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Podcast: Can you inherit more than half your genes from one parent? Debunking genomic myths and misconceptions – Genetic Literacy Project

Posted: March 17, 2020 at 6:42 pm

The Distaff Gospels, a collection of medieval Old Wives Tales, warns that if a pregnant woman eats hare shes likely to have a baby with a cleft palate, while eating fish heads leads to a trout pout. While these ideas certainly arent supported by modern science, there is still plenty of confusion surrounding genetics todayfor example, the idea that an inherited disease is the result of something bad happening in the family, that mutations are always bad, or that looking more like one parent than the other means youve inherited more of their genes.

Geneticist Kat Arney explores some of the myths and misconceptions about genetics, genomics and inheritance, in partnership with the Genomics Education Programme.

Genetic testsand increasingly, more detailed genomic analysisare providing an unprecedented amount of information about the underlying genetic variations and alterations that affect health. The pace at which genomic data and technologies are coming into the clinic is impressive. At the same time, it can leave patients, the public and healthcare providers feeling overwhelmed and trying to figure out what it all means.

Laura Boyes, Consultant Genetic Counselor for the West Midlands, explains where we get our ideas about inheritance from, and how they shape our family relationships. She also talks about the need to normalize the idea of genetic variation: nobody has a perfect genome, and we are all carrying our own unique alterations.

Anna Middleton, Head of Society and Ethics Research at the Wellcome Genome Campus in Cambridge, discusses whether media portrayals of genetics are helpful or harmful, and whether scientists should get worked up about bad science in the movies.

Finally, Arney speaks with Michelle Bishop, the Education Lead for the Genomics Education Programme, about the importance of providing accurate and understandable information about genomics, and the need for educators and healthcare professionals to keep up to date with advances in this fast-moving field.

The Genomics Education Programme is running a week of action from the 16th to the 20th March 2020, designed to raise awareness about the impact of genomics in healthcare and what we can all do to tackle some of the myths and misconceptions that are out there. Following @genomicsedu and #GenomicsConversation on Twitter or visit genomicseducation.hee.nhs.uk for more information.

Full transcript, links and references available online atGeneticsUnzipped.com

Genetics Unzippedis the podcast from the UKGenetics Society,presented by award-winning science communicator and biologistKat Arneyand produced byFirst Create the Media.Follow Kat on Twitter@Kat_Arney,Genetics Unzipped@geneticsunzip,and the Genetics Society at@GenSocUK

Listen to Genetics Unzipped onApple Podcasts(iTunes)Google Play,Spotify,orwherever you get your podcasts

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Genomics took a long time to fulfil its promise – The Economist

Posted: March 17, 2020 at 6:42 pm

Mar 12th 2020

THE ATOMIC bomb convinced politicians that physics, though not readily comprehensible, was important, and that physicists should be given free rein. In the post-war years, particle accelerators grew from the size of squash courts to the size of cities, particle detectors from the scale of the table top to that of the family home. Many scientists in other disciplines looked askance at the money devoted to this big science and the vast, impersonal collaborations that it brought into being. Some looked on in envy. Some made plans.

The idea that sequencing the whole human genome might provide biology with some big science of its own first began to take root in the 1980s. In 1990 the Human Genome Project was officially launched, quickly growing into a global endeavour. Like other fields of big science it developed what one of the programmes leaders, the late John Sulston, called a tradition of hyperbole. The genome was Everest; it was the Apollo programme; it was the ultimate answer to that Delphic injunction, know thyself. And it was also, in prospect, a cornucopia of new knowledge, new understanding and new therapies.

By the time the completion of a (rather scrappy) draft sequence was announced at the White House in 2000, even the politicians were drinking the Kool-Aid. Tony Blair said it was the greatest breakthrough since antibiotics. Bill Clinton said it would revolutionise the diagnosis, prevention and treatment of most, if not all, human diseases. In coming years, doctors increasingly will be able to cure diseases like Alzheimers, Parkinsons, diabetes and cancer by attacking their genetic roots.

Such hype was always going to be hard to live up to, and for a long time the genome project failed comprehensively, prompting a certain Schadenfreude among those who had wanted biology kept small. The role of genetics in the assessment of peoples medical futures continued to be largely limited to testing for specific defects, such as the BRCA1 and BRCA2 mutations which, in the early 1990s, had been found to be responsible for some of the breast cancers that run in families.

To understand the lengthy gap between the promise and the reality of genomics, it is important to get a sense of what a genome really is. Although sequencing is related to an older technique of genetic analysis called mapping, it produces something much more appropriate to the White House kitchens than to the Map Room: a recipe. The genes strung out along the genomes chromosomesbig molecules of DNA, carefully packedare descriptions of lifes key ingredients: proteins. Between the genes proper are instructions as to how those ingredients should be used.

If every gene came in only one version, then that first human genome would have been a perfect recipe for a person. But genes come in many varietiesjust as chilies, or olive oils, or tinned anchovies do. Some genetic changes which are simple misprints in the ingredients specification are bad in and of themselvesjust as a meal prepared with fuel oil instead of olive oil would be inedible. Others are problematic only in the context of how the whole dish is put together.

The most notorious of the genes with obvious impacts on health were already known before the genome was sequenced. Thus there were already tests for cystic fibrosis and Huntingtons disease. The role of genes in common diseases turned out to be a lot more involved than many had naively assumed. This made genomics harder to turn into useful insight.

Take diabetes. In 2006 Francis Collins, then head of genome research at Americas National Institutes of Health, argued that there were more genes involved in diabetes than people thought. Medicine then recognised three such genes. Dr Collins thought there might be 12. Today the number of genes with known associations to type-2 diabetes stands at 94. Some of these genes have variants that increase a persons risk of the disease, others have variants that lower that risk. Most have roles in various other processes. None, on its own, amounts to a huge amount of risk. Taken together, though, they can be quite predictivewhich is why there is now an over-the-counter genetic test that measures peoples chances of developing the condition.

In the past few years, confidence in sciences ability to detect and quantify such genome-wide patterns of susceptibility has increased to the extent that they are being used as the basis for something known as a polygenic risk score (PRS). These are quite unlike the genetic tests people are used to. Those single-gene tests have a lot of predictive value: a person who has the Huntingtons gene will get Huntingtons; women with a dangerous BRCA1 mutation have an almost-two-in-three chance of breast cancer (unless they opt for a pre-emptive mastectomy). But the damaging variations they reveal are rare. The vast majority of the women who get breast cancer do not have BRCA mutations. Looking for the rare dangerous defects will reveal nothing about the other, subtler but still possibly relevant genetic traits those women do have.

Polygenic risk scores can be applied to everyone. They tell anyone how much more or less likely they are, on average, to develop a genetically linked condition. A recently developed PRS for a specific form of breast cancer looks at 313 different ways that genomes vary; those with the highest scores are four times more likely to develop the cancer than the average. In 2018 researchers developed a PRS for coronary heart disease that could identify about one in 12 people as being at significantly greater risk of a heart attack because of their genes.

Some argue that these scores are now reliable enough to bring into the clinic, something that would make it possible to target screening, smoking cessation, behavioural support and medications. However, hope that knowing their risk scores might drive people towards healthier lifestyles has not, so far, been validated by research; indeed, so far things look disappointing in that respect.

Assigning a PRS does not require sequencing a subjects whole genome. One just needs to look for a set of specific little markers in it, called SNPs. Over 70,000 such markers have now been associated with diseases in one way or another. But if sequencing someones genome is not necessary in order to inspect their SNPs, understanding what the SNPs are saying in the first place requires that a lot of people be sequenced. Turning patterns discovered in the SNPs into the basis of risk scores requires yet more, because you need to see the variations in a wide range of people representative of the genetic diversity of the population as a whole. At the moment people of white European heritage are often over-represented in samples.

The first genome cost, by some estimates, $3bn

The need for masses of genetic information from many, many human genomes is one of the main reasons why genomic medicine has taken off rather slowly. Over the course of the Human Genome Project, and for the years that followed, the cost of sequencing a genome fell quicklyas quickly as the fall in the cost of computing power expressed through Moores law. But it was falling from a great height: the first genome cost, by some estimates, $3bn. The gap between getting cheaper quickly and being cheap enough to sequence lots of genomes looked enormous.

In the late 2000s, though, fundamentally new types of sequencing technology became available and costs dropped suddenly (see chart). As a result, the amount of data that big genome centres could produce grew dramatically. Consider John Sulstons home base, the Wellcome Sanger Institute outside Cambridge, England. It provided more sequence data to the Human Genome Project than any other laboratory; at the time of its 20th anniversary, in 2012, it had produced, all told, almost 1m gigabytesone petabyteof genome data. By 2019, it was producing that same amount every 35 days. Nor is such speed the preserve of big-data factories. It is now possible to produce billions of letters of sequence in an hour or two using a device that could easily be mistaken for a chunky thumb drive, and which plugs into a laptop in the same way. A sequence as long as a human genome is a few hours work.

As a result, thousands, then tens of thousands and then hundreds of thousands of genomes were sequenced in labs around the world. In 2012 David Cameron, the British prime minister, created Genomics England, a firm owned by the government, and tasked initially with sequencing 100,000 genomes and integrating sequencing, analysis and reporting into the National Health Service. By the end of 2018 it had finished the 100,000th genome. It is now aiming to sequence five million. Chinas 100,000 genome effort started in 2017. The following year saw large-scale projects in Australia, America and Turkey. Dubai has said it will sequence all of its three million residents. Regeneron, a pharma firm, is working with Geisinger, a health-care provider, to analyse the genomes of 250,000 American patients. An international syndicate of investors from America, China, Ireland and Singapore is backing a 365m ($405m) project to sequence about 10% of the Irish population in search of disease genes.

Genes are not everything. Controls on their expressionepigentics, in the jargonand the effects of the environment need to be considered, too; the kitchen can have a distinctive effect on the way a recipe turns out. That is why biobanks are being funded by governments in Britain, America, China, Finland, Canada, Austria and Qatar. Their stores of frozen tissue samples, all carefully matched to clinical information about the person they came from, allow study both by sequencing and by other techniques. Researchers are keen to know what factors complicate the lines science draws from genes to clinical events.

Today various companies will sequence a genome commercially for $600-$700. Sequencing firms such as Illumina, Oxford Nanopore and Chinas BGI are competing to bring the cost down to $100. In the meantime, consumer-genomics firms will currently search out potentially interesting SNPs for between $100 and $200. Send off for a home-testing kit from 23andMe, which has been in business since 2006, and you will get a colourful box with friendly letters on the front saying Welcome to You. Spit in a test tube, send it back to the company and you will get inferences as to your ancestry and an assessment of various health traits. The health report will give you information about your predisposition to diabetes, macular degeneration and various other ailments. Other companies offer similar services.

Plenty of doctors and health professionals are understandably sceptical. Beyond the fact that many gene-testing websites are downright scams that offer bogus testing for intelligence, sporting ability or wine preference, the medical profession feels that people are not well equipped to understand the results of such tests, or to deal with their consequences.

An embarrassing example was provided last year by Matt Hancock, Britains health minister. In an effort to highlight the advantages of genetic tests, he revealed that one had shown him to be at heightened risk of prostate cancer, leading him to get checked out by his doctor. The test had not been carried out by Britains world-class clinical genomics services but by a private company; critics argued that Mr Hancock had misinterpreted the results and consequently wasted his doctors time.

23andMe laid off 14% of its staff in January

He would not be the first. In one case, documented in America, third-party analysis of genomic data obtained through a website convinced a woman that her 12-year-old daughter had a rare genetic disease; the girl was subjected to a battery of tests, consultations with seven cardiologists, two gynaecologists and an ophthalmologist and six emergency hospital visits, despite no clinical signs of disease and a negative result from a genetic test done by a doctor.

At present, because of privacy concerns, the fortunes of these direct-to-consumer companies are not looking great. 23andMe laid off 14% of its staff in January; Veritas, which pioneered the cheap sequencing of customers whole genomes, stopped operating in America last year. But as health records become electronic, and health advice becomes more personalised, having validated PRS scores for diabetes or cardiovascular disease could become more useful. The Type 2 diabetes report which 23andMe recently launched looks at over 1,000 SNPs. It uses a PRS based on data from more than 2.5m customers who have opted to contribute to the firms research base.

As yet, there is no compelling reason for most individuals to have their genome sequenced. If genetic insights are required, those which can be gleaned from SNP-based tests are sufficient for most purposes. Eventually, though, the increasing number of useful genetic tests may well make genome sequencing worthwhile. If your sequence is on file, many tests become simple computer searches (though not all: tests looking at the wear and tear the genome suffers over the course of a lifetime, which is important in diseases like cancer, only make sense after the damage is done). If PRSs and similar tests come to be seen as valuable, having a digital copy of your genome at hand to run them on might make sense.

Some wonder whether the right time and place to do this is at birth. In developed countries it is routine to take a pinprick of blood from the heel of a newborn baby and test it for a variety of diseases so that, if necessary, treatment can start quickly. That includes tests for sickle-cell disease, cystic fibrosis, phenylketonuria (a condition in which the body cannot break down phenylalanine, an amino acid). Some hospitals in America have already started offering to sequence a newborns genome.

Sequencing could pick up hundreds, or thousands, of rare genetic conditions. Mark Caulfield, chief scientist at Genomics England, says that one in 260 live births could have a rare condition that would not be spotted now but could be detected with a whole-genome sequence. Some worry, though, that it would also send children and parents out of the hospital with a burden of knowledge they might be better off withoutespecially if they conclude, incorrectly, that genetic risks are fixed and predestined. If there is unavoidable suffering in your childs future do you want to know? Do you want to tell them? If a child has inherited a worrying genetic trait, should you see if you have it yourselfor if your partner has? The ultimate answer to the commandment know thyself may not always be a happy one.

This article appeared in the Technology Quarterly section of the print edition under the headline "Welcome to you"

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Progressive Genetics to suspend manual milk recording due to Covid-19 – Agriland

Posted: March 17, 2020 at 6:42 pm

Progressive Genetics is suspending its manual milk recording service from 12:00pm tomorrow, Tuesday, March 17, due to the ongoing developments with Covid-19.

Taking measures to prevent the spread of the novel coronavirus, the agricultural services firm sent out a text to customers of its manual milk recording service earlier today, Monday, March 16, to inform them of the development.

The manual milk recording will be suspended for a two-week period and is expected to resume on Monday, March 30, according to the company.

Speaking to AgriLand about the decision, Progressive Genetics milk recording manager Stephen Connolly explained: We have to be responsible.

We want to protect our staff, our contractors and our farmers. Thats whats most important.

The manager assured that Electronic do it yourself (EDIY) milk recording will continue over the two-week period, adding:

We have a protocol in place to minimise contact with the farmer and if a farmer is under pressure with a [somatic] cell count issue or anything like that we will get EDIY staff to drop bottles out so that the farmer can do samples themselves, if there is a spike in cell count.

Commenting on the suspension, Connolly said: It is unfortunate and regrettable, but you need a bit of common sense. We do need to put best practice in place and then hopefully after the next two weeks we can get back manual milk recording.

We all have to play our part. Its trying to minimise everything as much as possible. We all need to do our bit, whether it be Progressive Genetics or farmers or the public, just to minimise the risk.

The manager reiterated that EDIY services remain in place, adding that strict protocols are being adhered to regarding minimising contact and disinfecting equipment between farms.

If a farmer has a problem, we will get bottles out to them for milk recording and cell count; we wont leave anyone in the lurch.

Were available to be contacted in the office or our supervisors are available to be contacted if farmers have any issues or anything like that well be on call.

Its just unfortunate. Its a challenge but we have to put common sense and peoples safety before anything else, Connolly concluded.

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Dr. John T. Macdonald Foundation seeking to fund community-based organizations with major grant dollars – Miami’s Community Newspapers

Posted: March 16, 2020 at 8:49 pm

The Dr. John T. Macdonald Foundation is seeking to fund community-based organizations throughout Miami-Dade County with grants up to $50,000 each. Qualified tax-exempt 501(c)(3) organizations conducting grass-roots work that improves, preserves, or restores the health and healthcare of local area citizens have until April 15 to apply.

Since 1992, the Dr. John T. Macdonald Foundation has responded to identified community needs, said Aldo C. Busot, Chairman of the Coral Gables-based nonprofit foundation. Our board is appreciative of the work being done by our grant recipients throughout the community. The Board of Directors remains committed to sustaining its support in meeting the needs of our local community-based organizations. Busot is a senior vice president and financial advisor with Busot Group at Morgan Stanley in Coral Gables, and a graduate of the University of Miami.

From its earliest days, the foundation board wanted the foundation to serve the immediate grassroots needs of both children and adults and has successfully done so by awarding 468 grants to more than 300 community-based organizations over the years.

According to Charles Dunn, M.D., Chairman of the Community Grants Committee, The Community Grants program is the backbone of the foundation. The local organizations that receive funding are providing much-needed services and contribute to the well-being of our community. A graduate of University of Miami School of Medicine, Dr. Dunn is a long-established family medicine practitioner in Coral Gables.

Local organizations that qualified last year for the first-time, during the foundations 2019-20 funding cycle, included Friendship Circle of Miami offering behavioral physical and occupational therapies for children with special needs in Miami-Dade County; and Iam Able, with a county-wide reach for its Able 2 Adapt program that provides mentoring and exercise-based therapy for individuals with paralysis.

Whispering Manes Therapeutic Riding Center also has been funded in past years to support scholarships and new equipment for their equine-assisted program for special needs children all across the county.

Other award recipients include Wounded Veterans Relief Fund, , Fishing With Americas Finest, Miami Lighthouse for the Blind, Canine Assisted Therapy, Good Hope Equestrian Training Center, the Coral Gables Womens Club Childrens Dental Clinic, and Epilepsy Foundation of Florida, among many others.

In addition to community grants, the foundation also has undertaken three signature initiatives in conjunction with UMs Miller School of Medicines Dept. of Pediatrics with the establishment of the Dr. John T. Macdonald Foundation School Health Initiative, the Dr. John T. Macdonald Foundation Dept. of Human Genetics, and the Dr. John T. Macdonald Foundation Biomedical Nanotechnology Institute.

According to the Foundations Managing Director John Edward Smith, Since its inception as a grant-making institution, the Dr. John T. Macdonald Foundation has invested some $48 million into our community. Foundation grants serve as recognition of the admirable work so many community-based organizations are doing across the county to improve the quality of life for citizens.

The Dr. John T. Macdonald Foundation is accepting letters of inquiry for the 2020-21 grant cycle now through April 15, 2020. Funding priorities include:

Projects that promote health education and prevention, and early detection of disease;

Health related projects that assist children and the economically disadvantaged; and

Projects that target medical care.

Qualified organizations that propose to conduct projects or programs related to the health needs of the citizens of Miami-Dade County, and are seeking funding support from the Dr. John T. Macdonald Foundation, should first submit a letter of inquiry. Programs and projects are funded depending upon the budget in the $5,000 $50,000 range. Applications are available online at http://www.JTMacdonaldFDN.org.

ABOUT THE FOUNDATION

With a long legacy of service to the local community, Doctors Hospital in Coral Gables is the genesis of todays Dr. John T. Macdonald Foundation. The foundation grew from the sale of the hospital in 1992. Starting as a grant-making institution with an initial fund balance of $12 million, over the course of the past 20 years, the foundations fund balance has appreciably grown. Today, the foundation continues funding and invest in the healthcare and medical needs of the local community.

The Dr. John T. Macdonald Foundation is located at 1550 Madruga Ave., Suite 215, Coral Gables, FL 33146. For information, call 305-667-6017 or send an e-mail to info@jtmacdonaldfdn.org.

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Assistant professor says he’s been fired because he dared to talk about human population variation – Inside Higher Ed

Posted: March 16, 2020 at 8:49 pm

An assistant professor of psychology at Marietta College says his contract isnt being renewed because of what hes said and was alleged to have said about differences between ethnic groups.

Many academics believe that race is mere social construct -- that there is no meaning behind being black, white or anything else, beyond what society assigns to it. Others say that that is mere orthodoxy and that race is real; this group often points to research demonstrating group-based differences in complex traits such as intelligence.

Scientists at the cutting edge of studying race and complex traits, meanwhile, say that these traits are always a mix between genetics and environment. And as of now, these experts add, its impossible to tell in any genuine way just what the mix is, because babies cant be raised exactly the same way over two generations, as such experiments would require.

Bo Winegard falls in the middle camp and believes that purposely not talking about race-based differences is disingenuous and dangerous. The "rich, variegated tapestry of humanity" and its evolution have long interested him and ought to be among the truths that academics pursue, he said in a recent interview. Otherwise, he added, "literal racists" will fill the information void.

I do think theres an informational embargo on human population variation and certainly on race and IQ, he said. People have opinions, and they dont want those to get out publicly.

Whatever you think of Winegards ideas, he said in a recent essay in the conservative academic publication Quillette, you should care that hes effectively being fired for them.

If it can happen to me, then it can happen to any academic who challenges the prevailing views of their discipline, he wrote. You may disagree with everything I believe, say, and write, but it is in everyones interests that you support my freedom to believe, say and write it.

Trouble Begins

Winegard, who is in his second year at Marietta and is scheduled to leave at the end of the academic year, says the trouble started in October. That's when he was invited to address the University of Alabamas Evolution Working Group, which is affiliated with the universitys evolution studies program. Both parties agreed that Winegard would talk about population variation, or, in his words, the hypothesis that human biological differences are at least partially produced by different environments selecting for different physical and psychological traits in their populations over time.

The idea was to link the theory with natural selection, in line with a recent article Winegard co-wrote for Personality and Individual Differences. The article, called "Dodging Darwin: Race, Evolution and the Hereditarian Hypothesis," says, "Like most hereditarians (those who believe it likely that genes contribute to differences in psychological traits among human populations), we do not believe there is decisive evidence about the causes of differences in cognitive ability." Yet the "partial genetic hypothesis is most consistent with the Darwinian research tradition."

One class visit with students went well, Winegard recalled in Quillette. Then he received a number of texts from a campus host expressing concern about Winegards entry on the website RationalWiki. The website, like Wikipedia, is edited by volunteers, but is dedicated to debunking what it sees as junk science. And Winegard, according to RationalWiki, is guilty of writing racist bullshit for the right-wing online magazine Quillette.

Winegard told his hosts that he disagreed with the characterization. He has previously argued, for example, that racism isnt wrong because there arent races; it is wrong because it violates basic human decency and modern moral ideals.

This, of course, contradicts a broad literature asserting that race is a social construct, not a biological one, but it doesnt endorse racism. As Winegard said in the same co-written article, In fact, pinning a message of tolerance to the claim that all humans are essentially the same underneath the skin is dangerous. It suggests that if there were real differences, racism would be justified.

Despite the texts, Winegards main talk at Alabama went on as scheduled, followed by what he described as a rowdy question-and-answer period. Someone yelled that he was a racist, and another accused him of promoting phrenology, a discredited pseudoscience having to do with skull shape.

But Winegard said via telephone that that he never spoke about phrenology or on race and IQ at Alabama. The most controversial thing he said was that psychology may someday, in the aggregate, provide some explanation as to why East Asian societies tend toward collectivism, he added.

One of his slides, however, did say that groups may vary on socially significant traits (on average) such as intelligence, agreeableness, athleticism, cooperativeness [and] criminality.

Alabamas student newspaper published an article on the talk, vaguely linking the subject matter to eugenics, or reproduction to promote certain heritable traits. It also published an apology from the group that hosted him.

Winegard said this week that he never mentioned eugenics, and that he finds things such as forced sterilization morally repugnant. He didn't preclude having mentioned embryo selection once or twice on Twitter, he said, but he's never made a sustained argument.

Back at Marietta, Winegard was summoned to a meeting with his president and provost to discuss the article. While they werent pleased, Winegard wrote in Quillette, they told [him] to be more strategic in my navigation of such a sensitive topic. I agreed that I would try.

Months later, someone began emailing Winegards department and administration about things hes written and said on Twitter. One tweet, in particular, read, The greatest challenge to affluent societies is dealing openly, honestly, and humanely with biological (genetic) inequality. If we dont meet this challenge, I suspect our countries will be torn apart from the inside like a tree destroyed by parasites.

At a second, consequent meeting with his supervisors, Winegard explained (as he recapped in Quillette) that his tweet was not about groups, but rather about individual genetic differences, and the need to create a humane society for everyone, not just for the cognitive elite and hyper-educated (a theme I discuss often). The simile about parasites was a reference to political conflict and not a reference to some group of humans or another, he also said.

Winegard recalled his bosses expressing disappointment in me and particular dismay about the tweet I had deleted, which they said evoked anti-black and anti-Semitic tropes. He agreed and apologized but said he would continue to pursue potentially controversial research topics.

Termination

Termination never came up, even after Winegard published a co-written article on human population variation -- until two weeks ago.

My boss informed me, without any warning, that the college was not renewing my contract, he wrote in Quillette. I dont know if my paper was the proximate cause of my firing, but in the light of the foregoing weeks tumult, it was plausibly the last straw.

Did Winegard see it coming? I had worried vaguely about such an eventuality, but didnt really think it would happen, he wrote. I naively assumed that the norms of academic freedom would prevail. They did not.

Winegard told Inside Higher Ed that hes had strong teaching evaluations and high research productivity since hes been at Marietta. He sees no apparent reason for his effective termination, apart from the controversy surrounding what he has said and, more to the point, is alleged to have said.

In response to his Quillette article, some have argued that one should wait until tenure to pursue certain topics. But Winegard reiterated that he, perhaps navely, took academic freedom seriously. Beyond that, he said, if academics follow "pragmatic" advice about waiting until tenure to discuss controversial issues, it means waiting 10 or more years, through graduate school and the tenure track.

Im perplexed by the response, he said of Mariettas actions. The best response would have been to come out with a bold, affirmative statement for academic freedom, even if the college distanced itself from Winegards views in doing so.

Otherwise, he said, Youre incentivizing this trollish behavior. Trollish here refers to those Winegard says emailed his institution about him anonymously.

Marietta declined comment, saying Winegards case was a private personnel issue.

Relevant, widely followed American Association of University Professors policy says that even professors on probationary appointments should enjoy the same academic freedom as those with tenure, even if they don't have the same due process protections. Winegard said he's unaware of any paths to appeal, but AAUP policy also holds that a faculty committee should evaluate any concerns about non-reappointment related to a possible violation of academic freedom.

Winegard's department chair did not respond to a request for comment. Marietta's Faculty Council chair also did not respond to questions about the case.

Facts and Feelings

Attempts to link cognition to race have for decades happened mostly in academe's fringes. That's because it's either dog-whistle racist junk science or there is a conspiracy of silence surrounding it, depending on what you believe. In 1994, Richard Herrnstein and Charles Murray's The Bell Curve: Intelligence and Class Structure in American Life was immediately controversial, stirring concerns about lack of peer review and whether it represented mainstream science.

Race-based science debates don't just happen in psychology. In January, for example, Philosophical Psychology faced a boycott for publishing an article in defense of race-based research on intelligence. The gist of that article, written by Nathan Cofnas, a Ph.D. candidate in philosophy at the University of Oxford, was that when advances in science reveal genetic variants underlying individual differences in intelligence, we wont be ready for it.

One of the main criticisms of Cofnas's piece was that it speculated that these breakthroughs are close. They are not. So postulating about them is, in a sense, pseudoscience, critics maintain.

Cofnas said at the time that those "who argue that we should wait for the genetics and neuroscience of intelligence to become more advanced before we attempt to study this issue often claim that, in the meantime, we should accept the environmental explanation for the purpose of policy making" and more. But that is a "political, not a scientific, position."

Journalist Angela Saini, author of the 2019 book Superior: The Return of Race Science (which Winegard has reviewed), said that her research demonstrates there is simply "no conspiracy against talking about race and IQ in academia, largely because this matter was settled 70 years ago -- and reinforced by genetics since -- by the universal understanding that race is a social construct."

It's "impossible to say that any differences in attainment we may see between socially defined groups must be biological in origin," Saini added. "Scientists are overwhelmingly in consensus on this."

That a "few academics like to claim otherwise," she said, "in particular, a small number of social scientists on the margins of respectable academia, does nothing to undermine the scientific facts. The facts, Im afraid, dont care about their feelings."

Intelligence researcher Richard Haier, professor emeritus in the pediatric neurology division at the School of Medicine at the University of California, Irvine, said that the questions Winegard is working on are controversial and emotional -- and well within the bounds of reasonable debate.

What happened at Marietta is, therefore, an apparent violation of academic freedom, Haier said. I dont know all the details, but I do know that it is very hard to defend academic freedom for issues that are not just controversial but also extremely emotional. And a lot of people in academia are happy to say that they support academic freedom but there are many examples of occurrences that appear to violate academic freedom, and the local academic community has not stood up for academic freedom.

Haier added, The hard thing about science is to go where the data take you. Without tenure and even with tenure, its becoming increasingly difficult to address controversial ideas, where some points of view do not acknowledge the legitimacy of other points of view, and therefore shut down discussion. Thats not how science works.

Lee Jussim, distinguished professor of psychology at Rutgers University and co-author of a recent paper on political bias in social science research, said that the topic of race and IQ "is poison." Further, he said, "I see no reason to believe the methods are capable of answering the question of how much race differences in intelligence are genetic versus environmental versus some combination.

That doesn't mean that Winegard or anyone else should be fired for trying to do so, however, Jussim said. Of course he has a right to pursue the line of inquiry.

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Love Rivals Risk Having Offspring with a Greater Number of Harmful Mutations – Global Health News Wire

Posted: March 16, 2020 at 8:49 pm

A female (lower left) and male (top right) Callosobruchus maculatus mating. The mating typically lasts for 2-5 minutes during which the male transfers 40,000-60,000 sperm in an ejaculate weighing about 3-5% of his own body weight.

Males that face tougher competition for females risk having offspring with a greater number of harmful mutations in their genome than males without rivals. Researchers at Uppsala University have discovered this correlation in the beetle speciesCallosobruchus maculatus. Their study is published in the scientific journalNature Ecology & Evolution.

Many researchers working in the fields of human reproductive biology and more general evolutionary theory have taken an interest in this. The hypothesis is not new in itself but there have been few experiments conducted to test it. This is where we hope our study can contribute an important piece of the puzzle, says David Berger of Uppsala Universitys Department of Ecology and Genetics.

Just as with fish, birds and mammals, in the insect world several males often mate with the same female. This leads to a form of sexual selection in which the males sperm compete to fertilise the females eggs. Males that produce more numerous or more competitive sperm often win the competition and become fathers.

Research conducted at the Department of Ecology and Genetics at Uppsala University has succeeded in demonstrating that increased competition between males can lead to a higher rate of harmful mutations in offspring.

Genomic DNA is damaged with every cell division but this damage is usually prevented or repaired by an effective, but costly, cellular surveillance system. The new study shows that sperm production in competing males of the speciesCallosobruchus maculatus, or cowpea weevil, comes at the expense of this cellular surveillance.

In experiments, male beetles were exposed to radiation in order to damage their genome. After a period of recuperation, the males were allowed to mate with females and become fathers. The researchers then followed their offspring to measure the varying quality of subsequent generations and discovered that males kept in groups, with the concomitant risk of sperm competition, had offspring with a greater number of harmful new mutations than those that lived alone.

The researchers behind the study do however point out that competition between males need not lead to deteriorating gene health in the long term. This is because, as the study also shows, males from populations with high sperm competition over many generations adapt to the new conditions by producing more sperm and more viable offspring compared to males adapted to a life of monogamy.

Even if the direct effect of sperm competition is to increase the number of mutations in offspring, the paradoxical long-term effect of sexual selection may be a lower rate of mutation, explains David Berger.

The researchers behind the study explain that both of these mechanisms play important roles in how genetic variation arises and is maintained in species where males compete to mate. This in turn can affect the potential for evolutionary adaptation, which depends on genetic variation.

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A book that could save lives: Adam Rutherford’s How to Argue with a Racist reviewed – Spectator.co.uk

Posted: March 16, 2020 at 8:49 pm

How to Argue with a Racist: History, Science, Race and Reality

Adam Rutherford

Weidenfeld, pp. 206, 12.99

In the award-winning musical Avenue Q, filthy-minded puppets sang about schadenfreude, internet porn, loud sex, the uselessness of an English literature degree and racism. Or, more specifically, they sang about the ubiquitous human habit of

stereotyping people by race:

Everyones a little bit racist, sometimes.

The puppets were right: everyone makes judgments based on race. Humans are lazy creatures who like mental short cuts. Thinking in shades of grey is more effortful than thinking in black and white. Evaluating a new person afresh, based on their unique characteristics, is slower than falling back on a ready made judgment. If youve spent time with a two-year-old, or if youve used psychedelic drugs, you might have glimpsed what its like to see an individual blade of grass as itself, and not just as an exemplar of the category grass. Its exhausting.

In How to Argue with a Racist, Adam Rutherford uses his expertise in genetics to try to get us to see people the way a person on LSD might see a field of grass. That is, he wants us to see individual humans as themselves, rather than as exemplars of racial categories. Overcoming deeply ingrained patterns of mind, while also providing a crash course in genetic biology, is a tall order for any book, particularly one so brief. To accomplish his goal, Rutherford has densely packed each section of his book with scientific and historical details, all of which converge on a central theme its wickedly complicated.

Part I begins by challenging the apparent simplicity of racial distinctions based on skin colour or other observable physical characteristics. Consider, for instance, that two Africans, who would both be assigned the same race based on their skin colour, might be more different genetically than the Scots are from the Japanese.

Part II then challenges the idea of racial purity, the fiction that there are groups of people (like the Scots or the Japanese) who can trace their blood to just one set of ancestors living in one particular place. No such pure bloodlines exist; there really is no true Scotsman. Because people have had sex wherever and whenever they could, we dont have to go back too far in history to find a time when everyone alive then was the ancestor of everyone alive now. You and your immigrant neighbour are all part of the same family tree.

Next, parts III and IV challenge the idea that some racial groups are naturally more athletic, more musical or more intelligent. Do African-Americans dominate certain track and field events because they have a speed gene? Are the genetic diseases more common in Ashkenazi Jews evidence of selection for high intelligence? One by one, Rutherford picks up an apparently neat story about racial differences and turns it this way and that, exposing its holes and flaws and tattered seams.

Some of the science here has been explained in other books, including Rutherfords own A Brief History of Everyone Who Ever Lived, and more recently, David Reichs Who We Are and How We Got Here. What makes the organisation of the scientific material different in this book is right there in the opening sentence: This book is a weapon. Rutherford continues: These pages ... will provide a foundation to contest racism. Yet despite its confident title, How to Argue with a Racist is not entirely sanguine about the power of scientific argument. Arguing with racists, Rutherford says, is a fairly fruitless endeavour, and exhausting and he quotes Jonathan Swift: Reasoning will never make a man correct an ill opinion, which by reasoning he never acquired.

Rutherfords uncertainty regarding how useful science is for combatting racism reflects a deeper uncertainty about what, exactly, is the relationship between sciency-sounding ideas about biological differences between racial groups and the violence and vitriol that he calls avowed or overt or extreme racism. After all, as the puppets of Avenue Q cheerfully protested, the use of racial judgments doesnt mean we go around committing hate crimes.

But ideas about racial difference can, indeed, incite violence. Consider Dylann Roof, who gunned down nine black parishioners in a Charleston, South Carolina church after being radicalised on the internet. Before the massacre, Roof penned a racist screed that asked the exact same question about racial differences that How to Argue with a Racist considers at length: How could our faces, skin, hair and body structure all be different, but our brains be exactly the same?

It is tempting to answer that incendiary question by insisting that everyones brains really are exactly the same. As the great evolutionary biologist Theodosius Dobzhansky observed back in the 1960s, if you maintain that people should be equal, then it is convenient to argue that the differences between them are accidental and trivial. This, for instance, is the argument that Ibram Kendi made in his similarly titled How to Be an Antiracist. An anti-racist is someone who is expressing the idea that races are meaningfully the same in their biology.

Rutherford avoids the temptation of insisting that everyone is the same. Instead, he presents a more difficult but more accurate argument, describing both the reality of human genetic variation and the fiction of racial purity. Yes, genetic differences between people are important, not just for their bodies, but also for their brains and behaviours. But the physical characteristics that we use to lump people together into races are terrible indicators of how genetically similar those people are. And when considering achingly complex domains of human achievement, such as music, sport, art and science, it has proved nearly impossible to separate out genetics from the messiness of human history, from colonialism and culture.

Rereading How to Argue with a Racist a second time, I began to imagine it as a letter, directed to one racist in particular to a younger Dylann Roof, as he was being drawn into the darker corners of the internet, before he picked up a gun to commit mass murder. Could science and history, clearly presented, have cut through the thicket of poisonous ideas that ultimately choked off Roofs capacity for the most basic human empathy? Could arguing with that particular racist about genetics have saved lives? That possibility, slim as it might be, is why How to Argue with a Racist is an important book.

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Researchers study irregular horse heartbeats, hoping to find a cure – Minnesota Daily

Posted: March 16, 2020 at 8:49 pm

University of Minnesota researchers are looking at cardiac conditions in racehorses to point toward a solution for both horses and humans.

Researchers are examining the effects of irregular heartbeats in racehorses, which are more frequently affected than average horses. Many racehorses die suddenly on the racetrack for unexpected reasons that may be due to irregular heartbeats, known broadly as arrhythmias. Researchers said they can examine which arrhythmias cause disease and which ones are specific to horses or humans.

The prevalence in horses is not common, but in racehorses with poor performances, its about 2%, said Sian Durward-Akhurst, lead author of the study and a University graduate student. Atrial fibrillation is the most common form of irregular heartbeat in horses.

The researchers examined the genes of 534 horses and found greater variations of disease in them, she said. Researchers are analyzing the disease-causing variants identified in both horses and humans.

Its something thats really interesting because why is it causing disease in humans, but not in horses? Durward-Akhurst said.

They will test these variants in more horses this summer and aim to produce a research paper by next year. Earlier this month, the researchers presented their recent findings at the Santa Anita racetrack in Los Angeles, California.

Atrial fibrillation is the most common abnormal heart rhythm in humans, in cattle, in dogs. Its actually an interesting disease because of its impact on multiple species, including us, said Molly McCue, the principal investigator of the research and the associate dean of research in the Universitys College of Veterinary Medicine.

The irregular heartbeats of atrial fibrillation are sometimes referred to as a quivering heart due to how they affect the heartbeats pace. According to a veterinarian from the Paulick Report, the irregular heartbeat sounds like shoes in a dryer.

Racehorses are bred to have higher functioning cardiovascular systems than other horses, McCue said. Because of this, racehorses are expected to have a higher capacity for exercise.

They have this really frequent occurrence of arrhythmia, she said. The issue now is to figure out why. Then researchers can determine if arrhythmias are contributing to why racehorses are dying on the race track and if they can prevent it.

James Mickelson, a University professor in the Department of Veterinary and Biomedical Sciences, has studied the genetics of diseases in various animals for more than 20 years.

The condition of atrial fibrillation and heart arrhythmias is very likely responsible for sudden death of horses on race tracks, just like similar conditions in people, in human athletes, are responsible for sudden fatal deaths as well, he said.

If researchers can find a new mutation in horse genetics, they can use that to see if the same gene is responsible for any of the human cases, Mickelson said.

Lynn Hovda, chief commission veterinarian for the Minnesota Racing Commission, said horses dont have heart attacks like humans do because of their different cardiovascular systems.

[Horses] have cardiac rhythm disturbances, most often atrial fibrillation, that may result in sudden death. I say may as we dont really know yet, she said.

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New UNC computational tool boosts understanding of genetic disorders affecting the brain – WRAL Tech Wire

Posted: March 16, 2020 at 8:49 pm

CHAPEL HILL Scientists at the UNC School of Medicine and colleagues created a new computational tool called H-MAGMA to study the genetic underpinnings of nine brain disorders, including the identification of new genes associated with each disorder.

The research,published inNature Neuroscience, revealed that genes associated with psychiatric disorders are typically expressed early in life, highlighting the likelihood of this early period of life as critical in the development of psychiatric illnesses. The researchers also discovered that neurodegenerative disorder-associated genes are expressed later in life. Lastly, the scientists linked these disorder-associated genes to specific brain cell types.

By using H-MAGMA, we were able to link non-coding variants to their target genes, a challenge that had previously limited scientists ability to derive biologically meaningful hypotheses from genome-wide association studies of brain disorders, said study senior authorHyejung Won, PhD, assistant professor of genetics at the UNC School of Medicine and member of the UNC Neuroscience Center. Additionally, we uncovered important biology underlying the genetics of brain disorders, and we think these molecular mechanisms could serve as potential targets for treatment.

Hyejung Won, PhD UNC photo)

Brain disorders such as schizophrenia and Alzheimers disease are among the most burdensome disorders worldwide. But there are few treatment options, largely due to our limited understanding of their genetics and neurobiological mechanisms. Genome-wide association studies (GWAS) have revolutionized our understanding of the genetic architecture related to many health conditions, including brain-related disorders. GWAS is a technique that allows researchers to compare genetic sequences of individuals with a particular trait such as a disorder to control subjects. Researchers do this by analyzing the genetic sequences of thousands of people.

To date, we know of hundreds of genomic regions associated with a persons risk of developing a disorder, Won said. However, understanding how those genetic variants impact health remained a challenge because the majority of the variants are located in regions of the genome that do not make proteins. They are called non-coding genetic variants. Thus, their specific roles have not been clearly defined.

Prior research suggested that while non-coding variants might not directly encode proteins, they can interact with and regulate gene expression. That is, these variants help regulate how genes create proteins, even though these variants do not directly lead to or code for the creation of proteins.

Given the importance of non-coding variants, and that they make up a large proportion of GWAS findings, we sought to link them to the genes they interact with, using a map of chromatin interaction in the human brain, Won said. Chromatin is the tightly packed structure of DNA and proteins inside cells, folded in the nucleus in a way to maintain normal human health.

Won and colleagues used this map to identify genes and biological principles underlying nine different brain disorders, including psychiatric conditions such as schizophrenia, autism, depression, and bipolar disorder; and neurodegenerative disorders such as Alzheimers, Parkinsons, amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS).

Using the computational tool H-MAGMA, Won and colleagues could link non-coding variants to their interacting genes the genes already implicated in previous GWAS findings.

Another important question in brain disorders is to identify cellular etiology the cells involved in the root cause of disease. This is especially critical as the brain is a complex organ with many different cell types that may act differently in response to treatment. In the attempt of finding critical cell types for each brain disorder, the researchers found that genes associated with psychiatric disorders are highly expressed in glutamatergic neurons, whereas genes associated with neurodegenerative disorders are highly expressed in glia, further demonstrating how the two disorder clusters diverge from each other.

Moreover, we classified biological processes central to the disorders, Won said. From this analysis, we found that the generation of new brain cells, transcriptional regulation, and immune response as being essential to many brain disorders.

Won and colleagues also generated a list of shared genes across psychiatric disorders to describe common biological principles that link psychiatric disorders.

Amongst the shared genes, we once again identified the brains early developmental process as being critical and upper layer neurons as being the fundamental cell-types involved, Won said We unveiled the molecular mechanism that underscores how one gene can affect two or more psychiatric diseases.

H-MAGMA is publicly available so that the tool can be widely applicable and available to the genetics and neuroscience community to help expand research, with the ultimate goal of helping people who suffer with brain-related conditions.

The National Institute of Mental Health, the Brain and Behavior Research Foundation, and the Simons Foundation Autism Research Initiative funded this research.

Other authors were Nancy Sey, Benxia Hu, Won Mah, Harper Fauni, Jessica McAfee, all from UNC-Chapel Hill, and Prashanth Rajarajan, Kristen Brennand, and Schahram Akbarian from Mount Sinai Health System.

(C) UNC-Chapel Hill

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Validea’s Top Five Healthcare Stocks Based On Motley Fool – 3/15/2020 – Nasdaq

Posted: March 16, 2020 at 8:49 pm

The following are the top rated Healthcare stocks according to Validea's Small-Cap Growth Investor model based on the published strategy of Motley Fool. This strategy looks for small cap growth stocks with solid fundamentals and strong price performance.

ZYNEX INC. (ZYXI) is a small-cap growth stock in the Medical Equipment & Supplies industry. The rating according to our strategy based on Motley Fool is 76% based on the firms underlying fundamentals and the stocks valuation. A score of 80% or above typically indicates that the strategy has some interest in the stock and a score above 90% typically indicates strong interest.

Company Description: Zynex, Inc. operates through the Electrotherapy and Pain Management Products segment. The Company conducts its business through its subsidiaries and the operating subsidiary is Zynex Medical, Inc. (ZMI). Its other subsidiaries include Zynex Monitoring Solutions, Inc. (ZMS) and Zynex Europe, ApS (ZEU). ZMI designs, manufactures and markets medical devices that treat chronic and acute pain, as well as activate and exercise muscles for rehabilitative purposes with electrical stimulation. ZMS is in the process of developing its blood volume monitoring product for non-invasive cardiac monitoring. ZEU intends to focus on sales and marketing its products within the international marketplace, upon receipt of necessary regulatory approvals. It markets and sells Zynex-manufactured products and distributes private labeled products. Its products include NexWave, NeuroMove, InWave, Electrodes and Batteries. ZMI devices are intended for pain management to reduce reliance on drugs and medications.

The following table summarizes whether the stock meets each of this strategy's tests. Not all criteria in the below table receive equal weighting or are independent, but the table provides a brief overview of the strong and weak points of the security in the context of the strategy's criteria.

For a full detailed analysis using NASDAQ's Guru Analysis tool, click here

CHINA BIOLOGIC PRODUCTS HOLDINGS INC (CBPO) is a mid-cap growth stock in the Biotechnology & Drugs industry. The rating according to our strategy based on Motley Fool is 72% based on the firms underlying fundamentals and the stocks valuation. A score of 80% or above typically indicates that the strategy has some interest in the stock and a score above 90% typically indicates strong interest.

Company Description: China Biologic Products Holdings, Inc. is a biopharmaceutical company. The Company is principally engaged in the research, development, manufacturing and sales of human plasma-based biopharmaceutical products in China. It operates through the manufacture and sales of human plasma products segment. China Biologic has a product portfolio with over 20 various dosage forms of plasma products and other biopharmaceutical products across nine categories.The Company's products include human albumin, human immunoglobulin, immunoglobulin for intravenous injection (IVIG), human hepatitis B immunoglobulin, human rabies immunoglobulin, human tetanus immunoglobulin, placenta polypeptide, Factor VIII and human prothrombin complex concentrate (PCC).

The following table summarizes whether the stock meets each of this strategy's tests. Not all criteria in the below table receive equal weighting or are independent, but the table provides a brief overview of the strong and weak points of the security in the context of the strategy's criteria.

For a full detailed analysis using NASDAQ's Guru Analysis tool, click here

MEDPACE HOLDINGS INC (MEDP) is a mid-cap growth stock in the Biotechnology & Drugs industry. The rating according to our strategy based on Motley Fool is 72% based on the firms underlying fundamentals and the stocks valuation. A score of 80% or above typically indicates that the strategy has some interest in the stock and a score above 90% typically indicates strong interest.

Company Description: Medpace Holdings, Inc. is a clinical contract research organization. The Company provides clinical research-based drug and medical device development services. The Company partners with pharmaceutical, biotechnology, and medical device companies in the development and execution of clinical trials. The Company's drug development services focus on full service Phase I-IV clinical development services and include development plan design, coordinated central laboratory, project management, regulatory affairs, clinical monitoring, data management and analysis, pharmacovigilance new drug application submissions, and post-marketing clinical support. The Company also provides bio-analytical laboratory services, clinical human pharmacology, imaging services, and electrocardiography reading support for clinical trials. The Company's operations are principally based in North America, Europe, and Asia.

The following table summarizes whether the stock meets each of this strategy's tests. Not all criteria in the below table receive equal weighting or are independent, but the table provides a brief overview of the strong and weak points of the security in the context of the strategy's criteria.

For a full detailed analysis using NASDAQ's Guru Analysis tool, click here

FULGENT GENETICS INC (FLGT) is a small-cap growth stock in the Medical Equipment & Supplies industry. The rating according to our strategy based on Motley Fool is 69% based on the firms underlying fundamentals and the stocks valuation. A score of 80% or above typically indicates that the strategy has some interest in the stock and a score above 90% typically indicates strong interest.

Company Description: Fulgent Genetics, Inc. is a technology company. The Company offers genetic testing to provide physicians with clinically actionable diagnostic information to improve quality of patient care. The Company has developed a technology platform that integrates data comparison and suppression algorithms, adaptive learning software, advanced genetic diagnostics tools and integrated laboratory processes. As of December 31, 2015, the Company's test menu includes approximately 18,000 single-gene tests and over 200 pre-established, multi-gene, disease-specific panels that collectively test for approximately 7,500 genetic conditions, including various cancers, cardiovascular diseases and neurological disorders. The Company's gene probes are specifically engineered to generate genetic data that is optimized for its software, which enables to rapidly incorporate new genes into its test menu, develop new panels of disease-specific tests and customize tests for its customers.

The following table summarizes whether the stock meets each of this strategy's tests. Not all criteria in the below table receive equal weighting or are independent, but the table provides a brief overview of the strong and weak points of the security in the context of the strategy's criteria.

For a full detailed analysis using NASDAQ's Guru Analysis tool, click here

MASIMO CORPORATION (MASI) is a large-cap growth stock in the Medical Equipment & Supplies industry. The rating according to our strategy based on Motley Fool is 68% based on the firms underlying fundamentals and the stocks valuation. A score of 80% or above typically indicates that the strategy has some interest in the stock and a score above 90% typically indicates strong interest.

Company Description: Masimo Corporation is a medical technology company that develops, manufactures and markets a range of non-invasive patient monitoring technologies. The Company's business is Measure-through Motion and Low Perfusion pulse oximetry monitoring, known as Masimo Signal Extraction Technology (SET) pulse oximetry. Its product offerings include non-invasive monitoring of blood constituents with an optical signature, optical organ oximetry monitoring, electrical, brain function monitoring, acoustic respiration monitoring and exhaled gas monitoring. In addition, the Company has developed the Root patient monitoring and connectivity platform, the Radical-7 bedside and portable patient monitor, and the Radius-7 wearable wireless patient monitor. It offers Patient SafetyNet remote patient surveillance monitoring system, which allows patients to be monitored through a personal computer-based monitor or by care providers through their pagers, voice-over-Internet Protocol (IP) phones or smartphones.

The following table summarizes whether the stock meets each of this strategy's tests. Not all criteria in the below table receive equal weighting or are independent, but the table provides a brief overview of the strong and weak points of the security in the context of the strategy's criteria.

For a full detailed analysis using NASDAQ's Guru Analysis tool, click here

Since its inception, Validea's strategy based on Motley Fool has returned 413.50% vs. 172.71% for the S&P 500. For more details on this strategy, click here

About Motley Fool: Brothers David and Tom Gardner often wear funny hats in public appearances, but they're hardly fools -- at least not the kind whose advice you should readily dismiss. The Gardners are the founders of the popular Motley Fool web site, which offers frank and often irreverent commentary on investing, the stock market, and personal finance. The Gardners' "Fool" really is a multi-media endeavor, offering not only its web content but also several books written by the brothers, a weekly syndicated newspaper column, and subscription newsletter services.

About Validea: Validea is an investment research service that follows the published strategies of investment legends. Validea offers both stock analysis and model portfolios based on gurus who have outperformed the market over the long-term, including Warren Buffett, Benjamin Graham, Peter Lynch and Martin Zweig. For more information about Validea, click here

The views and opinions expressed herein are the views and opinions of the author and do not necessarily reflect those of Nasdaq, Inc.

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