Archive for the ‘Male Genetics’ Category

Every cat is unique and special, theres no denying that. But scientifically speaking, a male tortoiseshell cat is very special. And why is that? Well, because the genetics that control their coat pattern also controls their gender, and those chromosomes are what causes them to be female 99.9% of the time.

But just like Jeff Goldblum said as Dr. Ian Malcolm in Jurassic Park, well

And in this case, its in the form of an extremely adorable male tortoiseshell kitten named Cresta who just so happens to be a boy. The Cats Protection Wrexham Adoption Centre is currently housing the five-month-old kitten, who needless to say found a furever home in no time flat.

So, exactly how unique is little Cresta? Well, its believed that only 1 in 3,000 tortoiseshell kittens are born male. And this little diamond in the rough was found wandering the streets of Colwyn Bay in the UK by the RSPCA.

We couldnt believe it when we discovered Cresta was a boy. Certainly none of us here have ever seen a male tortoiseshell before, and its been many years since Cats Protection has had one in care, despite us helping 200,000 cats a year.

It wasnt difficult to find Cresta a home, and his new owners realise how special he is and are looking forward to him becoming part of the family.

Male tortoiseshell interesting fact: Male tortoiseshells are usually conceived as a result of an extra chromosome being present, and are usually sterile as a result (same with male calico cats).

From humble beginnings in 1927, Cats Protection has grown to become the UKs leading feline welfare charity.

We helparound 200,000 cats and kittens every yearthrough our network of over 250 volunteer-run branches and 36 centres.

Our work doesnt stop there, however: we also provide an array of cat care information via ourpublications,help and advicesection and National Information Line; promote the benefits of neutering to prevent unwanted litters from being born and becoming the abandoned cats of tomorrow and seek toeducatepeople of all ages about cats and their care.

The Cats Protection is certainly doing their part to make the world a better place for homeless cats, and we thank them for all that they do year after year. If youd like to learn more about them, you can visit their website here.

All Images Courtesy of The Cats Protection

STORY IN CONJUNCTION WITH CATTITUDEDAILY.COM

Related Story: Rescue Woman Hits 1:3000 Odds When She Discovers Her New Foster Kitten Is A Male Tortoiseshell!

Related Story: Male Sphynx Cat Found To Be Experiencing Gender Transition By Accident!

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Rare Male Tortoiseshell Kitten Picked Up As A Stray In The UK - Cole & Marmalade

MUC5B genetic variants and shorter telomeres or chromosome endings are risk factors associated with greater lung damage and poorer survival in Chinese patients with idiopathic pulmonary fibrosis (IPF), a study has revealed.

The study, The relationship between MUC5Bpromoter,TERT polymorphisms and telomere lengths with radiographic extent and survival in a Chinese IPF cohort, was published in the journal Nature Scientific Reports.

While a better understanding of the underlying processes and risk factors that lead to IPF are urgently needed, several genetic factors have been associated with the disease.

Research points to genetic alterations, or polymorphisms, in genes that provide instructions for making telomerase reverse transcriptase (TERT) and telomerase RNA component (TERC), as possible contributors to the development of pulmonary fibrosis. In fact, according to the the National Institutes of Health, 15% of all cases of IPF are related to mutations in these genes.

TERC and TERT are responsible for making components of telomerase, an enzyme that extends DNA caps at the end of chromosomes called telomeres. These structures are very important in protecting the genome from wearing down and cells from entering an aging-like process.

Maintaining telomere length is important because when telomeres get too short, cells irreversibly stop dividing and acquire features of aged cells.

In fact, telomere shortening has been linked to increased susceptibility and lower survival in IPF patients. For this reason, scientists report that IPF is the most frequent manifestation of telomerase-associated disease.

Prior studies have also linked variations at the mucin 5B gene (MUC5B) to the risk of IPF and poor prognosis of patients. However, most of these studies were conducted in Western countries or looked at genetic variants that are rare in Asian populations.

Recognizing the need to address risk factors in Asian patients, researchers investigated the association between genetic variations in MUC5B and TERT,as well as changes in telomere length, and the extent of lung fibrosis and survival in a group of Chinese IPF patients.

In total, 79 patients (86.08% males; mean age of 64.19 years) and 200 age- and sex-matched healthy controls were enrolled in the study at the Nanjing Drum Hospital in China. The mean follow-up time was 30.36 months.

Participants were screened for five small genetic variations (single-nucleotide polymorphisms, or SNPs) rs35705950 and rs868903 in MUC5B, rs2736100 and rs2853676 in TERT, and rs1881984 in TERC.Their telomere length was also determined using blood samples.

Variations within each participant were compared with the extent of radiographic lung fibrosis seen on chest high-resolution computed tomography scans (HRCT), and with survival data. The extent of lung fibrosis was specifically measured by scoring honeycombing (clustered air spaces), an abnormal HRCT finding characteristic of IPF, used by doctors to definitively diagnose the disease.

HRCT results showed that a minority of patients (13 patients; 16.46%) had mild honeycombing (in less than 10% of the lung), while 34 patients (43.04%) had moderate honeycombing (1050%), and 32 patients (40.51%) had severe honeycombing (more than 50% of the lung).

Patients who carried one of two genetic variants CT or CC at the MUC5B promoter rs868903 or those who had shorter telomeres had more extensive honeycombing on chest scans.

After adjusting for age, sex, and smoking status, the CT/CC variants in MUC5B also emerged as a genetic risk factor for poorer survival, linked to a higher risk of death over time in IPF patients. Of note, 38 (35.44%) of the total patients analyzed died during the follow-up period.

According to the team, this is the first study to find that MUC5B promoter variations and telomere size are associated with radiological features, and that MUC5B variations were a predictive factor for the prognosis in a Chinese IPF cohort.

Further investigations are needed to determine exactly potential role of MUC5B gene in the pathogenesis of IPF, and the regulation mechanisms of telomere shortening, they added.

Ana is a molecular biologist with a passion for discovery and communication. As a science writer she looks for connecting the public, in particular patient and healthcare communities, with clear and quality information about the latest medical advances. Ana holds a PhD in Biomedical Sciences from the University of Lisbon, Portugal, where she specialized in genetics, molecular biology, and infectious diseases

Total Posts: 110

Patrcia holds her PhD in Medical Microbiology and Infectious Diseases from the Leiden University Medical Center in Leiden, The Netherlands. She has studied Applied Biology at Universidade do Minho and was a postdoctoral research fellow at Instituto de Medicina Molecular in Lisbon, Portugal. Her work has been focused on molecular genetic traits of infectious agents such as viruses and parasites.

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MUC5B Genetic Variants, Short Telomeres Linked to Greater Lung Damage, Poorer Survival in Chinese Patients, Study Shows - Pulmonary Fibrosis News

Few topics arouse as much interest and controversy as sex. This is hardly surprising. The biological continuance of the species hinges on it if human beings stopped having sex, there would soon be no more human beings. Popular culture overflows with sex, from cinema to advertising to, yes, even politics. And for many, sex represents one of the most intimate forms of human connection.

Despite its universality, sex and its purpose have been understood very differently by different thinkers. I teach an annual course on sexuality at Indiana University, and this work has provided opportunities to ponder sex from some provocative angles, including the body, the psyche, and the spirit.

Alfred Kinsey (1894-1956) was an insect biologist whose alarm at widespread ignorance of sexual structure and physiology led him to become perhaps the first major American figure in the study of sex. The Kinsey Reports, published in 1948 and 1953, presented a highly statistical taxonomy of sexual preferences and practices. Despite draining sex of virtually all eroticism, the books managed to sell about three-quarters of a million copies.

The intellectual climate for Kinseys studies of sex had been powerfully shaped by the work of Sigmund Freud (1856-1939). Physician and founder of psychoanalysis, Freud created a model of the human psyche that placed libido or sex drive at its core and postulated that psychological and social life are powerfully shaped by its tensions with the conventions of civilized behavior. According to Freud, failure to adequately resolve such tensions could manifest in a variety of mental and physical ailments.

The stage for psychoanalysis had in turn been set by Charles Darwin (1809-1882). In Selection in Relation to Sex (1871), Darwin argued that human beings are animals, likening differences between males and females in body and behavior to those seen among species such as peacocks and emphasizing female choosiness and direct competition among males. From Darwins vantage point, and later that of Freud, even some of the most sophisticated trappings of human civilization reflect basic biological imperatives. The subject of non-heterosexual attraction requires a different account.

At first glance, sexual reproduction is a puzzle, since each member of an asexually reproducing species can produce its own genetically identical young at a lower biological cost. However, sexual reproduction allows a more rapid reshuffling of the genetic deck, increasing the probability that some individuals will be well-adapted to environmental changes. Because human beings reproduce sexually, the foundation is laid for sexual selection, the competition for mates of which Darwin wrote in such detail.

The writer Leo Tolstoy (1828-1910) presents a more broadly humanistic understanding of the purpose of sex. In Anna Karenina, often ranked as the greatest of all novels, sex provides the foundation for the family. Characters who treat sex as an adventure with no regard to family come to bad ends, while those who devote themselves to family happiness fare well. In Tolstoys view, the seemingly mundane joys of family life, made possible by sex, constitute the truest joys accessible to human beings.

Consider Tolstoys description of the life of a devoted mother, Dolly, troubled by the illnesses of her children:

Though hard it was for the mother to bear the dread of illness, the illnesses themselves, and the signs of evil propensities in her children the children themselves were even now repaying her in small joys for her sufferings. These joys were so small they passed unnoticed, like gold in sand, and at bad moments she could see nothing but the pain, nothing but sand; but there were good moments too, when she saw nothing but the joy, nothing but gold.

In the first book of Anna Karenina, two men discuss the theories of love in Platos (428-348 B.C.) dialogue, The Symposium. One of its characters, the comic poet Aristophanes, grounds sex in our desire for completeness. Aristophanes tells the story of once-whole creatures, who, because of their pride, were cut in two, creating human beings who now wander the Earth seeking completion in their other half. For Aristophanes, sex represents above all a desire for wholeness.

Augustine of Hippo (354-430), a saint in Catholicism, also subordinates sex to other purposes in human life. As a young man, Augustine had relished the pleasures of sexual life, even taking a concubine who bore him a son. Later in his Confessions, he describes his former self as a slave to his sexual impulses. He recognized that such impulses could find appropriate expression in marriage and family, but he treated his own preoccupation with sex as evil, because it prevented him from orienting his life around his ultimate purpose, God.

One of the most extraordinary books in the Bible is the Song of Songs. Unlike the other books, it does not mention the God of Israel or covenant, contains no prophecy, and does not represent a wisdom text, like Proverbs. Instead, it celebrates the mutual yearning of two lovers, each of whom waxes erotically on the others charms and the sexual intimacy they enjoy. More than any other text discussed here, this is love poetry in which lovers revel in one anothers allure and embrace.

In an era in which sex and religion are often portrayed as antagonists, it can be a bit hard to fathom the view of some rabbis that the Song of Songs represents the Holy of Holies, capturing the flow of divine love and the restoration of harmony between God and creation. Likewise, Christian interpreters have often read the Song of Songs as an analogy for the love between God and man, in which the two exist in full accord. In both traditions, sex is seen as an earthly sign of a higher union.

Today, we doctors take for granted that sex and health are linked. Sexually transmitted infections such as gonorrhea, chlamydia, and HIV/AIDS, immunization against human papillomavirus (HPV), and the health implications of pregnancy are rightly regarded as essential topics in sex education. Likewise, there is increasing interest in the health benefits of sex sex as a form of exercise good for the heart, intimacy as a way of relieving tension, and the benefits of sex for immune function and general sense of healthiness.

Yet the biologists, psychologists, and theologians of sex invite us to think more deeply about the purposes of sex. From a biological point of view, sex enables each human being to participate in the perpetuation of the species, interweaving each generation with its forebears and progeny. Psychologically speaking, sex brings us together in a way that makes 1 + 1 = 3, rendering us co-creators. And spiritually, sex serves as a rich metaphor for the union of earthly and higher orders.

How we see sex depends on our vantage point. Athletic and hedonistic perspectives offer relatively limited accounts of sex. If, on the other hand, we view sex as an opportunity to participate in something beyond ourselves, it may unexpectedly enrich our whole lives.

This article was originally published on The Conversation by Richard Gunderman. Read the original article here.

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What is sex really for? - Inverse

The facility lies midway between Munichs city center and its international airport, roughly 23 miles to the north. From the outside, it still looks like the state-run farm it once was, but peer through the windows of the old farmhouse and youll see rooms stuffed with cutting-edge laboratory equipment.

In a newer building at the back of the farm, Barbara Kessler pulls off her sneakers and sprays her bare feet and hands with antiseptic. The wiry veterinarian steps over a taped line in the shower room, leaving behind everything she can from the outside world: clothes, watch, earrings. She scrubs her body and haira buzz cut, so its easier to manage these frequent washings.

After the shower, she finds her size among the neat stacks of supplied clothes and pulls on a pair of black pants, a red shirt, and black Crocs. Outside the dressing room, she adds a black knit cap to keep even her short-cropped hair from passing on germs, and then strides down the hall to the boot room, where she carefully steps into knee-high rubber boots that are power-washed after each wearing.

LAETITIA VANCON

All these precautions are to protect animals not known for their cleanliness: pigs. And once Kessler opens the door to the indoor pens, the smell is unmistakable. Its a pigsty, after all.

When Kessler unlocks one pen to show off its resident, a young sow wanders out and starts exploring. Like other pigs here, the sow is left nameless, so her caregivers wont get too attached. She has to be coaxed back behind a metal gate. To the untrained eye, she acts and looks like pretty much any other pig, but smaller.

Its whats inside this animal that matters. Her body has been made a little less pig-like, with four genetic modifications that make her organs more likely to be accepted when transplanted into a human. If all goes according to plan, the heart busily pumping inside a pig like this might one day beat instead inside a person.

Different types of tissues from genetically engineered pigs are already being tested in humans. In China, researchers have transplanted insulin-producing pancreatic islet cells from gene-edited pigs into people with diabetes. A team in South Korea says its ready to try transplanting pig corneas into people, once it gets government approval. And at Massachusetts General Hospital, researchers announced in October that they had used gene-edited pig skin as a temporary wound covering for a person with severe burns. The skin patch, they say, worked as effectively as human skin, which is much harder to obtain.

But when it comes to life-or-death organs, like hearts and livers, transplant surgeons still must rely on human parts. One day, the dream goes, genetically modified pigs like this sow will be sliced open, their hearts, kidneys, lungs and livers sped to transplant centers to save desperately sick patients from death.

Laetitia Vancon

The death of Baby Fae

Today in the United States, 7,300 people die each year because they cant find an organ donortwo-thirds of them for want of a kidney. In many cases, the only hope is someone elses tragedy: an accident that kills someone whose organs can be harvested.

Surgeons looking for another source of organs at first looked to monkeys, because theyre the animals most similar to us. In 1984, a little girl known as Baby Fae received a baboon heart but died 20 days later, after her immune system attacked it. Baby Faes short life and quick death received global attention; many condemned the idea of killing our closest animal relatives to save ourselves. An opinion piece by a cardiologist in the Washington Post described the procedure as medical adventurism. Another, in the Journal of Medical Ethics, was headlined Baby Fae: A beastly business.

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Then, in the 1990s, researchers and biotech companies turned to pigs as the donor of choice. Since we eat pigs (120 million of them a year in the US alone), taking their organs seemed less morally fraught to many. Scientifically, their organs are roughly the right size, with similar anatomy, and pigs reach adulthood in about six monthsmuch faster than primates. But a problem arose: pigs harbor viruses that might make the jump to people. Whats more, with the simple genetic engineering available at the time, the transplanted organs didnt last long when they were tested in monkeys. They were simply, genetically speaking, too foreign.

When it comes to life-or-death organs, like hearts and livers, transplant surgeons still must rely on human parts.

More than two decades later, advances in genetic engineering have revived the prospect of so-called xenotransplants. The hottest source of debate in the field: exactly how many gene edits are needed in pigs like these to overcome the species barrier. A well-funded US company, eGenesis, which leads the more-is-better-camp, says it has made a double-digit number of changes to the pigs it raises with a sister company in China.

The Germans at the Munich facility are in the less-is-more camp. The pigs they work with have three key genetic modifications originally made more than a decade agoall designed to keep baboons and humans from rejecting their organs. Knocking out a gene that produces a sugar called galactosyltransferase prevented the recipients immune system from immediately rejecting an organ from a different species. The second change added a gene expressing human CD46, a protein that helps the immune system attack foreign invaders without overreacting and causing autoimmune disease; the third introduced a gene for a protein called thrombomodulin, which prevents the blood clots that would otherwise destroy the transplanted organ.

A smaller number of edits can be better controlled and measured, and their effects are easier to document, says Eckhard Wolf, who runs this former state farm on the outskirts of Munich, now called the Center for Innovative Medical Models. If something goes wrong, as often happens in xenotransplantation, it will be clear where the issue lies. With more edits come more potential problems. At some point, you are in a situation that you have no idea what an additional genetic modification does, he says.

The size of a heart

In 2018, the hearts of pigs from the Munich center were transplanted into 14 baboons. Two of the monkeys survived for six months, the longest any animal has lived with a heart from another species. In a report in Nature last December, the German researchers described their achievement as a milestone on the way to clinical cardiac xenotransplantation.

Laetitia Vancon

Of the first five baboons to get a pig heart, four died within a day or two, and when the fifth died after a month, its heart was diseased. In the next batch of baboons, Wolfs collaborator Bruno Reichart, a retired heart transplant surgeon, flooded the organ with nutrients, hormones, and red blood cells from the time it was removed from the pig until it was fully functional in the recipient animal. Three baboons treated with this approach lived for 18, 27, and 40days.

The last five baboons had the same procedure but were also kept on an immunosuppressant drug. Two lived for 182 and 195 days, but they had to be euthanized last year when still in good health, because it was so challenging to continue the anti-rejection therapy.It isnt practical to leave an intravenous line in a baboon for longer than six months. But neither is it a simple thing to convince a baboon to take drugs. Like young children, they resist drinking anything that smells like medication.

Reichart says he is working on a better delivery system that will enable the baboons to stay on the anti-rejection drugs for at least a yearthe amount of time he says is needed to prove that xenotransplantation is ready to be tested in people.

Midway through their baboon study, however, Wolf and Reichart noticed an unanticipated problem: the hearts, harvested from juvenile pigs to make sure they were small enough for baboons, kept on growing as if they were still destined to keep alive a 600-pound (270-kilogram) pig. The transplanted heart weighed 62% more than a typical baboon heart: massive cardiac overgrowth, as their paper described it. In the baboons, the new hearts crowded out other essential organs and, in a few cases, caused the animals death.

Laetitia Vancon

At the pig facility, Kessler showed me Wolfs solution to this problem: two sister sows, created with one more CRISPR gene edit. Researchers have turned off the animals growth hormone receptor(GHR) gene, leaving them roughly half the weight of a typical pig. Both tip the scales at about 175 pounds (79 kg),compared with nearly 400 pounds for a normal sow. The pregnant sister stood across the hall, alone in a pen facing the wall. Metal bars kept her from lying down against the wallsa precaution to protect the piglet litter. Though she was bred with a full-sized male pig, roughly half of her offspring should be missing their GHR gene.

The cost of saving a life

It isnt cheap to create a gene-edited pig and then raise it to the standard required by the US Food and Drug Administration and other agencies that would regulate pig-to-human transplants around the world. Kessler and her colleagues clone pig embryos by putting the desired genetic material into eggs collected Mondays and Tuesdays from a local slaughterhouse. To minimize germs, every new line of pigs must start by conceiving the animal in a lab dish, delivering it by Caesarean section, and separating it from its mother at birth. Later germ-free generations dont require as many precautions and cost only about 10 times the price of raising a pig for bacon and pork, Kessler says.

About 120 gene-edited adult pigs and 150 piglets live on this pig farm (one of only a handful worldwide), but even it cant afford to raise pigs to the standard that will be needed before an organ is transplanted into a person. Wolfs government grant wont cover the cost of HEPA filters to clean the air in every room of the pig facility, or to irradiate the special vegetarian feed pellets that are trucked in. The researchers lobbied for years for funding to build a perimeter fence to keep wild boarsand their germsoff the property.

LAETITIA VANCON

Reichart says he just needs funding to complete one more trial, keeping baboons alive for a full year with the pigs hearts, before hell be ready to test them in people. Other groups are also getting close. In Florida, transplant surgeon Joseph Tector, newly relocated to the University of Miami, says he just needs time to build a pig facility like Wolfs only stricter, and then hell be ready to test pig kidneys in people. The University of Alabama-Birmingham has a pig facility to support clinical transplants, with experts looking at both hearts and kidneys. Their first clinical trial of xenotransplantation might be in babies born with congenital heart malformations. A pig heart could serveas was hoped for Baby Faea bridge until they can receive a human heart.

Reichart says he doesnt need to be the first to successfully do a xenotransplant. But he believes hes likely to be among the first, since hes so close. After decades of research, the pigs in the Munich lab just might be the ones that allow surgeons to break the species barrier.

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Meet the pigs that could solve the human organ transplant crisis - MIT Technology Review

Fighting Blindness Canadas secure, clinical patient registry is a database dedicated to connecting people living with retinal eye diseases to clinical trials and research.Paffy69 / PNG

Blind and partially sighted people no longer have to wait passively for a research breakthrough in hope of treatment options. In fact, people living with genetic eye conditions can now actively drive vision research forward by enrolling in a patient registry and getting their genes tested.

There are 2.2 billion people living with visual impairment globally. Some are living with inherited retinal diseases that are progressive and can lead to complete blindness. Up until recent years, blind and visually impaired people were told that no treatment is available. This is changing as genetic testing is paving the way for a surge of gene therapies.

My doctoral dissertation at the University of B.C. was on drug therapy for retinitis pigmentosa. This progressive, blinding eye condition is the most common type of inherited retinal disease.

In people affected by retinitis pigmentosa, the light sensing cells in their retina photoreceptors die early. Unlike skin cells that regenerate, the body does not make more photoreceptors once they are damaged.

As a vision scientist affected by retinitis pigmentosa, I am passionate about finding the truth about the disease. Why do photoreceptors die? How can we stop it? How can science and medicine help?

When I was 12 years old, I realized while at summer camp that my night vision was disappearing. In the last two decades, I lost my peripheral vision, contrast sensitivity and depth perception.

I worked in Dr. Orson Moritzs lab at the UBC department of ophthalmology and visual sciences, which focuses on research using tadpoles that contain known human mutations for retinitis pigmentosa to understand the disease.

I made an alarming discovery in our animal model: knowing the genetic cause of retinitis pigmentosa is vital for treatment with one class of drugs histone deacetylase inhibitors. These determine how genes are switched on or off.

A similar study in mice showed that the same drug reacted differently to variations in a single mutant gene that also causes retinitis pigmentosa.

Treating retinitis pigmentosa is like extinguishing fire. To stop a fire, you need to know whether its water-based or grease-based. If you try to use water to stop a grease fire, the damage gets worse.

Blind and visually impaired people can advocate for eye health by enrolling in a patient registry. Participation in a registry benefits researchers by offering more information about the disease.

In Canada, individuals can self-refer to Fighting Blindness Canadas secure, clinical patient registry. This database is dedicated to connecting people living with retinal eye diseases to clinical trials and research.

When a gene therapy trial arises, researchers draw participants from this database. Since gene therapy aims to correct an underlying genetic mistake in DNA that causes disease, knowing the genetic cause of a disease is a criteria for most gene therapy trials.

Globally, other registries include My Retina Tracker in the United States, Target 5000 in Ireland, MyEyeSite in the United Kingdom, the Australian Inherited Retinal Disease Registry and Japan Eye Genetics Consortium. In New Zealand, Dr. Andrea Vincent has established the Genetic Eye Disease Investigation Unit. There is even a Blue Cone Monochromacy Patient Registry for one rare eye condition.

In the last two decades, the number of gene therapy trials has blossomed. Currently, 250 genes on inherited retinal diseases have been identified. In 2017, the first gene therapy for inherited retinal disease Luxturna was approved by the United States Federal Drug Administration.

To date, there are trials for: retinitis pigmentosa; Usher syndrome, a condition that involves hearing and vision loss; achromatopsia, a disease that causes colour blindness; X-linked retinoschisis, a dystrophy that causes splitting of the retina and affects mostly in males; and age-related macular degeneration, the third-largest cause of vision loss worldwide, caused by the interplay between genetics and environment.

Enrolment in a patient registry and genetic testing advance the design of gene therapy trials. This in turn benefits blind and visually impaired people.

Research advancement is a concerted effort across the globe blind and partially sighted people should know they have the power to push it forward.

Ruanne Vent-Schmidt is a PhD candidate in cell and developmental biology at the University of B.C.This article originally appeared online at theconversation.com, an independent source of news and views, from the academic and research community.

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Ruanne Vent-Schmidt: The blind and visually impaired can help researchers by getting their genes tested - Vancouver Sun

Tell me about your football career.

I started playing when I was eight years old. Ill have been playing for 15 years by the end of the season. Collegiately, I played JUCO, or Junior College, before I came here, which was really successful. We were a super good team, nationally ranked at American River College. I redshirted my freshman year there, and my second year I got injured. My third year wasnt a bad year, but a guy whos now at USC played ahead of me, so I didnt have the greatest success. After my third season, I was considering giving up because I had barely played the last season. Luckily, Luther had a recruiter that would not give up. He was super persistent. So I said, screw it and came out here for a visit. I came legitimately wanting to hate this place, and it slowly just won me over. That was over a J-term, and I committed the next day. I went from living in Sacramento with a job to moving out here within two weeks.

Describe your role on the team.

As a captain, my impact is just like being a big brother to a lot of the guys, especially because we have a really young team. The majority of our roster is freshmen and sophomores, with few juniors and even fewer seniors. I always preach that players play, coaches coach. Its not our job to chew guys out, as I see it. Trying to lead by example, doing all the right things, so guys can have a reference for how they should carry themselves.

How do you prepare for games?

Obviously, we practice every day as a team. But for me personally, Friday nights I try to settle in. Look over our notes from meetings. We always have a quiz to complete. I like to imagine myself in the game and create a mental image of myself in there, going through good and bad scenarios. On the actual game day, I just have laser focus. I dont look at social media. I send out a thank- you to people saying good luck, but other than that I dont do anything but focus. About an hour before the game, I get super intense and create a small goal for myself. Five tackles or a sack, something like that.

Do you usually accomplish your goals?

Depends on the game. Usually my bare minimum goal is five tackles and a sack, and if I get one or the other then Im happy. Then Ive had bad games as well. When those happen, the most important thing is that I gave it my all. Thats the one thing I care about more than anything. My position isnt super glorious, and when I do make a tackle its cool because I had to fight off a big, fat offensive linemen. If I do my best, I can live with it.

What are your thoughts on this season so far?

For our team, its been disappointing. Nobody likes losing. But we have a lot of room to grow. As I said, we have a lot of young players that are developing mentally and physically. Moving forward for the next few seasons, its gonna get better and better. If they do the right things, they will do big things in the future. For myself moving forward, we only have about three games left and this is my last season. My ultimate goal is to finish strong. I dont want to look back and say, man, I should have worked harder. When I dont work my hardest, it eats at me. When I was at JUCO, I almost gave up. Luckily, I was given this opportunity to finish strong here, and thats what I want to do. Win or lose, I just want to finish strong.

How has the team grown since you arrived at Luther?

We have a very young team, and Ive seen a few players step up and go in the right direction. Ive also seen young players with a lot of room to grow, which is okay since they have time. I thought our camp was much better this year in terms of keeping the game as the focus. Theres improvements and growth, but it will take time for it to show.

What are you looking forward to during the rest of your time at Luther?

Im looking forward to enjoying myself as a student for once. Ive played since I was eight, and I dont think Ive ever had a moment where Ive never played a sport before. With our next semester, I wont have that football commitment. It wont be easier, but it will be an interesting feeling. Itll be sad because I wont be doing what I love, but Ill get to experience something new and Im excited for that. Because I was a transfer, I have a bunch of freedom for what I can take, so Im very excited for that. Im excited to get involved in new things, as Im now freed up to do a little more.

Who is an athlete you look up to?

Theres a guy I played in JUCO with, and he recently got signed by the Carolina Panthers. Hes a linebacker, and his names Jordan Kunaszyk. We werent super close, but I knew him pretty well. He was a captain at my JUCO, and I admired the way he carried himself and his work ethic. A lot of the times when people talk about college athletics, they talk about genetics. He had a solid frame, but his work ethic alone is why hes at where hes at. And he made the actual team. He didnt get cut and he plays. His accomplishments and his work ethic are what I admire.

Whats a fun fact about yourself that isnt related to football?

I have club thumbs and people say they look like toes.

Photo courtesy of Luther FootballSefried hails from Lodi, CA.

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Norse of the Week: Tyler Sefried ('20) - Luther College Chips

KFOR via Fox News An Oklahoma journalist who chose to air her first-ever mammogram on Facebook Live last year was subsequently diagnosed with breast cancer, she said.

In October 2018, Ali Meyer, a reporter with Oklahomas News 4 (KFOR), chose to live-stream her mammogram because I thought it might remind some women to schedule theirs, she wrote in an essay posted to the news stations website.

When the day of her appointment arrived, I had no concerns, Meyer, 41, wrote. No lumps; no family history; no reason at all to think that my baseline mammogram would turn my world upside down.

But to her shock and dismay, Meyers mammogram results were abnormal.

Local radiologist Dr. Richard Falk, with the University of Oklahomas Breast Health Network, found cancerous calcifications in the reporters right breast, she said. More specifically, she was told she had non-invasive ductal breast cancer.

I will never forget that day. I will never forget telling my husband, my girls, she wrote.

One day after her diagnosis, Meyer took to Facebook Live to share the news.

This has been hard and shocking. It does rock you to your core, she said, according to KFOR. You guys have been really supportive and I appreciate it so much. This is not the news I was hoping to tell you about to raise breast cancer awareness.

Meyer, who was only 40 at the time of her diagnosis, did not have any genetic mutations that could explain why she developed breast cancer at such a young age.

Meyer later underwent a right side, skin and nipple-sparing mastectomy.

Even though [the] surgery was my choice, it felt like forced mutilation, she wrote in the essay. It felt like cancer was stealing part of my body away from me.

Luckily, because of how early her breast cancer was detected, Meyers prognosis was good.

"We found this when it was not invasive and not a mass when you are most likely to be completely cured and go on with a normal life," Falk told Meyer for the essay.

Meyers surgery was a success. Now one year later, she is cancer-free.

"I will never stop having mammograms, she wrote. I will never stop telling women to take care of their bodies and schedule their mammograms."

"This year I had my second, annual, 3D screening mammogram, she continued. I am thrilled and relieved to tell you my mammogram was clear, showing no signs of breast cancer.

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Oklahoma news anchor diagnosed with breast cancer after streaming first-ever mammogram on Facebook Live - msnNOW

Pick your products

The first few days, and even weeks, of moustache growth can be reminiscent of your pre-pubescent peach fuzz but persistence and the right products can help.

"No product is really going to help you grow a moustache quicker, but definitely taking care of your skin and your hair will promote natural growth," Fraser says.

Plus, using a good beard oil can also help you resist the itch that comes with growing facial hair.

"For the first 10 days of growth, your hair is actually sucking all the nutrients and essential oils out of your skin, so that's where the dry skin and all that itchiness comes from," he exaplins. "We actually refer to that as beardruff."

Don't be afraid to ditch the razor and go semi-caveman in the first stages.

"I definitely think for a moustache to look better when it's starting to grow out, you would grow your moustache, but then you'd grow a little bit of shadow under your bottom lip and also maybe on your chin, and then as that moustache starts to get a bit of length to it, then you could take your chin and the bit under your bottom lip a lot shorter. That'll make it look a lot more appealing."

Once your whiskers have settled in, it's time to trim. Fraser reckons around the second week mark for most Movember participants.

"I definitely recommend growing it until the 15th, at least, so a good 10 to 14 days growth, and then you would look at trimming up your lip line," he says.

"That's the most important part to any guy with a moustache, because as soon as it gets past your lip line, it becomes really annoying to eat or even just talking, you can feel these little pricks. Or with your partner, if you kiss your partner or anything like that you can get little sharp bits."

While upkeep can help, how your mo grows is pretty much out of your hands.

"At the end of the day, it comes down to genetics, which some people can't help," Fraser says.

If your handlebar is looking more like facial fur don't waste your time with potions and promises. Just wear your whiskers with confidence because whatever you grow will save a bro.

The Movember movement is taking on major men's health issues like prostate cancer, testicular cancer, mental health and suicide prevention. Your help in spreading awareness and raising money goes a long way in helping change the face of men's health. Literally.

emember the importance of what the message is, and what you're doing it for," Fraser says. "It's great that there's a bit of humour behind it and everyone has a bit of a laugh with the different moustaches created over the years for Movember, but at the end of the day, the underlying message is that we're doing this for a reason and for a charity so stick it out."

Head here for more information about Movember and how you can get behind the cause.

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4 Tips For Growing Your Moustache This Movember - Men's Health

Murdoch Childrens Research Institute (MCRI) in collaboration with Lineagen, a Utah-based diagnostic genetic testing and clinical information services company, has developed a new test, called Methylation Specific Quantitative Melt Analysis, for the more accurate and timely diagnosis of Fragile X syndrome.

Fragile X syndrome is a common genetic cause of intellectual disability and autism spectrum disorder.

This syndrome impacts about one in 4,000 children. Approximately 90,000 Australians and over one million Americans are impacted in some way by this syndrome.

A large section of these are women who may not be affected with Fragile X, but carry a DNA premutation in their FMR1 gene, which then impacts their children.

One major problem with Fragile X is that this syndrome is not clinically identifiable at a young age. An average age of diagnosis in Australia is about five years, while in the US, it is over three years, according to the Centers for Disease Control and Prevention.

Due to delayed diagnosis, impacted children often do not receive the medical care they need in time.

MCRIs associate professor and lead researcher of this international study David Godler said: The impact of delayed diagnosis is significant and potentially preventable not only to the families but also for our health system. This is why we developed our new test, called Methylation Specific Quantitative Melt Analysis (MS-QMA). This is a one step process, to assist in more accurate and timely diagnosis of Fragile X in affected children referred for genetic testing.

This one-step process looks at the number of chemical modifications or marks, called methylation, added to a patients FMR1 gene in Fragile X, that are not usually found in typically developing children without the syndrome.

An increase in these marks cut down the production of a protein called FMRP, which is needed for healthy brain development and function.

For the first time, this study shows that the number of these marks can be increased, even in people without the usual genetic changes seen in Fragile X syndrome (called CGG repeats).

Previously, this was not known, partly as the present standard testing does not involve looking at these marks as part of the initial CGG screen.

The existing regular testing examines these marks through a second separate test, and only on the restricted number of patients suspected with the typical genetic change (CGG repeats) linked with Fragile X, called full mutation, and large permutation alleles. A reason for this is because the second methylation test is expensive.

For this trial, Lineagen and MCRI compared DNA test results of over 300 patients from paediatric clinics in the US and Australia.

As per standard testing, these patients either had Fragile X mutations or did not have mutations.

Although the second group of patients had no Fragile X mutations diagnosed by standard CGG repeat testing, they were diagnosed by doctors as having a kind of intellectual disability with/or without autism.

The genetic testing was performed in associate professor Godlers laboratory at MCRI using MS-QMA on male and female samples blinded by Lineagen.

With the lifting of the blind, all male and female patients with known Fragile X diagnosis received exact diagnosis using MS-QMA.

Godler said: We also identified, for the first time, smaller more common FMR1 alleles that are not usually tested for methylation (a tell-tale sign of Fragile X), that had abnormal methylation signatures in a significant number of affected patients.

These abnormal signatures were confirmed to be present by the current standard confirmatory methylation test performed by Lineagen. These signatures may compromise function of the FMR1 gene, and potentially lead to Fragile X like clinical features, and is an active area of research for my group.

Contribution to the findings also came from researchers of the University of Melbourne, Victorian Clinical Genetics Services, Genetics of Learning Disability in Newcastle, and The Royal Childrens Hospital.

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Researchers develop new test to diagnose the genetic cause of autism - Medical Device Network

SALT LAKE CITY Mental health is blamed for a lot of issues plaguing society these days, but scientists and biologists still know very little about whats happening inside the brain that brings on problems in certain people.

A group of researchers at the University of Utah, however, may now have a clue.

Theyve identified a link between a group of specialized brain cells, called Hoxb8-lineage microglia, and obsessive compulsive disorder and anxiety in mice.

Similar to humans, female mice are more susceptible to the anxiety-related diseases, though symptoms were observed in male mice, too. The discovery could lead to the development of drugs better suited to treat and/or prevent anxiety and OCD.

It opens up a new avenue for thinking about anxiety, said Dimitri Trnkner, a lead author of the study and assistant biology professor at the U. Since we have this model, we have a way to test new drugs to help these mice and hopefully at some point, this will help people.

The findings suggest a link between biological sex hormones (estrogen and progesterone) and genetics, two major risk factors for anxiety-related disorders in humans, according to the study published this week in Cell Reports.

Until now, it was unknown whether this subset of microglia, which play a crucial role in brain development in the womb, had any other function at all. The new findings build upon previous mice studies conducted by Nobel laureate Mario Capecchi, also a lead author in the new research.

Capecchi had long suspected this subset of microglia was special in some way, but researchers didnt pick up on certain behaviors related to anxiety, such as overgrooming, until this time around its the first study to describe the role of microglia in OCD and anxiety in this way.

We didnt really know what to make of the fact that mice without Hoxb8 appear so normal, until we noticed that they groom significantly more and longer than what would be considered healthy, said Capecchi, a distinguished professor of human genetics at the U.

To test whether sex hormones drove OCD and anxiety symptoms, Trnkner and his colleagues manipulated estrogen and progesterone levels in the mice. They found that at male-levels, the OCD and anxiety behaviors in female mice resembled the male response, and at female hormone levels, the OCD behaviors in male mice looked more like the females severe symptoms, and showed signs of anxiety.

Scientists want to help these people to get their lives back.Dimitri Trnkner

We have a good understanding of how anxiety is produced in people, but cannot do experiments in people, Trnkner said. Of all models, I have great faith that mice are one of the best models, as they are so similar to people.

He said some of the mice had significant hair loss, were more easily stressed out, or lost their natural fight-or-flight response mechanisms without the protective presence of the microglia in their brains.

It shows that the two phenomena are related.

Researchers have long suspected that microglia have a role in anxiety and other neuropsychological disorders in humans because this type of cell can also release substances to harm neurons.

Its surprising to see that (the microglia) are not causing it, but they can protect from it, Trnkner said, adding that researchers and biologists now have an explanation as to why anxiety-related diseases are more common in women.

This news should give hope ... for many reasons, he said.

Science has long tried to find solutions for people who deal with the life-altering mental illnesses, and Trnkner said this puts everyone that much closer to new drugs to treat them, particularly anxiety.

Scientists want to help these people to get their lives back, he said.

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Utah researchers discover link between certain brain cells and anxiety, OCD - KSL.com

One thing that had been brought up time and time again, as a potential answer to the flood of male dairy calves coming from the expanding dairy industry, is sexed semen.

Again during an IFA discussion held in The Hotel Kilmore, Co. Cavan, last week the topic of sexed semen was brought up by farmers and discussed by both the Irish Cattle Breeding Federation (ICBF) and Teagasc.

Speaking at the event, Teagascs Dr. Pat Dillon the Head of the Animal and Grassland Research and Innovation Programme agreed with farmers that progress needs to be made on a sexing lab in Ireland as currently, there is none. He said:

We tried to fly the semen over to England to be sexed and it was a disaster. The conception rate was a disaster. So, the lab has to be in Ireland.

He also stated that he feels farmers are underestimating the benefit of sexed semen because they are getting a dairy calf versus a beef calf which, he said: Is of no value.

I think if we can solve the conception rate, it is a no brainer for all dairy farmers to use it; because of the relative difference between what a good dairy calf is worth last year they were worth about 250 and what a male calf is worth.

The differential is big, if the technology works, he added.

While going on to saythat 24% of semen used by dairy herds in the UK last year was sexed and in Denmark, from 2021 only sexed semen will be allowed to be used on Jersey cows.

However, he said that the issue Teagasc has found, with sexed semen, is around the handling of the semen. He stated: The handling is going to influence the performance of sexed semen.

Also shedding some light on the issue, Sean Coughlan, CEO of the ICBF, said: The challenge is we dont have a lab in the country. So, if you want to get significant volumes of semen from bulls you have to ship them to the UK.

That is an expensive process and the AI companies are not fully sure that there is a market for the semen, should they do that. So, there are significant logistical and financial challenges there at the moment.

Responding to the question: Why are the best bulls not being sexed? he said: The actual sexing process costs the same per straw. But, the number of straws you get is three or four times more for conventional semen, than it is for the sexed semen.

So, there is an opportunity cost on the AI companies. One jump from a bull will get between 200 and 250 straws for sexed versus four times as many for conventional.

Another challenge he mentioned was, because sexing cost more than conventional, the cost of discarding those straws if the bull drops or if there is no demand for that bull, is an issue.

That is why there has to be a broader industry solution to the sexing problem; the AI companies cant necessarily do it on their own, he added.

Pat reiterated this, when he said: The AI companies will not send their top bulls over to England to be sexed, in case they cant bring them back.

Aswell, he also agreed that the best genetics need to be available to farmers.

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Sexed semen: Why is it not there yet? - Agriland

When my sister suffered from Rett Syndrome, an old patterning table and a dubious therapy brought my community together and offered hope.

By: Adriana Knouf

For more than two decades, Sherry Turkle has challenged our collective imagination with her insights about how technology enters our private worlds. The moving essays in the The Inner History of Devices, edited and introduced by Turkle, bring together writings about devices that come supplied with sanctioned ways of understanding them objects ranging from cell phones to prosthetic eyes, from televisions to dialysis machines. By taking time to go further, its authors reveal how what we make is woven into our ways of seeing ourselves, often finding what they did not know they were looking for.

In Adriana Knoufs essay, featured below, a medical device, in its presence and absence, allows her to dream. Faced with her sister Robins illness the gravely debilitating Rett Syndrome Knouf and her family learn of a technique that offers some hope. The family moves Robins limbs rhythmically in crawling and walking movements on a specially built patterning table. While Robin lives, Knouf is immersed in the community around the table. After Robin dies, the tables absence opens a reflective space for Knouf to consider how it shaped her life. With Robin, says Knouf, the volunteers, the discredited therapy method, and the patterning table, we had tried to awaken cognition with care, with the soft sheepskin, the men and women gathered around. But the table has stood in the way of many things, and it takes her time to find her way after Robin and the table are gone. With loss, Knouf is able to re-integrate the past.

Our basement walls were covered with charts, schedules, and sets of instructions. In the southeast corner stood the patterning table. Made when I was eight years old by a friend of the family who lived in a nearby town, the patterning table came up to my chest. Supported on its four corners by thick wooden legs attached with massive bolts, the highly varnished table was strong enough for a 50-to-80 pound person to be moved around on its flat surface. That surface was padded with Naugahyde, which in turn was covered by sheepskin that fitted snugly around the edges.

At this table, every Monday through Saturday, three people (five, if we were training new volunteers) surrounded my sister, Robin. We gently took hold of her fragile arms, legs, and head. With a regular rhythm we moved her extremities in the motions of a crawl: one, turn the head to the left, bring the left arm away from the body and next to the head, bend the left leg next to the torso, and vice versa for the right side; two, keep the head where it was, pull the right arm back next to the body, extend the left leg, and vice versa for the right side; three, repeat as one, but switching left for right; four, repeat as two, but switching left for right. One, two, three, four, the count continued over the course of five minutes, and the patterning session was done, for this hour. The ding of a kitchen timer told us it was time to move on. Next hour we repeated it, on the same table with the same sheepskin cover, with different volunteers. All day this continued, according to the schedules, instructions, and charts that my mom wrote in thick strokes on butcher paper and taped to our recently sheetrocked basement walls. Patterning was combined with breathing exercises, using a mask designed to increase the blood flow to Robins brain.

When I was in first grade Robin was diagnosed with Rett Syndrome, a rare neurological disorder that may include devastating mental and physical symptoms. It afflicts only girls, most of whom are not expected to live past their 18th birthday. The girls often make rocking motions while sitting, wringing their hands. Many are able to develop some basic level of functioning, such as simple mobility or being able to feed themselves. Robin, however, could do none of these things; she was utterly dependent on us. Even so, there were still the smiles, tears, and frowns of any young girl, and in her eyes you could see thoughts she could not speak.

There were still the smiles, tears, and frowns of any young girl, and in her eyes you could see thoughts she could not speak.

Robins disease led our family to take on a major commitment: a full-time, in-home physical therapy program. Our location, rural Iowa, meant we had to develop everything ourselves. To build the equipment, to schedule the people who came in on a regular basis, week after week, we found volunteers, some local, some from afar.

The patterning table took up a good part of our basement, but at a certain point during Robins therapy we set up another apparatus for her, a jungle-gym-like contraption made by the same volunteer who built the patterning table. The new contraption reached from the floor to our seven-foot ceiling. The height of the jungle-gym bars was adjustable. At certain times the overhead bars were low enough so that Robin could walk her hands along them. When she was stronger, the bars were raised and Robin had to grab onto freely swinging handholds of thick nylon rope that hung from the bars; she wore specially designed Velcro footies that stuck to our short-pile institutional carpeting. The resistance from the Velcro was meant to make it harder for her to lift her foot, while the swinging rope was meant to improve her sense of balance. It was hoped that this would strengthen Robins legs and upper body in preparation for walking on her own.

Our work at the patterning table was based on the Doman-Delacato method. It laid out a series of therapies designed to help brain-damaged children toward better functioning. The method is based on an evolutionary metaphor: The individual develops in their lifetime just as the human evolved over generations. That is, development begins at the fish and reptilian stage (crawling) and moves through to mammals and primates (creeping, with the stomach off the ground). Doman-Delacato reasons that if you pattern a brain-damaged child with the motions that are involved in each of these stages, you will unlock the later stages of development. So the repetitive motions on the patterning table were supposed to teach Robins muscle memory to crawl. Yet she never was able to crawl on her own: She learned only to walk a step or two, lightly aided.

The Doman-Delacato method reasons that if you pattern a brain-damaged child with the motions that are involved in each of these stages, you will unlock the later stages of development.

The Doman-Delacato method has not found empirical support, and the American Academy of Pediatrics has issued a number of warnings about the technique over the years. As a child I never questioned our program. To me, it seemed natural that if we moved Robins arms and legs in a certain manner, we eventually would train her brain to move body parts on its own. And of course my parents, like so many others, seized on the programs marketing and the bits of anecdotal evidence that suggested it worked. The Doman-Delacato method provided hope, but I think back on it now with sadness, regret, anger, and resignation.

Robin began to experience seizures when I was in fifth grade, not unusual for Rett girls who often regress from their developmental plateau. I remember the huge stuffed rabbit that lay on the table the day Robin was rushed to the hospital because of her first, unexpected seizure. The seizures made it impossible to continue with the treatments on the patterning table. Yet the patterning table remained in the basement. We removed the sheepskin, and then the Naugahyde quilting, and used the table as any other flat surface, a place to store papers, books, and mail. Gradually the schedules and charts on the butcher-block paper began to come off our walls, but the patterning table remained, a reminder of what we had done, of what we had tried to do.

Even as a young child, I read the few journal articles our family had about Rett Syndrome. They were over my head, but I persisted in my efforts to figure out what was going on with my sister. I launched into my parents popular science book on genetics. A year or two before I took any proper biology class, I was discovering genotypes, phenotypes, and karyotypes, the genetic bases of diseases such as sickle-cell anemia and Parkinsons. At the time, the Human Genome Project was in its nascent stages and the hope for miracle cures was strong. With the insufficient knowledge I had, and bolstered by the arguments in the genetics book, I believed that finding the gene or genes that caused her disease would lead immediately to gene therapy that would reverse Robins genetic malfunction. Of course you had to have a way to get the genes into the cells, so I eagerly read about techniques to force the existing chromatin to take up new genetic materialretroviruses and exotic electro gene therapy. Then came the problem of how to reverse the damage in existing cells. Neuron regrowth in the brain is meager at best; there, repairing genes would not be enough.

The Doman-Delacato method provided hope, but I think back on it now with sadness, regret, anger, and resignation.

As a middle school student growing up with my sister, I thought these problems surmountable. And I determined that all of this would be my doctoral work: I would find the gene that caused Rett Syndrome and discover the necessary therapies to cure the disease. It was merely a matter of time. The summer before high school, I enrolled in a summer program in molecular biology at the state university, a first chance to work with the tools I had read about: restriction enzymes, plasmids, and ethidium bromide stains. I was in the throes of passion: I pored over books I could not understand; I persuaded other students to work unattended in laboratories full of dangerous reagents. I was in a hurry.

But Robin died in the fall of 1993, just short of her ninth birthday. I sunk into a world of grey and black, my schoolwork the only thing that kept me going. I remember the rush to finish assignments in my high-school biology course that were late because of Robins funeral and the time I took off after her death. I remember the fleeting thought that if I could complete my work faster, I could start college early and be on my way to finding the cure for other Rett girls.

I went to Caltech as an undergraduate to study molecular biology with one sole objective in mind: to find a cure for Robins disease. In high school I had performed in a chamber music group and had notions about attending a conservatory. I devoured literature and thought about being an English major and studying philosophy. But now, stronger than all of these were my memories of Robin and the patterning table. I was driven to discover the gene for Rett syndrome. I saw it as an achievable goal.

Then, on a gray California winter day during my sophomore year, I read that a group of researchers had discovered the gene responsible for Rett Syndrome. I posted the article outside my room. I told all of my friends. I wanted to be among the people in the article. But there was more work for me: turning the genetic discovery into a treatment for Rett patients. Soon after, experience as a research assistant convinced me that I was not suited for the biology workbench. I moved toward cognitive sciences, with its higher-level descriptions of perception, action, and emotion.

The patterning table, long unused even during Robins life, was finally removed from our basement, probably passed on to another family using the Doman-Delacato method. Its absence left a space. I had passed the patterning table and its volunteers in the early morning; I had looked toward it when I came home from school; I had walked to it when it was my turn to be part of the group that moved Robins head, legs, and arms.

The table was more than a focus for our thoughts; it anchored our love for Robin and the energy we put into giving her a future.

Without the steady presence of the table, where would we turn? Where would our efforts be channeled? Without Robins influence, what would be our purpose? The table was more than a focus for our thoughts; it anchored our love for Robin and the energy we put into giving her a future. Like the tables in traditional Midwestern churches or cafes, the volunteers who assembled chatted and gossiped and spoke about their lives. It brought Robin into a community. When Robin was happy and obedient, her attendants gave her praise; when she was cranky and ornery, they understood, but lightly scolded. The patterning table made life coherent, all of a piece. With Robin, the volunteers, the discredited therapy method, and the patterning table, we had tried to awaken cognition with care, with the soft sheepskin, the men and women gathered around.

I originally wrote this in 2005, and in the interim there has been a tremendous increase in research on Rett Syndrome in light of the gene discovery. I have moved away from cognitive science and into media arts and design, yet I still draw upon the scientific, social, and emotional experiences written about here in my work. Finally, this was written from the perspective of an assigned-male-at-birth person, however I have recently come out as a transgender woman. The experiences with Robin, the volunteers, and my family have all contributed to making me the woman that I am.

Adriana Knouf is an Assistant Professor of Art + Design in the Department of Art + Design in the College of Arts, Media, and Design at Northeastern University in Boston, MA.

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The Patterning Table That Changed My Life - The MIT Press Reader

Spanish Fork Jud Harwards first hemp crop dangles from his hay barn rafters, drying as it saturates the air with an eyebrow-raising cannabis aroma.

Though he hasnt sold much of it yet, the Utah County farmer is proud of how his 10-acre experiment turned out. Paging through pre-harvest cellphone photos, he shows off his neatly lined plants, some with stalks soaring above shoulder-height and crowned with what he calls the filet mignon of hemp buds.

As part of Utahs industrial hemp vanguard, he relied mainly on his instinct to coax the temperamental crop into flourishing. Little guidance was available, and there were few examples to follow. He was never sure if he was doing it right or wrong.

Its on the fly, says Harward, whos been farming sweet corn and hay for decades. Every day was new.

This legal sea-change coincided with the rising popularity of cannabidiol, or CBD oil, a hemp extract marketed for numerous purported health benefits and beautifying properties. The craze has spawned everything from CBD deodorant to CBD hamburgers, and with estimates that the U.S. market could grow to $20 billion by 2024 some Utah entrepreneurs saw a hemp license as a golden ticket.

In a time of financial struggle for farmers, some in Utah ripped up their hay fields and tossed out their lettuce plants to replace them with the new cash crop. David Lee, Harwards partner in the hemp venture, said hes heard of people mortgaging their farms for funds to get in on the business.

But any get-rich-quick hopes rapidly faded, and Harward said some threw in the towel because of crop failure. Three hemp cultivators separately said it felt like theyd strayed into the agricultural Wild West where reliable information was hard to come by and sketchy consultants and suppliers ran rampant.

They saw an opportunity and some doe-eyed entrepreneurs here in Utah, said Tom Paskett, executive director of the Utah Cannabis Association.

Ruston Peterson has grown hydroponic lettuce out of a greenhouse in Annabella for about a decade. Without a local market for his greens, hes had to drive most of his produce to Salt Lake City for sale, a commute that became tiring.

So, earlier this year, he decided to try his hand at industrial hemp. He shut down his lettuce operation in about a week and began growing hemp starts for a larger cultivator south of him.

People assured him that the cannabis plant is a weed and would grow anywhere. Peterson, along with many others, was about to have a different experience.

There are tons of ways to lose at this game, he said. And everybody, I think, found that out this year.

Some growers, he said, just saw money in their eyes and were victims of their own zeal, determined to plant even though theyd already missed the growing window. And even for people who did everything by the book, nature took its toll, with withering heat stunting one of Lees hemp grows in southern Utah and a September frost claiming plants in fields near Harward Farms.

And then there was the states mandated pre-harvest test to make sure the hemp plants didnt contain an illicit amount of THC, the psychoactive compound in marijuana.

The states Department of Agriculture and Food ordered the destruction of 16,323 plants this year after finding theyd tested hot, or above the 0.3% limit. While that was less than 1% of the states total harvest, the department estimates, it was a setback for the farmers who lost their expensive plants.

Its absolutely doable,"Rigby said. "But is it easy? No.

The difficulty in distinguishing hemp from marijuana, which look and smell the same, also created confusion for local police and passersby at the states hemp farms.

Michelle Finch, a hemp grower for Hansen Plants in Benjamin, said she found people snooping around her greenhouse, drawn by the cannabis scent. And Harward said he had to erect signs around his hemp crop to ward off thieves, who he suspects were passing off the plant as marijuana to gullible buyers.

For the states experienced farmers, cultivating hemp wasnt like growing hay or corn or wheat or anything that they were used to. The cannabis plants were finicky.

You have to be there. You have to baby it, Peterson said.

In Harwards case, he decided to spoon feed the hemp plants fertilizer. He sprayed molasses on them to give them a kick of sugar. And he and other farmers painstakingly harvested them by hand rather than by machine. Learning the ins and outs of the crop was no simple task because, in the nascent and chaotic industry, the farmers didnt know who they could trust.

"There's a lot of crooked people," Harward said. "Rip 'em off Ralph kind of guys."

Paskett said hes also heard from a number of farmers who complained they were taken for a ride by consultants or hoodwinked by out-of-state seed banks. Its possible that some cases could lead to legal action, he said, but thats a heavy lift for farmers who are already financially underwater because they took out a loan to buy seeds.

His group is stepping in to advocate for hemp farmers in some of these situations and has done some investigating and vetting of these suppliers.

We dont want these farmers who took the leap of faith and then got hosed to wash their hands and be done with it forever, he said.

The consequences for picking the wrong business partner can be disastrous, according to farmers.

Hemp plants carry sex chromosomes, and only the female varieties are preferred because they contain cannabinoids in much higher concentrations. Farmers carefully cull through their fields to uproot the male plants so that they dont pollinate the rest of the crop lowering the CBD content in the surrounding females.

To maximize their yield, farmers often sought after feminized seeds that yield mostly female plants. But many of them feel they were sold a bill of goods.

Peterson bought a batch of seeds that was marketed to him as feminized. To his dismay, when the plants grew up, about half of them were males.

So it was three days-worth of work or more because we had to pull plants, Peterson said.

The same thing happened to Amber Berry, who tried growing hemp with her husband near Cedar City. They, too, thought they were getting good seed and ended up with a disappointing blend of male and female plants.

I think everybody jumped in thinking they were going to get rich the first year, said Berry. But theres a reason the value is there. Its not easy to grow, its not easy to do. And I think a lot of people have been let down that way.

Planting an acre of wheat costs about $400 an acre, Harward estimates. Hay is more like $600 an acre, and corn is a little more expensive at $1,200 an acre.

But the price tag for growing hemp dwarfs the others it can easily cost farmers $15,000 an acre, he said. And Harward would guess hes spent more like $20,000 an acre on his crop, if you count the cost of drying the plants and stripping the leaves and flowers off the stems to prepare for CBD extraction.

Tyson Hinkins of Black Dragon Ranch landed one of the states hemp licenses, but the front-end costs were so high that he decided against planting the crop this year.

I was scared, said the Ferron hay farmer, whod been looking to grow hemp with his father, state Sen. David Hinkins, R-Orangeville.

So, hes waited to see how the first year plays out for other Utah farmers.

Berry already anticipates she and her husband wont turn a profit this season; theyll probably try again next year, but on a smaller scale. Even for Harward and Peterson, both of whom had a successful hemp harvest, the battle isnt over. The key to recouping their costs will be careful timing and finding the right buyers, they say.

Since the passage of the 2018 farm bill late last year, the total licensed acreage for hemp cultivation has shot up by more than 455% nationwide, according to Forbes. And the ballooning hemp supply has pushed down prices, especially now that the harvest is coming in.

The price of the oil is rock-bottom, said J.R. Carter, who co-owns Rooster Valley Botanicals in Salina, a company that extracts CBD from hemp. Its the lowest its been all year.

CBD oil that was selling for about $4,500 a liter last year is going for about $800 per liter now, he said. Carters strategy is to hold onto the majority of his oil until the glut subsides and the prices rebound.

That is, if he can discover a doorway into the market, something he and many Utah hemp growers are struggling to do.

I got flower at my house, but I havent had anybody buy it, Peterson said.

Until he does sell it, he wont know if his hemp experiment was worthwhile. Harward is in the same situation, searching for hemp buyers and still wondering if his first-year venture will pan out.

Our long-range goal, he said, is to get through today.

Read more:
Utah hemp farmers find success and struggles in their first year of growing - Salt Lake Tribune

Most U.S. Dairy Cows Are Descended from Just 2 Bulls. Thats Not Good, reads an NPR article. As I perused the article, it only took me a moment to make a connection to the young earth creationist teachings I was raised on.

A few years ago, Dechow and some of his colleagues at Penn State made a discovery that shocked a lot of people. All the Holstein bulls that farmers were using could trace their lineage back to one of just two male ancestors. Everything goes back to two bulls born in the 1950s and 1960s, he says. Their names were Round Oak Rag Apple Elevation and Pawnee Farm Arlinda Chief.

Or, to put it another way:

When researchers at the Pennsylvania State University looked closely at the male lines a few years ago,they discoveredmore than 99 percent of them can be traced back to one of two bulls, both born in the 1960s. That means among all the male Holsteins in the country, there are just two Y chromosomes.

There are just two Y chromosomes found among all Holstein dairy cows. Ponder that for a moment. And then consider this:According to young earth creationist doctrine, all humans after the flood could trace their lineage back to just one male ancestorNoah.

Think back to what you learned about genetics in high school. Most humans have either two X chromosomes or one X and one Y chromosome. Noah would have had one Y chromosome. His three sons would each have had the same Y chromosome. His grandchildren born after the Flood would also have had the same Y chromosome.Of course, there would have been only one Y chromosome to begin with anyway, hundreds of years before thisAdams.

Young earth creationists play fast and loose with genetics. Genetics does not work this way, and that its why researchers are worried about the U.S. dairy population.

What weve done is really narrowed down the genetic pool, saysChad Dechow, one of the researchers.

The females havent fared much better. In fact, Dechowan associate professor of dairy cattle geneticsand others say there is so much genetic similarity among them, the effective population size is less than 50. If Holsteins were wild animals, that would put them in the category of critically endangered species.

After the Flood, in young earth creationists telling, there was a human population size of 8. At creation, the human population size was 2. The level of inbreeding that would have to take place to end up with a population of millions (and, today, billions) starting with population sizes of 2 or 8 is mind numbing.

Theres a reason there are high rates of certain genetic defects among the Amish population.

Currently, more than 50,000 Lancaster County Amish can trace their lineage to just 80 ancestors

Fewer ancestors mean more sharing of genetic material and any genetic defects the same linked to potentially fatal hereditary diseases like SCID contained therein.

Meanwhile, genetic defects not found in the settler population remain locally non-existent.

This isthe founder effect, and evidence of it has been found in Amish and Mennonite populations from Pennsylvania and Ohio to Ontario, Canada.

The founder effect, population bottlenecksthese are real things that affect real, actual genetics. Again, you probably learned about these things in high school.

The thing about the founder effect and population bottlenecks is thatthey result in the loss of genetic information.That is simply how it works.

Any elementary science student knows that genetic homogeneity isnt good in the long term. It increases the risk of inherited disorders while also reducing the ability of a population to evolve in the face of a changing environment. Dairy farmers struggling to pay bills today arent necessarily focusing on the evolutionary prospects of their animals, but Dechow and his colleagues were concerned enough that they wanted to look more closely at what traits had been lost.

Young earth creationists typically respond to concerns about population bottlenecks in one of two ways. The either argue that the original couples genes contained far more genetic diversity than our genes today, effectively canceling the bottleneck entirely, or they argue that the genetic diversity we see today is the result of random mutations in DNA over time.

Lets take the first argument first. Genes simply do not work like that. A population can have more genetic diversity, but an individual person cant. A population of fifty adults living in Bozeman, Montana, for example, is going to have less genetic diversity than a group of fifty adults chosen at random from every country in the western hemisphere. But an individual adult in Bozeman is not going to have more genetic diversity than an individual adult in Brazil, Honduras, or Haiti. Genetics does not work like that.

Now, the second argumentthat the genetic diversity we see today is the result of mutations. Most scientists believe that all Y chromosomes that exist today can be traced back to one Y chromosome that existed around 150,000 years ago. In other words, all men living today have a common ancestor, sometimes termed Y-chromosomal Adam. Young earth creationists argue the same thing, but they put this ancestor only 4,000 years ago. And that matters!

Imagine the rate of mutation required to get all the Y chromosomes we have today, in only 4,000 years!Ive said it before and Im sure Ill say it again: young earth creationists are far stronger believers in evolution than any evolutionary scientist Ive ever met.

Ill leave you with one last thing, from an Answers in Genesis article titled The genetic effects of the population bottleneck associated with the Genesis Flood:

There is one other consideration to make before we conclude the discussion of created diversity, however: the introduction of mutations to the population prior to Babel. Mutational load in children increases with the age of the father (due to the fact that older men pass on gametes that have gone through many more generations/genome copying events than younger men). Thus, any child born to an ancient person could theoretically carry many genetic differences from other people. Extrapolating from the data of Crow, a man 500 years of age would donate approximately 10,000 mutations to a child (the current average is two orders of magnitude less than that). Konget al.concluded that every extra year of paternity adds an average of about 2 additional mutations. This would mean Noah would only contribute slightly more than 1,000 mutations (40 baseline mutations + 500 years x 2) after age 500. But they also discuss models with an exponential mutational increase over time and only studied men under age 50. Either way, it could be said that Noah, by far the oldest to have fathered children recorded in biblical history, was genetic poison to the future world population, as he would be expected to have contributed many new mutations to each of his three sons (and possibly his daughters-in-law, if they were daughters).

Yes. Yes, they really went there.Its ok that all humans are descended from one coupleNoah and his wifebecause Noah fathered his three sons when he was 500 years old, so they would have had lots and lots of mutations. Yep.

What was that I said about young earth creationists being stronger believers in evolution than any evolutionary scientist out there?

I guess that gives us a solution for the Holstein dairy cows, anywayresearchers should just breed them when theyre super old and their genetic diversity will come back. Because Im sure thats exactly what will happen. (It does not work like that.)

I have a Patreon! Please support my writing!

Read more here:
What Do Dairy Cows' Y Chromosomes Have to Do with Young Earth Creationism? Plenty. - Patheos

Dr. Peter Schlegel, M.D., urologist-in-chief at New York-Presbyterian/Weill Cornell Medical Center and president of the American Society for Reproductive Medicine, Jan. 6, 2019

Barbara Collura, president of RESOLVE: The National Infertility Association, Jan. 10, 2019

Dr. Gloria Bachmann, M.D., director of the Women's Health Institute at Rutgers Robert Wood Johnson Medical School in New Jersey, May 22, 2019

Dr. Marc Goldstein, M.D., director of the Center for Male Reproductive Medicine and Microsurgery at the NewYork-Presbyterian Hospital/Weill Cornell Medical Center, Jan. 4, 2019

Alice Domar, Ph.D., an associate professor of obstetrics, gynecology and reproductive biology at Harvard Medical School and director of Integrative Care at Boston I.V.F., Jan. 11, 2019

Paul Flynn, 46, a social worker in Sacramento, Calif., Jan. 17, 2019

Denny Ceizyk, 52, author of Almost a Father: A Memoir of Male Infertility, Jan. 19, 2019

Diagnostic Evaluation of the Infertile Male: A Committee Opinion, Fertility & Sterility, March 2015

Treatment of Male Infertility (Beyond the Basics), UpToDate, September 2019

Temporal trends in sperm count: a systematic review and meta-regression analysis, Human Reproduction Update, November 2017

Maternal, infant and childhood risks associated with advanced paternal age: The need for comprehensive counseling for men, Maturitas, July 2019

The Negative Impact of Higher Body Mass Index on Sperm Quality and Erectile Function: A Cross-Sectional Study Among Chinese Males of Infertile Couples, The American Journal of Mens Health, Jan. Feb. 2019

Tobacco smoking and semen quality in infertile males: a systematic review and meta-analysis, BMC Public Health, January 2019

Habitual alcohol consumption associated with reduced semen quality and changes in reproductive hormones; a cross-sectional study among 1221 young Danish men, BMJ Open, September 2014

Type of underwear worn and markers of testicular function among men attending a fertility center, Human Reproduction, September 2018

Diet and men's fertility: does diet affect sperm quality? Fertility & Sterility, September 2018

Report on varicocele and infertility: a committee opinion, Fertility & Sterility, December 2014

Mens Experience of Infertility: Findings from a Qualitative Questionnaire Study, Fertility Network U.K., November 2017

Originally posted here:
Male Infertility: What to Know and How to Cope - NYT Parenting

Studies have shown that there is a link between cardiovascular health and brain health, but it is unclear whether genetic or environmental factors are most important in determining them both. A new study in twins suggests that nurture, rather than nature, may be decisive.

Evidence from different studies has suggested that there is a strong link between cardiovascular health and brain health.

Researchers have explained that poor cardiovascular health can, with age, contribute to dementia mechanisms, affecting cognitive function.

But what predisposes a person to poorer or better cardiovascular and brain health? So far, scientists have been unable to answer this question with any degree of certainty.

Generally speaking, there are two types of factors that could influence aspects of heart and brain health in the long term. These are genetic (nonmodifiable) factors and environmental (modifiable) factors, a conjuncture that people sometimes refer to as the "nature vs. nurture" conundrum.

To try to determine whether genes or environmental factors play a more important role in long term health outcomes for the heart and brain, researchers from Emory University in Atlanta, GA, decided to study a cohort able to provide more solid answers: pairs of twins.

Identical (monozygotic) twins have the same genetic profile, while fraternal (dizygotic) twins share about 50% of their genes. As a result, pairs of twins can allow researchers to compare the effects of nature with those of nurture more effectively than other populations.

In the current study the findings of which appear in the Journal of Alzheimer's Disease the researchers analyzed the data of 272 male pairs of monozygotic and dizygotic twins, which they were able to access via the Vietnam Era Twin Registry. All of the participants were free of both cardiovascular disease and dementia at baseline.

More specifically, the investigators looked at the relationship between cardiovascular health which they determined by scoring blood sugar and cholesterol, blood pressure, body mass index (BMI), physical activity, diet, and cigarette smoking and cognitive performance.

"Our study across the entire sample of twins confirmed that better [cardiovascular health] is associated with better cognitive health in several domains," notes senior author Dr. Viola Vaccarino, Ph.D.

"The analyses further suggested that familial factors shared by the twins explain a large part of the association and thus could be important for both cardiovascular and brain health," she adds.

According to the findings of the study, the association between heart and brain health was similar among all pairs of twins, regardless of whether they were identical or fraternal.

The researchers believe that some of the modifiable factors that contribute to a predisposition toward certain heart and brain health outcomes include factors relating to early family life, as well as socioeconomic status and education.

"Improving population-level [cardiovascular health] scores, which are extremely low in the United States, has the potential to reduce the burden of dementia along with heart disease," notes co-author Dr. Ambar Kulshreshtha, Ph.D.

"Because [cardiovascular health] factors are modifiable, prevention of cardiovascular risk factors and promotion of a healthy lifestyle beginning early in life should achieve the best results for promoting not only cardiovascular health but also cognitive health."

Dr. Ambar Kulshreshtha, Ph.D.

The findings, the investigators add, are relevant in the context of the American Heart Association's 2020 Strategic Impact Goal. This goal is a 20% improvement in cardiovascular health and a 20% reduction in deaths from cardiovascular diseases and stroke in the U.S., both by next year.

Read this article:
Heart and brain health are connected, but what influences both? - Medical News Today

While Gunnison Sage-grouse population numbers have declined over the last four years, federal agents are penciling out what recovery looks like for the species listed as threatened under the Endangered Species Act (ESA).

The U.S. Fish and Wildlife Service (FWS) soon will release its draft Recovery Plan for the bird, whose greatest population lies in the Gunnison Basin.

After the bird was determined to be threatened in 2015, local conservation efforts have been underway in an attempt to preserve the species and avoid a potential endangered listing, which carries much more stringent restrictions. The draft Recovery Plan is the next step in fulfilling requirements under the threatened listing and sets both population and habitat goals which must be achieved for the bird to be delisted.

Things can change over time its not set in stone forever, said FWS Regional Director Noreen Walsh.

FWS representatives met with stakeholders in Gunnison last week to explain the three-step process for Recovery Planning and Implementation under the ESA. While the draft Recovery Plan has yet to be released, FWS officials outlined its contents during the meeting.

The first step in the planning process a Species Status Assessment (SSA) was completed last April. It includes details about each of the eight populations of grouse, said FWS biologist Allison Vendramel.

The SSA informs the second step the Recovery Plan which outlines criteria, actions, time and cost involved in achieving target population and habitat goals. Once released, the public will have 60 days to offer input on the Recovery Plan.

Finally, a Recovery Implementation Strategy will be created to fulfill delisting criteria. Vendramel noted that each step can be revised and expanded as more information is learned in the process.

The road to recovery

The current draft Recovery Plan, Vendramel said, calls for resiliency, redundancy and representation for the species, and that objective and measurable thresholds would signify when recovery likely has been met.

Resiliency, she said, is dependent upon population numbers and the birds ability to adapt to annual climate fluctuations, while redundancy is reliant upon the number of grouse and their distribution. Finally, representation is indicated by the birds ability to adapt to change, its genetic make-up, behavior and ecological conditions. All three qualities must be demonstrated for the bird to be delisted.

The plan sets population and habitat goals as well. Five of the eight grouse populations will be subject to high-male count targets and habitation requirements. For the high-male count target, a running three-year average was determined over the course of at least seven consecutive years.

During the time period used for the calculation, the birds population numbers were highest. From the high-male count, population estimates are generated.

Populations which must achieve high-male count and habitat targets are located in the Gunnison and San Miguel basins, Pion Mesa, Crawford and Monticello. The Gunnison Basin, Vendramel said, demonstrates the greatest resiliency.

Two of the Gunnison Sagegrouse populations Dove Creek and the Cerro Summit-Cimarron-Sims Mesa (CSCSM) will only be required to have the amount of habitat which could potentially support a high-male count target, without actually requiring the number of males.

High-male count for Dove Creek is set at 30 while the same target for CSCSM is only seven.

Efforts to improve some populations

Colorado Parks and Wildlife (CPW) Grouse Conservation Coordinator Kathy Griffin estimates the Gunnison Basins population at 2,862 and the birds population throughout its entire range at 3,299. Those numbers have declined from high estimates in 2016 of 4,440 and 5,141, respectively.

She speculated that the decline was due to two years of drought followed by a harsh winter with late and heavy snows.

Griffin said grouse numbers for both the Gunnison and greater sage-grouse are down across their range in virtually every state, indicating it may be due to normal population fluctuations.

In Gunnison County, efforts have focused on improving habitat and minimizing future impacts to the grouse. In 2006, the county adopted regulations that seek to minimize development conflicts through its landuse review process.

By way of comparison, San Miguel County has taken a different approach than Gunnison County to preserve habitat and protect the bird by focusing on conservation easements. However, like other satellite populations, county leaders have only seen a declining trend in the annual counts, said San Miguel County Commissioner Hilary Cooper.

The San Miguel Basin population, she said, continues to be threatened by oil and gas activity, powerlines, habitat fragmentation and weather changes, and her county is learning from Gunnison Countys example.

Much of our Gunison Sagegrouse habitat is on BLM land and we are actively engaged in protests and litigation against Bureau of Land Management actions that directly impact occupied habitat and threaten the bird, specifically with oil and gas activity, Cooper told the Times. The county is currently developing a GIS analysis in order to guide the most effective actions based on the latest science and lessons learned from the more successful efforts in the Gunnison Basin population.

Steps toward delisting

Recovery actions offered in the draft Recovery Plan include site-specific interventions. Areas prioritized to minimize stressors such as noise and development would be within the four-mile radius of an active lek, according to the plan.

The draft recommends improving public awareness, offering incentives and resources to conserve and improve habitat quality and quantity and better data collection. Recovery actions include relocating Gunnison Basin birds to other populations which have enough habitat to sustain them, and conserving existing habitats by improving management plans.

Finally, delisting the bird was defined during last weeks meeting. Once a species is delisted, Vendramel said a community must decide if it wants to maintain measures which have resulted in recovery.

Delisting is the Fish and Wildlife using a biological rationale to say, This species does not need the protection of the ESA, said Vendramel, noting that when targets are achieved the federal agency exits the picture.

Still, she questioned whether communities would have the will to keep a species such as the grouse from being relisted.

Weve reached a threshold, she said of the situation that exists when targets are met. Does a community want to stay above that threshold?

Recovery Implementation Strategy workshops are scheduled throughout the birds population area in January. The final draft of the Recovery Plan is slated for approval in October 2020.

(Chris Rourke can be contacted at 970.641.1414 or at chris.rourke@gunnisontimes.com .)

See the original post here:
Steps outlined for grouse recovery - Gunnison Country Times

Cheetah Conservation Station keepers at the Smithsonians National Zoo are celebrating the arrival of a male lesser kudu calf, who was born Oct. 14 to 5-year-old mother Rogue and 9-year-old father Garrett. During their routine animal health assessments, keepers found that Rogue had given birth and observed the calf nursing, moving well and exploring his environment. A neonatal veterinary exam the following day, Oct. 15, found the calf to be healthy and strong. He is steadily gaining weight, growing from about 13 pounds at the time of his exam to about 19 pounds at 9 days old.

Animal care staff are allowing the calf to bond with mom in a quiet enclosure behind the scenes. His 10-month-old brother, Kushukuru, was present for the birth and continues to spend evenings with the calf and their mother. The younger kudu will make his public debut later this fall, weather permitting.

Keepers describe the calf as bold and alert, and they are looking forward to watching the young brothers explore the habitat, chase one another and spar with each other and their father. The Zoo will provide details about the calfs debut on its Facebook, Instagram and Twitter accounts as the date approaches. Meantime, visitors can view Garrett and Kushukuru at the Cheetah Conservation Station, along with two Abyssinian ground hornbills named Karl and Karoline that share their habitat.

Rogue arrived at the Zoo in October 2016 from the St. Louis Zoo in Missouri, per a recommendation to breed with Garrett. Most of the Zoos animals participate in the Association of Zoos and Aquariums Species Survival Plan (SSP). The SSP scientists determine which animals to breed by considering their genetic makeup, nutritional and social needs, temperament and overall health. This is the second calf for both Rogue and Garrett.

Native to arid and semi-arid areas of northeastern Africa, including parts of Ethiopia, Somalia, Kenya, Sudan, Uganda and Tanzania, lesser kudu are listed as near threatened by the International Union for Conservation of Nature. Lesser kudu number about 100,000 in the wild, but the population is decreasing due to habitat loss from human and livestock expansion, hunting and disease.

# # #

Caption: Lesser kudu female Rogue with her newborn male calf behind the scenes at the Zoos Cheetah Conservation Station.

Continued here:
Lesser Kudu Born at Smithsonian's National Zoo - Smithsonian's National Zoo and Conservation Biology Institute

In a recent article for Current Affairs, Nathan Robinson describes Harvard psychologist Steven Pinker as the most annoying man in the world because Pinker is the type of person who constantly insists hes Just Being Reasonable while he is actually being extremely goddamn unreasonable. Although Robinsons article was a bit harsh in tone, it gestures at something very real: were in the midst of an epidemic of intellectuals, almost entirely white men, who claim to embody Reason and Rationality while flagrantly and habitually succumbing to the same tribalistic tendencies that they identify as the Ultimate Enemy.

My own experience with Pinker and his ilk exemplifies the problem. Last January, I published an article here at Salon that summarized some extremely detailed criticisms that I wrote of Pinker's book "Enlightenment Now!" More specifically, I examined a few pages in the books Existential Threats chapter, one line or passage at a time, since my own research focuses on existential threats (that is, threats to civilization and humanity) and thus I have some knowledge of the topic.

Although Pinker is widely known, or at least was at one point, as a clear-headed, objective intellectual of the highest caliber, his chapter on existential threats was overflowing with quotes taken out of context, misrepresented ideas, false dichotomies, blatantly inaccurate claims, poor reasoning, dubious citations, condescending straw-man attacks and cockamamie ad hominems. If the chapter had been a first-year undergraduate term paper, and if the professor were an exceptionally easy grader who habitually dished out As for poorly researched papers, Pinkers chapter might have received a C.

(The popularity of poor scholarship seems to be on the rise, incidentally. Just consider the egregious mistakes made by Jared Diamond in his most recent book, "Upheaval.")

What was most telling, though, was the response to my article. For example, the founding editor of Skeptic magazine, Michael Shermer, tweeted this in response to my critique:

Where @RichardDawkins had his fleas (The Dawkins Delusion etc.), @sapinker has his cockroaches (the oleaginous Phil Torres desperate for attention), artfully squashed here:

Shermer then linked to a blog post by Jerry Coyne, which contained a response from Pinker. Before getting to that, though, Shermers tweet is notable for a couple of reasons. First, not only does it contain a personal attack, but the personal attack is overtly uncivil. Thats a bit humorous given that Shermer, as well as Pinker, are famous for accusing progressives, especially those who care about women and people of color, of incivility. For example, in May of this year, Pinker tweeted:

Are you concerned about the growing illiberalism, incivility, intellectual conformity, and repression of debate in today's universities? Join us at the meeting of the society set up to encourage viewpoint diversity and constructive debate on campuses. Ill be giving the keynote.

But Pinker did nothing to call out Shermer for his patently crude, puerile behavior, which has also included calling people he disagrees with (seriously) namby-pamby bedwetters and (seriously) losers. This is perhaps unsurprising when one realizes the Pinker has unwaveringly supported Shermer despite multiple women accusing Shermer of sexual harassment, assault and even rape. To my knowledge, Pinker has made no effort to contact any of Shermers purported victims. And why would he? What does truth have to do with standing by your comrades? Instead, Pinker has repeatedly de-emphasized the issue of rape in society and college campuses by tendentiously pointing to opinions that support his preferred views rather than by honestly examining the totality of evidence, which gives a quite different perspective. All of this is very worrisome, tribalistic behavior. But it gets worse.

Back to the blog that Shermer references. The particular post was published by Jerry Coyne, a biologist at the University of Chicago who has become something of Pinkers bulldog, defending him against any and all criticisms no matter what, with (almost) no questions asked. One of the most recent examples is Coyne coming to Pinkers defense after a picture emerged of Pinker with Jeffrey Epstein, the child sex-trafficker who recently killed himself in a New York jail cell.

Coyne quickly dismissed criticisms of Pinker hanging out with Epstein as mere slander and character assassination, writing that suggestions that Pinker should have known better disturbed me so much since Pinker is a friend whose character I respect. The problem is that Pinker appears in the photo with Epstein and he tweeted out an affidavit defending Epstein after Epstein was convicted of sex crimes, which happened in 2008. That is inexcusable and gross but not to Coyne, whose allegiance is rooted not in evidence but loyalty.

So it should be no surprise that Coyne tore into my critique of the existential threats chapter, inaccurately calling it a hit piece. Indeed, by any reasonable account, the article was a substantive critique of shoddy scholarship. In fact, I was in touch with four scholars or writers whose work Pinker misrepresents within just a few pages of the chapter. All of them were unhappy with the quality of Pinkers work, so its not like this was just me being a grump.

For example, the political economist Eric Zency, whom Pinker incorrectly describes as an engineer, was livid that Pinker had used a line from one of his papers to mean the exact opposite of what Zency had intended. In an email to me about Pinkers misuse of his quote, Zency remarked, How this guy managed to become a public intellectual in fields so far removed from his expertise is something to wonder at. I agree.

Pinker also wrote a response to my critique, but it only further justifies the view that Pinker is or has become, sadly an ideologue who cant acknowledge when hes wrong. Just consider that the second sentence of his response makes an ad hominem claim that Im trying to make a career out of warning people about the existential threat that AI [i.e., artificial intelligence] poses to humanity. Since ['Enlightenment Now'] evaluates and dismisses that threat, it poses an existential threat to Phil Torress career.

This is obvious nonsense. First of all, the same thing could be said about Pinker: Since his career these days is based on claiming that things have been going quite well for humanity, convincing people that AI poses an existential threat itself could be seen as an existential threat to Pinkers reputation. How Pinker and Coyne both missed this obvious flaw suggests that they werent wearing their critical-thinking hats. The aim of Pinkers comment was to discredit a critique without having to engage with its substance.

Once again, I contacted four scholars or writers who affirmed errors in a small handful of pages in Pinkers chapter. I have no doubt that if someone were to find the same problems in a chapter written by, say, Reza Aslan or Linda Sarsour, both of whom are loathed by the Pinker-Coyne crew, theyd be hailing the critique as proof that Aslan and Sarsour are intellectual frauds.

Pinker then defended one of his most flagrant mistakes: classifying a computer scientist at UC Berkeley, Stuart Russell, as someone who isnt worried about AI. The exact opposite is true! Pinker then doubled down, insisting that his description of Russell was accurate, even though Russell himself told me in an email, which I quote in my article, that hed seen this [mention in Pinker's book] and I agree its an incorrect characterization. So, you have Pinker on one side refusing to acknowledge that he incorrectly characterized a person who says he has been incorrectly characterized. This led Julia Galef, a notable effective altruist who hosts the Rationally Speaking podcast and has knowledge of the relevant issues, to tweet:

Im frustrated Steven Pinker wont admit an error in Enlightenment Now.Summary:- Pinker names Stuart Russell as an expert whos skeptical of AI risk- Someone points out that's exactly backwards; Russell is one of the main experts warning about AI risk- Pinker doubles down

She concludes that the point is its bad that Pinker got this fact wrong and wont admit it. This encapsulates the central problem: Pinker and his ilk dont acknowledge errors when they make them; they are ideologues rather than truth-seekers, willing to bend the facts, launch personal attacks and censor critics to win debates. At exactly the moment in history when we need true intellectual leadership, people who exemplify intellectual honesty and integrity, the most, we get stubborn tribespeople.

But the problem is hardly confined to those mentioned above: Shermer, Coyne and Pinker. Consider another Intellectual Dark Web (IDW) luminary, Sam Harris, one of the most famous atheists in the world because of his book "The End of Faith." Previously, I never had any reason to believe that Harris was racist but I do now. He has spent a massive amount of time and energy defending Charles Murray, author of "The Bell Curve," which argues that black people are inherently inferior to white people.

Over and over again, ad nauseam, Harris has used his large platform to suggest that Murray isnt a junk scientist peddling cowardly racist memes, but someone whos been victimized by those anti-truth progressives. Even more, Harris apparently believes Murrays claim that blacks are genetically dumber than whites. In a podcast with Josh Zepps, Harris opines the following with a wholly unjustified degree of epistemic confidence:

As bad luck would have it, but as youd absolutely predict on the basis of just sheer biology, different populations of people, different racial groups, different ethnicities, different groups of people who have been historically isolated from one another geographically, test differently in terms of their average on this measure of cognitive function. So if youre gonna give the Japanese and the Ashkenazi Jews, and African Americans, and Hawaiians youre gonna take populations who differ genetically and we know they differed genetically, thats not debatable and you give them IQ tests, it would be a miracle if every single population had the same mean IQ. And African Americans come out about a standard deviation lower than white Americans. A standard deviation for IQ is about 15 points. So, if its normed to the general population, predominantly white population for an average of 100, the average in the African American community has been around 85.

In other words: black people are dumber than white people. Why? Because of genetic evolution, meaning that IQ is in the genes and the genes of white people are, well, just plain better. What a bold stance, especially amid the ongoing rise of white nationalism in the U.S. and Europe!

In all seriousness, the irresponsibility of being a public intellectual with a large following and spouting unsupported claims with the sort of certainty you might expect from someone reciting the second law of thermodynamics is shocking. If Pinker is annoying, as Robinson claims, then Harris is intolerably obnoxious, constantly demeaning people for not being Rational and Reasonable while simultaneously making anintellectual fool of himself with claims like those above.

Other examples could be adduced, but I dont have an extra 20,000 words to spare. The point is that the entire IDW movement is annoying. Its really, really annoying its champions misrepresent positions without their (mostly white male) audience knowing, and then proceed to embarrass the opposition. They embrace unsupported claims when it suits their narrative. They facilely dismiss good critiques as hit jobs and level ad hominem attacks to undercut criticism. And they refuse they will always refuse, its what overconfident white men do to admit making mistakes when theyre obviously wrong. I am annoyed, like Robinson, mostly because I expected so much better from the most popular intellectuals of our time.

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Steven Pinker, Sam Harris and the epidemic of annoying white male intellectuals - Salon

Women wait with their malaria-struck babies for treatment in Angola. Will opponents of gene ... [+] engineering deny prevention to families like these?

Mosquitoes are not just obnoxious summer pests they are a serious health threat to most of the world. In fact, the WHO calls mosquitoes one of the deadliest animals in the world.

Why? Mosquitoes carry and spread diseases to humans that cause millions of deaths every year. The biggest threat is malaria: a half a million lives are lost annually, and Africa alone loses $12 billion in health care, productivity, investment, and tourism to the disease. Then theres Zika, dengue, chikungunya, and yellow fever each carried by mosquitoes, and each extracting their toll in human lives and livelihood.

But now, there is hope that biotechnology can help solve this crisis. The solution lies in genetically modifying a small population of mosquitoes and releasing them into malaria-prone areas. These mosquitoes carry a lethal gene that kills larvae before they reach adulthood and carry malaria to others, just stunting human illness.

Oxitec is a British biotechnology company doing just this. Over the last fifteen years or so the company has introduced Friendly Technology. Oxitecs latest results back up historic successes in Brazil, which saw dengue cases in one area reduced by 91% in a small trial. Their latest study showed a 96% reduction in mosquito numbers, this time using a more effective strategy of targeting the biting, egg-laying females - albeit leaving non-biting males to survive and reproduce. A great success, on the face of it.

The anti-GM backlash

However, Oxitec and others are taking a lot of flak from the anti-GM lobby, which according to the Genetic Literacy Project spent $850 million in the last five years alone opposing everything from the way we label genetically engineered food to fabric thats fermented from sugar.

The backlash was triggered by a paper that, ironically, seems likely to be retracted (or at least highly modified) due to exaggerated predictions of more robust mosquitoes, among others. Though reports of genetic mixing between surviving introduced mosquitoes and local mosquitoes were valid, the lethal gene was not actually present - which was the most likely outcome considering the lethality of the gene in question. A lethal gene will naturally diminish in frequency among a population.

But another consideration is to ask: does it even matter, all things considered, when eradication of disease should be the goal?

The risk of inaction

Mosquitoes are utterly deadly, and even when theyre not they provide among the largest disease burden on the planet. Tuberculosis may kill more people (around 1.3 million per year, compared with around 450,000 for malaria). But malaria infects 20 times that number of people.

Those 219 million annual malaria cases cost low income countries a significant chunk of their GDP up to 1.3% in the worst affected while just a 10% reduction in malaria was associated with a 0.3% growth in a much cited study on the economic burden of malaria. For Uganda, the economic gain from eradicating malaria would total around $50 million USD.

This doesnt take into account emerging diseases such as dengue and Zika virus, among others. In Brazil, the focus of Oxitecs recent trials aiming to reduce numbers of Aedes aegypti, 1.2 million people were infected with dengue in the first six months of 2019 six times more than in 2018 with an associated 388 deaths. Zika virus, carried by the same mosquito, exploded onto the scene in 2015 and has been associated with a range of effects on babies born to infected mothers in 10% of cases.

Yes, there are likely some knock-on ecosystem effects of releasing Oxitec mosquitoes. There might well be reduced prey for fish that eat the larvae, or less food for some of the birds that eat the flying insects. However, mosquitoes are not irreplaceable as far as the wider ecosystem is concerned, especially pests such as Aedes aegypti. There are another 3000 species of mosquito other than the three which primarily cause disease in people.

The World Health Organization (WHO) brands Aedes aegypti mosquitoes as being exquisitely adapted to city life, and that they prefer to breed in artificial containers. Given this information, it makes it even less important that lethal genes might persist among the wider population of these costly pests, less so that they might be eradicated - an opinion seemingly shared by researchers who have looked into the potential environmental costs associated with getting rid of the worst species of disease-bearing mosquitoes.

It all boils down to a cost/benefit analysis. Is the risk of some genetically modified mosquitoes passing on transgenes to wild populations worse than the risk of millions of people being infected with haemorrhagic fever and malaria, or babies being born with abnormally small heads (microcephaly)?

In any case, we will always have to take measures to reduce the burden of disease. What about the alternative forms of pest control and their relatively indiscriminate, off-target effects?

What is natural?

Oxitec, the company responsible for releasing genetically modified mosquitoes, have always known and stated - explicitly so - that some mosquitoes would survive to breed and pass on their genes. They have also taken measures to ensure that populations containing the lethal gene eventually go their predestined way.

In fact, their latest mosquitoes are meant to pass on genes to wild populations, this time to reverse the naturally occurring genetic mechanisms that render mosquitoes resistant to pesticides such as DEET. (Incidentally, multi drug resistance in the malaria parasite itself is also increasing).

To put our collective minds at ease, its worth pointing out that nature is weirder than what Oxitec is doing. mosquitoes perform their own version of enforced sterilisation, whereby male tiger mosquitoes (of the species Aedes albopictus) can mate with, and sterilize, female Aedes aegypti mosquitoes.

The fact that diseases such as Zika and dengue are present in Brazil in the first place is evidence that we are about as far removed from whatever natural used to mean as we can possibly be. Zika was introduced by a traveller from French Polynesia. The only way it got to Brazil was by aeroplane.

Its not just Zika traversing the globe in such a manner. There are emergent diseases popping up left, right and center, and it is not an easy task to keep them in check. The WHO warned us over ten years ago that infectious diseases are emerging at a rate not seen before. (One example is West Nile Virus, a mosquito-borne disease first described in 1937 in Uganda but discovered in New York in the summer of 1999. It is becoming more prevalent in California and will soon reach Silicon Valley and the San Francisco biotech region.)

It is no wonder. We live in a globally connected world with a rapidly expanding population that is a hotbed for disease-causing agents to emerge, mix, and spread (from viruses and bacteria to malaria parasites), which means that we need highly innovative, modern solutions to control them. Its an evolutionary arms race, and we need all the tools we can muster. If one of them happens to include lethal genes that successfully wipe out local populations of disease-causing mosquitoes, so be it.

Mosquito-borne diseases already threaten half of the global population.And as the climate warms and favors the mosquito, these diseases could spread to a billion more people.

Clearly, our current methods of control havent quite been enough to stop 219 million people becoming afflicted with malaria each year, or an increasing number suffering and dying from dengue and other diseases. Its not genes escaping that is the problem, but the sheer difficulty in eradicating mosquitoes and their diseases at all.

We must proceed carefully with new genetic engineering technologies, but we must also weigh the risks of inaction: each year hundreds of millions of people mostly children needlessly die, get sick, or suffer genetic defects. GMO mosquitoes are something we can do about it.

So what would you rather have: GMO mosquitoes or dying babies?

Acknowledgement: Thank you to Peter Bickerton for additional research and reporting in this post.

Please note: I am the founder ofSynBioBeta, and some of the companies that I write about are sponsors of theSynBioBeta conference(click herefor a full list of sponsors).

The rest is here:
British Biotech Company Sees Hope In Reducing Mosquito-Borne Diseases And Deaths With GMOs - Forbes

COLUMBUS, Ohio The first overmatched victim ofOhio State defensive end Chase Youngflashes on a projector screen in the Buckeyes football facility. Defensive coordinator Jeff Hafley hits pause to single out an offensive tackle from Florida Atlantic, frozen in game-film infamy amid an autopsy of Youngs sacks.

Hafley see-saws the film until it stops in the precise place that shows Young vaulting a half-step toward the quarterback an instant after the snap. Theres a tone of pity in Hafleys voice, as the Florida Atlantic linemen are still lined up perfectly still like a row of folding chairs.

A half-step advantage for a defensive lineman is like a 10-yard cushion for a wide receiver, and Young appears poised to bull-rush past the line with the ease of fans flowing through a turnstile.

Not one of the offensive linemen is moving, Hafley said, shaking his head. Its. Over. Doesnt it look like hes running out of the blocks in a track meet?

When the film resumes, Young proceeds to barrel around the edge virtually unimpeded for one of his 9.5 sacks, a total thats tied for No. 1 in college football. The frozen moments of singular dominance have come in flourishes through seven games, as the image of Youngs blond dreadlocks splayed out behind him as he mauls helpless quarterbacks has seemingly played on a loop this season.

Young is a 6-foot-6, 270-pound freak who appears to be darting toward greatness like, well, a sprinter coming out of the blocks. Former BuckeyeNick Bosacompares Youngs skill set to elite NFL rush endsKhalil MackandVon Miller, two generational pass-rush talents. That type of get-off, Bosa told Yahoo Sports recently. He has that speed first, power second.

Youngs potential invokes the hyperbole of an athlete that can change the paradigm of the position. Along with consistently mangling quarterbacks, he can also fluidly drop back into coverage, block kicks and has an imposing physique that one NFL scout likens toLeBron James.

The natural comparison for Young in Columbus remains the Bosa brothers, former Buckeyes who went No. 2 in the 2019 draft (Nick) and No. 3 overall in 2016 (Joey). Both Bosas have performed at a level that justify those lofty picks, but former OSU coach Urban Meyer says that Young may be the most talented of the three.

The guy looks like the Predator, said FAU coach Lane Kiffin,mimicking Youngs popular nickname. Theres only 10 guys like him in the world.

NFL scouts see him the same way, as hes widely considered the most talented prospect in all college football. His draft position will be reflective of the quarterback desperation among the NFLs most despondent franchises. Hes what you want from a guy who is going to be the No. 1 pick, said a veteran NFL scout. Hes a super athlete, hes massive and hes been productive.

Youngs emergence is a combination of fortunate genetics, conscientious parenting and a flurry of bold-faced mentors. They begin with Carla and Greg Young, his exacting mother and father who shepherded his journey through do-your-own-laundry discipline and strict regiments of pushups and tough love. Young also learned along the way from No. 1 NBA draft pick Markelle Fultz and No. 2 NFL pick Nick Bosa, and lapped up all the lessons of Larry Johnson, the Buckeyes defensive line Yoda.

As Ohio State (7-0) pursues its first College Football Playoff bid since 2016, Young is simultaneously sprinting toward meeting Fultz, his old DeMatha Catholic High School hoops teammate, in the rarest of airs. I used to tell him when I was younger that I was going to be the No. 1 pick in basketball, Fultz said. And he was going to try and meet me up top and be the No. 1 pick in football.

How didChase Younggrow into the most feared player in all of college football? It all starts with how he grew up.

The stories of Chase Youngs accelerated trajectory begin at age 3, at his familys home in Cheltenham, Maryland. When Young first jumped off the diving board at the familys housing development, he debuted with a front flip. From there, Young kept somersaulting ahead of his peers.

The evolution of Chase Young into a generational prospect starts with his parents, who provided both outsized genetics and a diverse plan for success. Greg Young is 6-foot-10, a lunar eclipse of a human who played college basketball at Bowie State and still holds the burly build of a 1980s NBA power forward. Carla Young is 6-foot, and while she didnt play sports, she helped set the tone of work ethic and competitiveness in the family.

Greg is retired from Arlington County Sheriffs Office after years of working the 7 p.m. to 7 a.m. shift. Carla has worked the last 32 years for the Department of Transportation and 34 overall years for the federal government. Greg Young worked 15 days a month, a schedule that allowed him to train his kids. (Chases sister, Weslie, played college basketball at North Carolina Wesleyan). The Youngs believed in both physical and mental development, with specialization frowned upon and weights and trainers not necessary.

The training began soon after their kids could walk. Greg and Carla insisted their kids play outside, with skateboards, sandboxes and trampolines luring their kids out of the house. They didnt do video games, Carla said, proudly.

Ohio State star Chase Young has been building up to this moment his whole life. (Yahoo Sports illustration/Photos courtesy of Young family)

Chase Young played soccer until eighth grade, played basketball until his junior year of high school and ran track into high school, developing the footwork, speed and dexterity inherent to those sports. Chase even played the piano, saxophone and violin. In high school, he sang in the choir at St. Vincent Pallotti (Maryland) before transferring to DeMatha Catholic.

Chase may be the most physically blessed player in college football, but he didnt begin seriously lifting weights until late in high school. He built a strong core with 100 pushups and 200 sit-ups a day, as Greg believed in Herschel Walkers philosophy that physique could be built on the weight of the body.

Greg insisted on toughness, including enrolling Chase to play football with older kids. Chase played quarterback for the Patuxent Rhinos, a team of 9-year-olds, easily memorizing and executing the full assortment of plays. There was just one issue. Every time he got hit, he would get up crying, Greg said. They were like, Why's he always crying? I said, He's 6!

Chase didnt get a cell phone until high school, never had a television in his bedroom and wasnt allowed to grow out his dreadlocks until 10th grade. Attendance at Sunday church was mandatory, as was family dinner with Carla cooking up meatloaf, mac-and-cheese and greens, piled high for growing kids. Privileges came with accomplishment, as Chase was allowed to get tattoos only after he got to Ohio State. Carla relented after a memorable text: Are you still gonna love me if I get a tattoo? Chase asked. Carla lets out her hearty trademark laugh. Of course!

Chase began washing and ironing his own clothes at age 7, with the unappealing alternative of having to wear dirty clothes. He began mowing the lawn at age 10 and he and his sister both were in charge of packing their own lunch.

A lot of parents can learn from them, said Randy Ransom, one of Chases youth coaches and a family friend. I wouldnt say they sheltered him, but they told him the rules and he abided by them.

As Chase navigates the final stretch of college until his vast potential will collide with professional riches, he looks back with appreciation. What my parents did, he says, it's the reason why I am who I am today.

Nick Bosa laughed on the other end of the phone. He knew the question was coming and chuckled upon its arrival. Hed grown up in the five-star shadow of his brother, Joey, so hes had years of refining his dodging technique. Chase can be as good as he wants, Nick Bosa said. I dont want to compare.

The making of Chase Young into a prospect that can inhabit the same rare conversational sphere as the Bosas continued upon his arrival at Ohio State in 2017. At that time, Joey Bosa was a burgeoning star on a defensive line where every starter Jalyn Holmes, Tyquan Lewis, Sam Hubbard and Nick Bosa ended up getting drafted.

Nick Bosa most appreciated how Youngs desire to learn and grow into a star matched his physical promise, as he jokes Young showed up at 270 pounds with a six pack. After a lifetime as Joeys little brother, Nick enjoyed the role reversal in mentoring Young.

He saw me as a role model, I guess, which was cool, Nick Bosa said. I was always looking up to people. To have someone younger than me looking up to me was cool.

The education of Chase Young came at the feet of Bosa, the loaded defensive line room and its wise leader, Johnson, the 68-year old position coach who has tutored a daunting eight first-round defensive linemen. The best evidence of Johnsons wizardry could be seen on a recent Monday in the Ohio State football facility, as his players sat outside his office, eager to seek his counsel and grandfatherly advice.

Johnson saw a unique inquisitiveness in Young during his recruitment, as Young would constantly text him during recruiting to ask question normal recruits wouldnt ask. What was it like recruiting this guy? Where do you see my weight? Where do you see me playing?

Hes probably the most intriguing guy Ive ever recruited, Johnson said.

Chase Young (2) chases down the ball carrier during the Ohio State Buckeyes' win over the Florida Atlantic Owls. (Getty)

It has become a perfect marriage of teacher and student, as Hafley calls Johnson one of the best pass-rush coaches hes ever been around. Young has evolved from a raw athlete to a nuanced pass rusher, mastering techniques like Johnsons trademark side-scissoring the offensive linemans hands away to be able to turn his hips and flip to the quarterback. Thats why some guys make $30 million and some guys dont, said Meyer, now a Fox analyst, of Youngs hips. Chase has the speed, size and flexibility.

Strength coach Mickey Marotti saw the final stages of Youngs evolution come this winter. He began paying forward the advice Nick Bosa passed onto him, motivating and teaching young linemen like former five-star Zach Harrison and redshirt freshman Javontae Jean-Baptiste. In the circle of life in the Buckeye defensive line room that Johnson calls moving the yardstick, Bosa still sends clips of good rushes to Young on Snapchat. Young passes on the message to the next generation.

Ohio State coach Ryan Day noticed Youngs off-field development a few days into summer camp, when the Buckeyes came out with low energy during pre-practice stretching. Without any prodding from coaches, Young got in front of the team and barked at them to follow his juice and energy.

Hes prompted other guys to take the lead, and you see guys coming out of their shells, Day said. In this day and age, with this generation, thats not easy to do.

When asked about Youngs physical dominance, Marotti keeps steering the conversation back to his personal attributes. Marotti teases Young that he needs a hair net for his blond locks. Young shoots back by poking fun at Marottis size-12 feet, abnormally large for a man of modest height. Marotti jokingly calls Young a newscaster politician, as their conversations veer to topics like the secrets of Marottis marriage. Its really fun, Marotti says. Hes very inquisitive, its like hes a grown-up.

Young isnt nave to the NFL riches that potentially await him in the upcoming months. He went on YouTube before the season to learn to meditate to help with focus. What hes doing right now, hes leaving a legacy, Day said. In a day and age when people get caught up in whats next, he really wants to leave a legacy here. That makes him special.

Greg Young beams when relaying the genesis of one of his sons best pass-rushing attributes, a first-step toward that Marotti calls ginormous. Greg declares: The first step came from basketball.

Young transferred to DeMatha, the erudite school outside Washington D.C., midway through his sophomore year in 2014. The move came primarily because of his football potential, but he also played one season of JV hoops and one on varsity. That coincided with Fultzs senior season of 2015-16, around the time hed emerged as a favorite to become the No. 1 pick in the 2017 NBA draft.

Youngs time playing basketball for veteran coach Mike Jones wont invoke memories of DeMatha legends like Danny Ferry, Victor Oladipo or Adrian Dantley. But Young says he entered high school at 5-foot-6 and still was growing into his body. I definitely had to struggle, Young said. I wasnt always this big, this fast in high school.

Young backed up Josh Carlton, a 6-foot-11 forward who has gone on to become a starter at UConn. Jones insists that Young earned more playing time than he was given, but Jones said he wanted to showcase the players who specialized in basketball to help their futures. Even then, Chases football future was clear.

Chase was a luxury, Jones said. I dont say that negatively at all. If we needed someone to go into the game and knock the snot out of someone, wed put him in. But he was a much better player than that. His role for us was definitely not consistent with what his ability was.

Markelle Fultz and Chase Young look on before a DeMatha Catholic High School basketball game. (Photo credit: Mike Jones)

That role meshed philosophically with how Greg taught Chase to play, as he wanted his son to test opponents by fouling them as hard as possible early in the game. Theyre either going to want to fight you, Greg reasoned, or theyre going to cry.

Jones recalls Young accepting his role, admiring how both he and his family never complained about playing time. Jones remembers Young just as fondly in the classroom, as Jones teaches public speaking at DeMatha. He complimented Youngs engagement in the class Young would be the first to offer concise feedback or say, Yo pay attention, before a classmates presentation. When he said it, Jones said with a laugh, everyone straightened up and fixed their ties.

Fultz and Young, who were friends prior to DeMatha, still stay in close touch. They trade texts, including mutual support, as they share a unique bond. I always tell him, Young said, its a matter of time before he gets healthy and its a wrap for the whole NBA.

Fultz has gone through what Young is facing, and hes told him to keep his circle tight.

[I want to make sure he] doesnt let all the hype and stuff get to him, which I dont think will happen, Fultz said. Hes a humble young man who works extremely hard. I tell him to be himself and watch the people around you.

That giant first step for Chase Young is leading to his scintillating final steps, as collegiate glory and professional riches all loom within reach. As he aims to meet his old teammate atop a different draft, Chase Young is secure in acknowledging who guided him there one pushup and laundry load at a time.

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Why freaky OSU DE Chase Young is the best player in college football: Theres only 10 guys like him in the world - Yahoo Sports

The local Association of Psychology is working to address some of the myths and misconceptions about ADHD during this, ADHD Awareness Month.

Dr. Janine Hubbard says despite extensive clinical and medical studies, many people still question whether Attention Deficit Hyperactivity Disorder is a real medical condition.

She says ADHD conservatively affects about 5 per cent of the overall population and has a very strong genetic component.

Dr. Hubbard says ADHD is a chronic disorder affecting both males and females relatively equally that persists throughout a persons lifetime.

She says symptoms change over time, and the environments also change but you dont grow out of ADHD it just looks different.

She says that child who couldnt sit still in class might grow up to be someone who can sit when socially appropriate, but theyre fidgeting, clicking their pen or shaking their foot.

While many think of ADHD as manifesting in hyperactivity, brain scans show that the brain is actually less active. Dr. Hubbard says the disorder is best managed with medication if symptoms interfere with regular activities like school or work.

She says many people pour a cup of coffee if they want to help focus, stimulants prescribed for patients are similar in that they help to wake up the brain.

Dr. Hubbard says while a diagnosis of ADHD can mean that school or certain work environments might be more challenging for some, people with ADHD do succeed, especially when they choose a profession that keeps them engaged and stimulated.

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Association of Psychology Addressing Myths and Misconceptions about ADHD - VOCM

PEORIA People often think of breast cancer as a disease that exclusively targets women. While it is true that a great majority of breast cancer cases are women, Doctor Jessica Guingrich, a medical radiologist for OSF HealthCare and the Susan G. Komen Breast Center, says the disease doesnt discriminate against men.

Men and women both have breasts, so men and women can both get breast cancer. Its just significantly less common in a man because of the way their breasts develop, compared to the way a womans breast develops, said Dr. Guingrich.

Breast cancer in men is rare; about 1% of all breast cancers are diagnosed in males. According to the American Cancer Society, in 2019 about 2,670 invasive breast cancers will be diagnosed in men, and 500 men will die from the disease.

65 year old Allen Smith of Canton is part of that 1%. Smith, a prostate cancer survivor, was going through testing when a CT scan found an area of density in his chest wall. Doctors recommended a mammogram, which was a strange request to Smith.

I thought, everybodys going to look at me. Theres a guy coming in here, you know hes going to have a mammogram or whatever, and I felt a little odd, he said. I wasnt embarrassed by it, but I just felt a little odd because, you know this is kind of just like a new thing. I mean, you just dont hear of this.

Soon after his scan at the Susan G. Komen Breast Center in Peoria, Smith was diagnosed with stage zero breast cancer.

You could have knocked me on the floor with a feather, said Smith. I had no idea. I had no lump, I had no problem whatsoever there that I knew of.

Because of the rarity of breast cancer in men, many dont know the signs of a potential problem. Dr. Guingrich says a lump in the breast area, usually behind the nipple, is the main symptom for men to look for.

Its important to get that lump checked out because in a man, that lump, if it is a cancer, just has a greater chance of getting into the chest wall and into the muscle, into the nipple, into the lymph nodes much quicker than in a female because there just isnt much tissue buffer around a mass thats developing, she warned.

Men can also experience skin dimpling or puckering around the breast area, nipple retraction, redness or scaling of the nipple or breast skin, or even discharge from the nipple.

Dr. Guingrich also says, as in women, family history of breast cancer needs to be considered for men. Both Smiths mother and grandmother had breast cancer.

If a man has a really strong family history, or if a man maybe has a family member who is a BRCA gene carrier, its really important to be aware of that risk, said Dr. Guingrich. You need to talk to your doctor about what can be done. A man should consider having genetic testing perhaps if they have a very strong family history of breast cancer.

According to the American Cancer Society, the best strategies for reducing the number of deaths caused by the disease is early detection and prompt treatment.

Smith says, there is no reason to delay if you think you have a problem.

If you think theres something wrong with you, follow up. Dont think youre going to bother the doctors, dont think youre going to be a pain, follow up. Get it checked, Smith urged.

Dr. Guingrich agrees.

I think the important thing is that if a man notices a change to just be reassured that the physicians at breast facilities are there to help and to solve problems and give reassurance that things are okay, and if something needs to be biopsied, then we biopsy it and try to make it as comfortable of an environment as possible, she said.

OSF Saint Anthonys HealthCare recently opened the OSF HealthCare Moeller Cancer Center at 2200 Central Ave., Alton.

Link:
Our Health: Breast Cancer in men: What you need to know - Alton Telegraph

Growing up in a family of entomologists, bankruptcy lawyer Mark Sterling was always interested in moths. He could never quite kick the habit despite being busy rescuing troubled businesses. Now, at 61, the retired Briton is back to chasing moths-and his pursuit has brought him to India.

Sterling is an (unpaid) scientific associate at the Natural History Museum, London. His current project is to look at certain material in the museum since British entomologist Edward Meyricks time which has so far remained uncurated and undescribed on the basis of morphological analysis and DNA sequencing.

Meyrick was an entomologist with a passion for butterflies and small moths. He is believed to have described more species than anyone and his collection of around 100,000 specimens is housed at the London museum.

The work that I am doing at the moment involves a group of which 25 species were described between 1894 and 1934, Sterling said. Almost all of them were described by Meyrick, in almost all cases in India and Sri Lanka except for a pest species described by another scientist from Japan.

Speaking to Mongabayon the sidelines of the recently-concluded Asian Lepidoptera Conservation Symposium at the Zoological Survey of India, Kolkata, Sterling said this group is known as the Metathrinca group small white moths within the family Xyloryctidae.

Butterflies and moths make up the order of insects called Lepidoptera. Xyloryctidae is a family of moths contained within the superfamily Gelechioidea, described by Edward Meyrick in 1890.

Theres been very little work done on that group [Metathrinca] since, Sterling told Mongabay. The work so far shows that this is actually a very large group that occurs from New Guinea to Japan, including most of southern Asia, India, and China.

One aim of his Kolkata visit, said Sterling, is to find some modern material (specimens) from India.

There is no recorded specimen from India of any Metathrinca group moth since 1934, he said. I am hoping to find fresh specimens because the historic Indian specimens are too old to produce viable DNA sequences at a realistic cost, if at all. I am hoping to find live specimens from India which will allow me to sequence modern materials.

Sterling observed it is impossible to know exactly what type of habitats the old Indian materials were collected from. All we know from their data is that they were collected from Meghalaya/the Khasi Hills/Shillong but from this, we can assume that they are classical northeast Indian hill and forest species, he said.

However, the British NHM also has species from southern Asia, in the 1970s and 1980s, which are a mixture of hill and forest species including a number of mangrove forest species, so Sterling said he is hoping to find some modern Indian specimens at the forest site in Dalma and the mangrove forest site in the Sunderbans.

Whether I find any is largely a matter of luck as I have no real insights into the exact sorts of habitats in which these species occur, said Sterling, describing what he calls a hit and miss approach. So I will be putting out light traps at night, as the males, in particular, are attracted to light. I am hoping I may find a few females. I will be putting out my lights hoping for the best but, if I dont find at least some specimens on this trip, I will be disappointed, given the diversity of the group and the richness of the Indian species. If I find the material I will need to collaborate with scientists in India in order to sequence and/or describe them and will undoubtedly need to find an excuse to come back to Kolkata in order to find further materials.

Sterling said he is keen on examining the genetic difference between the described Indian species and the species he is describing from the rest of Asia.

If I can find fresh Indian specimens which are morphologically identical to already described Indian species I will be able to obtain sequences from the fresh specimens and form a view as to the genetic divergence of the Indian species from the species from other parts of Asia, he said.

Sterling acknowledged that discovering and describing moth species may not be a huge benefit to mankind, but knowledge of biodiversity is critically important.

Its not something which will make the difference between economic riches for large corporations and it is not something which will improve agriculture so I cant claim it will be a huge benefit to mankind, argued Sterling. But knowledge of biodiversity is critically important. Biodiversity in itself should be regarded as an important resource in its own right and we will be contributing to the knowledge of biodiversity.

He also stressed on balancing conservation with real needs.

We need to conserve biodiversity but that cant be the only aim of the government; you have to balance conservation with very real needs of feeding a massive population, elaborated Sterling. You need to know how to conserve, what is most important to conserve, and how to do it and in order to do that as a starting point, you need to understand what the biodiversity is, and to understand the biodiversity you need to know what species are in a place.

Sterling grew up in England, Germany, and Belgium in a family of lepidopterists and has always been interested in moths and smaller moths because butterfly diversity in England is very low. There are only 64 species of resident butterflies in England, he said. Moths are more of a challenge and interesting and smaller moths were not very well known when I was younger so they were an obvious area of interest.

Unlike other family members, Sterling became a lawyer but always kept an interest in moths. When I became a partner in my firm I was sent to Hong Kong to set up an Asian bankruptcy business so I started working on smaller moths of Asia in my spare time, he recounted. I never managed to kick the habit. Now that I am retired I can go back to the family passion.

The older brother of well-known entomologist Phil Sterling, lead author of the acclaimed micro-moth guide The Field Guide to the Micro-moths of Great Britain and Ireland, Mark Sterling finds smaller moths challenging.

Smaller moths are challenging because there are very few people working on them, compared to larger moths and even more so if compared to butterflies, Mark Sterling noted. For example, if I go out on the field somewhere in Hong Kong, Malaysia or North East India I will expect that 50% to 80% of the smaller moths I see will be undescribed species.

Sterling says there could be at least 20,000 to 30,000 species of Lepidoptera waiting to be discovered only in India.

In India, there are about 10,000 species of Lepidoptera described, he said. Published estimates range between a further 10,000 to 20,000 which are undiscovered. On the basis of old historical records in NHM on which I am working, I would have thought the 10,000 to 20,000 number is a significant underestimate so there could be at least 20,000 to 30,000 species [of Lepidoptera] only in India.

But with a dearth of taxonomists, how do you get people to take an interest in conservation?

Sterling believes an appreciation of the natural environment and biodiversity should be an important part of everyday life. In some countries, this is beginning to happen. For example, in England, membership of the Royal Society for the Protection of Birds exceeds the aggregate membership of the three main British political parties. Appreciation of moths and butterflies should be an important and exciting recreational activity open to everyone, he emphasised.

Seeing a rare beautiful butterfly or moth ought to be as exciting as watching [Indian cricketing legend] Sachin Tendulkar score a century, observed Sterling. The starting point is introducing people, children who want to do recreational activities in the evening, when they are not working, to the spectacular diversity of moths and butterflies.

If they are regarded as something to be treasured then research into them is going to be much easier to find funding so the starting point is educational and proselytization of natural resource as something which is there to be appreciated and enjoyed as a relaxation from what we do in our working lives, Sterling signed-off.

This article first appeared on Mongabay.

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A Briton chasing moths comes to India: Its as exciting as watching Tendulkar score a century - Scroll.in

Two recent papers- The Formation of Human Populations in South and Central Asia ( Vageesh Narasimhan et al) and An Ancient Harappan Genome lacks Ancestry from Steppe Pastoralists or Iranian Farmers (Vasant Shinde et al) - have sparked different interpretations on what they reveal about the genetics of ancient Indians. The papers were authored by a team of geneticists from Harvard Medical School working with Indian scientists. They studied ancient DNA from sites in Europe, Central Asia and South Asia, including a sample from the Indus Valley Civilisation site of Rakhigarhi, before drawing their conclusions. One of which was the contested claim that descendants of pastoralists from Eurasian steppes migrated to the Indian subcontinent in the first half of the second millenium BCE, "almost certainly" bringing Indo-European languages. Their studies also claim the Steppe migrants eventually contributed 0-30% of the genes of groups living in India today. In an email interview, Harvard geneticist Prof David Reich breaks down the findings. Excerpts.

1) What are the big takeaways from the 2 recent studies you co-authored - Vasant Shinde et al 2019, and Narasimhan et al 2019?

1. At least some of the people of the ancient people of the Indus Valley Civilization were a mixture of south/southeast Asian-related hunter gatherers and Iranian-related hunter-gatherers. I say Iranian-related because their ancestors may actually have lived in South Asia rather than the Iranian plateau for many thousands of years before the time of the IVC. We just dont know yet where they lived because of lack of ancient DNA from the relevant times and places.

2. A population like the people we call the Indus Valley Cline - consisting of a Harappan individual from the site of Rakhigarhi, plus 11 individuals who were buried at the sites of Gonur in Turkmenistan and Shahr-i-Sokhta in Iran and as likely migrants from the Indus Valley Civilization is the primary source population of both North and South India.

3. Some time in the first half of the second millennium BCE, descendants of Steppe pastoralists entered South Asia from the north, eventually contributing 0-30% of the genes of groups living today (varying depending on the present-day group), and also almost certainly bringing Indo-European languages. There is no evidence that the actual people who brought these genes to South Asia were pastoralists by occupation - their ancestors were pastoralists.

2) What more can you tell us from your studies about this Steppe migration? Mostly male? Was it a significant number - so as to make such drastic changes in the gene pool of such a large area?

It is entirely plausible, and in my opinion even likely, that the movement of people bringing this ancestry to the Indian subcontinent was not sex-biased, and involved both males and females. However, the process by which people carrying this ancestry mixed with people with ancestry like the individual from Rakhigarhi, was a sex-biased one, whereby most of the Steppe ancestry to mixed population was contributed by males. Note that according to our paper, in the Swat Valley, Steppe ancestry mixes into South Asia in a sex-biased way but in the REVERSE pattern, that is, most of the Steppe ancestry is coming from females.

"In the Late Bronze Age and Iron Age individuals of the Swat Valley, we detect a significantly lower proportion of Steppe admixture on the Y chromosome (only 5% of the 44 Y chromosomes of the R1a-Z93 subtype that occurs at 100% frequency in the Central_Steppe_MLBA males) compared with ~20% on the autosomes (Z = 3.9 for a deficiencyfrom males under the simplifying assumption that all the Y chromosomes are unrelated to each other since admixture and thus are statistically independent), documenting how Steppe ancestry was incorporated into these groups largely through females (Fig. 4). However, sex bias varied in different parts of South Asia, as in present-day South Asians we observe a reverse pattern of excess Central_Steppe_MLBArelated ancestry on the Y chromosome compared with the autosomes (Z = 2.7 for an excess from males).

These differences could be explained by a non-sex-biased migration from Central Asia into South Asia of people carrying Steppe ancestry, followed (at some point later) by preferential incorporation of females from this population into the Swat Valley peoples, and preferential incorporation of males from this population into the ancestors of most present-day South Asians.

3) When did they reach the Indian subcontinent?

We know this rather precisely from our analysis: the first half of the second millennium BCE.

4) Was this the 'collision' that formed present day Indian populations?

This is one of at least four major collisions we now know about:

a. The mixture of Iranian-related ancestry and South/Southeast Asian hunter-gatherer-related ancestry that formed the Indus Valley Cline on average 7400-5700 years ago.

b. The mixture of people on the Indus Valley Cline with people from the southeast carrying relatively more South/Southeast Asian hunter-gatherer-related ancestry after the decline of the mature Indus Valley Civilization around 4000-3000 years ago

c. The mixture of people on the Indus Valley Cline with people from the north carrying Steppe ancestry after the decline of the mature Indus Valley Civilization around 4000-2000 years ago

d. The mixture of these two mixed populations (b and c)

There are surely more collisions yet to be discovered!

5) And what was the route to the Indian subcontinent? From the Yamnaya culture in Eastern Europe to the Central steppes (BMAC) and then to South Asia?

The exact routes are currently unknown. Almost certainly it started in far eastern Europe more than 5000 years ago (with the Yamnaya or their close relatives), then 4500-4000 years ago moved possibly west to east-central Europe (but this westward-before-eastward deviation is not certain), and then moved far to the east across the Urals to the central Steppe (Kazakhstan) and Central Asia (places like Turkmenistan) before moving into South Asia 4000-3500 years ago.

It is likely, based on our analysis, that the population that contributed genetic material to South Asia was (roughly) ~60% Yamnaya, ~30% European farmer-like ancestry, and ~10% Central Steppe hunter-gatherer ancestry.

6) What difference, according to your study, did it make to the Indus Valley Civilisation gene pool ?

This ancestry admixed with people like those we sequenced from the Indus Valley Civilization, eventually contributing 0-30% Steppe-derived ancestry to present-day populations.

7) Was it the contrast in the genetic profiles of later Indian (South Asian) people and that of the 2600 BC Rakhigarhi woman and the 11 other Indus Valley people (discovered at sites related to IVC) that helped you get this picture?

Yes. With these individuals, we for the first time found ancient people who could serve as a statistically fitting genetic source for the largest component of ancestry in South Asian (the Iranian-related ancestry)

8) Does your Rakhigarhi study 'An Ancient Harappan Genome lacks Ancestry from Steppe Pastoralists or Iranian Farmers' in any way contrast the findings of your other ( Narasimhan et al) study 'The Formation of Human Populations in South and Central Asia'.

The two studies are fully consistent. I am confident that there are no contradictions.

9) Digs at the Indus Valley site Rakhigarhi, from where the woman's skeletal remains were discovered show an archaeological continuity. No signs of destruction. Is it possible to have a shift in a population and even possibly a change in civilisation without a disruption in material culture? Have you see that happen elsewhere?

This is entirely possible. We discuss this explicitly in our paper by making an analogy to a major and slightly earlier cultural and genetic transformation in western Europe, where we know more accurately what happened because of a richer ancient DNA record

If the spread of people from the Steppe in this period was a conduit for the spread of South Asian Indo-European languages, then it is striking that there are so few material culture similarities between the Central Steppe and South Asia in the Middle to Late Bronze Age (i.e., after the middle of the second millennium BCE). Indeed, the material culture differences are so substantial that some archaeologists report no evidence of a connection. However, lack of material culture connections does not provide evidence against spread of genes, as has been demonstrated in the case of the Beaker Complex, which originated largely in western Europe but in Central Europe was associated with skeletons that harbored ~50% ancestry related to Yamnaya Steppe pastoralists (18). Thus, in Europe we have an unambiguous example of people with ancestry from the Steppe making profound demographic impacts on the regions into which they spread while adopting important aspects of local material culture. Our findings document a similar phenomenon in South Asia, with the locally acculturated population harboring up to ~20% Western_Steppe_EMBAderived ancestry according to our modeling (via the up to ~30% ancestry contributed by Central_Steppe_MLBA groups)

10) You've said that people who formed the population of the IVC is the single largest genetic contributor to people living in South Asia today? Can you elaborate?

The great majority of present-day South Asians are a mixture of two source populations that formed after the decline of the Indus Valley Civilization: the Ancestral South Indians (ASI) and the Ancestral North Indians (ANI). In our paper (Figure 4D), we show that the ASI and ANI both have high proportions of Indus Valley Cline ancestry (similar to that of the Rakhigarhi individual). Depending on the particular model used, this number could range from 30-60% for the ASI, and very roughly around 70% for the ANI. Since present-day South Asians are largely a mixture of ANI and ASI who in turn both have major proportions of Indus Valley Cline-type ancestry, this is the largest source of ancestry in present-day South Asians.

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Steppe migration to India was between 3500-4000 years ago: David Reich - Economic Times