Category Archives: Genetics

Maize is a staple food all over the world. In the United States, where its better known as corn, nearly 90 million acres were planted in 2018, earning $47.2 billion in crop cash receipts.

But, under the effects of climate change, this signature crop may not fare so well. As the world tries to feed a population skyrocketing to nine billion by 2050, that has major implications. So, what can we do about it? The answer might be exotic.

A multi-institutional team led byUniversity of Delaware plant geneticist Randy Wisserdecoded the genetic map for how maize from tropical environments can be adapted to the temperate U.S. summer growing season. Wisser sees these exotic varieties, which are rarely used in breeding, as key to creating next-era varieties of corn.

The research team included scientists from UD, North Carolina State University, University of Wisconsin, University of Missouri, Iowa State University, Texas A&M University and the U.S. Department of Agriculture-Agricultural Research Service.The resulting study, highlighted by the editorial board of Genetics, provides a new lens into the future viability of one of the worlds most important grains.

If we can expand the genetic base by using exotic varieties, perhaps we can counter stresses such as emerging diseases and drought associated with growing corn in a changing climate, says Wisser, associate professor in UDsDepartment of Plant and Soil Sciences. That is critical to ensuring ample production for the billions of people who depend on it for food and other products.

Modern maize strains were created from only a small fraction of the global maize population. This limited infusion of diversity raises concerns about the vulnerability of American corn in a shifting climate. TheU.S. Department of Agriculture (USDA) seed bankincludes tens of thousands of varieties, but many are just not being used.

We know that the tropical maize varieties represent our greatest reservoir of genetic diversity, says study co-author Jim Holland, a plant geneticist with the USDA Agricultural Research Service at North Carolina State. This study improved our understanding of those genetics, so we can use this information to guide future breeding efforts to safeguard the corn crop.

Certain exotic strains of maize better handle drought or waterlogging or low-nitrogen soil, for example. But because these strains have evolved outside the U.S., they are not immediately suited to states like Delaware. So, exotics first need to be pre-adapted.

In prior work, Wisser and his colleagues showed how 10 years of repeated genetic selection was required to adapt a tropical strain of maize to the temperate U.S. Co-author Arnel Hallauer spent a decade adapting the population through selective breeding, so it could flourish in an environment like Delaware.

Whats so cool now is that we could go back to the original generations from Hallauer and grow them side by side in the same field, Wisser says of the first-of-its-kind experimental design. This allows us to rule out the influence of the environment on each trait, directly exposing the genetic component of evolution. This has opened a back to the future channel where we can redesign our approach to developing modern varieties.

While extremely impressive, a decade to adapt exotic maize to new environments is a lot of time when the climate change clock is ticking.

Unfortunately, this process takes 10 years, which is not counting ongoing evaluations and integrating the exotic variations into more commonly used types of maize, Wisser says. With the climate threats we face, thats a long time. So, gaining insights into this evolutionary process will help us devise ways to shorten the time span.

Accelerating Adaptation

Wisser isnt wasting any time as he explores ways to bolster corns ability to survive and thrive. He and Holland are working on a new project to cut that time span in half.

In cutting-edge research funded by theU.S. Department of Agricultures National Institute of Food and Agriculture, the team is analyzing how corn genomes behave in a target environment as they aim to formulate a predictive model for fitness.

What were doing is sequencing the genomes and measuring traits like flowering time or disease for individuals in one generation. From this, we can generate a lookup table that allows us to foresee which individuals in the next generation have the best traits based on their genetic profiles alone, Wisser says. And our lookup table can be tailored to predict how the individuals will behave in a particular environment or location like Delaware.

That means plant breeders could grow a second generation of corn anywhere outside of Delaware, but still predict which individuals would be the most fit for Delawares environment.

For instance, even if the plants are grown at a location where a disease is not present, our prediction model can still select the resistant plants and cross them to enrich the genes that underlie resistance, Wisser says.

With this approach, researchers dont have to wait out a Delaware winter, so they can continue to pre-adapt the population for at least one extra generation per year. Thats how 10 years of selective breeding for pre-adaptation could become five, providing a quicker route to access exotic genes.

This new effort connects to theGenomes To Fields (G2F) Initiative, developed in 2013 for understanding and capitalizing on the link between genomes and crop performance for the benefit of growers, consumers and society.

If Wisser and Holland can develop a method to rapidly pre-adapt exotics, this opens a lane for G2F to test the impact of these unique genomes on crop performance.

Our goal is to advance the science so breeders can draw on a wider array of the diversity that has accumulated across thousands of years of evolution, explains Wisser, who has been involved in the public-private initiative since its beginning. In turn, they can produce improved varieties for producers and consumers facing the challenges of climate change.

Visit link:
Researchers Uncover the Genetics of How Corn Can Adapt Faster to New Climate - Seed World

Dr. Yujen Edward Ted Hsia, a pioneer in medical genetics at the University of Hawaii who shepherded his patients and students through that challenging field with warmth and grace, has died at age 88.

Ted had an uncanny ability to praise, scold and teach in one sentence all with a smile on his face, said Janet Berg, a genetic metabolic nurse who was one of his protegees. He was passionate about his patients and his colleagues and treated us all as family.

Hsia suffered a brain bleed and fall Feb. 11 at his residence in Arcadia, where he had moved a few months ago, according to Duncan Hsia, one of his five sons.

He is definitely the father of genetics in Hawaii, said Dr. Laurie Seaver, a geneticist and former colleague. He essentially built the clinical genetics program at Kapiolani (Medical Center). He was as smart as anyone I have ever known.

Medical genetics involves diagnosing, treating and managing hereditary and metabolic disorders, from birth defects to genetic diseases.

Each patient that came to him was like a puzzle, and he was trying to put all the pieces together to figure out what was going on with them, Berg said. He was never afraid to try something new.

Its body, mind and spirit he told me that all the time, she added. We can do the science all we want, but if the rest isnt OK, we are not going to get very far.

Born in Shanghai on Nov. 24, 1931, Hsia was educated in England, earning his undergraduate and medical degrees from Oxford University. He taught genetics at Yale University for a decade before joining the University of Hawaii, where he was a professor of genetics and pediatrics.

He started and ran the medical genetics program in Hawaii from 1977 to 1998, teaching genetics to all the medical students and also treating and counseling many children and their families, Duncan Hsia said.

Ted Hsia helped launch Hawaii Community Genetics, a clinical collaboration among Kapiolani Medical Center, the Department of Health and the UH Medical School.

In retirement, Hsia shared his expertise with an eager set of learners often overlooked by society: the inmates at the Womens Community Correctional Facility.

For 18 years he visited the prison weekly, helping the women understand issues such as the genetic components of disease, from cancer to bipolar disorder, as part of the Total Life Recovery Program.

He was super dedicated, said Tammy Turcios, chaplain and director of that program. Even up to the last week before he passed away, he was trucking on up that hill.

He taught them about what drugs do to their brain, about any kind of disease, she said. He always came prepared with a lesson that captivated the women. They just loved his class.

His son Duncan said his personality as well as his intelligence set him apart: He was always smiling and so friendly and generous.

As word spread of his death, former patients weighed in with social media posts. Im alive because of him, wrote Jason Taylan.

Hsias faith anchored his life. He and his late wife, Juliet, a pioneering genetics counselor herself, joined Calvary-by-the-Sea Lutheran Church when they arrived in Honolulu. He gave keiki talks at services, calling children to the front of the sanctuary and offering lessons for them and the congregation.

A baritone, Hsia was a devoted member of the church choir, and he also performed with the Honolulu Symphony Choir.

Everybody just loves his smile, said Gordon Hsia, his youngest son. The main reason why my father was smiling was that he always had faith with God in his heart. The balance of being a geneticist and having such a strong faith in the Lord is just amazing.

Seaver, who visited Hsia a few weeks ago from her home in San Antonio, said he was proud to tell her that his former students were now taking care of him as doctors.

His survivors include sons Martin, Calvin, Franklin, Duncan and Gordon; and 12 grandchildren.

A memorial service will be held Sunday at 4 p.m. at Calvary-by-the-Sea Lutheran Church. In lieu of flowers, donations may be made to the Ted &Juliet Hsia Foundation, 1177 Queen St. No. 2002, Honolulu 96814.

Read more:
Dr. Y. Edward 'Ted' Hsia is remembered as 'father of medical genetics in Hawaii' - Honolulu Star-Advertiser

A genetics engineering company in Texas, US, has come forth with claims that it has developed a vaccine for the Novel Coronavirus (COVID-19).

As reported by the New York Post, Greffex Inc. says it has completed the vaccine this week at its laboratory in Aurora, Colorado. These comments were made by the companys Chief Executive Officer, John Price, who recently spoke to the Houston Business Journal.

In the report, Price explained that what they have is a possible cure that was developed using adenovirus-based vector vaccines. What this means is that the vaccine was not developed using a living or killed virus.

The trick in making a vaccine is can you scale the vaccine that youve made to be able to make a certain number of doses, can you test that vaccine quickly and efficiently and then can you get it into patients. And thats where we have an edge as well on the other companies that are out there, Price claimed in the report.

Price further reported that the vaccine will go to animal trials, overseen by the Food and Drug Administration (FDA) in the US and other regulatory bodies in China and other heavily affected countries.

At this time, the World Health Organisation (WHO) has not released any comments in this regard.

South Korea has become the second country, outside of China, with the highest number of reported coronavirus cases. Currently, the number of infected patients stands at 204.

On Friday, South Korean health officials confirmed 100 new cases, 87 of which were connected to a church in Daegu, a city with a population of 2.5 million people.

As reported by the New York Times, the church has more than 200 000 members worldwide and at this time, it is not known if there are any others from the church who may be infected.

According to the latest figures that came in from WHO on Friday, the coronavirus has claimed an estimated 2,247 lives, with tens of thousands more infected.

Here is the original post:
Coronavirus: Texas genetics company claims to have created a vaccine - The South African

DNA testing kits for humans and their pets are a growing business. The draw for consumers ranges from understanding why their dog looks like a Labrador but acts like a German Shepherd, or what diseases they might be prone to.

For a nominal fee, individuals collect saliva from their pet and mail it to the testing company. A lab extracts DNA from the sample, which is then analyzed at many sites within the genome, called single nucleotide polymorphisms (SNPs, and pronounced snips). SNPs are places in the DNA sequence where there is a genetic variant.

In humans, SNPs occur approximately every 1,000 base pairs of DNA, which means there are about five million SNPs in each person. Dog testing kits may analyze more than 20,000 SNPs to determine breeds.

We can apply the same approaches used in these DNA testing kits to wildlife conservation and management. My research in conservation genetics has used genetic testing in several projects, including tracking raccoons movements to understand the spread of raccoon rabies.

Because DNA is inherited from parents, siblings will share more genetic variants with each other than they would with anyone else. The more related individuals are, the more variants they have in common. Through analyzing known dog breeds, DNA testing companies know which SNP variants are more common within a breed.

For dog testing kits to be most effective, they require a large database of DNA samples from individuals of known breeds to develop baseline data. This is a challenge for wildlife researchers because access to samples is difficult. Wildlife researchers often employ creative techniques to obtain DNA samples, such as hair traps for bear samples or collecting caribou scat.

Another obstacle is knowing where the genetic variants are found in the genomes of most wildlife species. Thankfully, the importance of genomic information for human health has driven advances in DNA sequencing. This has lowered the costs and improved access to technology that was once too expensive.

Knowing where individuals originate can be very important for wildlife conservation and management. For example, researchers used SNPs to identify different stock populations of Atlantic cod throughout the North Atlantic. Their genetic assessment of populations could be used to track fisheries activities and identify illegal harvesting, which is nearly impossible to do without DNA information yet critical to ensure healthy stocks into the future.

To identify risk factors in dogs, researchers compare genetic variation in individuals with and without the disease or condition, such as the potentially devastating rupture of the anterior cruciate ligament. These are called genome-wide association studies.

There are a number of examples in nature where disease is resulting in significant loss of species biodiversity. The chytrid fungus (Batrachochytrium dendrobatidis) affects amphibian populations worldwide, resulting in global declines. White-nose syndrome, caused by the fungus Pseudogymnoascus destructans, has resulted in declining bat populations in North America. Chronic wasting disease, which affects deer, is considered an emerging threat to global biodiversity.

The identification of genetic variants that are associated with disease resistance in these systems would help wildlife managers understand disease spread. This could, in turn, identify what options may be available for management of the disease and the affected species.

There are a growing number of examples that demonstrate the feasibility of this approach, such as in the case of infectious upper respiratory tract disease in gopher tortoises. Researchers can use this information to identify tortoises that are resistant to the infection and include them in breeding programs for this endangered species.

The importance of genomic research for humans has helped to drive improvements in the technology that make it more cost-effective to study wildlife species. While there are a number of challenges that researchers face in using DNA, the benefits to wildlife conservation and management are clear.

Continue reading here:
How genetic testing is helping scientists save animals from disease and illegal hunting - The Conversation CA

Seattle Genetics in-licenses antibodies from Five Prime. Credit: Pixnio.

California-based Five Prime Therapeutics has signed a global license agreement with Seattle Genetics regarding a family of monoclonal antibodies for a single solid tumour target.

According to the terms of the agreement, Seattle Genetics will pay Five Prime $5m for exclusive rights to the antibodies, which the former will use to develop and commercialise novel antibody drug conjugate (ADC) therapies.

Seattle Genetics will be solely responsible for the research, development, manufacturing and commercialisation of the ADCs. However, Five Prime will be eligible for up to $525m in future development and regulatory milestone payments, as well as single-digit tired royalties.

Five Prime chairman and interim chief executive officer William Ringo said: We are pleased to enter into this license agreement with Seattle Genetics, a global leader that develops and commercializes transformative targeted cancer therapies that utilize its industry-leading ADC technology.

This agreement allows Five Prime to realize value from our pre-clinical pipeline while prioritizing our clinical investments based on upcoming data readouts for our programs.

Looking to the future, we will continue to seek strategic partnerships that allow us to maximize the value of our assets and the long-term potential of the company.

Seattle Genetics has a proprietary ADC technology platform, which it has leveraged for a range of biotech and pharma collaborations, including AbbVie, Roches Genentech and Genmab.

Five Prime also has a strong history of pharma collaborations, most notably with Bristol-Myers Squibb (BMS). The core of the BMS-Five Prime partnership is combining the formers Opdivo with Cabira in various solid cancers.

Most recently, Five Prime announced investigational antibody Cabira (cabiralizumab) plus Opdivo failed to meet its primary endpoint in a Phase II trial.

Five Prime vice-president and chief medical officer Helen Collins said: Pancreatic cancer is a difficult disease to treat, and unfortunately the combination of cabiralizumab and Opdivo with and without chemotherapy did not show any meaningful benefit over standard of care chemotherapy in this randomized, controlled Phase 2 trial.

We are disappointed by this outcome and appreciate the participation of the investigators, staff, patients, caregivers, and our development partner who all contributed to the conduct and completion of this Phase 2 clinical trial.

Follow this link:
Seattle Genetics in-licenses some of Five Prime's antibodies for $5m - pharmaceutical-technology.com

The key to a better understanding of schizophrenia may exist in a genetic disorder so rare that researchers havent been able to conduct an adequate study until now.

The genetic disorder 22q11.2 deletion syndrome (22q11DS), caused by a small segment of missing DNA on chromosome 22, is the strongest known genetic risk factor for developing schizophrenia. About a quarter of people with the disorder develop schizophrenia or experience psychotic symptoms, so studying it provides a unique window into how such psychiatric problems develop over time.

But theres one problem: Only about one in 4,000 people have it. Even a large city like Los Angeles may hold just a few hundred people with the condition.

Fortunately, the Enhancing Neuro Imaging Genetics through Meta-Analysis (ENIGMA) consortium, led by Paul M. Thompson, PhD, associate director of the Mark and Mary Stevens Neuroimaging and Informatics Institute (INI) at the Keck School of Medicine of USC, has spent the past 10 years uniting researchers around the world to pool data and insights on rare diseases. Now, ENIGMA has launched a new working group to study 22q11DS using data collected by researchers across the U.S., Canada, Europe, Australia and South America.

Weve pieced together many of the major research centers studying 22q11DS around the world to create the largest-ever neuroimaging study of the disorder, said Christopher Ching, PhD, a postdoctoral researcher at the INI and lead author of the working groups latest study.

Thompson, Ching and the ENIGMA 22q11.2 Deletion Syndrome Working Group published their results in the American Journal of Psychiatry on Feb. 12.

Correlations become clear with advanced neuroimaging

To get a clear picture of the brain abnormalities associated with schizophrenia in individuals with 22q11DS, the studys authors examined magnetic resonance imaging (MRI) scans from 533 people with the disorder and 330 healthy control subjects. Using advanced analytic techniques developed at the USC INI, the authors measured and mapped structural differences between the brains of the two groups.

Overall, individuals with 22q11DS had significantly lower brain volumes, as well as lower volumes in specific structures including the thalamus, hippocampus and amygdala, compared with the control group. They also had higher volumes in several brain structures. The magnitude of these abnormalities, especially in those 22q11DS individuals that had psychosis, was larger than is typical in many other common psychiatric conditions.

Notably, the brain changes seen in people with 22q11DS and psychosis significantly overlapped with the brain changes observed in the largest-ever neuroimaging studies of schizophrenia and other serious mental illnesses including bipolar disorder, major depression and obsessive-compulsive disorder.

Thats important because these overlapping brain signatures add evidence to support 22q11DS as a good model for understanding schizophrenia in the wider population, Ching said. And thanks to these large ENIGMA studies, we now have a way to directly compare standardized brain markers across major psychiatric illnesses on an unprecedented scale.

This powerful connection means that studying 22q11DS may provide a clear path toward finding a biomarker, or a reliable biological indicator, of schizophrenia. Because of the large sample size used in the analysis, the researchers also found that larger segments of missing DNA in 22q11DS are linked to more extensive brain abnormalities.

Next steps in research

Looking forward, the studys authors aim to explore the similarities between brain abnormalities in individuals with 22q11DS and those with schizophrenia, bipolar disorder, major depressive disorder and obsessive-compulsive disorder, drawing on data from other ENIGMA groups to better understand whether various psychiatric illnesses may share common origins and affect similar or distinct brain circuits.

The group also plans to use these new analytic tools to explore 22q11DS in animal models, where they can conduct more controlled experiments to better understand the effects of the missing DNA segments across development.

We can even experimentally manipulate specific genes within the locus to better understand how and when they are affecting the development of these brain structures, said Carrie Bearden, PhD, professor of psychiatry and biobehavioral science and psychology at the University of California, Los Angeles, chair of the working group and corresponding author of the study.

Zara Greenbaum

The study was funded by NIHgrantU54EB020403 from the Big Data to Knowledge (BD2K) Program, NIMH Grant RO1 MH085953, and NIA T32AG058507.

Go here to read the rest:
Remote collaborative research drives new insights on a rare genetic disorder linked to schizophrenia - USC News

Dwarf woolly mammoths that lived on Siberia's Wrangel Island until about 4,000 years ago were plagued by genetic problems, carrying DNA that increased their risk of diabetes, developmental defects and low sperm count, a new study finds.

These mammoths couldn't even smell flowers, the researchers reported.

"I have never been to Wrangel Island, but I am told by people who have that in the springtime, it's just basically covered in flowers," study lead researcher Vincent Lynch, an assistant professor of biological sciences at the University at Buffalo in New York, told Live Science. "[The mammoths] probably couldn't smell any of that."

Related: Mammoth resurrection: 11 hurdles to bringing back an ice age beast

Wrangel Island is a peculiarity. The vast majority of woolly mammoths died out at the end of the last ice age, about 10,500 years ago. But because of rising sea levels, a population of woolly mammoths became trapped on Wrangel Island and continued living there until their demise about 3,700 years ago. This population was so isolated and so small that it didn't have much genetic diversity, the researchers wrote in the new study.

Without genetic diversity, harmful genetic mutations likely accumulated as these woolly mammoths inbred, and this "may have contributed to their extinction," the researchers wrote in the study.

The team made the discovery by comparing the DNA of one Wrangel Island mammoth to that of three Asian elephants and two other woolly mammoths that lived in larger populations on the mainland.

"We were lucky in that someone had already sequenced the [Wrangel mammoth's] genome," Lynch said. "So, we just went to a database and downloaded it."

After comparing the mammoths' and elephants' genomes, the researchers found several genetic mutations that were unique to the Wrangel Island population. The team had a company synthesize these tweaked genes; then, the researchers popped those genes into elephant cells in petri dishes. These experiments allowed the researchers to analyze whether the proteins expressed by the Wrangel Island mammoth's genes carried out their duties correctly, by sending the right signals, for instance, in the elephant cells.

The team tested genes involved in neurological development, male fertility, insulin signaling and sense of smell. In a nutshell, the Wrangel Island mammoths were not very healthy, the researchers found, as none of those genes carried out their tasks correctly.

That said, the study looked at only one Wrangel Island mammoth, so it's possible that this individual's comrades didn't have similar genes. But "it's probably unlikely that it was just this one individual that had these defects," Lynch said.

In fact, the case of the Wrangel Island mammoths is a cautionary tale about what can happen to a population that is too small and therefore lacks genetic diversity, he said.

The findings build on those from a study published in 2017 in the journal PLOS Genetics that found that the Wrangel Island mammoth population was accumulating damaging mutations.

The new study was published online Feb. 7 in the journal Genome Biology and Evolution.

Originally published on Live Science.

Originally posted here:
The last woolly mammoths on Earth had disastrous DNA - Livescience.com

It was funny once. The perfectly square bit of dirt on the window. The shocked reactions of Craggy Islands Chinese community. The local farmer who doesnt have much time to be a racist, because he just likes to have a cup of tea in the evening. The feckin Greeks

Dermot Morgans finest televisual moment that evocation of Nazi speech-making in front of the greatest window in comedy is perhaps a little less funny now that prime minsters or presidents of Hungary, Turkey, the United Kingdom and the United States are happy and comfortable to spout racist statements, and not merely get away with it but be applauded for it by their supporters.

How have we reached this point? Its the very question asked by geneticist and broadcaster Dr Adam Rutherford. Hes the Rutherford in the BBCs popular radio programme The Curious Cases of Rutherford and Fry, in which he and Dr Hannah Fry try to solve listeners scientific queries.

In the case of the resurgence of publicly acceptable racism, Rutherford decided that a radio show was insufficient and that a book would be needed. How to Argue with a Racist is published this week, and Rutherford will be delivering a lecture on the subject during the Northern Ireland Science Festival.

So, how did we get back here? I find myself asking the same question, Rutherford says. I find myself in lectures thinking how strange it is that Im now talking about this, because these are mostly questions that were parked, in my field genetics years ago. Maybe decades ago. And we keep discovering interesting things about evolution and population differences, and migration, and so on, but the question of how race as a concept relates to biological diversity, that ended a while back.

Having these conversations in the academy is one thing, but as someone who tries to communicate science, to talk about it, as a broadcaster and as a writer, I found I was suddenly having very different conversations. Conversations about race, when we were talking about ancestry In some ways, science has failed to convey to the public what is correct, and so I want to equip people with what current scientific thinking is, so that when the question comes up, they have the tools to respond. To say, Yes, there hasnt been a white man in the Olympic 100m final since 1980, but no thats not because of any lack of African-American ancestry.

Its precisely that sort of casual, inauspicious racism that Rutherford looks to quash with his book. The idea that Olympic athletes with African heritage are somehow better because their genes are imbued with extra strength is rubbish, he says. For a kick-off, using athletes as a test sample is a daft idea because anyone with the sort of genetic gifts that allow them to perform at the highest level is a poor sample of what a broader population is like. Beyond that, theres a simpler rebuttal if those with African heritage are inherently genetically better at running very quickly than others, then where are the Olympic 100m champions from South America, Europe or elsewhere with populations that can trace heritage to Africa?

Besides, tracing your genetic lineage in that manner, looking for secrets and answers to why you are so underprivileged compared with others, is a nonsense, says Rutherford. I do think that part of the change in culture which means I kind of had to write this book is to do with the rise of nationalism and the more open discussion of race. Certainly there are more open discussions of public racism than at any point I can remember in my lifetime. There are other factors, though, such as the rise in genetic ancestry testing kits. Now, theyre not pernicious in themselves, but I argue that they have fostered a misunderstanding of what genetics means, and specifically in the form of a sort of reversion to essentialism. So a notion that were determined by our genes and our ancestry, which as a geneticist I just dont think are scientifically valid nor verifiable to the extent that people adopt them.

So, when you take one of these tests and it comes back saying that youre 10 per cent Swedish, or 15 per cent Irish, these are very broad strokes, that are not scientifically meaningless, but they are of only trivial relevance. But people attribute very great significance to them. For instance, I sometimes talk about the fact that, genetically speaking, there is no such coherent ancestral group as Celts. But try telling that to an audience in Glasgow and see what happens.

Over in Ireland youve got some of the best genetic genealogists in the world, people like Dan Bradley [head of the school of genetics at Trinity College Dublin] who has been tracking the story of the Irish for years, and thats really important work, its important to understand the movement of peoples and the migration of peoples. But theyre always complex. Ancestry is a matted web, not linear family trees.

For example, I have a friend who told me that hes descended from Niall of the Nine Hostages, and they can trace their ancestry back to him. Well, theres two things about that. One, no one is actually really sure if Niall of the Nine Hostages existed, which is problematic for a starter.

The second thing, though, is that if he did exist, he lived in the fourth or fifth century, and thats a date which comes before the isopoint, which is the time at which everyone in Europe is descended from everyone else. So if Niall did exist, and if my friend Bill is directly descended from him, then so too am I. And so are you. And so is a guy in southern Italy, and in Turkey, and literally everyone else in Europe. So if you can attach some kind of tribal identity to that, that idea that youre descended from some fifth-century Irish king, well everyone else is too.

This is a relatively recent revelation. One that has the power to stun those who claim kinship with any royal lineage, or who might have notions of racial purity. The simple, genetic, fact is that your family tree isnt a neat family tree at all. Its more like an overgrown shrub, especially the farther back you go. And because everyone elses is, too, it means that the family shrubs intertwine and merge until, once you go back a surprisingly few generations, were all related to everyone else.

Thus the late actor Christopher Lees claim to be directly descended from Charlemagne is accurate, but also meaningless. Not everyone can prove it using family trees. Christopher Lee could, because he was the descendent of an Italian contessa, so they had the paper trail of her family going back. The whole Danny Dyer story, which showed that he was a direct descendent of Edward III, they were able to paper-trail that too, and very few people can actually do that, but I calculated out a mathematical proof that anyone with long-standing English heritage is also 100 per cent descended from Edward III.

At which point I suggest that we should use our now undisputed and mathematically proven royal lineage to, shall we say, take back control, but Rutherford politely declines my invitation to insurrection. The point is, of course, more profound than working out where you stand in line for a throne. Its the fact that every white supremacist has, if you trace their genetic code back, African ancestry. Every Nazi has Jewish heritage. Every Briton is a mish-mash of European bloodlines.

The problem, of course, is that while all of this science is correct and provable, its also useless in the face of racism. As someone once said: You can argue with a racist; you can argue with a Labrador retriever, too, for all the good it will do you.

Rutherford agrees, but says theres a more important battle, on two fronts, to be fought. Part of the book discusses actual neo-Nazis and white supremacists, because they are obsessed with genetics. And their misunderstanding of genetics makes them think that they can prove some sort of racial purity, which is a nonsense. Arguing with those guys using science is a demonstration of the old Jonathan Swift maxim that you cant reason someone out of a position that they didnt reason themselves into, he says.

Who Im really interested in reaching, though, are those who arent racists, and who dont think like that. But because of relying on stereotypes, or myths, or the cultural sphere that says that race is real, or that some factors are biologically encoded and that those factors segregate by race, I want those discussions to be the ones that are informed by science. Because those people arent fundamentally racist, so when youre armed with facts, and youre armed with a knowledge of history, then I think that is your best route to change. Science is a powerful ally, its the best ally we have, I think. But whats the Bob Dylan line? I know my song well before I start singing.

One of the ideas I explore is that scientists need to get more involved. Its no longer good enough to simply say: Heres the data and let society decide. Racists have no such compunctions, and will use every tool at their disposal to spread their message. So if we. as scientists, sit back and say, Hey, its just the data and I dont know what the political ramifications are, thats for others to discuss, then were volunteering ourselves to defeat, and for our voices to be silenced in favour of populist, emotive arguments, and thats the political landscape in which we now live.

Racism isnt wrong because its drawn from and based on a misunderstanding, or specious scientific ideas. Racism is wrong because its an affront to basic human dignity. What Im saying is, if you want to be a racist, fine, fill your boots, go ahead, but you cant have my scientific tools, my weapons, to justify your position.

How to Argue with a Racist by Adam Rutherford is published by Orion. Northern Ireland Science Festival runs February 13th-23rd. nisciencefestival.com

The rest is here:
How to turn racists genetic arguments against them - The Irish Times

MEDIA CONTACT

Available for logged-in reporters only

Feature

MEDICINE

Newswise (Indianapolis, IN) Nearly half of all U.S. adults have some type of cardiovascular disease. Its a heartbreaking statistic literally and figuratively. People often believe their risk for heart disease cannot be reduced if they have a genetic predisposition. In honor of American Heart Month, the American College of Sports Medicine (ACSM) and ACSM Fellow Beth A. Taylor, Ph.D., have teamed up to shatter this heart myth.

The truth about the heritability (or genetic component) of heart disease is a glass far more full than empty, as long as we look at it accurately, says Dr. Taylor, associate professor of kinesiology at the University of Connecticut and the director of exercise physiology research at Hartford Hospital.

Genetics do play a significant role in increasing heart disease risk. Research shows that individuals at high genetic risk have a 91% higher chance of experiencing a cardiac event, yet that risk can be cut nearly in half by adopting healthy lifestyles.

We may have genes that predispose us to cardiovascular disease, but when, how and to what extent those genes express themselves is highly influenced by lifestyle, says Dr. Taylor. Being more physically active, aiming for a healthy weight, eating a heart healthy diet and avoiding smoking can improve heart health and reduce the risk of coronary events by 46% for high genetic risk individuals.

The outlook looks even better when considering being healthy across the lifespan rather than at a single age. The Framingham Heart Study, a project of Boston University and the National Heart, Lung and Blood Institute (NHLBI), has sought to identify common factors contributing to cardiovascular disease (CVD) by following CVD development in three generations of participants.

Dr. Taylor adds, When those three generations of the Framingham Heart Study were reviewed, investigators concluded that the heritability of ideal cardiovascular health was only 13-18%, with health behaviors and lifestyle factors being much more influential.

She says other studies have found that adhering to just four out of five of healthy lifestyle factors (e.g., avoiding smoking and excessive alcohol intake, performing 30 or more minutes a day of moderate-to-vigorous physical activity, eating a heart healthy diet) increased the likelihood of living free of cardiovascular disease, as well as cancer and Type 2 diabetes, by more than 10 years in women and seven years in men.

For Dr. Taylor, the take-home message is simple. You cant completely cure a broken heart; however, you can make it better or worse based on your lifestyle. The choice is yours!

Find more heart health resources from ACSM at https://www.acsm.org/read-research/trending-topics-resource-pages/heart-health-resources.

# # #

About the American College of Sports Medicine

The American College of Sports Medicine is the largest sports medicine and exercise science organization in the world. More than 50,000 international, national and regional members and certified professionals are dedicated to advancing and integrating scientific research to provide educational and practical applications of exercise science and sports medicine. More details at acsm.org.

Visit link:
ACSM Tackles Myth on Genetics and Heart Disease as Part of American Heart Month - Newswise

On Thursday, Seattle Genetics(NASDAQ:SGEN) shared some good news regarding an experimental breast cancer drug called tucatinib. The U.S. Food and Drug Administration (FDA) will give tucatinib's new drug application a priority review.

Patients with HER2-positive breast cancer tumors that keep growing after treatment multiple rounds of standard care could have another treatment option this summer.

Image source: Getty Images

Instead of the standard 10-month process, the FDA granted tucatinib a priority review that will shave four months off the timeline. The agency's expected to announce a decision on or before Aug. 20, 2020.

The priority review the FDA gives tucatinib will most likely result in a positive approval decision on or before the FDA's action date. During the HER2Climb study that's supporting Seattle Genetics' new drug application, adding tucatinib to a standard regimen of chemotherapy plus Herceptin reduced patients' risk of death significantly. Two years after beginning treatment, 44.9% of patients given tucatinib plus standard care were still alive compared to a 26.6% survival rate for patients given standard care alone.

Roughly half of all patients with HER2-positive breast cancer develop brain tumors that are incredibly difficult to treat. Seattle Genetics' potential new cancer therapy appears to give this underserved population a fighting chance for long-term survival. During the HER2Climb trial, none of the patients with brain metastases given standard care survived past one year without signs of their disease worsening compared to an impressive 24.9% of those treated with the tucatinib-containing regimen.

Read more from the original source:
Seattle Genetics' Experimental Breast Cancer Drug Receives Priority Review From the FDA - Motley Fool