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Archive for the ‘Molecular Genetics’ Category

Orf Expression Clones Market Healthy Pace Throughout The Forecast Throughout 2017-2025 – Zebvo

Sunday, November 24th, 2019

DNA is transcribe into messenger RNA, messenger RNA is translated into protein ORF. During translation, the combination of three nucleotide codons are required for protein synthesis. The nucleotide that starts translation and stops translation is known as ORF. Every DNA has six open reading frame and it is important to determine the correct open reading frame so that the protein is expressed properly. An Open Reading Frame starts with ATG (Met), which is known as start codon and ends with DNA sequence such as TAA, TAG, TGA known as stop codon. ORF clones are eliminates the wearisomesteps of RNA isolation, DNA synthesis, PCR amplification and other tedious sequencing and validation procedures.

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The ORF expression clones are plasmid that contains protein coding DNA, the DNA contains the coding sequence without 5 and 3 end untranslated regions. The ORF expression clones helps to save as it moves directly protein expression and protein analysis. The ORF clones aids to get protein expression and analysis faster. The ORF allows to get gene of interest and expressed protein quickly, and help researchers to conduct clinical and medical applications. Clinical laboratory are highly equipped with assay and instrument systems used for the detection and classification of various disease type such as cancer and risk of cancer progressions, cardiovascular diseases, and others. The advancement in the molecular genetics, bioinformatics, proteomics, increasing number of infection rate is prompting manufacturers to seek newer methods of research, has led to the revenue growth over the forecast period.

Increased demand for research and development for early detection and diagnosis of disease, increased expenditure on healthcare sector, growing number of hospitals and diagnostic laboratories, increased demand for personalized medicines requires the study of individual cell structure and function, rise in prevalence of cell based diseases such as cancer and autoimmune diseases requires the detection and diagnosis of specific cell and tissue, rise in number of biopsy procedures. Technological advancement in the diagnostic and treatment process of infectious diseases, advancement in molecular techniques are the factors fueling the demand of ORF expression clone market in the near future.

The global ORF expression clones market is segmented on basis of expression system,application, end user and geography

Segment by Expression System

Segment by Application

Segment by End User

Global ORF expression clones is segmented by expression system, application and end user. On the basis of expression system the, ORF expression clones market is segmented as mammalian expression system, lentiviral expression system, bacterial expression system, yeast expression system, insect, wheat germ cell and others. Based on the application type, global ORF expression clones market is segmented as recombinant protein expression, functional assays, protein characterization, In vitro transcription and other application for research and study purpose. On the basis of end user, the global ORF expression clones market is segmented into biotechnological companies, pharmaceutical companies, contract research organizations, academic/ research institutes. Increasing outsourcing by pharmaceutical and biotechnological companies, declining R&D productivity and patent cliff sales drop leading to increasing research intensity in the pharmaceuticals sector, rapid process/product development due to fewer steps, increased awareness about new product launch and others are some of the factors drive the global ORF expression clones market during the forecast period. Whereas high cost and short reaction scale, low protein expression, inadequate access to health care, lack of standardized tools for research and development are some of the factors that may hamper the growth of global ORF expression clones market.

By Geography, the global ORF Expression Clones market is segmented into five broad regions viz. North America, Latin America, Europe, Asia-Pacific, and the Middle East & Africa. North America is estimated to lead the global ORF expression clones market due to increasing focus on protein expression and production, growing demand for simple and efficient protein production methods, government funding for research and development in developed countries and others. Europe market is also projected to experience high growth due to emphasis on up-scaling and industrial application in the near future. Asia Pacific market is anticipated to grow at the fastest growth rate during the forecast period, owing to factors such as focusing on healthcare expenditures, rise in research and development facilities and others.

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Some of the major players in global ORF expression clones market are Thermo Fisher Scientific, GeneCopoeia, Inc. Dharmacon, Inc., BioCat GmbH, Source BioScience, Kabushiki Kaisha DNAFOR, GenScript, OriGene Technologies, Inc. Sino Biological Inc. Promega Corporation and Others.

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Medical News Today: Targeting this protein could help combat aging – Stock Daily Dish

Sunday, November 24th, 2019

Scientists have discovered an unknown genetic mechanism of cell metabolism that becomes increasingly dysfunctional with aging. Is it possible to combat aging?

Researchers at the cole Polytechnique Fdrale de Lausanne (EPFL) in Switzerland suggest that their findings could lead to new targets for treatments to combat aging and age-related conditions.

Their discovery concerns a protein that alters the function of mitochondria, which are the tiny power units inside cells that give them their energy.

The EPFL team found that brain and muscle tissue from aged animals had high levels of the protein, which is called pumilio RNA binding family member 2 (PUM2).

A in the journal Molecular Cell describes how aging induces higher levels of PUM2, which, in turn, reduce levels of another protein called mitochondrial fission factor (MFF).

MFF helps cells break large mitochondria into smaller units and clear them away. The tissue samples from the aged animals also had lower levels of MFF.

The researchers suggest that as animals age, the PUM2/MFF pathway becomes more and more dysregulated.

As PUM2 levels rise, they bring down levels of MFF. The result is that cells become increasingly unable to break up and clear away smaller mitochondria. As time goes by, cells and tissues accumulate more and more large, unhealthy mitochondria.

PUM2 is an RNA-binding protein. These molecules alter gene expression by binding to the messenger RNA (mRNA) molecules that carry DNA code for cells to process.

In the recent study, the team discovered that when PUM2 binds to mRNA molecules that carry the DNA code for MFF, it blocks cells ability to make MFF protein from those mRNA molecules.

Most research on the molecules that influence aging in cells and tissues tends to focus on gene transcription into mRNA. However, this is just the first step in the complex process of transferring information held in genes into the workings of cells.

The EPFL researchers discovered the PUM2/MFF pathway when they decided to investigate the step that occurs after gene transcription.

When they screened animal cells to identify RNA-binding proteins that changed with age, they found that PUM2 was particularly elevated in older animals.

PUM2 binds only to mRNA molecules that have sites that it recognizes. When it attaches to the mRNA, it stops the translation of the code into the corresponding protein.

By employing a systems genetics approach, the team discovered a previously unknown mRNA that PUM2 binds to. This was the mRNA that carries the code for cells to make MFF.

In another part of the study, the researchers demonstrated how it might be possible to reverse the age-related effect of PUM2 on cells and tissues.

Using CRISPR-Cas9 gene-editing technology, they reduced PUM2 in the muscles of old mice by silencing its corresponding encoding gene.

This led to higher levels of MFF protein, which through increased breakup and waste-clearing improved mitochondrial function in the aged mice.

The team also investigated a similar mechanism in the roundworm Caenorhabditis elegans, which is a model that scientists often use to study molecular pathways.

In the roundworm, aging induces higher levels of the RNA-binding protein PUF-8. The researchers found that silencing the corresponding gene for PUF-8 in older worms improved the functioning of their mitochondria and extended their lifespan.

Other studies have linked RNA-binding proteins to neuromuscular degenerative diseases. They have also demonstrated that they often collect into clumps called pathological granules.

The EPFL researchers found that PUM2 has a similar tendency, with aging, to clump into particles that bind and capture MFF mRNA.

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Medical News Today: Targeting this protein could help combat aging - Stock Daily Dish

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Mapping human antibodies to develop protein therapeutics spotlighted at Feinstein Institutes Marsh Lecture – P&T Community

Sunday, November 17th, 2019

MANHASSET, N.Y., Nov. 15, 2019 /PRNewswire/ --The Feinstein Institutes for Medical Researchhosted a Marsh Lecture given by George Georgiou, PhD, of the University of Texas at Austin, to discuss human antibody repertoire and the development of protein therapeutics to help treat cancer, viral infection and autoimmune disorders.

Dr. Georgiou, the Laura Jennings-Turner Chair Professor in the departments of Chemical Engineering and Molecular Biosciences at Texas, researches and develops methods to observe and analyze, at the molecular-level, human antibody immune responses which ultimately leads to more efficient vaccines and other engineered enzyme therapeutics.

"To create more effective antibodies and vaccines for some of the most complicated medical conditions, we must better understand the body's molecular immune system," said Dr. Georgiou at the lecture on November 14.

TheMarsh Lectureis given by visiting prominent scientists who share their expertise and establish collaborations with Feinstein Institutes investigators. In his lecture, Dr. Georgiou emphasized the need to continue work in the discovery and preclinical development of protein therapeutics, the mapping of serological antibody repertoire in human health, disease and the methods to engineer second generation antibodies.

The lecture was co-hosted by the Feinstein Institutes' president and CEO, Kevin J. Tracey, MD,and the director of the Institute of Molecular Medicine, Betty Diamond, MD.

"Dr. Georgiou is a leader in defining how to exploit fundamental molecules of the immune system to make new therapies for patients with cancer and other disabling conditions," said Dr. Tracey.

The Feinstein Institutes' Marsh Lecture was established as a forum for renowned scientists to share their expertise with Feinstein Institutes investigators. The series was made possible by an endowment from the late Leonard Marsh and his family, the Marsh Lecture honors the memory of Leonard Marsh, co-founder of Snapple Beverage Corporation and a major supporter of the Feinstein Institutes. Leonard Marsh's legendaryenthusiasm for new ideas and innovations continue to inspire the Feinstein Institutes scientific faculty and staff.

For more information on this and upcoming Marsh Lectures,click here.

About the Feinstein Institutes The Feinstein Institutes for Medical Researchis the research arm of Northwell Health, the largest health care provider and private employer in New York. Home to 50 research labs, 2,500 clinical research studies and 4,000 researchers and staff, the Feinstein Institutes is raising the standard of medical innovation through its five institutes of behavioral science, bioelectronic medicine, cancer, health innovations and outcomes, and molecular medicine. We're making breakthroughs in genetics, oncology, brain research, mental health, autoimmunity, and bioelectronic medicine a new field of science that has the potential to revolutionize medicine. For more information about how we're producing knowledge to cure disease, visit feinstein.northwell.edu.

Contact: Matthew Libassi 516-465-8325mlibassi@northwell.edu

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SOURCE The Feinstein Institutes for Medical Research

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8,000 British species to be sequenced as 9.4m from Wellcome funds first phase of Darwin Tree of Life project – Cambridge Independent

Sunday, November 17th, 2019

Funding of 9.4million has been confirmed by Wellcome to begin the Darwin Tree of Life project, which will sequence all species in the British Isles.

In this first phase, 10 organisations will be involved in collecting and sequencing around 8,000 British species of animal, plant and fungi, and delivering the genomes of 2,000, giving an unprecedented insight into the evolution of life on Earth.

It will also uncover new genes, proteins and metabolic pathways that could help develop new drugs, while supporting the conservation of global biodiversity amid the threats posed by climate change and human development.

Professor Richard Durbin, in the University of Cambridges Department of Genetics, who will lead the universitys involvement in the collaboration. said: This project is the start of a transformation for biological research. It will change our relationship to the natural world by enabling us to understand life as never before. It will create a knowledge resource for others to build on, just as weve seen with the Human Genome Project for human health.

Ultimately, the aim is sequence all 60,000 species that live in the British Isles - a launchpad for the ambitious Earth Biogenome Project - a moonshot for biology that aims to do the same for all life on the planet.

Dr Michael Dunn, head of genetics and molecular sciences at Wellcome, said: The mission to sequence all life on the British Isles is ambitious, but by bringing together this diverse group of organisations we believe that we have the right team to achieve it.

Well gain new insights into nature that will help develop new treatments for infectious diseases, identify drugs to slow ageing, generate new approaches to feeding the world and create new bio-materials.

The UK organisations involved are:

University of Cambridge

Earlham Institute (EI)

University of Edinburgh

EMBLs-European Bioinformatics Institute (EMBL-EBI)

The Marine Biological Association (Plymouth)

Natural History Museum

Royal Botanic Gardens Kew

Royal Botanic Garden Edinburgh

University of Oxford

Wellcome Sanger Institute.

Professor Mark Blaxter, lead of the Tree of Life programme at the Wellcome Sanger Institute, said: The Darwin Tree of Life Project will change biology forever, delivering new insights into the numerous animals, plants, fungi and protists that call the British Isles home. The impact of this work will be equivalent to the effect the Human Genome Project has had on human health over the last 25 years.

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Scientists aim to sequence all 1.5 million known species on Earth - and Wellcome Sanger Institute will play leading role

25 species genomes have been sequenced to mark Wellcome Sanger Institute's 25th anniversary

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8,000 British species to be sequenced as 9.4m from Wellcome funds first phase of Darwin Tree of Life project - Cambridge Independent

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Is sexual orientation genetic? Yes and no, an extensive study finds – Haaretz

Friday, November 15th, 2019

The international group of scientists knew they were setting out to investigate an explosive subject: the hereditary basis of human same-sex behavior. Even so, the members of the prestigious Broad Institute in Cambridge, Massachusetts, may not have anticipated the magnitude of the public furor that erupted when they published their study, which identified several markers in certain genetic loci in the human genome related to same-sex sexual experience. The storm of reactions ranged from those who welcomed something seen as heralding significant progress in the field, to others who maintained that it would have been better if the scientists hadnt published anything.

The research results were published in full in the journal Science, at the end of August. This was the most extensive study of its kind ever conducted (there were about a half a million subjects), in which use was made of the GWAS (genome-wide association studies) method to analyze genetic big data. The researchers discovered five genetic markers (frequent, minor changes in the DNA segments of certain chromosomes) that appeared repeatedly among individuals who reported having had same-sex sexual experiences. Slight and frequent genetic variations were identified in both women and men, two others in men only and one more only in women.

No less important in the study, entitled Large-scale GWAS reveals insights into the genetic architecture of same-sex sexual behavior, is the scientists claim that a large number of genetic markers, perhaps even thousands, might operate simultaneously together although each in and of itself is of minuscule weight and influence ones same-sex orientation. Moreover, their study led the researchers to the conclusion that human genetics can explain up to 32 percent of same-sex sexual behavior.

What is at issue here, however, is not what the study contains but what it does not contain. As Melinda Mills, a sociology professor at Oxford, writes in the same issue of Science, there is no way that the researchers findings can be used as a tool to accurately predict same-sex behavior. Specifically, the fact that genetics can explain up to 32 percent of the fact that someone is gay or lesbian, does not mean that sexual identity is determined primarily by environmental factors not to mention social ones. This story is far more complex and has not yet been fully deciphered. Mills views are shared by Andrea Ganna, one of the chief authors of the new study.

What we basically do is statistical associations between having and not having these genetic markers and having or not having same-sex behavior, Ganna told Haaretz in a phone interview. Because we had this uniquely large study, he continued, which allowed us to have robust conclusions, and because we had the technology to measure the genetic markers of so many individuals, the time was right to confirm something that we expected: There is no one specific gay gene. Instead there are a lot of relatively common genetic markers, genetic mutations, that have a small effect on same-sex behavior.

At the same time, adds Ganna, a geneticist at Harvard Medical School and at Finlands Institute of Molecular Medicine, Not everyone is interpreting the fact that theres no single gay gene in the right way.

Gannas concern is shared by scientists around the world. Theyre worried that the researchers findings will fuel prejudice and discrimination against the LGBTQ community, and even spark calls for genetic engineering and genetic diagnosis among its members. So serious are these apprehensions that some have wondered whether the study would not do more harm than good.

As a queer person and a geneticist, I struggle to understand the motivations behind a genome-wide association study for non-heterosexual behavior, Joseph Vitti, a postdoctoral researcher at the Broad Institute, wrote on its blog, adding, I have yet to see a compelling argument that the potential benefits of this study outweigh its potential harms [T]he results presented not only oversimplify the question of biological causality, but also threaten direct damage by perpetuating the stereotype of LGBTQIA+ people as imprudent, while also likening same-sex attraction to a medical or psychological disorder.

Moreover, a website called The American Conservative posted an article entitled Not Born This Way After All? which wondered, skeptically: If the study proves that homosexuality is related to the environment, above all, and not to heredity why isnt it right and proper, in scientific terms, to allow those who so desire to undergo treatment in order to reduce their same-sex desires, which have now been shown not to be genetic?

That, however, is a simplistic reading of the studys findings. According to Michael Bailey, a professor of psychology at Northwestern University in Illinois, who was not involved in the study but has been conducting research on sexual orientation for 30 years, Its very important to understand that environment does not simply refer to social surroundings, like what your parents teach you and what kids you know, trauma and so on theres also a biological environment that begins right after conception.

Three years ago, Bailey and several colleagues published a survey of all the studies and professional literature in the field. The best studies have shown that genes are probably important but not overwhelmingly important, he tells Haaretz. We estimated in our 2016 review that 30 percent of the variation in sexual orientation is due to genetic variations. It may be this finding that led him to conclude that it is the biological environment that is mostly important. Bailey is convinced that men are born with their sexual orientation and that it is not subsequently acquired at any stage. He notes that there are several cases, I think there are seven throughout the professional literature, in which a baby boy was changed into a girl for medical reasons and was raised as a girl. When you follow these individuals through adulthood, you find that they are attracted to women and not to men.

In Baileys view, the best example of how biological-environmental factors can influence sexual orientation is the fraternal birth order effect. The phenomenon, whose existence is well established, he says, shows that the more older brothers a man has, the more likely he is to be homosexual. In practice, every older biological brother increases the probability that the youngest brother will be gay by about 33 percent. Thus, if the probability that a man with no older brothers will be gay is 2 percent, one older brother will increase the probability to 2.6 percent, and a second, third and fourth brother to 3.5 percent, 4.6 percent and 6 percent, respectively. Whats not yet clear is the reason for this.

In my mind, Bailey suggests, the best hypothesis as to why this happens is that a mothers immune system becomes increasingly active and produces antibodies against male proteins over successive births.

Fingers and hands

Behind this hypothesis is one of the most influential figures in the field, American-Canadian clinical psychologist and sexologist Ray Milton Blanchard. He was also among those who linked the fraternal birth order effect to another phenomenon of interest to scientists: the connection between being left-handed and having a same-sex orientation. The most extensive study in this regard was conducted in 2000, incorporating 20 different studies involving 7,000 gay male and female subjects and 16,000 heterosexual ones. It was found that gay men were 34 percent more likely to be left-handed. The situation was more extreme among lesbians: They were seen to have a 91 percent greater chance than straight women of writing with their left hand.

As a result, six years later, a research team led by Blanchard argued that the fraternal birth-order effect is relevant only among right-handed men. The reason is that, in any case, left-handed men who dont have older brothers already have a greater likelihood of being gay than right-handed men with such siblings.

A persons dominant hand turns out to be significant in another sense as well. An article published two years ago (about a study in which all the subjects had taken part in a gay pride parade in Toronto) found a connection between that hand and the gay persons role in bed: that is, the proportion of left-handed gays who defined their sexual behavior as passive or versatile (i.e., sometimes passive, sometimes not) was significantly higher than among those who described themselves as actives who clearly tended to be right-handed.

In research conducted over the years on the subject of the connection between sexual orientation and other attributes of the body, the hand holds a place of honor. But while Blanchard developed his theory on the basis of the whole hand, sometimes a few fingers are also enough: two, to be exact. In his 1998 study, British biologist John Manning confirmed a relatively old hypothesis, first put forward in Germany almost 150 years ago. Its gist is that the proportion between the length of index and ring fingers is, typically, different in men and women. Manning found that this phenomenon was detectable as early as age 2, which led to the observation that its source lies in the differences in testosterone and estrogen levels that already exist in the womb hereinafter: a biological-environmental factor.

Manning did not emphasize the element of sexual orientation in the two books and over 60 articles he wrote on this subject, but in the two decades that have elapsed since his study, more than 1,400 papers have been written on the ratio between the length of the second and fourth fingers (known as 2D:4D) and the connection between it and the level of risk of contracting certain diseases, as well as personality traits, cognitive and athletic abilities and sexual orientation.

One such study, published in 2010, maintained that straight and lesbian women are differentiated by the ratio between the length of the index and ring fingers, with lesbians tending to show a more masculine ratio i.e., closer to the average difference between the length of the fingers, among men. However, no such differences were found between gay and straight men.

Last year a team of scientists led by a British psychologist measured the fingers of 18 pairs of identical female twins, one lesbian, the other straight. Overall, differences in proportion were documented only in the lesbians and only in their left hand, and were comparable to the situation among men. This fact, the team concluded, could indicate a heightened exposure to testosterone in the womb but their study was based on a very small sample and drew much criticism. The critics charged that the conclusion was based on an overly simple means of measurement: of the way only two variables impacted each other. And, they added to bolster their argument, findings of studies involving those fingers have not been replicated in scientific experiments.

The field of gay science has been on a roll in recent years, but has a far longer history. Its modern phase dates to the early 1990s, when scientists began to publish increasing numbers of studies arguing that sexual orientation has a biological component. A leading scientist in this field is British-American neurobiologist Simon LeVay, who in 1990 performed autopsies on the bodies of 41 people: 19 gay men, 16 straight men and nine women. He discovered that the brain cells known as INAH-3 among the deceased gay men were relatively small, and closer in size to those of women than to heterosexual males.

In 1991, LeVay told Haaretz in a phone conversation, I published a study that got a lot of media attention, related to my observation that there was a region inside the hypothalamus that was different in size between men and women, and also between gay and straight men My additional finding was the difference in size between gay and straight men in this region inside the hypothalamus that is involved in the regulation of sexual behavior.

Adds LeVay, My general feeling is that there are certainly strong biological influences on peoples sexual orientation, but we cant say everything is genetic.

In the spirit of the period, and in light of the AIDS epidemic at the time, LeVay tried to be as cautious as possible about his conclusions. Its important to stress what I didnt find, he said in an interview to Discover magazine, in 1994. I did not prove that homosexuality is genetic, or find a genetic cause for being gay. I didnt show that gay men are born that way, [which is] the most common mistake people make in interpreting my work.

Three decades after publishing his study, he still thinks media coverage is doing an injustice to research even if its not his. Ive seen some headlines saying, basically, that this study [i.e., that of Ganna and his associates] shows its not genetic, or that are no gay genes, or something like that; and, of course, its not what the study shows at all.

Truly gay

In recent decades, scientific research (on men and women alike) in this realm has relied on an additional field: molecular genetics. The pioneer is geneticist Dean Hamer, who in 1993 conducted the first study of its kind.

We noticed that being gay, for males, tended to pass down through the mothers side of the family, he told Haaretz. And that is characteristic in genetics of something on the X chromosome because males get their X chromosomes from their moms That led us to look in families where there were gay brothers, to see if they shared anything on the X chromosome.

And thus, recalls Hamer, he and his team discovered Xq28: a genetic marker that plays a part in determining whether a person will be heterosexual or gay. He emphasizes that this is a factor, its not the factor and actually, overall, its not even the most important factor. He adds, Whats good about genetic studies, is that you know that whatever you find is a causal factor, because of course people are born with their genes, and its not something that changes over time.

LeVay, he explains, is looking directly at the brain, and were looking at what we think is building the brain and genes. Yet, its very difficult to know whether one was born with a brain like that, or whether that brain developed that way because of your behavior the causality is rather unknown.

At the same time, Hamer adds, That doesnt mean there arent specific pathways, because there has to be some sort of a pathway in the brain that controls sexual orientation. We know, for example, that the reason you become a male or a female is very simple: If you have a certain gene on the Y chromosome, you will produce male hormones, and if you have those you make a penis and scrotum and you become male. Accordingly, Theres probably some pathway in the brain that does same thing for sexual orientation, but were not going to discover it from genetics The answer will probably emerge from some sort of very sophisticated brain and developmental studies.

For 35 years, Hamer accumulated experience as a scientist at the National Institutes of Health in Bethesda, Maryland. That period is behind him. He doffed the white coat and now lives in Hawaii, where he makes films. But even if hes no longer occupied with research, it still occupies him.

Hamer: Back in the 1990s, I, along with all the scientists involved, believed that if we did good genetic studies wed find the important genes. For example, well find a gene that is responsible for the production of testosterone, and if its functioning was low, it would be possible to say that this is the cause of homosexuality in a particular person. But it turns out that it doesnt work that way. For every mental trait that has been studied everything you can imagine in the brain, for every single trait, theres a [vast number of] genes not to mention a host of complex societal and environmental factors.

For his part, Hamer has much praise for the Broad Institute study: The new GWAS study is really important, because for the very first time they used a huge sample and they mapped every inch of the genome. And this has never been done before. All the other studies were much smaller, or used many fewer genetic markers. But he also demurs: Whats very important is to look at what they actually analyzed. They didnt analyze people who were gay or lesbian, but anyone who had one single same-sex experience, which is quite different... They were measuring something more like openness to sexual experimentation.

As Hamer sees it, If you look for those five markers, or even just the three strongest markers, they are not necessarily found in people who actually identify as gay or lesbian. If you take people who are gay, like me, and look for those markers theyre not significantly there.

Hamer thinks that the whole field is lagging behind because of insufficient research, owing to the stigmas that plague the subject. I dont think sexuality is any more complicated than many other areas of human personality and individual differences, he observes, noting, We formally established that male sexuality is something that is deeply ingrained in people, its not any sort of choice really. It starts really early in life, and it has a major biological component to it. But, how it works? What the biological component is? Were completely unaware and dont know anything, and we barely know more than we did 25 years ago, or in the 1940s, when Kinsey did his work, to be honest.

Hamer was referring to biologist Alfred Kinsey, who in 1948 stunned the American public with his book, Sexual Behavior in the Human Male, which addressed previously taboo subjects, and challenged the traditional beliefs and existing knowledge about human sexuality. Kinsey had conducted a survey of men, which found that 37 percent of his subjects said they had undergone a homosexual experience of some kind, and 10 percent said they had been exclusively gay for three years of their adult life a statistic which to this day is generally said to represent the proportion of people engaging in same-sex behavior.

At the same time, subsequent studies reveal that the percentage of people who define themselves as exclusively homosexual is far lower, though it fluctuates from one article to the next. For example, a 2011 survey of nine different studies on the subject revealed that approximately 3.5 percent of Americans identify themselves as gays, lesbians or bisexuals. A poll involving 1,000 Jewish Israelis in 2012 found that 11.3 percent of the male respondents and 15.2 percent of the female ones said they felt an attraction to members of the same sex. However, only 8.2 percent of the men categorized themselves as gay or bisexual, while 4.8 percent of the women said they were lesbian or bisexual.

For his part, Ganna, of the Broad Institute, understands some of the criticism of his research. What we studied is not related directly to the biology, but to extended environmental factors related to it. Its not about our sample size once you have a lot of individuals, you can capture very small effects. But are these directly influencing same-sex behavior, or other things related to this topic? As a medical example, think about a study that looks for associations between genetic markers and lung cancer. In that example, what we found are genetic variants regarding how much you smoke, which is related to lung cancer.

One of the lessons, and one of the most interesting points arising from the study has to do, says Ganna, with the mode of measurement that had been in use since 1948, when Kinseys scale ranked individuals as being between 0 (totally heterosexual) and 6 (totally homosexual).

Ganna: Basically, the tendency is to locate individuals on a continuum. You can supposedly be anywhere between 100 percent heterosexual to 100 percent homosexual, which implies that the more youre homosexual, the less youre heterosexual, and vice versa. We show that this assumption actually doesnt hold water: When we look at the genetic data, its not that straightforward, theres no simple continuum of sexuality.

So, actually, you are refuting the Kinsey scale?

Ganna: Thats exactly one of our conclusions. What were now doing is, rather than asking people to put themselves on a scale somewhere between being exclusively heterosexual or exclusively homosexual, we ask them how much theyre attracted to men and women. You could be attracted to either of them, very attracted to both of them or to one more than the other. And that information will be crossmatched with genetic markers.

In the final analysis, he adds, We showed that this is just another natural human variation. Sexual orientation, similar to many other behavioral traits, is complicated and is composed of different factors. The interesting thing is how genetics and environment work together. If you think about how much more prevalent same-sex behavior has become lately, people engage in it more than in the past. And thats clearly not because our genetics are changing. Its because of the environment, because society is becoming more open and laws are changing.

Further research should focus on the relationship between environmental factors and genetics, Ganna says, and on how they interact. Its somewhat misleading to think of nature and nurture as separate aspects; they both contribute. So, it would be wrong to say that you can use only DNA to predict if someone will engage in same-sex behavior, but you also cant say its simply a [matter of] choice.

In summary, he says, I think that the more people who will understand that there are genetic and environmental components to sexual behavior, the better and this is a message that goes beyond just sexuality.

Choice and lifestyle

However, the relationship between science and the environment, and particularly the people living in it, is a complicated one. The subject definitely should be studied, but the social aspect of it is problematic, says LeVay, the neurobiologist. I am gay myself, and I feel strongly that gay people should be valued and accepted into society, regardless of what caused their sexual orientation. I dont think its vital for gay liberation to prove that gay people cant help but be gay there are plenty of other reasons [for accepting them], including basic human rights.

At the same time, he adds, this issue is socially relevant, because of traditional notions that see same-sex relations as a choice, a lifestyle or sinful behavior.

In recent years, there have been many studies showing that peoples attitudes toward homosexuality are closely tied to their beliefs about what makes people gay, says LeVay, citing a survey that showed there was a high probability that people who think homosexuality is a choice will object to a gay person being their childrens teacher which in a way might make sense, he adds: If you think being gay is something infectious, socially contagious, and you didnt want your kid to be gay, then you wouldnt want their teacher to be gay ... It follows that demonstrating that biological factors are involved, helps counter those ideas. Still, Im a bit ambivalent about the use of this type of research as some sort of a political weapon in the struggle for gay rights.

The Broad Institute study contains a reminder of the problems and stigmas that still exist with regard to the LGBTQ community. One of the parameters it considers are genetic correlations between genes that are ascribed to homosexuality, and certain psychological problems.

Bailey, the psychologist: One thing that was perceived as controversial, was to look for and find a genetic overlap between homosexual sex genes and genes associated with depression. Its not the same as saying all people who engage in homosexual sex are depressed for genetic reasons, but its also not something that can be easily ignored. There are assumptions that the higher rates of depression among gay men and lesbians is due to the way they are mistreated by society, but the evidence for that is not so overwhelming. There is also the fact, for example, that you have as high a rate of depression among homosexual men in the Netherlands, which is very tolerant, as you have in some less tolerant places, like the United States.

Ganna, for his part, tries to soften that criticism: Even if we see genetic overlap, or correlation, it is not set in stone that weve found a biological mechanism that causes depression and same-sex behavior, he says. There are many explanations for why this one genetic marker is associated with both things. But finding these correlations help us study human traits in general.

In the meantime, there is a price to be paid for conducting research in this realm, which all those involved must be aware of. Reminders of this abound, and are almost routine. In some cases whats at stake is not even a groundbreaking study or one of tremendous scientific importance. In 2017, for example, two researchers from Stanford published an article stating that gay men are predicted to have smaller jaws and chins, slimmer eyebrows, longer noses, and larger foreheads; the opposite should be true for lesbians. In the next stage, they created a facial-recognition program with the aid of more than 14,000 images taken from a singles site of straights and LGBTQs. The program was able to distinguish between gays and lesbians and heterosexuals with an accuracy of 81 percent for men and 71 percent for women, in contrast to an average rate of successful human guesses of 61 percent and 54 percent, respectively. Even though the program achieved relatively impressive results, the study as such drew widespread criticism not unusual for researchers engaged in such studies.

The Stanford gays identification program may be an extreme example, in this respect, but its also a byproduct of the considerable surge in studies in this field, a trend that began in the early 1990s. Together with the scientific community, media interest in the subject of same-sex orientation and its causes has contributed substantially to transmitting messages and shaping public opinion.

In the United States, this can be seen in a series of polls conducted by Gallup, Inc. The first one, conducted in 1977, found that only 13 percent of the respondents believed that homosexuality is an innate tendency, while 56 percent attributed it to environmental factors. This approach remained largely constant until the period between 1989 and 1996, when the rate of those supporting the innate thesis leaped from 19 percent to 31 percent; by 2001, it stood at 40 percent. Almost a decade and a half later, the annual poll produced, for the first time, a larger proportion who agreed with the innate argument. The latest survey, from the end of last year, showed this trend continuing: More than half of the American public believes that gay people are born with their sexual orientation, whereas only 30 percent attribute it to environmental factors (10 percent said both factors play a part, 4 percent cited other factors and 6 percent said they werent sure).

Changes in the perceptions of the origins of sexual orientation are having a pronounced effect on the struggle LGBTQ individuals are waging for equal rights. The latest Gallup poll shows that an absolutely majority (88 percent) of those who believe that homosexuality is an innate trait also support legitimizing same-sex marriages. In contrast, most of those who see this orientation as being environmentally driven (61 percent) are against.

When it comes to public opinion, which is very important, the born this way idea has been really resonant and has had a very positive impact on society, Hamer maintains. Public opinion polls asked people whether they think [gays] were born this way or not, and we know that believing that homosexuality is innate correlates with having positive feelings toward gay rights. Overall, its been important in educating the public about who we are, as gay people.

Such messages are reaching Israel as well. A poll conducted by the Dialog Institute for Haaretz at the end of 2013 found that 70 percent of those questioned favored full rights for same-sex couples, while 64 percent specifically backed their right to surrogacy. However, two polls conducted in the wake of the surrogacy law protest in July 2018 presented slightly lower numbers: About 57 percent of respondents expressed support for the right of same-sex male couples to surrogacy.

These polls did not ask Israelis whether they believe the origin of same-sex orientation is innate or environmental. If you ask Bailey, though, that doesnt really matter.

Ive gone to great lengths to try to persuade people not to base equal rights for gay people on the causal hypothesis, he says. Its a terrible idea to say gay people should have equal rights because they were born that way. Its terrible in part because some criminals might be born that way, and you dont want to them to have the same rights. Being gay doesnt harm anybody, other than people who are close-minded and easily offended. Preventing people from expressing their homosexuality is quite destructive for them. Thats true whether gay people are born that way or not.

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Bayer and Dewpoint Therapeutics Ink $100 Million Research Partnership – BioSpace

Friday, November 15th, 2019

Germany-based Bayer and Dewpoint Therapeutics, located in Boston, announced a research deal that could hit $100 million. The research pact will leverage Dewpoints biomolecular condensates technology platform and Bayers small molecule compound library to identify and develop new therapies for cardiovascular and gynecological diseases.

Biomolecular condensates are droplet-like membrane-less organelles that form in a dynamic fashion with many proteins in order to function within cells. About 80% of proteins in humans are considered unreachable with small molecule drugs. The companies believe that with Dewpoints platform, they will broaden the reach of small molecule therapeutics, identifying new drug targets.

As we continue to broaden our capabilities in Research & Development, the collaboration with Dewpoint gives us access to breakthrough innovation potential, said Joerg Moeller, member of Bayers executive committees Pharmaceuticals Division and head of Research and Development. New analytic tools and a growing understanding of biomolecular condensates could provide new insights into cellular functions that previously have not been considered by scientists in drug development, enabling us to identify novel pharmacological targets for future therapies.

Under the terms of the deal, Bayer picks up an option to exclusively license a specific number of novel therapeutics that come out of the research. In addition to access to Bayers small molecule compound library, it brings R&D capabilities including high throughput screening and medicinal chemistry. No other financial details were disclosed. Nor was the length of the pact.

In January 2019, Bayer participated in Dewpoints $60 million Series A financing via the Leaps by Bayer investment unit.

Dewpoint has locations in Boston and Dresden, Germany. Part of the agreement is to expand Dewpoints presence in Germany outside of Dresden.

This partnership is an exciting opportunity to advance treatments for diseases that have long evaded the industry, said Amir Nashat, Dewpoints chief executive officer. We look forward to combining Bayers expertise in chemistry and drug development and Dewpoints novel platform and insights into the role of biomolecular condensates in disease. We also look forward to working closely with Bayer to expand our capabilities in Germany and put the local biotech ecosystem at the forefront of this important and emerging area.

Dewpoint was founded by Anthony Hyman of the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden, Germany, and Richard Young of the Whitehead Institute in Cambridge, Massachusetts. At the Series A, additional investors besides Bayer included founding investor Polaris Partners, Samsara BioCapital, 6 Dimensions Capital, EcoR1 Capital, and Alexandria Venture Investments.

Although the research partnership between Dewpoint and Bayer will focus on cardiovascular and gynecologic diseases, numerous other diseases are affected by condensates including cancer, neurodegenerative disorders, immunology and virology.

At the time of the launch, Hyman said, Insights into biomolecular condensates could provide answers to fundamental mysteries in biology, and we are eager to begin using these to discover new therapeutic approaches to diseases.

The companys scientific advisors include Simon Alberti, professor and chair of Cellular Biochemistry at the Technical University Dresden; Arup Chakraborty, Robert T. Haslam Professor of Chemical Engineering and Professor of Physics and Chemistry at MIT; Bradley Hyman, John B. Penny, Jr. Professor of Neurology at Harvard Medical School and Director of the Alzheimers unit at Mass General Institute for Neurological Disease; Rudolf Jaenisch, Whitehead Institute Founding Member and Professor of Biology at MIT; Robert Langer, David H. Koch Institute Professor at MIT; Timothy Mitchison, Hasib Sabbagh Professor of Systems Biology at Harvard Medical School and Director of the Harvard Therapeutics Innovation Hub; and Rohit Pappu, Edwin H. Murty Professor of Engineering in the Department of Biomedical Engineering and Director of the Center for the Science & Engineering of Living Systems at Washington University in St. Louis.

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Here’s a better way to convert dog years to human years, scientists say – Science Magazine

Friday, November 15th, 2019

A biological clock governs aging in dogs just as in humans.

By Virginia MorellNov. 15, 2019 , 3:42 PM

Our Scotch collie, Buckaroo, is just shy of 14 years old. Following the long-debunked but still popular idea that one dog year equals seven human years, hes almost a centenarian. (This formula may be based on average life spans of 10 and 70 years for dogs and people, respectively.) Now, researchers say they have a new formula (see calculator below)to convert dog years to human yearsone with some actual science behind it.

The work is based on a relatively new concept in aging research: that chemical modifications to a persons DNA over a lifetime create what is known as an epigenetic clock. Scientists have built a case that one such modification, the addition of methyl groups to specific DNA sequences, tracks human biological agethat is, the toll that disease, poor lifestyle, and genetics take on our bodies. As a result, some groups have converted a persons DNA methylation status to an age estimateor even a prediction of life expectancy (worrying ethicists, who say the data could be misused by forensic investigators and insurance companies).

Other species also undergo DNA methylation as they age. Mice, chimpanzees, wolves, and dogs, for example, all seem to have epigenetic clocks. To find out how those clocks differ from the human version, geneticist Trey Ideker of the University of California, San Diego, and colleagues started with dogs. Even though mans best friends diverged from humans early in mammalian evolution, theyre a good group for comparison because they live in the same environments and many receive similar healthcare and hospital treatments.

All dogsno matter the breedfollow a similar developmental trajectory, reaching puberty around 10 months and dying before age 20. But to increase their chances of finding genetic factors associated with aging, Idekers team focused on a single breed: Labrador retrievers.

They scanned DNA methylation patterns in the genomes of 104 dogs, ranging from 4 weeks to 16 years of age. Their analysis revealed that dogs (at least Labrador retrievers) and humans do have similar age-related methylation of certain genomic regions with high mutation rates; those similarities were most apparent when the scientists looked at young dogs and young humans or old dogs and old humans. Most importantly, they found that certain groups of genes involved in development are similarly methylated during aging in both species. That suggests at least some aspects of aging are a continuation of development rather than a distinct processand that at least some of these changes are evolutionarily conserved in mammals, Ideker and colleagues report in a preprint posted online at bioRxiv.

We already knew that dogs get the same diseases and functional declines of aging that humans do, and this work provides evidence that similar molecular changes are also occurring during aging, says Matt Kaeberlein, a biogerontologist at the University of Washington in Seattle, who was not involved with this research. Its a beautiful demonstration of the conserved features of the epigenetic age clocks shared by dogs and humans.

The research team also used the rate of the methylation changes in dogs to match it to the human epigenetic clock, although the resulting dog age conversion is a bit more complex than multiply by seven. The new formula says a canines human age = 16 ln(dog age) + 31. (Thats the natural logarithm of the dogs real age, multiplied by 16, with 31 added to the total.)

Calculate

(*Enter numbers whose value is 1 or greater)

If your dog were a human, it would be:

Using that formula, dogs and humans life stages seem to match up. For example, a 7-week-old puppy would be equivalent to a 9-month-old human baby, both of whom are just starting to sprout teeth. The formula also nicely matches up the average life span of Labrador retrievers (12 years) with the worldwide lifetime expectancy of humans (70 years).

Theyve shown that theres a gradual increase in DNA methylation in both species with age, says Steve Austad, an evolutionary biologist and aging expert at the University of Alabama in Birmingham. He doesnt find that especially surprising, but he thinks the technique could reveal far more interesting results if applied to issues like the different life spans among different dog breeds.

Thats one goal of Kaeberlein, whose groups new Dog Aging Project (open to all breeds) will include epigenetic profiles of its canine subjects. He hopes to find out why some dogs develop disease at younger ages or die earlier than normal, whereas others live long, disease-free lives.

So, how does our Buckaroo fare? Happily, the epigenetic clock calculation goes in his favor. Hes now only 73 in human yearsand a spry 73 at that.

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Mapping human antibodies to develop protein therapeutics spotlighted at Feinstein Institutes Marsh Lecture – BioSpace

Friday, November 15th, 2019

MANHASSET, N.Y., Nov. 15, 2019 /PRNewswire/ --The Feinstein Institutes for Medical Researchhosted a Marsh Lecture given by George Georgiou, PhD, of the University of Texas at Austin, to discuss human antibody repertoire and the development of protein therapeutics to help treat cancer, viral infection and autoimmune disorders.

Dr. Georgiou, the Laura Jennings-Turner Chair Professor in the departments of Chemical Engineering and Molecular Biosciences at Texas, researches and develops methods to observe and analyze, at the molecular-level, human antibody immune responses which ultimately leads to more efficient vaccines and other engineered enzyme therapeutics.

"To create more effective antibodies and vaccines for some of the most complicated medical conditions, we must better understand the body's molecular immune system," said Dr. Georgiou at the lecture on November 14.

TheMarsh Lectureis given by visiting prominent scientists who share their expertise and establish collaborations with Feinstein Institutes investigators. In his lecture, Dr. Georgiou emphasized the need to continue work in the discovery and preclinical development of protein therapeutics, the mapping of serological antibody repertoire in human health, disease and the methods to engineer second generation antibodies.

The lecture was co-hosted by the Feinstein Institutes' president and CEO, Kevin J. Tracey, MD,and the director of the Institute of Molecular Medicine, Betty Diamond, MD.

"Dr. Georgiou is a leader in defining how to exploit fundamental molecules of the immune system to make new therapies for patients with cancer and other disabling conditions," said Dr. Tracey.

The Feinstein Institutes' Marsh Lecture was established as a forum for renowned scientists to share their expertise with Feinstein Institutes investigators. The series was made possible by an endowment from the late Leonard Marsh and his family, the Marsh Lecture honors the memory of Leonard Marsh, co-founder of Snapple Beverage Corporation and a major supporter of the Feinstein Institutes. Leonard Marsh's legendaryenthusiasm for new ideas and innovations continue to inspire the Feinstein Institutes scientific faculty and staff.

For more information on this and upcoming Marsh Lectures,click here.

About the Feinstein Institutes The Feinstein Institutes for Medical Researchis the research arm of Northwell Health, the largest health care provider and private employer in New York. Home to 50 research labs, 2,500 clinical research studies and 4,000 researchers and staff, the Feinstein Institutes is raising the standard of medical innovation through its five institutes of behavioral science, bioelectronic medicine, cancer, health innovations and outcomes, and molecular medicine. We're making breakthroughs in genetics, oncology, brain research, mental health, autoimmunity, and bioelectronic medicine a new field of science that has the potential to revolutionize medicine. For more information about how we're producing knowledge to cure disease, visit feinstein.northwell.edu.

Contact: Matthew Libassi516-465-8325mlibassi@northwell.edu

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SOURCE The Feinstein Institutes for Medical Research

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How maternal Zika infection results in newborn microcephaly – Baylor College of Medicine News

Friday, November 15th, 2019

The current study was initiated when a patient presented with a small brain size at birth and severe abnormalities in brain structures at the Baylor Hopkins Center for Mendelian Genomics (CMG), a center directed by Dr. Jim Lupski, professor of pediatrics, molecular and human genetics at Baylor College of Medicine and attending physician at Texas Childrens Hospital, said Dr. Hugo J. Bellen, professor at Baylor, investigator at the Howard Hughes Medical Institute and Jan and Dan Duncan Neurological Research Institute at Texas Childrens Hospital.

This patient and others in a cohort at CMG had not been infected by Zika virus in utero. They had a genetic defect that caused microcephaly. CMG scientists determined that the ANKLE2 gene was associated with the condition. Interestingly, a few years back the Bellen lab had discovered in the fruit fly model that ANKLE2 gene was associated with neurodevelopmental disorders. Knowing that Zika virus infection in utero can cause microcephaly in newborns, the team explored the possibility that Zika virus was mediating its effects in the brain via ANKLE2.

In a subsequent fruit fly study, the researchers demonstrated that overexpression of Zika protein NS4A causes microcephaly in the flies by inhibiting the function of ANKLE2, a cell cycle regulator that acts by suppressing the activity of VRK1 protein.

Since very little is known about the role of ANKLE2 or VRK1 in brain development, Bellen and his colleagues applied a multidisciplinary approach to tease apart the exact mechanism underlying ANKLE2-associated microcephaly.

The team found that fruit fly larvae with mutations in ANKLE2 gene had small brains with dramatically fewer neuroblasts brain cell precursors and could not survive into adulthood. Experimental expression of the normal human version of ANKLE2 gene in mutant larvae restored all the defects, establishing the loss of Ankle2 function as the underlying cause.

To understand why ANKLE2 mutants have fewer neuroblasts and significantly smaller brains, we probed deeper into asymmetric cell divisions, a fundamental process that produces and maintains neuroblasts, also called neural stem cells, in the developing brains of flies and humans, said first author Dr. Nichole Link, postdoctoral associate in the Bellen lab.

Asymmetric cell division is an exquisitely regulated process by which neuroblasts produce two different cell types. One is a copy of the neuroblast and the other is a cell programmed to become a different type of cell, such as a neuron or glia.

Proper asymmetric distribution and division of these cells is crucial to normal brain development, as they need to generate a correct number of neurons, produce diverse neuronal lineages and replenish the pool of neuroblasts for further rounds of division.

When flies had reduced levels of Ankle2, key proteins, such as Par complex proteins and Miranda, were misplaced in the neuroblasts of Ankle2 larvae. Moreover, live imaging analysis of these neuroblasts showed many obvious signs of defective or incomplete cell divisions. These observations indicated that Ankle2 is a critical regulator of asymmetric cell divisions, said Link.

Further analyses revealed more details about how Ankle2 regulates asymmetric neuroblast division. They found that Ankle2 protein interacts with VRK1 kinases, and that Ankle2 mutants alter this interaction in ways that disrupt asymmetric cell division.

Linking our findings to Zika virusassociated microcephaly, we found that expressing Zika virus protein NS4A in flies caused microcephaly by hijacking the Ankle2/VRK1 regulation of asymmetric neuroblast divisions. This offers an explanation to why the severe microcephaly observed in patients with defects in the ANKLE2 and VRK1 genes is strikingly similar to that of infants with in utero Zika virus infection, Link said.

For decades, researchers have been unsuccessful in finding experimental evidence between defects in asymmetric cell divisions and microcephaly in vertebrate models. The current work makes a giant leap in that direction and provides strong evidence that links a single evolutionarily conserved Ankle2/VRK1 pathway as a regulator of asymmetric division of neuroblasts and microcephaly, Bellen said. Moreover, it shows that irrespective of the nature of the initial triggering event, whether it is a Zika virus infection or congenital mutations, the microcephaly converges on the disruption of Ankle2 and VRK1, making them promising drug targets.

Another important takeaway from this work is that studying a rare disorder (which refers to those resulting from rare disease-causing variations in ANKLE2 or VRK1 genes) originally observed in a single patient can lead to valuable mechanistic insights and open up exciting therapeutic possibilities to solve common human genetic disorders and viral infections.

Others who contributed in this study are Hyunglok Chung, Angad Jolly, Marjorie Withers, Burak Tepe, Benjamin R. Arenkiel, Priya S. Shah, Nevan J. Krogan, Hatip Aydin, Bilgen B. Geckinli, Tulay Tos, Sedat Isikay, Beyhan Tuysuz, Ganesh H. Mochida, Ajay X. Thomas, Robin D. Clark and Ghayda M. Mirzaa. They are affiliated to one or more of the institutions: Baylor College of Medicine, Texas Childrens Hospital and the Jan and Dan Duncan Neurological Research Institute in Houston, TX; University of California at Davis and San Francisco; Zeynep Kamil Maternity and Children's Training and Research Hospital, Istanbul, Turkey; Marmara University School of Medicine, Istanbul, Turkey; Dr. Sami Ulus Research and Training Hospital of Women's and Children's Health and Diseases, Ankara, Turkey; Boston Childrens Hospital; Harvard Medical School, Boston, MA; Massachusetts General Hospital, Boston, MA; Loma Linda University Medical Center, Loma Linda, CA; University of Washington, Seattle, WA; and Seattle Children's Research Institute, Seattle, WA.

The study was funded by the National Institutes of Healths F32NS092270, NIH/NINDS R35NS105078, NIH U54NS093793, NIH R24OD022005, NIH/NINDS K08NS092898, Howard Hughes Medical Institute (HHMI), Medical Research Fellowship, Jordans Guardian Angels, a jointly funded NHGRI and NHLBI grant to the Baylor-Hopkins Center for Mendelian Genomics (UM1 HG006542) and the Huffington Foundation.

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Kadimastem to Present Interim Results of Cohort A of Its Phase 1/2a Clinical Trial in ALS at the 7th International Stem Cell Meeting, in Tel-Aviv,…

Friday, November 15th, 2019

NESS ZIONA, Israel, Nov. 11, 2019 /PRNewswire/ --Kadimastem Ltd.(TASE: KDST),a clinical stage cell therapy company, today announced that it will present the interim results of Cohort A of its ongoing Phase 1/2a Clinical Trial in ALS (as published in Company's press release) at the 7th International Stem Cell Meeting, to be held on November 12-13 at the Dan Panorama Hotel in Tel Aviv, Israel.

The International Stem Cell Meeting, hosted by the Israel Stem Cell Society, is a highly reputed conference, participated by international world leaders in stem cell research.

Presentation Details:

Title: "FIRST IN HUMAN CLINICAL TRIALS WITH HUMAN ASTROCYTES AS A NOVEL CELL THERAPY FOR THE TREATMENT OF ALS"

Session:ONGOING CLINICAL TRIALS WITH CELL THERAPY

Presenter:Arik Hasson, PhD, Executive VP, Research and Development, Kadimastem

Date:Wednesday, November 13, 2019

Time:1:50 pm Israel

Location: Dan Panorama Hotel, Tel Aviv, Israel

Rami Epstein, CEO of Kadimastem, stated: "We are pleased to share these results with global leaders in the cell therapy and stem cells industry,demonstrating the potential of AstroRx, our astrocyte-based cell therapy product,to bring treatment to ALS patients, and possibly other neurodegenerative diseases. We look forward to further share data of this ongoing trial, with final results of cohort A expected by year-end 2019and results of cohort B expected in Q3, 2020."

About the Phase 1/2a ALS Clinical Trial

The Phase 1/2a trial is an open label, dose escalating clinical study to evaluate the safety, tolerability and preliminary efficacy of AstroRxcells in patients with ALS. The trial is expected to include 21 patients and is being conducted at the Hadassah Medical Center, Jerusalem, Israel. The primary endpoints of the trial are safety evaluation and tolerability of a single administration of allogeneic astrocytes derived from human Embryonic Stem Cells (hESC), administered in escalating low, medium and high doses (100x106, 250x106, and 500x106 cells, respectively). The medium dose will also be administered in 2 consecutive injections separated by an interval of ~60 days. Secondary end points include efficacy evaluation and measurements. Treatment is administered in addition to the appropriate standard-of-care.

About AstroRx

AstroRx is a clinical grade cell therapy product developed and manufactured by Kadimastem in its GMP-compliant facility, containing functional healthy astrocytes (nervous system support cells) derived from human Embryonic Stem Cells (hESC) that aim to protect diseased motor neurons through several mechanisms of action. The Company's technology enables the injection of AstroRxcells into the spinal cord fluid of patients suffering from Amyotrophic Lateral Sclerosis (ALS) with the goal of supporting the malfunctioning cells in the brain and spinal cord, in order to slow the progression of the disease and improve patients' quality of life and life expectancy. AstroRxhas been shown to be safe and effective in preclinical studies. AstroRxhas been granted orphan drug designation by the FDA.

About ALS

Amyotrophic Lateral Sclerosis (ALS) is a rapidly progressive fatal neurodegenerative disease causing disfunction in the upper and lower motor nerves that control muscle function. ALS leads to muscle weakness, loss of motor function, paralysis, breathing problems, and eventually death. The average life expectancy of ALS patients is 2-5 years. According to the ALS Therapy Development Institute, it is estimated that there are approximately 450,000 ALS patients worldwide of which 30,000 reside in the US. According to the ALS Foundation for Life, the annual average healthcare costs of an ALS patient in the US are estimated at US$ 200,000. Thus, the annual healthcare costs of ALS patients in the US alone amount to US$ 6 Billion.

About Kadimastem

Kadimastem is a clinical stage cell therapy company, developing and manufacturing "off-the-shelf" allogeneic proprietary cell products based on its platform technology for the expansion and differentiation of Human Embryonic Stem Cells (hESCs) into clinical grade functional cells. AstroRx, the Company's lead program, is a clinical-grade astrocyte cell therapy for the treatment of ALS, currently undergoing a Phase 1/2a clinical trial. In addition, preclinical trials are ongoing with the Company's IsletRx pancreatic functional islet cells for the treatment of insulin dependent diabetes. Kadimastem was founded by Prof. Michel Revel, CSO of the Companyand Professor Emeritus of Molecular Genetics at the Weizmann Institute of Science. Prof. Revel received the Israel Prize for the invention and development of Rebif, a multiple sclerosis blockbuster drug sold worldwide. Kadimastem is traded on the Tel Aviv Stock Exchange (TASE: KDST).

Company Contacts:Yossi Nizhar, CFO y.nizhar@kadimastem.com+972-73-797-1613

Investor and Media Contact:Meirav Gomeh-Bauermeirav@bauerg.com+972-54-476-4979

Global Media Contact:Dasy (Hadas) MandelDirector of Business Development, Kadimastemd.mandel@kadimastem.com+972-73-797-1613

SOURCE Kadimastem

https://www.kadimastem.com/

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More Ways of Information Sharing Found in Living Things – Discovery Institute

Friday, November 15th, 2019

Sharing of information is not evolution. Its like sharing library books instead of writing new ones. Biologists are continuing to uncover ways that living things pass around what they know. This is not good for Darwinism, which requires new information to arise by chance.

Science Daily uses the analogy of fishing with rod and reel to illustrate what bacteria do to acquire information they need.

A new study from Indiana University has revealed a previously unknown role a protein plays in helping bacteria reel in DNA in their environment like a fisherman pulling up a catch from the ocean.

The discovery was made possible by a new imaging method invented at IU that let scientists see for the first time how bacteria use their long and mobile appendages called pili to bind to, or harpoon, DNA in the environment. The new study, reported Oct. 18 in the journal PLOS Genetics, focuses on how they reel their catch back in. [Emphasis added.]

Pili (singular, pilus) are tiny extensions from the cell membrane that grow out and then retract. Why should a bacterium invent a way to defeat antibiotics when it can fish for it? The paper indicates two issues for ID vs Darwinism: (1) information is shared, and (2) molecular motors do the work.

Almost all bacterial species use thin surface appendages called pili to interact with their environments. These structures are critical for the virulence of many pathogens and represent one major way that bacteria share DNA with one another, which contributes to the spread of antibiotic resistance. To carry out their function, pili dynamically extend and retract from the bacterial surface. Here, we show that retraction of pili in some systems is determined by the combined activity of two motor ATPase [i.e., ATP-spending] proteins.

This is a far cry from claims by Darwinians decades ago that the rise of antibiotic resistance represents Darwinian evolution in action before our eyes.

The promise of making your own household goods by 3-D printing them hasnt quite arrived, but in theory, you could make a complex object of any shape, like a car part or tool, on your 3-D printer if you had the code for it. A recent paper in PNAS suggests that something similar happens in yeast. In this case, a prokaryote shares information with a eukaryote. Carla and Paula Gonalves found a way that eukaryotic yeasts which lost the code for vitamin B1 can retrieve it from bacteria and make their own again.

Food is the only source of the essential vitamin B1 for humans, but many microorganisms such as yeast and bacteria can synthetize it themselves. Here we report on a group of yeasts that have lost part of the vitamin B1 biosynthetic pathway in the past but have managed to rebuild it by capturing multiple genes from bacteria through horizontal gene transfer (HGT). We show a mosaic pathway composed of yeast and bacterial genes working coordinately to accomplish the synthesis of an essential nutrient. This involved adaptation of the bacterial genes to the very different expression rules in their new environment using several different mechanisms. Our results endorse HGT as an important mechanism for evolutionary adaptation in eukaryotes.

The authors can call it evolutionary adaptation to please the censors, but its really information sharing. Nothing evolved. The yeast didnt re-invent the vitamin B1 synthesis pathway; they lost it (as Behe would say, they devolved), and so they borrowed genetic instructions from bacteria to get back to where they used to be. The authors very few instances of the words evolved and evolution in the paper seem superfluous to any serious consideration of causation or explanation.

Picture information-sharing tunnels at the nanometer scale. These would be way too small to see, so it would require indirect imaging techniques to observe them in action. A team of scientists possibly uncovered a novel mechanism in mammalian inter-cellular cytoplasmic transfer and communication between mammalian cells. Its just a preprint in bioRxiv, so the story will need further verification, but if observations confirm what the scientists think they are seeing, tunneling nanotubes and fine and often branching cell projections pass organellar cargo from cell to cell. In their experiments, healthy cells were found pumping material to malignant cells.

Discrete, rapid and highly localized transfer events, evidenced against a role for shed vesicles. Transfer coincided with rapid retraction of the cell-projections, suggesting a hydrodynamic mechanism. Increased hydrodynamic pressure in retracting cell-projections normally returns cytoplasm to the cell body. We hypothesize cell-projection pumping (CPP), where cytoplasm in retracting cell-projections partially equilibrates into adjacent recipient cells via micro-fusions that form temporary inter-cellular cytoplasmic continuities.

Cells can not only use protrusions to pump but also to poke neighboring malignant cells. In Nature, Kendall Powell discusses the growing realization among microbiologists that cells can evict, kill or cannibalize less-fit rivals. To do that, cells must have methods of sensing who is good and who is bad, and cooperating as a team. The burgeoning field of cell competition uses the Darwinian lingo of fitness and competition, but this really sounds more like a case of what Marcos Eberlin calls Foresight: the ability to foresee problems and have mechanisms in advance to deal with them.

The best-known case of genetic information sharing is, of course, sexual reproduction. Humans are all one species, Homo sapiens, so everyone is genetically compatible. But what about alleged human ancestors with other species names? Can they share genes?

One of the most astonishing developments in paleoanthropology in the last two decades was the discovery of Neanderthal DNA within us. As the myth of Neanderthals being other members of Homo began to crumble, first it was small bits of Neanderthal DNA, then more and larger segments. Next, Denisovan DNA was found mixed in with Neanderthal and living human genomes. Now, New Scientist reports, Long strand of DNA from Neanderthals found in people from Melanesia. Some paleoanthropologists are thinking that all three groups were genetically compatible with Homo erectus and other archaic humans.

Michael Marshall suggests that theres function, not just randomness, in these cases of genetic mixing:

The archaics have contributed to the success of humans that left Africa, says Eichler. Neanderthals and Denisovans lived in Europe and Asia for hundreds of thousands of years before modern humans emerged from Africa, so they would have evolved adaptations to the different climates, foods and diseases. These useful genes were kind of test-run in our precursors, says Eichler. Theyre basically borrowed.

Predictably, Marshall remains Darwinian in his thesis, but its not necessary to assume that the Africans invented their adaptations by chance mutations and natural selection. ID research could approach the same observations with Foresight in mind: humans have always had engineered mechanisms that could adapt to a wide variety of circumstances. If African meets European and they get twinkles in their eyes, why, theres a quick way to share their library books.

So, scientists continue to find ways that organisms share pre-existing genetic information. Old Darwinian paradigms continue to fall as observations reveal useful information passing through tunneling nanotubes, pili, and secretion systems from cell to cell. Organisms wouldnt borrow useless junk. If they are found reeling in DNA or passing it through secret passageways, it must be a good read.

Photo: Library shelves, bySusan YinviaUnsplash.

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Is Protein Therapeutic Market Trapped Between Growth Expectations and Uncertainty? – Daily Market Headlines

Friday, November 15th, 2019

AMA recently published a detailed study of over 180+ pages in its repository on Protein Therapeutic market covering interesting aspects of market with supporting development scenario till 2025. The study provides market size break-up by revenue and volume* for emerging countries and important business segments along with commentary on trending factors, growth drivers. Profiled players in study from the coverage used under bottom-up approach are Merck KGaA (Germany),Thermo Fisher Scientific Inc. (United States),Becton, Dickinson & Company (United States),Agilent Technologies, Inc. (United States),QIAGEN N.V. (Netherlands),Takara Bio Inc. (Japan) ,Lonza Group Ltd. (Switzerland), Bio-Rad Laboratories, Inc. (United States),GenScript Biotech Corporation (China) ,Lucigen Corporation (United States),Synthetic Genomics Inc. (United States),Promega Corporation (United States),New England Biolabs, Inc. (United States) ,Sengenics (Singapore)

Request a sample report @ https://www.advancemarketanalytics.com/sample-report/85549-global-protein-therapeutic-market

Protein Therapeutic refers to proteins which are engineered in the laboratory so it can be used in pharmaceutical use. These are an important class of drugs which serves patient in need of novel therapies. Protein Therapeutics treat a wide array of clinical indication which includes cancer, infectious diseases, genetic disorder and metabolic disorder.

Market Segmentation:by Type (Monoclonal Antibodies, Insulin, Fusion Protein, Erythropoietin, Interferon, Human Growth Hormone, Follicle Stimulating Hormone), Application (Cancer, Metabolic Disorders, Immunologic Disorders, Hematological Disorders, Hormonal Disorders, Genetic Disorders, Others), End User (Pharmaceutical and Biotechnology Companies, Healthcare service providers, Research Organizations and Academic Research Institutes, Other)

Make an enquiry before buying this Report @ https://www.advancemarketanalytics.com/enquiry-before-buy/85549-global-protein-therapeutic-market

Whats Trending in Market:Technological Advancements Such As Mass Spectrometry, Advances In Molecular Genetics, And Progress In Production Technologies

Growth Drivers:

Increase In Prevalence Of Chronic Diseases

Government Initiative to Improve The Healthcare Services

Rising Demand For High-Quality Recombinant Therapeutics

Rising Research Activities On Protein Therapeutics

Restraints:

High Costs Associated With Therapeutic Proteins

Binding Government Regulations For Protein Therapeutics

View Detailed Table of Content @ https://www.advancemarketanalytics.com/reports/85549-global-protein-therapeutic-market

Country level Break-up includes:North America (United States, Canada and Mexico)Europe (Germany, France, United Kingdom, Spain, Italy, Netherlands, Switzerland, Nordic, Others)Asia-Pacific (Japan, China, Australia, India, Taiwan, South Korea, Middle East & Africa, Others)

* Customized Section/Chapter wise Reports or Regional or Country wise Chapters are also available.

Strategic Points Covered in Table of Content of Global Protein Therapeutic Market:

Chapter 1: Introduction, market driving force product Objective of Study and Research Scope the Protein Therapeutic market

Chapter 2: Exclusive Summary the basic information of the Protein Therapeutic Market.

Chapter 3: Displaying the Market Dynamics- Drivers, Trends and Challenges of the Protein Therapeutic

Chapter 4: Presenting the Protein Therapeutic Market Factor Analysis Porters Five Forces, Supply/Value Chain, PESTEL analysis, Market Entropy, Patent/Trademark Analysis.

Chapter 5: Displaying the by Type, End User and Region 2013-2018

Chapter 6: Evaluating the leading manufacturers of the Protein Therapeutic market which consists of its Competitive Landscape, Peer Group Analysis, BCG Matrix & Company Profile

Chapter 7: To evaluate the market by segments, by countries and by manufacturers with revenue share and sales by key countries in these various regions.

Chapter 8 & 9: Displaying the Appendix, Methodology and Data Source

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KWASU advocates increased agric production to meet global population by 2020 – NIGERIAN TRIBUNE

Friday, November 15th, 2019

A professor of molecular genetics and plant breeding in the department of crop production, College of Agriculture, Kwara State University (KWASU), Olawale Aliyu, had said that agricultural production must increase by 80 per cent to meet world population of 7.7 billion to 10 billion by 2020.

Delivering sixth inaugural lecture of the university, titled, Decoding the secret of life: Plant, sex and sustainable food production, Professor Aliyu said that innovative breeding technologies for improving existing crops for better adaptation, among other measures, should be embarked upon to achieve the task ahead.

The KWASU don, who charged the federal government to give urgent priority to research by providing resources for functional laboratories, said that such labs should be equipped with modern technologies.

Theres the urgent need for the federal government to give priority to research by providing resources for functional laboratories, equipped with modern technologies and training of manpower that will carry out advanced research in agricultural production for sustainable food security.

The government should also strengthen the capacity of Nigerian scientists to embark on genetic engineering of our major food crops in addition to the conventional system being used.

ALSO READ:Changing outdated curriculum

The government should put in place monitoring mechanism to prevent the influx of GMO crops into the country because of its effect on the biodiversity of our plant and animal resources. Our national breeding programmes on cereals and grain legumes should consider integrating the use of apomixis technology for hybrid seed development because of its potential to revolutionize agriculture, he said.

Professor Aliyu, who said that advances in genetic research are moving at jet speed, added that there is an urgent need to review training curriculum in plant breeding and genetics for students in Nigerian universities to reflect current realities.

The KWASU don also said that cashew has the potential to transform the economy of Kwara state, adding that the sector should be properly organized and the industry is supported.

There is an urgent need for the Kwara state government to develop a 10-year strategic plan for the transformation of an agricultural commodity, especially cashew, where it has a competitive advantage. I am aware that the state government initiated a farmer-ownership cashew project that targeted 5,000 hectares per local government area with processing plants in each senatorial district in 2005, but this project was aborted before takeoff. The current administration can revisit this as part of the effort to lay a solid foundation for a sustainable economy of our dear state. The state government should partner with the federal government to stop the illegal shipment of nuts across porous borders to neighbouring countries, he said.

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Paper Used in Creationist Teaching Retracted After 30 Years – The Scientist

Wednesday, November 13th, 2019

A 1989 paper by Russian researcher Dmitrii Kuznetsov on the genetics of wild timber voles has been retracted, decades after a scientist alerted the journal to concerns, according to Retraction Watch. The paper, published in the International Journal of Neuroscience, has been touted by creationists as evidence of their beliefs, and Kuznetsov has repeatedly been accused of scientific misconduct, The Scientist reported in 2013.

In the paper, Kuznetsov reportedly identified an mRNA from one vole species that blocked protein synthesis in a related vole species. That same mRNA, however, did not block translation in the original vole species or another species that was more distantly related. The finding, Kuznetsov wrote in his report, supported the general creationist concept on the problems of the origin of boundless multitudes of different and harmonically functioning forms of life.

Five years after the paper was published, Dan Larhammar, a cell and molecular biologist at Uppsala University in Sweden, wrote to the journal editors discounting Kuznetsovs paper, saying his approach goes against established scientific experience and his claimed results are not qualitatively demonstrated, and that Kuznetsovs critique of a modern molecular-genetic concept of biological evolution has no scientific basis whatsoever. Larhammar learned last year that despite his criticism more than two decades earlier, Kuznetsovs paper was still available without a retraction label, he tells Retraction Watch, which was especially concerning given that repeated accusations of fraudallegedly making up citations and fabricating the sources of samplesled to Kuznetsovs ouster as editor-in-chief of two journals in 2013.

After a series of emails between Larhammar, now president of the Royal Swedish Academy of Sciences, and the International Journal of Neurosciences editor, the Kuznetsov paper now has a retraction stamp, which states: The above article has been retracted due to the unreliable nature of the experimental results presented.

Ashley Yeager is an associate editor at The Scientist. Email her at ayeager@the-scientist.com.

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Important New Joint Consensus Recommendation from the ACMG and ClinGen Provides Technical Standards for the Interpretation and Reporting of…

Wednesday, November 13th, 2019

BETHESDA, Md., Nov. 13, 2019 /PRNewswire/ --The American College of Medical Genetics and Genomics (ACMG) and the Clinical Genome Resource (ClinGen) have released an important new joint consensus recommendation that will guide the evaluation of constitutional copy number variants (CNVs), encourage consistency and transparency across clinical laboratories, and lead to improved quality of patient care.

The extensive and detailed recommendation, "Technical standards for the interpretation and reporting of constitutional copy number variants: a joint consensus recommendation of the American College of Medical Genetics and Genomics (ACMG) and the Clinical Genome Resource (ClinGen)," is the result of a joint collaborative working group of ACMG and ClinGen, working together since 2015, to update the existing ACMG clinical laboratory practice standards for evaluating CNVs. Copy number analysis is recommended as a first-tier approach for the evaluation of individuals with neurodevelopmental disorders, such as intellectual disability, developmental delay and autism spectrum disorder, as well as for individuals with multiple congenital anomalies and for fetuses with ultrasound abnormalities.

"It is our hope that having standards that are widely available, up to date, and flexible enough to incorporate lessons learned from the ever-evolving clinical genomics knowledge base will help to reduce discordance in clinical classifications and will improve clinical care," said Christa Lese Martin, PhD, FACMG, the paper's senior author.

The recommendation represents a significant update from previous recommendations published in 2011 entitled "American College of Medical Genetics standards and guidelines for interpretation and reporting of postnatal constitutional copy number variants," and is intended to complement the widely cited 2015 paper for sequence variants, "Standards and Guidelines for the Interpretation of Sequence Variants: A Joint Consensus Recommendation of the American College of Medical Genetics and Genomics and the Association for Molecular Pathology."

The updated technical standards include several major changes from the previous document. The first major change is using the same five-tier system used in sequence variant classification: pathogenic, likely pathogenic, uncertain significance, likely benign, and benign. The previous standards recommended utilizing "likely pathogenic" and "likely benign" as sub-categories under "uncertain significance" (essentially a 3-tier system). Harmonizing copy number and sequence variant terminology will become increasingly important as the identification and classification of both types of variants within a single platform becomes more commonplace.

The second major change encourages laboratories to uncouple the classification of the variant from the clinical significance for the patient. While the patient's phenotype may be an important piece of evidence to consider when determining the classification of the variant, it should not override other evidence for or against the pathogenicity of the variant, and it should not be used to justify different classifications of the same variant in different individuals. For example, loss of function variants in a particular gene are known to cause hearing loss; there is enough evidence to warrant calling deletions of this gene pathogenic. A deletion of this gene in an individual not reported to have hearing loss should not be called "uncertain significance" solely because hearing loss was not their reason for referral; this could represent an incidental finding with potential implications for the individual's future health, or a cause for a phenotype that was not reported. The practice of changing the variant classification based on whether it explained the stated reason for referral has the potential to result in both inter- and intra-laboratory variant classification discrepancies; this change is intended to help reduce this issue.

The most substantial change is the incorporation of points-based scoring metrics to systematically guide laboratories through the classification of copy number losses and gains. In this scoring system, the various types of evidence considered when evaluating CNVs are awarded points based on their relative strengths, with positive point values for evidence for pathogenicity and negative point values for evidence against pathogenicity. At the end of the evaluation, the sum of all accumulated points leads to a suggested classification. "The scoring metrics are intended to be a guide to provide more structure and transparency to the CNV evaluation," said Erin Rooney Riggs, MS, CGC, the paper's lead author. "We have developed this type of quantitative metric for other types of curation within ClinGen which are being used successfully to increase consistency in data interpretation. With education and experience, we anticipate that the use of these metrics, as well as the other recommendations in these updated technical standards, will lead to increased consistency in constitutional CNV classification."

The recommendation states, "Although these standards attempt to comprehensively incorporate commonly available resources and processes used in CNV classification and interpretation, it is important to recognize that no singular algorithm will be applicable in all potential scenarios.The semi-quantitative scoring framework is meant to serve as a guide. Professional judgment should always be used when evaluating the evidence surrounding a particular genomic variant and assigning a classification."

The working group and authors on the new joint consensus recommendations include: Erin Rooney Riggs, MS, CGC; Erica F. Andersen, PhD; Athena M. Cherry, PhD; Sibel Kantarci, PhD; Hutton Kearney, PhD; Ankita Patel, PhD; Gordana Raca, MD, PhD; Deborah I. Ritter, PhD; Sarah T. South, PhD; Erik C. Thorland, PhD; Daniel Pineda-Alvarez, MD; Swaroop Aradhya, PhD and Christa Lese Martin, PhD.

About the American College of Medical Genetics and Genomics (ACMG) and ACMG Foundation for Genetic and Genomic Medicine

Founded in 1991, the American College of Medical Genetics and Genomics (ACMG) is the only nationally recognized medical society dedicated to improving health through the clinical practice of medical genetics and genomics and the only medical specialty society in the US that represents the full spectrum of medical genetics disciplines in a single organization. The ACMG is the largest membership organization specifically for medical geneticists, providing education, resources and avoice for more than 2,300 clinical and laboratory geneticists, genetic counselors and other healthcare professionals, nearly 80% of whom are board certified in the medical genetics specialties. ACMG's mission is to improve health through the clinical and laboratory practice of medical genetics as well as through advocacy, education and clinical research, and to guide the safe and effective integration of genetics and genomics into all of medicine andhealthcare,resulting in improved personal and public health. Four overarching strategies guide ACMG's work: 1) to reinforce and expand ACMG's position as the leader and prominent authority in the field of medical genetics and genomics, including clinical research, while educating the medical community on the significant role that genetics and genomics will continue to play in understanding, preventing, treating and curing disease; 2) to secure and expand the professional workforce for medical genetics and genomics; 3) to advocate for the specialty; and 4) to provide best-in-class education to members and nonmembers. Genetics in Medicine, published monthly, is the official ACMG peer-reviewed journal. ACMG's website (www.acmg.net) offers resources including policy statements, practice guidelines, educational programs and a 'Find a GeneticService' tool. The educational and public health programs of the ACMG are dependent uponcharitable gifts from corporations, foundations and individuals through the ACMG Foundation forGenetic and Genomic Medicine.

About the Clinical Genome Resource

The Clinical Genome Resource (ClinGen)is a National Institutes of Health (NIH)-funded resourcededicated to building an authoritative central resource that defines the clinical relevance of genesand variants for use in precision medicine and research. Since 2012, ClinGen has worked tofacilitate responsible genomic and phenotypic data sharing between clinicians, clinicallaboratories, researchers, and patients; to develop and implement standards to support clinicalannotation and interpretation of genes and variants; to enhance and accelerate expert review ofthe clinical relevance of genes and variants; and to disseminate and integrate ClinGen knowledgeand resources to the broader community. ClinGen is primarily funded by the National HumanGenome Research Institute (NHGRI) through the following three grants: U41HG006834,U41HG009649, and U41HG009650.

Kathy Moran, MBA

kmoran@acmg.net

SOURCE American College of Medical Genetics and Genomics

http://www.acmg.net

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I Still Live Off the Land – Havana Times

Wednesday, November 13th, 2019

By Osmel Ramirez Alvarez

HAVANA TIMES I have quite a few intellectual projects on the backburner because Ill have a bit more time in the future: many interesting and useful books that I would like to read and I cant get a few pages in; jobs around the house that demand my attention; and dozens of other things that I put off for a bit or entirely because I prioritize whats important, urgent.

The three most pressing things right now are:

First of all, support my family with the basic, at least, because I have three children, a wife who depends on me financially, and I even have to support my parents from time to time. A great odyssey, theres no doubt about that, in this difficult country, where peoples work is the only dirt-cheap thing there is here.

Secondly, trying to be useful to my country, to the change that Cuba needs to move towards a democracy, contributing ideas, pushing consensus among Cubans, helping people to understand our complex reality and cooperating to try and get our citizens active in public affairs.

Its just that I dream of a better country, where we wouldnt need to emigrate or steal in order to have what we dream of and in order for that to be a possibility, we have to stop delegating responsibility and learn to take part ourselves.

Third of all, its my life mission to be happy, or as happy as I can be amidst all of these problems. Keeping myself as healthy as I can in both body and mind, without hate, resentment, regrets and resignation. On the contrary, with a lot of resilience, faith in the future and confidence in the value of what I and we do. Without such a life philosophy, youd get dragged into the daily confusion and being efficient and proactive becomes impossible.

And where does farming come into all of this?

I really like agriculture, but more as a hobby. If I do it commercially, or to make a living, its because tough economic times force me to. As a result, it fits in with my three life priorities, which are the foundation of my life strategy.

I farm as an extra to make ends meet and support my family, because what I earn from my intellectual endeavors would only be enough to support myself, and it wouldnt be enough for my large family. But, its not a burden. My family is my oasis. My childrens and wifes love is an incomparable refuge. As well as my parents company, who live next to me or my sisters and nephews and nieces, cousins, aunts and uncles, everything, is extra. This is how I live my life, surrounded by family and I feel loved.

Quite regularly, someone who knows me will talk sadly when they see me farming, dirty sometimes, with my old palm leaf hat and old work clothes. They say things like: With everything you studied, its a crime that youre out here working the land. But I tell them that Im as happy out here in the field as I am when I was behind a microscope or a laminar flow bench in the labs when I worked as a biologist. I even sing when Im farming. But they dont get me.

I understand crops and the work it takes to get a good harvest, just like I know about the human anatomy, molecular genetics or ecology. I dont really think of myself as a farmer, because thats not my main identity. However, I have always had the countryside around me, ever since I was born. Even though my father and grandfather were workers, of trades and at a sugar mill respectively, they never broke all ties with farming.

We inherited two hectares of land from my grandmother, which she had inherited herself from her father, and he from his, my great-great-grandfather called Ramon Segura, a son of the Spanish who didnt support the Mambises in their cause, because he preferred to keep ties with Spain. That was his right. The 1902 Republic respected private property and it is still privately-owned today, being a horse ranch, and then divided among the descendants.

The alluvial soil is very fertile, one of the best in Cuba for tobacco farming (and Im not exaggerating). My plot isnt very big, in commercial terms, but it helps us to get by. It would be a great help if we were able to sow what we need to, but we cant because of high theft rates. Only tobacco, which you cant eat, and is hard to steal because of the process it needs to be of high commercial value, and little patches of other things.

I will plant tobacco again this year. My problems from two or three years ago still havent been completely resolved, which made this business riskier than gambling for me and I was forced to retire. However now the most important thing is that the company is valuing the product a lot more fairly because of a lapse in its production. And because there are very few options to invent on the side, Im trying to get a loan for a small plot, which is hard to do amid so much bureaucracy.

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Gene patenting reform in the US and the knock-on effect in Europe – Health Europa

Wednesday, November 13th, 2019

This year there has been quite some talk about patenting the discovery of new genes. The patency eligibility criteria for this is set to undergo major reform in the US, which is likely to have a huge impact on a number of companies offering genetic testing kits, including 23andMe and AncestryDNA. Here, McDowell of EIP, an IP and patent law firm, shares her thoughts on the reform and the potential far-reaching impact it might have in the world of genetics, gene patenting and beyond.

The question of what should and should not qualify as patent eligible subject matter has, for several years, drawn sharp debate in the United States. Since 2012, the US Supreme Court has operated under the Alice/Mayo framework, which has sought to prevent patenting of abstract ideas and naturally occurring phenomena. This has had broad repercussions within the biotechnology sector and beyond; for example, resulting in the widespread proliferation of mail-order spit-kit operations like 23andMe.

Reform of the Alice/May framework has seen strong support from parts of the biotech industry, citing lack of investment as a barrier to greater research into diagnostic methods. However, a more general concern from stakeholders in the United States is that the unpredictability caused by the Alice/Mayo framework puts the US at a disadvantage compared to International competitors; particularly in respect of some of the most cutting-edge technologies, such as AI and molecular diagnostics. A lack of patent availability is allegedly driving investment to other countries, where such inventions are more clearly patent-eligible.

Battle lines have been drawn between the biotechnology and software industries, with calls for less restrictive eligibility criteria coming from the former. The financial input needed to develop new technologies differs substantially between these industries. Lone inventors and small businesses in the software industry, with the ability to develop their products cheaply, felt stifled by overbroad patents granted to others before 2012.

Meanwhile, even small players in the biotech industry rely on high value investment before diagnostic and curative treatments can be brought to patients. Intellectual property protection is key to ensuring that investors in this sector feel secure that the vast sums of money they contribute will be recouped through effective commercialisation.

The Executive Director of Cleveland Clinic Innovations recently explained that: Ability to gain patent protection is the first factor in our assessment of whether a product can reach the market; if an invention cannot get intellectual property protection, usually that is a fatal flaw and the invention is canned at that point.

With this being a widespread stance in the pharmaceutical and diagnostics industries, it is easy to see how the current restrictions to patentability could lead to fewer treatments being developed in the US. What is more, Internationally, the US is no longer top of the list for biopharma companies launching their products; with companies citing inability to protect their ideas as a key reason for not entering the US market.

On the other hand, there are those within the biotechnology sector who side with the software industry in favouring the status quo. Genetic testing companies have reaped the benefits of a restrictive patent eligibility criteria, which has resulted in the invalidation of patents to isolated gene products, and so removed the barriers to developing genetic testing kits.

Since 2013, aided by this provision, the cost of genetic testing kits has decreased significantly leading to a boom in popularity and numerous spit-kit companies have crowded the genetic testing market. This new Bill, if enacted, will likely prove problematic for US companies such as 23andMe, who offer customers the ability to test their DNA to uncover their ancestry or genetic vulnerabilities. Consequently, this might open the door for a widespread change in the industry.

The proposed Bill stuttered when a sticking point emerged during consultations with stakeholders. A last-minute amendment to 35 U.S.C. 112F, which governs how patentees may claim their invention in functional terms (as opposed to reciting specific physical structures), has been criticised by members of the biotech industry for watering down patent protections.

The draft Bill provided that, if any patent claim element is expressed as a specified function without the recital of structure, material, or acts in support thereof, then that claim element will be limited to the corresponding structure, material, or acts described in the specification and their equivalents.

This was offered to assuage concern that overruling the patent-eligible-subject-matter case law would herald a return of nuisance patents directed to business methods and software, which often contain functionally defined terms. However, rather than reassuring stakeholders in the software industry, the proposal seems to have succeeded mainly in frightening the biotechnology sector.

Several witnesses from both sides of the debate raised concerns about the burden that drafters and inventors will face from having to enumerate every way of carrying out a claimed method under the proposed amendment to 112F.

Conflicting views on the draft proposal has meant that the initial momentum for reform has been lost for the time being. This will frustrate those in the biotech industry who are keen to see a return the ability to obtain patent protection for their products and processes, which they hope will boost research, and drive investment back into the United States.

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Method for Measuring Animal Personality Developed to Explore Connections Between Genes and Behavior – SciTechDaily

Wednesday, November 13th, 2019

We might refer to someones personality as mousy, but in truth, mice have a range of personalities nearly as great as our own. Prof. Alon Chen and members of two groups he heads one in the Weizmann Institute of Sciences Department of Neurobiology and one in the Max Planck Institute of Psychiatry in Munich, Germany decided to explore personality specifically in mice. This would enable the scientists to develop a set of objective measurements for this highly slippery concept. A quantitative understanding of the traits that make each animal an individual might help answer some of the open questions in science concerning the connections between genes and behavior. The findings of this research were published in Nature Neuroscience.

Each mouse could be seen to have a unique, individual personality that consistently informed its behavior.

Dr. Oren Forkosh, then a postdoctoral fellow who led the research in Prof. Chens group in Germany, explains that understanding how genetics contribute to behavior has remained an open question. Personality, scientists hypothesized, might be the glue that binds the two together: both genes and epigenetics (which determines how the genes are expressed) contribute to personality formation; in turn, ones personality will determine, to a great extent, how one behaves in any given situation.

Personality is, by definition, something that is individual for each animal and something that remains fairly stable for an animal over its lifetime. Human subjects are generally given personality scores based on multiple-choice questionnaires, but for mice, the researchers needed to start with their behavior and work backward. The mice were color-coded for identification, placed in small groups in regular lab environments with food, shelter, toys, etc. and allowed to interact and explore freely. These mice were videoed over several days, and their behavior analyzed in depth. All together, the scientists identified 60 separate behaviors, including approaching others, chasing or fleeing, sharing food or keeping others away from food, exploring or hiding.

Four mice in a well-stocked cage exhibited around 60 different behaviors for evaluation. Credit: Weizmann Institute of Science

Next, the team created a computational algorithm to extract personality traits from the data on the mices behavior. This method works something like the five-part personality score used for humans in which subjects are graded on sliding scales that rate extroversion, agreeableness, conscientiousness, neuroticism, and openness to experience. For mice, the algorithms the group developed revealed four such sliding scales, and although the researchers refrained from assigning anthropomorphic labels to these ratings, they can be applied very much like the human ones. That is, each scale is linear, with opposites at either end; when the group assigned the mice personality types based on their scores for these traits, they found that each mouse could be seen to have a unique personality that consistently informed its behavior. To see if these traits were indeed stable, the researchers mixed up the groups a stressful situation for the mice. They found that some of the behaviors changed sometimes drastically but what they had assessed as personality remained the same.

What can now be learned from a method for assessing a mouses personality? Working with Prof. Uri Alon of the Institutes Department of Molecular Cell Biology, the team used the linear scales they had developed to plot a personality space in which two of the traits were compared. This sort of analysis yields a triangle in which archetypes inhabit the corners (for example, highly dominant and non-commensal [country mice that are not human-friendly], dominant but commensal [city mice], and subordinate).

When traits are viewed this way, they can point to evolutionary tradeoffs for example, in the need to survive and thrive in a dominance hierarchy. In fact, says Dr. Forkosh, we see that these archetypes and all the shades in between are quite natural. These traits have not been bred out of our mice, even though they have lived for generations in labs and could probably not survive in the wild.

The researchers also mapped gene expression patterns in the brains of these mice, and found that they could identify a number that were associated with certain personality traits they had identified.

Based on the 60 behaviors, an algorithm found those relevant to personality, and mapped out four scales for assessing mouse personality. Credit: Weizmann Institute of Science

This method will open doors to all sorts of research, says Dr. Forkosh. If we can identify the genetics of personality and how our children inherit certain aspects of their personalities, we might also be able to diagnose and treat problems when these genes go wrong. We might even, in the future, be able to use these insights to develop more personalized psychiatry; for example, to be able to prescribe the proper treatments for depression. In addition, we can use the method to compare personality across species, and thus to gain insight into the animals that share our world.

###

Reference: Identity domains capture individual differences from across the behavioral repertoire by Oren Forkosh, Stoyo Karamihalev, Simone Roeh, Uri Alon, Sergey Anpilov, Chadi Touma, Markus Nussbaumer, Cornelia Flachskamm, Paul M. Kaplick, Yair Shemesh and Alon Chen, 4 November 2019, Nature Neuroscience.DOI: 10.1038/s41593-019-0516-y

Prof. Alon Chen is the President-Elect of the Weizmann Institute of Science. Also participating in this research were Stoyo Karamihalev, Sergey Anpilov, and Yair Shemesh of the Weizmann Institute of Science and the Max Planck Institute of Psychiatry; Markus Nussbaumer, Cornelia Flachskamm, Paul M. Kaplick, and Simone Roeh of the Max Planck Institute of Psychiatry; and Chadi Touma of the University of Osnabrck, Germany.

Prof. Alon Chens research is supported by the Vera and John Schwartz Professorial Chair in Neurobiology; the Ruhman Family Laboratory for Research in the Neurobiology of Stress; the Perlman Family Foundation, founded by Louis L. and Anita M. Perlman; the Fondation Adelis; Bruno Licht; and Sonia T. Marschak.

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Method for Measuring Animal Personality Developed to Explore Connections Between Genes and Behavior - SciTechDaily

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Shape Therapeutics, Inc. Raises $35.5M Series A Financing, Led by NEA and Announces the Formation of a World-Class Scientific Advisory Board, to…

Sunday, November 10th, 2019

SEATTLE--(BUSINESS WIRE)--Shape Therapeutics, Inc. (ShapeTx), a development-stage biotechnology company leading the field of RNA-editing gene therapy, announces $35.5M in Series A financing, led by New Enterprise Associates (NEA), with additional participation from CureDuchenne Ventures. The new capital will enable the company to extend its growing portfolio of intellectual property, recruit and hire top scientific talent and advance its groundbreaking RNA and protein targeting platforms focused on curing human diseases.

These platforms include the proprietary ShapeTx RNAfix technology that enables direct in vivo targeting and modification of RNA by leveraging proteins such as Adenosine Deaminases Acting on RNA (ADARs), suppressor tRNAs, and engineered adeno-associated viruses (AAVs). The RNAfix platform differentiates from other contemporary genome engineering technologies by engaging natural human cellular machinery to modify RNA.

ShapeTx was founded on the work of Dr. Prashant Mali, Assistant Professor of Bioengineering at UCSD, who during his postdoctoral fellowship in the George Church laboratory at Harvard Medical School pioneered the use of CRISPR in human cells. ShapeTx RNAfix platform is built upon his lab's most recent work demonstrating in vivo use of guide RNAs to recruit native ADARs and to fix mutations in multiple rare genetic disease mouse models.

Our technology can correct mutations or target specific genes in neurodegenerative, oncology, metabolic and rare genetic disorders by hijacking naturally occurring proteins such as ADARs present in our cells using just a short guide RNA. Our proprietary new platform avoids the risk of in vivo immunogenicity and permanent off-target damages commonly associated with CRISPR-based approaches, explained Francois Vigneault, Ph.D., President and CEO, who was previously VP of Research at Juno Therapeutics after a successful co-acquisition of AbVitro, Inc. by Juno and Celgene.

Ed Mathers, Partner at NEA and Board member at ShapeTx, said, One rarely comes across a proprietary technology platform with such transformative potential led by a focused and data-driven scientific group with a successful track record in pre-clinical and clinical development. The team has shown us an exciting demonstration of the technology in multiple in vivo models, alongside one of the strongest IP estates we have seen in the field. NEA looks forward to backing the company in future rounds as they move the technology toward the clinic.

While the ShapeTx platform will be enabling for many other genetic diseases, Dr. Malis in vivo proof of concept in Duchenne Muscular Dystrophy was quite exciting and could potentially lead to a cure for families suffering from such a debilitating disorder, said Debra Miller, CEO and Founder of CureDuchenne and CureDuchenne Ventures.

The ShapeTx Series A financing coincides with the formation of a world-class Scientific Advisory Board comprised of foremost global experts in genomics, bioengineering, and gene editing, including George Church Ph.D., James Collins Ph.D., and Don Cleveland Ph.D. The scientific advisory board will serve as strategic advisors and ensure that the research and development of its platforms meet the highest standards of scientific merit.

Prashant and Francois are some of the most innovative and brilliant individuals that have come through my lab over the years, and it will be impressive to see these two disrupt the field of gene therapy with this paradigm-shifting technology, said Dr. George Church, Professor in Genetics at Harvard Medical School and member of the ShapeTx Scientific Advisory board.

Shape Therapeutics Scientific Advisory Board Members:

George Church, Ph.D.

George Church Ph.D., world-famous geneticist, molecular engineer, and chemist. He developed the methods used for the first genome sequence & million-fold cost reductions since, as well as pioneered many of the CRISPR advances in genome editing. He is currently a Professor of Genetics at Harvard Medical School and Professor of Health Sciences and Technology at Harvard and the Massachusetts Institute of Technology (MIT). He is Director of the U.S. Department of Energy Technology Center and Director of the National Institutes of Health Center of Excellence in Genomic Science. He has received numerous awards, including the 2011 Bower Award and Prize for Achievement in Science from the Franklin Institute and election to the National Academy of Sciences and Engineering.

James Collins, Ph.D.

James Collins Ph.D., is one of the pioneers of the field of synthetic biology and has made multiple synthetic biology and bioengineering breakthroughs in biotechnology and biomedicine. He serves as the Termeer Professor of Medical Engineering & Science and Professor of Biological Engineering at MIT, as well as a member of the Harvard-MIT Health Sciences & Technology Faculty, and core member of the Wyss Institute. His many awards include a Rhodes Scholarship, a MacArthur Genius Award, a National Institutes of Health Directors Pioneer Award. Jim is also an elected member of the National Academy of Sciences, the National Academy of Engineering, the National Academy of Medicine, the American Academy of Arts & Sciences, as well as a charter fellow of the National Academy of Inventors.

Don Cleveland Ph.D.

Don Cleveland Ph.D. is an award-winning inventor and pioneer in the field of Antisense Oligonucleotide (ASO) and their uses in gene therapy. He was recently awarded the Breakthrough Prize in Life Sciences for his work on the pathogenesis of disease and ASO-mediated treatment approaches in ALS and Huntingtons disease. Don is currently Professor of Medicine and Department Chair of Cellular and Molecular Medicine and Neurosciences at the University of California at San Diego, and Head, Laboratory for Cell Biology at the San Diego branch of Ludwig Cancer Research. He has made pioneering discoveries on the mechanisms of chromosome movement and cell-cycle control during normal cellular division, as well as the principles of neuronal cell development and the relationship to defects that contribute to inherited neurodegenerative disease.

About Shape Therapeutics, Inc.

Shape Therapeutics, Inc. is creating the worlds leading RNA and protein targeting platforms focused on the cure of human diseases. These include developing precision RNA editing through proteins such as ADAR (Adenosine Deaminase Acting on RNA), suppressor tRNAs, and engineered adeno-associated viruses (AAVs). The RNAfix technology allows for the editing of RNA using natural human cellular machinery, limiting the risk associated with immunogenicity, cellular toxicity, or off-target DNA editing. The teams founders include Prashant Mali, Ph.D., Francois Vigneault, Ph.D., and John Suliman. ShapeTx is headquartered in Seattle, Washington, with a satellite site opening in Cambridge, Massachusetts. For additional information, visit http://www.ShapeTx.com.

About NEA

New Enterprise Associates, Inc. (NEA) is a global venture capital firm focused on helping entrepreneurs build transformational businesses across multiple stages, sectors, and geographies. With more than $20 billion in cumulative committed capital since the firm's founding in 1978, NEA invests in technology and healthcare companies at all stages in a company's lifecycle, from seed stage through IPO. The firm's long track record of successful investing includes more than 225 portfolio company IPOs and more than 375 acquisitions. For additional information, visit http://www.nea.com.

About CureDuchenne Ventures

CureDuchenne Ventures supports Duchenne research by using philanthropic donations to encourage the development of new Duchenne drugs. Through an impact financing model, we can provide equity or royalty financing to biotech and pharmaceutical companies. CureDuchennes portfolio includes 16 wide-ranging projects with several successful exits. Investments from CureDuchenne Ventures have successfully de-risked and leveraged more than $2.3 billion in follow-on financing from venture capital, biotech, and pharmaceutical companies to fund emerging projects to find treatments for Duchenne. For additional information, visit https://www.cureduchenne.org/ventures/.

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Shape Therapeutics, Inc. Raises $35.5M Series A Financing, Led by NEA and Announces the Formation of a World-Class Scientific Advisory Board, to...

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Reddit’s r/science community is one of science writing’s biggest outlets, with the stats to prove it – Massive Science

Sunday, November 10th, 2019

Have you ever wondered why you wash your rice or soak it overnight before cooking it? Perhaps you wash your rice grains to enhance taste, reduce starch levels, or maybe that's just the way your family has always prepped rice. Thanks to a tip from science communicator Samantha Yammine who came across Dr. Nausheen Sadiq's neat finding while live-tweeting a forum on Diversity and Excellence in Science it turns out there is another reason why, as washing rice actually helps reduce the concentration of heavy metals, like chromium, cadmium, arsenic, and lead.

Heavy metal contamination in crops can be caused by human activities, such as mining, fertilizers, pesticides, and sewage sludge. Compared to most cereal crops though, rice (Oryza sativa L.) actually accumulates more heavy materials, like cadmium or arsenic, where long-term heavy metal intake can cause health risks. For example, long-term arsenic exposure leads to skin disease, high blood pressure, and neurological effects. This is especially important to consider as rice is a staple food across the globe.

Heavy metal contamination in crops can be caused by human activities, such as mining, fertilizers, pesticides, and sewage sludge.

Photo by TUAN ANH TRAN on Unsplash

In a recent study, researchers investigated the effects of different cooking methods (normal, high-pressure and microwave cooking) on the concentration, bio-accessibility and health risks posed by three heavy metals (cadmium, arsenic and lead) in two strains of brown rice. After cooking 100 grams of brown rice grains, researchers evaluated bioaccessibility (i.e. how much of the heavy metal is released for absorption) by mixing rice samples with simulated gastric fluid, and then used spectrometery to measure heavy metal concentration. Lastly, the researchers calculated the health risk posed by the heavy metals by calculating values such as the average daily dose.

Overall, the researchers found that instead of the three different cooking methods, it was the washing process which significantly reduced concentrations of cadmium, arsenic and lead, suggesting that the reduction may be due to rice morphology. For example, lead is found largely in the outer compartments of rice kernels, so lead is more likely to be removed during rice washing.

In contrast, the three cooking methods did impact bioaccessibility i.e. how much of the heavy metal would be released for absorption by the body. Here, washing and soaking isn't enough as rice absorbs water poorly at 25C. This finding was also reflected in calculated values: the average daily doses of cadmium, arsenic and lead were lower in washed and cooked rice, compared to raw rice.

It's worth noting that the European Commission has enforced limits on heavy metal levels - for example, arsenic is currently limited to 200 parts per billion (ppb) for adults and 100 ppb for infants. Both the U.S. and Canada currently have no limits in place for arsenic in food though Canada is currently reviewing a proposal to add maximum levels for arsenic found in white and brown rice, while the U.S. FDA has previously released a (non-binding) risk assessment, suggesting the same 100 ppb levels as Europe.

So the takeaway here is that yes, your family and all those professional chefs have been right all along. Yes, washing rice involves sacrificing some of its nutritional value, but doing so means you can reduce the levels of heavy metals present in grains, and still enjoy dishes like rice cakes. And returning back to Yammine's reporting, Saudiq actually shared that by soaking and washing rice for ~5 mins, you can get rid of 50-100% of these elements. (Thanks Sam!)

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Reddit's r/science community is one of science writing's biggest outlets, with the stats to prove it - Massive Science

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