all-found-murdered/

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Dr. Bradstreet, Nagalase, and the Viral Issue in Autism

In the past months Dr. Bradstreet has become interested in nagalese, which he describes as an enzyme "produced by cancer cells and viruses."  He thinks it unlikely that children with autism have undiagnosed cancers, and thus suspicion falls on a viral etiology.  Dr. Bradstreet writes, "Viruses make the nagalese enzyme as part of their attachment proteins.  It serves to get the virus into the cell and also decreases the body's immune reaction to the virus-thereby increasing the odds of viral survival."

Further on Dr. Bradstreet writes, "It is reasonable and likely that the nature of the immune dysfunction and the frequently observed autoimmune problems in autism are mediated by persistent, unresolved viral infections."  He claims to have tested approximately 400 children with autism for the viral marker, nagalese, and found that nearly 80% have significantly elevated levels.  He hopes to publish soon on this study and believes this information "is one of the most important developments in the clinical treatment of children on the spectrum that I have experienced in the last 15 years."


Dr. Bradstreet also discusses a substance called GcMAF, which I don't have enough information about to make an informed judgment, and that after viral clearance, the possibility of using neuronal stem cells which can cross the blood-brain barrier.  I really can't comment on the advisability of either suggestion.


http://www.ageofautism.com/2011/10/dr-bradstreet-nagalase-and-the-viral-issue-in-autism.html


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VACCINE INGREDIENTS (POISONS)


[These are injected directly into the body, more so in combination. You can see these listed on the Package Inserts, apart from well hidden ones such as Peanut oil and Msg. Poisons deplete nutrients that are crucial defences against infections!  Then you have Contaminants like SV40 that is still in the polio vaccines1. Then you may get a badly made batch (see: Vaccine production/manufacturing Vaccination mistakes  Vaccine storage), called Hot lots  leading to Vaccine Disasters. Then you may get one of their bioweapons, see: Nagalase Vaccine attack.  Then the risk rises if your child is ill, they reject sick kids in vaccine trials (see: Healthy trial babies only), then give it to all and sundry including mercury containing flu vaccines for pregnant women 1. Hence the term vaccine roulette, where you take ALL the risk, they get ALL the benefit (see: Why Vaccination Continues.]


VACCINE "CELL LINE" INGREDIENTS:
[2015 pdf] Vaccine contents Included in U.S. Vaccines, by Vaccine  this table includes not only vaccine ingredients (e.g., adjuvants and preservatives), but also substances used during the manufacturing process, including vaccine-production media, that are removed from the final product and present only in trace quantities.  In addition to the substances listed, most vaccines contain Sodium Chloride (table salt).

"(Vaccine ingredients) 1. Micro-organisms, either bacteria or viruses, thought to be causing certain infectious diseases and which the vaccine is supposed to prevent. These are whole-cell proteins or just the broken-cell protein envelopes, and are called antigens.  2. Chemical substances which are supposed to enhance the immune response to the vaccine, called adjuvants.   3. Chemical substances which act as preservatives and tissue fixatives, which are supposed to halt any further chemical reactions and putrefaction (decomposition or multiplication) of the live or attenuated (or killed) biological constituents of the vaccine."--Viera Scheibner

Articles
Aluminium
Thimerosal
ArticlesQuote banners
Thimerosal/Mercury
Aluminium
Alzheimer's
Ingredients
Quotes
Quotes
Thimerosal
Synergistic toxicity
Proteins (Vaccine ingredient)
Vaccine ingredients 1
Vaccine ingredients 2
[2015] Excipients Included in U.S. Vaccines, by Vaccine
Sterilising
Beta human chorionic gonadotropin (b-HCG)
Estradiol
Tween 80
Contaminants
Adjuvants
Aluminium
Squalene
  Monophosphoryl lipid A (MPL, ASO4)
  MF59
65

Freund's (FCA)
Sodium borate
QS-21
AS03:
Squalene,
Tween 80
(Polysorbate 80)
DL-α-tocopherol
Preservatives:
Alcohols
Glycerine
Neomycin
2-phenoxyethanol (2-PE)
Streptomycin
Polymyxin B
Mercury

Formaldehyde
Antibiotics
Neomycin
Streptomycin
Detergents
Sodium deoxycholate
Stabiliser/solvent:
Tween 80
Triton X-100
Bovine
Canine kidney cells
Aborted fetal DNA
Gelatin
Methiolate
Monkey kidney cells
MSG
Phenol
Allergy reactions
Allergies
Anaphylaxis
Vaccines used to induce disease in animals
A-Z
2-phenoxyethanol (2-PE)
65
Aborted fetal DNA
Alcohols
  Benzyl alcohol
Allergy reactions
Allergies
Aluminium
  Articles
  Quotes
  Banners
  Citations

 
Anaphylaxis
Antibiotics
  Neomycin
  Streptomycin
Articles

Benzyl alcohol
Beta human chorionic gonadotropin (b-HCG)
Bovine
Canine kidney cells
Chicken
Contaminants
Estradiol
Freund's (FCA)
Formaldehyde
Gelatin
Glutaraldehyde
Glycerine
Histidine
Human Cancer Tumors
Human DNA

Human fetal cells
Latex
Mercury (Thimerosal)
  Articles
  Quotes
  Quote banners

  Boyd Haley Ph.D. quotes
Methiolate
Monkey kidney cells
M
onophosphoryl lipid A (MPL, ASO4)
MF59
MSG
Nagalase
Nano particles

Neomycin
Parasites
Peanut oil
Phenol
Polymyxin B
Polysorbate 80
Proteins (Vaccine ingredient)
Quotes
QS-21
Sodium borate
Sodium deoxycholate
Sorbitol
Soy
Squalene
Streptomycin
Synergistic toxicity
Triton X-100
Tween 80
Vaccines used to induce disease in animals
Vaccine ingredients 1
Vaccine ingredients 2
Yeast




 http://www.whale.to/vaccine/vaccines/ingredients.html


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 GcMAF research (Vaccines)


https://gcmaf.se/


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GcMAF


 Update July 16 2015: GcMAF is no longer available as the company that made it was shutdown by overseas regulatory agencies.  As always, consult your doctor before making any medical decisions on any therapy you may be considering.

http://www.betterhealthguy.com/gcmaf


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Lyme Disease and GcMAF

 Sep 2, 2012

David Noakes talks about the treatment of Lyme Disease with First Immune GcMAF


 https://www.youtube.com/watch?v=rjhC6YqIatM

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WHO Ranks Antibiotics To Fight Life-Threatening Antibiotic Resistance

WHO say some drug companies will take a financial hit

Mike Barrett | Infowars.com - August 3, 2017

 https://www.infowars.com/who-ranks-antibiotics-to-fight-life-threatening-antibiotic-resistance/


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Breaking: Interview with Vaxxed Producer who was Banned from Australia

Doctors, medical bureaucrats, and government officials in Australia are foaming at the mouth

Jon Rappoport | Infowars.com - August 9, 2017
Polly Tommey, producer of the famous documentary, Vaxxed (trailer), has been banned from Australia. If that sounds quite insane—it is.
Vaxxed has been screening across the world. It is an explosive revelation about egregious fraud at the US Centers for Disease Control (CDC).

The film focuses on the 2014 public confession of a long-time researcher at the CDC, William Thompson. Thompson admits that he and his colleagues committed a crime, by manipulating data to give the MMR vaccine a free pass, “proving” it had no connection to autism—when in fact, as Thompson states, the vaccine does raise the risk of autism in children.


 https://www.infowars.com/breaking-interview-with-vaxxed-producer-who-was-banned-from-australia/

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Five Dangerous Dog Vaccine Ingredients

1. Aluminium

2. Thimerosal

3. Contaminants

Contaminants found in vaccines are also behind many of the adverse reactions we see in dogs. “Contaminant” means anything that shouldn’t be there. That’s anything impure or unclean, is toxic or poisonous, or has the ability to create disease. Vaccines contain contaminants that can cause cancer, leukemia, autoimmune diseases and a myriad of other unwanted conditions.
An important scientific paper was published in April 2010 in the Journal of Virology (Isolation of an Infectious Endogenous Retrovirus [RD-114] in a Proportion of Live Attenuated Vaccines for Pets, Journal of Virology, April 2010, p 3690-3694, Vol 84, No 7). It showed how two teams of scientists, in Japan and the UK, isolated a feline retrovirus (called RD-114) in both feline and canine vaccines in the UK and Japan. Had teams from America, or Germany, or Kazakhstan also been looking, they would probably have found the retrovirus, too. The contamination involved seed stock – the witches’ brew of disease shared amongst vaccine manufacturers internationally, from which they make their vaccines.
The following are extracts from a related paper appearing in Biologicals in 2010. “RD-114 was first isolated from a human tumor cell line (RD cells) derived from a human rhabdomyosarcoma after passage through fetal cats, and is thought to be xenotropic.”
Translation: they found this cat retrovirus in a highly malignant human tumor. “Xenotropic” means that it will be harmless in the original host species, but will cause problems (like tumors) in a different species.
In her article on Vaccine Contaminants in the January 2013 issue of Dogs Naturally Magazine, author Catherine O’Driscoll continues, “One of the authors of this paper wrote to me privately: “If the ERV induces diseases in vaccinated animals and humans, it will take more than five years (in animals) to ten years (in humans) when the first patient appears. But it will take additional time to relate some diseases with specific vaccines because expected diseases are very common (such as cancers, lymphoma and autoimmune diseases). If so, when we are aware of the real risk of ERVs, it is too late because millions are infected with the viruses by the contaminated vaccines.””
The only official checks made for contaminants in vaccines are for a few known pathogens, potentially missing a vast host of unknown, unstudied, small particles and chemicals. It’s simply impossible to remove contaminants from vaccines.

4. Animal Protein

Disease micro-organisms are often cultured on animal tissue including embryonic chickens or cow fetuses. When a vaccine is manufactured, it is impossible to divide the wanted virus from the unwanted animal tissue. It all gets ground up together and injected into your dog’s body.
If a dog eats animal flesh or an egg, it is digested into simpler amino acids before entering the bloodstream. The digestive process in most cases changes protein molecules so they don’t trigger an immune reaction. This is not the case for vaccines. They are injected undigested, directly into the bloodstream, where the foreign protein matter circulates throughout the body.


An immune response is triggered when the body detects foreign proteins. Killer cells (white blood cells) are sent out to consume the cells containing the foreign proteins and protein fragments. This process is nature’s way of protecting the body from being overwhelmed by invading organisms and eventually succumbing to them. The foreign protein fragments are not always destroyed by the body as it is busy cleaning up the multiple viruses that have just been injected, along with the serious chemicals aluminum, Thimerosal, formaldehyde and more. So the foreign protein matter gets absorbed into body cells. T-Cells, sensing they are there, but unable to reach them directly, attack the body cells that harbor them. This can lead to autoimmune disorders including cancer, allergies, arthritis and more.
“Our ongoing studies of dogs show that following routine vaccination, there is a significant level of antibodies dogs produce against their own tissues…Some of these antibodies have been shown to target the thyroid gland, the connective tissue such as that found in the valves of the heart, red blood cells, DNA etc.” Larry Glickman DVM, referring to the results of the


5. Money

The final vaccine ingredient to be discussed isn’t injected into dogs, but the concept of vaccination itself. In 2005, the global vaccine market was $6 billion. In 2012, it is $34 billion. It’s not surprising that more vaccines are manufactured for dogs and media hype frightens pet owners into using them. The canine influenza vaccine is an example.
In 2011, the media heavily covered canine influenza and the need for vaccination. At the center of most of the media articles reporting the need to vaccinate for canine influenza was Dr Cynda Crawford. Dr Crawford is a veterinarian at the University of Florida (UF) who led the research team that first identified the canine influenza virus in 2004.
Interestingly, Crawford, along with colleagues at UF, Cornell University and the U.S. Centers for Disease Control and Prevention (CDC), share intellectual rights to the canine influenza virus; Merck has licensed the right to use the virus to make a vaccine. However, Crawford maintains that she and the others do not receive compensation from vaccine sales.

 http://www.dogsnaturallymagazine.com/five-vaccine-ingredients-that-can-harm-your-dog/

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CDC Knew Its Vaccine Program Was Exposing Children to Dangerous Mercury Levels Since 1999

 Uncovered documents show that the U.S. Food and Drug Administration (FDA) and the Centers for Disease Control and Prevention (CDC) knew that infant vaccines were exposing American children to mercury far in excess of all federal safety guidelines since 1999. The documents, created by a FDA consulting toxicologist, show how federal regulators concealed the dangerous impacts and lied to the public.



In 1997, Congress passed the FDA Modernization Act. A provision of that statute required the FDA to "compile a list of drugs that contain intentionally introduced mercury compounds, and provide a quantitative and qualitative analysis of the mercury compounds on the list." In response, manufacturers reported the use of the mercury-based preservative, thimerosal, in more than 30 licensed vaccines.
FDA's Center for Biologics Evaluation and Research (CBER) was responsible for adding up the cumulative exposure to mercury from infant vaccines, a simple calculation that, astonishingly, had never been performed by either the FDA or the CDC. When the agency finally performed that basic calculation, the regulators realized that a six month-old infant who received thimerosal-preserved vaccines following the recommended CDC vaccine schedule would have received a jaw dropping 187.5 micrograms of mercury.
Instead of immediately ordering the removal of thimerosal, FDA officials circled the wagons treating the public health emergency as a public relations problem. Peter Patriarca, then director of the FDA Division of Viral Products, warned his fellow bureaucrats that hasty removal of thimerosal from vaccines would:
" … raise questions about FDA being 'asleep at the switch' for decades by allowing a potentially hazardous compound to remain in many childhood vaccines, and not forcing manufacturers to exclude it from new products. It will also raise questions about various advisory bodies regarding aggressive recommendations for use. We must keep in mind that the dose of ethylmercury was not generated by "rocket science." Conversion of the percentage thimerosal to actual micrograms of mercury involves ninth grade algebra. What took the FDA so long to do the calculations? Why didn't CDC and the advisory bodies do these calculations when they rapidly expanded the childhood immunization schedule?"

 https://www.ecowatch.com/cdc-mercury-vaccines-kennedy-2199157054.html

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The Most Dangerous Vaccine

 Dec 11, 2002

Dan Rather Reports On The Debate Over Safety Of Smallpox Vaccine

The smallpox vaccine is made from a weak biological cousin of the smallpox virus. When you get vaccinated with the weaker virus, you become immune to the smallpox virus.
But once in a while, the vaccine does more harm than good. If you scratch where the smallpox is at the surface, and you put it to the eye, you can transfer the smallpox to your eye. That occurs in about 500 people for every million that get the vaccine. If you get "progressive vaccinia," your immune system is compromised. The virus just continues to grow and grow, and is often the cause of death.
No one is certain how many people will be hurt by the vaccine. A 1969 study found that, out of every one million people vaccinated, 74 will suffer serious complications, and at least one will die.

 http://www.cbsnews.com/news/the-most-dangerous-vaccine/

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It's officiall: HPV vaccine, the most dangerous vaccine yet




Anyone daring to suggest that a vaccine might present a risk, especially to children as the most vulnerable members of our society, are usually shot down in flames. Health authorities have tried their best to continue telling everyone that HPV vaccines (note use of plural as there are three different types available) are safe, despite  ongoing research suggesting otherwise.
A study just released by a World Health Organization (WHO) monitoring centre in Sweden shows that adverse event reports received from national authorities — and these will represent only a fraction of those actually experienced — show a tendency to produce clusters of serious adverse events that include complex regional pain syndrome (CRPS), postural orthostatic tachycardia syndrome (POTS) and chronic fatigue syndrome (CFS) that exceeds any other vaccine.

GMO vaccine released a decade ago

The genetically engineered vaccine, first introduced for mass vaccination around 10 years ago, has been delivered to around 80 million girls, women and, in some countries, boys.
By August 2014 58 countries had introduced the vaccine into their immunisation schedules. According to the WHO, 80% of all cases of cervical cancer are linked to HPV, the key justification for giving the vaccine to young girls, occur in developing countries and are linked to sexual encounters at very young ages.
Concerns around the safety of the vaccine began to arise in 2013 with reports of CRPS in Japan, POTS in Denmark and CFS in Holland.
This study, which explores global reporting patterns of Adverse Reactions (AEs) for HPV vaccines shows that these different types of effects are often clustered, i.e. they are more likely to occur together, and so are likely related.

The science bit

The study looked at case safety reports for HPV Vaccine in VigiBase, the WHO International database of suspected adverse drug reactions. Reports are received from pharmacovigilance centres in 124 countries who participate in the WHO Programme for International Drug Monitoring up to 1st January 2015. Cases including at least 2 reporting terms were included in the study.


 http://anhinternational.org/2017/01/18/official-hpv-vaccine-vaccine-dangerous-yet/


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Kids Given Vaccines Have 22 Times the Rate of Ear Infections

November 01, 2011


32 times the rate of sinusitis, 4x allergies, 2x asthma, 4x hayfever, 3x ADHD and 19 times higher odds of Autism based on this 7,850 person survey. Yet 98% of parents give it to their children -...

Vaccinated vs. Unvaccinated: Survey Reveals Who's Healthier

However, that doesn't mean there is a total absence of evidence about the health of vaccinated versus unvaccinated children to give us an indication of whether or not the use of many more vaccines by children is contributing to their being chronically ill. In December 2010, a survey was initiated by VaccineInjury.info3 to compare the health of vaccinated children with unvaccinated children. To date, over 7,850 surveys have been submitted, and the study is ongoing, so if you have an unvaccinated child (or are unvaccinated yourself) and would like to submit your child's health data, you can do so here.
Though this is obviously not a double-blind controlled study, and depends on the individuals submitting the data to give accurate information, it is still revealing. So far, the results show:

 

Health Condition     Prevalence in Vaccinated Children     Prevalence in Unvaccinated Children

Allergies:               40% report at least one allergy                                  |           Less than 10%
Asthma:                  6%                                                                                        |       2.5%
Hay fever:               10.7% of German children                                                  |        2.5%
Neurodermatitis (an autoimmune disorder):           13% of German children     |        7%
ADHD:               8% of German children, and another nearly 6% with borderline cases   |  1-2%
Middle ear infections:                11% of German children           |                 Less than 0.5%
Sinusitis:                         Over 32% of German children             |                  Less than 1%
Autism:                   Approximately 1 in 100                               |           Only 4 cases out of 7,800+ surveys (one child tested very high for metals, and another's mother tested very high for mercury)


http://articles.mercola.com/sites/articles/archive/2011/11/01/more-parents-waking-up-to-vaccine-dangers.aspx

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Dawn of the Bionic Age: Body Hackers let Chips get Under their Skin

‘It can emulate every card in your wallet, so you can chuck your wallet away’

McClatchy DC - August 4, 2017

 https://www.infowars.com/dawn-of-the-bionic-age-body-hackers-let-chips-get-under-their-skin/


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Scientists Hack a Computer Using DNA

 August 10, 2017

Malware can be encoded into a gene and used to take over a computer program.

 In what appears to be the first successful hack of a software program using DNA, researchers say malware they incorporated into a genetic molecule allowed them to take control of a computer used to analyze it. 

To carry out the hack, researchers led by Tadayoshi Kohno (“see “Innovators Under 35, 2007”) and Luis Ceze encoded malicious software in a short stretch of DNA they purchased online. They then used it to gain “full control” over a computer that tried to process the genetic data after it was read by a DNA sequencing machine.

The researchers warn that hackers could one day use faked blood or spit samples to gain access to university computers, steal information from police forensics labs, or infect genome files shared by scientists.

https://www.technologyreview.com/s/608596/scientists-hack-a-computer-using-dna/

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THE NICHOLAS GONZALEZ FOUNDATION


http://www.dr-gonzalez.com/index.htm



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Chapter 6: Autism



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Autism-Vaccine Link: Evidence Doesn't Dispel Doubts


http://www.webmd.com/brain/autism/searching-for-answers/vaccines-autism


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BPA exposure linked to autism spectrum disorder, study reports


March 2, 2015


https://www.sciencedaily.com/releases/2015/03/150302150723.htm



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Pesticide exposure during pregnancy linked to higher autism risk


June 23, 2014


http://www.latimes.com/science/sciencenow/la-sci-sn-study-finds-link-between-pesticide-exposure-pregnancy-autism-20140623-story.html


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Fine particulate air pollution linked with increased autism risk


December 18, 2014


http://www.hsph.harvard.edu/news/press-releases/fine-particulate-air-pollution-linked-with-increased-autism-risk/


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The "Western disease": Autism and Somali parents' embodied health movements.

Mar 2017

https://www.ncbi.nlm.nih.gov/pubmed/28171816

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Ambient Air Pollution and Autism in Los Angeles County, California


http://ehp.niehs.nih.gov/1205827/


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MIT Scientist Uncovers Link Between Glyphosate, GMOs And The Autism Epidemic


May 11, 2015


http://reset.me/story/mit-scientist-uncovers-link-between-glyphosate-gmos-and-the-autism-epidemic/


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Sleep quality influences the cognitive performance of autistic and neurotypical children


 May 28th, 2015


https://www.sciencedaily.com/releases/2015/05/150528123855.htm


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Brain study reveals insights into genetic basis of autism


July 13th, 2015


https://www.sciencedaily.com/releases/2015/07/150713113336.htm


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Growing Micro-Brains From Skin Cells Sheds Light On Autism


 July 16, 2015


http://www.popsci.com/autism-might-be-result-dampened-brain-signal


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 Researchers unravel a genetic link with autistic behaviors—and find a way to undo it


 May 28, 2015


http://www.buffalo.edu/news/releases/2015/05/045.html

-----------------


Full Show - What The MSM Won't Cover - 07/23/2015


https://www.youtube.com/watch?v=k7U-1vtjg3c


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Busted: Gov't Admits Vaccines Cause Autism


 ( Mar 31, 2016 )


 https://www.youtube.com/watch?v=a0glbc0S3sA


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Monsanto’s Glyphosate Found in California Wines, Even Wines Made With Organic Grapes


March 27, 2016


http://ecowatch.com/2016/03/27/monsanto-glyphosate-wine/


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WIN! California to List Glyphosate as a Carcinogen

 California will add glyphosate, the main ingredient in Monsanto’s blockbuster herbicide RoundUp, to its list of chemicals known to cause cancer, effective July 7, 2017.


 http://naturalsociety.com/win-california-list-glyphosate-carcinogen-1555/


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Honeybees Are Being Killed off in Europe by 57 Different Pesticides, Study Finds


April 5, 2016


http://www.alternet.org/environment/honeybees-are-being-killed-europe-57-different-pesticides-study-finds


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Autism Study: More Evidence Linking Altered Gut Bacteria to ASD -


https://www.autismspeaks.org/science/science-news/autism-study-more-evidence-linking-altered-gut-bacteria-asd


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[Different reports claim that different hazards can cause a number of birth defects, this includes autism from air pollution. Many reports and evidence have also suggested that certain chemicals found in vaccines, can lead to birth defects, this would include autism. Different groups now claim that vaccines do not cause autism, while other groups are still claiming that a multiple number of things could be causing autism. However, It is the job of the media, to bring you all sides of the story, and try to figure out scientifically, what is causing many birth defects in children.]


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Chapter 7: Genome mining & editing


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 Genome mining effort discovers 19 new natural products in four years


September 8, 2015

  It took two postdoctoral researchers, a lab technician, four undergraduates and their faculty advisors only four years - a blink of an eye in pharmaceutical terms - to scour a collection of 10,000 bacterial strains and isolate the genes responsible for making 19 unique, previously unknown phosphonate natural products, researchers report. Each of these products is a potential new drug. One of them has already been identified as an antibiotic.


Read more at: http://phys.org/news/2015-09-genome-effort-natural-products-years.html#jCp


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Scientists discover new system for human genome editing


September 25, 2015


A team including the scientist who first harnessed the revolutionary CRISPR-Cas9 system for mammalian genome editing has now identified a different CRISPR system with the potential for even simpler and more precise genome engineering.

In a study published today in Cell, Feng Zhang and his colleagues at the Broad Institute of MIT and Harvard and the McGovern Institute for Brain Research at MIT, with co-authors Eugene Koonin at the National Institutes of Health, Aviv Regev of the Broad Institute and the MIT Department of Biology, and John van der Oost at Wageningen University, describe the unexpected biological features of this new system and demonstrate that it can be engineered to edit the genomes of human cells.

http://phys.org/news/2015-09-scientists-human-genome.html#jCp


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First results of CRISPR gene editing of normal embryos released


9 March 2017

A team in China has corrected genetic mutations in at least some of the cells in three normal human embryos using the CRISPR genome editing technique. The latest study is the first to describe the results of using CRISPR in viable human embryos, New Scientist can reveal.

 https://www.newscientist.com/article/2123973-first-results-of-crispr-gene-editing-of-normal-embryos-released/

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Chinese scientists genetically modify human embryos

April 22, 2015


In a world first, Chinese scientists have reported editing the genomes of human embryos. The results are published1 in the online journal Protein & Cell and confirm widespread rumours that such experiments had been conducted — rumours that sparked a high-profile debate last month2, 3 about the ethical implications of such work.


http://www.nature.com/news/chinese-scientists-genetically-modify-human-embryos-1.17378


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The First Human-Pig Hybrid Embryo Has Been Created in The Lab

A big step towards lab-grown organs.


 Jan. 26, 2017


http://www.sciencealert.com/it-s-alive-the-first-human-pig-hybrid-has-been-created-in-the-lab


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Human-Pig Hybrid Created in the Lab—Here Are the Facts

January 26, 2017

Scientists hope the chimera embryos represent key steps toward life-saving lab-grown organs.


http://news.nationalgeographic.com/2017/01/human-pig-hybrid-embryo-chimera-organs-health-science/


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Human-animal hybrid embryos

Bioethics: Human-animal hybrid embryos


In May 2008 a cross-party attempt to ban hybrid human animal embryos was defeated on a free vote in the House of Commons, by 336 to 176. MPs had been debating the Human Fertilisation and Embryology Bill, which would allow regulated research using hybrid or 'admix' embryos, where the nuclei of human cells are inserted into animal eggs. The resulting embryos would be kept for up to 14 days to harvest stem cells.

In the present state of science, hybrid embryos are produced as research tools, and only kept alive for 14 days or fewer. The article below only deals with the ethical issues of this case, and not with the ethics of producing new creatures that are a combination of animal and human.

Possible types of animal/human hybrid embryos

    Cytoplasmic hybrid embryos: embryos created through cell nuclear replacement using animal eggs
    Hybrid embryos: embryos created by mixing human sperm and animal eggs or human eggs and animal sperm
    Human chimera embryos: human embryos which have animal cells added to them during early development
    Animal chimera embryos: animal embryos which have human cells added to them during early development
    Transgenic human embryos: human embryos which have animal genes inserted into them during early development

http://www.bbc.co.uk/ethics/animals/using/hybridembryos_1.shtml


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Mouse egg cells made entirely in the lab give rise to healthy offspring

 Oct. 17, 2016


In work that raises the prospect of new infertility treatments and designer babies, researchers have used stem cells to grow fertile mouse egg cells for the first time entirely in a lab dish. The eggs gave rise to pups after being fertilized and implanted into rodent foster mothers. The method—which sometimes produced defective eggs and had a success rate of less than 1%—won’t be producing human egg cells any time soon, but the technique could help researchers identify key genes involved in egg development and maturation.


http://www.sciencemag.org/news/2016/10/mouse-egg-cells-made-entirely-lab-give-rise-healthy-offspring


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FDA approves genetically modified chicken — but not as food
Gathering a drug from chicken egg whites

Dec 9, 2015,


This isn't the first time that the FDA has approved a transgenic animal for drug production. Six years ago, the US government approved genetically modified goats that can make a drug in their milk that prevents blood clots. And in 2014, the FDA approved Ruconest — a drug that's collected from rabbit milk.

But yesterday's approval doesn't rely on milk production. To collect the active protein, researchers have to purify it from the whites of the chicken's eggs. Kanuma works by replacing a malfunctioning enzyme in people with lysosomal acid lipase deficiency.

As part of the approval process for the drug, the government officials looked at whether the alterations made to the chicken's genetic material would cause it harm. They also examined whether these changes are stable enough to be passed on to future generations.


https://www.theverge.com/2015/12/9/9879678/gmo-chicken-transgenic-fda-approved-kanuma-drug-eggs


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Brit scientists create genetically modified chickens that can lay eggs from different breeds

18 Feb 2017

The aim is to preserve rare chicken breeds that may be resistant to global infections like bird flu in the future or have highly desirable features such as excellent meat quality


http://www.mirror.co.uk/science/brit-scientists-create-genetically-modified-9842348


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                    Genetically Modified Birds


IOSR Journal of Pharmacy and Biological Sciences

http://iosrjournals.org/iosr-jpbs/papers/Vol9-issue6/Version-3/D09631629.pdf


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Researchers Engineer Hens that Make Drugs in Eggs


 January 19, 2007


 Scientists at the Roslin Institute, which produced Dolly the cloned sheep, have genetically engineered chickens to produce drugs in their egg whites. Helen Sang, the lead scientist at the Roslin Institute in Midlothian, Scotland, talks about the findings.


For instance, they have tweaked cows to produce drugs in their milk so every time the cows give milk, they also give a fresh supply of drugs. But in a twist on this approach, scientists at the Roslin Institute - that's the institute that created Dolly, the cloned sheep - well scientists at Roslin have genetically engineered chickens now to produce drugs in their egg whites. Some of them - some of these drugs that are used to fight cancer.

With every batch of eggs comes a fresh supply of drugs. Unfortunately, getting the drugs isn't as easy as scrambling up an omelet. The researchers report on their research in the current issue of the journal Proceedings of the National Academy of Sciences, and the leader of the team joins us now to talk about their work and its potential to change the way drugs are made.


http://www.npr.org/templates/story/story.php?storyId=6921969


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Targeted mutagenesis in chicken using CRISPR/Cas9 system

 23 October 2015

 The CRISPR/Cas9 system is a simple and powerful tool for genome editing in various organisms including livestock animals. However, the system has not been applied to poultry because of the difficulty in accessing their zygotes. Here we report the implementation of CRISPR/Cas9-mediated gene targeting in chickens. Two egg white genes, ovalbumin and ovomucoid, were efficiently (>90%) mutagenized in cultured chicken primordial germ cells (PGCs) by transfection of circular plasmids encoding Cas9, a single guide RNA, and a gene encoding drug resistance, followed by transient antibiotic selection. We transplanted CRISPR-induced mutant-ovomucoid PGCs into recipient chicken embryos and established three germline chimeric roosters (G0). All of the roosters had donor-derived mutant-ovomucoid spermatozoa, and the two with a high transmission rate of donor-derived gametes produced heterozygous mutant ovomucoid chickens as about half of their donor-derived offspring in the next generation (G1). Furthermore, we generated ovomucoid homozygous mutant offspring (G2) by crossing the G1 mutant chickens. Taken together, these results demonstrate that the CRISPR/Cas9 system is a simple and effective gene-targeting method in chickens.

https://www.nature.com/articles/srep23980

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Genetic modification of chicken germ cells

 Oct, 2012


 Over the past two decades numerous reports have demonstrated that the genetic modification of poultry genomes has great potential for improving poultry production; moreover, it may be used as a powerful tool for the production of industrial proteins. To date, transgenic techniques have been established for generating transgenic birds that express recombinant human proteins in hen eggs, as well as tissue-specific genes as an animal model. The production of transgenic birds is a promising approach that could have practical applications in agriculture and biopharmacology, in addition to advancing our understanding of avian biology. Finally, germ cell–mediated transgenesis could provide a more efficient strategy for creating gene-targeted insertions and deletions in avian species.


 Recently, van de Lavoir et al.21 genetically modified chicken PGCs by the electroporation of a nonviral expression vector to produce transgenic offspring through germline transmission. However, the frequency of transgene integration into the genome as well as the rate of gene transfer into germ cells remain insufficient for generating transgenic birds using virus-independent conventional methods. For efficient transgene integration into the genome of chicken PGCs, Leighton et al.22 used phiC31 integrase and specific elements. phiC31 integrase catalyzes site-specific recombination between an attB site and an attP site; thus, the co-transfection of an integrase and attB-containing plasmid could improve genomic insertion into chicken PGCs. They showed increased frequencies of transgene integration into endogenous pseudo attP sites in the chicken PGC genome when phiC31 integrase was co-introduced; however, there is no report of the production of transgenic chickens using phiC31 integrase and an attB element. In addition, the in vitro and in vivo silencing of transgene expression following nonviral transfection has hampered the stable expression of antibiotic genes for selection and specific expression in target tissues.21–23 Leighton et al.22 demonstrated that the usage of phiC31 integrase and an attB element could be an efficient tool for genomic insertion; however, they also reported the transcriptional silencing of a transgene in chicken PGCs even after the co-transfection of phiC31 integrase and attB sequences. We previously showed that the methylation of a transgenic promoter in the transgenic chicken could lead to transgene transcriptional silencing in a tissue-specific manner in vivo, although little is known about the control of gene expression in avian species via DNA methylation.23 To overcome this transcriptional repression, HS4 insulator, which is the first insulator identified in vertebrates, derived from the 5' end of the chicken ß-globin locus, has been used in chicken PGCs.


 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3499655/



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 Chapter 8: Bioweapons


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US Intelligence Director Says Genome Editing is a WMD

Gene Editing with CRISPR/Cas-9 Can Heal or Kill

Genetic modification using new technologies like CRISPR has been called a “weapon of mass destruction and proliferation” by James Clapper, U.S. Director of National Intelligence, in his annual Worldwide Threat Assessment report.

Gene editing is the latest brainchild of the biotechnology industry. It has been touted as entirely different from gene insertion, the genetic modification technique used over the past several decades to create GM crops and GM animals. Gene editing technology alters the DNA inside living cells. The biotech industry says it is an easy and cheap way to mess with Mother Nature – but, as with other GM technology, the outcomes can’t be precisely controlled.


http://naturalsociety.com/us-director-national-intelligence-genome-editing-wmd-67384/


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Biological weapons and designer babies: 15 years of decoding humanity’s DNA

On 26th June 2000, the Human Genome Project announced that they had a sequence of the human genome. Here’s how our understanding of DNA has changed the world since
Build-a-baby

If you’ve always dreamed of a baby with green eyes and curly brown hair, then the link between our DNA and appearance could make designer babies a disconcerting reality. Dr Claes says he’s received emails from fertility clinics who want to use his technology to help future parents build their perfect baby.

Biological weapons

The science that allows us to create DNA-based personalised medicine can also be used for a far more sinister flipside: biological weapons. Battles have been fought using biological toxins or viruses for hundreds of years..


 http://www.telegraph.co.uk/news/science/science-news/11700454/Biological-weapons-and-designer-babies-15-years-of-decoding-humanitys-DNA.html



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Genetically Engineered Bioweapons: A New Breed of Weapons for Modern Warfare

March 10, 2013

 http://dujs.dartmouth.edu/applied_sciences/genetically-engineered-bioweapons-a-new-breed-of-weapons-for-modern-warfare#.VXU2dEa-2zk

Genome sequencing has given rise to a new generation of genetically engineered bioweapons carrying the potential to change the nature of modern warfare and defense.

Introduction

Biological weapons are designed to spread disease among people, plants, and animals through the introduction of toxins and microorganisms such as viruses and bacteria. The method through which a biological weapon is deployed depends on the agent itself, its preparation, its durability, and the route of infection. Attackers may disperse these agents through aerosols or food and water supplies.

Although bioweapons have been used in war for many centuries, a recent surge in genetic understanding, as well as a rapid growth in computational power, has allowed genetic engineering to play a larger role in the development of new bioweapons. In the bioweapon industry, genetic engineering can be used to manipulate genes to create new pathogenic characteristics aimed at enhancing the efficacy of the weapon through increased survivability, infectivity, virulence, and drug resistance. While the positive societal implications of improved biotechnology are apparent, the “black biology” of bioweapon development may be “one of the gravest threats we will face”

Limits of Past Bioweapons

Prior to recent advances in genetic engineering, bioweapons were exclusively natural pathogens. Agents must fulfill numerous prerequisites to be considered effective military bioweapons, and most naturally occurring pathogens are ill suited for this purpose. First, bioweapons must be produced in large quantities. A pathogen can be obtained from the natural environment if enough can be collected to allow purification and testing of its properties. Otherwise, pathogens could be produced in a microbiology laboratory or bank, a process which is limited by pathogen accessibility and the safety with which the pathogens can be handled in facilities. To replicate viruses and some bacteria, living cells are required. The growth of large quantities of an agent can be limited by equipment, space, and the health risks associated with the handling of hazardous germs. In addition to large-scale production, effective bioweapons must act quickly, be environmentally robust, and their effects must be treatable for those who are implementing the bioweapon.

Recent Advances

As researchers continue to transition from the era of DNA sequencing into the era of DNA synthesis, it may soon become feasible to synthesize any virus whose DNA sequence is known (4). This was first demonstrated in 2001 when Dr. Eckard Wimmer re-created the poliovirus and again in 2005 when Dr. Jeffrey Taubenberger and Terrence Tumpey re-created the 1918 influenza virus (1). The progress of DNA synthesis technology will also allow for the creation of novel pathogens. According to biological warfare expert Dr. Steven Block, genetically engineered pathogens “could be made safer to handle, easier to distribute, capable of ethnic specificity, or be made to cause higher mortality rates.”

The growing accessibility of DNA synthesis capabilities, computational power, and information means that a growing number of people will have the capacity to produce bioweapons. Scientists have been able to transform the four letters of DNA—A (adenine), C (cytosine), G (guanine), and T (thymine)—into the ones and zeroes of binary code. This transformation makes genetic engineering a matter of electronic manipulation, which decreases the cost of the technique (4). According to former Secretary of State Hillary Clinton, “the emerging gene synthesis industry is making genetic material more widely available […] A crude but effective terrorist weapon can be made using a small sample of any number of widely available pathogens, inexpensive equipment, and college-level chemistry and biology.”



---------------------------



Genetic engineering and biological weapon


shttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC1326447/



Indeed, the insights into the nature of infectious diseases gained by Louis Pasteur and Robert Koch in the nineteenth century did not actually represent a great breakthrough in the use of infectious organisms as biological weapons. Similarly, the development of a bioweapon does not necessarily require genetic engineering—smallpox, plague and anthrax are deadly enough in their natural states. But the revolution in biotechnology, namely the new tools for analysing and specifically changing an organism's genetic material, has led to an increased risk of biowarfare due to several factors. First, the expansion of modern biotechnology in medical and pharmaceutical research and production has led to a worldwide availability of knowledge and facilities. Many countries and regions, where 30 years ago biotechnology merely meant brewing beer and baking bread, have established high-tech facilities for vaccine or single-cell-protein production that could be subverted for the production of biological weapons. Today, nearly all countries have the technological potential to produce large amounts of pathogenic microorganisms safely (Fig. 1). Second, classical biowarfare agents can be made much more efficiently than their natural counterparts, with even the simplest genetic techniques. Third, with modern biotechnology it becomes possible to create completely new biological weapons. And for technical and/or moral reasons, they might be more likely to be used than classical biowarfare agents. These possibilities have generated new military desires around the world, including within those countries that have publicly renounced biological weapons in the past. This paper deals predominantly with the last two factors, and with the use of real-life examples, we shall discuss the possibilities for such military abuse of biotechnology.


--------------


Is Monsanto doing secret biowar research on Maui?


by Jon Rappoport

April 4, 2015


 “According to the Sunshine Project, a nonprofit arms control watchdog operating out of Austin, Texas, among corporations holding back information about their [biowarfare research] activities are:

“Abbott Laboratories, BASF Plant Science, Bristol-Myers Squibb, DuPont Central Research and Development, Eli Lilly Corp., Embrex, GlaxoSmithKline, Hoffman-LaRoche, Merck & Co., Monsanto, Pfizer Inc., Schering-Plough Research Institute, and Syngenta Corp. of Switzerland.

“In case you didn’t know it, the White House since 9/11 has called for spending $44-billion on biological warfare research, a sum unprecedented in world history, and an obliging Congress has authorized it.”

Notice that the above list of corporations includes some of the biggest names in biotech: BASF, DuPont, Syngenta, and, of course, Monsanto, who manufactured the highly toxic Agent Orange sprayed in Vietnam.

https://jonrappoport.wordpress.com/2015/04/04/is-monsanto-doing-secret-biowarfare-research-on-maui/


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We can see why some governments want to ban experiments with GMO's in homes and in private labs.


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GENETIC DISCRIMINATION

A Position Paper Presented by the Council for Responsible Genetics


*GENETIC TESTS CAN BE USED TO HELP . . . AND TO HARM


*THE EXPANSION OF GENETIC TESTS MEANS THAT THE DISCRIMINATION WILL LIKELY INCREASE.


*THE SOCIAL COSTS OF GENETIC DISCRIMINATION


*INSURANCE DISCRIMINATION


http://www.councilforresponsiblegenetics.org/ViewPage.aspx?pageId=85


-----------------------------


Genetic Engineering and Its Dangers


TENTH ANNIVERSARY YEAR
SITE FOUNDED IN 1996


 
ESSAYS ABOUT GENETIC ENGINEERING GENETICALLY ENGINEERING 
HUMAN BEINGS
GENETICALLY ENGINEERED 
PLANTS AND FOOD
INTERNET LINKS
GENETIC ENGINEERING AND BIOWARFARE BOOKS ON THE DANGERS OF GENETIC ENGINEERING

 
ESSAYS ABOUT GENETIC ENGINEERING
"What is Genetic Engineering?" by Dr. Ricarda Steinbrecher
"The Rest Of The Story Behind Genetic Engineering: An Interview with Brian Tokar" by Mark Oshinskie

"PR for the 'Book of Life'" by Jackie Stevens
"Synthetic Life" by W. Wayt Gibbs
"Unraveling the DNA Myth: The Spurious Foundation of Genetic Engineering" by Barry Commoner

"Data Stored in Multiplying Bacteria" by Natasha McDowell
"Genetic Copy of Cat Not a Copycat after All" by Kristen Hays
GM Microbes Invade North America
"Mice 'make human proteins in semen'" by Dr David Whitehouse
"Mice produce sperm from monkeys" by Dr David Whitehouse
"Killer virus: An engineered mouse virus leaves us one step away from the ultimate bioweapon" by Rachel Nowak
"Rebellious Bodies Dim the Glow of `Natural' Biotech Drugs" by Andrew Pollack
"Klebsiella planticola--The Gene-Altered Monster That Almost Got Away" by Elaine Ingham
"Biohazards: The Next Generation?" by Brian Tokar
"Biotech at 25--Too Soon to Celebrate"
"Splicing the Sting Out of Bugs" by Aaron Zitner
Ethical and Religious Questions
Technical Information

GENETICALLY ENGINEERED PLANTS AND FOOD
General Information

True Food Shopping List: How to Avoid Genetically Engineered Food

5 reasons to keep Britain [and the rest of the world] GM-free

"Super Organics" by Richard Manning "GM TRIALS TO FIND MEDICINE RAISE NEW ETHICAL FEARS; HUMAN GENE CROP FURY" by JOHN INGHAM AND TOBY MOORE
"Genetically Modified Foods: Are They a Risk to Human/Animal Health?" By Arpad Pusztai, Ph.D.
"Transgenic DNA introgressed into traditional maize landraces in Oaxaca, Mexico" by David Quist and Ignacio H. Chapela

Worldwide Initiatives Against GMOs
"Bad Bad seeds in court: when genetically modified plants contaminate their crops, organic farmers fight big biotech" by Thomas Hayden
"GM Trials to Find Medicine Raise New Ethical Fears; Human Gene Crop Fury" by John Ingham and Toby Moore
"THE 'GOLDEN RICE' HOAX  -When Public Relations replaces Science" by Dr. Vandana Shiva "NASA's Earth plants could invade Mars" by David Perlman
USDA Says Yes to Terminator
Technical Information

GENETIC ENGINEERING AND BIOWARFARE

Bioterror Researchers Build a More Lethal Mousepox
"Now for GM weapons: It's time to get tough with the biotech firms over germ warfare" by Jeremy Rifkin
Bioterrorism issue of Emerging Infectious Diseases (July/August, 1999, v5n4)
"The Demon in the Freezer" by Richard Preston
"Ebola Virus Could Be Synthesised" by Sylvia Pagàn Westphal
"Scientists Create a Live Polio Virus" by Andrew Pollack
"Bioterror And Biosafety" by Vandana Shiva
"US Non-lethal Weapon Reports Suppressed" by Debora MacKenzie
"Single Gene Leap Led to Flea-Borne Transmission of Plague Bacterium" by Laurie K. Doepel
"A Terrifying Power" by Philip Cohen
"Prepare for the Worst" By Rachel Nowak
"With Biotechnology, a Potential to Harm" by Andrew Pollack
"Now for GM weapons: It's time to get tough with the biotech firms over germ warfare" by Jeremy Rifkin Project Censored: Human Genome Project Opens the Door to Ethnically Specific Bioweapons
"Secret U.S. Germ Tests Threat to Treaty" by Roland Watson

GENETICALLY ENGINEERING HUMAN BEINGS
"Engineering Humans" by Rachel Massey
"The New Eugenics: The Case Against Genetically Modified Humans" by Marcy Darnovsky
"Scientists Raise Spectre of Gene-Modified Athletes" by James Randerson
"Gods and Monsters: Talking apes, flying pigs, superhumans with armadillo attributes, and other strange considerations of Dr. Stuart Newman's fight to patent a human/animal chimera" by Mark Dowie
FRONTLINE "Organ Farm: The Risks of Xenotransplantation"
"The Threshold Challenge of the New Human Genetic Technologies"
"Governing the Genome" by Ralph Brave
"The Human Genome Map: The Death of Genetic Determinism and Beyond" by Mae-Wan Ho
"Genetically Altered Babies Born" by Dr. David Whitehouse


http://online.sfsu.edu/rone/GEessays/gedanger.htm


---------------


Ethnic bioweapon

 https://en.wikipedia.org/wiki/Ethnic_bioweapon


An ethnic bioweapon (biogenetic weapon) is a type of weapon that aims to harm only or primarily people of specific ethnicities or genotypes.
Genetic weapons

In 1997, U.S. Secretary of Defense William Cohen referred to the concept of an ethnic bioweapon as a possible risk. In 1998 some biological weapon experts considered such a "genetic weapon" a plausible possibility, and believed the former Soviet Union had undertaken some research on the influence of various substances on human genes.


In 2004, The Guardian reported that the British Medical Association (BMA) considered bioweapons designed to target certain ethnic groups as a possibility, and highlighted problems that advances in science for such things as "treatment to Alzheimer's and other debilitating diseases could also be used for malign purposes".

In 2005, the official view of the International Committee of the Red Cross was "The potential to target a particular ethnic group with a biological agent is probably not far off. These scenarios are not the product of the ICRC's imagination but have either occurred or been identified by countless independent and governmental experts."

In 2012, The Atlantic wrote that a specific virus that targets individuals with a specific DNA sequence is within possibility in the near future. The magazine put forward a hypothetical scenario of a virus which caused mild flu to the general population but deadly symptoms to the President of the United States. They cite advances in personalized gene therapy as evidence.

In 2016, Foreign Policy magazine suggested the possibility of a virus used as an ethnic bioweapon that could sterilize a "genetically-related ethnic population.

Israeli "ethno-bomb" controversy

In November 1998, The Sunday Times reported that Israel was attempting to build an "ethno-bomb" containing a biological agent that could specifically target genetic traits present amongst Arab populations. Wired News also reported the story, as did Foreign Report.

Microbiologists and geneticists were skeptical towards the scientific plausibility of such a biological agent. The New York Post, describing the claims as "blood libel", reported that the likely source for the story was a work of science fiction by Israeli academic Doron Stanitsky. Stanitsky had sent his completely fictional work about such a weapon to Israeli newspapers two years before. The article also noted the views of genetic researchers who claimed the idea as "wholly fantastical", with others claiming that the weapon was theoretically possible.


Russian ban on export of biological samples

In May 2007, a Russian newspaper Kommersant reported that the Russian government banned all exports of human biosamples. The report claims that the reason for the ban was a secret FSB report about on-going development of "genetic bioweapons" targeting Russian population by Western institutions. The report mentions the Harvard School of Public Health, American International Health Alliance, Department of Medical Biotechnology of Jagiellonian University, United States Department of Justice Environment and Natural Resources Division, Institute of Genetics and Biotechnology Warsaw University, and United States Agency for International Development.


---------------



Israel is Developing 'Ethnic Bomb' for Growing Biological Weapons Arsenal


http://www.ihr.org/jhr/v17/v17n6p24_weber.html


---------------

Clinton warns of bioweapon threat from gene tech

December 7, 2011

 (AP) -- New gene assembly technology that offers great benefits for scientific research could also be used by terrorists to create biological weapons, U.S. Secretary of State Hillary Rodham Clinton warned Wednesday.

 https://phys.org/news/2011-12-clinton-bioweapon-threat-gene-tech.html


-------------

Bill Gates Warns Of Virus Worse Than Ebola: “We Are Simply Not Prepared To Deal With A Global Epidemic”

March 20th, 2015


http://www.shtfplan.com/headline-news/bill-gates-warns-of-virus-worse-than-ebola-we-are-simply-not-prepared-to-deal-with-a-global-epidemic_03202015


-------------------


Infectious diseases and bioweapons

2003 Jun


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1326435/

---------------------


Genetically Engineered Bioweapons: A New Breed of Weapons for Modern Warfare

 March 10, 2013

The growing accessibility of DNA synthesis capabilities, computational power, and information means that a growing number of people will have the capacity to produce bioweapons. Scientists have been able to transform the four letters of DNA—A (adenine), C (cytosine), G (guanine), and T (thymine)—into the ones and zeroes of binary code. This transformation makes genetic engineering a matter of electronic manipulation, which decreases the cost of the technique (4). According to former Secretary of State Hillary Clinton, “the emerging gene synthesis industry is making genetic material more widely available […] A crude but effective terrorist weapon can be made using a small sample of any number of widely available pathogens, inexpensive equipment, and college-level chemistry and biology.”

Techniques to Enhance Efficacy of Bioweapons

Scientists and genetic engineers are considering several techniques to increase the efficacy of pathogens in warfare.

1. Binary Biological Weapons

This technique involves inserting plasmids, small bacterial DNA fragments, into the DNA of other bacteria in order to increase virulence or other pathogenic properties within the host bacteria (2).

2. Designer Genes

According to the European Bioinformatics Institute, as of December 2012, scientists had sequenced the genomes of 3139 viruses, 1016 plasmids, and 2167 bacteria, some of which are published on the internet and are therefore accessible to the public (6). With complete genomes available and the aforementioned advances in gene synthesis, scientists will soon be able to design pathogens by creating synthetic genes, synthetic viruses, and possibly entirely new organisms (2).

3. Gene Therapy

Gene therapy involves repairing or replacing a gene of an organism, permanently changing its genetic composition. By replacing existing genes with harmful genes, this technique can be used to manufacture bioweapons (2).

4. Stealth Viruses

Stealth viruses are viral infections that enter cells and remain dormant for an extended amount of time until triggered externally to cause disease. In the context of warfare, these viruses could be spread to a large population, and activation could either be delayed or used as a threat for blackmail (2).

5. Host-Swapping Diseases

Much like the naturally occurring West Nile and Ebola viruses, animal viruses could potentially be genetically modified and developed to infect humans as a potent biowarfare tactic (2).

6. Designer Diseases

Biotechnology may be used to manipulate cellular mechanisms to cause disease. For example, an agent could be designed to induce cells to multiply uncontrollably, as in cancer, or to initiate apoptosis, programmed cell death (2).

7. Personalized Bioweapons

In coming years it may be conceivable to design a pathogen that targets a specific person’s genome. This agent may spread through populations showing minimal or no symptoms, yet it would be fatal to the intended target (4).

Biodefense

In addition to creating bioweapons, the emerging tools of genetic knowledge and biological technology may be used as a means of defense against these weapons.

1. Human Genome Literacy

As scientific research continues to reveal the functions of specific genes and how genetic components affect disease in humans, vaccines and drugs can be designed to combat particular pathogens based on analysis of their particular molecular effect on the human cell (2).

2. Immune System Enhancement

In addition to enabling more effective drug development, human genome literacy allows for a better understanding of the immune system. Thus, genetic engineering can be used to enhance human immune response to pathogens. As an example, Dr. Ken Alibek is conducting cellular research in pursuit of protection against the bioweapon anthrax (2).

3. Viral and Bacterial Genome Literacy

Decoding the genomes of viruses and bacteria will lead to molecular explanations behind virulence and drug resistance. With this information, bacteria can be engineered to produce bioregulators against pathogens. For example, Xoma Corporation has patented a bactericidal/permeability-increasing (BPI) protein, made from genes inserted into bacterial DNA, which reverses the resistance characteristic of particular bacteria against some popular antibiotics (2).

4. Efficient Bio-Agent Detection and Identification Equipment

Because the capability of comparing genomes using DNA assays has already been acquired, such technology may be developed to identify pathogens using information from bacterial and viral genomes. Such a detector could be used to identify the composition of bioweapons based on their genomes, reducing present-day delays in resultant treatment and/or preventive measures (2).

5. New Vaccines

Current scientific research projects involve genetic manipulation of viruses to create vaccines that provide immunity against multiple diseases with a single treatment (2).

6. New Antibiotics and Antiviral Drugs

Currently, antibiotic drugs target DNA synthesis, protein synthesis, and cell-wall synthesis processes in bacterial cells. With an increased understanding of microbial genomes, other proteins essential to bacterial viability can be targeted to create new classes of antibiotics. Eventually, broad-spectrum, rather than protein-specific, anti-microbial drugs may be developed (2).

Future of Warfare

“The revolution in molecular biology and biotechnology can be considered as a potential Revolution of Military Affairs (RMA),” states Colonel Michael Ainscough, MD, MPH (2). According to Andrew Krepinevich, who originally coined the term RMA, “technological advancement, incorporation of this new technology into military systems, military operational advancement, and organizational adaptation in a way that fundamentally alters the character and conduct of conflict” are the four components that make up an RMA. For instance, the Gulf War has been classified as the beginning of the space information warfare RMA. “From the technological advances in biotechnology, biowarfare with genetically engineered pathogens may constitute a future such RMA,” says Ainscough (2).

In addition, the exponential increase in computational power combined with the accessibility of genetic information and biological tools to the general public and lack of governmental regulation raise concerns about the threat of biowarfare arising from outside the military (7). The US government has cited the efforts of terrorist networks, such as al Qaida, to recruit scientists capable of creating bioweapons as a national security concern and “has urged countries to be more open about their efforts to clamp down on the threat of bioweapons”


 http://dujs.dartmouth.edu/2013/03/genetically-engineered-bioweapons-a-new-breed-of-weapons-for-modern-warfare/#.WWvmc-llDIV



---------------



10 Scariest Bioweapons

Smallpox

Anthrax

Ebola Hemorrhagic Fever

Plague

Tularemia

Botulinum Toxin

Rice Blast

Rinderpest

Nipah Virus

Chimera Viruses


http://www.stufftoblowyourmind.com/blogs/10-scariest-bioweapons.htm


-------------


Virions at the Gates: Receptors and the Host–Virus Arms Race

 May 28, 2013

Abstract

All viruses need to bind to specific receptor molecules on the surface of target cells to initiate infection. Virus–receptor binding is highly specific, and this specificity determines both the species and the cell type that can be infected by a given virus. In some well-studied cases, the virus-binding region on the receptor has been found to be unrelated to the receptor's normal cellular function. Resistance to virus infection can thus evolve by selection of mutations that alter amino acids in the binding region with minimal effect on normal function. This sort of positive selection can be used to infer the history of the host–virus “arms race” during their coevolution. In a new study, Demogines et al. use a combination of phylogenetic, structural, and virological analysis to infer the history and significance of positive selection on the transferrin receptor TfR1, a housekeeping protein required for iron uptake and the cell surface receptor for at least three different types of virus. The authors show that only two parts of the rodent TfR1 molecule have been subject to positive selection and that these correspond to the binding sites for two of these viruses—the mouse mammary tumor virus (a retrovirus) and Machupo virus (an arenavirus). They confirmed this result by introducing the inferred binding site mutations into the wild-type protein and testing for receptor function. Related arenaviruses are beginning to spread in human populations in South America as the cause of often fatal hemorrhagic fevers, and, although Demogines et al. could find no evidence of TfR1 mutations in this region that might have been selected as a consequence of human infection, the authors identified one such mutation in Asian populations that affects infection with these viruses.


 http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1001574


-------------


Next Generation Bioweapons: Genetic Engineering and BW


 http://www.au.af.mil/au/awc/awcgate/cpc-pubs/biostorm/ainscough.pdf

-------------


Is All Fair in Biological Warfare? The Controversy over Genetically Engineered Biological Weapons

J. M. Appel

Journal of Medical Ethics

Vol. 35, No. 7 (Jul., 2009), pp. 429-432

http://www.jstor.org/stable/27720364?seq=1#page_scan_tab_contents


----------------------------------

Bioweapons, Biodiversity, and Ecocide: Potential Effects of Biological Weapons on Biological Diversity: Bioweapon disease outbreaks could cause the extinction of endangered wildlife species, the erosion of genetic diversity in domesticated plants and animals, the destruction of traditional human livelihoods, and the extirpation of indigenous cultures

July, 2002

https://academic.oup.com/bioscience/article/52/7/583/247983/Bioweapons-Biodiversity-and-Ecocide-Potential

Government-sponsored scientific research into the development of technologically sophisticated applications of biological weapons for use against humans, livestock, and crops began during the early decades of the 20th century. Most government bioweapons programs included research on the culture and testing of disease agents intended specifically for use against livestock and food crops (Ban 2000). During World War I, Germany investigated techniques for using anthrax, glanders, cholera, and fungal diseases of wheat as biological weapons. German espionage agents attempted to create outbreaks of anthrax among livestock in Romania and Argentina and spread glanders among horses and mules—then still critically important as cavalry mounts and draft animals for the transport of artillery, ordnance, and supplies—in Mesopotamia, France, Argentina, and the United States. Germany was also implicated in an attempt to precipitate an epidemic of plague among humans in St. Petersburg, Russia (Dire and McGovern 2002). Japan developed and used biological weapons against human and animal populations in Asia during the period 1932–1945 (Kortepeter et al. 2001). Plague-infected fleas were reportedly used by the Japanese to precipitate plague epidemics in China during World War II, and it has been estimated that some 10,000 human subjects were used for bioweapon experiments in China involving anthrax, plague, tularemia, and smallpox (Christopher et al. 1997).

During the 1980s and 1990s, Soviet scientists used newly developed genetic engineering techniques to create antibiotic-resistant and vaccine-subverting strains of smallpox, anthrax, plague, and tularemia for bioweapon applications (Alibek and Handelman 2000). Genetically modified zoonotic and epizootic diseases of humans and animals (plague, tularemia, anthrax) and virulent cultivated or wild strains of natural livestock diseases (e.g., foot and mouth disease [FMD], rinderpest, brucellosis) represent potentially serious threats to livestock, wildlife, and endangered species populations. Plant diseases developed for bioweapons applications against food crops, opium poppies, and coca plants may, however, infect nontarget species of wild plants and become established locally subsequent to their introduction to new environments (Madden and van den Bosch 2002).

Bioterrorist uses of enzootic livestock diseases and emerging zoonotic diseases (diseases that can be transmitted between animal and human populations) represent a potentially serious threat to livestock and wildlife populations never previously exposed to these diseases. This risk holds true even, and perhaps especially in some instances, for wildlife species that may become infected by serious livestock diseases without exhibiting overt clinical signs of infection. Many formerly ubiquitous diseases that have been eradicated from livestock populations in the United States and Western Europe over the past century are still common elsewhere and readily accessible to individuals and terrorist organizations. Vaccines for many animal diseases still common in developing countries have been phased out in Europe and North America, and these vaccines, along with drugs for routine treatment, may not be readily available in sufficient quantities to suppress large-scale disease outbreaks among animals and livestock.


Biological warfare and bioterrorism

Zoonotic and epizootic disease organisms known to have been cultivated and tested in bioweapon research programs include Bacillus anthracis (anthrax), Yersinia pestis (plague), Brucella abortus (brucellosis), Clostridium botulinum, Apthovirus (FMD), Burkholderia mallei (glanders), morbilliviruses (measles, canine distemper, rinderpest), Staphylococcus, Francisella tularensis (tularemia), rabies virus, Venezuelan equine encephalomyelitis virus, and several virulent hemorrhagic fever viruses (Ebola, Marburg, Lassa fever, Rift Valley fever) (OTA 1993, Kortepeter et al. 2001, CNS 2002). Plant bioweapons cultured and tested for disrupting agriculture and food production have included fungal diseases (Fusarium spp., Tilletia spp.), viral diseases, and even insect pests (e.g., Colorado potato beetle, Leptinotarsa decemlineata).

The former USSR sponsored extensive research on possible bioweapons applications of a variety of fungal diseases of important food crops (wheat stem rust, rice blast), viral and bacterial diseases of domesticated livestock (e.g., anthrax, tularemia, malignant catarrhal fever), and insect disease vectors (mosquitoes, ticks, fleas) (Bozheyeva et al. 1999). The Soviet bioweapons program tested plant and livestock bioweapon diseases for potential deployment, with the goal of disrupting food production and food processing infrastructures and damaging the agricultural sector of national economies (Alibek and Handelman 2000). Soviet scientists reportedly used newly developed genetic engineering techniques to create vaccine-subverting and antibiotic-resistant strains of anthrax, plague, tularemia, and smallpox for attacks against military forces and civilian populations (Bozheyeva et al. 1999, Alibek and Handelman 2000). Most, perhaps even all, of the cultivated and potentially weaponized diseases identified by the Office International des Epizooties as possible major threats to livestock and wildlife species (FMD, rinderpest, Newcastle disease, African swine fever, sheep pox, and Rift Valley fever; OIE 2001) were experimentally tested for bioweapons applications under the Soviet bioweapons research and development program (Bozheyeva et al. 1999, Kortepeter et al. 2001)

Countries believed to have active biowarfare research programs during recent years include some former USSR states (i.e., Russia, Kazakstan), Syria, Iraq, Iran, Libya, North Korea, Israel, Egypt, Taiwan, China, South Africa, Libya, Cuba, Romania, Bulgaria, Pakistan, India, United Kingdom, France, Germany, the Netherlands, Norway, Sweden, and the United States (Leitenberg 2000). Several major international terrorist organizations, including but not restricted to the Al Qaeda network, are believed to have the financial resources and political contacts needed to access state-of-the-art bioweapon disease cultures and production technologies. Aum Shinrikyo, a Japanese terrorist group that used sarin gas for a terrorist attack on the Tokyo subway system, was also involved in developing terrorist bioweapons employing anthrax spores, botulism toxin, Q fever, and Ebola virus (Christopher et al. 1997).

Recent advances in molecular biology and genetic engineering have opened the way for a potential Pandora's box scenario, in which the unforeseen proliferation of a bioweapon organism could severely affect human and animal populations at regional, continental, or even global levels. Recent gene-transfer experiments with viral interleukin4 and viral diseases of the house mouse (Mus musculus) have demonstrated that even carefully controlled and monitored genetic engineering experiments may produce entirely unanticipated results, generating viruses or organisms with unwanted, deleterious, and sometimes extremely dangerous properties (Jackson et al. 2001).


-------------------------------------


Iranians, Bioweapons in Mind, Lure Needy Ex-Soviet Scientists


Dec, 1998


Iran is scouring the former Soviet Union to hire scientists who once worked in
             laboratories tied to Moscow's vast germ warfare program and has succeeded in recruiting some of
        them to take jobs in Teheran, according to Russian scientists and American officials.


http://online.sfsu.edu/rone/GEessays/Iranians%20Bioweapons%20ExSoviet%20Scientists.htm

------------------


British scientists granted permission to genetically modify human embryos

1 February 2016


British scientists have been granted permission to genetically modify human embryos by the fertility regulator.

The Francis Crick Institute could begin the controversial experiments as early as March after the Human Fertilisation and Embryology Authority (HFEA) gave the green light this morning.

The scientists want to deactivate genes in leftover embryos from IVF clinics to see if it hinders development.


http://www.telegraph.co.uk/science/2016/03/12/british-scientists-granted-permission-to-genetically-modify-huma/


-----------------


Genetic Engineering Now Allows Parents to Select the Gender and Eye Color of Their Children

 Feb 25, 2015

 http://www.popularmechanics.com/science/a19313/genetic-engineering-allow-parents-select-gender-eye-color-children/


---------------

First Genetically Engineered Salmon Sold in Canada

Aug 7, 2017

US firm AquaBounty Technologies says that its transgenic fish has hit the market after a 25-year wait


https://www.infowars.com/first-genetically-engineered-salmon-sold-in-canada/

---------------


‘Stop GMOs’: Russian scientists urge 10-year ban on genetically modified products

 16 Dec, 2013


 https://www.rt.com/news/gmo-ban-russian-scientists-293/


----------


Scientists Argue the US Ban on Human Gene Editing Will Leave It Behind


 Aug 4 2016


After a ban on germline editing, researchers say the US 'is ceding its leadership in this arena to other nations.'

As the biotech revolution accelerates globally, the US could be getting left behind on key technological advances: namely, human genetic modification.

A Congressional ban on human germline modification has "drawn new lines in the sand" on gene editing legislation, argues a paper published today in Science by Harvard law and bioethics professor I. Glenn Cohen and leading biologist Eli Adashi of Brown University. They say that without a course correction, "the United States is ceding its leadership in this arena to other nations."


https://motherboard.vice.com/en_us/article/nz7dp8/scientists-argue-the-us-ban-on-human-gene-editing-will-leave-it-behind


-----------------


[We should have an international moratorium on the use of Genetically modified organisms in food, chemicals, including genetically modified animals and humans.]


-----------------

UNESCO panel of experts calls for ban on “editing” of human DNA to avoid unethical tampering with hereditary traits

 A UNESCO panel of scientists, philosophers, lawyers and government ministers has called for a temporary ban on genetic “editing” of the human germline, calling for a wide public debate on genetic modification of human DNA.

http://en.unesco.org/news/unesco-panel-experts-calls-ban-editing-human-dna-avoid-unethical-tampering-hereditary-traits

---------


Are We Violating Biological Weapons Bans?

 August 21, 2016


https://www.laprogressive.com/biological-weapons-attack-plan/


--------


Biological Weapons Convention

 The Convention on the Prohibition of the Development, Production and Stockpiling of Bacteriological (Biological) and Toxin Weapons and on their Destruction (usually referred to as the Biological Weapons Convention, abbreviation: BWC, or Biological and Toxin Weapons Convention, abbreviation: BTWC) was the first multilateral disarmament treaty banning the production of an entire category of weapons.


https://en.wikipedia.org/wiki/Biological_Weapons_Convention


----------------

Putin’s Influential Top Advisor Warns of Plan to Destroy Humanity

AI leads to tecehnotronic takeover

Infowars.com - August 5, 2017
https://www.infowars.com/putins-top-advisor-warns-world-of-globalist-satanic-ai-takeover-plan/

----------


Is genetic engineering (crispr, gene drive, etc.) advanced enough to kill or save billions of people?

If not, how long until a bad actor could design a killer virus with the contagion of measles and the lethality of Ebola?  Or a positive actor end Malaria?  Could George Church (or another genetic scientist) single handedly kill tens of millions of people?

Millions of gamers across the world enjoy playing Plague Inc: Evolved (PC). The object of the game is to eradicate the human species by evolving pathogens via a complex set of variables to simulate the severity and spread of the plague. Tomorrow's CRISPR-based "gene drives" (cf. Gene Drive FAQ - Sculpting Evolution) have the capacity to kill billions of sentient beings or make the world a radically better place.

https://www.quora.com/Is-genetic-engineering-crispr-gene-drive-etc-advanced-enough-to-kill-or-save-billions-of-people

----------------


Could you make a genetically targeted weapon?

 Oct, 2004

- The BMA, which dismissed the idea of genetic weapons in a 1999 report (Biotechnology, Weapons and Humanity I), has lifted its new concerns from the work of a German group called the Sunshine Project. It looked at how mutations in our genome called single nucleotide polymorphisms (SNPs) differ between specific ethnic groups and concluded: "Genome data in public databases revealed that hundreds, possibly thousands, of target sequences for ethnic specific weapons do exist. It appears that ethnic specific biological weapons may indeed become possible in the near future."

Rather than specifically triggering the toxic effects of organisms such as anthrax, the Sunshine project warned that weapons based on a new medical technique called RNA interference could shut down vital genes. If the sequence of the target gene varies between two different populations the technique could be used to interrupt key body functions in one population and not the other. "If as little as 10% or 20% of a target population would be affected, this would wreak havoc among enemy soldiers on a battlefield or in an enemy society as a whole," the group said.

Others say the concerns are exaggerated. "Trying to find a weapon that affects quite a few of one ethnic group and none of another ethnic group is just not going to happen," says David Goldstein, who studies population genetics at University College London. "Because all groups are quite similar you will never get something that is highly selective. The best you would probably do is something that kills 20% of one group and 28% of another."

https://www.theguardian.com/science/2004/oct/28/thisweekssciencequestions.weaponstechnology

----------------


Ethnic specific weapons: The real story behind the murder of Dr David Kelly

July 27, 2010


https://www.sott.net/article/212776-Ethnic-specific-weapons-The-real-story-behind-the-murder-of-Dr-David-Kelly


----------------

Many people ask if bioweapons can be used against a specific group of people. We can see that certain groups of people can react differently to certain chemicals and pesticides. These types of chemical, biological and genetically modified experiments with weapons and viruses can cause harm to the environment, including all people, animals, as well as other types of beneficial organisms and bacteria. Others claim that the research on biological and genetically modified viruses, could help solve many of the diseases that harm millions of people a year.

We can see the problems with many bioweapons that could be targeted against specific living beings. We are for using medical technology for good, and for promoting life on this planet. With many of the current genetic diseases and disorders, we should concentrate on solving many of these problems, instead of creating them. We now would like to give an example of how humans are all very similar and also very different, with unique genetic traits for scientists to study.


----------------

----------------


 Chapter 9: Genetic disorders and diseases


----------------

----------------

We are for promoting and expanding all human races to live together in peace and harmony. We even believe that all human races should be able to travel to space, and expand all the races on different planets and moons. We could even gather and harvest many ideas, from trillions of people in the Universe. We can eliminate disease and poverty, and work on making the Universe a better place for all to live.


----------------


List of genetic disorders

 https://en.wikipedia.org/wiki/List_of_genetic_disorders

Sortable table
Disorder name Mutation type Chromosome
1p36 deletion syndrome D 1p36
18p deletion syndrome D 18p
21-hydroxylase deficiency
6p21.3
47,XXX
see triple X syndrome
C X
47,XXY
see Klinefelter syndrome
C X
5-ALA dehydratase-deficient porphyria
see ALA dehydratase deficiency


AAT
see alpha 1-antitrypsin deficiency

14q32
aceruloplasminemia
3p26.3
Achondrogenesis type II
12q13.11
achondroplasia substitution 4p16.3
Acrocephaly
see Apert syndrome

10q26.13
acute intermittent porphyria

adenylosuccinate lyase deficiency

Adrenoleukodystrophy

Alagille syndrome

Albinism

Alexander disease

alkaptonuria

ALS
see amyotrophic lateral sclerosis


Alström syndrome

Alzheimer's disease

Amelogenesis imperfecta

androgen insensitivity syndrome

Anemia

Angelman syndrome

ataxia telangiectasia

B variant of the Hexosaminidase GM2 gangliosidosis
see Sandhoff disease


Beare-Stevenson cutis gyrata syndrome
10q26
Benjamin syndrome

biotinidase deficiency

Birth Defects

Bloom syndrome
15q26.1
Birt–Hogg–Dubé syndrome
17
Broad Thumb-Hallux syndrome
see Rubinstein-Taybi syndrome


CADASIL syndrome P 3
CGD Chronic granulomatous disorder

Campomelic dysplasia C 17q24.3-q25.1
Canavan disease

Cancer

Caylor cardiofacial syndrome
see 22q11.2 deletion syndrome
D 22q
CF
see cystic fibrosis[1]
D (most common);
or substitution
CFTR (7q31.2)
Charcot–Marie–Tooth disease

CHARGE syndrome

Chondrodystrophy with dysplasia
see otospondylomegaepiphyseal dysplasia


Cockayne syndrome

Coffin–Lowry syndrome

collagenopathy, types II and XI

Cowden syndrome

CPO deficiency
see hereditary coproporphyria


Cri du chat D 5p
Crohn's disease, P 16q12
Crouzon syndrome
FGFR2 (10q25.3-q26)
Crouzon syndrome with acanthosis nigricans
see Crouzonodermoskeletal syndrome


cutis gyrata syndrome of Beare-Stevenson
see Beare-Stevenson cutis gyrata syndrome


Genetic hypercalciuria
see Dent's disease

Xp11.22
de Grouchy syndrome 1
see De Grouchy syndrome
D 18p
Di George's syndrome D 22q
distal hereditary motor neuropathy

Ehlers–Danlos syndrome

Erythroblastic anemia
see beta-thalassemia


FA
see fanconi anemia


Fabry disease P Xq22.1
factor V Leiden thrombophilia

familial adenomatous polyposis

familial dysautonomia

FG syndrome

Friedreich's ataxia

G6PD deficiency

galactosemia

Gaucher disease

Glioma, retinal
see retinoblastoma


Glycine encephalopathy
see Nonketotic hyperglycinemia


Haemochromatosis
see hemochromatosis


Harlequin type ichthyosis

hemophilia

hepatoerythropoietic porphyria

Hereditary coproporphyria P 3q12
Hereditary hemorrhagic telangiectasia (HHT)

Hereditary Inclusion Body Myopathy
see skeletal muscle regeneration


Hereditary multiple exostoses

Hereditary spastic paraplegia
see infantile-onset ascending hereditary spastic paralysis


Hereditary spinal ataxia
see Friedreich's ataxia


HNPP
see hereditary neuropathy with liability to pressure palsies


homocystinuria

Huntington's disease T 4p16.3
Hutchinson–Gilford progeria syndrome
see progeria


hyperoxaluria, primary

hyperphenylalaninemia

Hypochondrogenesis

Hypochondroplasia
4p16.3
ICF syndrome
see Immunodeficiency, centromere instability and facial anomalies syndrome

20q11.2
Incontinentia pigmenti P Xq28
infantile-onset ascending hereditary spastic paralysis

Isodicentric 15
see isodicentric 15
Inv dup 15q11-14
Jackson–Weiss syndrome

Joubert syndrome

JPLS
see Juvenile Primary Lateral Sclerosis

ALS2
Keloid disorder

Kniest dysplasia

Krabbe disease

Lesch-Nyhan syndrome

Li-Fraumeni syndrome

lipoprotein lipase deficiency, familial

Marfan syndrome
15
McCune–Albright syndrome
20 q13.2-13.3
McLeod syndrome
X
MEDNIK[2][3] D AP1S1
Mediterranean fever, familial

Menkes disease

Mental retardation with osteocartilaginous abnormalities
see Coffin–Lowry syndrome


Methemoglobinemia

methylmalonic acidemia

Micro syndrome
2q21.3
Microcephaly P 1q31 (ASPM)
Mowat-Wilson syndrome

Mucopolysaccharidosis (MPS I)

Muenke syndrome

Muscular dystrophy

Muscular dystrophy, Duchenne and Becker type

myotonic dystrophy

Neurofibromatosis type I
17q11.2
Neurofibromatosis type II

Niemann-Pick
see Niemann–Pick disease
NPA, NPB, NPC1, NPC2,
Sphingomyelin phosphodiesterase 1
SMPD1
Nonketotic hyperglycinemia
see Glycine encephalopathy


nonsyndromic deafness

Noonan syndrome

Ogden syndrome P X
osteogenesis imperfecta

pantothenate kinase-associated neurodegeneration

Patau Syndrome (Trisomy 13)

PCC deficiency
see propionic acidemia


PCT
see porphyria cutanea tarda


Pendred syndrome

Peutz-Jeghers syndrome

Pfeiffer syndrome

phenylketonuria

Polycystic kidney disease P 16 (PKD1) or 4 (PKD2)
Polycystic Ovarian Syndrome (PCOS)

porphyria

Prader-Willi syndrome

Primary ciliary dyskinesia (PCD)

primary pulmonary hypertension

protein C deficiency

protein S deficiency

protoporphyria
see erythropoietic protoporphyria


Prion disease

pseudo-Gaucher disease

pseudoxanthoma elasticum

Rett syndrome

RSTS
see Rubinstein-Taybi syndrome


Schwartz–Jampel syndrome

SED congenita
see spondyloepiphyseal dysplasia congenita


sickle cell anemia P 11p15
Siderius X-linked mental retardation syndrome
caused by mutations in the PHF8 gene
PD Xp11.22
Smith-Lemli-Opitz syndrome

Smith Magenis Syndrome

spinal muscular atrophy

spinocerebellar ataxia

SSB syndrome
see SADDAN


Stickler syndrome

Strudwick syndrome
see spondyloepimetaphyseal dysplasia, Strudwick type


Tay-Sachs disease

tetrahydrobiopterin deficiency

thanatophoric dysplasia

Treacher Collins syndrome
5q32-q33.1
Trisomy 21
see Down syndrome


Tuberous Sclerosis Complex (TSC) see Tuberous sclerosis
TSC1, TSC2
Turner's syndrome
see Turner syndrome

X
Usher syndrome

variegate porphyria

von Hippel-Lindau disease

Waardenburg syndrome

Weissenbacher-Zweymüller syndrome

Williams Syndrome

Wilson disease

Wolf–Hirschhorn syndrome D 4p
Xeroderma pigmentosum ERCC4 15
X-linked mental retardation and macroorchidism
see fragile X syndrome

X
X-linked spinal-bulbar muscle atrophy
see spinal and bulbar muscular atrophy

X
X-SCID
see X-linked severe combined immunodeficiency

X
XLSA
see X-linked sideroblastic anemia

X
XXXX syndrome
see 48, XXXX

X
XXXXX syndrome
see 49, XXXXX

X
XYY syndrome
see 47,XYY syndrome

X

https://en.wikipedia.org/wiki/List_of_genetic_disorders



-------------------------------------------




Genetic Disorders in Arab Populations


 http://www.cags.org.ae/cbc02ga.pdf


Genetic disorders in Arab populations as for OMIM.

http://www.cags.org.ae/cbc02ga.pdf

1.
100100
Abdominal Muscles, Absence of, with Urinary Tract Abnormality and Cryptorchidism
Lebanon
-
2.
100640
Aldehyde Dehydrogenase 1 Family, Member A1
Egypt
-
3.
102600
Adenine Phosphoribosyltransferase
?
-
4.
102610
Actin, Alpha, Skeletal Muscle 1
Oman
-
5.
102700
Adenosine Deaminase
KSA
-
6.
102730
Adenosine Deaminase, Elevated, Hemolytic Anemia due to
Libya
-
7.
103000
Adenylate Kinase 1
?
-
8.
103050
Adenylosuccinase Deficiency
Morocco
-
9.
103600
Albumin
Iraq
-
10.
104170
Alpha-Galactosidase B
Morocco
-
11.
104210
Alpha-2A-Adrenergic Receptor
Algeria
-
12.
104300
Alzheimer Disease
?
-
13.
105400
Amyotrophic Lateral Sclerosis 1
Tunisia
-
14.
106150
Angiotensin I
UAE
-
15.
107300
Antithrombin III Deficiency
Algeria
-
16.
107470
Interferon, Gamma, Receptor 1
Algeria, Tunisia, Sudan
-
17.
107680
Apolipoprotein A-I
UAE
-
18.
107730
Apolipoprotein B
?
-
19.
107777
Aquaporin 2
Palestine
-
20.
109150
Machado-Joseph Disease
Yemen
-
21.
109400
Basal Cell Nevus Syndrome
Egypt
-
22.
109535
Tumor Necrosis Factor Receptor Superfamily, Member 5
KSA
-
23.
110700
Blood Group--Duffy System
Yemen
-
24.
111000
Blood Group--Kidd System
Tunisia
-
25.
113100
Brachydactyly, Type C
Iraq
-
26.
113610
Branchial Myoclonus with Spastic Paraparesis and Cerebellar Ataxia
Kuwait
-
27.
113705
Breast Cancer 1 Gene
Morocco, Iraq, Yemen
-
28.
113900
Progressive Familial Heart Block, Type I
Lebanon
-
29.
114240
Calpain 3
Lebanon
-
30.
114830
Carbonyl Reductase 1
Sudan
-
31.
117000
Central Core Disease of Muscle
Algeria
-
32.
117550
Sotos Syndrome
?
-
33.
118450
Alagille Syndrome
?
-
34.
119100
Cleft Hand And Absent Tibia
Algeria
-
35.
120131
Collagen, Type IV, Alpha-4
Algeria
-
36.
120160
Collagen, Type I, Alpha-2
Libya, Lebanon
-
37.
120250
Collagen, Type VI, Alpha-3
Morocco
-
38.
120290
Collagen, Type XI, Alpha-2
Morocco
-
39.
120700
Complement Component 3
Palestine, Lebanon, Kuwait
-
40.
121011
Gap Junction Protein, Beta-2
Tunisia, Egypt, Palestine, Jordan
-
41.
122100
Corneal Dystrophy, Juvenile Epithelial, of Meesmann
KSA
-
42.
122470
Cornelia de Lange Syndrome
?
-
43.
123400
Creutzfeldt-Jakob Disease
Tunisia, Libya, Egypt
-
44.
124030
Cytochrome P450, Subfamily IID
KSA
-
45.
125630
Dermodistortive Urticaria
Lebanon
-
46.
125700
Diabetes Insipidus, Neurohypophyseal Type
Palestine
-
47.
126650
Solute Carrier Family 26, Member 3
Kuwait, KSA
-
48.
130070
Ehlers-Danlos Syndrome, Progeroid Form
?
-
49.
130500
Erythrocyte Membrane Protein Band 4.1
Algeria
-
50.
131244
Endothelin Receptor, Type B
Tunisia
-
51.
131760
Epidermolysis Bullosa Herpetiformis, Dowling-Meara Type
?
-
52.
133530
Excision-Repair, Complementing Defective, in Chinese Hamster, 5
Morocco
-
53.
134570
Factor XIII, A1 Subunit
Morocco, Syria
-
54.
134790
Ferritin Light Chain
Egypt
-
55.
135100
Fibrodysplasia Ossificans Progressiva
Tunisia, Syria
-
56.
136435
Follicle-Stimulating Hormone Receptor
Morocco
-
57.
136850
Fumarate Hydratase
Morocco
-
58.
137167
Gamma-Glutamyl Carboxylase
Lebanon
-
59.
137280
Gastritis, Familial Giant Hypertrophic
Jordan
-
60.
137290
Tumor-Associated Calcium Signal Transducer 2
Tunisia
-
61.
137800
Glioma of Brain, Familial Glioblastoma Multiforme
?
-
62.
138350
Glutathione S-Transferase, MU-1
KSA
-
63.
139090
Gray Platelet Syndrome
Palestine
-
64.
139191
Growth Hormone-Releasing Hormone Receptor
Morocco
-
65.
139250
Growth Hormone 1
KSA
-
66.
140300
Hashimoto Thyroiditis
Tunisia
-
67.
141800
Hemoglobin-Alpha Locus 1
Mauritania, Morocco,
Algeria, Tunisia, KSA,
Qatar, UAE
-
68.
141850
Hemoglobin--Alpha Locus 2
Algeria, Tunisia, Iraq,
KSA, Yemen
-
69.
141900
Hemoglobin--Beta Locus
Morocco, Algeria, Tunisia,
Egypt, Lebanon, Syria,
Iraq, Kuwait, KSA, Qatar,
Oman, Sudan
-
70.
142200
Hemoglobin, Gamma A
Tunisia
-
71.
142250
Hemoglobin, Gamma G
Algeria, KSA, UAE
-
72.
142309
Hemoglobin--Variants for which the Chain Carrying the Mutation is Unknown or Uncertain
KSA
-
73.
142461
Heparan Sulfate Proteoglycan of Basement Membrane
Tunisia
-
74.
142470
Heterocellula
-
75.
142800
Major Histocompatibility Complex, Class I, A
Egypt
-
76.
142900
Holt-Oram Syndrome
Jordan
-
77.
143100
Huntington Disease
Morocco, Sudan
-
78.
143890
Hypercholesterolemia, Autosomal Dominant
Lebanon, Syria
-
79.
144200
Palmoplantar Keratoderma, Epidermolytic
Kuwait
-
80.
145420
Hypertelorism, Teebi Type
?
-
81.
145900
Hypertrophic Neuropathy of Dejerine-Sottas
Lebanon
-
82.
147000
IgA Constant Heavy Chain 2
Tunisia
-
83.
147100
IgG Heavy Chain Locus
Tunisia
-
84.
147120
Immunoglobulin Gm3
Tunisia
-
85.
147920
Kabuki Syndrome
?
-
86.
148820
Waardenburg Syndrome, Type III
Egypt, Yemen
-
87.
150330
Lamin A/C
Morocco, Algeria
-
88.
150590
Leg Ulcers, Familial, of Juvenile Onset
Iraq
-
89.
150900
Lentigines
Lebanon
-
90.
151443
Leukemia Inhibitory Factor Receptor
UAE, Oman
-
91.
151600
Leukonychia Totalis
?
-
92.
152200
Apolipoprotein(a)
Sudan
-
93.
153454
Procollagen-Lysine, 2-Oxoglutarate 5-Dioxygenase
Qatar
-
94.
153670
Bernard-Soulier Syndrome, Benign Autosomal Dominant
Algeria
 -
95.
154045
Lens Intrinsic Membrane Protein 2, 19-kD
Iraq
-
96.
154550
Mannosephosphate Isomerase
Lebanon
-
97.
154570
Mannose 6-Phosphate Receptor Recognition Defect, Lebanese Type
Lebanon
-
98.
155255
Medulloblastoma
Morocco
-
99.
156225
Laminin, Alpha-2
KSA
-
100.
157660
Mitochondrial RNA-Processing Endoribonuclease, RNA Component of
KSA
-
101.
158000
Monilethrix
?
-
102.
159980
Myogenic Factor 4
Oman
-
103.
160900
Dystrophia Myotonica 1
Morocco, Egypt, Yemen
-
104.
161200
Nail-Patella Syndrome
Palestine
-
105.
161561
Interleukin 12B
KSA
-
106.
161900
Renal Failure, Progressive, with Hypertension
Iraq
-
107.
162700
Neutropenia, Chronic Familial
Yemen
-
108.
164500
Spinocerebellar Ataxia 7
Morocco
-
109.
164831
Leukemia Viral BMI-1 Oncogene, Mouse, Homolog of
Morocco
-
110.
166210
Osteogenesis Imperfecta Congenita
Algeria
-
111.
166800
Otosclerosis
Tunisia
-
112.
169500
Leukodystrophy, Adult-Onset, Autosomal Dominant
Sudan
-
113.
170200
Peptidase E
Syria
-
114.
170261
Transporter, ATP-Binding Cassette, Major Histocompatibility Complex, 2
Morocco
-
115.
173470
Integrin, Beta-3
Iraq
-
116.
175100
Adenomatous Polyposis of the Colon
?
-
117.
175200
Peutz-Jeghers Syndrome
Iraq
-
118.
176100
Porphyria Cutanea Tarda
Tunisia
-
119.
176261
Potassium Channel, Voltage-Gated, ISK-Related Subfamily, Member 1
Lebanon
-
120.
176640
Prion Protein
Morocco, Tunisia, Libya
-
121.
176670
Hutchinson-Gilford Progeria Syndrome
Libya, Egypt
-
122.
176860
Protein C Deficiency, Congenital Thrombotic Disease due to Protein C
?
-
123.
177070
Protein 4.2, Erythrocytic
Tunisia
-
124.
177850
Pseudoxanthoma Elasticum, Autosomal Dominant
Morocco
-
125.
179280
Radial-Renal Syndrome
Morocco
-
126.
180090
Retinaldehyde-Binding Protein
KSA
-
127.
180700
Robinow Syndrome
Algeria, Kuwait, KSA
-
128.
180860
Silver-Russell Syndrome
Lebanon
-
129.
180901
Ryanodine Receptor 1
Algeria
-
130.
180960
S-Adenosylhomocysteine Hydrolase
Tunisia
-
131.
181450
Ulnar-Mammary Syndrome
Yemen
-
132.
182380
Solute Carrier Family 5 (Sodium/Glucose Cotransporter), Member 1
Lebanon, Syria
-
133.
182601
Spastic Paraplegia 4, Autosomal Dominant
Tunisia
-
134.
182860
Spectrin, Alpha, Erythrocytic 1
Morocco, Algeria, Tunisia
-
135.
182870
Spectrin, Beta, Erythrocytic
Algeria
-
136.
183090
Spinocerebellar Ataxia 2
Tunisia
-
137.
184253
Spondylometaphyseal Dysplasia, Algerian Type
Algeria
-
138.
186970
T-Cell Antigen Receptor, Gamma Subunit
Tunisia, Lebanon
-
139.
187300
Telangiectasia, Hereditary Hemorrhagic, of Rendu, Osler, and Weber
?
-
140.
187500
Tetralogy of Fallot
Lebanon
-
141.
187600
Thanatophoric Dysplasia
Morocco
-
142.
188250
Thymidine Kinase, Mitochondrial
?
-
143.
188455
Thyroglossal Duct Cyst, Familial
?
-
144.
188540
Thyroid-Stimulating Hormone, Beta Chain
Egypt
-
145.
188570
Thyroid Hormone Resistance
Algeria
-
146.
190160
Thyroid Hormone Receptor, Beta
Algeria
-
147.
191315
Neurotrophic Tyrosine Kinase, Receptor, Type 1
UAE
-
148.
191720
5-Prime,3-Prime-@Nucleotidase, Cytosolic
Syria
-
149.
191740
Udp-Glycosyltransferase 1 Family, Polypeptide A1
Tunisia
-
150.
192340
Arginine Vasopressin
Palestine
-
151.
192500
Long QT Syndrome 1
Tunisia
-
152.
192600
Cardiomyopathy, Familial Hypertrophic
Lebanon
-
153.
193230
Vitreoretinal Degeneration, Snowflake Type
Algeria
-
154.
193700
Whistling Face-Windmill Vane Hand Syndrome
Morocco
-
155.
201100
Acrodermatitis Enteropathica, Zinc-Deficiency Type
Egypt, Jordan
-
156.
201300
Neuropathy, Hereditary Sensory and Autonomic, Type II
?
-
157.
201710
Lipoid Congenital Adrenal Hyperplasia
Palestine
-
158.
201910
Adrenal Hyperplasia, Congenital, due to 21-Hydroxylase Deficiency
Kuwait
-
159.
202010
Adrenal Hyperplasia, Congenital, due to 11-Beta-Hydroxylase Deficiency
Morocco, Tunisia, KSA
-
160.
202370
Adrenoleukodystrophy, Autosomal Neonatal Form
Egypt
-
161.
202400
Afibrinogenemia, Congenital
Morocco, Iraq
-
162.
203500
Alkaptonuria
Egypt
-
163.
203700
Alpers Diffuse Degeneration of Cerebral Gray Matter with Hepatic Cirrhosis
?
-
164.
203740
Alpha-Ketoglutarate Dehydrogenase Deficiency
Algeria, Tunisia
-
165.
203750
Alpha-Methylacetoaceticaciduria
Tunisia
-
166.
203800
Alstrom Syndrome
Algeria
-
167.
204200
Ceroid Lipofuscinosis, Neuronal 3, Juvenile
Morocco
-
168.
204500
Ceroid Lipofuscinosis, Neuronal 2, Late Infantile
Lebanon
-
169.
204870
Corneal Dystrophy, Gelatinous Drop-Like
Tunisia
-
170.
205100
Amyotrophic Lateral Sclerosis 2, Juvenile
Tunisia, Kuwait, KSA
-
171.
206500
Anencephaly
Iraq
-
172.
208050
Arterial Tortuosity
Morocco
-
173.
208100
Arthrogryposis Multiplex Congenita, Neurogenic Type
?
-
174.
208230
Arthropathy, Progressive Pseudorheumatoid, of Childhood
Jordan
-
175.
208250
Arthropathy-Camptodactyly Syndrome
KSA
-
176.
208400
Aspartylglucosaminuria Aspartylglucosaminidase
Tunisia, Palestine
-
177.
208850
Ataxia-Deafness-Retardation Syndrome
Kuwait
-
178.
208870
Ataxia-Microcephaly-Cataract Syndrome
?
-
179.
208900
Ataxia-Telangiectasia
Morocco
-
180.
209500
Atrichia with Papular Lesions
?
-
181.
209900
Bardet-Biedl Syndrome
Kuwait
-
182.
209920
Bare Lymphocyte Syndrome, Type II
Morocco, Algeria, Tunisia
-
183.
210000
Behr Syndrome
Iraq
-
184.
210200
3-@Methylcrotonyl-CoA Carboxylase 1 Deficiency
Tunisia
-
185.
210600
Seckel Syndrome
Iraq, Yemen
-
186.
210745
Blepharophimosis with Ptosis, Syndactyly, and Short Stature
Yemen
-
187.
211530
Bulbar Palsy, Progressive, with Sensorineural Deafness
Lebanon
-
188.
211770
Cahmr Syndrome
Egypt
-
189.
211890
Campomelia, Cumming Type
Egypt
-
190.
211900
Calcinosis, Tumoral, with Hyperphosphatemia
Lebanon
-
191.
211960
Camptodactyly with Muscular Hypoplasia, Skeletal Dysplasia, and
Morocco, Libya
Abnormal Palmar Creases
-
192.
212110
Cardiomyopathy, Dilated, Autosomal Recessive
KSA
-
193.
212112
Cardiomyopathy, Congestive, with Hypergonadotropic Hypogonadism
Lebanon
-
194.
212135
Cardioskeletal Syndrome, Kuwaiti Type
Kuwait
-
195.
212138
Solute Carrier Family 25 (Carnitine/Acylcarnitine Translocase), Member 20
KSA
-
196.
213200
Cerebellar Ataxia 1
Lebanon
-
197.
213700
Cerebrotendinous Xanthomatosis
Morocco
-
198.
213980
Cerebrofaciothoracic Dysplasia
Morocco
-
199.
214100
Zellweger Syndrome
Algeria
-
200.
214150
Cerebrooculofacioskeletal Syndrome
Egypt
-
201.
214300
Cervical Vertebral Fusion, Autosomal Recessive
Iraq
-
202.
214400
Charcot-Marie-Tooth Disease, Type 4A
Tunisia
-
203.
214700
Chloride Diarrhea, Familial
Kuwait
-
204.
215518
Ciliary Discoordination due to Random Ciliary Orientation
Lebanon
-
205.
216550
Cohen Syndrome
Lebanon
-
206.
216900
Achromatopsia 2
Morocco, Iraq
-
207.
217070
Complement Component 7 Deficiency
Morocco, Tunisia, Yemen
-
208.
217080
Cone-Rod Dystrophy and Amelogenesis Imperfecta
?
-
209.
217400
Corneal Dystrophy and Perceptive Deafness
Morocco
-
210.
218350
Craniofacial Dyssynostosis with Short Stature
?
-
211.
219200
Cutis Laxa with Growth and Developmental Delay
KSA
-
212.
219550
Cysteine Peptiduria
Iraq
-
213.
219600
Cystic Disease of Lung
Yemen
-
214.
219700
Cystic Fibrosis
Morocco, Libya, Iraq,
KSA, Yemen
-
215.
219721
Cystic Fibrosis with Helicobacter Pylori Gastritis, Megaloblastic Anemia,
?
and Subnormal Mentality
-
216.
220100 Cystinuria
Libya
-
217.
220150 Hypouricemia, Renal
Iraq
-
218.
220290 Deafness, Neurosensory, Autosomal Recessive 1
Tunisia, Egypt, Palestine
-
219.
220500 Deafness, Congenital, and Onychodystrophy, Recessive Form
Oman
-
220.
220900 Deafness, Congenital, with Total Albinism
Morocco
-
221.
221745 Mitochondrial Deafness Modifier Gene 1
?
-
222.
221950 Dextrocardia with Unusual Facies and Microphthalmia
?
-
223.
222300 Wolfram Syndrome
Sudan
-
224.
222400 Diaphragm, Unilateral Agenesis of Diaphragmatic Defects, Familial Congenital
Egypt, Kuwait
-
225.
222448 Donnai-Barrow Syndrome
KSA
-
226.
222700 Lysinuric Protein Intolerance
Morocco, KSA
-
227.
222748 Dihydropyrimidinase
Lebanon
-
228.
223800 Dyggve-Melchior-Clausen Disease
Morocco, Lebanon
-
229.
223900 Dysautonomia, Familial
Algeria
-
230.
224120 Anemia, Dyserythropoietic Congenital, Type I
Kuwait, KSA
-
231.
224230 Dyskeratosis Congenita, Autosomal Recessive
Syria
-
232.
224400 Dyssegmental Dwarfism
Palestine, Lebanon, Jordan
-
233.
224500 Dystonia Musculorum Deformans 2
?
-
234.
224900 Ectodermal Dysplasia, Anhidrotic
Morocco
-
235.
225280 Eem Syndrome
Yemen
-
236.
225400 Ehlers-Danlos Syndrome, Type VI
?
-
237.
225750 Aicardi-Goutieres Syndrome 1
Algeria
-
238.
226300
Enteropathy, Protein-Losing
?
-
239.
226400
Epidermodysplasia Verruciformis
Algeria
-
240.
226980
Epiphyseal Dysplasia, Multiple, with Early-Onset Diabetes Mellitus
Oman
-
241.
227090
Erythroderma, Lethal Congenital
Oman
-
242.
227260
Facial Ectodermal Dysplasia
Oman
-
243.
227300
Factor V and Factor VIII, Combined Deficiency of
Algeria, Tunisia
-
244.
227310
Factor V and Factor VIII, Combined Deficiency of, with
Syria
Normal Protein C and Protein C Inhibitor
-
245.
227320
Faciothoracogenital Syndrome
?
-
246.
227330
Faciodigitogenital Syndrome, Recessive
Kuwait
-
247.
227400
Factor V Deficiency
Morocco
-
248.
227500
Factor VII Deficiency
Morocco
-
249.
227645
Fanconi Anemia, Complementation Group C
Iraq
-
250.
228000
Farber Lipogranulomatosis
Tunisia
=
251.
228250
Femur, Unilateral Bifid, with Monodactylous Ectrodactyly
?
-
252.
228400
Fever, Familial Lifelong Persistent
Lebanon
-
253.
228550
Fibromatosis, Congenital Generalized
Morocco
-
254.
228980
Fleck Retina, Familial Benign
Palestine
-
255.
229200
Fragilitas Oculi with Joint Hyperextensibility
Tunisia, Syria
-
256.
229300
Friedreich Ataxia 1
Tunisia
-
257.
229800
Fructosuria Ketohexokinase
?
-
258.
229850
Fryns Syndrome
Sudan
-
259.
230740
Gapo Syndrome
Algeria, Egypt
-
260.
230800
Gaucher Disease, Type I
Palestine
-
261.
231005
Gaucher-Like Disease
?
-
262.
231070
Geroderma Osteodysplastica
Morocco
-
263.
231090
Hydatidiform Mole
Lebanon
-
264.
231550
Achalasia-Addisonianism-Alacrima Syndrome
KSA
-
265.
231670
Glutaricacidemia I Glutaryl-CoA Dehydrogenase
?
-
266.
232200
Glycogen Storage Disease I Glucose-6-Phosphatase, Catalytic
?
-
267.
232300
Glycogen Storage Disease II
Palestine
-
268.
232700
Glycogen Storage Disease VI Glycogen Phosphorylase, Liver
?
-
269.
233710
Granulomatous Disease, Chronic, Autosomal Cytochrome-b-Positive Form II
Palestine, Jordan
-
270.
234050
Hair-Brain Syndrome
Morocco
-
271.
235200
Hemochromatosis
Algeria, Egypt
-
272.
235510
Hennekam Lymphangiectasia-Lymphedema Syndrome
?
-
273.
236200
Homocystinuria
KSA
-
274.
236450
Hutterite Cerebroosteonephrodysplasia Syndrome
Yemen
-
275.
236600
Hydrocephalus
Palestine, Kuwait
-
276.
236700
McKusick-Kaufman Syndrome
Lebanon
-
277.
236730
Urofacial Syndrome
?
-
278.
236792
L-2-@Hydroxyglutaricacidemia
Morocco, Tunisia
279.
236800
Hydroxykynureninuria
Algeria
-
280.
237300
Carbamoyl Phosphate Synthetase I Deficiency, Hyperammonemia due to
?
-
281.
237500
Dubin-Johnson Syndrome
Morocco, Iraq
-
282.
237900
Hyperbilirubinemia, Transient Familial Neonatal Breastfeeding Jaundice
Yemen
-
283.
238310
Aminomethyltransferase
?
-
284.
239000
Paget Disease, Juvenile
Iraq
-
285.
239500
Hyperprolinemia, Type I
Algeria
-
286.
239710
Acrofrontofacionasal Dysostosis, Severe
Kuwait
-
287.
239840
Hypertrichosis, Congenital Anterior Cervical, with Peripheral
?
Sensory and Motor Neuropathy
-
288.
241080
Hypogonadism, Diabetes Mellitus, Alopecia, Mental Retardation,
KSA
and Electrocardiographic Abnormalities
-
289.
241410
Hypoparathyroidism-Retardation-Dysmorphism Syndrome
KSA, Qatar
-
290.
242300
Ichthyosis, Lamellar, 1
Egypt
-
291.
242870
Immunodeficiency, Partial Combined, with Absence of HLA
Algeria
Determinants and Beta-2-Microglobulin from Lymphocytes
-
292.
243060
Infertility Associated with Multi-Tailed Spermatozoa and Excessive DNA
Libya
-
293.
243110
Interleukin 1, Defective T-Cell Response to
Lebanon
-
294.
243320
Intrinsic Factor and R Binder, Combined Congenital Deficiency of
Algeria
-
295.
243600
Jejunal Atresia
?
-
296.
243800
Johanson-Blizzard Syndrome
KSA
-
297.
244400
Kartagener Syndrome
?
-
298.
244460
Kenny-Caffey Syndrome, Type 1
Kuwait, KSA
-
299.
245000
Papillon-Lefevre Syndrome
Jordan
-
300.
245200
Krabbe Disease
Egypt, Lebanon, Syria
-
301.
245552
Lambotte Syndrome
Morocco
-
302.
245590
Laron Syndrome, Type II Growth Hormone Insensitivity with Immunodeficiency
Palestine
-
303.
245600
Larsen Syndrome, Recessive
UAE
-
304.
245800
Laurence-Moon Syndrome
Kuwait
-
305.
246200
Leprechaunism
Yemen
-
306.
246450
3-@Hydroxy-3-Methylglutaryl-CoA Lyase Deficiency
Morocco, KSA
-
307.
247100
Lipoid Proteinosis of Urbach and Wiethe
Lebanon
-
308.
248110
Macrosomia with Microphthalmia, Lethal
Kuwait
-
309.
248250
Hypomagnesemia, Primary
?
-
310.
248300
Mal de Meleda
Algeria
-
311.
248500
Mannosidosis, Alpha B, Lysosomal
Palestine
-
312.
248600
Maple Syrup Urine Disease
Tunisia, Egypt
-
313.
248800
Marinesco-Sjogren Syndrome
Kuwait
-
314.
249100
Familial Mediterranean Fever
Morocco, Libya, Palestine,
Lebanon, Syria, Jordan,
Iraq, Kuwait, KSA
Country
-
315.
249240
Megalencephaly with Dysmyelination
Iraq
-
316.
249270
Thiamine-Responsive Megaloblastic Anemia Syndrome
?
-
317.
249420
Ter Haar Syndrome
Syria
-
318.
249500
Mental Retardation, Autosomal Recessive
Algeria
-
319.
250100
Metachromatic Leukodystrophy Pseudoarylsulfatase A Deficiency
?
-
320.
250220
Metaphyseal Chondrodysplasia, Congenital Lethal
Yemen
-
321.
250450
Metaphyseal Dysplasia, Anetoderma, and Optic Atrophy
Egypt
-
322.
250790
Methemoglobinemia due to Deficiency of Cytochrome B5
Yemen
-
323.
250800
Methemoglobinemia due to Deficiency of Methemoglobin Reductase
Algeria
-
324.
250951
3-@Methylglutaconicaciduria, Type IV
Iraq
-
325.
251260
Nijmegen Breakage Syndrome Berlin Breakage Syndrome
?
-
326.
251270
Microcephaly with Chorioretinopathy
Kuwait
-
327.
251280
Microcephaly with Spastic Quadriplegia
Palestine
-
328.
251450
Desbuquois Syndrome
Morocco, UAE
-
329.
251600
Microphthalmos, Autosomal Recessive
?
-
330.
251850
Microvillus Inclusion Disease
Iraq
-
331.
252010
Complex I, Mitochondrial Respiratory Chain, Deficiency of Myopathy,
Morocco
Mitochondrial, with Deficiency of Respiratory Chain NADH-CoQ Reductase Activity
-
332.
252350
Moyamoya Disease
?
-
333.
252650
Mucolipidosis IV
Sudan
-
334.
252800
Alpha-L-Iduronidase
Morocco, Libya, Egypt,
Lebanon, Syria
-
335.
252920
Mucopolysaccharidosis Type IIIb N-Acetylglucosaminidase, Alpha-
?
-
336.
253220
Mucopolysaccharidosis Type VII
Algeria
-
337.
253250
Mulibrey Nanism
Egypt
-
338.
253270
Multiple Carboxylase Deficiency
Jordan
-
339.
253290
Multiple Pterygium Syndrome, Lethal Type
Morocco
-
340.
253300
Spinal Muscular Atrophy, Type I
Kuwait
-
341.
253550
Spinal Muscular Atrophy, Type II
Kuwait
-
342.
253600
Muscular Dystrophy, Limb-Girdle, Type 2A
?
-
343.
253601
Muscular Dystrophy, Limb-Girdle, Type 2B
Yemen
-
344.
253700
Muscular Dystrophy, Limb-Girdle, Type 2C
Morocco, Algeria,
Tunisia, Libya, Egypt
-
345.
254130
Miyoshi Myopathy
Tunisia
-
346.
254210
Myasthenia Gravis, Familial Infantile
Iraq
-
347.
254780
Myoclonic Epilepsy of Lafora Epilepsy
Palestine
-
348.
254800
Myoclonic Epilepsy of Unverricht and Lundborg
?
-
349.
255800
Schwartz-Jampel Syndrome, Type 1
Algeria, Tunisia, UAE
-
350.
256000
Leigh Syndrome
Mauritania
-
351.
256020
Nail-Patella-Like Renal Disease
Palestine
-
352.
256370
Nephrotic Syndrome, Early-Onset, with Diffuse Mesangial Sclerosis
?
-
353.
256450
Nesidioblastosis of Pancreas Persistent Hyperinsulinemic
KSA
Hypoglycemia of Infancy due to Focal Adenomatous Hyperplasia
-
354.
256520
Neu-Laxova Syndrome
Egypt
-
355.
256800
Insensitivity to Pain, Congenital, with Anhidrosis
Kuwait
-
356.
256850
Giant Axonal Neuropathy 1
Tunisia
-
357.
256851
Neuropathy, Giant Axonal, Tunisian Form
Tunisia
-
358.
257300
Nondisjunction
Kuwait
-
359.
257320
Lissencephaly Syndrome, Norman-Roberts Type
KSA
-
360.
257980
Odontoonychodermal Dysplasia
Lebanon
-
361.
258501
3-@Methylglutaconicaciduria, Type III
Iraq
-
362.
258860
Oral-Facial-Digital Syndrome, Type IV
Lebanon
-
363.
258870
Ornithine Aminotransferase Deficiency
Algeria, Lebanon, Iraq
-
364.
259700
Osteopetrosis, Autosomal Recessive
Palestine
-
365.
259730
Osteopetrosis with Renal Tubular Acidosis
Tunisia, Kuwait, KSA
-
366.
259775
Osteoclerotic Bone Dysplasia, Lethal
?
-
367.
260600
Pelizaeus-Merzbacher Disease, Acute Infantile Type
Yemen
-
368.
260650
Pellagra-Like Syndrome
Sudan
-
369.
260800
Pentosuria
Lebanon
-
370.
260920
Hyper-IgD Syndrome
?
-
371.
261100
Megaloblastic Anemia 1
KSA
-
372.
261500
Peroxidase and Phospholipid Deficiency in Eosinophils
Yemen, Sudan
-
373.
261550
Persistent Mullerian Duct Syndrome, Types I and II
?
-
374.
261600
Phenylketonuria
Kuwait, Yemen
-
375.
261630
Phenylketonuria II
Tunisia
-
376.
261750
Phosphorylase Kinase Deficiency of Liver and Muscle, Autosomal Recessive
?
-
377.
262400
Pituitary Dwarfism I
Iraq, Yemen
-
378.
262500
Pituitary Dwarfism II
?
-
379.
263630
Polysyndactyly with Cardiac Malformation
Oman
-
380.
263650
Popliteal Pterygium Syndrome, Lethal Type
Qatar, UAE
-
381.
263700
Porphyria, Congenital Erythropoietic
Algeria
-
382.
264300
17-@Beta Hydroxysteroid Dehydrogenase III Deficiency Polycystic
?
Ovarian Disease due to 17-Ketosteroid Reductase Deficiency
-
383.
264600
Pseudovaginal Perineoscrotal Hypospadias
Jordan
-
384.
264900
Pta Deficiency Coagulation Factor XI
Iraq
-
385.
265000
Pterygium Syndrome
Kuwait
-
386.
265100
Pulmonary Alveolar Microlithiasis
Lebanon
-
387.
265380
Pulmonary Hypertension, Familial Persistent, of the Newborn
Tunisia
-
388.
265800
Pycnodysostosis
?
-
389.
265950
Pyloric Atresia
Iraq
-
390.
266140
Pyropoikilocytosis, Hereditary
KSA
-
391.
266150
Pyruvate Carboxylase Deficiency
Egypt
-
392.
266200
Pyruvate Kinase Deficiency of Erythrocyte
Lebanon
-
393.
266265
Congenital Disorder of Glycosylation, Type IIc
?
-
394.
267000
Renal Hamartomas, Nephroblastomatosis, and Fetal Gigantism
Yemen
-
395.
267430
Renal Tubular Dysgenesis
Palestine
-
396.
267700
Reticulosis, Familial Histiocytic
Iraq
-
397.
268020
Retinitis Pigmentosa, Deafness, Mental Retardation, and Hypogonadism
Morocco
-
398.
268050
Retinopathy, Pigmentary, and Mental Retardation
Lebanon
-
399.
268130
Revesz Syndrome
Sudan
-
400.
268200
Rhabdomyolysis, Acute Recurrent
Kuwait
-
401.
268250
Rhizomelic Syndrome
?
-
402.
268310
Robinow Syndrome, Autosomal Recessive
Kuwait, Oman
-
403.
268800
Sandhoff Disease
Lebanon
-
404.
269000
SC Phocomelia Syndrome
Lebanon
-
405.
269150
Schinzel-Giedion Midface-Retraction Syndrome
Egypt
-
406.
269700
Lipodystrophy, Congenital Generalized, Type 2
Lebanon, Oman
-
407.
269950
Sideroblastic Anemia, Autosomal
Libya
-
408.
270200
Sjogren-Larsson Syndrome
Egypt
-
409.
270300
Skin Peeling, Familial Continuous
Kuwait
-
410.
270550
Spastic Ataxia, Charlevoix-Saguenay Type
Tunisia
-
411.
270750
Spastic Paraplegia 23
Jordan
-
412.
270800
Spastic Paraplegia 5A, Autosomal Recessive
Tunisia
-
413.
271322
Spinocerebellar Degeneration with Slow Eye Movements
Palestine, Kuwait
-
414.
271550
Spondyloenchondrodysplasia
Iraq
-
415.
271640
Spondyloepimetaphyseal Dysplasia with Joint Laxity
?
-
416.
271665
Spondylometaepiphyseal Dysplasia, Short Limb-Hand Type
Egypt
-
417.
271900
Canavan Disease
KSA
-
418.
272300
Sulfocysteinuria
Algeria
-
419.
272440
Syndactyly, Type I, with Microcephaly and Mental Retardation
Tunisia
-
420.
272450
Syndesmodysplasic Dwarfism
Algeria
-
421.
272460
Spondylocarpotarsal Synostosis Syndrome
Lebanon
-
422.
272750
Tay-Sachs Disease, AB Variant
KSA
-
423.
272800
Tay-Sachs Disease
Morocco, Lebanon, Syria
-
424.
272950
Teebi-Shaltout Syndrome
Tunisia
-
425.
273150
Testes, Rudimentary
Lebanon
-
426.
273250
Testicular Regression Syndrome
Tunisia
-
427.
273395
Tetra-Amelia with Pulmonary Hypoplasia
Palestine
-
428.
273800
Thrombasthenia of Glanzmann and Naegeli
Jordan, Iraq
-
429.
275000
Graves Disease
Tunisia
-
430.
275200
Thyrotropin, Unresponsiveness to
Egypt, Syria
-
431.
275210
Tight Skin Contracture Syndrome, Lethal
Algeria
-
432.
275350
Transcobalamin II Deficiency
Morocco
-
433.
275595
Trigonobrachycephaly, Bulbous Bifid Nose, Micrognathia,
Palestine
and Abnormalities of the Hands and Feet
-
434.
275630
Triglyceride Storage Disease with Impaired Long-Chain Fatty Acid Oxidation
Egypt
-
435.
275900
Spastic Paraplegia 20, Autosomal Recessive
Kuwait
-
436.
276600
Tyrosine Transaminase Deficiency
KSA
-
437.
276820
Ulna And Fibula, Absence of, with Severe Limb Deficiency
Jordan
-
438.
276821
Ulnar Hypoplasia with Mental Retardation
?
-
439.
276901
Usher Syndrome, Type IIA
Tunisia
-
440.
276902
Usher Syndrome, Type III
Yemen
-
441.
276903
Myosin VIIA
Tunisia, Yemen
-
442.
276905
Usher Syndrome, Type IIB
Tunisia
-
443.
277300
Spondylocostal Dysostosis, Autosomal Recessive, 1
?
-
444.
277320
Visceral Myopathy, Familial, with External Ophthalmoplegia
Iraq
-
445.
277350
Vitamin A Metabolic Defect
Lebanon
-
446.
277440
Vitamin D-Resistant Rickets with End-Organ Unresponsiveness to
?
1,25-Dihydroxycholecalciferol
-
447.
277450
Vitamin K-Dependent Clotting Factors, Combined Deficiency of,
?
1 Chondrodysplasia Punctata with Coagulation Factor Deficiency
-
448.
277460
Vitamin E, Familial Isolated Deficiency of
Tunisia
-
449.
277465
Vitiligo, Progressive, with Mental Retardation and Urethral Duplication
Algeria
-
450.
277580
Waardenburg-Shah Syndrome
Yemen
-
451.
277600
Weill-Marchesani Syndrome, Autosomal Recessive
Lebanon
-
452.
277900
Wilson Disease
?
-
453.
278250
Wrinkly Skin Syndrome
Iraq, KSA
-
454.
278300
Xanthinuria, Type I
Lebanon, Kuwait
-
455.
278700
Xeroderma Pigmentosum, Complementation Group A
Tunisia, Egypt, Palestine
-
456.
279000
Young Syndrome
Yemen
-
457.
300265
Zinc Finger Protein of Cerebellum, 3
Lebanon
-
458.
300331
Thrombocytosis, Familial X-Linked
?
-
459.
300383
Properdin P Factor, Complement
Tunisia
-
460.
300392
WAS Gene
Lebanon, Syria
-
461.
300419
Mental Retardation, X-Linked 54
Tunisia
-
462.
300463
Polyglutamine-Binding Protein 1
Morocco
-
463.
301090
Amelia, X-Linked
?
-
464.
301900
Borjeson-Forssman-Lehmann Syndrome
KSA
-
465.
304790
Immunodysregulation, Polyendocrinopathy, and Enteropathy, X-Linked
Morocco
-
466.
305900
Glucose-6-Phosphate Dehydrogenase
Algeria, Egypt, Lebanon,
Syria, Jordan, Iraq, KSA,
Sudan
-
467.
308050
Congenital Hemidysplasia with Ichthyosiform Erythroderma and Limb Defects
Egypt
-
468.
309200
Major Affective Disorder 2
Iraq, Yemen
-
469.
309550
Fragile Site Mental Retardation 1 Gene
Tunisia
-
470.
309900
Mucopolysaccharidosis Type II
Morocco
-
471.
310400
Myotubular Myopathy 1
Yemen
-
472.
312060
Properdin Deficiency, X-Linked
Tunisia
-
473.
312550
Retinal Dysplasia, Primary
Iraq
-
474.
313700
Androgen Receptor
Kuwait
-
475.
313900
Thrombocytopenia 1
KSA
-
476.
561000
Ribosomal RNA, Mitochondrial, 12S
?
-
477.
580000
Streptomycin Ototoxicity
?
-
478.
600060
Deafness, Neurosensory, Autosomal Recessive 2
Tunisia
-
479.
600116
Parkinson Disease, Juvenile, Autosomal Recessive
Algeria
-
480.
600118
Warburg Micro Syndrome 1
Lebanon
-
481.
600146
Spastic Paraplegia 5B, Autosomal Recessive
Tunisia
-
482.
600160
Cyclin-Dependent Kinase Inhibitor 2A
Tunisia
-
483.
600179
Guanylate Cyclase 2D, Membrane
Algeria, Tunisia
484.
600185
Breast Cancer 2 Gene
Yemen
-
485.
600252
Lowry-Maclean Syndrome
Kuwait
-
486.
600262
Prostaglandin-Endoperoxide Synthase 2
Algeria
-
487.
600266
Solute Carrier Family 11 (Proton-Coupled Divalent Metal Ion Transporter),
Sudan
Member 1
-
488.
600301
Acyl-CoA Dehydrogenase, Short/Branched Chain
Eritrea
-
489.
600360
Aplasia Cutis Congenita of Limbs, Recessive
Yemen
-
490.
600374
BBS4 Gene
KSA
-
491.
600502
Immunoglobulin MU Binding Protein 2
Lebanon
-
492.
600509
ATP-Binding Cassette, Subfamily C, Member 8
KSA
-
493.
600514
Reelin
KSA
-
494.
600529
AU-Specific RNA-Binding Protein
Morocco, Lebanon
-
495.
600617
Steroidogenic Acute Regulatory Protein
Palestine, Jordan, Kuwait
-
496.
600650
Carnitine Palmitoyltransferase II
Morocco
-
497.
600662
Mads Box Transcription Enhancer Factor 2, Polypeptide C
Oman
-
498.
600737
Inclusion Body Myopathy 2, Autosomal Recessive
Palestine
-
499.
600760
Sodium Channel, Nonvoltage-Gated 1, Beta Subunit
?
-
500.
600794
Spinal Muscular Atrophy, Distal, Type V
Algeria
-
501.
600805
Laminin, Alpha-3
KSA
-
502.
600818
Transgelin
Algeria
-
503.
600850
Schizophrenia 4
Algeria
-
504.
600863
Casein Kinase I, Epsilon
Syria
-
505.
600900
Sarcoglycan, Beta
Tunisia
-
506.
600918
Cystinuria, Type III
Libya
-
507.
600923
Protoporphyrinogen Oxidase
Lebanon
-
508.
600957
Anti-Mullerian Hormone
Morocco
-
509.
601007
Leptin Receptor
Algeria
-
510.
601015
NPC2 Gene
Algeria
-
511.
601067
Usher Syndrome, Type ID
Morocco
-
512.
601071
Deafness, Autosomal Recessive 9
Lebanon
-
513.
601105
Cathepsin K
Morocco
-
514.
601107
ATP-Binding Cassette, Subfamily C, Member 2
Morocco
-
515.
601145
Cystatin B
?
-
516.
601146
Growth/Differentiation Factor 5
Oman
-
517.
601170
Muscular Dystrophy, Congenital, with Severe Central Nervous
?
System Atrophy and Absence of Large Myelinated Fibers
-
518.
601214
Naxos Disease
?
-
519.
601277
Ichthyosis, Lamellar, 2
Morocco
-
520.
601386
Deafness, Autosomal Recessive 12
Syria
-
521.
601441
Diacylglycerol Kinase, Zeta, 104-kD
Jordan
-
522.
601451
Nevo Syndrome
?
-
523.
601537
Microcephaly, Retinitis Pigmentosa, and Sutural Cataract
Morocco
-
524.
601549
Alacrima
Jordan
-
525.
601552
Ectopia Lentis, Spontaneous Filtering Blebs, and Craniofacial Dysmorphism
Lebanon
-
526.
601553
Hypotrichosis, Congenital, with Juvenile Macular Dystrophy
Egypt
-
527.
601559
Stuve-Wiedemann Syndrome/Schwartz-Jampel Syndrome, Type 2
UAE, Oman
-
528.
601596
Charcot-Marie-Tooth Disease, Type 4C
Algeria
-
529.
601601
Transcription Factor AP2-Beta
Palestine
-
530.
601604
Interleukin 12 Receptor, Beta-1
Morocco
-
531.
601618
SRY-Box 18
Oman
-
532.
601623
Ubiquitin-Protein Ligase E3A
Iraq
-
533.
601691
ATP-Binding Cassette, Subfamily A, Member 4
KSA
-
534.
601706
Yemenite Deaf-Blind Hypopigmentation Syndrome
Yemen
-
535.
601769
Vitamin D Receptor
KSA
-
536.
601771
Cytochrome P450, Subfamily I, Polypeptide 1
Morocco, Algeria, KSA
-
537.
601843
Solute Carrier Family 5 (Sodium Iodide Symporter), Member 5
Algeria
-
538.
601993
Nuclear Receptor Coactivator 2
Oman
-
539.
602078
Fibrosis of Extraocular Muscles, Congenital, 2
KSA
-
540.
602097
Usher Syndrome, Type IE
Morocco
-
541.
602099
Amyotrophic Lateral Sclerosis 5
Tunisia
-
542.
602109
Matrilin 3
?
-
543.
602201
Extracellular Matrix Protein 1
Kuwait
-
544.
602229
SRY-Box 10
Yemen
-
545.
602247
Xanthomatosis, Susceptibility to
Syria
-
546.
602302
Hairless, Mouse, Homolog of
Palestine, Oman
-
547.
602337
Receptor Tyrosine Kinase-Like Orphan Receptor 2
Oman
-
548.
602400
Ichthyosis, Follicular Atrophoderma, Hypotrichosis, and Hypohidrosis
UAE
-
549.
602401
Ectodermal Dysplasia, Hidrotic, Autosomal Recessive
Lebanon
-
550.
602419
Early Growth Response 3
Syria
-
551.
602421
Cystic Fibrosis Transmembrane Conductance Regulator
?
-
552.
602459
Deafness, Autosomal Dominant Nonsyndromic Sensorineural 15
Tunisia, Libya, Egypt
-
553.
602544
Parkin
Algeria
-
554.
602557
Spondyloepimetaphyseal Dysplasia, Shohat Type
Iraq
-
555.
602574
Tectorin, Alpha
Lebanon
-
556.
602593
Corneodesmosin
Yemen
-
557.
602643
Tumor Necrosis Factor Receptor Superfamily, Member 11B
Iraq
-
558.
602753
Aristaless Homeo Box, Drosophila, Homolog of
KSA
-
559.
602768
Delta-Like 3
?
-
560.
602956
X-Ray Repair, Complementing Defective, in Chinese Hamster, 9
Lebanon
-
561.
602976
Max-Like Protein X
Egypt
-
562.
603009
Dysferlin Libya, Palestine,
Yemen
-
563.
603033
Collagenic Tail of Endplate Acetylcholinesterase
Palestine, Iraq
-
564.
603034
Endplate Acetylcholinesterase Deficiency
Palestine, Iraq
-
565.
603098
Deafness, Autosomal Recessive 13
Lebanon
-
566.
603133
Dislocated Elbows, Bowed Tibias, Scoliosis, Deafness, Cataract,
Lebanon
Microcephaly, and Mental Retardation
-
567.
603194
Meckel Syndrome, Type 2
Tunisia
-
568.
603266
Diabetes Mellitus, Insulin-Dependent, 17
?
-
569.
603335
Dynein, Axonemal, Heavy Chain 5
Lebanon
-
570.
603400
WNT1-Inducible Signaling Pathway Protein 3
Jordan, KSA
-
571.
603438
Radioulnar Synostosis with Short Stature, Microcephaly, Scoliosis,
?
and Mental Retardation
-
572.
603552
Hemophagocytic Lymphohistiocytosis, Familial, 1
KSA
-
573.
603554
Omenn Syndrome
Morocco
-
574.
603557
Myotubularin-Related Protein 2
KSA
-
575.
603593
Solute Carrier Family 7, Member 7
Tunisia
-
576.
603629
Deafness, Autosomal Recessive 21
Lebanon
-
577.
603642
Atrial Septal Defect, Secundum, with Various Cardiac and Noncardiac Defects
Lebanon
-
578.
603650
Bardet-Biedl Syndrome 5
Kuwait, KSA
-
579.
603678
Deafness, Autosomal Recessive 14
Lebanon
-
580.
603681
Otoferlin
Lebanon
-
581.
603707
Molybdenum Cofactor Synthesis 1
?
-
582.
603708
Molybdenum Cofactor Synthesis 2
Egypt
-
583.
603720
Deafness, Autosomal Recessive 16
Palestine, Syria
-
584.
603813
Hypercholesterolemia, Autosomal Recessive
Syria
-
585.
603824
UDP-N-Acetylglucosamine 2-Epimerase/N-Acetylmannosamine Kinase
Palestine
-
586.
603868
Ras-Associated Protein RAB27A
?
-
587.
603896
Leukoencephalopathy with Vanishing White Matter
Algeria
-
588.
603903
Sickle Cell Anemia
Oman
-
589.
603968
Polymerase, DNA, ETA
Lebanon
-
590.
604032
Eukaryotic Translation Initiation Factor 2-Alpha Kinase 3
Tunisia
-
591.
604110
G Protein-Coupled Receptor 56
Palestine, Qatar
-
592.
604144
Solute Carrier Family 7, Member 9
Libya
-
593.
604161
G Protein-Coupled Receptor 54
KSA
-
594.
604201
Hepatic Fibrosis, Severe, Susceptibility to, due to Schistosoma Mansoni Infection
Sudan
-
595.
604228
Partial Albinism and Immunodeficiency Syndrome
KSA
-
596.
604232
Leber Congenital Amaurosis, Type III
KSA
-
597.
604320
Spinal Muscular Atrophy with Respiratory Distress 1
Lebanon
-
598.
604321
Microcephaly, Primary Autosomal Recessive, 4
Morocco
-
599.
604327
Xylosylprotein 4-Beta-Galactosyltransferase, Polypeptide 7
?
-
600.
604490
Sacsin
Tunisia
-
601.
604559
Progressive Familial Heart Block, Type I, Locus 1
Lebanon
-
602.
604563
Charcot-Marie-Tooth Disease, Type 4B2
Tunisia
-
603.
604571
Bare Lymphocyte Syndrome, Type I
Morocco
-
604.
604595
Cholesterol-Lowering Factor
Syria
-
605.
604611
RECQ Protein-Like 2
Syria
-
606.
604780
Comparative Gene Identification 58
Morocco, Algeria, Tunisia
-
607.
604801
Muscular Dystrophy, Congenital, 1B
UAE
-
608.
604934
Tubulin-Specific Chaperone E
?
-
609.
605156
Nodulosis-Arthropathy-Osteolysis Syndrome
KSA
-
610.
605195
Mesoderm Posterior 2
Lebanon
-
611.
605203
Multiple Pterygium Syndrome, Aslan Type
Qatar
-
612.
605225
Inflammatory Bowel Disease 7
Iraq
-
613.
605239
ATPase, H+ Transporting, Lysosomal, V0 Subunit A, Isoform 4
KSA
-
614.
605242
USH1C Gene
Lebanon
-
615.
605248
Mucolipin 1
?
-
616.
605316
Deafness, Congenital Neurosensory, Autosomal Recessive 10
Palestine
-
617.
605378
Aladin
Algeria
-
618.
605379
Gigaxonin
Tunisia
-
619.
605511
Transmembrane Protease, Serine 3
Tunisia, Palestine
-
620.
605573
17-@Beta Hydroxysteroid Dehydrogenase III
Syria
-
621.
605588
Charcot-Marie-Tooth Disease, Axonal, Type 2B1
Morocco, Algeria
-
622.
605597
Forkhead Transcription Factor FOXL2
Algeria
-
623.
605646
Solute Carrier Family 26, Member 4
Tunisia
-
624.
605678
Williams-Beuren Syndrome Chromosome Region 14
Egypt
-
625.
605685
Cutis Verticis Gyrata, Retinitis Pigmentosa, and Sensorineural Deafness
Lebanon
-
626.
605725
Periaxin
Lebanon
-
627.
605726
Neuropathy, Distal Hereditary Motor, Jerash Type
Jordan
-
628.
605747
Autosomal Recessive Hypercholesterolemia Gene
Lebanon, Syria
-
629.
605799
Amnionless, Mouse, Homolog of
Tunisia
-
630.
605818
Deafness, Autosomal Recessive 27
UAE
-
631.
605822
Spondyloocular Syndrome, Autosomal Recessive
Iraq
-
632.
605828
Epidermodysplasia Verruciformis Gene 1
Algeria
-
633.
605829
Epidermodysplasia Verruciformis Gene 2
Algeria
-
634.
605881
GDP-Fucose Transporter 1
?
-
635.
605899
Glycine Encephalopathy
?
-
636.
605908
Megalencephalic Leukoencephalopathy with Subcortical Cysts Gene 1
Libya
-
637.
606054
Propionicacidemia
KSA
-
638.
606119
Secreted Ly6/uPAR-Related Protein 1
Algeria, Tunisia, Palestine,
UAE
-
639.
606125
Tripartite Motif-Containing Protein 8
Egypt
-
640.
606158
BerardinellI-Seip Congenital Lipodystrophy Gene 2
Lebanon
-
641.
606201
Wolfram Syndrome Gene 1
KSA
-
642.
606220
Mental Retardation, Short Stature, Facial Anomalies, and Joint Dislocations
Lebanon
-
643.
606324
Parkinson Disease, Type 7, Autosomal Recessive Early-Onset
Lebanon
-
644.
606352
Alsin
Tunisia, Kuwait
645.
606397
USH3A Gene
Yemen
-
646.
606412
BSND Gene
Lebanon
-
647.
606416
CIAS1 Gene
Algeria
-
648.
606438
Huntington Disease-Like 2
Morocco, KSA
-
649.
606463
Glucosidase, Acid Beta
Lebanon, KSA
-
650.
606527
Megarbane Syndrome
Iraq
-
651.
606530
Cytochrome P450, Subfamily XXVIIa, Polypeptide 1
Morocco
-
652.
606545
Ichthyosis, Lamellar, 5
?
-
653.
606555
Tripartite Motif-Containing Protein 9
Egypt
-
654.
606556
Tripartite Motif-Containing Protein 14
Egypt
-
655.
606559
Tripartite Motif-Containing Protein 22
Egypt
-
656.
606580
Optic Atrophy 3 Gene
Iraq
-
657.
606596
Fukutin-Related Protein
Algeria, Tunisia, Libya
-
658.
606597
Paired Box Gene 3
Yemen
-
659.
606598
Ganglioside-Induced Differentiation-Associated Protein 1
Morocco, Tunisia
-
660.
606612
Muscular Dystrophy, Congenital, 1C
Algeria, Tunisia
-
661.
606693
Parkinson Disease 9
Jordan
-
662.
606709
Protease, Serine, 12
Algeria
-
663.
606744
Seckel Syndrome 2
Iraq
-
664.
606808
Myosin IIIA
Iraq
-
665.
606810
Proline Dehydrogenase
Algeria
-
666.
606824
Glucose/Galactose Malabsorption
Iraq
-
667.
606844
Alstrom Syndrome Gene
Algeria
-
668.
606854
Polymicrogyria, Bilateral Frontoparietal
Palestine
-
669.
606869
Hexosaminidase A
Morocco, Algeria,
Lebanon, Iraq
-
670.
606873
Hexosaminidase B
?
-
671.
606879
Phosphoglycerate Dehydrogenase
Morocco
-
672.
606883
Interleukin 1 Receptor-Associated Kinase 4
KSA
-
673.
606897
Lysosomal Trafficking Regulator
Kuwait
-
674.
606937
Cerebellar Ataxia with Mental Retardation, Optic Atrophy, and Skin Abnormalities
Lebanon
-
675.
606943
Usher Syndrome, Type IG
Tunisia, Palestine, Jordan
-
676.
606945
Low Density Lipoprotein Receptor
Algeria, Lebanon, Syria,
Kuwait, Bahrain
-
677.
607009
Transient Receptor Potential Cation Channel, Subfamily M, Member 6
?
-
678.
607038
Otoancorin
Palestine, Lebanon,
Jordan, Yemen
-
679.
607039
Deafness, Autosomal Recessive 22
Palestine
-
680.
607042
CLN3 Gene
Morocco
-
681.
607059
Solute Carrier Family 39 (Zinc Transporter), Member 4
Tunisia, Egypt
-
682.
607067
Saitohin
Algeria
-
683.
607084
Deafness, Autosomal Recessive 31
Palestine, Jordan
-
684.
607088
Spinal Muscular Atrophy, Chronic Distal, Autosomal Recessive
Lebanon
-
685.
607095
Anauxetic Dysplasia
Jordan
-
686.
607101
Deafness, Autosomal Recessive 30
Iraq
-
687.
607131
Macrocephaly with Multiple Epiphyseal Dysplasia and Distinctive Facies
Oman
-
688.
607139
Fanconi Anemia Complementation Group A Gene
Morocco, Tunisia
-
689.
607155
Muscular Dystrophy, Limb-Girdle, Type 2I
Tunisia
-
690.
607198
Tyrosyl-DNA Phosphodiesterase 1
KSA
-
691.
607239
Deafness, Autosomal Recessive 33
Jordan
-
692.
607250
Spinocerebellar Ataxia, Autosomal Recessive, with Axonal Neuropathy
KSA
-
693.
607306
Steroid 5-Alpha-Reductase 2
Lebanon
-
694.
607358
Autoimmune Regulator
Egypt
-
695.
607473
Vitamin K-Dependent Clotting Factors, Combined Deficiency of, 2
Lebanon
-
696.
607483
Basal Ganglia Disease, Biotin-Responsive
Syria, Yemen
-
697.
607564
Tripartite Motif-Containing Protein 6
Egypt
-
698.
607574
Arylsulfatase A
Lebanon, KSA
-
699.
607584
Spastic Paraplegia 24, Autosomal Recessive
KSA
-
700.
607585
Ataxia-Telangiectasia Mutated Gene
Morocco, Tunisia, Palestine
-
701.
607590
BBS7 Gene
KSA
-
702.
607608
Sphingomyelin Phosphodiesterase 1, Acid Lysosomal
Morocco, Algeria, Tunisia,
KSA
-
703.
607624
Griscelli Syndrome, Type 2
?
-
704.
607625
Niemann-Pick Disease, Type C2
Algeria
-
705.
607626
Ichthyosis, Leukocyte Vacuoles, Alopecia, and Sclerosing Cholangitis
Morocco
-
706.
607690
Sar1a, S. Cerevisiae, Homolog 2
Algeria
-
707.
607694
Leukodystrophy With Oligodontia
Syria
-
708.
607696
USH1G Gene
Tunisia, Jordan
-
709.
607697
Set-Binding Factor 2
Morocco, Tunisia
-
710.
607731
Charcot-Marie-Tooth Disease, Axonal, Type 2H
Tunisia
-
711.
607739
Charcot-Marie-Tooth Disease, Type 4B2, With Early-Onset Glaucoma
Morocco, Tunisia
-
712.
607759
Integrin, Alpha-2B
Iraq
-
713.
607764
3-@Beta-Hydroxy-Delta-5-C27-Steroid Oxidoreductase
KSA
-
714.
607765
Cholestasis, Progressive Familial Intrahepatic 4
KSA
-
715.
607800
ATP-Binding Cassette, Subfamily A, Member 12
Morocco, Algeria
-
716.
607812
Craniolenticulosutural Dysplasia
KSA
-
717.
607817
COH1 Gene
Lebanon, Oman
-
718.
607831
Charcot-Marie-Tooth Disease, Axonal, Type 2K
Morocco
-
719.
607868
Tripartite Motif-Containing Protein 11
Egypt
-
720.
607900
Kindlin 1
Oman
-
721.
607928
Whirlin
Jordan
-
722.
608027
Cerebellar Atrophy with Progressive Microcephaly
Oman
-
723.
608034
Aspartoacylase
?
-
724.
608041
Anthrax Toxin Receptor 2
Morocco
-
725.
608091
Cerebellooculorenal Syndrome 2
UAE
-
726.
608097
Heterotopia, Periventricular, Autosomal Recessive
Yemen
-
727.
608107
Familial Mediterranean Fever Gene
Morocco, Lebanon,
Jordan, Iraq
-
728.
608115
Ovarian Hyperstimulation Syndrome
Morocco
-
729.
608132
Tetratricopeptide Repeat Domain 8
KSA
-
730.
608154
Lipodystrophy, Generalized, with Mental Retardation, Deafness,
Oman
Short Stature, and Slender Bones
-
731.
608156
Nablus Mask-Like Facial Syndrome
Palestine
-
732.
608207
Kala-Azar, Susceptibility to
Sudan
-
733.
608222
Adenylosuccinate Lyase
Morocco
-
734.
608358
Myopathy, Myosin Storage
KSA
-
735.
608367
Myopia 4
Algeria
-
736.
608395
Karak Syndrome
Jordan
-
737.
608443
Mental Retardation, Nonsyndromic, Autosomal Recessive, 3
?
-
738.
608465
Senataxin
Algeria
-
739.
608487
Tripartite Motif-Containing Protein 5
Egypt
-
740.
608509
Alopecia Universalis Congenita, XY Gonadal Dysgenesis, and Laryngomalacia
Jordan
-
741.
608515
Neutrophil Cytosolic Factor 2
Palestine, Jordan
-
742.
608547
Vitamin K Epoxide Reductase Complex, Subunit 1
Lebanon
-
743.
608585
Brachial Palsy, Familial Congenital
Egypt
-
744.
608630
Roundabout, Drosophila, Homolog of, 3
?
-
745.
608637
Spondyloepiphyseal Dysplasia, Omani Type
Oman
-
746.
608653
Deafness, Autosomal Recessive 32
Tunisia
-
747.
608681
Spondylocostal Dysostosis, Autosomal Recessive 2
Lebanon
-
748.
608728
Spondyloepimetaphyseal Dysplasia, Matrilin-3 Related
?
-
749.
608801
Glutaryl-CoA Dehydrogenase
?
-
750.
608845
ADP-Ribosylation Factor-Like 6
?
-
751.
608911
Choanal Atresia, Posterior
Yemen
-
752.
608931
Myasthenic Syndrome, Congenital, Associated with Acetylcholine Receptor Deficiency Iraq

http://www.cags.org.ae/cbc02ga.pdf




-----------------------------------


Medical genetics of Jews

 https://en.wikipedia.org/wiki/Medical_genetics_of_Jews

The medical genetics of Jews is the study, screening, and treatment of genetic disorders more common in particular Jewish populations than in the population as a whole.[1] The genetics of Ashkenazi Jews have been particularly well-studied, resulting in the discovery of many genetic disorders associated with this ethnic group. In contrast, the medical genetics of Sephardic Jews and Mizrahi Jews are more complicated, since they are more genetically diverse and consequently no genetic disorders are more common in these groups as a whole; instead, they tend to have the genetic diseases common in their various countries of origin.[1][2] Several organizations, such as Dor Yeshorim,[3] offer screening for Ashkenazi genetic diseases, and these screening programs have had a significant impact, in particular by reducing the number of cases of Tay–Sachs disease.
Ashkenazi diseases

The most detailed genetic analysis study of Ashkenazi was published in September 2014 by Shai Carmi and his team at Columbia University.[14] The results of the detailed study show that today's 10 million Ashkenazi Jews descend from a population of only 350 individuals who lived about 600–800 years ago. That population derived from both Europe and the Middle East.[15] There is evidence that the population bottleneck may have allowed deleterious alleles to become more prevalent in the population due to genetic drift.[16] As a result, this group has been particularly intensively studied, so many mutations have been identified as common in Ashkenazis.[17] Of these diseases, many also occur in other Jewish groups and in non-Jewish populations, although the specific mutation which causes the disease may vary between populations. For example, two different mutations in the glucocerebrosidase gene causes Gaucher's disease in Ashkenazis, which is their most common genetic disease, but only one of these mutations is found in non-Jewish groups.[4] A few diseases are unique to this group; for example, familial dysautonomia is almost unknown in other populations.[4]
Genetic disorders common in Ashkenazi Jews[1]


Genetic disorders common in Ashkenazi Jews[1]
Disease Mode of inheritance Gene Carrier frequency
 Favism X-linked G6PD
 Bloom syndrome Autosomal recessive BLM 1/100
 Breast cancer and ovarian cancer Autosomal dominant BRCA1 or BRCA2 1/100 and 1/75, respectively
 Canavan disease Autosomal recessive ASPA 1/60
 Congenital deafness Autosomal recessive GJB2 or GJB6 1/25
 Cystic fibrosis Autosomal recessive CFTR 1/25
 Haemophilia C Autosomal recessive F11 1/12
 Familial dysautonomia Autosomal recessive IKBKAP 1/30
 Familial hypercholesterolemia Autosomal dominant LDLR 1/69
 Familial hyperinsulinism Autosomal recessive ABCC8 1/125–1/160
 Fanconi anemia C Autosomal recessive FACC 1/100
 Gaucher disease Autosomal recessive GBA 1/7–1/18
 Glycogen Storage Disease type 1a Autosomal recessive G6PC 1/71
 Mucolipidosis IV Autosomal recessive MCOLN1 1/110
 Niemann–Pick (type A) Autosomal recessive SMPD1 1/90
 Nonclassical 21 OHase deficiency Autosomal recessive CPY21 1/6
 Parkinson's disease Autosomal dominant LRRK2 1/42[18]
 Tay–Sachs Autosomal recessive HEXA 1/25–1/30
 Torsion dystonia Autosomal dominant DYT1 1/4000
 Usher syndrome Autosomal recessive PCDH15 1/72

Tay–Sachs disease

Tay–Sachs disease, which can present as a fatal illness of children that causes mental deterioration prior to death, was historically more prevalent among Ashkenazi Jews, although high levels of the disease are also found in some Pennsylvania Dutch, southern Louisiana Cajun, and eastern Quebec French Canadian populations.[20] Since the 1970s, however, proactive genetic testing has been quite effective in eliminating Tay–Sachs from the Ashkenazi Jewish population.

Lipid transport diseases

Gaucher's disease, in which lipids accumulate in inappropriate locations, occurs most frequently among Ashkenazi Jews; the mutation is carried by roughly one in every 15 Ashkenazi Jews, compared to one in 100 of the general American population. Gaucher's disease can cause brain damage and seizures, but these effects are not usually present in the form manifested among Ashkenazi Jews; while sufferers still bruise easily, and it can still potentially rupture the spleen, it generally has only a minor impact on life expectancy.

Ashkenazi Jews are also highly affected by other lysosomal storage diseases, particularly in the form of lipid storage disorders. Compared to other ethnic groups, they more frequently act as carriers of mucolipidosis[24] and Niemann–Pick disease, the latter of which can prove fatal.

The occurrence of several lysosomal storage disorders in the same population suggests the alleles responsible might have conferred some selective advantage in the past. This would be similar to the hemoglobin allele which is responsible for sickle-cell disease, but solely in people with two copies; those with just one copy of the allele have a sickle cell trait and gain partial immunity to malaria as a result. This effect is called heterozygote advantage.

Some of these disorders may have become common in this population due to selection for high levels of intelligence (see Ashkenazi intelligence). However, other research suggests no difference is found between the frequency of this group of diseases and other genetic diseases in Ashkenazis, which is evidence against any specific selectivity towards lysosomal disorders.

Familial dysautonomia


Diseases inherited in an autosomal recessive pattern often occur in endogamous populations. Among Ashkenazi Jews, a higher incidence of specific genetic disorders and hereditary diseases have been verified, including:

Non-Ashkenazi disorders

In contrast to the Ashkenazi population, Sephardic and Mizrahi Jews are much more divergent groups, with ancestors from Spain, Portugal, Morocco, Tunisia, Algeria, Italy, Libya, the Balkans, Iran, Iraq, India, and Yemen, with specific genetic disorders found in each regional group, or even in specific subpopulations in these regions.

Genetic disorders common in Sephardic and Mizrahi Jews
Disease Mode of inheritance Gene or enzyme Carrier frequency Populations
 Oculocutaneous albinism Autosomal recessive TYR 1/30 Morocco
 Ataxia telangiectasia Autosomal recessive ATM 1/80 Morocco, Tunisia
 Creutzfeldt–Jakob disease Autosomal dominant PRNP 1/24,000 Libya
 Cerebrotendinous xanthomatosis Autosomal recessive CYP27A1 1/70 Morocco
Cystinuria Autosomal recessive SLC7A9 1/25 Libya
Familial Mediterranean fever Autosomal recessive MEFV 1/5–7 All MENA (Middle Eastern and North African countries).
 Glycogen storage disease III Autosomal recessive AGL 1/35 Morocco, North Africa
 Limb girdle muscular dystrophy Autosomal recessive DYSF 1/10 Libya
 Tay–Sachs Autosomal recessive HEXA 1/110 Morocco
 11-β-hydroxylase deficiency Autosomal recessive CYP11B1 1/30–1/128 Morocco
 
 
 
                                           Genetic disorders common in Mizrahi Jews

 
Disease Mode of inheritance Gene or enzyme Carrier frequency Populations
 Beta-thalassemia Autosomal recessive HBB 1/6 Iran, Iraq, Kurdistan
 Factor VII deficiency Autosomal recessive F7 1/40 Iran
 Familial Mediterranean fever Autosomal recessive, but heterozygous carriers also can show clinical manifestations. MEFV 1/5–1/7 Iraq, Iran, Armenia, North African Jews, Ashkenazi[49]
 Glucose-6-phosphate dehydrogenase deficiency X-linked G6PD 1/4 Iraq, esp. Kurdistan, Syria and all MENA countries. Female heterozygotes can also show clinical symptoms due to lyonization (X-inactivation) especially during pregnancy.[50]
 Inclusion body myopathy Autosomal recessive GNE 1/12 Iran
 Metachromatic leukodystrophy Autosomal recessive ARSA 1/50 Yemen
 Oculopharyngeal muscular dystrophy Autosomal, recessive or dominant PABPN1 1/7 Bukhara
 Phenylketonuria Autosomal recessive PAH 1/35 Yemen

https://en.wikipedia.org/wiki/Medical_genetics_of_Jews



-----------------------------------------------------



Ashkenazi Jewish Genetic Panel (AJGP) - What Are Ashkenazi Jewish Genetic Diseases?


Ashkenazi Jewish genetic diseases are a group of rare disorders that occur more often in people of Eastern European (Ashkenazi) Jewish heritage than in the general population. Even though most of these diseases are severe and can cause early death, some can be treated to reduce symptoms and prolong life. Some of these diseases can be found during pregnancy through chorionic villus sampling (CVS) or amniocentesis. This testing is done usually if one or both parents are carriers of a genetic disease.

Diseases in this group include:

    Bloom syndrome. Babies with this disease are born small and remain shorter than normal as they grow. Their skin may look red, and they have more lung and ear infections than children normally have.
    Canavan disease. This disease gradually destroys brain tissue.
    Cystic fibrosis. This disease causes very thick mucus in the lungs and problems with digesting food.
    Familial dysautonomia (FD). People with this problem cannot feel pain, they sweat a lot, and they have trouble with speech and coordination.
    Fanconi anemia. People with this problem do not have enough blood cells and have problems with the heart, kidneys, arms, or legs. They also are more likely to get cancer.
    Gaucher disease. This disease causes a type of fat called glucocerebroside to build up in certain cells of the liver, spleen, and bone marrow.
    Mucolipidosis IV. This problem causes the nervous system to deteriorate, or break down, over time.
    Niemann-Pick disease (type A). This disease causes a type of fat called sphingomyelin to build up in cells of the liver, spleen, lymph nodes, and bone marrow.
    Tay-Sachs disease. This disease causes a type of fat called ganglioside to build up in the cells of the brain and nervous system.
    Torsion dystonia. People with this problem have ongoing spasms that twist the muscles in their arms, legs, and sometimes their body. Testing for this condition may not always be done.

About 1 out of 4 people of Ashkenazi Jewish heritage is a carrier of one of these genetic conditions, most commonly of Gaucher disease, cystic fibrosis, Tay-Sachs disease, familial dysautonomia, or Canavan disease.1


 http://www.webmd.com/children/tc/ashkenazi-jewish-genetic-panel-ajgp-what-are-ashkenazi-jewish-genetic-diseases



-----------------------------


Jewish Genetic Disease Consortium (JGDC)
Sephardic and Mizrahi Diseases

There is no single preconception carrier-screening panel for people of Sephardic or Mizrahi background. Carrier screening is dependent upon country of origin. People of Sephardic or Mizrahi background should seek genetic counseling.


http://www.jewishgeneticdiseases.org/jewish-genetic-diseases/



---------------------------------



All About Genetic Diseases That Strike Sephardic Jews


 The Forward Staff has compiled a guide to the most common heritable “Sephardic Jewish diseases,” with information on symptoms, causes and carrier rates for each, as well as the geographic regions from which affected Jewish populations originate.


These diseases are mostly caused by recessive genetic mutations, meaning that mutations must be present in both copies (alleles) of the gene for the associated condition to be expressed. When both parents carry a given mutation, each child of theirs has a 25% of developing the associated disease. This is why couples with at least one partner of Sephardic or Mizrahi origin are encouraged to undergo screening if they plan to have children.


Unlike Ashkenazi Jews, who share ethnic commonalities regardless of country of origin,” Sephardi” is a broad label. Subgroups like Moroccan Jews or Iranian Jews have distinct characteristics, making universal screening panels for inherited genetic diseases for all Sephardic and Mizrahi Jews impractical. Therefore, it’s best to discuss one’s family heritage with a doctor or genetic counselor in order to receive screening recommendations.


The Sephardic Health Organization for Referral and Education recommends that non-Ashkenazi Jewish couples get tested for the 19 most common Ashkenazi Jewish diseases as well — because some of the diseases, such as cystic fibrosis and spinal muscular atrophy, can also be found among non-Ashkenazi populations. Screenings usually require blood samples.

Data on the estimated carrier frequency and the affected Jewish population are courtesy of the Jewish Genetic Disease Consortium in New York.


Dr. Adele Schneider, the medical director of the Einstein Victor Center for the Prevention of Jewish Genetic Diseases in Philadelphia, Pennsylvania, has contributed to this section.


   (1) Alpha Thalassemia

   (2) Ataxia Telangiectasia

   (3) Beta Thalassemia

   (4) Corticosterone Methyloxidase Type 2 Deficiency

   (5) Costeff Optical Atrophy

   (6) Cystic Fibrosis

   (7) Familial Mediterranean Fever

   (8) Glycogen Storage Disease Type 3

   (9) G6PD Deficiency

   (10) Hereditary Inclusion Body Myopathy

   (11) Limb-Girdle Muscular Dystrophy Type 2B

   (12) Metachromatic Leukodystrophy

   (13) Normophosphatemic Familial Tumoral Calcinosis

   (14) Polyglandular Deficiency Syndrome

   (15) Pseudocholinesterase Deficiency

   (16) Spinal Muscular Atrophy Type 1A

   (17) Wolman's Disease



http://forward.com/culture/203321/all-about-genetic-diseases-that-strike-sephardic-j/



-----------------------------------------------


Genetic Diseases

Jewish

There are several genetic disease mutations that occur at increased frequencies in the Ashkenazi Jewish (Central & Eastern European), Sephardi Jewish (Southern European and Northern African), and Mizrahi Jewish (Middle Eastern/Arab) populations. The Mount Sinai Comprehensive Jewish Carrier Screening Panel covers 96 conditions that fall into this category. Some disorders are specific to one of the 3 sub-populations; however, there are certain diseases that are relevant to all Jewish sub-groups. Because these disorders are inherited in an autosomal recessive or X-linked manner, if you are of Jewish descent you may be at risk for being a carrier for a genetic disorder without even knowing it. Some of the most common diseases are listed below.
Abetalipoproteinemia
Alport Syndrome
Arthrogryposis Multiplex Congenita
Bardet-Biedl Syndrome
Bloom Syndrome
Canavan Disease
Carnitine Palmitoyltransferase II Deficiency
Congenital Amegakaryocytic Thrombocytopenia
Congenital Disorder of Glycosylation Ia
Dyskeratosis Congenita
Ehlers-Danlos VIIC
Familial Dysautonomia
Familial Hyperinsulinism
Fanconi Anemia
Galactosemia (also more frequent among people of Irish descent)
Gaucher Disease (Type I)
Glycogen Storage Disease Type 1a
Joubert Syndrome 2
Lipoamide Dehydrogenase Deficiency (E3)
Maple Syrup Urine Disease
Mucolipidosis Type IV
Nemaline Myopathy
Niemann-Pick Type A
3-Phospoglycerate Dehydrogenase Deficiency
Polycystic Kidney Disease
Retinitis Pigmentosa 59
Smith-Limli-Opitz Syndrome
Spinal Muscular Atrophy
Tay-Sachs Disease (also more frequent among French Canadians, Cajuns, and people of Irish/British descent)
Tyrosinemia I (also more frequent in Norwegians, Finnish, French Canadians)
Usher Syndrome (IF & III)
Walker-Warburg Syndrome
Wilson Disease
Zellweger Syndrome

http://www.geneticdiseasefoundation.org/genetic-diseases/

-----

The population genetics of the Jewish people

Oct 2012

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3543766/

----

Creutzfeldt-Jakob Disease among Libyan Jews

Sep 1991

https://www.jstor.org/stable/3520745?seq=1#page_scan_tab_contents

-------------------

Jewish Genetics: 75% of Jews Are Lactose Intolerant and 11 Other Facts

July 8, 2015

Almost half of Ashkenazim carry at least one of 38 genetic diseases, and our closest genetic relatives are Druze, Bedouin, Palestinians - and Italians.

Is there such a thing as a “Jewish gene”? No, there isn't.

http://www.haaretz.com/israel-news/science/.premium-1.664967


-----------------------


Genetic studies on Arabs

The Centre for Arab Genomic Studies (CAGS) oversees genetic analyses on the populations of the Arab world. Based in Dubai, United Arab Emirates, it indicates that Arab countries have among the highest rates of genetic disorders in the world. Some 906 pathologies are endemic to the Arab states, including thalassaemia, Tourette's syndrome, Wilson's disease, Charcot-Marie-Tooth disease, mitochondrial encephalomyopathies and Niemann-Pick disease.


Genetic diseases Databases in Arabic countries and studies

Several organizations maintain genetic databases for each Arabic country. The Centre for Arab Genomic Studies (CAGS) is the main organization based in the United Arab Emirates. It initiated a pilot project to construct the Catalogue for Transmission Genetics in Arabs (CTGA) database for genetic disorders in Arab populations. At present, the CTGA database is centrally maintained in Dubai, and hosts entries for nearly 1540 Mendelian disorders and related genes. This number is increasing as researchers are joining the largest Arab scientific effort to define genetic disorders described in the region. The Center promotes research studies on these emergent disorders. Some of the genetic disorders endemic to the Arab world are: hemoglobinopathy, sickle cell anemia, glucose-6-phosphate dehydrogenase deficiency, and fragile X syndrome (FXS), which is an inherited genetic condition with critical consequences. The Centre provide information about specific countries, and maintain a list of Genomic diseases.

Specific rare autosomal recessive diseases are high in Arabic countries like Bardet Biedl syndrome, Meckel syndrome, congenital chloride diarrhea, severe childhood autosomal recessive muscular dystrophy (SMARMD) Lysosomal storage diseases and PKU are high in the Gulf states. Dr Teebi's book provides detailed information and by country. Even the Middle East respiratory syndrome coronavirus (MERS-CoV) that was first identified in Saudi Arabia last year, it has infected 77 people, mostly in the Middle East and Europe. Forty of them - more than half - have died. But MERS is not yet a pandemic, could become pervasive in genetic disease patient.

Dr Thurman' guidebook about Rare genetic diseases  another book Arabic genetic disorders layman guide Suadi Journal article about genetic diseases in Arabic countries The highest proportion of genetic disorders manifestations are: congenital malformations followed by endocrine metabolic disorders and then by Neuron disorders (such as Neuromotor disease)and then by blood immune disorders and then neoplasms. The Mode of Inheritance is mainly autosomal recessive followed by autosomal dominant. Some of the diseases are beta-thalassemia mutations, sickle-cell disease, congenital heart-disease, glucose-6-phosphate dehydrogenase deficiency, alpha-thalassemia, molecular characterization, recessive osteoperosis, gluthanione-reducatsafe DEf. A study about sickle cell anemia in Arabs article about Birth defects  6Glucose Phisphate isomere deficiency responsible for unexpected hemolytic episodes. one of late Dr Teebi's syndromes. flash cards guide. NY times article In Palestinian Arabs study study about potential on pharmacology  another study on Arab Palestinians Database of Genetic disorders in Arabs study In Palestinians[26] new general study about databases Database for B thalassemia in Arabs Israeli National genetic bank contains genetic mutations of Arabs Teebi database 2002  2010 genes responsible for genetic diseases among Palestinian Arabs The next Pan-Arab conference Nov 2013


 https://en.wikipedia.org/wiki/Genetic_studies_on_Arabs


---------------


Genetic disease in the Arab world

 Oct, 2006


 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1618432/


-------------------


Sickle-cell Anemia and Consanguinity among the Saudi Arabian Population


June 15, 2016


Abstract

Sickle Cell Disease (SCD) is one of the most common severe autosomal recessively inherited blood disorders. In Saudi Arabia, the prevalence of this disease is significantly varied in different regions of the country, and the highest prevalence in the Eastern province of the country. A consanguineous marriage has been linked to the high incidence and prevalence of Sickle Cell Anemia (SCA), which, accounts more than 50%, with the rate of marriage between first cousins ranging from 40% to 50%. However, the last few years showed no increase in the prevalence of sickle cell disease among Saudi’s. This might be related to the remarkable scientific progress in the understanding of the complex pathophysiology of the disease, improving knowledge regarding SCA among community, better medical care, and the efforts of Saudi’s government to provide genetic counselling services and implementing of mandatory premarital screening program. This review therefore is about the epidemiology, history of SCA among Saudi’s, clinical complications, and consanguinity marriage and SCA, with a focus on its local premarital screening program.



http://www.archivesofmedicine.com/medicine/sicklecell-anemia-and-consanguinity-among-the-saudi-arabian-population.php?aid=9701


----------------


Sickle Cell Anemia: It's Not a 'Black Disease'
How Sickle Cell is Acquired - Inheritance

As we've become more knowledgeable about sickle cell anemia we've discovered that it is not infectious but rather genetic. In other words you can't get sickle cell from exposure to a toxin, infection, virus, or parasite. People with sickle cell are born with the disease. It is inherited when parents pass it on to their children.
Location of Sickle Cell Carriers
Sickle Cell in the United States

We've also discovered that sickle cell is, in the United States, very prevalent among dark skinned people and almost completely absent in "white" populations. This is why sickle cell anemia has been, for a very long time, associated with people of dark skin color. This association has been based on the partially correct assumption that sickle cell originates in Africa and those who are of African descent (and therefore very often dark skinned) are the only people who can carry the gene for the disease and pass it on genetically.
Sickle Cell in the World

While it is true that sickle cell is very prevalent in much of Africa it is entirely untrue that it is confined just to that region. In fact sickle cell is prevalent in parts of all of the following areas:

    Africa
    Mediterranean countries (such as Greece, Turkey, and Italy)
    The Arabian peninsula
    India
    Spanish-speaking regions (South America, Central America, and parts of the Caribbean)

In each region both dark and light skinned people have been found to be sickle cell carriers. The explanation for this particular distribution lies in explanation for the survival of sickle cell over time.


 http://www.netwellness.org/healthtopics/sicklecell/sicklecellblackdisease.cfm


----------


The epidemiology of thyroid diseases in the Arab world: A systematic review


2015


 The  review  showed that the prevalence of different types of thyroid disease varied between the

reported studies in  Arab world ranging from 6.18 to 47.34% prevalence of goiter  reported  by

several studies conducted in Arab world, such as Egypt, Algeria and Bahrain with 25.25,  86  and  1.7%, respectively. Gender,  dietary  factors,  iodine  deficiency, family history, diabetes and x-ray radiation were reported as risk factors associated with different type of thyroid diseases.


The most prevalence of thyroid disease was concluded to be thyroid lesions which varied in different  regions of Arab and the burden of thyroid  cancer is very high and very common in different Arab region, and further longitudinal studies are still needed to investigate the prognosis and determinants of these thyroid diseases in the Arab world.


http://www.academicjournals.org/journal/JPHE/article-full-text-pdf/0C73CDC56758


[Eating Iodine can help fight thyroid cancer, seaweed has a lot of Iodine.]


----------


Centre for Arab Genomic Studies, Dubai, United Arab Emirates

GENETIC DISORDERS IN ARABS


Genetic  and  inherited  disorders  have  accompanied  humanity  since  its  earliest  existence.    Many  prehistoric and   historic   sites   have   revealed   archeological remains  with  pathologies  suggestive  of  inherited disorders. Paleopathology studies  -  the  identification of  pathological  conditions  in  ancient  skeletal  remains -  from  many  world  sites  revealed  the  presence  of

various  hereditary  or  congenital  conditions  including Paget’s  disease,  neurofibromatosis,  cleft  lip  and  cleft palate,  juvenile  kyphosis  (Scheuermann’s  disease), scoliosis, spina bifida, achondroplasia, Hurler syndrome (mucopolysaccharidosis  type  I),  Hunter’s  syndrome,

(mucopolysaccharidosis  type  II),  Morquio’s  syndrome (mucopolysaccharidosis type IV), osteogenesis imperfecta (types III and IV), cleidocranial dysostosis, osteopetrosis,

diaphyseal  sclerosis  (Camuratoi-Engelmann  disease), osteopoikilosis,  and  many  others  (reviewed  in Ortner, 2003).  One of the oldest of such records includes a 1.5

million year old fossil of a 2-year-old Homo erectus child with amelogenesis imperfecta (

Zilberman et al., 2004).  In  Indonesia,  the  skeleton  of  a  25-30  year-old  Homo

floresiensis, discovered in 2003 on the island of Flores, featured a small skull that could be due to microcephaly (Jacob et al., 2006).  In Egypt, scientific investigation of mummies  from  the  huge  necropolis  of Thebes-West  in Upper Egypt revealed osseous manifestations suggestive of metabolic and chronic anemia in high frequencies in populations of the “Middle Kingdom” (2050-1750 BCE;

Nerlich et al., 2002).  In addition, bizarre physical features were shared by many members of Egypt’s 18th Dynasty, including the Pharaoh Akhenaten, suggestive of possible familial  disorders  possibly  including  the  aromatase excess syndrome, the sagittal craniosynostosis syndrome, or a variant of the Antley-Bixler syndrome (Braverman et al., 2009).  Interestingly, ancient DNA analysis revealed

a b-thalassemia  mutation  in  the  skeletal  remains  of  an Ottoman child with severe porotic hyperostosis (Filon et al., 1995).


The Early Farmers


Around 12,000 years ago, Neolithic human populations adapted  agricultural  technologies  that  allowed  them to establish permanent  sizeable  settlements and to adapt  a  far-reaching shift  in  subsistence and lifestyle. Undoubtedly, improvement of the climatic conditions in the area along with the practice of agriculture helped in the establishment of major historical settlements with sizeable densities that could have contributed enormously to the genetic makeup of modern Arab populations.  Yet, farming was almost always associated with settlements near mosquito-infested soft and marshy soil causing large malarial outbreaks (Grmek, 1994; de Zulueta, 1994; Joy et al., 2003).  These outbreaks imposed selective pressure on the human genome and amplified the frequencies of

several  genetic  disorders  including  sickle  cell  disease, b-thalassemia,  and  glucose-6-phosphate  dehydrogenase (G6PD)  deficiency  (Angel,  1966 ;Carter  and  Mendis, 2002 Kwiatkowski, 2005).


http://www.cags.org.ae/cb404c1.pdf



------------


Lifestyle disorders top health issues in Arab world

 January 2014


PARIS: Heart disease and stroke have replaced infectious disease as the top causes of early death in the Arab world, tracking the West in a trend toward lifestyle disorders, The Lancet reported Monday.

An international consortium of scientists compared the state of health in the 22 countries of the Arab League in 1990 and in 2010, using data from a vast study — the 2010 Global Burden of Diseases report.

In 1990, respiratory infection headed the list of concerns, accounting for 11 percent of deaths, while stillbirths and poor nutrition also featured high on the mortality list.

These problems still persist in the low-income countries of the Comoros, Djibouti, Mauritania, Somalia and Yemen, the investigators found.


 http://www.arabnews.com/news/515126


----------------



Arab countries living longer but battling chronic disease

In the region as a whole, important changes occurred over those two decades. Burden attributable to non-communicable disease, including ischemic heart disease, mental disorders such as depression and anxiety, and musculoskeletal disorders increased, while the premature death and disability from most newborn, nutritional, and maternal disorders decreased. Basically, there were tremendous improvements in what is killing people but not in what is ailing them.

Of the 10 leading causes of health loss, combining both premature mortality and years lived with disability, between 1990 and 2010, lower respiratory infections remained the first, while ischemic heart disease rose to second. Major depressive disorder rose from eighth to fifth place, and low back pain, which was not among the top causes of health loss in 1990, was ranked seventh in 2010. The rise of non-communicable disease in the Arab world mirrors similar changes in the US, Western Europe, and Canada.


http://www.healthdata.org/news-release/arab-countries-living-longer-battling-chronic-disease


-----------------------


Frequently asked questions on Middle East respiratory syndrome coronavirus (MERS-CoV)

 May, 2017


1. What is Middle East respiratory syndrome (MERS)?

Middle East respiratory syndrome (MERS) is a viral respiratory illness caused by a coronavirus (Middle East respiratory syndrome coronavirus, or MERS-CoV) that was first identified in Saudi Arabia in 2012. Coronaviruses are a large family of viruses that can cause diseases in humans, ranging from the common cold to Severe Acute Respiratory Syndrome (SARS).



http://www.who.int/csr/disease/coronavirus_infections/faq/en/


-----------

Population structure and the burden of disease in the United Arab Emirates

 2012

 http://www.sciencedirect.com/science/article/pii/S2210600612000214

-------------


Saudi Arabia Awakes to the Perils of Inbreeding

 MAY 1, 2003


Health officials and genetic researchers here say there is no way to stop inbreeding in this deeply conservative Muslim society, where marrying within the family is a tradition that goes back hundreds of years.

Today, when most unions are still arranged by parents, marrying into wealth and influence often means marrying a relative. Social lives are so restricted that it is virtually impossible for men and women to meet one another outside the umbrella of an extended family. Courtships without parental supervision are rare.

Among more educated Saudis, marrying relatives has become less common and younger generations have begun to pull away from the practice. But for the vast majority, the tradition is still deeply embedded in Saudi culture.


http://www.nytimes.com/2003/05/01/world/saudi-arabia-awakes-to-the-perils-of-inbreeding.html



------------



 Hemoglobinopathies in the United Arab Emirates


       Genetic Disorders in the UAE Autosomal recessive disorders are common in the UAE.   

        Hemoglobinopathies are one of the most common disorders among the UAE nationals. Other

   diseases include congenital abnormalities, cancers, metabolic disorders, chromosomal aberrations and mental retardation. Monogenic diseases such as cystic fibrosis, fragile-X and G6PD also exist at appreciable levels.  During the last  two years  alone, the author's laboratory has carried out  mutational  identification and  characterization  of  more  than  50  cases  of  cystic

Fibrosis, predominantly among the UAE nationals.


ß-Thalassemia


ß-Thalassemia  (ß-thal)  is  one  of  the  most  common single gene disorders affecting almost all the countries in  the  Mediterranean  Basin, the  Middle East,  SouthbEast  Asia,  Far  East,  Australasia,  the  Americas  and Africa.  It is characterized by the deficiency or absence of ß-globin chain production.  More than 200 different mutations  have  so  far  been  reported  that  result  in

ß- thalassemia.


    a-Thalassemia and HbH Disease

a-Thalassemia (a-thal) is generally caused by the deletion of one (-a/

a   a) or both (-a/-a or --/a) func-tional a-globin genes leading to a-thal-2

     (-a/a) and a-thal-1 (--/a) conditions, respectively. Individuals who inherit two or three functional a-genes (-a/a; -a-a; --/) have a-thal trait with a mild hypochromic, microcytic anemia. Those who inherit a single a-gene (--/-a) have HbH (ß4) disease, a moderately severe hemolytic anemia with a variable clinical course. HbH Disease is the most severe form of the a-thal syndromes compatible with life. Hb Bart's Hydrops Fetalis syndromes arise from total absence of four a-globin genes (--/--) and such condition is incompatible with life. The majority of a-thal and HbH cases in the Gulf Region are caused by point mutations characterized by relatively severe phenotype.

HbH disease is a moderately severe hemolytic anemia with microcytosis, hypochromia, low HbA and HbF levels, and varying quantities of HbH (ß4; 2-30%).

Most of the HbH syndromes were thought to be caused by the deletion or inactivation of three of the four a-globin genes. However, in the last decade, numerous reports have been published demonstrating an increasing number of non-deletional (aT)a-thal as

the molecular basis for many of the HbH syndromes, particularly from the Middle East.

For decades, hematological evaluation and gene mapping techniques have been used to

identify these anomalies at the molecular level. More recently, novel techniques such as PCR have been devised which enable the molecular characterization of such patients rapidly, easily and accurately.

Several studies were conducted in the author's laboratory in an attempt to elucidate the frequency of a-thal in the UAE. Cord blood samples were collected from 418 consecutive UAE national newborns. The PCR-based analysis of the a

-globin gene status demonstrated that the incidence of a-thal, particularly the -a3.7 deletion, was extremely high.


The DNA-based newborn screening survey demonstrated that 49  %  of  the  neonates  had 
α-thal, one  of  the  highest  in  the  world.  The  distribution of mutations was as follows: 
αα/αα:  51%;  -α3.7/αα:34%; -α3.7/-α3.7: 11%; -
α4.2/αα: 1.0% and one newborn was  compound  heterozygous  for  the  -α3.7/-α4.2geno-
type.  The  remaining  3%  of  the  chromosomes  were
identified with the non-deletional type of αthal (αT). Four  different  αT alleles  were  identified;  PolyA-1[αPA-1(AATAAA→AATAAG)],      PolyA-2      [αPA-2(AATAAA→AATGAA)], Hb Constant Spring [HbCS(αCSα/αCSα) TAA→CAA]  and  pentanucleotide  deletion [α-5nt del(GAGGTGAGG→GAGG)]


https://www.dha.gov.ae/en/SpecialtyCentres/GeneticsCenter/Documents/Hemoglobinopathies%20in%20the%20UAE%20By%20Dr.%20E.%20Baysal.pdf


------------------


In Middle East and North Africa, Health Challenges are Becoming Similar to Those in Western Countries

 September 4, 2013


WASHINGTON, September 4, 2013 - In the Middle East and North Africa region, non-communicable diseases such as heart disease (up by 44%), stroke (up 35%), and diabetes (up 87%) are causing more premature death and disability than they did in the past. Potentially preventable risk factors such as poor diets, high blood pressure, high body mass index (an indicator of obesity and overweight), and smoking are contributing to the growing burden of non-communicable diseases in the region.


 http://www.worldbank.org/en/news/press-release/2013/09/04/middle-east-north-Africa-health-challenges-similar-western-countries


---------------------

Cardiovascular diseases on the increase in Arab states

March 2012


Children in the Arab Gulf region are more at risk of developing cardiovascular diseases (CVD) than those in other Arab states, according to a new report from the World Heart Federation.

The rapid urbanisation of Arab Gulf states means children are increasingly living in densely populated cities and suffering exposure to air and water pollution. Many are being denied access to green spaces and their health is further compromised by passive smoking and fast food.

Kuwait is the most urbanised Arab state, with 98% of its population living in cities, followed closely by Qatar with 96%. Neighbouring Saudi Arabia and the United Arab Emirates (UAE) come next, with 84% and 78% of people living in cities respectively.


 http://www.natureasia.com/en/nmiddleeast/article/10.1038/nmiddleeast.2012.36


-----------


About the Epidemiology of IBD

June, 2012


Epidemiology is the study of the frequency and distribution of diseases in the population.

It is estimated that 1.4 million Americans suffer from Crohn's disease or ulcerative colitis (collectively known as inflammatory bowel diseases, or IBD). The search for risk factors in IBD has been frustrating, and the difficulty in diagnosing these diseases has been a further hindrance. However, epidemiologists have gathered enough information to know a good deal about the distribution of IBD in the United States and Western Europe. Current evidence suggests that both genetic and environmental factors contribute to these diseases.
Genetics

In 2001, Nod2, the first gene linked to Crohn's disease, was discovered. This breakthrough was funded in part by a CCFA research grant. Most researchers agree that there is a strong genetic component in IBD. If a person has a relative with the disease, his/her risk is estimated to be at least 10 times that of the general population -- 30 times greater if the relative is a sibling. New technologies, including a genome-wide search, are helping researchers to close in on the genes that predispose people to IBD.
Race and Ethnicity

    American Jews of European descent are four to five times more likely to develop IBD than the general population.
    IBD has long been considered a predominantly white disease. The prevalence rate among whites is 149 per 100,000. Among African Americans, however, there has been a steady increase in reported cases of both Crohn's disease and ulcerative colitis. An HMO with two million members reported hospitalization rates per 100,000 by race, over a six-year period, as:
        10.2 - Whites
        10.2 - African Americans

According to this study, prevalence rates among Hispanics and Asians were lower than those for whites and African Americans.


http://www.crohnscolitisfoundation.org/resources/epidemiology.html


-----------



Prevalence and Risk Factors of Postpartum Depression in Middle Eastern/Arab Women

 Postpartum Depression (PPD) affects women around the world and it is estimated that its prevalence runs at about 10-15% (Fuggle, Glover, Khan & Haydon, 2002). Some studies show that PPD may affect up to 30% of all women after delivery (Evins, Theofrastous & Galvin, 2000; WHO, 2003), and has a significant impact on the mother and long-term consequences on the cognitive and emotional development of children (Tammentie, Tarka, Astedt-Kurki & Paavilainen, 2002). It is generally also agreed that while this illness can turn into major depression and carries substantial risk of morbidity and death, it is an underdiagnosed and underrated illness. Mathers & Loncar (2006) project that by the year 2030, depression will be one of the top three leading causes of death in the world; yet PPD is one of the least addressed types of depression today. Additionally, for women who have experienced PPD, up to 50% will face a reoccurrence during subsequent pregnancies (Nonacs and Cohen, 2000).\


http://quod.lib.umich.edu/j/jmmh/10381607.0009.104/--prevalence-and-risk-factors-of-postpartum-depression?rgn=main;view=fulltext


-----------

Indian genetic disease database

 Indians, representing about one-sixth of the world population, consist of several thousands of endogamous groups with strong potential for excess of recessive diseases. However, no database is available on Indian population with comprehensive information on the diseases common in the country. To address this issue, we present Indian Genetic Disease Database (IGDD) release 1.0 (http://www.igdd.iicb.res.in)—an integrated and curated repository of growing number of mutation data on common genetic diseases afflicting the Indian populations. Currently the database covers 52 diseases with information on 5760 individuals carrying the mutant alleles of causal genes. Information on locus heterogeneity, type of mutation, clinical and biochemical data, geographical location and common mutations are furnished based on published literature. The database is currently designed to work best with Internet Explorer 8 (optimal resolution 1440?×?900) and it can be searched based on disease of interest, causal gene, type of mutation and geographical location of the patients or carriers. Provisions have been made for deposition of new data and logistics for regular updation of the database. The IGDD web portal, planned to be made freely available, contains user-friendly interfaces and is expected to be highly useful to the geneticists, clinicians, biologists and patient support groups of various genetic diseases.



 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3013653/



----------

Prevalence of common disease-associated variants in Asian Indians

2008

    Trevor J Pemberton,
    Niyati U Mehta,
    David Witonsky,
    Anna Di Rienzo,
    Hooman Allayee,
    David V Conti and
    Pragna I PatelEmail author

BMC Genetics20089:13

DOI: 10.1186/1471-2156-9-13

©  Pemberton et al; licensee BioMed Central Ltd. 2008
Background

Asian Indians display a high prevalence of diseases linked to changes in diet and environment that have arisen as their lifestyle has become more westernized. Using 1200 genome-wide polymorphisms in 432 individuals from 15 Indian language groups, we have recently shown that: (i) Indians constitute a distinct population-genetic cluster, and (ii) despite the geographic and linguistic diversity of the groups they exhibit a relatively low level of genetic heterogeneity.


Results

We investigated the prevalence of common polymorphisms that have been associated with diseases, such as atherosclerosis (ALOX5), hypertension (CYP3A5, AGT, GNB3), diabetes (CAPN10, TCF7L2, PTPN22), prostate cancer (DG8S737, rs1447295), Hirschsprung disease (RET), and age-related macular degeneration (CFH, LOC387715). In addition, we examined polymorphisms associated with skin pigmentation (SLC24A5) and with the ability to taste phenylthiocarbamide (TAS2R38). All polymorphisms were studied in a cohort of 576 India-born Asian Indians sampled in the United States. This sample consisted of individuals whose mother tongue is one of 14 of the 22 "official" languages recognized in India as well as individuals whose mother tongue is Parsi, a cultural group that has resided in India for over 1000 years. Analysis of the data revealed that allele frequency differences between the different Indian language groups were small, and interestingly the variant alleles of ALOX5 g.8322G>A and g.50778G>A, and PTPN22 g.36677C>T were present only in a subset of the Indian language groups. Furthermore, a latitudinal cline was identified both for the allele frequencies of the SNPs associated with hypertension (CYP3A5, AGT, GNB3), as well as for those associated with the ability to taste phenylthiocarbamide (TAS2R38).
Conclusion

Although caution is warranted due to the fact that this US-sampled Indian cohort may not represent a random sample from India, our results will hopefully assist in the design of future studies that investigate the genetic causes of these diseases in India. Our results also support the inclusion of the Indian population in disease-related genetic studies, as it exhibits unique genotype as well as phenotype characteristics that may yield new insights into the underlying causes of common diseases that are not available in other populations.


https://bmcgenet.biomedcentral.com/articles/10.1186/1471-2156-9-13




---------


Diet, Genetics, and Disease: A Focus on the Middle East and North Africa Region


 2012


https://www.hindawi.com/journals/jnme/2012/109037/



----------


An Overview of Human Genetic Disorders with Special Reference to African Americans

 October 27, 2015


 Diabetes

 Hypertension

 Pancreatic Cancer

 Prostate Cancer

 Alzheimer’s Disease

 Sickle Cell Disease

 Kidney Disease

 Inflammatory Bowel Disease

 AIDS

 Sarcoidosis

[Glucose-6-Phosphate Dehydrogenase Deficiency]

[Beta-thalassemia]




 https://www.omicsonline.org/open-access/an-overview-of-human-genetic-disorders-with-special-reference-to-africanamericans-2155-9821-1000e139.php?aid=63273



-----------


Genetic disorders in Southern Africa.


Abstract

Certain uncommon genetic disorders occur relatively frequently in the various population groups of Southern Africa. Prominent among these are porphyria, colonic polyposis and sclerosteosis in the Afrikaner community, Huntington's chorea in the British, Gaucher's and Tay-Sachs diseases in the Jewish population, glucose-6-phosphate dehydrogenase deficiency (G-6-PD deficiency) and thalassaemia in the Greek community, various skeletal dysplasias in the Black group, lipoid proteinosis and cleidocranial dysostosis in the Cape Coloured population, diabetes mellitus in the Indian community and retinitis pigmentosa in the Tristan da Cunha islanders. In addition, 'private' syndromes have been encountered in virtually every group. Awareness of the ethnic distribution of unusual genetic conditions is of considerable practical importance during the differential diagnosis of obscure disease.

https://www.ncbi.nlm.nih.gov/pubmed/959924



---------------------------------------------


GENETIC ANALYSIS OF AFRICAN

POPULATIONS: HUMAN EVOLUTION

AND COMPLEX DISEASE


http://bioinformatics.bc.edu/~marth/BI820-2004S/files/Tishkoff-AfricanPop-NRG-2002.pdf



---------------------------------------------------

Moroccan Genetic Disease Database

Database content

Disease325
Gene389
Mutation532
Polymorphism305
Article399

http://mgdd.pasteur.ma/

--------------------------------

Genetics and genomic medicine in Morocco: the present hope can
make the future bright

http://onlinelibrary.wiley.com/doi/10.1002/mgg3.255/pdf

-------------------------

Consanguinity and genetic disorders in Egypt

Jan 2012

http://journals.lww.com/mejmedgen/Fulltext/2012/01000/Consanguinity_and_genetic_disorders_in_Egypt.3.aspx

------------------------

Profile of genetic disorders prevalent in northeast region of Cairo, Egypt

February 2012

http://www.sciencedirect.com/science/article/pii/S1110863011000620

---------------------------

The genetic affinities of Ethiopians

January 10, 2011

http://blogs.discovermagazine.com/gnxp/2011/01/the-genetic-affinities-of-ethiopians/#.WXDzxullDIU

-------------------------


Hereditary neurodegenerative disorders in Nigerian Africans.

1984

https://www.ncbi.nlm.nih.gov/pubmed/6230542

--------------------


Oldest genetic disorder few Kenyans know about

April 16th 2017

 https://www.standardmedia.co.ke/health/article/2001236551/oldest-genetic-disorder-few-kenyans-know-about


--------------------

Congo’s Uncharted Territory

Aug 19, 2013

http://blogs.discovermagazine.com/bodyhorrors/2013/08/19/congos-neglected-tropical-diseases/#.WXDxSOllDIU

--------------------

Genetic Disorders in Sudan

April 2010

https://link.springer.com/chapter/10.1007/978-3-642-05080-0_20/fulltext.html

---------------------


Blacks More Prone to Colon Cancers That Arise Between Colonoscopies: Study

May 22, 2017


A new study finds that older black Americans are far more likely than whites to develop a colon cancer in the decade-long gap between these screenings.

Some of this may be due to where black patients receive their colonoscopy, the researchers said.

"Blacks and other minorities more frequently received colonoscopies from physicians with lower [colon] polyp detection rates, suggesting there was lower quality of care," said study lead author Stacey Fedewa, a researcher with the American Cancer Society.


http://health.usnews.com/health-care/articles/2017-05-22/blacks-more-prone-to-colon-cancers-that-arise-between-colonoscopies-study


------------

African Americans at Increased Risk for Eye Diseases

Cataracts

Cataracts are a clouding of the lens of the eye. African Americans are 1.5 times more likely to develop cataracts than the general population and five times more likely to develop related blindness.
Glaucoma
Glaucoma refers to a family of diseases that affect the optic nerve and cause vision loss. African Americans are five times more likely than whites to develop glaucoma and four times more likely to develop related blindness.
Diabetes
African American adults are twice as likely as non-Hispanic whites to be diagnosed with diabetes and twice as likely to develop and die from diabetes-related complications. Diabetes can cause diabetic retinopathy, a condition that can lead to retinal damage and permanent vision loss.
Hypertension
Even though hypertension may not seem to be related to the eyes, high blood pressure can cause vision problems and vision loss. African American adults are more likely to be diagnosed with hypertension but less likely to have the condition under control (Source: Vision Problems).
Black History Month is truly a time to celebrate, so what better way to celebrate than to schedule a comprehensive eye exam? An eye exam does much more than evaluate the clarity of your vision; it can serve as a window into your overall health. Celebrate good health this February by getting a thorough vision screening!

http://yoursightmatters.com/african-americr-eye-diseases/


--------------------


Glaucoma in the African American and Hispanic Communities

Yvonne Ou, MD

University of California, San Francisco, UCSF Medical Center

Thursday, January 1, 2015

African Americans and Hispanics are at increased risk of developing glaucoma. Find out why and learn about important steps that can prevent vision loss from this eye disease. 


http://www.brightfocus.org/glaucoma/article/glaucoma-african-american-and-hispanic-communities


--------



Blacks Seem More Vulnerable to Deadly Blood Infection

By Jenifer Goodwin

HealthDay Reporter


TUESDAY, June 22 (HealthDay News) -- Black patients are more likely to develop the life-threatening blood infection sepsis and have a greater chance of dying from it than whites, new research suggests.


http://www.medicinenet.com/script/main/art.asp?articlekey=117445


-----------


High Blood Pressure in African-Americans

High blood pressure, also known as hypertension, affects African-Americans in unique ways:

    African-Americans develop high blood pressure at younger ages than other groups in the U.S.
    African-Americans are more likely to develop complications associated with high blood pressure. These problems include stroke, kidney disease, blindness, dementia, and heart disease.

http://www.webmd.com/hypertension-high-blood-pressure/guide/hypertension-in-african-americans#1


------------


Blacks still dying more from cancer than whites

 February 18, 2009


Three years ago, the American Cancer Society (ACS) broke some exciting news: for the first time in decades, U.S. cancer deaths fell. The trend continued the following year. But new research today shows that the milestone has been a mixed bag for one segment of the population, African-Americans. They’re also dying less of cancer—in some cases, their gains are coming at a faster pace than for whites—but the disease still kills them more often.


https://blogs.scientificamerican.com/news-blog/blacks-still-dying-more-of-cancer-t-2009-02-18/


------------


Prostate cancer risk in African Americans


African Americans are more likely to develop — and die from — prostate cancer than others. But why?

This year, the American Cancer Society estimates that nearly 1.5 million Americans will be diagnosed with some form of cancer — and that figure doesn’t even include more than 1 million cases of certain skin cancers. The organization estimates that cancer will also claim 562,340 lives in 2009. Scientific evidence shows that about one-third of those deaths could have been prevented by making lifestyle changes. Smoking, being overweight or obese, not exercising, and eating a poor diet — all modifiable risk factors — have been linked to cancer (as well as heart disease, diabetes, and many other conditions).


http://www.harvardprostateknowledge.org/prostate-cancer-risk-in-african-americans


------------


 Racial Differences in Reported Lyme Disease Incidence

2000

In the United States, the incidence of Lyme disease is considered to be disproportionately high among Whites because of risk of exposure. For assessment of racial differences in Lyme disease incidence and the role of risk

exposure, incidence rate ratios (IRRs) for Lyme disease and its manifestations between Whites and African Americans in Maryland and in its focus of endemicity, the Upper Eastern Shore, were calculated. Calculations were based on reported cases of Lyme disease in Maryland during the years 1992–1996. The IRR for Lyme disease between Whites and African Americans was 6.3 (95% confidence interval (CI): 5.0, 8.0), decreasing to 1.8 (95% CI: 1.2, 2.7) for the Upper Eastern Shore. Statewide, there was a significant difference between the White to African American IRR for erythema migrans and for Lyme disease-associated arthritis, at 17.7 (95% CI: 11.2, 27.8) and 2.3 (95% CI: 1.7, 3.2), respectively. On the Upper Eastern Shore, the IRR for arthritis

reversed, indicating higher incidence among African Americans than among Whites: IRR = 5.7 (95% CI: 2.4,13.9) for erythema migrans and IRR = 0.7 (95% CI: 0.4, 1.1) for arthritis. White patients were more likely to have erythema migrans (risk ratio = 2.8, 95% CI: 1.9, 4.1) and less likely to have arthritis than were African Americans(risk ratio = 0.4, 95% CI: 0.3, 0.5). Among all patients, there was a significant negative association between arthritis and erythema migrans. Although much of the racial disparity in incidence rates diminishes in a rural, endemic area, consistent with exposure risk being responsible for much of the variation, a difference remains.

This may be due to failure to recognize early disease (erythema migrans) among African Americans, resulting in increased rates of late manifestations. Geographic spread of the disease warrants efforts to increase awareness of Lyme disease and its manifestations among people of color and the health care providers who serve them.

 https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/aje/152/8/10.1093/aje/152.8.756/2/756.pdf?Expires=1500258112&Signature=F1DoMlshZnNEHWu~2fUwXIR1oKQq4~R2DNIiCIc5GXfui4gPyBRd0~98cDAx74Sda~2DqPTtQAOshONXI1fZHWYUIWMj8LbDZkFeFupFdQfZ-ceP-Akto8-CrB4Uq7B-4wd1qDq0zKQrhks0vKDFJGd3Cvxe7ySA-b2L1zzRdiRDEEQJwYOpl5Wvuf9MIsQ5BSzzlQPA~woJXRfkZJ3p0Cno1o4erPBQiAOs4ngIKLYjafnTnVIhPnve2YvMt54lXG7kWfKLDioAhxZMxup9fCo5dPj5Fa8gXi-iCnvusIW62cb9ytVGhBwicoNIKETVwz9wEhkKZUYo7bOKZ~0YGQ__&Key-Pair-Id=APKAIUCZBIA4LVPAVW3Q


-----------------------------


Alzheimer's Affects Races Differently: Researchers

Thursday, 16 Jul 2015


Alzheimer's disease seems to develop differently in the brains of black patients than in whites.

And, black people seem more likely to suffer different types of brain changes that also contribute to dementia, a new study reports.

Alzheimer's disease dementia is generally associated with a build-up of substances known as plaques and tangles inside the brain.

But, there are other brain changes that can also contribute to dementia, the study authors noted.

For example, the brains of people with dementia sometimes contain infarcts -- tiny areas of dead tissue caused by micro-strokes, the researchers explained.

They also might contain Lewy bodies -- another form of abnormal protein build-up in the brain that's usually associated with Parkinson's disease.

Autopsies of black and white Alzheimer's patients revealed that blacks were more likely than whites to experience a mix of dementia-related changes, as opposed to the damage usually associated with "pure" Alzheimer's dementia, according to the study.

"We were surprised that the African Americans were much more likely to have a mixed picture," said lead author Lisa Barnes, a professor of neurology and behavioral science at Rush University Medical Center in Chicago. "The underlying brain changes were different, which indicates that they probably had different risk factors."

The study findings were published online July 15 in advance of print publication in the journal Neurology.

http://www.newsmax.com/Health/Health-News/alzheimers-dementia-races-blacks/2015/07/16/id/657369/


------------------------



How Alzheimer’s Is Different in African-Americans

Jul 15, 2015

 The hallmark signs of Alzheimer’s are well-established—plaques of amyloid protein and tangles of tau protein in the brain, which work to suffocate and eventually destroy neurons that are dedicated to higher level functions such as memory and reasoning.But in a study published in the journal Neurology, researchers show that there may be important differences in the way Alzheimer’s appears in the brains of African-American and white patients. When Lisa Barnes, a neurologist at the Rush Alzheimer’s Disease Center at Rush University Medical Center and her colleagues compared the brains of 41 black patients who had died of the disease to the brains of 81 white patients, they found a much more complex picture of Alzheimer's in the brains of the African-Americans.


These patients were more likely to have not just the familiar plaques and tangles, but also other signs of neurological abnormalities, including Lewy bodies, signs of infarcts and blood vessel disease. In fact, 71% of the African-American patients showed this mixed picture compared to 50% of the white patients.


The most common—and surprising, says Barnes—connection involved the Lewy bodies. These are clumps of proteins that aggregate inside nerve cells, particularly those involved in movement. They are common in Parkinson’s patients and can contribute to tremors as well as hallucinations and sleep disruptions. Because the black population is known to have higher risk of circulatory disorders, including stroke and hypertension, Barnes expected to find more infarct-related differences when comparing the brains of African-Americans to those of whites. “We did not find that,” she says. “We found a much more mixed picture than just infarcts, and that was a little bit surprising.”


http://time.com/3959295/alzheimers-african-americans/


--------------------


UNC study: Frequency of foot disorders differs between African Americans and whites

Monday, November 8, 2010 — African Americans in the study age 45 or older were three times more likely than whites of the same age to have corns or flat feet. In people who were not obese, African Americans were twice as likely to have bunions and hammer toes than whites.


http://www.med.unc.edu/www/newsarchive/2010/november/unc-study-frequency-of-foot-disorders-differs-between-african-americans-and-whites


--------------------


Asthma in African Americans: What can we do about the higher rates of disease? 

March, 2012

To remedy disparities such as greater disease severity and higher rates of hospitalization and death, we need to ensure that all patients receive proper care and the knowledge they need to control their asthma.

 ABSTRACTAfrican Americans not only have a higher prevalence of asthma than whites, they also are encumbered with higher rates of asthma-associated morbidity and death. Factors such as genetics, socioeconomic status, health maintenance behaviors, air quality, and obesity likely contribute in combination to these burdens. Further work is needed to better understand these complex risk factors. To remedy these disparities, we need to ensure that patients at higher risk are given proper care and the knowledge to control their asthma.


http://www.mdedge.com/ccjm/article/95718/pulmonology/asthma-african-americans-what-can-we-do-about-higher-rates-disease


----------------------


Genetics key to African-Americans' hypertension

Stanford Report, January 26, 2005

National health records have shown that African-Americans are more prone to high blood pressure than Caucasians, but pinning down the roots of that difference has proven elusive. Now, researchers at the School of Medicine have narrowed down the search for genes that contribute to this difference in disease risk.

Finding such a gene could have several benefits for African-Americans and other ethnic groups. One is that by knowing the normal role of the gene, doctors can better understand the disease and devise new drugs or treatments to keep blood pressure under control. It could also lead to genetic tests to help identify people at higher risk of heart disease.


http://news.stanford.edu/news/2005/january26/med-hypertension-012605.html


-----------------------



Metabolic Syndrome in African Americans: Implications for Preventing Coronary Heart Disease

2007


        Summary:

The metabolic syndrome represents a specific

clustering of cardiovascular risk factors in the same individu-

al (abdominal obesity, atherogenic dyslipidemia, elevated

blood pressure, insulin resistance, a prothrombotic state, and

a proinflammatory state). Almost 50 million American adults

(about one in four) have the metabolic syndrome, which puts

them at increased risk for the development of diabetes melli-

tus and cardiovascular disease. African Americans, especial-

ly African-American women, have a high prevalence of the

metabolic syndrome. This is attributable mainly to the dis-

proportionate occurrence in African Americans of elevated

blood pressure, obesity, and diabetes. Management of the

metabolic syndrome consists primarily of modification or re-

versal of the root causes (overweight/obesity and physical in-

activity) and therapy to reduce or control the risk factors.

Although all components of the metabolic syndrome should

be addressed, optimal control of atherogenic dyslipidemia

and elevated blood pressure may reduce cardiovascular risk

by more than 80%.


http://onlinelibrary.wiley.com/doi/10.1002/clc.20003/pdf


-----------------


Food Allergies Among Kids Vary by Race: Study

Researchers find blacks and Hispanics more likely to be allergic to corn and shellfish, for instance.


TUESDAY, Nov. 22, 2016 (HealthDay News) -- Black and Hispanic children are much more likely to have corn, shellfish and fish allergies than white children, according to a U.S. study.
The study also found that compared to whites, black children have much higher rates of asthma, eczema and allergies to wheat and soy.


https://consumer.healthday.com/respiratory-and-allergy-information-2/food-allergy-news-16/food-allergies-among-kids-vary-by-race-study-717085.html


--------------------------


Why Black Children May Be More Likely to Develop Food Allergies

 Sept. 05, 2011


New research suggests that race and ancestry may play an important role in food allergies.

Dr. Rajesh Kumar, a pediatrician at Northwestern University Medical School, and his team report in the journal Pediatrics that black children are more than twice as likely as white children to have sensitivities to eight foods that commonly cause allergic reactions, and that they are especially vulnerable to peanut allergies.

While other studies have linked African American ethnicity to a higher risk of asthma, Kumar’s group was interested in investigating whether race also affects children’s risk of allergy to certain foods. Using a multi-ethnic database of 1,104 children who participated in regular health checkups at 6 months, then again at 1, 2, 4 and 6 years old, the scientists measured the youngsters’ antibodies to egg white, cow’s milk, peanut, soy, shrimp, walnut, wheat and cod.


http://healthland.time.com/2011/09/05/why-black-children-might-be-more-likely-to-develop-food-allergies/


------------

Are People of Certain Races and Ethnicities More Susceptible to Food Allergies

 Nov, 2015


https://www.premierallergyohio.com/doctors-blog/are-people-of-certain-races-and-ethnicities-more-susceptible-to-food-allergies


-----------


Racial Differences in Allergic Sensitization: Recent Findings and Future Directions

 June, 2013


 Racial disparities are present in many facets of health and disease. Allergy and asthma are no exceptions. Secondary results from cross-sectional and cohort studies have provided information on the scope of racial disparities in allergic sensitization in the United States. African American/Black individuals tend to be sensitized more frequently than White individuals. Little is known about rates in other race groups. Genetics are unlikely to be the sole or major cause of the observed differences. Home dust allergen and endotoxin levels cannot explain the differences. Studies that have been designed to specifically address the sources of these racial disparities are needed. A “Multilevel Framework” that considers the roles of the individual, family and community presents an excellent approach to guide design of future studies of the causes of these disparities. Understanding the causes of the disparities could lead to interventions that would improve the health of all individuals.


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4888051/


-------

Ethnic differences in coronary atherosclerosis

February 2002


Conclusions

As compared with whites, blacks and Hispanics had significantly lower prevalence of CAC and obstructive coronary disease. Ethnic differences in risk-factor profiles do not explain these differences. This study demonstrated that whites have a higher atherosclerotic burden than blacks and Hispanics, independent of risk-factor differences among symptomatic patients referred for angiography.


http://www.sciencedirect.com/science/article/pii/S073510970101748X


--------------


Why Are African-Americans at Greater Risk for Heart Disease?

African-Americans are at higher risk for heart disease, yet they're less likely to get the care they need.

African-Americans and Heart Failure

In a startling 2009 study published in the New England Journal of Medicine, researchers found that African-Americans have a much higher incidence of heart failure than other races, and it develops at younger ages. Heart failure means that the heart isn't able to pump blood as well as it should.

Before age 50, African-Americans' heart failure rate is 20 times higher than that of whites, according to the study. Four risk factors are the strongest predictors of heart failure: high blood pressure (also called hypertension), chronic kidney disease, being overweight, and having low levels of HDL, the "good" cholesterol. Three-fourths of African-Americans who develop heart failure have high blood pressure by age 40.


 http://www.webmd.com/heart-disease/features/why-african-americans-greater-risk-heart-disease#1


--------------

Black Women Have Worse Breast Cancer Survival Rates Compared to Whites and Hispanics


http://www.breastcancer.org/research-news/black-women-have-worse-survival-rates


----------------


Race, Ancestry, and Development of Food-Allergen Sensitization in Early Childhood

2011 Oct

RESULTS:

In this predominantly minority cohort (60.9% black and 22.5% Hispanic), 35.5% of subjects exhibited food sensitizations. In multivariate models, both self-reported black race (odds ratio [OR]: 2.34 [95% confidence interval [CI]: 1.24–4.44]) and African ancestry (in 10% increments; OR: 1.07 [95% CI: 1.02–1.14]) were associated with food sensitization. Self-reported black race (OR: 3.76 [95% CI: 1.09–12.97]) and African ancestry (OR: 1.19 [95% CI: 1.07–1.32]) were associated with a high number (=3) of food sensitizations. African ancestry was associated with increased odds of peanut sIgE levels of =5 kUA/L (OR: 1.25 [95% CI: 1.01–1.52]). Similar ancestry associations were seen for egg sIgE levels of =2 kUA/L (OR: 1.13 [95% CI: 1.01–1.27]) and milk sIgE levels of =5 kUA/L (OR: 1.24 [95% CI: 0.94–1.63]), although findings were not significant for milk.
CONCLUSIONS:

Black children were more likely to be sensitized to food allergens and were sensitized to more foods. African ancestry was associated with peanut sensitization.


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3182844/


------------------------------------------



 1.What Is Sarcoidosis?


Sarcoidosis involves inflammation that produces tiny lumps of cells in various organs in

your body. The lumps are called granulomas because they look like grains of sugar or sand.

They are very small and can be seen only with a microscope. These tiny granulomas can grow and

clump together, making many large and small groups of lumps. If many granulomas form in

an organ, they can affect how the organ works


          Who Gets It?

Sarcoidosis affects people of all ages and races worldwide.

It occurs mostly in:

Adults between the ages of 20 and 40

African Americans (especially women)


http://www.nyc.gov/html/doh/wtc/downloads/pdf/wtc/SarcoidosisFS.pdf


 -----------------------------------



Coccidioidomycosis in African Americans

 Jan, 2011


 Coccidioidomycosis is caused by Coccidioides species, a fungus endemic to the desert regions of the southwestern United States, and is of particular concern for African Americans. We performed a PubMed search of the English-language medical literature on coccidioidomycosis in African Americans and summarized the pertinent literature. Search terms were coccidioidomycosis, Coccidioides, race, ethnicity, African, black, and Negro. The proceedings of the national and international coccidioidomycosis symposia were searched. All relevant articles and their cited references were reviewed; those with epidemiological, immunologic, clinical, and therapeutic data pertaining to coccidioidomycosis in African Americans were included in the review. Numerous studies documented an increased predilection for severe coccidioidal infections, coccidioidomycosis-related hospitalizations, and extrapulmonary dissemination in persons of African descent; however, most of the published studies are variably problematic. The immunologic mechanism for this predilection is unclear. The clinical features and treatment recommendations are summarized. Medical practitioners need to be alert to the possibility of coccidioidomycosis in persons with recent travel to or residence in an area where the disease is endemic.


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3012635/


---------------------

5 Diseases More Common in Minorities

Oct 13, 2011

Although more and more people are living longer with colorectal cancer, new research has found that black people with the disease aren't living as long as whites.

In an analysis of more than 14,000 patients with stage 2 and 3 colorectal cancer who had surgery to remove tumors, followed by treatment to prevent recurrence, the 1,218 African-American patients had a lower five-year survival rate than their white counterparts, according to researchers, led by Greg Yothers of the National Surgical Adjuvant Breast and Bowel Project Biostatistical Center in Pittsburgh.

Five years after diagnosis, 72.8 percent of white patients survived cancer, but only 68.2 percent of blacks survived.

Colorectal cancer isn't the only medical condition that disproportionately affects certain races. Black people, for example, have much poorer health outcomes for a number of diseases.

"Across the board, if you look at the 15 leading causes of death in the U.S., blacks have higher death rates than whites in about 12 of them, including heart disease, cancer and stroke," said David Williams, the Norman professor of public health at the Harvard School of Public Health.
Cancer
Heart disease
HIV/AIDS

Diabetes


Osteoporosis


http://abcnews.go.com/Health/diseases-common-minorities/story?id=14722258



----------


Why 7 Deadly Diseases Strike Blacks Most

Health care disparities heighten disease differences between African-Americans and white Americans.

Several deadly diseases strike black Americans harder and more often than they do white Americans.

Fighting back means genetic research. It means changing the system for testing new drugs. It means improving health education. It means overcoming disparities in health care. It means investments targeted to the health of black Americans. And the evidence so far indicates that these investments will pay health dividends not just for racial minorities, but for everyone.

Yet we're closer to the beginning of the fight than to the end. Some numbers:

    Diabetes is 60% more common in black Americans than in white Americans. Blacks are up to 2.5 times more likely to suffer a limb amputation and up to 5.6 times more likely to suffer kidney disease than other people with diabetes.
    African-Americans are three times more likely to die of asthma than white Americans.
    Deaths from lung scarring -- sarcoidosis -- are 16 times more common among blacks than among whites. The disease recently killed former NFL star Reggie White at age 43.
    Despite lower tobacco exposure, black men are 50% more likely than white men to get lung cancer.
    Strokes kill 4 times more 35- to 54-year-old black Americans than white Americans. Blacks have nearly twice the first-time stroke risk of whites.
    Blacks develop high blood pressure earlier in life -- and with much higher blood pressure levels -- than whites. Nearly 42% of black men and more than 45% of black women aged 20 and older have high blood pressure.
    Cancer treatment is equally successful for all races. Yet black men have a 40% higher cancer death rate than white men. African-American women have a 20% higher cancer death rate than white women.

http://www.webmd.com/hypertension-high-blood-pressure/features/why-7-deadly-diseases-strike-blacks-most#1


--------------------------------


A Genetically Engineered Live Attenuated Vaccine of Coccidioides posadasii Protects BALB/c Mice against Coccidioidomycosis

 2007

ABSTRACT

Coccidioidomycosis (also known as San Joaquin Valley fever) is an occupational disease. Workers exposed to outdoor dust which contains spores of the soil-inhabiting fungus have a significantly increased risk of respiratory infection. In addition, people with compromised T-cell immunity, the elderly, and certain racial groups, particularly African-Americans and Filipinos, who live in regions of endemicity in the southwestern United States have an elevated incidence of symptomatic infection caused by inhalation of spores of Coccidioides posadasii or Coccidioides immitis. Recurring epidemics and escalation of medical costs have helped to motivate production of a vaccine against valley fever. The major focus has been the development of a defined, T-cell-reactive, recombinant protein vaccine. However, none of the products described to date have provided full protection to coccidioidal disease-susceptible BALB/c mice. Here we describe the first genetically engineered, live, attenuated vaccine that protects both BALB/c and C57BL/6 mice against coccidioidomycosis.

http://iai.asm.org/content/77/8/3196.full

---------------------------

Who Gets Lupus

It has been estimated that lupus affects 1.5 million Americans, and millions more worldwide.

Although the cause of lupus is unknown, genetics and hormones are thought to play a role.
Ninety percent are young women

The majority of people with lupus—90 percent—are female, and most first develop signs and symptoms of the illness between the ages of 15 and 44.

As adults, far fewer males than females develop lupus.

The scenario is much different under age 18 and over age 50, when as many males as females have the disease.

Many men struggle with the idea that they have a “woman’s disease,” in fact the diagnosis has no connection to manliness. Find out more about lupus in men
Lupus discriminates against African American, Latina, and Native American women

African-American women are three times more likely than Caucasian women to get lupus and develop severe symptoms, with as many as 1 in every 250 affected.

And the disease is two times more prevalent in Asian-American and Latina women than it is in Caucasian women. Women of  Native American descent are also disproportionately affected.

The famous Lupus in Minorities: Nature Versus Nurture (LUMINA) study—a large multi-ethnic, multi-regional, and multi-institutional examination of lupus begun in 1993—found that genetic and ethnic factors are more important than socioeconomic ones in influencing disease activity.

The study tracked death, damage, disability, and disease activity.

The results also suggest that there are probably other genetic factors affecting the presentation of the disease in the African-American and Latino communities.

The researchers have published numerous papers reporting study findings on the relative contribution of genetic and socioeconomic factors on the course and outcome of lupus in Latinos, African Americans, and Caucasians.

LUMINA findings include:

    African-Americans and Latinas with lupus tend to develop the disease earlier in life, experience greater disease activity such as kidney problems, and, overall, have more complications than Caucasian patients.
    Latinas had a poorer prognosis overall than Caucasian women, were more likely to have kidney involvement and damage, and showed a more rapid rate of kidney failure.
    African-Americans have a higher frequency of neurological problems such as seizures, hemorrhage, and stroke.
    Latinas experience a higher level of cardiac disease.

What have we learned from a 10-year experience with the LUMINA (Lupus in Minorities; Nature vs. nurture) cohort? Where are we heading? Read the PubMed abstract


http://www.lupusny.org/about-lupus/who-gets-lupus


-----------------------------

Ethnicity-Related Skeletal Muscle Differences Across the Lifespan

Jan, 2010

Abstract

Despite research and clinical significance, limited information is available on the relations between skeletal muscle (SM) and age in adults, specifically among Hispanics, African Americans (AA), and Asians. The aim was to investigate possible sex and ethnic SM differences in adults over an age range of 60 years. Subjects were 468 male and 1280 female adults (=18 years). SM was estimated based on DXA-measured appendicular lean-soft tissue using a previously reported prediction equation. Locally weighted regression smoothing lines were fit to examine SM trends and to localize age cutoffs; piecewise multiple linear regression models were then applied, controlling for weight and height, to identify age cutoffs for sex-specific changes in SM among the ethnic groups. The age of 27 years was identified for women and men as the cut-off after which SM starts to show a negative association with age. Both sexes had a similar ethnic pattern for expected mean SM at the age cutoff, with AA presenting the highest SM values, followed by Whites, Hispanics, and Asians. After the age cutoffs, the lowering of SM differed by ethnicity and sex: AA women showed the greatest SM lowering whereas Hispanic women had the least. Hispanic men tended to show a higher negative association of SM with age followed by AA and Whites. To conclude, significant sex and ethnic differences exist in the magnitude of negative associations of SM with age >27 years. Further studies using a longitudinal design are needed to explore the associations of ethnicity-related decline of SM with health risks.


 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2795070/


-----------


Do Black People Have Better Genetics For Building Muscle?

Is it true that race can influence muscle size?

It’s Not About Race. It’s About Personal Muscle Genetics

The black community is gifted in the field of athletics. This is backed by the fact that almost all top level running athletes are black. Track and field has always been dominated by black people, and it doesn’t look like the hegemony will end.

The fact that black people are good at fast and explosive sports such as sprinting has a direct effect on bodybuilding since both activities rely on fast twitch muscle fibers.

Fast twitch fibers have more potential for muscular growth than slow twitch fibers. This partially explains why people carrying a predominant amount of fast twitch fibers have larger musculatures.

However, there are “highs” and “lows” in every community. Some black people have good genetics for building muscle, but there are also many who don’t.

The fact that you’re black does not mean that you have superior genetics for building muscle mass by default. Muscle size depends on your personal genes and overall potential for growth rather than race.


Victor

March 20, 2017 at 11:42 pm


I think blacks are better for muscle building and whites are better for strength. Most of the powerlifters are white people. You don’t see any black domain in powerlifting and see in bodybuilding. Simples as that.

Black = size

White = strength


    Reply

    Abg

    March 30, 2017 at 12:07 am


    *facepalm*

    End your bro science idiot ie mr victor

    Reply

    Conway

    July 6, 2017 at 11:01 pm


    This is a very near-sighted comment my friend. I think culturally powerlifting has always been a Caucasian males sport in the US. Don’t forget people like Ronnie Coleman and CT Fletcher. We can’t take singular, anecdotal points of view and apply it to genetic statistics without scientific evidence. Cheers!


Reply

Scott

April 16, 2017 at 2:49 am


Such a baseless argument. I’m an African and not muscular like you think. White black or Asian we are the same.

Reply

Stephen

June 25, 2017 at 6:12 pm


Agree with Scott. We are all pretty much the same.




---------------------------



Not Politically Correct

Human Biodiversity, IQ, Evolutionary Psychology, and Evolution


https://notpoliticallycorrect.me/2016/10/19/blacks-are-not-stronger-than-whites/



--------------------------------


Race and health

 Race and health refers to the relationship between individual health and one's race and ethnicity. Differences in health status, health outcomes, life expectancy, and many other indicators of health in different racial and ethnic groups is well documented, referred to as health disparities. Race is a complex concept, and the two major competing theories of race use biological definitions and social construction to define racial difference. Although this relationship can vary depending on the definitions used, race is generally used in the context of health research as a fluid concept to group populations of people according to various factors that include but are not limited to ancestry, social identity, visible phenotype, and genetic makeup.[1] Determinants of health include environmental, social, and genetic factors, as well as the person's individual characteristics and behaviors.


 https://en.wikipedia.org/wiki/Race_and_health


------------------------------------


Inequality in disease

 While rates of incidence for many diseases vary based on biological factors and inheritable characteristics, a larger disparity, which cannot be explained by biological factors, exists in disease rates among varying racial and socioeconomic groups in the United States (for example, lower-income African-Americans and upper-class Caucasians). This suggests that social and economic factors play a role in determining who acquires certain diseases in the United States. For example, heart disease is the most dangerous disease in America, followed closely by cancer, with the fifth most deadly being diabetes. The general risk factors associated with these three diseases include obesity and poor diet, tobacco and alcohol use, physical inactivity, and access to medical care and health information. While some of these risk factors are individual health choices, all of them are also correlated with socioeconomic factors, such as gender, race, income, environment, and education, and consequently, a person’s likelihood for developing heart disease, cancer, or diabetes is in part correlated with these social factors. Men are more likely than women to die from heart disease. Likewise, African-Americans and other racial minorities have higher mortality rates from heart disease, cancer, and diabetes than their white counterparts. Among all racial groups, individuals who are impoverished or low income, have lower levels of educational attainment, and live in lower-income neighborhoods are all more likely to develop heart disease, cancer, and diabetes.


https://en.wikipedia.org/wiki/Inequality_in_disease


-----------------------------


Environmental racism


https://en.wikipedia.org/wiki/Environmental_racism


-----------------


Beauty Products Marketed to Black Women May Contain More Hazardous Chemicals: Report

 Dec 06, 2016


Beauty and hair products marketed to black women are more likely to contain potentially harmful chemicals and ingredients, according to a new report from a nonprofit environmental research group.


http://time.com/4591079/beauty-products-marketed-to-black-women-may-contain-more-hazardous-chemicals-report/



--------------------


Prenatal Exposure To Flame Retardants Linked With Lower IQ In Children

A risk found to be greater than lead exposure

 August 9, 2017

https://www.infowars.com/prenatal-exposure-to-flame-retardants-linked-with-lower-iq-in-children/

---------------

For more information on toxins in food and cosmetics, view our book titled "The DuPont Investigation" - DuPontInvestigation.Blogspot.com

----------


Secret World War II Chemical Experiments Tested Troops By Race

 June 22, 2015


As a young U.S. Army soldier during World War II, Rollins Edwards knew better than to refuse an assignment.

When officers led him and a dozen others into a wooden gas chamber and locked the door, he didn't complain. None of them did. Then, a mixture of mustard gas and a similar agent called lewisite was piped inside.

"It felt like you were on fire," recalls Edwards, now 93 years old. "Guys started screaming and hollering and trying to break out. And then some of the guys fainted. And finally they opened the door and let us out, and the guys were just, they were in bad shape."



Edwards was one of 60,000 enlisted men enrolled in a once-secret government program — formally declassified in 1993 — to test mustard gas and other chemical agents on American troops. But there was a specific reason he was chosen: Edwards is African-American.

"They said we were being tested to see what effect these gases would have on black skins," Edwards says.


http://www.npr.org/2015/06/22/415194765/u-s-troops-tested-by-race-in-secret-world-war-ii-chemical-experiments


----------

The Depo Provera shot exposed! Present day eugenics

 The Depo Provera has proven side effects that the FDA overlook and target non whites with this product

https://www.youtube.com/watch?v=YDqHtPtTmjI

-------



New Documentary Alleges CDC Withheld Proof of Link Between Vaccines and Autism in Black Boys

 Jan 26, 2016

A controversial scientist says the data was omitted from an official CDC report a decade ago. The agency says the link doesn't exist.


There has long been a debate about the link between vaccinations and autism, beginning with a now widely discredited study from British medical researcher Andrew Wakefield. Now, a new documentary from TruthInMedia.com alleges that not only is there a link, but that the Centers for Disease Prevention and Control (CDC) covered it up.
In 2014, CDC doctor William Thompson sent Congress paperwork that he said was proof that the agency withheld data that suggested that Black boys who received the measles, mumps and rubella (MMR) vaccine before the age of 36 months were at increased risk of developing autism. The CDC maintains that there was not enough data to draw race-based conclusions, and Snopes.com has an extensive post meant to debunk Thompson’s claims.
 https://www.colorlines.com/articles/new-documentary-alleges-cdc-withheld-proof-link-between-vaccines-and-autism-black-boys

-----

Is Swine Flu A Race-Specific Virus?

April 29, 2009


First death in U.S. is Mexican toddler, prompting questions about why only hispanics have died despite outbreak spreading to at least ten countries.


The first swine flu death in the United States has been confirmed, but the victim is a Mexican toddler who caught the illness in Mexico before traveling to Texas. Serious questions must now be asked about why a virus that has spread across at least 10 countries and is suspected in many others has only killed hispanics, and whether a race-specific bio-weapon is being beta-tested.


https://www.prisonplanet.com/is-swine-flu-a-race-specific-virus.html


-----


Can genes be patented?

A gene patent is the exclusive rights to a specific sequence of DNA (a gene) given by a government to the individual, organization, or corporation who claims to have first identified the gene. Once granted a gene patent, the holder of the patent dictates how the gene can be used, in both commercial settings, such as clinical genetic testing, and in noncommercial settings, including research, for 20 years from the date of the patent. Gene patents have often resulted in companies having sole ownership of genetic testing for patented genes.

On June 13, 2013, in the case of the Association for Molecular Pathology v. Myriad Genetics, Inc., the Supreme Court of the United States ruled that human genes cannot be patented in the U.S. because DNA is a "product of nature." The Court decided that because nothing new is created when discovering a gene, there is no intellectual property to protect, so patents cannot be granted. Prior to this ruling, more than 4,300 human genes were patented. The Supreme Court's decision invalidated those gene patents, making the genes accessible for research and for commercial genetic testing.

The Supreme Court's ruling did allow that DNA manipulated in a lab is eligible to be patented because DNA sequences altered by humans are not found in nature. The Court specifically mentioned the ability to patent a type of DNA known as complementary DNA (cDNA). This synthetic DNA is produced from the molecule that serves as the instructions for making proteins (called messenger RNA).


 https://ghr.nlm.nih.gov/primer/testing/genepatents


----------------

How did patenting cause conflicts within the Human Genome Project?

Some scientists involved in the Human Genome Project upset the collaborative nature by trying to patent sections of the DNA sequence for their own financial gain.

Despite the collaborative atmosphere established during the years of the Human Genome Project?, it was not without its conflicts and disagreements.

Some scientists displayed differing ideas that threatened the progress of the project. Many were keen to achieve the scientific recognition of making an important discovery whilst also wanting to accommodate the needs of their corporate partners and make money!

    “Through patenting, companies could gain ownership over specific sequences of DNA or genes.

Patenting was one way individuals were able to make commercial profit from the Human Genome Project. Through patenting?, companies could gain ownership over specific sequences of DNA? or genes?. This meant the company would have full rights over that sequence, allowing them to decide who can profit from carrying out research on it (and how much they charge them to access it) and how much to charge individuals wanting to be tested for those genes.


 http://www.yourgenome.org/stories/how-did-patenting-cause-conflicts-within-the-human-genome-project


----------------


Chinese Scientists Genetically Modify Human Embryos—Again

 4/8/16

Just one year after scientists in China made history by modifying the DNA of human embryos, a second team of Chinese researchers has done it again. Using CRISPR/Cas9, the researchers introduced HIV-resistance into the embryos, showcasing the tremendous potential for gene-editing.

In that earlier work, the Chinese scientists modified a gene responsible for a fatal blood disorder, but the embryos were quickly destroyed after the experiment. It was a watershed moment in biotechnology, showcasing the tremendous potential of CRISPR—a powerful gene editing tool—to alter our offspring at the genetic level. Should this technology ever reach the clinical stage, it could be used to eliminate all sorts of genetic diseases, but it could also be used to introduce entirely new capacities.


 http://gizmodo.com/chinese-scientists-genetically-modify-human-embryos-aga-1769884160


-----

Massive DNA Collection Campaign in Xinjiang, China

https://soylentnews.org/article.pl?sid=17/05/26/0254237&from=rss


-------


GOP Bill Would Allow Genetic Testing Demands By Employers
It Might Soon Be Legal for Employers to Force You Into a Genetic Test

Mar 10, 2017


http://fortune.com/2017/03/10/genetic-testing-workplace-wellness-bill/

--------


Employees who decline genetic testing could face penalties under proposed bill

 March 11, 2017


http://www.journalnow.com/news/local/employees-who-decline-genetic-testing-could-face-penalties-under-proposed/article_ec4136ca-650a-5ecd-9963-f5fb91acf1d4.html


--------------


 Completely unconstitutional bill proposes forced genetic screening for employees


https://voat.co/v/pizzagate/comments/1710447


---------------------



Bill S-201: Liberal Backbenchers Defy Trudeau To Approve Genetic Testing Bill


OTTAWA — Liberal backbenchers have defied Prime Minister Justin Trudeau, voting in favour of a bill that would bar health and life insurance companies from forcing clients to disclose the results of genetic testing.

Just hours before the vote late Wednesday in the House of Commons, Trudeau said the proposed law is unconstitutional because it intrudes on provincial jurisdiction. He recommended that MPs vote against it.

But most Liberal backbenchers, along with Conservative and New Democrat MPs, ignored Trudeau's warning. The bill passed by a vote of 222-60.

It was a free vote, meaning Liberal backbenchers were not required to toe the party line. They did, however, come under pressure from the government, including Trudeau.


 http://www.huffingtonpost.ca/2017/03/08/trudeau-bill-s-201-unconstitutional-_n_15246810.html



-----------------


Many say that genetic testing is being done for several reasons, such as the government wanting to have your DNA, and for Obamacare or health insurance companies to have your information as well. This is also being done, because the government would like to also be able to do more scientific research, with many of these chemicals, including pollution being introduced in our society, and that can even change your DNA over a period of time. If your DNA can change or mutate, then you would think that the government would want to have an update on your DNA. Many claim that evolution in animals is caused by a DNA mutation, this can be a good thing. DNA mutations can also be bad, and can lead to health problems, including cancer. Radiation can even cause a mutation in the DNA of different organisms. Many say that one of the goals of many of these agencies such as MI5 and other security agencies, is to master the genetic coding, sequence and structure of DNA, through various techniques, including with genetic modification. To many, DNA is considered one of the great mysteries in our universe and even a miracle of life. Many even talk how the government wants everyone's DNA, in order to have a database to track people. You can even put DNA in a database, for drones to find people with just pointing a lazer at you, to identify you, and even harm or detain an individual. Some question if this is being done to verify certain races of people as well.


-------

Russia 'collects DNA samples' of Muslim women

2013

Saliva samples of conservative women taken in wake of spate of suicide attacks in run-up to Sochi Winter Olympics.

 Russia is allegedly taking saliva samples from religiously conservative Muslim women to help its security forces identify remnants of suicide bombers in case of an attack sabotaging the Sochi Winter Olympics, Reuters news agency has reported, quoting locals in the North Caucasus.


 http://www.aljazeera.com/news/europe/2013/10/russia-collects-dna-samples-muslim-women-2013103181444480202.html


--------------------


 [For more information about the crisis of radical Islam in the Middle East and around the globe, view our book titled Islamic Sharia Law & Genocide - "The Middle East Conflict Investigation." - IslamicShariaGenocide.Blogspot.com ]



-----------------------


Your DNA Changes

 https://www.genisyss.com/dna-changes/


Many people are not aware that their DNA changes over time. Because DNA can be used for identification purposes, people assume that it remains the same over the course of their life. Although the pattern of the nucleotides (AGCT) doesn’t change, a process called DNA methylation describes the important changes that can occur and have been associated with the appearance of various medical conditions. An entire field of science, epigenetics, studies DNA and how it chemically changes. Every day, we encounter numerous factors that change our DNA including the sun’s radiation, pollution, chemicals in our foods and surroundings, and even stress. These DNA changes contribute to the expression of genetic and lifestyle-linked diseases including heart disease, cancer, diabetes, autism and a long list of others. Many of these diseases are incurable, but with the rapid progress that genetic research is making, this is changing. Already, DNA is being used therapeutically, and its usage is becoming an integral part of precision medicine. Stem cell research has identified ways to deliver therapeutic DNA to specific sites in your body. DNA is central to disease prevention and treatment.


---------------------


Isolated populations and complex disease gene identification

 2008























Table 1
Recent genetic studies of complex diseases and traits in special populations

Complex disease/trait
Gene/locus
Population/isolate
Reference
Affective disorders
Several loci
Northern Sweden
[34]
Asthma
IRAK-M (interleukin-1 receptor-associated kinase M)
Sardinia
[74]
Asthma
CHI3L1 (chitinase 3-like 1)
Hutterites
[25]
Asthma
NPSR1 (neuropeptide S receptor 1)
Finland
[24]
Atrial fibrillation
4q25
Iceland
[11]
Bipolar disorder
5q31-34
Antioquia (Colombia), Central Valley of Costa Rica
[29]
Bone mineral density
Several loci
Iceland
[75]
Breast cancer
5p12, 2q35, 16q12
Iceland
[76, 77]
Myocardial infarction
9p21
Iceland
[8, 78]
Coronary heart disease
8p22
French Canadians
[79]
Crohn's disease
Several loci
French Canadians
[80]
Fasting glucose levels
G6PC2 (glucose-6-phosphatase, catalytic, 2)/ABCB11 (ATP-binding cassette, sub-family B (MDR/TAP), member 11) region
Finland, Sardinia
[81]
Exfoliation glaucoma
LOXL1 (lysyl oxidase-like 1)
Iceland
[82]
Height
Several loci
Iceland
[13]
Height
GDF5 (growth differentiation factor 5)/UQCC (ubiquinol-cytochrome c reductase complex chaperone) locus
Finland, Sardinia, Amish
[83]
Nicotine dependence and smoking-related diseases
15q24
Iceland
[84]
Obesity
FTO (fat mass and obesity associated), PFKP (phosphofructokinase, platelet)
Sardinia
[28]
Parkinson's disease
GBA (β-glucocerebrosidase)
Ashkenazi Jews
[37]
Pigmentation
Several genes
Iceland
[14, 15]
Prostate cancer
Xp11.22, 2p15, 17q
Iceland
[12, 85]
Psychotic and bipolar spectrum disorders
TSNAX (translin-associated factor X)/DISC1(disrupted in schizophrenia 1) locus
Finland
[86]
Psychosis
TGIF (TGFB-induced factor)
Central Valley of Costa Rica
[87]
Schizophrenia
DRD2 (dopamine D2 receptor)
Basques
[30]
Type 2 diabetes
CDKAL1 (CDK5 regulatory subunit associated protein 1-like 1)
Iceland
[10]

 https://genomebiology.biomedcentral.com/articles/10.1186/gb-2008-9-8-109




---------------------- -


Finnish heritage disease

Finnish heritage diseases include:

    APECED (autoimmune polyendocrinopathy—candidiasis—ectodermal dystrophy)
    Aspartylglucosaminuria, a lysosomal storage disease
    Congenital adrenal hyperplasia[6]
    Congenital nephrotic syndrome,[7] a kidney disease of newborn babies
    Congenital chloride diarrhea
    Congenital stromal corneal dystrophy
    GRACILE syndrome
    Lethal arthrogryposis with anterior horn cell disease
    Lethal congenital contracture syndrome 1
    Meretoja syndrome
    Meckel syndrome
    Myotonia congenita
    Nonketotic hyperglycinemia
    Salla disease,[8] a lysosomal storage disease
    PEHO syndrome
    Rapadilino syndrome
    Retinoschisis
    Usher syndrome

Three rare causes of dwarfism are included in the Finnish heritage: cartilage–hair hypoplasia, diastrophic dysplasia and Mulibrey nanism.

Four genetically distinct subtypes of neuronal ceroid lipofuscinosis are found in the Finnish heritage: CLN1, CLN3, CLN5, and CLN8. Names for conditions associated with these subtypes include infantile neuronal ceroid lipofuscinosis, Jansky–Bielschowsky disease and northern epilepsy syndrome. As of 2001, CLN5 and CLN8 had been reported almost exclusively in Finland.

Meckel syndrome type 1 (MKS1[10]), a lethal condition, is known in 48 Finnish families.
Other genetic diseases

The European Organization for Rare Diseases (EURORDIS) estimates that there are between 5,000 and 7,000 distinct rare diseases, affecting between 6% and 8% of the population of the European Union. The majority of genetic diseases reported in Finland are not part of the Finnish disease heritage and their prevalence is not higher in Finland than worldwide.

Some genetic diseases are disproportionately rare in Finns. These include cystic fibrosis and phenylketonuria. In Finland, about 1 in 80 persons are carriers of a cystic fibrosis mutation, compared with an average of 1 in 25 elsewhere in Europe.


https://en.wikipedia.org/wiki/Finnish_heritage_disease


----------------------------------


Finland's Fascinating Genes

 April. 2005

The people in this land of lakes and forests are so alike that scientists can filter out the genes that contribute to heart disease, diabetes, and asthma

 http://discovermagazine.com/2005/apr/29-finlands-fascinating-genes


------------------------------



Unique disease heritage of the Dutch-German Mennonite population.

 April 15, 2008


https://www.ncbi.nlm.nih.gov/pubmed/18348259


--------------------------------



 Molecular diagnosis of some common genetic diseases in Russia and
the former USSR: present and future.


1993


 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1016272/pdf/jmedgene00004-0055.pdf



---------------------------------


Prevalences of hereditary diseases in different populations of Russia

 Sep 2007


 https://link.springer.com/article/10.1134/S1022795407090104



------------------------------



The Vikings and Baron Dupuytren's disease

Oct, 2001


Dupuytren’s disease (DD) is an ancient affliction of unknown origin. It is defined by Dorland as shortening, thickening, and fibrosis of the palmar fascia producing a flexion deformity of a finger. Tradition has it that the disease originated with the Vikings, who spread it throughout Northern Europe and beyond as they traveled and intermarried. After being present for hundreds of years, DD was named in the 19th century after a famous French surgeon, who was not the first to describe it. This article reviews the history of DD and describes its incidence, clinical manifestations, and treatment.


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1305903/



---------------------------


Vikings could be to blame for why Scots have highest levels of multiple sclerosis in the world, say scientists

December 10, 2012

    Study found one in every 170 women in the Orkney Islands suffers from multiple sclerosis
    It is the highest rate in the world and has been linked with their Norse ancestry
    Scientists say Vitamin D deficiency could also be to blame


http://www.dailymail.co.uk/health/article-2245978/Vikings-blame-Scots-highest-levels-multiple-sclerosis.html



-----------------------------

Human genetics: lessons from Quebec populations.

 2001


 https://www.ncbi.nlm.nih.gov/pubmed/11701644

---------


Hereditary disorders in the French Canadian population of Quebec. I. In search of founders.

1994


https://www.ncbi.nlm.nih.gov/pubmed/8194844


--------


Europe's most common genetic disease is a liver disorder

Feb 6, 2012


https://www.embl.de/aboutus/communication_outreach/media_relations/2008/080205_heidelberg/



----------------------------------

Ethnicity and adverse drug reactions

Personalised drug treatment is getting closer but will not replace good clinical judgment

May 2006

Whether ethnicity is an important contributor to the variable outcome of drug treatment is still a matter of debate. Research evidence on such associations is limited in quantity and variable in quality. Too often patients' ethnicity is classified by using poorly defined criteria or an inadequate scientific basis. Indeed, both skin colour and self identification of ethnic origin seem to be poorly correlated with molecular genetics, and most genetic variability is found within, rather than among, continental populations. In addition, ethnic differences in drug response might originate from cultural or environmental factors.


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1463978/


----------------------------------------------


Lupus in AfroCaribbeans and Other Ethnic Groups


1997


http://www.lupus-support.org.uk/Ethnic.htm


------------------------------------------------



 The HPV Vaccine and the Case for Race-Based Medicine


Nov 1, 2013


The human papillomavirus (HPV) vaccine, approved in 2006, protects against strains of the virus responsible for 70% of cervical cancers. But what about the remaining 30%?

It turns out that those strains circulate more frequently among African-American and non-white Hispanic women, meaning that even if they are properly immunized, these populations aren’t protected against the sexually transmitted virus and the cancer it can cause...


http://healthland.time.com/2013/11/01/the-hpv-vaccine-and-the-case-for-race-based-medicine/

--------


Study: Whites with muscular dystrophy live up to 12 years longer than blacks

Sep 13, 2010

Whites with muscular dystrophy live up to 12 years longer than their African American counterparts, according to a study published Monday in Neurology.

Although medical advancements over a period of 20 years increased the life span of patients with the debilitating muscle disease, those improvements haven’t been equal among different groups.White women with muscular dystrophy had a median death age of 63, versus 51 for African American women.  For men, their median age at death was 33, versus 23 for African American males.


http://thechart.blogs.cnn.com/2010/09/13/study-whites-with-muscular-dystrophy-live-up-to-12-years-longer-than-blacks/



------


Health Disparities in Hormone Disorders

Oct 2013

What are health disparities?

Health disparities refer to unequal health status or health care between groups of people due to differences in their background, physical traits, or their environment. Group differences include race/ethnicity, country of origin, sex, income, and disability. These and other differences can affect how often people in a group get a disease, how sick they are, and their chance of dying from the disease. Some people may not be able to get good health care or have the opportunity to make healthy lifestyle choices.

Unfortunately, health disparities affect large and diverse groups of people. They exist for many types of illnesses, including endocrine (hormone) disorders and diseases.

Type 2 diabetes

Compared with white adults, minority adults are more likely to

    Develop type 2 diabetes
    Have diabetic complications such as diabetes eye disease and kidney disease
    Die from diabetes


Gestational diabetes

Women who have new diabetes during pregnancy are more apt to develop type 2 diabetes later. Gestational diabetes is more common in Hispanics, Asians, and Native Americans than in whites or blacks. Yet, for some reason, black women who do get this type of diabetes are even more likely to develop type 2 diabetes than women of other races. This holds true even when the groups have the same body mass index, or BMI (a measure of body size).


Osteoporosis

Fracture frequency: Fractures (broken bones) due to the bone-thinning disease osteoporosis are more common in white women than minorities. Yet black women are more likely to die than white women after breaking a hip. This may be because blacks are older and more often have other severe health problems at the time of fracture.

Gaps in diagnosis and treatment: Compared with whites, black women who had a fracture are less likely to receive a diagnosis of osteoporosis. And if they are at risk for fracture, black women receive preventive osteoporosis medicine less often than whites do.
Low vitamin D

A shortage of vitamin D in the body worsens bone health and may raise the risk for some other diseases. Low vitamin D is a common problem among all races and ethnic groups, but blacks have lower vitamin D levels than others. There likely are many reasons for blacks’ higher risk for vitamin D shortage. One reason is their dark skin lessens their ability to make vitamin D from the sun. Compared with whites, blacks also tend to have less intake of vitamin D from supplements and their diet.




 http://www.hormone.org/hormones-and-health/scientific-statements/health-disparities


--------------------------


Study Links Disparities in Pain Management to Racial Bias

 April 04, 2016

https://news.virginia.edu/content/study-links-disparities-pain-management-racial-bias


------------------------------


The Impact of Race or Ethnicity in Crohn's Disease


Edward V. Loftus, Jr., M.D.

Professor of Medicine

Mayo Clinic

Rochester, Minnesota, USA


Caucasians, especially northern European

ancestry


Scandinavia


Northern Europe


British Isles



United States and Canada



Increased risk in Jews


Uncommon in African Americans and other

racial minorities in U.S.

http://www.gihealthfoundation.org/GI_news_and_library/library/ppts/IBD/impactofraceethnicity.pdf



--------------------------------------------------


How Does Race Affect COPD?

 Oct 8, 2015


 Chronic obstructive pulmonary disorder (COPD) is one of the many chronic lung diseases that can leave sufferers struggling to breathe. It is the fourth leading cause of death in the United States, and while it is estimated that 12.7 million people have COPD, it is also assumed that there is a vast number of individuals with COPD who are not diagnosed. Many of the individuals who are undiagnosed may not fit into the majority racial profile. Currently, there are more Caucasian individuals diagnosed with COPD than those of African decent—despite newer research showing that the gap may not actually be significant. By having a larger volume of white individuals diagnosed with COPD, scientists previously accepted the notion that white individuals are more susceptible to COPD than black individuals. Surprisingly, new research refutes this finding as African American individuals are more likely to receive a COPD diagnosis at a younger age and with less of a cumulative-smoking background, or less years with first-hand smoke.  Theoretically, this supports the idea that African Americans are more susceptible to COPD. With findings pointing in different directions, scientists are baffled by the potential connection between COPD and race.


https://lunginstitute.com/blog/how-does-race-affect-copd/



-------------------------------


Genetics and Genomic Medicine in Colombia

Mar 5, 2015


Genetic Disorders in Colombia

We have evidence from the pre-Columbian era on the recognition of certain disorders from the Tumaco-La Tolita culture, a group of Amerindians settled in what is now the Colombian and Ecuador coast circa the year 600 bc. A collection of clay figurines have preserved in incredible detail the representation of what are thought to be prevalent genetic syndromes in the population at that time, such as: Morquio, Down syndrome, and Treacher-Collins


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367080/


---------------------------------


Medical genetics and genomic medicine in Chile: opportunities for improvement

 14 July 2015


http://onlinelibrary.wiley.com/doi/10.1002/mgg3.166/full

----------------------------------


Ethical issues in genetics and public health in Latin America with a focus on Argentina

 July, 2015


http://pubmedcentralcanada.ca/pmcc/articles/PMC4524838/


----------------------------------


Rare disease landscape in Brazil: report of a successful experience in inborn errors of metabolism

2016

The LSD Brazil network

A particular group of genetic metabolic conditions—the lysosomal storage diseases, LSDs—has received a disproportionate attention among the IEM, compared to their relative size (there are around 60 LSDs among the 600 IEM), as specific treatments—as enzyme replacement therapies, substrate reduction therapy and molecular chaperones—became available for many of these conditions. As the investigation for LSDs usually follows a relatively different strategy compared to the investigation for the other IEM, we decided to create a separate network:

The NPC Brazil network

As Niemann-Pick type C (NPC) disease requires for its diagnosis an invasive technical tool, the Filipin staining test performed in fibroblasts, we set up an independent network to deal with the protocol to diagnose this challenging disease.


https://ojrd.biomedcentral.com/articles/10.1186/s13023-016-0458-3


----------------------------------


 Movement disorders in Latin America


June 29, 2005


      Contents

1.

Introduction

....................................................................................126

2.

Idiopathic Parkinson’s disease and parkinsonism

.........................................................127

3.

Dystonia

.......................................................................................127

4.

Tics

..........................................................................................128

5.

Tremor

........................................................................................128

5.1.

Chin tremor .

..............................................................................128

6.

Infectious-parasitic and autoimmune

..................................................................128

6.1.

HIV infection and AIDS

......................................................................129

6.2.

Meningitis . .

..............................................................................129

6.3.

Neurocysticercosis

..........................................................................129

6.4.

Malaria

..................................................................................130

6.5.

Paracoccidioidomycosis

......................................................................130

6.6.

Sydenham’s chorea (SC)

......................................................................130

6.7.

Prion disease

..............................................................................131

6.8.

Subacute sclerosing panencephalitis (SSPE)

........................................................131

7.

Environmental and lifestyle

.........................................................................132

7.1.

Central and peripheral trauma

..................................................................132

7.2.

Drug-induced movement disorders (DIMD)

........................................................132



7.3.

Exposure to toxins—occupational neurology

.......................................................132

7.4.

The parkinsonism complex of Guadeloupe

.........................................................133

8.

Cerebrovascular disorders

..........................................................................133

9.

Inherited movement disorders .

......................................................................133

9.1.

Huntington’s disease . . .

......................................................................133

9.2.

Spinocerebellar ataxias .

......................................................................134

9.2.1.

SCA3—Machado–Joseph disease

.........................................................134

9.2.2.

SCA 2

.............................................................................134

9.2.3.

SCA 10

............................................................................135

9.2.4.

Other SCAs . . .

......................................................................135


 http://www.neurologia.ufsc.br/wp-content/uploads/2008/08/mdla.pdf


----------------------------------


Medical genetics and genomic medicine in Chile: opportunities for improvement

 July 14, 2015


http://onlinelibrary.wiley.com/doi/10.1002/mgg3.166/full


----------------------------------


Latin-Americans with different Native-American ancestry show different health risks

May 26, 2017

A genetic study of Chileans finds Mapuche and Aymara ancestry linked to different diseases


 Latin Americans originate from a mix of people with Native American, European and African ancestry. A new study finds that different types of original Native American ancestry can be associated to different causes of death. Justo Lorenzo Bermejo and Felix Boekstegers from Heidelberg University in Germany, and their Chilean colleagues report these findings in a new study published May 26th, 2017 in PLOS Genetics.


https://www.eurekalert.org/pub_releases/2017-05/p-law051817.php


-----------------------------------


Respiratory diseases in the world


https://www.ersnet.org/pdf/publications/firs-world-report.pdf


-----------------------------------

Next generation sequencing: Coping with rare genetic diseases in China

 2016 August


Each year in China, we estimate that there are around 26,000 new DS patients added to the population. This estimate is based on an annual birth rate of 18 million newborn and a disease incidence of DS of 1 in 700 births. Factoring in the life expectancy of DS patients which today is generally over 50 years of age and, adjusting for population growth rate over the last 50 years, we estimate that DS patients alone currently account for around 1.4 million people. After DS, sex chromosomal diseases, such as Turner (45,X), Klinefelter (47,XXY), Triple X syndrome (47,XXX) and Jacob (47,XYY) syndromes have a combined incidence of 1 in 1,000 births (4). With a near normal life expectancy, the number of Chinese individuals with sex chromosome disease syndromes is estimated to exceed 2 million. In a review of chromosome disease incidence in the United Stated (US), it has been estimated that the combined number of patient's with other types of chromosome disease syndromes far exceeds that of DS and sex chromosome disease patients (5). On this basis, we estimate that the number of Chinese patients with rare genetic disease caused by chromosomal abnormalities alone is well over 10 million.


Although monogenic diseases are less prevalent than chromosome diseases, based on population size, they still represent a significant proportion of the overall genetic disease burden in China. On top of the list are blood disorders such as alpha- and beta- Thalassemia, Sickle Cell Anemia (SCA) and Hemophilia, the muscle disorders Duchenne Muscular Dystrophy (DMD) and Spinal Muscular Atrophy (SMA), the metabolic disease Phenylketonuria (PKU), the sensory disorder Hereditary Hearing Loss (HHL) and mental disabilities such as Fragile X Syndrome (FXS). In southern China, the incidence rates of alpha-and beta- thalassemia are among the highest in the world, with a combined carrier rate of 11% and 23% in Guangdong and Guangxi provinces respectively (6,7), making thalassemia the number one rare genetic disease in these regions. However, since the average life expectancy is less than 10 years, we estimate that the number of living thalassemia patients in these provinces would not exceed more than 25,000. For the other monogenic diseases mentioned, disease incidence is much lower, ranging from as high as 1 in 3,000 to as low as 1 in 10,000 individuals. Despite the low incidence rate of each individual single gene disease, their combined total still represents a large body of patients in China because of the sheer magnitude of the population size. We estimate that the number of existing patients afflicted with monogenic diseases exceeds well over a million in China.


 http://pubmedcentralcanada.ca/pmcc/articles/PMC4995420/


---------------------------------


Prevalence of congenital malformations and genetic diseases in Korea.


 1999


 A nationwide investigation of congenital malformations and genetic diseases in Korea was conducted by analyzing Medical Insurance data for infants aged under 1 year. Medical Insurance data were obtained for 1993 and 1994 and the ICD-9 (International Classification of Diseases, Ninth Revision) code was used to classify the diseases. The coverage rate of medical insurance was approximately 95% of the total population. Anomalies of the cardiovascular, musculoskeletal, and gastrointestinal systems, in descending order of frequency, were more frequent than anomalies in other systems. The average prevalence of cardiovascular anomalies for 1993 and 1994 was 15 per 1000 infants, and ventricular septal defect, with an average prevalence of about 3.50 per 1000 for 1993 and 1994, was the most frequent cardiovascular anomaly in infants. Polydactyly was the most frequent musculoskeletal anomaly, with an average prevalence, for 1993 and 1994, of about 1.20 per 1000 infants. Anencephaly had the highest frequency of nervous system anomalies. Congenital hypertrophic pyloric stenosis was the most common of the gastrointestinal anomalies. The prevalence of the congenital malformations and genetic diseases examined was similar to that reported in other countries. Total medical expenses for the care of patients with each disease entity were also estimated. The highest medical expenses were incurred for ventricular septal defect, congenital coagulation factor VIII disorders, atrial septal defect, tetralogy of Fallot, and spinal anomalies, in descending order of magnitude. This investigation could be helpful in planning social welfare systems, as well as for elucidating the current status of congenital malformations and genetic diseases in Korea, and in other Asian countries.


https://www.ncbi.nlm.nih.gov/pubmed/9929974


------------------------------


The Genome of a Mongolian Individual Reveals the Genetic Imprints of Mongolians on Modern Human Populations

Dec 8, 2014


https://academic.oup.com/gbe/article/6/12/3122/546344/The-Genome-of-a-Mongolian-Individual-Reveals-the


----------------------------

Genetic disease patterns in Japan: a review.

1992

 https://www.ncbi.nlm.nih.gov/pubmed/1427743


---------------------------


Eugenics in Japan

https://en.wikipedia.org/wiki/Eugenics_in_Japan#Abolition_of_eugenics_laws


---------------------

Eugenics

 https://en.wikipedia.org/wiki/Eugenics


---------------------


 Native Hawaiian and Pacific islander Health Disparities


 http://www.apiahf.org/sites/default/files/NHPI_Report08a_2010.pdf


 -------------


      New insights into ancestry and health of Polynesians and

     New Zealand Mäori

     http://scientists.org.nz/files/posts/justinhodgkiss/NZSR73_1_Chambers.pdf


----------------


Ancient Denisovan DNA excavated in modern Pacific Islanders
Substantial genomic remnants of the extinct Denisovans recovered in Oceania populations

    March 17, 2016

Source:: University of Washington Health Sciences/UW Medicine


--------------


Differences in disease frequency between Europeans and Polynesians: directions for future research into genetic risk factors.

March, 2001

 The purpose of this review is to identify complex genetic diseases that might be common in Polynesian ethnic groups because of a high frequency of susceptibility genes. Since a number of Polynesian ethnic groups are descended from recent founder populations, they may be especially suitable for studies designed to identify these genes. We have reviewed the epidemiological literature looking for diseases that i) have a higher frequency in at least two Polynesian groups than in Europeans living in the same geographic areas, ii) are not at high frequency in Polynesia entirely because of high levels of known environmental risk factors, and iii) are known to be inherited in other ethnic groups. Twenty-one diseases fulfilling these three criteria were identified. It may be possible to design studies to identify the genes that cause these diseases in Polynesian ethnic groups.
https://www.ncbi.nlm.nih.gov/pubmed/12017815


-------------

How a Powerful Obesity Gene Helped Samoans Conquer the South Pacific


By studying the genomes of more than 5,000 Samoans, researchers have uncovered a single gene that boosts a person’s obesity risk by upwards of 40 percent. Remarkably, this gene—which appears in a quarter of all Samoans—may have arisen in the population as they colonized the South Pacific.

As described in the latest edition of Nature Genetics, this “thrifty” genetic variant, called CREBRF, is associated with a 1.5 percent increase in Body Mass Index (BMI). So, for a person of average height weighing around 180 pounds, this gene corresponds to an extra 10 pounds. As noted by the researchers in their study, CREBRF promotes more efficient storage of fat and features “an effect size much larger than that of any other known common BMI risk variant.”


Working with colleagues from several universities, Stephen McGarvey from Brown University made the discovery while scanning the genomes of thousands of Samoans. This populations has some of the highest obesity rates in the world, a fact that prompted the scientists to conduct a genetic investigation. Around a quarter of all Samoans involved in the study had the genetic variant, which was associated with 30 to 40 percent increased odds of being obese compared to those who don’t have the gene. At the same time, this gene is virtually non-existent in European and African populations and occurs at very low frequencies among East Asians.

“Although we have found a genetic variant with a reasonable biological mechanism, this genetic variant is just one part of the many reasons for the high levels of BMI and obesity among Samoans,” noted McGarvey in a press statement.


 http://gizmodo.com/how-a-powerful-obesity-gene-helped-samoans-conquer-the-1784266550


------------------

Asian genetic killer found in Polynesian men

 June 16, 2003


A mysterious genetic disease that kills Asian men in their sleep also affects Polynesians, researchers have discovered.

Known as sudden unexplained death syndrome, or SUDS, it is an inherited disorder that strikes South East Asian men aged 40 to 60 while they sleep. The discovery of SUDS in a new population was announced at the American Heart Association's second Asia Pacific Scientific Forum last week.

Called Lai Thai in Thailand, it rarely affects women. As a result, in some rural Thai villages, men at risk sleep in womens' nightclothes to ward off the 'ghoul' they believe is responsible for killing men during sleep.

But scientists know SUDS is caused by a condition called ventricular fibrillation, when the heart's electrical activity is out of synch, preventing the heart from pumping enough blood to the body.


 http://www.abc.net.au/science/articles/2003/06/16/877742.htm


--------------

Pacific islanders pay heavy price for abandoning traditional diet

Replacing traditional foods with imported, processed food has contributed to the high prevalence of obesity and related health problems in the Pacific islands. Jane Parry reports.

Scattered across the Pacific Ocean are thousands of islands which make up three regions known as Melanesia, Micronesia and Polynesia. Beyond the image of white sandy beaches and carefree lifestyles, the Pacific islands are facing serious health problems, the prime culprit being imported foods.


http://www.who.int/bulletin/volumes/88/7/10-010710/en/

-------------

How does Asian ancestry affect heart disease risk?

 January 19, 2016


The world is picking up the bad habits of Western culture when it comes to health. Lifestyle – especially what you eat and how much you exercise – has a big impact on heart disease. Unfortunately, many people are consuming too many calories and getting too little exercise. Across the globe, people are abandoning their traditional diets and lifestyles and are suffering the consequences.

For reasons that are unclear, Asians and Asian Americans tend to develop diabetes at a lower body mass index (BMI) than Caucasians. People of Asian descent who carry 20 extra pounds are at risk of developing diabetes, whereas Caucasians usually need to carry 40 or more extra pounds before they are at risk. This is true for people of Asian descent regardless of where in the world they live.

The literature indicates that an astonishing 11 percent of Chinese have diabetes. Perhaps even more amazing, 50 percent of Chinese have prediabetes, a condition that typically emerges into diabetes. Out of 1.3 billion human beings, that’s 143 million people with diabetes and 650 million with prediabetes!


http://www.utswmedicine.org/stories/articles/year-2016/heart-disease-asian.html


---------------------------------------



Leading Causes of Death among Asian American Subgroups (2003–2011)

Methods and Findings

We examined national mortality records for the six largest Asian subgroups (Asian Indian, Chinese, Filipino, Japanese, Korean, Vietnamese) and non-Hispanic Whites (NHWs) from 2003-2011, and ranked the leading causes of death. We calculated all-cause and cause-specific age-adjusted rates, temporal trends with annual percent changes, and rate ratios by race/ethnicity and sex. Rankings revealed that as an aggregated group, cancer was the leading cause of death for Asian Americans. When disaggregated, there was notable heterogeneity. Among women, cancer was the leading cause of death for every group except Asian Indians. In men, cancer was the leading cause of death among Chinese, Korean, and Vietnamese men, while heart disease was the leading cause of death among Asian Indians, Filipino and Japanese men. The proportion of death due to heart disease for Asian Indian males was nearly double that of cancer (31% vs. 18%). Temporal trends showed increased mortality of cancer and diabetes in Asian Indians and Vietnamese; increased stroke mortality in Asian Indians; increased suicide mortality in Koreans; and increased mortality from Alzheimer’s disease for all racial/ethnic groups from 2003-2011. All-cause rate ratios revealed that overall mortality is lower in Asian Americans compared to NHWs.
Conclusions

Our findings show heterogeneity in the leading causes of death among Asian American subgroups. Additional research should focus on culturally competent and cost-effective approaches to prevent and treat specific diseases among these growing diverse populations.

 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4411112/



------------------------------------


Rare Autoimmune Disease attacks People of Asian Descent

6-Sep-2012


Newswise — There has been an outbreak of an adult-onset immunodeficiency syndrome in Southeast Asia. The autoimmune disease causes AIDS-like symptoms but is not associated with HIV and is not contagious.

The disease causes patients’ bodies to produce antibodies that attack their own immune systems. Dr. Sarah Browne, a clinical investigator at the National Institute of Allergy and Infectious Diseases at NIH and the lead author on the study, says that we all have molecules and proteins that tell different immune cells when to start fighting infection. A large number of the patients studied with serious opportunistic infections make an antibody that blocks the function of one of these molecules. The molecule is called interferon-gamma. Without functioning interferon-gamma, people become more susceptible to certain types of infections -- infections people with working immune systems normally don't get. Interferon-gamma is a protein that helps the body fight off infections. In those diagnosed, the immune system has begun treating interferon-gamma as an enemy and makes an autoantibody against it, thus making it an autoimmune condition.

“These findings provide new opportunities to understand the relationship between immunodeficiency and autoimmune diseases, the topic of a recent AARDA-sponsored international symposium,” says Dr. Noel Rose, the director of the Johns Hopkins Autoimmune Disease Research Center.


http://www.newswise.com/articles/rare-autoimmune-disease-attacks-people-of-asian-descent



--------------------------------------------


Researchers find distinctive patterns of cancer in Asian-Americans

 July 11, 2007


Asian-Americans, both those born in the United States and new immigrants, have distinctive patterns of cancer incidence that doctors should consider when treating them, researchers have found.

A report appearing Wednesday in the journal CA is "one of the most comprehensive summaries of cancer among Asian-Americans," according to the American Cancer Society, which publishes the journal. The report is based on information on cancer cases collected by the state of California from 2000 to 2002 and focuses on five ethnic groups: Chinese, Filipino, Japanese, Korean and Vietnamese. The state has a large Asian population, 3.7 million, and carefully sorts its cancer data by ethnic group.

When all cancers are combined, Asian-Americans actually have lower rates than other groups in the United States. But cancer is still a major cause of death for Asians, killing more of them than heart disease. Different groups appear prone to different types of cancer.

Groups that have been in the United States the longest are likely to develop cancers that are most common there, like breast and colorectal cancer, although their rates are still significantly below those of non-Hispanic whites. The risk of those cancers may be increased by obesity, inactivity, high alcohol intake and diets rich in fat and low in fruits and vegetables, and the rates in Asians seem to rise gradually as they adopt more American habits.


Recent immigrants, by contrast, tend to suffer from the same types of cancer that are predominant in their native countries, like stomach and liver cancer. In developing countries, those cancers are often caused by chronic infections with certain bacteria and viruses that are routinely treated or prevented in the United States.

"I was surprised to see the diversity in cancer among the ethnic groups," said Melissa McCracken, an epidemiologist with the cancer society and the first author of the report. "The group is not homogeneous. Clinicians need to be aware of that and to really extend their scope of attention to cancer due to infectious agents, not just typical chronic conditions."

Among the more striking findings in the report are that Vietnamese men have incidence and death rates from liver cancer that are seven times the rate in non-Hispanic white men, and Korean men and women are 5 to 7 times as likely as whites to develop stomach cancer. Other Asians are also prone to these cancers, but their rates are generally not as high.

The hepatitis B virus is endemic in Asia, McCracken said, and chronic infection is a major cause of liver cancer there and in recent immigrants.


 http://www.nytimes.com/2007/07/11/health/11iht-cancer.4.6617221.html




--------------------------


10 Top Asian American Health Risks

- The Asian American population has the highest tuberculosis case rate of any ethnic group: 24 times greater than Caucasians. Additionally, 80% of the population in many Asian countries test positive in tuberculin tests, while only 5-10% of the US population test positive.

20% of Asian women older than 50 have osteoporosis and over 50% of them are at risk. Asian American women are at a higher risk for developing osteoporosis compared with Caucasian women.

Asian American women older than 65 have a suicide rate of 11.6 per 100,000—more than double the rate for Caucasian women in that age group. Out of over 2,000 Asian Americans aged 18 or older, 2.7% reported having attempted suicide at some point in their lives and 9.1% of the group reported having had suicidal thoughts.

Lung cancer is the second most prevalent cancer among Asian American men and third among Asian American women. Lung cancer rates among Southeast Asian Americans are 18% higher than among Caucasians and Chinese Americans have the highest death rates for lung cancer among Asian American groups.

Asian Americans are a high –risk group for diabetes type 2. The risk for type 2 diabetes occurs at a lower BMI for Asian Americans compared to other ethnic groups. Additionally, while diabetes was the seventh leading cause of death in the US in 2006, it ranked as the fifth among Asian Americans.

The incidence rates of liver cancer in Asian American groups are 1.7 to 11.3 times higher than the rate among Caucasians. Additionally, Vietnamese American males have the highest incidence rates of liver cancer out of any other group in the US. Asian Americans are three times more likely to die of liver cancer than Caucasians.

Asian American women have one of the highest rates of cervical cancer in the US and Vietnamese American women in particular have an incidence rate five times higher than Caucasian women.


http://goldsea.com/Text/index.php?id=1596


-------------------------



Ethnic Differences in BMI and Disease Risk


The chance of developing diabetes, heart disease, and other weight-related health risks increases with increasing body mass index (BMI). But theres strong evidence that at any given BMI, these health risks are markedly higher in some ethnic groups than others.

The Nurses Health Study, for example, tracked patterns of weight gain and diabetes development in 78,000 U.S. women, to see if there were any differences by ethnic group. (1) All women were healthy at the start of the study. After 20 years, researchers found that at the same BMI, Asians had more than double the risk of developing type 2 diabetes than whites; Hispanics and blacks also had higher risks of diabetes than whites, but to a lesser degree. Increases in weight over time were more harmful in Asians than in the other ethnic groups: For every 11 pounds Asians gained during adulthood, they had an 84 percent increase in their risk of type 2 diabetes; Hispanics, blacks, and whites who gained weight also had higher diabetes risks, but again, to a much lesser degree than Asians. Several other studies have found that at the same BMI, Asians have higher risks of hypertension and cardiovascular disease than their white European counterparts, and a higher risk of dying early from cardiovascular disease or any cause. (2–4)


 https://www.hsph.harvard.edu/obesity-prevention-source/ethnic-differences-in-bmi-and-disease-risk/


------------------------------


Kidney Disease Most Common In Asian Populations

Researchers have identified five genomic regions that increase susceptibility to IgA nephropathy, a major cause of kidney failure worldwide.


AsianScientist (Apr. 4, 2011) - Researchers have identified five regions in the human genome that increase susceptibility to immunoglobulin A (IgA) nephropathy, a major cause of kidney failure worldwide.

The findings, a result of long-term collaborations among investigators in the United States, Italy, and China, was published in the April issue of Nature Genetics.

The researchers looked at the genes of 3,144 people of Chinese and European ancestry, all of whom have IgA nephropathy. The disease occurs when abnormal IgA antibodies deposit on the delicate filtering portion of the kidney and form tangles. The immune system tries to get rid of the tangles, but the kidneys are caught in the crossfire, further destroying the delicate filters.

Worldwide prevalence of IgA nephropathy appears highest in Asia and southern Europe, and rare in Africans. The frequency of genetic risk variants was similarly highest in Chinese people, intermediate in Europeans and lowest in Africans.

The "beauty" of this study, according to Dr. Rebekah Rasooly, was that nobody had suspected the association of the immune basis of IgA nephropathy with kidney diseases.



https://www.asianscientist.com/2011/04/health/kidney-disease-common-asian-populations/



-------------------------------

Chronic diseases: Asia's emerging health threat

Jan 29, 2013


Two in three deaths worldwide (34.5 million) were from chronic diseases in 2010 - an increase of about eight million between 1990 and 2010, according to the landmark Global Burden of Disease Study 2010 published in The Lancet last month, a collaborative project by nearly 500 scientists from more than 300 institutions in 50 countries..


http://www.scmp.com/lifestyle/health/article/1137943/chronic-diseases-asias-emerging-health-threat


-------------------------------

Inherited metabolic disorders in Thailand.

Aug 2002

 https://www.ncbi.nlm.nih.gov/pubmed/12403250

---------------------

Genetic Hemoglobin Disorders, Infection, and Deficiencies of Iron and Vitamin A Determine Anemia in Young Cambodian Children

 

 April 2012

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3301994/

------------------


Genetic disorders in a paediatric hospital in Cambodia.

 March 2005

https://www.ncbi.nlm.nih.gov/pubmed/16096216

-------------------

 Rare Disorders in Malaysia: Rare and Special

http://www.mrds.org.my/2008%20Rare%20Disorders%20MRDS.pdf

------------------

Genetics and genomic medicine in Indonesia

 March 2017

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5370234/

------------------

Indonesia's Many Human Physical Deformities: A Closer Look

 February 6, 2016

http://www.acsh.org/news/2016/02/06/matt-whats-up-in-indonesia

-----------------

 Indonesia lacks qualified doctors, medication to treat rare diseases

 March 8, 2017

 https://www.pressreader.com/indonesia/the-jakarta-post/20170308/281603830260773

----------------

Birth  Defects  In  South-east  Asia 
A  Public  Health  Challenge

http://apps.searo.who.int/PDS_DOCS/B4962.pdf

----------------

 Blood Mercury Reporting in NHANES: Identifying Asian, Pacific Islander, Native American, and Multiracial Groups

 Sep 2005


 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1367827/



----------------


Shift from traditional foods takes toll on Alaska Native populations

2016

 https://www.adn.com/rural-alaska/article/processed-food-comes-diabetes-obesity-alaska-natives/2014/09/29/



---------------


Man-made chemicals blamed as many more girls than boys are born in Arctic

2007

· High levels can change sex of child during pregnancy
· Survey of Greenland and east Russia puts ratio at 2:1

Twice as many girls as boys are being born in some Arctic villages because of high levels of man-made chemicals in the blood of pregnant women, according to scientists from the Arctic Monitoring and Assessment Programme (Amap).

The scientists, who say the findings could explain the recent excess of girl babies across much of the northern hemisphere, are widening their investigation across the most acutely affected communities in Russia, Greenland and Canada to try to discover the size of the imbalance in Inuit communities of the far north.


https://www.theguardian.com/world/2007/sep/12/gender.sciencenews


--------------

Health Problems in Chinese Children Are Different


Introduction

"Different race has different face",1 this saying obviously applies to Chinese children, as they do look different from children of other ethnic origins. In fact, many health problems are different in Chinese children also.2-6 Genetic conditions account for some of the differences. Well-known examples can be found in the thalassaemia syndromes which are highly prevalent in southern Chinese,7,8 or cystic fibrosis which is very rare in Chinese,2 although it is the most common chronic lung problem in Caucasians.9

Traditions usually exert major influences on all kinds of child-care practices in the Chinese culture.2-6,10-13 Many medical and health problems demonstrate strong cultural characteristics. As improvement in socio-economic conditions and changes in life-style together with trends towards westernization have occurred in many Chinese communities2,4,5,10,12,13 in recent years, there are associated significant changes of disease pattern in the children also.2,4,10,12,13 Such changes appear to occur in children who have migrated to take up residence in overseas places as well.

This paper reviews some of the documentations and the author's personal observations on the differences commonly identified in children of Chinese origin.


Background

Chinese people comprise of five major ethnic groups,14 viz. Han (?), Man (Manchurians ?), Mong (Mongolians ?), Hwei (Islamics ?), Zhuang (Tibetans ?). Han is the majority. There are many other "ethnic minority groups" whose features sometimes draw some similarities to the people of the bordering countries. For example, a small group in south-western China has some Persian features; a few people in the North-west look Russian. Most of the Manchurians, Mongolians and Hweis have integrated into the Han society and have become indistinguishable from the Hans, from whom most of the reports regarded as Chinese are based.


External Features

At birth, the Chinese infant has a broader face, often with depressed nasal bridge (Table 1).1,2,5,10,15-24 He does not look "yellow", as his skin pigmentation usually takes days, often weeks to establish. More than one in ten infants have up-slanting eyes. One in four has "low-set ears" by Western standard. The head is usually not as elongated as the Caucasians. This could be due to the supine-sleeping position2,12,25,26 resulting in flattening of the occiput rather than an oblong shape assumed by the head lying on its sides from the prone-sleeping posture.

Of the many external features as listed in Table 1, particularly note-worthy are the "Mongolian blue spots" which are present in nearly all newborns.15 These skin patches, many of them can be quite large around the buttocks, persist till 5-6 years old; and such features should not to be mistaken for "child abuse" by the inexperienced. It is interesting also to note that Chinese children born or raised in temperate regions such as North America are generally less pigmented and not as "yellow" as their cousins who live in China.


Child Growth

"Chinese are born small and remain small all through childhood",27-29 this is a common misconception. Such belief was apparently based on observations made in days when the nutritional status and health care facilities were poor. Recent studies conducted in more developed Chinese communities, like Hong Kong, have indicated that both the intra-uterine30 and childhood growth grids are similar if not identical to the National Council of Health Standards (NCHS) curves of U.S.A. These secular changes appear not influenced by previously presumed genetic and ethnic factors as some workers have suggested.

Already Chinese teenagers of Hong Kong in the late 1980s were 4.2 - 6.7 cm taller than those in the late 1960s.31 Similar secular growth trends are occurring in various big cities in Mainland China29,33-35 and Taiwan.36 One study showed that the femur length was shorter,37 and several surveys have shown that Chinese children in certain big cities of North America are shorter and lighter26,38 than the Caucasian-Americans. These findings could be the result of certain traditional feeding practices which have been found to provide less than optimal dietary intake for the growing Chinese children rather than because of their ethnic endowment.


Congenital Abnormalities

Congenital anomalies as listed in Table 3 are some examples quite unique in Chinese. Uncommon occurrences of neural-tube defects50-52 appear to be due to the plentiful vegetables with folic acid in the southern Chinese diet.51 In a study of supplementing women with folic acid in several northern provinces in China, significant reduction of neural tube disorders has resulted.53 Other conditions like meconium ileus and meconium-plug syndrome from cystic fibrosis2,5,6,9 are extremely rare occurrences,5,6 very different from the experience drawn from Europe and North America.

Congenital conditions which are much less common in Chinese also include congenital dislocation of hips (CDH) which was found to be ten times less common compared with the Caucasians,54 pulmonary hypoplasia from renal agenesis and congenital hypertrophic pyloric stenosis.55,56 Strictly speaking, pyloric stenosis is an acquired condition, as most infants only develop symptoms days, sometimes even weeks, after birth. Local experience has indicated its occurrence is on the rise in recent years. If such observation holds true, it may suggest an etiologic relationship to many recently introduced perinatal interventional therapies which may be stressful to the infants, resulting in increased vagal discharges and smooth muscle hypertrophy as a response around the pylorus.

The incidence of congenital heart defects is similar to Caucasians, but the pattern of heart defects is different.57,58 There are more right heart obstructive lesions and less hypoplastic left heart syndrome (Table 4). Cardiovascular defects associated with Chinese children with Down syndrome are also different (Table 4);59 the commonest problem is not atrio-ventricular cushion defect as noted in the western literature but ventricular septal defect. Although the frequency of congenital heart block has not been clearly documented, one might suspect that it would be higher, as there are many more young Chinese women with systemic lupus erythematosis.60,61

Hydrops fetalis due to a-thalassaemia is common.7 4.5% and 4% of a southern Chinese school-age population have been found to be carriers of the a & b thalassaemia genes respectively.8 While infants with hydrops fetalis due to a-thalassaemia either die in-utero or soon after birth, children with b-thalassaemia major usually require monthly blood-transfusions and daily chelation therapy to sustain life. 4.42% boys and 0.45% girls62 were found to be severely deficient in glucose-6-phosphate dehydrogenase (G-6-P D). Such enzyme defect had accounted for a very high incidence of neonatal jaundice and kernicterus (Figure 1) in the past;63-66 even in older children haemolytic anaemia often occurs in association with an infection, in particular with hepatitis and typhoid fever, or precipitated by an oxidizing agent. Hare-lips and cleft palate which were noted to be more prevalent in Chinese previously49,67 have recently been found to be similar in incidence67 as in other reports.



Conclusion

Chinese children are different from other ethnic people, not only in their look but also in many medical and health conditions. Genetic disorders account for some differences, most of the other conditions appear to be affected by environmental factors and traditional practices. As there are much movements of Chinese people to take up residence in overseas places in recent years, it is important for child care workers to be alerted to some of the unique features of Chinese children to avoid misunderstanding and even possible mis-management--------------


http://www.cchi.com.hk/specialtopic/case3/

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South Asian health issues
Diabetes and heart disease

People in the UK from south Asian communities are about twice as likely to develop diabetes compared with people from white European backgrounds.

South Asian people are also more likely to develop diabetes at a younger age.

Coronary heart disease (CHD) is also more common in south Asian people, as is the risk of dying early from CHD.

Experts aren’t sure why this is the case, but it may be linked to diet, lifestyle and different ways of storing fat in the body.
Children and diabetes

Children of south Asian origin in the UK are more likely to develop type 2 diabetes than white European children.

Weight gain caused by eating traditional foods high in sugar and fat, alongside Western "fast foods", is thought to be a contributing factor, according to Diabetes UK.
Eye health and kidney health

The eye condition acute glaucoma and chronic kidney disease can affect anybody, but people from south Asian communities have a higher risk.

Having diabetes increases the chances of developing kidney disease, and research suggests that diabetes can also raise the risk of glaucoma.


 http://www.nhs.uk/Livewell/SouthAsianhealth/Pages/Overview.aspx


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Bai fu mei: China’s obsession with white skin and ‘trophy’ partners may stem from genetic mutation 15,000 years ago, scientists say

Jan 12, 2016

Men in the country can often seem obsessed with fair skin, especially in a partner, while many women have in the past favoured a Caucasian or “trophy” husband. This has long been dismissed as a social, economic or cultural problem, but new evidence suggests it may stem from a genetic predisposition.

New international study led by Chinese team finds the diverging complexions of Han Chinese and native Africans and Southeast Asians was caused by a mutation of the OCA2 gene 15,224 years ago


For thousands of years, China was ruled by pale-looking nobles in the north, and the invasion of Europeans in its more modern history further added to the perception that a white skin colouring was somehow superior.


But the new study found that the phenomenon could have a biological explanation dating back to prehistoric times as the relatively light skin colouring of the Han Chinese may derive from the same gene held responsible for a number of diseases.


The researchers from China, the United States and Europe analysed genetic samples from more than 1,000 individuals and found that the fairer skin of the Han Chinese in comparison to people from Africa and Southeast Asia was caused by a mutation of the OCA2 gene.

One of the gene’s main functions is to help transport tyrosine, an amino acid used as a raw material in synthesising melanin, a pigment that determines skin colouration .


The mutated version of the gene has been linked to many diseases, such as albinism, acute eye inflammation, Angelman syndrome (characterised by mental disability and jerky movements), learning difficulties and obsessive eating, to name but a few.


The team of researchers were led by Professor Su Bing at the Kunming Institute of Zoology in Yunnan province, and Meng Anming from Tsinghua University in Beijing.

They estimated that the mutated genes which led to the fairer skin of the Han Chinese occurred some 15,224 years ago. This happened after that group’s ancestors migrated up north from Southwest China and Southeast Asia about 25,000 – 30,000 years ago.



This dark colouring would have served as a natural form of defence “against the harmful effects of UV radiation, including protection against sunburn and folate destruction”, according to the team’s paper published in the latest issue of the journal Molecular Biology and Evolution.

But in north China, which experiences less sunshine than other parts of the country, the whiter skin allowed the body to absorb more sunlight to prevent a deficiency of vitamin D. A shortage of this can lead to fragile or brittle bones, cardiovascular problems and cognitive impairments.


According to the laws of natural selection, those with lighter skin were fitter for survival in the new environment. They may also have enjoyed other physical advantages such as being taller with stronger bones and perhaps a greater intelligence, studies show.

Another interesting discovery of the latest study was that the same OCA2 mutation was not detected among Europeans, who also underwent a shift to paler skin after the first modern humans moved out of Africa.

But the evolution of people’s skin colour in Europe took place on a completely different set of genes such as SLC24A5 and SLC45A2, according to other studies.


The genetic difference between Han Chinese and Europeans implied “independent skin-lightening in both East Asians and Europeans”, the scientists said.

But they said other environmental and biological factors could not be ruled out, either.

“Dietary changes and/or sexual selection … may also have created selective pressure in skin lightening,” they wrote.

And that “selective pressure” has shown scant sign of easing up.

A quick pore through a Chinese search engine quickly reveals what many modern Chinese woman aspire to be: Bai-fu-mei. This portmanteau of three Chinese characters - “white”, “rich”, “beautiful” - puts white first, even though in today’s China, wealth is for many the most desirable quality.

A study by market research company Mintel last year found that more than 95 per cent of Chinese women aged 20 to 49 had used facial masks to whiten their face - or three times as many as in Britain.



http://www.scmp.com/tech/science-research/article/1900084/bai-fu-mei-chinas-obsession-white-skin-and-trophy-partners-may

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What genetics reveals about traditional Chinese medicine

January 6, 2017


Impacting genes

Can Chinese medicine impact the human genome, and deliver on its promises? A variety of individual responses to these therapies might be explained by epigenetic influences on gene expression.

    A Korean research team found in mice that stimulating a specific acupuncture point associated with neurostimulation and Parkinson’s disease changed the expression levels of 799 genes. These genes could become biomarkers that indicate changes in neuronal activity and possibly point to treatments for the disease.
    A Chinese group found changes in mRNA and protein expression in mouse lung tissue after stimulation of three acupoints with acupuncture needles. These expression changes appear to affect regulation of macromolecular biosynthesis, transportation and metabolism, the team reported.
    A Taiwanese team analyzing 3,294 medicinal herbs and other compounds found that 36 percent of them worked with histone-modifying enzymes, and one-third of those promoted chromatin condensation, which compacts chromosomes and affects DNA repair and gene expression.

Natural isn’t harmless

Not all traditional medicines are beneficial, however. In fact, any responsible practitioner or specialist will warn that herbal treatments can be hazardous.

Aristolochic acid, which is part of many traditional Chinese preparations for menstrual cramps, rheumatism and (sometimes) weight loss, was also associated with kidney failure and urinary tract cancer, two studies reported.

In addition, traditional Chinese preparations have been found to contain heavy metals and plant toxins. Cases of adverse reactions have been reported, including some deaths. These concoctions are not regulated in either the US or Europe as drugs, but they can have powerful actions by themselves and equally powerful interactions with prescription drugs.

Another issue with Chinese traditional medicines has been identifying the ingredients of any individual herbal preparation. This issue has stemmed from either contaminants or the use of a substitute compound from similar, but not identical, species of plant. Since more than 5,000 species are used for therapies, and most of them are animal- or plant-derived organics, such identification has been difficult. But high-throughput screening and new whole-exome or whole-genome sequencing analysis has permitted scientists to more precisely determine what’s in the mix.


 https://geneticliteracyproject.org/2017/01/06/what-genetics-reveals-about-traditional-chinese-medicine/


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Simple blood test can detect genetic diseases early in pregnancy

 Together, single-gene disorders are more common than Down’s syndrome. Now there’s a safe prenatal test that can help prospective parents decide what to do

 https://www.newscientist.com/article/mg23331074-100-simple-blood-test-can-detect-genetic-diseases-early-in-pregnancy/


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