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

November 17th, 2019 12:47 am

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

November 17th, 2019 12:47 am

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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Scientists reveal why we feel so tired in the morning – Yahoo Sports

November 17th, 2019 12:46 am

If youre the type of person who snoozes your alarm every morning or cant function before (or even after) yourmorning coffee, there might be a genetic reason for that.

New research by DNA testing company,23andMe, has discovered that genetic programming plays a part in our wake up time.

The research studied over 1,500 British people to determine that 7.55am was the UKs average genetic wake up time.

This means that the average Brit willwake upnaturally just before 8am each day.

READ MORE: Drinking tea or coffee has no impact on sleep, according to study

Many people set their alarms for much earlier than that, hence our feelings of tiredness and lack of productivity.

Interrupting your bodys circadian rhythm (which is the official term for our body clock) can leave us feeling out of sorts at the beginning of the day.

If you dont feel tired first thing, it doesnt mean youre immune to these feelings. Many people have tiredness slumps at different points in the day.

READ MORE: Parents can buy children anti-nightmare mist

TheNHShas found that one in five of us get unusually tired and have suggested some good ways to wake yourself up when the slump sets in.

Exerciseis cited as one of the key ways to bolster your energy reserve. Aside from the psychological benefits of exercise, it alsolowers your risk of early death by 30%.

Cutting down oncaffeineis another recommended way to beat the tiredness. As a nation of tea drinkers, we are all at risk of being over-stimulated by the affects of caffeine. Switching to decaffeinated tea and coffee could make all the difference.

Getting into a routine of having daytime naps may also interrupt your bodys circadian rhythm. If you go to sleep every time you feel a bout of tiredness, you may struggle to get to sleep at night, so says the NHS.

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Should this deer be culled? The answer may not be what you think. – Clarion Ledger

November 17th, 2019 12:46 am

Mississippi has produced some giant bucks and even a world record. Here are the top six deer on record in Mississippi by category. Brian Broom

Studies show genetics can't be controlled in wild deer populations

It's a common debate on social media.

A hunter gets a photo on a game camera that shows a deer with a spike on one side and a normal antler on the other and asks if the deer should be removed.

Many will say the buck needs to be taken to prevent the continuation of its genesinto future generations, but biologists say that's probably not the correct answer.

Many hunters feel a buck with a spike on one side should be removed from the herd to improve genetics, but biologists say that's not the case.(Photo: Special to Clarion Ledger)

"That's almost always related to some kind of injury," said Kip Adams, Quality Deer Management Association director of conservation. "It's usually not genetic.

"Most of those are injury-related. Deer just aren't genetically built to have crazy antlers like that. Most of the time, if the animal is allowed to live, he'll drop those antlers and you won't see it in future years."

However, there are times when a malformed antler caused by injury will return after antlers are shed.

"It could," Adams said. "It could be an injury to the base. If the injury is right at the base of the antler, it could recur in future years."

Adams said a serious injury to the body can also cause a recurring abnormal antler.

"Again, none of that is genetic-related," Adams said. "So, it's not passed on.

"If you remove them you're not doing anything to change the genetics of the deer herd. The only gain you're making is providing more food for the rest of the herd by removing them."

One of the causes of pedicle, or antler base damage, that seems to be more common is what has been called "dirty sheds."

Gabriel Karns, who is currently avisiting assistant professor in the School of Environment and Natural Resources at Ohio State University, wrote an article published by QDMA about his work examining skulls of bucks with spikes on one side.

"Most commonly, it appeared that antlers had failed to cleanly separate from the pedicles, as in normally shed antlers,and that the antler base had fractured off portions of the pedicle and sometimes even the surrounding cranium those dirtysheds I mentioned earlier," Karns wrote."Although the antlerogenic periosteum tries to heal itself in advance of the next antler growing season, the integrity of the pedicle is compromised and becomes a messy combination of intact pedicle and callus tissue.

"Picture how water flows out of the end of a garden hose, then picture what happens when you partially block the nozzle with your thumb. The blood supply and nutrient flow necessary for normal antler development is impeded leading to stunted growth and irregular antler configurations due to the animals prior injury. Complicating the issue once initial damage occurs, subsequent antler cycles tend to re-aggravate the injury, resulting in repetitive abnormal antlers."

So, a spike on one side or otherwise deformed antler is likely caused by injury, but what if it isn't? What if it really is a genetic trait? Shouldn't the buck be harvested to prevent passing along that genetic trait? You can remove him, but you're not doing anything other than putting meat in the freezer.

"It's been shown over and over that you can't alter genetics in the wild," Adams said. "A buck with big antlers can sire a buck with small antlers and vice-versa. Those antler traits aren't 100 percent inheritable."

Adams' statement is backed by a study in Texas. Wild bucks were captured andmicrochipped. Samples of DNA were taken from them and they were released. Family trees of bucks were developed through DNA samples taken over a number of years. What the researchers discovered isin the wild there is no correlation between a buck's antler size and that of its offspring.

"Don't think you're making an improvement in the deer herd from a genetic standpoint," Adams said. "Hunters don't need to concern themselves or worry about it."

Deer hunting: 'It just made a good day that much better.' Father and son double down on big bucks

Win big money: You can win a share of $1,500 in the Big Bucks Photo Contest sponsored by Van's

Please, shoot them: 12 bucks on MSU Deer Lab's most wanted list. Here's why.

ContactBrian Broomat 601-961-7225 orbbroom@gannett.com. FollowClarion LedgerOutdoors on Facebookand @BrianBroom onTwitter.

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Cocker spaniel with cancer to receive stem cells from mother living 4,000 miles away – Fox News

November 17th, 2019 12:44 am

A 6-year-old cocker spaniel in California that was recently diagnosed with cancer is slated to receive stem cells from her mother living 4,000 miles away in the United Kingdom.

Coco the cocker spaniel gave birth to a litter of puppies six years ago. One of those puppies, Millie, was adopted by Serena and Andrew Lodge, who now live in San Francisco. They may live across the world from each other, but the mother and daughter will soon be reunited for the rare treatment, reported South West News Service, or SWNS, a British news agency.

CHEAPER MEDICATION FOR DOGS WITH SEPARATION ANXIETY NOW APPROVED, FDA SAYS

Coco, left, and daughter, Millie. (SWNS)

The transplant will occur at the North Carolina State Veterinary Hospital in Raleigh. The facility isreportedly one of only a few animal hospitals in the world to offer the treatment, which involves taking healthy stem cells from Cocos bone marrow and injecting them intoMillies.

"Serena and Andrew started chemo on Millie three months ago but they've been told the only chance they'll have of curing her is if they find a positive donor so she can have a transplant, said Cocos owner, Robert Alcock, 52. He arrived with Coco in North Carolina on Wednesday.

Millie while in an animal hospital. (SWNS)

"They contacted us, and we sent some blood samples for testing, along with samples from one of Coco's other pups, he added. They both came back positive but because Coco is Millie's mother the vet said she would be a better match."

"Coco will go into hospital on Sunday for the procedure and then the cells will be donated on Monday, he continued, noting the Lodges have paid for everything.

Robert Alcock and his cocker spaniel, Coco. (SWNS)

BLACK LAB GIVES BIRTH TO 13 PUPPIES, SHOCKS OWNERS: 'THEY WERE JUST FLYING OUT'

Coco is expected to make a full recovery following the procedure. However, there is only a 50 percent chance Millie will be cured even if the treatment is successful, according to SWNS.

Stem cell therapy for pets is costly, typically setting an owner back between $2,000 and $3,000, according to Pet WebMD.

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Is Stem Cell Therapy for Hip Arthritis Safe and Effective? – The African Exponent

November 17th, 2019 12:44 am

What are stem cells?

Stem cells are the raw cells of the body. Essentially, this means that the stem cells are the cells from which all other specialized cells are derived. The specialty of stem cells is that they are able to become any cell in the body. The cells of the heart, the cells of the liver, the cells of the kidney all come from the basic stem cells. Any cell that has been derived from a stem cell is called a daughter cell. Stem cells can be made to develop and divide into daughter cells in the right laboratory conditions. In recent years, there have been a lot of research about stem cell transplant for arthritis.

Is stem cell therapy safe?

Stem cell therapy is considered much safer than traditional procedures that may involve implantations. The reason for this increased safety is because of the bodys immune system. The bodys immune system is always on high alert to intercept and destroy any foreign particle in the body. Because in an implant, you are placing a foreign object in the body, there are chances that there will be rejection or high wear and tear of these objects. The success rate of stem cell therapy for hips is very high because stem cells are a part of our own body. They have our DNA, and because of that, they are not considered as foreign particles.

How do stem cells help in managing and curing arthritis?

When they are applied to an arthritic joint, the stem cells might start becoming cartilage cells that are required in the hip joint. The main reason for extreme pain in the hip joints of a person with arthritis is the degeneration of cartilage. The cartilage is a tissue that is similar to bone and helps keep the bones intact, and the hip to move freely.

The cartilage cells often become hard and brittle because of old age and start wearing out with passing time. Stem cell transplant for arthritis works by considering that the stem cells can become any specialized cell in the human body, doctors think that the stem cells will either become new cartilage cells and replace the old ones. Or the stem cells will help in slowing down the aging of the cartilage by releasing certain proteins (called cytokines). This slowing down will help reduce the pain of arthritis in the patient. When it comes to stem cell therapy vs. hip replacement surgery, It looks like stem cell therapy has a smaller number of complications that are associated with it.

The only risk of complication with using stem cell therapy for hip arthritis is swelling and infection. Infection and swelling are also major risks of having traditional hip replacement surgery. Swelling can be controlled with a few drugs that help in blood flow and will not hamper the healing of the patient. Infection, on the other hand, may pose a bigger problem and threat later on for the health. In stem cell therapy, the infection could happen if the wrong types of stem cells, for example. Pluripotent stem cells are used instead of adult stem cells. When it comes to traditional hip replacement surgery, the infection can be because of the implantation of an infected hip joint or because of the entry of any foreign particle through the cuts that have been made for the implant surgery. Considering all these factors, stem cell transplant for arthritis looks like a safer and better option.

Am I eligible for stem cell therapy for hip arthritis?

Firstly, there are not many centers around the world that have mastered the art of treating hip arthritis with stem cell therapy. There are a few surgeons and doctors who have performed stem cell therapy successfully for hip arthritis with satisfactory results. You should try and approach doctors who have already done this treatment first and have performed them with ease.

There are a lot of serious conditions that have been met with the patient who wants to take the option for stem cell transplant for arthritis. Firstly, the patient must be stable enough to undergo stem cell therapy. The stem cells have to be harvested first for this treatment to work. Harvesting may not be possible in all patients, and the patient may not be able at times to take this route of treatment for curing hip arthritis.

Is there any research going on for stem cell therapy for hip-related conditions?

There is a lot of research that is going on to identify diseases that can be cured by stem cell therapy. One of the hotly researched topics is stem cell transplant for arthritis. It will not be a very long time before stem cell therapy will become the go-to option to cure people of hip-related arteritis and other related conditions. Extensive research is happening in all major universities as well as pharmaceutical companies regarding stem cell transplant for arthritis.

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Leading Alternative Healing Director of Total Health Institute Reviews and Receives 3rd Fellowship in Stem Cell Therapy – Financialbuzz.com

November 17th, 2019 12:44 am

Chicago, IL, Nov. 14, 2019 (GLOBE NEWSWIRE) Dr. Keith Nemec the clinic director ofTotal Health Institute in Chicago has received yet another fellowship in his advanced research. Most recently Dr. Nemec received his fellowship in Stem Cell Therapy to add to his other fellowships in Regenerative Medicine and Integrative Cancer Therapies.

Dr. Nemec has overseen patient care for the last thirty-five years at Total Health Institute which is an alternative and integrative medical facility. Total Health Institute has seen over 10,000 patients who have traveled from around the world to seek Dr. Nemecs guidance in their healing journey.

Total Health Institute uses unique approach developed by Dr. Nemec called theSystems Sequence Approach to balance cellular communication between the cells, tissues, organs, glands and systems of the body. Dr. Nemec explains It is like knowing the combination to open the lock to complete healing. To open this lock, you must not only know the right systems to balance but also in the right sequence.

Dr. Keith Nemec is very excited about the research in stem cells and stem cell therapy that is why he focused his concentration in this area. According to Dr. Nemec All health and healing starts at the stem cell level. Whether a person has cancer, autoimmune disease or chronic diseases of aging they are all involving stem cells. In cancer, an inflammatory environment has mutated a normal stem cell into a cancer stem cell which is not killed with either chemotherapy nor radiation. This is why many times with conventional cancer treatment alone one tends to see improvements for a season but then return the cancer stem cell retaliates with a vengeance. Dr. Nemec also states Since all cells come from a base stem cell then the answer to all chronic disease can be found in activating the stem cells to produce an anti-inflammatory niche and continual healthy cell renewal.

Dr. Nemec is a member of the American Academy of Anti-Aging Medicine which is the largest and most prestigious group of Regenerative and Anti-Aging Medicine doctors in the world. He received his masters degree in Nutritional Medicine from Morsani College of Medicine. He has also published 5 books including: The Perfect Diet, The Environment of Health and Disease, Seven Basic Steps to Total Health and Total Health = Wholeness. Dr. Nemec has also published numerous health articles including: The Single Unifying Cause of All Disease and The answer to cancer is found in the stem cell and for 18 years he hosted the radio show Your Total Health in Chicago AM1160.

Total Health Institute boasts all 5 starreviews on RateMDs, an A+ rating onBBBand is top rated on Manta.

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The genetic basis of Peruvians’ ability to live at high altitude – Ars Technica

November 15th, 2019 8:46 pm

Enlarge / Many Peruvians are well adapted to high-altitude life in the Andes.

Eric Lafforgue/Art in All of Us

Sherpas are physiologically adapted to breathing, working, and living in the thin air of the Himalayas, enabling them to repeatedly schlep stuff up and down Mount Everest. The Quechua, who have lived in the Andes for about 11,000 years, are also remarkably capable of functioning in their extremely high homes. New work suggests that these adaptations are the result of natural selection for particular genetic sequences in these populations.

Both populations live above 14,000 feet (4,267m), under chronic hypoxialack of oxygenthat can cause headaches, appetite suppression, inability to sleep, and general malaise in those not habituated to altitude. Even way back in the 16th century, the Spaniards noted that the Inca tolerated their thin air amazingly well (and then they killed them).

Metabolic adaptations give these highlanders a notably high aerobic capacity in hypoxic conditionsthey get oxygenated blood to their muscles more efficiently. But the genetic basis for this adaptation has been lacking. Genome Wide Association Studies, which search the entire genome for areas linked to traits, had found tantalizing clues that one particular gene might be a site of natural selection in both Andeans and Tibetans. It encodes an oxygen sensor that helps cells regulate their response to hypoxia.

This new work looked for genetic variants that were more common in the Quechua population compared to white lowlanders from Syracuse, New York. The researchers then tried to correlate the variants with the Quechuas high aerobic capacity at altitude. But none of the genetic differences showed a significant association with high aerobic capacity, probably because the sample size429 Quechua and 94 lowlanderswas too small to detect one.

So the researchers subjected the data to a more sensitive statistical analysis. This analysis found five variants of the gene that were significantly associated with the Quechuas adaptive high aerobic capacity in hypoxic conditions; they also appeared significantly more frequently in the Quechua population than in lowlanders. This observation was buttressed by analysis of a second, independent cohort of Quechua compared to global populations from the 1000 Genomes Project.

All of the adaptive variants were in the regulatory region of the geneDNA that controls when and where the gene is active. None were in the part of the gene that encodes a protein. So, the location and timing of the protein's activity seems to be more important than the protein itself in the Quechua.

A number of conditions must be met to claim that a population is genetically adapted to specific conditions. First, there must in fact be an adaptation: in this case, enhanced aerobic capacity under hypoxia. Check. Next, that adaptation must be associated with a genetic variant, and that variant must occur in the population of interest at rates indicating that it is being selected for. Thats what this most recent work did.

But it has not shown that the adaptation has increased the groups fitness, in terms of improving fertility and/or limiting mortality. And it is not absolutely certain that aerobic capacity is the trait being selected for; it is possible that this gene does something else oxygen-related that is really the trait being selected for, and the observed enhanced aerobic capacity is just a bonus side-effect.

Tibetans have alterations to the protein encoded by this gene, which is intriguing. Even more intriguing is that the Tibetan variants are not associated with high aerobic capacity in hypoxia, but with low hemoglobin. Counterintuitively, this seems to help Tibetans at altitude by increasing their blood flow to an extent that compensates for the fact that the blood carries less oxygen.

PNAS, 2019. DOI: 10.1073/pnas.1906171116 (About DOIs).

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A new study hopes to prevent disease before it starts through genetics – KSL.com

November 15th, 2019 8:46 pm

HURRICANE What would life be like if you knew you would get cancer one day, but could prevent it beforehand? Clinicians in Utah are hoping to accomplish just that through a new study.

One St. George man said he's participating for the health of his posterity.

Durward Wadsworth, 76, grew up on a farm in Southern Utah. He worked alongside his family tending to the fruits trees, horses, and other animals.

"We had to milk cows and bring hay in," he said.

The farm has remained, but things have changed.

"I have a brother that passed away. I have a sister that passed away, Wadsworth said.

They both died from cancer. Wadsworth was also diagnosed with colon cancer and finished chemo only a year ago.

It's not a fun treatment, he said. He went to the Dixie Regional Cancer Center for 12 rounds of chemo.

As a teenager Wadsworth was exposed to radiation during nuclear testing at the Nevada National Security Site.

"As kids, we didn't know any different, so we would go up on the hill and watch when one would explode and you could actually see the mushroom and hear the boom, he said.

Both his family history of cancer and heart disease, and his exposure to radiation, had him concerned.

His son encouraged him to participate in Intermountain Healthcare's HerediGene population study. Clinicians hope this study, in collaboration with deCODE Genetics of Iceland, will help them better understand the human genome.

Dr. Lincoln Nadauld, Chief of Precision Health at Intermountain Healthcare, said the study is unprecedented. He said it looks at the link between genes and human disease.

"This study is the largest of its kind. It's an attempt to map the genomes of 500,000 people over the next five years, Nadauld said. There is no genetic study in health care that has ever been reported or ever attempted that compares in size or scope.

Nadauld said this study will impact generations to come.

(It) will allow us and subsequent generations to better understand health and the origins of disease and health care-related issues, he said. It's going to change the way that we deliver health care for the better.

Nadauld hopes the study will help doctors better predict and prevent disease before someone is ill.

So let's intervene with either a medicine or a lifestyle change so that you never have to experience heart failure or heart attack or a stroke, he explained.

While this type of precision genomics started in oncology, Nadauld said his team has applied it to all of their medical disciplines, including cardiovascular and neurodegenerative disorders, metabolic issues and even mental illness.

This study could uncover the link between mental illness and genes, and could identify new treatments for mental illness, he said.

Even though Wadsworth still has a lot of life to live, he knows he probably won't personally benefit from the study by the time its completed. "But, you know, my posterity will benefit, he said.

That's enough motivation for him. Wadsworth said he doesn't want his five children and 18 grandchildren to suffer through cancer like he did.

"We want the best health care for them, he said. He also hopes they'll carry on the family farm.

Nadauld said the study isn't just for people who have been sick, but will include mostly healthy individuals.

He said it just takes a simple blood draw to participate. Nadauld said by the end of the year there will be 25 different walk-in clinics across the entire state.

Nadauld said he anticipates a very small percentage of the participants will be informed of a health issue, in which doctors and patients need to take action.

We expect that will happen in about 3% of our participants, he said.

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Genetic study reveals the family secrets of people in the 1800s – New Scientist News

November 15th, 2019 8:46 pm

By Michael Le Page

Celebrating the Birth by Jan Steen, 1664. The Wallace Collection, London

In the 19th century, poorer families living in cities in Europe had a higher rate of children who werent biologically related to their legal fathers. This is according to a genetic study that looked at how this rate differs for different socio-economic groups.

It is widely assumed many men arent the biological fathers of their children. The rate of extra-pair paternity, as this is called, has been claimed to be as high as 30 per cent today. They look just like the milkman, goes the popular joke that no parent finds funny.

However, over the past two decades DNA studies in several countries have shown the average rate is low around 1 per cent. Maarten Larmuseau at KU Leuven in Belgium, who authored one of these studies, wondered whether there was a difference between groups.

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He suspected, for example, that the rate was higher among aristocrats in the 17th century, as there was often a large age gap between husband and wife. Extra-pair paternity is depicted in the 1664 painting Celebrating the Birth by Jan Steen, which shows a wealthy Dutch father holding his newborn child. But behind him a man is making the sign of the cuckolds horns, meaning the child was fathered by another.

Larmuseaus team identified 500 pairs of men in Belgium and the Netherlands where, according to genealogical records, each pair descended from the same male ancestor through a male lineage. Half of these ancestors were born before 1840 and the oldest was from 1315.

The men in each pair should have inherited their shared ancestors Y chromosome, as it comes from the father. When DNA testing revealed a mismatch, the team tested other male descendants to narrow down when a son had been fathered by someone other than the husband. All the men were volunteers and the team didnt test close relatives to avoid uncovering recent cases.

What we found was completely the opposite to what we expected, says Larmuseau.

The rate of extra-pair paternity among farmers and more well-to-do craftsmen and merchants was about 1 per cent, rising to 4 per cent among labourers and weavers and nearing 6 per cent among working class people who lived in densely populated cities in the 19th century. This was in comparison to a rate of around 0.5 per cent among the more well-off.

What the study cannot reveal is why people were more likely to be in this situation. We cannot give an explanation, Larmuseau says. We cannot interview them.

One possibility is that poorer women in cities were more vulnerable to male sexual violence and exploitation.

The overall rate was still low, at 1.6 per cent per generation. But that still means a very large number of people alive today may not be aware of their biological parentage. Larmuseau says 30 million people worldwide have done ancestry tests, which suggests up to 500,000 could have made a shocking discovery about their father. Companies offering these tests dont provide any counselling, he says.

Journal reference: Current Biology, DOI: 10.1016/j.cub.2019.09.075

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Genetics may be the reason why you hate vegetables, study shows – Yahoo Food

November 15th, 2019 8:46 pm

Cant stand the taste of vegetables? Your genes may be to blame.

Preliminary newresearchpresented at the American Heart Association (AHA) Scientific Sessions shows that a specific gene makes certain foods especially, broccoli, cauliflower, cabbage, and Brussels sprouts taste extremely bitter to some people.

The gene in question is calledTAS2R38. Everyone inherits two copies of this taste gene, but which variant of the gene you get makes all of the difference. According to the AHA: People who inherit two copies of the variant called AVI arent sensitive to bitter tastes from certain chemicals. Those with one copy of AVI and another called PAV perceive bitter tastes of these chemicals; however, individuals with two copies of PAV, often called super-tasters, find the same foods exceptionally bitter.

In the study, researchers analyzed questionnaires from 175 men and women about how often they ate certain foods and found that those with the PAV form of the gene who are more sensitive to bitter tasting foods were more than two and a half times as likely to eat the least amount of vegetables.

For super-tasters, the bitterness they taste in vegetables goes beyond being mildly annoying. A super-taster is a person who experiences a bitter taste with a much greater intensity than others,Tina Sindher, MD, an allergist and immunologist with Stanford Health Care, tells Yahoo Lifestyle, noting that super-tasters have many more visible taste papillae (bumps on the tongues surface) with more taste receptor cells compared to others.

Or as the lead author of the study,Jennifer L. Smith, PhD, RN, put it to theAHA: Were talking a ruin-your-day level of bitter when they tasted the test compound.

Super-tasters have the hardest time eating brassica vegetables broccoli, cauliflower, Brussels sprouts, cabbage, turnips, collards, kale, bok choy along with spinach, coffee, and tart citrus flavors. Studies show that bitter tasters eat fewer soy products and drink less green tea, and rated these foods to be more bitter than non-tasters, says Sindher.

That bitterness is getting in the way of super-tasters eating their vegetables, which may mean losing out on some health benefits. An overall healthy diet thats rich in vegetables and fruits may reduce the risk ofheart disease, including heart attack andstroke, according to theU.S. Department of Agriculture. Vegetables are also a good source ofdietary fiber, which helps reduce blood cholesterol levels and may lower risk of heart disease.

And in case you were wondering, just because you hate cilantro doesnt mean youre a super-taster. Disgust with that particular herb, which some find smells like soap, is a combination of two genetic variants (one of which is tied to sensing odors), according toNature. Cilantros aroma is created by several substances, which include fragments of fat molecules called aldehydes the same (or similar) aldehydes youll find in soap and lotions, according to aNew York Timesreport.

Super-tasters are individuals who are sensitive to specific bitter compounds, none of which are found in cilantro, explains Sindher. In fact, an aversion to cilantro occurs due to genetic variants associated with sensing smells and sensitivity to the aldehyde chemicals that give cilantro its distinctive flavor.

But for true super-tasters, how can they make sure to eat their vegetables? Unfortunately, theres no obvious way to disguise the bitter taste, explains Sindher. However, some strategies may be to sprinkle some sweetness to help mask bitter flavors, she says. Spices can help enhance flavor. Adding a little fat can also decrease bitterness.

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Aversion to Broccoli May Have Genetic Roots – Scientific American

November 15th, 2019 8:46 pm

If you have heart disease, your doctor might tell you, eat more vegetables. A tactic that haslimited success.

Getting people to change their diets is actually pretty hard. These are lessons I would give over and over again. And I would think, Why is this so hard to do?

Jennifer L. Smith is a nurse researcher at the University of Kentucky who now has a preliminary answer about why change is so hard: it might depend on your genes. Specifically, whether or not youre genetically predisposed to perceive bitternessand therefore bitter veggies.

So broccoli is definitely one of them. They tend to be cruciferous vegetables, like broccoli, cauliflower, cabbage, brussels sprouts, asparagus."

If you ever took that test in science class where you put a piece of paper on your tongue to see if it tastes bitter, you might already know your bitter status.

Smith took saliva samples from 175 adults known to be at risk of cardiovascular disease. She then did a genetic test to determine whether they had a copy of a bitter-taste gene variant. She also had them fill in a questionnaire about their eating habits.

After controlling for factors like age, gender, income, and so on, Smith found that people with a copy of the bitter-sensitive gene variant were just 40 percent as likely to report eating a lot of veggies as were the folks without the gene variant.

Shes presenting the results this week at the American Heart Association Scientific Sessionsin Philadelphia. [Jennifer L. Smith et al., TAS2R38 haplotype predicts vegetable consumption in community dwelling adults at risk for cardiovascular disease]

If these findings hold up to more testing, Smith says, perhaps doctors could advise patients with this gene variant to avoid the most offensively bitter veggies but to try the others. Or perhaps certain herbs and spices might counteract the bitterness, she says.

Of course, chefs already figured this outwith cheesy broccoli. But for heart patients, the better flavor might not be a favor.

Christopher Intagliata

[The above text is a transcript of this podcast.]

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Endangered birds leave genetic clues in their drinking water – Cosmos

November 15th, 2019 8:46 pm

By Natalie Parletta

Australian researchers have worked out how to trace an endangered bird species by analysing water samples from its drinking holes.

Using environmental DNA (eDNA), a team led by Karen Gibb from Charles Darwin University identified the movements of the stunning rainbow-coloured Gouldian finch (Erythrura gouldiae), a species native to tropical savanna woodlands in Australias north.

Once numbering in the millions, there are now just 2500 adults as a result of the illegal bird trade, altered habitat, predators and wildfires, and the species is listed as endangered.

eDNA is used to detect the locations and numbers of rare and threatened species from water samples and to date has mostly been applied to freshwater animals.

Gibbs and team, including colleagues from the University of Western Australia, saw an opportunity to track the Gouldian finch using water sample analysis, as it needs to drink several times a day.

To do this, they developed a test that can identify estrildid finches from a fragment of mitochondrial DNA, and a probe specifically designed to detect Gouldian finch DNA.

This was necessary to distinguish the colourful finches from masked finches (Poephila personata) and long-tailed finches (P. acuticauda) other estrildid species that often flock together at the same waterholes.

Its a much more accurate test, says Gibb. By having primers that pick up other finches it tells us the eDNA is good enough quality to be amplified. If the Gouldian test is then negative, we can be confident that the eDNA test worked, but there just werent Gouldian finches at that site.

First, they piloted it in wildlife park aviaries before doing field trials at the Yinberrie Hills in the Northern Territory, where scientists and rangers had good observation data to validate the tests.

With a 200-millilitre water sample they could successfully detect Gouldian finch eDNA from waterholes the birds had visited in the previous 48 hours, and where there were lots of birds, it was still measurable from the samples two weeks later.

When it worked in the real world at the waterholes, even where the water was poor quality in places where it was hot and looked a bit oily we were really excited, says Gibb.

The study opens new options for rangers and scientists to keep track of the birds movements by simply collecting small water samples during their explorations, which will help inform conservation efforts.

People who are travelling around will be able to put a cup of water into an appropriate container and then into a car fridge, and be able to take a lot of samples, Gibbs says. We can cover a much larger area.

The study is published in the journal Endangered Species Research.

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Invitae Launches Invitae Discover Research Platform on Apple Watch; First Study on Platform Will Investigate Genetic Causes of Cardiovascular Disease…

November 15th, 2019 8:45 pm

--Study announced in conjunction with American Heart Association's Scientific Sessions--

--Researchers also presenting data on limitations of highly targeted screening strategies in familial hypercholesterolemia--

PHILADELPHIA, Nov. 15, 2019 /PRNewswire/ --Invitae Corporation (NVTA), a leading medical genetics company, today announced Invitae Discover, a clinical research platform that leverages biometric data available through Apple Watch to provide better understanding of the genetic causes of disease. The first study on the platform will evaluate genetics in cardiovascular disease and was announced in conjunction with the American Heart Association's Scientific Sessions where researchers are presenting data on genetic screening in familial hypercholesterolemia.

Invitae's (NVTA) mission is to bring comprehensive genetic information into mainstream medical practice to improve the quality of healthcare for billions of people. http://www.invitae.com (PRNewsFoto/Invitae Corporation)

"The creation of the Invitae Discover platform will make it easier to conduct studies that assess genetic test results alongside the biometric data that is now easily available on Apple Watch, thereby joining basic electrophysiological data with genetic information in order to advance our understanding of the genetic underpinnings of disease and help improve clinical care," said Robert Nussbaum, M.D., chief medical officer of Invitae. "Our first study on the platform is designed to determine the contribution of certain genetic variants to clinical presentations of atrial fibrillation and other cardiovascular conditions associated with abnormal heart rhythms, as well as to improve the interpretation of genetic testing results."

The first study on Invitae Discover is the Afib CAUSE Study. Patients who have genetic testing through Invitae can enroll in the study via the Invitae Discover app. The study will combine health and activity data from Apple HealthKit with clinical genetic testing results. In addition to assessing known genetic variants, the study will specifically evaluate biometric data for patients whose genetic testing included variants of uncertain significance (VUS) to help build preliminary data that improves variant classification and, ultimately, provide evidence to support resolution. The Invitae Discover app is available on the Apple app store. The Afib CAUSE study is open to U.S. residents 18 years of age and older and enrollment criteria can be accessed through the Invitae Discover app.

The study will be conducted under the supervision of an Institutional Review Board (IRB). As a medical genetics company, Invitae is subject to and fully complies with the privacy and security requirements under HIPAA for all its patients.

Separately at the AHA Scientific Sessions, Invitae researchers will be participating in a moderated poster session at the AHA meeting to discuss research quantifying the low diagnostic yield of highly targeted, direct-to-consumer genetic screening strategies in familial hypercholesterolemia. The study will be presented on November 17th during the Cardiovascular Genomic Medicine session at 2:20pm.

About InvitaeInvitae Corporation (NVTA) is a leading medical genetics company, whose mission is to bring comprehensive genetic information into mainstream medicine to improve healthcare for billions of people. Invitae's goal is to aggregate the world's genetic tests into a single service with higher quality, faster turnaround time, and lower prices. For more information, visit the company's website atinvitae.com.

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Safe Harbor StatementsThis press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, including statements relating to the attributes and potential benefits of the company's clinical research platform; and the design and potential benefits of the company's first study on the platform. Forward-looking statements are subject to risks and uncertainties that could cause actual results to differ materially, and reported results should not be considered as an indication of future performance. These risks and uncertainties include, but are not limited to: the company's history of losses; the company's ability to compete; the company's failure to manage growth effectively; the company's need to scale its infrastructure in advance of demand for its tests and to increase demand for its tests; the company's ability to use rapidly changing genetic data to interpret test results accurately and consistently; security breaches, loss of data and other disruptions; laws and regulations applicable to the company's business; and the other risks set forth in the company's filings with the Securities and Exchange Commission, including the risks set forth in the company's Quarterly Report on Form 10-Q for the quarter ended September 30, 2019. These forward-looking statements speak only as of the date hereof, and Invitae Corporation disclaims any obligation to update these forward-looking statements.

Contact:Laura D'Angelo pr@invitae.com (628) 213-3283

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Correlation Found Between Left-Handedness and Genetic Markers Associated with Neurological Disease – JD Supra

November 15th, 2019 8:45 pm

Updated: May 25, 2018:

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Investigative Genetic Genealogy Used to Charge Man With Murder, Rape in 1980s SoCal Killings of 2 Women – KTLA Los Angeles

November 15th, 2019 8:45 pm

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Prosecutors have charged a man with murder and rape in the killings of two women during the 1980s, after using investigative genetic genealogy to solve the crimes, Los Angeles County District Attorney Jackie Lacey said in a news release Friday.

The charges filed Friday are the first in L.A. County to use the forensic technology, authorities said.

Thanks to advances in technology and forensics, we are now able to virtually reach back in time and find those responsible for these vicious crimes, District Attorney Lacey said.

Horace Van Vaultz Jr., 64, was charged with two counts of murder, with special circumstance allegations of multiple murders, crimes committed during a rape and sodomy, and with lying in wait for each victim, the news release said.

Van Vaultz is accused of murdering Mary Duggan, 22, on June 9, 1986. Duggan's body was found in the trunk of a car in a Burbank parking lot, authorities said. She was bound, sexually assaulted and died from asphyxia because a tissue was stuffed down her throat, according to the release.

The second murder charge is for the killing of Selena Keough, 20, on July 16, 1981. Keough was found under some bushes in Montclair in San Bernardino County. She was also bound, sexually assaulted and strangled, authorities said.

Van Vaultz faces the death penalty or life in prison with the possibility of parole if convicted of the charges, the DA's office said.

His arraignment is expected to take place on Monday.

Investigators have reached out to other law enforcement agencies to determine if Van Vaultz is responsible for other unsolved murders in the state, the release said.

With dedicated resources and rapidly advancing technology, we can unmask the cowardly murderers who have remained hidden in our community and bring justice to the grief-stricken families who have waited too long for answers, Lacey said in the release.

The case remains under investigation by the Burbank and Montclair police departments and the FBI's Forensic Genetic Genealogy Team, authorities said.

Anyone with information is asked to contact the Burbank Police Department tip line at 818-238-3086.

34.052227-118.243660

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

November 15th, 2019 8:45 pm

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

November 15th, 2019 8:45 pm

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

November 15th, 2019 8:45 pm

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

View original content to download multimedia:http://www.prnewswire.com/news-releases/mapping-human-antibodies-to-develop-protein-therapeutics-spotlighted-at-feinstein-institutes-marsh-lecture-300959137.html

SOURCE The Feinstein Institutes for Medical Research

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

November 15th, 2019 8:45 pm

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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Here's a better way to convert dog years to human years, scientists say - Science Magazine

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