Category Archives: Human Genetics

Asthma is a chronic condition that causes your airways to become inflamed leading them to swell and narrow. This makes it harder for you to breathe and can cause dangerous asthma attacks.

Asthma is often linked to other health conditions like hay fever and environmental factors including air pollution. However, research also shows that carrying certain genes can put you at greater risk of developing asthma.

Here's what you need to know about what causes asthma and how it can be passed down through families.

Scientists have identified more than one hundred specific genes that may play a role in whether or not a person develops asthma. In fact, a person with at least one biological parent with asthma is 3 to 6 times more likely to develop the condition than someone whose parents don't have asthma.

However, even if you are born with asthma-related genes, you may not develop asthma unless those genes are "turned on," likely by something in your environment. "Multiple genes may be involved and they could be triggered by a number of factors, such as viral infections," says Stanley Szefler, MD, the Director of the Pediatric Asthma Research Program at Children's Hospital Colorado.

This means that if you have asthma-related genes and suffer a bad respiratory infection as a child, this could kickstart a lifelong asthma condition. However, experts say that more research is needed to fully understand how these genes interact with the environment to cause asthma in the first place.

Doctors have identified several different types of asthma including adult-onset asthma, allergic asthma, and exercise-induced asthma. Scientists have not linked any specific genes to a particular type of asthma, Szefler says. However, there is evidence that every type of asthma has a genetic component.

In a study, published in 2008 in Twin Research and Human Genetics, researchers compared the incidence of asthma in twins to determine how strongly genes affect the likelihood of developing asthma, compared with environmental factors. The results showed that genetics plays a very large role the genes account for about 70% of your risk of developing asthma.

It's important to remember that even though genes are an important risk factor for asthma:

About half of all asthma sufferers start having symptoms as children age 5 and younger. But for people who develop asthma later in life, genes are less likely to play a role. This may be because some older people develop asthma due to lifestyle choices like smoking.

In addition to genetics, asthma may be caused by:

In many cases, experts don't know why some people develop asthma while others don't. However, there are risk factors that can increase your risk. These include:

There is no way to prevent asthma, even if you start treatment early on after your symptoms develop, says Szefler. Researchers are starting to look at whether using biologic medications containing live bacteria could work to prevent asthma, Szelfer says, "but the results are several years off."

However, even if you can't prevent asthma, there are steps you can take to prevent asthma attacks:

Asthma is an ongoing condition and you should "maintain good medical follow-up to keep the disease under control," Szefler says. You will need to make an individual treatment plan with your doctor, designed to target your symptoms and help avoid your asthma triggers.

Continued here:
There is a strong genetic component to asthma, but it's not the only risk factor - Insider - INSIDER

Common wisdom has long held that each dog year is equivalent to seven human years. But a new equation developed to measure how a dog ages finds the family pup may be a lot older than we realize.

Researchers studying chemical changes to canine DNA found that dogs age very quickly during their first five years and much more slowly later on.

The findings, published recently in the journal Cell Systems, calculate that a 5-year-old dog would be pushing 60 in human years.

Puppies age super quickly, said Trey Ideker, the studys senior author and a professor of genetics at the University of California, San Diego, School of Medicine. By the time a dog is a year old, at a molecular level, hes much more like a 30-year-old human. Retrospectively, we did know these things. It didnt make any sense that the equivalent to a 7-year-old human would be able to have puppies.

Ideker and colleagues noticed that dogs, just like humans, have chemical marks on their DNA, called methylation marks, that change with age.

The genome itself doesnt change with age, Ideker said. "What does change is marks on the genes that control a dog or human's growth pattern."

The methylation marks, or as Ideker calls them wrinkles on the genome, change in predictable ways as we and dogs age.

We are able to quantify this at the molecular level and tell how fast someone is aging, and we can align it across dogs and humans, Ideker said. But we dont know exactly what it all means.

To find the mathematical relationship connecting dog aging to human aging, Ideker and his colleagues studied 104 Labrador retrievers whose ages ranged from weeks-old puppies to 16-year-old dogs.

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When they compared the dog DNA data to information from humans, the researchers came up with a new equation to figure out the dog's comparable human age.

The equation: 16 ln(dog age) + 31 = human age.

For iPhone calculators that have the natural logarithm, or "ln," function, first type in the dog's age. Then hit the "ln" button. Multiply that result by 16; then add 31.

If you're using Googles scientific calculator: First, hit "ln," then type in the dogs age, then equal it out. Next, multiply by 16, and then add 31.

Using that equation:

By this time, dog aging has slowed down, so an 8-year-old dog is like a 64-year-old human.

According to this equation, the average 12-year Labrador lifespan is equivalent to a human living to about 70.

Ideker suspects there will be some variation based on dog breed but that they will all follow a similar pattern.

The new dog-age math has given Ideker some pause when he thinks about taking his own dogs on runs: He now realizes his 6-year-old dog is actually pushing 60 in human years.

Margret Casal, a specialist in veterinary genetics, said the new calculations match what shes observed in her dog patients.

It validates what a lot of other researchers have been saying, said Casal, a professor of medical genetics, pediatrics and reproduction at the University of Pennsylvania School of Veterinary Medicine.

Researchers knew the 1-to-7 comparison was off, but they did not know what the specific relationship was, she added.

It will be interesting to look at different breeds," Casal said. "We know that some smaller breeds live longer and some larger ones dont live quite as long.

For owners hoping to help a beloved dog live as long as possible, Casal offered a few tips:

Lastly, take your dog for yearly wellness visits.

Thats really important, Casal said. I can say as an owner of a dog, sometimes you dont see something is wrong and your vet might be able to see it better.

Linda Carroll is a regular health contributor to NBC News and Reuters Health. She is coauthor of "The Concussion Crisis: Anatomy of a Silent Epidemic" and "Out of the Clouds: The Unlikely Horseman and the Unwanted Colt Who Conquered the Sport of Kings."

Original post:
How old is your dog? New equation shows how to calculate its age in human years - NBC News

The formulation of what has come to be known as moral foundations theory has been crucial to a deeper understanding of this process. The theory

proposes that the human mind is organized in advance of experience so that it is prepared to learn values, norms, and behaviors related to a diverse set of recurrent adaptive social problems.

Leading proponents argue that there are

five foundations of intuitive ethics: care/harm; fairness/cheating; loyalty/betrayal; authority/subversion; and sanctity/degradation.

The theory is described in detail in Moral Foundations Theory: The Pragmatic Validity of Moral Pluralism, a 2013 paper by Jesse Graham of the University of Utah; Jonathan Haidt of N.Y.U.; Sena Koleva, a research consultant; Matt Motyl of the University of Illinois at Chicago; Ravi Iyer, chief data scientist for Ranker, a consumer internet platform; Sean P. Wojcik, a senior data scientist at the news site Axios; and Peter H. Ditto, of the University of California-Irvine.

What makes moral foundations theory especially relevant now is that in recent decades liberal and conservative partisans have divided over the importance they place on these five moral foundations:

Liberals valued Care and Fairness more than did conservatives, whereas conservatives valued Loyalty, Authority and Sanctity more than did liberals.

These differences mattered little for politics when both parties included liberals and conservatives, but beginning around 1964, this disagreement between left and right on moral values began to coincide more strongly with party affiliation.

A number of scholars have put forth ideas in an effort to understand these developments.

Kevin Smith, a political scientist at the University of Nebraska whose research explores the biology and psychology of individual-level differences in political attitudes and behavior, emailed in response to my inquiry:

Fights about abortion, gay rights, gun rights etc. are less about policy than about underlying core values, values that for many are not up for discussion or compromise because they are deeply held indeed, given the genetic influences on such attitudes, its probably fair to say they are at least partly biologically instantiated.

Smith, who is a co-author of Predisposed: Liberals, Conservatives and the Biology of Political Differences, argues that as political parties have coalesced along ideologically consistent lines, especially on issues related to race, they have

created a political environment where genetically influenced predispositions, what most people would experience as gut feelings that one side or the other is right or wrong on a given set of issues of the day, made partisanship something that was much more likely to become a central part of someones identity.

Smith is quite explicit that he does not posit that there is biological determinism of political views or anything else, but he does contend that

theres little doubt that ideological orientations are genetically influenced, and to a surprisingly high degree studies consistently estimate roughly 40-60 percent of the population level variance in ideology is under genetic influence.

The ideological realignment of the parties that has pushed many liberal Republicans into the Democratic camp and conservative Democrats in the opposite direction, Smith writes, has created a political environment in which

those with strong predispositions to lean one way or the other can readily mate those instinctual feelings to a political party that espouses and affirms those predispositions.

At that point, he continues,

Youve got a recipe for deeply polarized politics that is going to feed on its own dynamics and be hard to change. And that sounds awfully like the political environment we have right now.

In Predisposed, Smith and John Hibbing and John Alford, his co-authors, stress that we are not making a nature versus nurture argument.

Instead, they write, innate forces combine with early development and later powerful environmental events to create attitudinal and behavioral tendencies. A predisposition can be altered. Nonetheless,

predispositions nudge us in one direction or another, often without our knowledge, increasing the odds that we will behave in a certain way, but leaving plenty of room for predispositions to be contravened.

Kevin Arceneaux, a political scientist at Temple, stressed in an email that

It is important to resist the tendency to see heritability of eye color, for example, as the same thing as the heritability of an attitude. I cannot change my eye color, but I can change my attitudes.

Some of the most interesting work in the field of behavioral genetics, Arceneaux continues, shows how

context interacts with genetic influences. If you change the context, the heritability of behavioral constructs changes. So, I would caution against drawing a straight line from heritability to unchanging/intractable.

Along the same lines, Yuan Chang Leong, a postdoctoral fellow in the psychology department at Berkeley, emailed me that

What is heritable is unlikely to be ideology per se, but something more akin to personality traits or a predisposition to respond to certain information in a particular way.

The relationship between these factors and policy positions, Leong continued,

are not set in stone. There is evidence that partisans can be persuaded by political messages, especially when the messages are framed in a manner that appeals to them, so efforts at persuasion are not futile.

Ariel Malka, a professor of psychology at Yeshiva University, believes that religiosity, authoritarianism, and conservative cultural attitudes are rooted in personality traits that have some heritable components.

In an email, Malka noted that

Increased partisan polarization in the U.S. has coincided with the parties placing greater (and opposing) emphases on racial and culture war positions. So its certainly plausible that American polarization stems from partisan conflict having expanded into the racial and cultural areas, aligning this heritable attitude syndrome with partisanship.

Malka cited the work of Amanda Friesen and Aleksander Ksiazkiewicz, political scientists at Indiana University-Purdue University Indianapolis and the University of Illinois-Urbana, who are the authors of Do Political Attitudes and Religiosity Share a Genetic Path?

Friesen and Ksiazkiewicz are persuaded that

certain religious, political, and first principle beliefs on social organization can be explained by genetic and unique environmental components, and that the correlation between these three trait structures is primarily due to a common genetic path.

Malka also points to the work of Steven Ludeke, Wendy Johnson and Thomas J. Bouchard Jr., psychologists at the University of Southern Denmark, the University of Edinburgh and the University of Minnesota, whose findings are described in the title of their 2014 paper, Obedience to traditional authority: A heritable factor underlying authoritarianism, conservatism and religiousness.

In Malkas view, the strength of these predispositions to authoritarianism, religiousness and conservatism has been crucial to the success of Republicans in winning support from white middle-class and working-class voters, many of whom hold strongly liberal views on economic policy.

Originally posted here:
How Could Human Nature Have Become This Politicized? - The New York Times

Every three seconds, someone in the world develops dementia. The most common form of dementia is Alzheimers disease. While researchers have identified a number of risk factors that are linked to dementia including genetics, smoking, and high blood pressure there is currently still no cure.

Part of the reason for this is because of how complicated it is to test potential Alzheimers drugs. In order to conduct clinical trials participants need to have symptoms. But by the time symptoms appear, its usually too late for treatments to have a large effect as many of their brain cells have already died.

But our latest research developed a new human cell model that is able to rapidly simulate the development of Alzheimers disease in the lab. This allowed us to identify a gene, called BACE2, that is naturally able to suppress the signs of Alzheimers disease in human brain cells. Our research is the result of around five years work, and was the collaborative effort of teams based in London, Singapore, Sweden and Croatia.

Researchers already know a lot about which genes cause Alzheimers disease or make someone more likely to develop it. These genes contribute to certain toxic proteins accumulating in the human brain. So our team thought that the opposite must also be true: our brain cells must also have proteins that can naturally slow down the development of Alzheimers.

One gene that can definitely cause Alzheimers disease is a gene found on the 21st pair of human chromosomes that is responsible for making the amyloid precursor protein (APP). Research shows that 100% of people born with just one extra copy of the APP gene (called DupAPP) will develop dementia by age 60.

People with Downs syndrome are born with three copies of APP because they have a third 21st chromosome. But by age 60, only 60% of them will develop clinical dementia. We wanted to know why some people with Downs syndrome have delayed development of or never develop Alzheimers dementia compared to those who have one extra DupAPP gene.

The simple answer for this is because they have an extra dose of all other genes located in chromosome 21. We believed that there could be some dose-sensitive genes on chromosome 21 that, when triplicated, protect against Alzheimers disease by counteracting the effects of the third APP gene.

These genes must then appear to delay the onset of clinical dementia in some people with Downs syndrome by approximately 20 years. Studies have even shown that any future drug able to delay dementia onset by just five years would reduce the prevalence of Alzheimers in the general population by half.

To study the potential of the extra genes, we took hair follicle cells from people with Downs syndrome and re-programmed the cells to become like stem cells. This allowed us to turn them into brain cells in a Petri dish.

We then grew them into 3D balls of cells that imitated the tissue of the grey matter (cortex) of the human brain. The 3D nature of the culturing allowed misfolded and toxic proteins to accumulate, which are crucial changes that lead to Alzheimers disease in the brain.

We found all three major signs of Alzheimers disease (plaque build-up in the brain, misfolded tau proteins and dying brain neurons) in cell cultures from 71% of people with Downs syndrome who donated samples. This proportion was similar to the percentage of clinical dementia among adults with Downs syndrome.

We were also able to use CRISPR a technology that allows researchers to alter DNA sequences and modify a genes function to reduce the number of BACE2 genes from three copies to two copies on chromosome 21. This was only done in cases where there were no indications of Alzheimers disease in our cellular model. Surprisingly, reducing the number of BACE2 genes on chromosome 21 provoked signs of the disease. This strongly suggest that having extra copies of a normal BACE2 gene could prevent Alzheimers.

The protective action of BACE2 reduces the levels of toxic amyloid proteins. This was verified in our cellular models, as well as in cerebrospinal fluid and post-mortem brain tissue from people with Downs syndrome.

Our study provides proof that natural Alzheimers-preventing genes exist, and now we have a system to detect new potential protective genes. Importantly, recent research showed the protective action of BACE2 might also be relevant to people who dont have Downs syndrome.

Our results also show that all three signs of Alzheimers disease can be potentially detected in cells from live donors. Though this requires a lot more research, it means we may be able to develop tests that identify which people are at higher risk of Alzheimers disease by looking at their cells.

This would allow us to detect the disease before it starts developing in a persons brain, and could make it possible to design personalised preventative treatments. However, we are still a long way from reaching this goal.

Most importantly, our work shows that all three signs of Alzheimers disease detected using our model could be prevented by drugs known to inhibit the production of the toxic amyloid protein and this can be detected in as little as six weeks in the lab. We hope our discovery could lead to the development of new drugs aimed at delaying or preventing Alzheimers disease, before it causes brain cell death.

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Alzheimer's disease: protective gene uncovered in human cell model bringing promise for new drug discoveries - The Conversation UK

Genetic testing comprises examination of ones DNA. The term DNA refers to the chemical database that is responsible for conveying the instructions for functions that need to be performed by the body. Genetic testing is capable of revealing changes or mutations in the genes of living beings, which might result in any kind of disease or illness in the body.

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Predictive genetic testingrefers to the utilization of genetic testing methods in an asymptomatic individual to make a prediction about risk of contacting particular disease in future. These tests are regarded as representation of emerging class of medical tests, which differ in fundamental ways from the usual diagnostic tests.

The global predictive genetic testing and consumer/wellness genomics marketis likely to gather momentum owing to the benefits offered by predictive genetic testing.

The benefits of predictive genetic testing are

The global predictive genetic testing and consumer/wellness genomics marketis influenced by reducing cost of genetic sequencing and technological advancement in the field of genetics. North America is expected to emerge as a prominent region for the global predictive genetic testing and consumer/wellness genomics market in years to come due to high adoption rates of latest technologies in all fields.

Over centauries human DNA has undergone tremendous alteration due to evolutionary and lifestyle changes. They have led to both, advantages and disadvantages over the years. Some have given the mankind a deserving edge over other creatures while the others have led to disorders and diseases. Predictive genetic testing and consumer/wellness genomics market thrives on the growing demand for understanding the lineage of a certain gene pool to identify disorders that could manifest in the later or early stage of a human life. The surging demand for understanding the family history or studying the nature of certain diseases has given the global market for predictive genetic testing and consumer/wellness genomics market adequate fodder for growth in the past few years.

This new class of medical tests are aimed at reducing the risk of morbidity and mortality amongst consumers. The thorough surveillance and screening of a certain gene pool can allow an individual to avoid conditions that disrupt normal existence through preventive measures. The clinical utility of these tests remains unassessed. Therefore, increasing research and development by pharmaceutical companies to develop new drugs by understanding diseases and disorders is expected to favor market growth.

Unlike conventional diagnostic testing, predictive genetic testing identifies the risk associated with potential conditions. In certain cases it is also capable of stating when the disease may appear and the how severe will it be. Thus, this form of testing is expected to allow consumers to take up wellness measurements well in time to lead a life of normalcy, characterized by good health.

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Global Predictive Genetic Testing and Consumer/Wellness Genomics Market: Overview

Predictive genetic testing are used to identify gene mutations pertaining to the disorders that surface at a considerably later stage in life after birth. These tests are particularly beneficial for people from a family with a history of genetic disorder, although they themselves show no symptoms of the disorder at the time of testing. Genetic testing promises to revolutionize the healthcare sector, providing crucial diagnostic details related to diverse verticals such as heart disease, autism, and cancer. As the healthcare sector touches new peaks, the global predictive genetic testing and consumer/wellness genomics market is projected to expand at a healthy growth rate during the forecast period of 2017 to 2025.

This report on the global market for predictive genetic testing and consumer/wellness genomics analyzes all the important factors that may influence the demand in the near future and forecasts the condition of the market until 2025. It has been created using proven research methodologies such as SWOT analysis and Porters five forces. One of the key aspect of the report is the section on company profiles, wherein several leading players have been estimated for their market share and analyzed for their geographical presence, product portfolio, and recent strategic developments such as mergers, acquisitions, and collaborations.

The global predictive genetic testing and consumer/wellness genomics market, on the basis of test type, can be segmented into predictive testing, consumer genomics, and wellness genetics. The segment of predictive testing can be sub-segmented into genetic susceptibility test, predictive diagnostics, and population screening programs, whereas the segment of wellness genetics can be further divided into nutria genetics, skin and metabolism genetics, and others.

By application, the market can be segmented into breast and ovarian cancer screening, cardiovascular screening, diabetic screening and monitoring, colon cancer screening, Parkinsons or Alzheimers disease, urologic screening or prostate cancer screening, orthopedic and musculoskeletal screening, and other cancer screening. Geographically, the report studies the opportunities available in regions such as Asia Pacific, Europe, North America, and the Middle East and Africa.

Global Predictive Genetic Testing and Consumer/Wellness Genomics Market: Trends and Opportunities

Increasing number of novel partnership models, rapidly decreasing cost of genetic sequencing, and introduction of fragmented point-solutions across the genomics value chain as well as technological advancements in cloud computing and data integration are some of the key factors driving the market. On the other hand, the absence of well-defined regulatory framework, low adoption rate, and ethical concerns regarding the implementation, are expected to hinder the growth rate during the forecast period. Each of these factors have been analyzed in the report and their respective impacts have been anticipated.

Currently, the segment of predictive genetic cardiovascular screening accounts for the maximum demand, and increased investments in the field is expected to maintain it as most lucrative segment. On the other hand, more than 70 companies are currently engaged in nutrigenomics, which is expected to further expand the market.

Global Predictive Genetic Testing and Consumer/Wellness Genomics Market: Regional Outlook

Owing to robust healthcare infrastructure, prevalence of cardiovascular diseases, and high adoptability rate of new technology makes North America the most lucrative region, with most of the demand coming from the country of the U.S. and Canada. Several U.S. companies hold patents, which further extends the outreach of the market in the region of North America.

Companies mentioned in the research report

23andMe, Inc, BGI, Genesis Genetics, Illumina, Inc, Myriad Genetics, Inc, Pathway Genomics, Color Genomics Inc., and ARUP Laboratories are some of the key companies currently operating in global predictive genetic testing and consumer/wellness genomics market. Various forms of strategic partnerships with operating company and smaller vendors with novel ideas helps these leading players maintain their position in the market.

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Predictive Genetic Testing and Consumer/Wellness Genomics Market Analysis On Trends & Need 2025 - Daily Research Chronicles

Since the coronavirus disease (COVID-19) and its virus SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) emerged in Wuhan in the Hubei Province of China, global attention has focused on itscontrol and containment.

Its rapid spread and the absence of an effective treatment or vaccine has caused COVID-19 to overwhelm even the most robust health systems in the world.

From January 2020 to date, the cumulative number of cases is over 8.

5 million with more than 450,000 deaths globally.

Conceivably, therefore COVID-19 has the potential to decimate large populations especially those of low and middle-income countries with limited health infrastructure, personnel and resources, and thus a reason for the unrelenting efforts to control and prevent its spread.

Among those who have died from the condition are senior government officials, policy makers and key front line health workers who are critical in the fight against the disease.

The virus, as has been well established, spreads through contaminated surfaces, droplets from saliva, sneezes and coughs and through aerosols (micro droplets) in breath.

Public health measures adopted so far to contain COVID-19 have thus focused mainly on preventing the virus from entering the nasal and oral cavities.

These include the isolation and quarantining of confirmed and suspected individuals, physical distancing, staying at home, regular hand washing with soap under running water, rubbing hands withalcohol-based sanitizers and the use of face masks.

The provision of personal protective equipment for frontline staff has been key, considering their increased risk of contracting the disease.

MOUTH AND THROAT EXPOSUREWith growing numbers of asymptomatic individuals increasing the spread of the virus in communities as well as increasing concerns among dentists about its potential spread especially during aerosol generating procedures , it is extremely difficult to restrict the virus from entering the oral and nasal cavities, even with the available protective measures for clinicians especially surgeons (Dental, Oropharyngeal, ENT) not to mention anesthetists, physicians, nurses and support staff in critical care.

In that regard, attention should therefore focus also on interventions that prevent viruses that have gained access to these cavities from invading host cells to cause disease.

Such a measure, which is our present focus, could protect especially contacts of infected persons and at the same time, reduce viable viral load shed in saliva by asymptomatic carriers and cases.

Notably, the virus attaches to the angiotensin-converting enzyme 2 (ACE2) receptors in the most superficial cells in the non-keratinized epithelium of the oral cavity and oropharynx.

It then uses its signaling and trafficking pathways to gain further access to infect the body.

These ACE2 receptors are also found in several other areas including the epithelial cells of the respiratory tract down to the alveoli.

The incubation period of COVID-19 is 14 days with an average of 6.

4 days.

How long the virus takes on entering the oral cavity and oropharynx to invade host cells is uncertain.

If it is assumed that the whole of the infective process in the upper respiratory and the oropharynx regions takes 2-5 days, there is very little time, albeit a day or two, to intervene to prevent the virus from infecting an individual who has been exposed to it through the oral cavity.

This demonstrates how speedily action should be taken to prevent a contact of COVID-19 from being infected.

Therapeutic mouthwashes that inactivate microbes in the oral cavity, the palatine fossa and the oropharynx include hydrogen peroxide.

This communication is advocating its use to limit the infectivity and spread of SARS-CoV-2 especially in countries and communities with inadequate healthcare delivery systems.

HYDROGEN PEROXIDEHydrogen peroxide has been used in dental practice for nearly 100 years and has been considered safe when used in low concentrations.

[13] In a review on its safety, it had been noted that 3% hydrogen peroxide daily use for up to six years, showed only occasional or transient irritations in a minimal number of subjects who also had pre-existing lesions.

Even though this solution has mutagenic potential through its reactive oxygen species that could induce DNA damage, there has been no substantive evidence in the literature to support assertions that it causes cancer in humans.

It has been stated that there is strong evidence for the safety of low concentrations of hydrogen peroxide products when used on daily basis and over an extended period Earlier, the International Agency for Research on Cancer also concluded after reviewing animal and human studies that hydrogen peroxide is not classifiable as to its carcinogenicity in humans.

In a recent study assessing carcinogenicity associated with exposure to hydrogen peroxide neither tissue irritation nor tumor promotion was observed in animal models.

The efficacy of hydrogen peroxide has not been in doubt, especially about its capacity to inactivate corona and influenza viruses.

A recent review of studies on human coronaviruses has suggested that 0.

5% hydrogen peroxide will inactivate SARS-CoV-2 on surfaces.

Furthermore, a suggestion has been made quite recently to buttress the view that 1% hydrogen peroxide may serve to prevent entry of the virus into susceptible cells and reduce the possibility of severe disease.

We are proposing, therefore, that use of 1% hydrogen peroxide mouthwash and gargle, at least twice a day be added to the established WHO preventive protocols for SARS-CoV-2.

This could augment protection of frontline health personnel, contacts of COVID-19 cases, and the highly vulnerable individuals such as the aged, security personnel, media staff, persons with underlying health issues and individuals in communities where the burden of COVID-19 is high.

Furthermore, since there is evidence that even 0.

5% hydrogen peroxide could inactivate the SARS-CoV-2 on surfaces, this lower concentration could be used by individuals who may be more susceptible to tissue irritation, considering that its prophylactic use might be required over a long period.

To further limit the risk of infecting others, asymptomatic individuals and mild to moderate cases could use hydrogen peroxide mouthwash and gargle to inactivate SARS-CoV-2 shed.

In conclusion, Hydrogen Peroxide that has been in use in dental practice with proven safety and efficacy could be employed in limiting the infectivity and spread of SARS-CoV-2 whilst awaiting the emergence of fail-proof prophylactic and therapeutic measures.

We have planned a clinical trial of mouthwash and gargle with hydrogen peroxide compared with mouthwash or gargle with water only, in asymptomatic cases ofCOVID-19.

Rev.

Emeritus Professor Andrews Seth Ayettey MB.

ChB.

PhD.

Retired Professor, University of Ghana Medical School, College of Health Sciences.

University of Ghana, Legon.

Ghana.

Email: seth.

ayettey@gmail.

com Twitter@ayettey_sethEmerita Professor, Isabella A.

Quakyi.

PhD.

FGA.

School of Public Health, College of Health Sciences, University of Ghana, Legon.

Ghana.

Hannah N.

G.

Ayettey-Anie.

BSc (Med Sc) MB ChB FGCP, Senior Specialist, National Radiotherapy Oncology and Nuclear Medicine Centre, Korle Bu Teaching Hospital, Accra, Ghana.

Kwamena W.

Sagoe.

MSc PhD.

Associate Professor, Department of Medical Microbiology, University of Ghana Medical School, College of Health Sciences.

University of Ghana, Legon.

Ghana.

Mary N.

B.

Ayettey-Adamafio.

BSc (Med Sc) BDS FGCS FWACS.

Senior Specialist, Department of Dentistry, Korle Bu Teaching Hospital, Korle Bu, Accra.

Ghana.

Merley Newman-Nartey BDS MClD FGCS.

Senior Lecturer, University of Ghana Dental School, College of Health Sciences, University of Ghana.

Ruth N.

A.

Ayettey Brew BSc (Med Sc), MB.

ChB.

Resident, Department of Obstetrics and Gynecology, Korle Bu Teaching Hospital, Accra.

Ghana.

Nii Otu Nartey BDS MSc FAAOP MRCD FWACS FGCS Retired Associate Professor, University of Ghana Dental School, College of Health Sciences, University of Ghana.

Albert G.

B.

Amoah MB ChB, PhD, FWACP, FGCP, FGA.

Retired Professor, University of Ghana Medical School, College of Health Sciences, University of Ghana.

Felix I D Konotey-Ahulu MD (Lond) FRCP(Lond & Glasg) DTMH(L'pool) Distinguished Professor of Human Genetics University of Cape Coast, Honorary Consultant Physician Specialist to Ghana Ministry of Health through Commissioner of Health Brigadier Odartey-Wellington 1976, and Former Consultant Physician, Korle Bu Teaching Hospital, Accra, and Phoenix Hospital Group 9 Harley St, London W1G 9AL.

*Corresponding Author Professor Seth Ayettey: Twitter@ayettey_sethAcknowledgement: The authors acknowledge Mr.

Benjamin Yankah of Accra, Ghana, for encouragement.

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OBITUARY of Amged El-Hawrani.

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(Born 1964; Qualified 1993), died from COVID-19 on 28 March 2020.

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Covid-19: what treatments are being investigated? - BusinessGhana

Genetics is that the study of genes, their functions and their effects. Among the varied sorts of biology like genetic science, developmental genetic science, population genetics and quantitative genetic science, human genetics is that the study that deals with the inheritance happens in folks. It encompasses a range of overlapping fields like classical biology, genetics, genetic science, genetics and plenty of additional.

The Human Genetics Market is expected to exceed at a CAGR of 9.5% in the given forecast period.

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The Human Genetics Market is segmented on the lines of its methods, product, applications, end-users and regional. Based on methods segmentation it covers cytogenetic, molecular, presymptomatic and prenatal. Based on product it covers Consumables, devices and accessories. Based on end-user analysis it covers hospitals, clinics, research centers and forensic departments. Based on application it covers research, diagnostic and forensic science and others. Based on Others it covers Hysteroscopy Instruments Market on geographic segmentation covers various regions such as North America, Europe, Asia Pacific, Latin America, Middle East and Africa. Each geographic market is further segmented to provide market revenue for select countries such as the U.S., Canada, U.K. Germany, China, Japan, India, Brazil, and GCC countries.

This report provides:

1) An overview of the global market for Human Genetics Market and related technologies.2) Analyses of global market trends, with data from 2015, estimates for 2016 and 2017, and projections of compound annual growth rates (CAGRs) through 2024.3) Identifications of new market opportunities and targeted promotional plans for Human Genetics Market.4) Discussion of research and development, and the demand for new products and new applications.5) Comprehensive company profiles of major players in the industry.

Report Scope:

The scope of the report includes a detailed study of Human Genetics Market with the reasons given for variations in the growth of the industry in certain regions.

The report covers detailed competitive outlook including the market share and company profiles of the key participants operating in the global market. Key players profiled in the report include Agilent Technologies, Bode Technology, GE Healthcare, Illumina, LGC Forensics, Orchid Cell mark, Inc., Promega Corporation, QIAGEN N.V., Thermo Fisher Scientific, Inc. Company profile includes assign such as company summary, financial summary, business strategy and planning, SWOT analysis and current developments.

The Human Genetics Market has been segmented as below:

The Human Genetics Market is Segmented on the lines of Application Type, Methods, Product Type, End-user and Regional Analysis. By Application Type this market is segmented on the basis of Research, Diagnostic, Forensic science and Others. By Methods this market is segmented on the basis of Cytogenetic, Molecular, Presymptomatic and Prenatal.

By Product Type this market is segmented on the basis of Consumables, Devices and Accessories. By End-user this market is segmented on the basis of Hospitals sector, Clinics sector, Research centers sector and Forensic departments sector. By Regional Analysis this market is segmented on the basis of North America, Europe, Asia-Pacific and Rest of the World.

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Human Genetics Market 2020: Challenges, Growth, Types, Applications, Revenue, Insights, Growth Analysis, Competitive Landscape, Forecast- 2025 - Cole...

A friend of mine with Central American, Southern European and West African ancestry islactose intolerant. Drinking milk products upsets her stomach, and so she avoids them. About a decade ago, because of her low dairy intake, she feared that she might not be getting enough calcium, so she asked her doctor for abone density test. He responded that she didnt need one because blacks do not get osteoporosis.

My friend is not alone. The view that black people dont need a bone density test is a longstanding and common myth. A2006 studyin North Carolina found that out of 531 African American and Euro-American women screened for bone mineral density, only 15 percent were African American women despite the fact that African American women made up almost half of that clinical population. A health fair in Albany, New York, in 2000,turned into a ruckuswhen black women were refused free osteoporosis screening. The situationhasnt changed muchin more recent years.

Meanwhile,FRAX, a widely used calculatorthat estimates ones risk of osteoporotic fractures, is based on bone density combined with age, sex and, yes, race. Race, even though it is never defined or demarcated, is baked into the fracture risk algorithms.

Lets break down the problem.

First, presumably based on appearances, doctors placed my friend and others into a socially defined race box called black, which is a tenuous way to classify anyone.

Race is a highly flexible way in which societies lump people into groups based on appearance that is assumed to be indicative of deeper biological or cultural connections. As a cultural category, the definitions and descriptions of races vary. Color lines based on skin tone can shift, which makes sense, but the categories are problematic for making any sort of scientific pronouncements.

Second, these medical professionals assumed that there was a firm genetic basis behind this racial classification, which there isnt.

Third, they assumed that this purported racially defined genetic difference would protect these women from osteoporosis and fractures.

Some studies suggestthat African American women meaning women whose ancestry ties back to Africa may indeed reach greater bone density than other women, which could be protective against osteoporosis. But that does not mean being black that is, possessing an outward appearance that is socially defined as black prevents someone from getting osteoporosis or bone fractures. Indeed, this same research also reports that African American women are more likely to die after a hip fracture. The link between osteoporosis risk and certain racial populations may be due to lived differencessuch as nutritionandactivity levels, both of which affect bone density.

But more important:Geographicancestry is not the same thing as race. African ancestry, for instance, does not tidily map onto being black (or vice versa). In fact, a2016 studyfound wide variation in osteoporosis risk among women living in different regions within Africa. Their genetic risks have nothing to do with their socially defined race.

When medical professionals or researchers look for ageneticcorrelateto race, they are falling into a trap: They assume thatgeographic ancestry, which does indeed matter to genetics, can be conflated with race, which does not. Sure, different human populations living in distinct places may statistically have different genetic traits such as sickle cell trait (discussed below) but such variation is aboutlocal populations(people in a specific region), not race.

Like a fish in water, weve all been engulfed by the smog of thinking that race is biologically real. Thus, it is easy to incorrectly conclude that racial differences in health, wealth and all manner of other outcomes are the inescapable result of genetic differences.

The reality is that socially defined racial groups in the U.S. and most everywhere else do differ in outcomes. But thats not due to genes. Rather, it is due to systemic differences in lived experience and institutional racism.

Communities of color in the United States, for example, often have reduced access to medical care, well-balanced diets andhealthy environments. They are often treated more harshly in their interactions withlaw enforcement and the legal system. Studies show that they experience greater social stress, includingendemic racism, that adversely affects all aspects of health. For example, babies born to African American women are more thantwice as likely to diein their first year than babies born to non-Hispanic Euro-American women.

Systemic racism leads to different health outcomes for various populations. The infant mortality rate, for example, for African American infants is double that for European Americans. (Credit: Kelly Lacy/Pexels)

As a professor of biological anthropology, I teach and advise college undergraduates. While my students are aware of inequalities in the life experiences of different socially delineated racial groups, most of them also think that biological races are real things. Indeed, more than half of Americans still believe that their racial identity is determined byinformation contained in their DNA.

For the longest time, Europeans thought that the sun revolved around the Earth. Their culturally attuned eyes saw this as obvious and unquestionably true. Just as astronomers now know thats not true,nearly all population geneticistsknow that dividing people into races neither explains nor describes human genetic variation.

Yet this idea of race-as-genetics will not die. For decades, it has been exposed to the sunlight of facts, but, like a vampire, it continues to suck blood not only surviving but causing harm in how it can twist science to support racist ideologies. With apologies for the grisly metaphor, it is time to put a wooden stake through the heart of race-as-genetics. Doing so will make for better science and a fairer society.

In 1619, the first people from Africa arrived in Virginia and became integrated into society. Only after African and European bond laborers unified in various rebellions did colony leaders recognize the need to separate laborers.Race dividedindentured Irish and other Europeans from enslaved Africans, and reduced opposition by those of European descent to the intolerable conditions of enslavement. What made race different from other prejudices, including ethnocentrism (the idea that a given culture is superior), is that it claimed that differences were natural, unchanging and God-given. Eventually, race also received the stamp of science.

Over the next decades, Euro-American natural scientists debated the details of race, asking questions such as how often the races were created (once, as stated in the Bible, or many separate times), the number of races and their defining, essential characteristics. But they did not question whether races were natural things. They reified race, making the idea of race real by unquestioning, constant use.

In the 1700s, Carl Linnaeus, the father of modern taxonomy and someone not without ego, liked to imagine himself asorganizing what God created. Linnaeus famously classified ourown species into racesbased on reports from explorers and conquerors.

The race categories he created includedAmericanus,Africanus, and evenMonstrosus(for wild and feral individuals and those with birth defects), and their essential defining traits included a biocultural mlange of color, personality and modes of governance. Linnaeus describedEuropeausas white, sanguine and governed by law, andAsiaticusas yellow, melancholic and ruled by opinion. These descriptions highlight just how much ideas of race are formulated by social ideas of the time.

Swedish taxonomist Carl Linnaeus divided humanity up into racial categories according to his notion of shared essences among populations, a concept researchers now recognize has no scientific basis. (Credit: Wikimedia Commons/Public Domain)

In line with early Christian notions, these racial types were arranged in a hierarchy:a great chain of being, from lower forms to higher forms that are closer to God. Europeans occupied the highest rungs, and other races were below, just above apes and monkeys.

So, the first big problems with the idea of race are that members of a racial group do not share essences, Linnaeus idea of some underlying spirit that unified groups, nor are races hierarchically arranged. A related fundamental flaw is that races were seen to be static and unchanging. There is no allowance for a process of change or what we now call evolution.

There have been lots of efforts since Charles Darwins time to fashion the typological and static concept of race into an evolutionary concept. For example, Carleton Coon, a former president of the American Association of Physical Anthropologists, argued inThe Origin of Races(1962) that five racesevolved separatelyand became modern humans at different times.

One nontrivial problem with Coons theory, and all attempts to make race into an evolutionary unit, is that there is no evidence. Rather, all the archaeological and genetic data point to abundant flows of individuals, ideas and genes across continents, withmodern humansevolving at the same time, together.

Afew pundits such asCharles Murrayof the American Enterprise Institute and science writers such asNicholas Wade, formerly ofThe New York Times, still argue that even though humans dont come in fixed, color-coded races, dividing us into races still does a decent job ofdescribinghuman genetic variation. Their position is shockingly wrong. Weve known for almost 50 years that race does not describe human genetic variation.

In 1972, Harvard evolutionary biologist Richard Lewontinhad the idea to testhow much human genetic variation could be attributed to racial groupings. He famously assembled genetic data from around the globe and calculated how much variation was statistically apportioned within versus among races. Lewontin found that only about 6 percent of genetic variation in humans could be statistically attributed to race categorizations. Lewontin showed that the social category of race explains very little of the genetic diversity among us.

Furthermore, recent studies reveal that the variation between any two individuals isverysmall, on the order of onesingle nucleotide polymorphism(SNP), or single letter change in our DNA, per 1,000. That means that racial categorization could, at most, relate to 6 percent of the variation found in 1 in 1,000 SNPs. Put simply, race fails to explain much.

In addition, genetic variation can be greaterwithingroups that societies lump together as one race than it is between races. To understand how that can be true, first imagine six individuals: two each from the continents of Africa, Asia and Europe. Again, all of these individuals will be remarkably the same: On average, only about 1 out of 1,000 of their DNA letters will be different. A study by Ning Yu and colleaguesplaces the overall difference more precisely at 0.88 per 1,000.

The researchers further found that people in Africa had less in common with one another than they did with people in Asia or Europe. Lets repeat that: On average, two individuals in Africa aremoregenetically dissimilar from each other than either one of them is from an individual in Europe or Asia.

Homo sapiensevolved in Africa; the groups that migrated out likely did not include all of the genetic variation that built up in Africa. Thats an example of what evolutionary biologists call thefounder effect, where migrant populations who settle in a new region have less variation than the population where they came from.

Genetic variation across Europe and Asia, and the Americas and Australia, is essentially a subset of the genetic variation in Africa. If genetic variation were a set of Russian nesting dolls, all of the other continental dolls pretty much fit into the African doll.

What all these data show is that the variation that scientists from Linnaeus to Coon to the contemporary osteoporosis researcher think is race is actually much better explained by a populationslocation. Genetic variation is highly correlated togeographic distance. Ultimately, the farther apart groups of people are from one another geographically, and, secondly, the longer they have been apart, can together explain groups genetic distinctions from one another. Compared to race, those factors not only better describe human variation, they invoke evolutionary processes to explain variation.

Those osteoporosis doctors might argue that even though socially defined race poorly describes human variation, it still could be a useful classification tool in medicine and other endeavors. When the rubber of actual practice hits the road, is race a useful way to make approximations about human variation?

When Ive lectured at medical schools, my most commonly asked question concerns sickle cell trait. Writer Sherman Alexie, a member of the Spokane-Coeur dAlene tribes, put the question this wayin a 1998 interview: If race is not real, explain sickle cell anemia to me.

OK! Sickle cell is a genetic trait: It is the result of an SNP that changes the amino acid sequence of hemoglobin, the protein that carries oxygen in red blood cells. When someone carries two copies of the sickle cell variant, they will have the disease. In the U.S., sickle cell disease is most prevalent in people who identify as African American, creating the impression that it is a black disease.

(Credit: SciePro/Shutterstock)

Yet scientists have known about the much more complexgeographic distributionof sickle cell mutation since the 1950s. It is almost nonexistent in the Americas, most parts of Europe and Asia and also in large swaths of Northern and Southern Africa. On the other hand, it is common in West-Central Africa and also parts of the Mediterranean, Arabian Peninsula, and India. Globally, it does not correlate with continents or socially defined races.

Inone of the most widely citedpapers in anthropology, American biological anthropologist Frank Livingstone helped to explain the evolution of sickle cell. He showed that places with a long history of agriculture and endemic malaria have a high prevalence of sickle cell trait (a single copy of the allele). He put this information together with experimental and clinical studies that showed how sickle cell trait helped people resist malaria, and made a compelling case for sickle cell trait being selected for in those areas.Evolution and geography, not race, explain sickle cell anemia.

What about forensic scientists: Are they good at identifying race? In the U.S., forensic anthropologists are typically employed by law enforcement agencies to help identify skeletons, including inferences about sex, age, height and race. The methodological gold standards for estimating race are algorithms based on a series of skull measurements, such as widest breadth and facial height. Forensic anthropologists assume these algorithms work.

The origin of the claim that forensic scientists are good at ascertaining race comes from a 1962 study of black, white and Native American skulls, which claimed an 8090 percent success rate. That forensic scientists are good at telling race from a skull is a standard trope of both thescientific literatureandpopular portrayals.But my analysisof four later tests showed that the correct classification of Native American skulls from other contexts and locations averaged about two incorrect for every correct identification. The results are no better than a random assignment of race.

Thats because humans are not divisible into biological races. On top of that, human variation does not stand still. Race groups are impossible to define in any stable or universal way. It cannot be done based on biology not by skin color, bone measurements or genetics. It cannot be done culturally: Race groupings have changed over time and place throughout history.

Science 101: If you cannot define groups consistently, then you cannot make scientific generalizations about them.

Skull measurements are a longstanding tool in forensic anthropology. (Credit: Internet Archive Book Images/Flickr/Public Domain)

Wherever one looks, race-as-genetics is bad science. Moreover, when society continues to chase genetic explanations, it misses the larger societal causes underlying racial inequalities in health, wealth and opportunity.

To be clear, what I am saying is that human biogenetic variation is real. Lets just continue to study human genetic variation free of the utterly constraining idea of race. When researchers want to discuss genetic ancestry or biological risks experienced by people in certain locations, they can do so without conflating these human groupings withracial categories. Lets be clear that genetic variation is an amazingly complex result of evolution and mustnt ever be reduced to race.

Similarly, race is real, it just isnt genetic. Its a culturally created phenomenon. We ought to know much more about the process of assigning individuals to a race group, including the category white. And we especially need to know more about the effects of living in a racialized world: for example, how a societys categoriesand prejudiceslead to health inequalities. Lets be clear that race is a purely sociopolitical construction with powerful consequences.

It is hard to convince people of the dangers of thinking race is based on genetic differences. Like climate change, the structure of human genetic variation isnt something we can see and touch, so it is hard to comprehend. And our culturally trained eyes play a trick on us by seeming to see race as obviously real. Race-as-genetics is even more deeply ideologically embedded than humanitys reliance on fossil fuels and consumerism. For these reasons, racial ideas will prove hard to shift, but it is possible.

Over 13,000 scientistshave come together to form and publicize a consensus statement about the climate crisis, and that has surely moved public opinion to align with science. Geneticists and anthropologists need to do the same for race-as-genetics. The recent American Association of Physical AnthropologistsStatement on Race & Racismis a fantastic start.

In the U.S., slavery ended over 150 years ago and the Civil Rights Law of 1964 passed half a century ago, but the ideology of race-as-genetics remains. It is time to throw race-as-genetics on the scrapheap of ideas that are no longer useful.

We can start by getting my friend and anyone else who has been denied that long-overdue bone density test.

Alan Goodmanis a professor of biological anthropology at Hampshire College in Massachusetts. This story was originally posted onSAPIENS. Read the original articlehere.

Read more from the original source:
Race Is Real, But It's Not Genetic - Discover Magazine

The combination of genomics, transcriptomics and proteomics sheds light on autoimmune thyroid disease, other autoimmune diseases and AML

REYKJAVIK, Iceland, June 24, 2020 /PRNewswire/ -- Scientists at deCODE genetics, a subsidiary of Amgen, and their collaborators from the Icelandic healthcare system, University of Iceland and the Karolinska Institute in Sweden, today publish a studyin Nature, comparing over 30 thousand patients with autoimmune thyroid disease from Iceland and UK with 725 thousand controls. Autoimmune thyroid disease (AITD) is the most common autoimmune disease and is highly heritable. The scientists found 99 sequence variants that associate with autoimmune thyroid disease and 84 of those had not been associated with the disease before.

One of the newly discovered sequence variants is in a gene that codes for the FLT3 receptor (fms-related tyrosine kinase 3) on blood cells and immune cells, and is of large interest for several reasons.

First, it strongly increases the risk of autoimmune thyroid disease and other autoimmune diseases, both systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and celiac disease. Thesediseases are all characterized by autoantibodies and are more common in women than men. Furthermore, patients with thesediseases are quite often affected by autoimmune thyroid disease as well.

Second, it is known that activating somatic mutations in the FLT3 gene associate with acute myeloid leukemia (AML). Therefore, the scientists tested whether this FLT3 germline variant, affects the risk of AML like it increases the risk of autoimmune diseases. It turned out that it almost doubles the risk of AML, but not the risk of cancer overall.

Third, it is quite remarkable that this variant in FLT3, which is in anintron of the gene and does not directly affect coding sequence, can have so strong effect on disease risk. It turns out that the variant introduces a stop codon in one-third of the transcripts, which results in a shorter protein that lacks the kinase part, which is essential for its function.

Finally, this variant in FLT3 affects the plasma levelsof several other proteins in the body, especially the ligand of FLT3, resulting in almost double the level in carriers. This molecular couple, the FLT3 receptor and its ligand, has a key role in the development of blood cells that are important in both acute myeloid leukemia and immune responses. Hence, this variant is a loss of function mutation that through compensatory increase in the level of the ligand, acts as a gain of function.

"This report describes a novel major risk gene for several autoimmune diseases, discovered through a genome-wide study on autoimmune thyroid disease, and how the risk variant affects the gene product, FLT3, and consequently the level of the ligand to the FLT3 receptor in blood, thereby demonstrating its functional importance," says Prof. Saedis Saevarsdottir, scientist atdeCODEgenetics and first author on the paper

"The discoveries presented in this paper are based on the sequential application of genomics, transcriptomics and proteomics; the combination of these three omics in a hypothesis independent manner yields a remarkably powerful approach to the study of human disease," says Kari Stefansson, CEO of deCODE genetics and senior author on the paper.

Based in Reykjavik, Iceland, deCODE is a global leader in analyzing and understanding the human genome. Using its unique expertise in human genetics combined with growing expertise in transcriptomics and population proteomics and vast amount of phenotypic data, deCODE has discovered risk factors for dozens of common diseases and provided key insights into their pathogenesis. The purpose of understanding the genetics of disease is to use that information to create new means of diagnosing, treating and preventing disease. deCODE is a wholly-owned subsidiary of Amgen (NASDAQ: AMGN).

Video - https://www.youtube.com/watch?v=Wa4OGAejKTs Photo - https://media.zenfs.com/en/prnewswire.com/65959edb04d7e824e88686a3d5635154 Logo - https://media.zenfs.com/en/prnewswire.com/5c073ade5135fe6bbd51ce8b6019cb27

Contact: Thora Kristin AsgeirsdottirPR and CommunicationsdeCODE geneticsthoraa@decode.is+354 894 1909

Story continues

Link:
deCODE Genetics: Loss of Function Variant in FLT3 Strongly Increases the Risk of Autoimmune Thyroid Disease and Other Autoimmune Diseases - Yahoo...

Scientists, biotech companies, and medical societies are reacting with outrage and dismay to President Trumps executive order (EO), signed on June 21, 2020, that restricts the issuance of new work visas for skilled workers and managers (and au pairs) through the end of 2020.

The visas affected include the H-1B, H-4, H-2B, L-1, and J categories. The EO means that foreign graduate students and postdocs would be banned from entering the United States. Almost every major research lab includes a diverse mix of research talent from around the world. Many of these scientists eventually lead their own groups, move to industry, and/or become naturalized U.S. citizens.

In the science community, many are reacting and expressing their concerns about the future of labs, and how the EO will affect research and innovation. Akiko Iwasaki, PhD, who is a professor in the department of immunobiology and department of molecular, cellular, and developmental biology at Yale University (and an investigator of the Howard Hughes Medical Institute) expressed her dismay.

Iwasaki tweeted: This is the worst thing thats happened to U.S. science and innovation. Banning immigrant scientists will lead to a devastating loss in creativity and productivity. Pretty much every lab in the U.S. will suffer.

The EO also extends Trumps April 22 order denying green cards to applicants in several immigrant visa categories. The Trump Administration says its goal is to protect 520,000 jobs and get Americans back to work. We have a moral duty to create an immigration system that protects the lives and jobs of our citizens, stated President Trump.

But many scientists in academia and industry not only disagree with the executive order but also highlight how their labs would look without their immigrant postdocs. Samantha Morris, PhD, an assistant professor of genetics, and developmental biology at Washington University School of Medicine, expressed her frustrations on Twitter.

I invest a lot of energy trying to recruit postdocs to my lab. I haven't received a SINGLE non-immigrant postdoc application in the past five years

Samantha Morris (@morris_lab) June 23, 2020

Florian Krammer, PhD, professor of microbiology at the Icahn School of Medicine at Mount Sinai in New York, expressed concern about colleagues working on SARS-CoV-2. I am about to hire a postdoc from Spain who is specialized in vaccine production and a postdoc from Japan who is specialized in mucosal immunity to virus infections. I might not be able to hire them if this is signed. Both would have worked on SARS-CoV-2 and influenza virus. Krammer also posted a picture of his lab with and without immigrants, and the image paints a picture of what research labs may look like.

My lab with and without immigrants. pic.twitter.com/aLJmUQFXEM

Florian Krammer (@florian_krammer) June 15, 2020

Lars Dietrich, PhD, associate professor, Department of Biological Sciences at Columbia University, who came to the U.S. through a work visa expressed his thoughts on the EO. The visa situation is disturbing. I came to the U.S. on a J1 visa, then transferred to H-1B before becoming faculty at Columbia University. Ive always been inspired by the way that, in U.S. academia, people of diverse backgrounds can come together to do transformative science. It reflects values that the U.S. can be proud of, and it sets an example. It really saddens me to see the erosion of this commitment to diversity.

Rebecca Bernhard, a partner at the law firm Dorsey & Whitney in immigration, labor and employment practices, highlighted some exemptions in the EO. One key exemption is for workers involved in the U.S. food supply system. This exemption should cover people involved in meatpacking and processing plants, as well as all aspects of the food supply chain from production to transportation and logistics, Bernhard said.

Another key exemption is for medical personnel working on COVID-19 research or treatment. Most physicians, nurses, and other medical personnel should still be able to obtain visas, Bernhard stated.

But what will this mean for companies working on vaccines and treatments for COVID-19? Major companies such as Moderna Therapeutics, GlaxoSmithKline, Inovio, and others who are currently working on a vaccine or treatment for COVID-19, had received approvals from the Department of Labor to hire foreign workers with either green cards or H-1B work visas more than 11,000 times from 2010 to 2019.

The American Society of Human Genetics (ASHG), the worlds largest genetics organization, is urging the White House to rescind their executive order as it will hinder the progress of science and better human health. They also point out the importance of connecting globally especially with the coronavirus crisis.

ASHG is deeply committed to a diverse and inclusive research workforce and honors those who come to U.S. labs from across the world to contribute to genetics and genomics advances in this country, said ASHG president Anthony Wynshaw-Boris, MD, PhD. Their experiences enrich American science and global science, and it is precisely Americas commitment to international collaboration that has made the U.S. a recognized global scientific leader. As the SARS-CoV-2 pandemic illustrates, we should be expanding global research connections that harness all minds to solve a problem, not closing our doors.

In a strongly worded statement, Kevin Wilson, director of public policy and media relations at the American Society for Cell Biology (ASCB), said the EO will hurt science in the United States. The decision by the Trump Administration to freeze through 2020 important U.S. visa programs that allow future scientists from around the world to come to the United States to learn is reprehensible. It goes against everything the United States stands for and violates the principle that scientific excellence requires collaboration, regardless of nationality.

The ASCB statement continued: It is American science and scientists who are the real victims of these policies. Without these talented individuals from around the globe, American biomedical research will not remain the world leader it is. If these policies are allowed to remain in place, the United States will no longer lead but will have to settle for the role of runner up.

H-1B visas are used for skilled workers and are common in the technology industry; H-4 visas are given to spouses of H-1B visa holders. H-2B visas apply to seasonal workers; L-1 visas are used for managers or executives transferring to the United States from positions abroad; and J-1 visas are given to scholars, researchers, and au pairs. The EO stops the issuance of all J-1s except for those going to physicians, medical researchers, or secondary school students. The order does not apply to immigrants already living and working in the United States nor to permanent residents seeking to become citizens.

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Scientists and Societies Decry Trump Executive Order on Immigration Visas - Genetic Engineering & Biotechnology News