Archive for the ‘Male Genetics’ Category

The ensuing gold rush was catastrophic for fish and porpoise alike. At first, the totoabas were so plentiful that they could be harpooned from the beach, butchered for their mawswhich, when dried, resemble colossal potato chips with unappetizing tendrilsand left to rot. But as the population dwindled, fisherman turned to new methods. Near the Colorado River estuary, they laid gill nets, aquatic weapons of mass destruction designed to hang in the water column and ensnare passing prey. Vaquitas have the fatal misfortune of being nearly the same size as totoabas, so the nets were disastrous for them.

Lorenzo Rojas-Bracho, head of the International Committee for the Recovery of the Vaquita, at his home in Ensenada, Mexico.

The Mexican government banned totoaba fishing in the 1970s, but the killing never really stopped. By 2017, Rojas-Bracho and Taylor faced a difficult decision. With vaquitas stuck in critical decline, what else could be done? They'd talked about setting up a captive breeding program for years, but the expense and complexity had never seemed worth the risk. Now, though, it was time for a Hail Mary. That summer, Rojas-Bracho's boss, the Mexican environment minister, gave him the go-ahead to assemble his armada.

The team had four weeks to pull it all off. Early on in the effort, the vaquitas showed a knack for slipping past the researchers' nets, or just disappearing altogether. Then, with one week remaining, everything changed. It was a gorgeous day, Rojas-Bracho recalled, sinking into his sofa. I was far away from the action, but I could follow by radio. They were saying, We have the vaquita, it's behaving very nicely, it's coming to the net. We've got it on board, it's a female, it's a great animal, it's very calm. Rojas-Bracho motored over to take a look. It was the closest he'd ever been to a live vaquita. I could see my eyes in her eyes, he said.

As the sun set and the sea darkened, the team introduced the vaquita to its temporary home, el Nido. At first, it swam erratically, taking the measure of its new surroundings. Then it started to adapt. Rojas-Bracho was seated on deck, taking it all in. He heard one of the vets say to the vaquita, You're doing well, baby, so he stood up and walked away to call the environment minister. By the time he hung up, the situation had changed dramatically.

The animal started behaving wildly, and then it stopped breathing and it started to kind of sink, he said. Then there was a decision to take it out of the water and do CPR for three hours until it died, and that was painful. Jesus, it was painful. Seeing the best vets in the world trying to prevent the vaquita from dying, saying, Come on sweetie, you can do it, you can do it, it was He sighed quietly and lifted his glasses to wipe his eyes.

Conservationists must ask unpleasant questions: How to triage so many at-risk creatures? How to decide what lives and what dies?

The scientists' terrible night wasn't over. They took the vaquita onshore and performed a necropsy. Rojas-Bracho didn't sleep. The next morning, everyone agreed to shelve the captivity project.

The rest is here:
How a Pudgy Porpoise May Save Other Animals From Extinction - WIRED

The single biggest threat to mans continued dominance on the planet is thevirus. Joshua Lederberg, Nobel Prize in Physiology or Medicine, 1958

One of the most terrifying aspects of the COVID-19 pandemic is that we dont know what makes one person die, another suffer for weeks, another have just a cough and fatigue, and yet another have no symptoms at all. Even the experts are flummoxed.

Ive been puzzled from the beginning by the sharp dichotomy of who gets sick. At first it was mostly older people with chronic disease, and then a young person with low risk would show up. It can be devastating and rapid in one individual but mild in another, said Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Disease on a media webinar.

What lies behind susceptibility to COVID-19? Gender? Genetics? Geography? Behavior? Immunity? All of these factors may be at play, and they overlap.

Comedian Bill Maher blames poor immunity on eating too much sugar, and a thriving industry pitches immune-boosters, but much of the strength or weakness of an individuals immune response arises from specific combinations of inherited gene variants. Thats my take as a geneticist, and Dr. Faucis. Perhaps genetics and the immune response play a role in why one person has a mild response, yet another rapidly deteriorates into viral pneumonia and respiratory failure, he said.

During the first weeks of the pandemic, the observation that many victims were either older, had certain chronic medical conditions, or both, fed a sense of denial so widespread that young people flocked to Spring Break beaches as older folks boarded cruise ships in Florida as recently as early March. And then the exceptions began to appear among the young people.

While clinicians on the front lines everywhere are saving as many lives as possible, researchers are racing to identify factors that the most vulnerable, and the most mildly affected, share, especially the asymptomatic carriers. And as the numbers continue to climb and more familiar possible risk factors are minimized or dismissed age, location, lifestyle habits genetics is emerging as an explanation for why otherwise young, strong, healthy people can die from COVID-19.

Following are possible genetic explanations for why some people become sicker than others. These are hypotheses, the language of science: ideas eventually fleshed out with observations and data. Proof is part of mathematics; in science, conclusions can change with new data. The public is getting a crash course in the scientific method.

The most obvious genetic risk factor in susceptibility to COVID-19 is being male. The details of disease demographics change daily, but males are about twice as likely to die if theyre infected as are women: 4.7% versus 2.8%.

At first people blamed the sex disparity on stereotypes, like the riskier habits of many a male compared to females. But the sex difference comes down to chromosomes.

In humans, a gene, SRY, on the X chromosome determines sex. Males have one X and a puny Y; females have two Xs. Fortunately, nature takes care of this fundamental inequality of the sexes, which I detailed hereand in every biology textbook Ive ever written.

To compensate for the X deficit of the male, one X in every cell of a female is silenced beneath a coating of methyl groups, an epigenetic change. But which X is silenced differs, more or less at random. In a liver cell, the turned off X might be the one that the woman inherited from her father; in a skin cell, the silenced X might be the one inherited from her mother.

The immune system seems to benefit from the females patchwork expression of her X-linked genes, with a dual response. Gene variants on one X may recognize viruses, while gene variants on the other X may have a different role, such as killing virally-infected cells.

Women also make more antibodiesagainst several viral pathogens. But some of us pay the price for our robust immune response with the autoimmune disorders that we are more likely to get.

People with type O blood may be at lower risk, and with type A blood at higher risk, of getting sick from SARS-CoV-2, according to results of a recent population-based study. But the idea of type O blood protecting against viral infections goes back years.

We have three dozen blood types. Theyre inherited through genes that encode proteins that dot red blood cell (RBC) surfaces, most serving as docks for sugars that are attached one piece at a time. The RBCs of people with type O blood do not have an extra bit of a sugar that determines the other ABO types: A, B, or AB.

The unadorned RBCs of people with type O blood, like me, are less likely to latch onto norovirus (which explains why I rarely throw up), hepatitis B virus, and HIV.

An investigation of ABO blood types from the SARS epidemic of 2002 to 2003 provides a possible clue to the differences. People with blood types B and O make antibodies that block the binding of the SARS viruss spikes to ACE2 receptors on human cells growing in culture. Since the novel coronavirus enters our cells through the same receptors, are people with type O blood less likely to become infected?

Thats what researchers from several institutions in China have found in the new study. They compared the blood types of 2,173 patients with COVID-19 from three hospitals in Wuhan and Shenzhen to the distribution of blood types in the general population in each area.

People with type A blood were at higher risk than people with type 0 blood for both infection and severity of the illness.

In the general population 31% of the people are type A, 24% are type B, 9% are type AB, and 34% are type O. But among infected individuals, type A is up to 38%, type B up to 26%, AB at 10%, and type O way down to 25%.

The researchers conclude that the findings demonstrate that the ABO blood type is a biomarker for differential susceptibility of COVID-19. I think thats a bit strong for a trend, considering the exceptions. But the researchers suggest that their findings, if validated for more people, can be used to prioritize limited PPE resources and implement more vigilant surveillance and aggressive treatment for people with blood type A.

Immunity and genetics are intimately intertwined. Links between mutations both harmful and helpful and immunity to infectious diseases are well known.

Mutations in single genes lie behind several types of severe combined immune deficiencies (SCIDs), like bubble boy disease. Sets of human leukocyte antigen gene variants (HLA types) have long been associated with increased risk of autoimmune conditions such as celiac disease, type 1 diabetes, and rheumatoid arthritis, and were for many years the basis of tissue typing for transplants.

In HIV/AIDS, two specific mutations in theCCR5 gene remove a chunk of a co-receptor protein to which the virus must bind to enter a human cell. The mutation has inspired treatment strategies, including drugs, stem cell transplants, and using CRISPRto recreate the CCR5 deletion mutation by editing out part of the gene.

Might variants of the gene that encodes ACE2, the protein receptor for the novel coronavirus, protect people in the way that a CCR5 mutation blocks entry of HIV? The search is on.

Another clue to possible genetic protection against the novel coronavirus may come from the SARS experience from years ago and parasitic worm diseases in Africa. (This hypothesis I came up with on my own so Im prepared to be shouted down.)

In a human body, the SARS virus disrupts the balance of helper T cells, boosting the number of cells that fight parasitic worms (the Th2 response) while depleting the cells that protect against bacteria and viruses (the Th1 response). The resulting Th2 immune bias, in SARS as well as in COVID-19, unleashes the inflammatory cytokine storm that can progress to respiratory failure, shock, and organ failure.

In subSarahan Africa alone, a billion people have intestinal infections of parasitic worms, the most common of which is schistosomiasis. Its also called snail fever because the worms are released into fresh water from snails and burrow into peoples feet when they wade in the water.

The worms mate inside our blood vessels, releasing eggs that leave in urine and feces into the water supply. Remaining eggs can inflame the intestines and bladder. The infection begins with a rash or itch, and causes fever, cough, and muscle aches in a month or two. A drug treatment is highly effective.

Genetics determines susceptibility, or resistance to, schistosomiasis. And thats what got me thinking about COVID-19.

People who resist the flatworm infection have variants of eight genes that ignite a powerful Th2 immune response that pours out a brew of specific interferons and interleukins. Could the Th2 immune bias of the novel coronavirus SARS-CoV-2 not be as devastating to people who already have the bias, to resist schistosomiasis? If so, then places in Africa where many people are immune to schistosomiasis might have fewer cases of COVID-19.

So far parts of Africa have reported low incidence of the new disease. On April 7, the World Health Organization reported approximately 10,000 cases in all of Africa. Thats similar to the number of deaths in New York City, although Africa could be on track for the exponential growth seen elsewhere. But if the lower number in Africa persists, then maybe those eight genes are protecting people. Adding to the evidence is that the 8-gene set varies more between West Africans and Europeans than do other sets of genes.

Like the ABO blood type study, if the 8-gene signature that protects against schistosomiasis protects against COVID-19, then the signature should be overrepresented among those exposed to the virus who do not get very sick, and underrepresented among those who do. However, its possible that Africa is just behindthe rest of the world in reporting COVID-19 cases. So, a thought experiment for now.

Before researchers zero in on a highly predictive genetic signature of COVID-19 risk, we can think about how the information would best be used:

I hope that discovery of a genetic basis for COVID-19 vulnerability or resistance will not inspire discrimination unfortunately, genetic information has had a legacy of misuse.

Ricki Lewis is the GLPs senior contributing writer focusing on gene therapy and gene editing. She has a PhD in genetics and is a genetic counselor, science writer and author of The Forever Fix: Gene Therapy and the Boy Who Saved It, the only popular book about gene therapy. BIO. Follow her at her website or Twitter @rickilewis

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Can genetics explain the degrees of misery inflicted by the coronavirus? - Genetic Literacy Project

The premise of my latest novel, Virgin & Child, will no doubt be seen as so outrageous and provocative that it calls for some explanation.

Its a novel that arose out of a thought experiment, which I wrapped up as a literary thriller. It was long in the writing and brings together all the different aspects of my own life and work, and yet the idea came to me in one instant, more than 10 years ago.

I was studying for my masters in theology, having come to faith after a long struggle between my head and my heart, wanting to understand it better. We had a task: to review the then Pope Benedicts first encyclical, Deus Caritas Est (God is Love). What was praised by the Catholic Church and many commentators for what Ruth Gledhill called its beautiful and passionate writing and theological rigour seemed to me to set up such an idealised nature of love that no human being could possibly come close to it.

An encyclical is addressed to the world, not just the Catholic Church, and this one had nothing to say to anyone who doesnt support the churchs position that only in a heterosexual marriage and when open to procreation can sex be approved.

The encyclical failed to address any of the new approaches to gender, embodiment, sexuality and sexual orientation in our postmodern or transmodern world. There was nothing either to help or offer guidance with all the difficult and complex moral and ethical dilemmas faced in the modern age by us imperfect beings in an imperfect world. In short, it was an epic fail.

I had spent a great deal of my early career involved in womens reproductive rights. I worked for various charities and sat on the Committee to Defend the 1967 Abortion Act, and worked with Spanish groups trying to set up contraception and abortion services after Francos death.

I saw at first hand the very real pain and suffering and the struggles faced by women who found themselves unwantedly pregnant, and the moral conflicts they faced. The language used by the Catholic Church around abortion, as well as on issues such as homosexuality and transgender, is dismissive and horrible.

What could happen to shake these popes and cardinals in the Vatican, wrapped in their dogma, surrounded by medieval walls and completely divorced from the reality of peoples ordinary lives, desires and problems? How, in particular, could they ever understand a womans lived experience, what it is like to be unwantedly pregnant, or the lives of those who feel different?

And then the idea came to me. It was only if one of them became mysteriously pregnant, I thought, if they desired to end it and were afraid of childbirth, if they discovered that they were not male as they had thought, that they would understand. And I liked the idea that they could be intersex, since I had been a tomboy as a child and had felt frustrated with the gender roles in our society when I was growing up, especially since my then ambition was to become an astronaut.

Yes, this seemed an absurd idea for a novel. Was this even possible? Could I make it convincing? Happily, my first degree was in biochemistry, which included a module in molecular genetics. I looked at scientific papers and found that a rare condition exists where two early embryos fuse, one male and one female, and then go on to develop as one individual, but with a random distribution of male and female cells and characteristics.

One case study caught my eye a person with one ovary and one testis, who appeared to be male. And there had been 11 live births to such people. So, while of course it was extremely unlikely, it was indeed possible and so it neednt be a miracle, though of course people would suspect that it was.

My Pope, Patrick, is the first Irish Pope. I chose an Irish Pope because there has never been one, so I felt that he couldnt be thought to be based on anyone specific; and because I have always identified as a Celt rather than English, as my Welsh, Scottish, and distant Irish ancestry far outweighs my English blood.

It also seemed appropriate in terms of the enormous changes that have taken place in Irish society in the last few years, with the diminishing power of the church, tarnished by child abuse scandals, and the legalisation of abortion, which happened towards the end of the writing of the novel.

At first, it was hard to like my Pope Patrick. He started off as dogmatic, rigid, fussy, a bit like Benedict himself. And then Benedict resigned and we had Pope Francis a different kind of character altogether. My Pope changed too as I recreated his childhood.

As I wandered round Cork where my cousin lives, and where it was therefore convenient for Patrick to have grown up, he began to become human. I realised that as a child he had been mocked for being different, something I had always felt at school. He was desperate for human love and connection, and found himself in a position where this was impossible to achieve.

This human love is of course mediated through touch, something withheld from him by his mother and father; his difficult relationship with his parents rested on secrets which he uncovered only after his fathers death.

As the cardinals in my novel opposed him and threatened his position, even took steps to remove him, I felt more and more sympathy with his predicament. And as the story unfolded, and his faith was shaken, it reflected my own struggles with Christianity, something which as a scientist I had always found hard to believe, and yet which constantly tugged at my heart till I could no longer resist it.

I tried to write the book with humanity, and respect. I dont have any wish to denigrate religion, and indeed, there are passages in the book based on my own experience of prayer and Gods presence. The Catholic Church today is torn, as is my novel, between those who want things to stay as they are and those who want to make the faith more relevant in the modern world. My novel is a way of engaging with this debate, asking questions and inviting people to share in the experience, rather than giving any definitive answers.Virgin & Child is published by Barbican Press, priced 16.99

Read the original here:
Meet Pope Patrick Irish, intersex and pregnant - The Irish Times

THE number of people dying from coronavirus across the world is continuing to rise every day - with just under 130,000 deaths in 210 countries.

And in the UK alone,the total of deathspushed past the 12,000 barrier yesterday - with the grim total expected to be 15 per cent higher than reported due to people dying outside of hospital.

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However, scientists have now revealed that there are some key factorsthat people who pass away from Covid-19have in common.

A team of researchers from eight institutions in China and the United States including the Chinese Peoples Liberation Army General Hospital in Beijing, and the University of California Davis recently looked at the data of 85 patients who died of multiple organ failure after having received care for severe Covid-19.

All individuals whose data the study used received care at either the Hanan Hospital or the Wuhan Union Hospital between January 9 and February 15, 2020.

And the researchers who conducted the study,that appears in the American Journal of Respiratory and Critical Care Medicine,uncovered a series of factors that the majority of these patients shared.

Here, we outline these key factors...

The killer new coronavirus appears to be posing a particularly deadly threat to men.

In fact, the researchers found that 72.9 per cent of those who died from the new coronavirus were male.

Experts believe there are a few reasons for more men dying than women, including some biological and other lifestyle choices.

Hand washing is one of the best ways to prevent infection - but multiple studies show that women are much more likely to wash their hands and use soap than men.

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Akiko Iwasaki, a professor of immunology at Yale University, told the New York Times that men may have a "false sense of security" about coronavirus.

Meanwhile, Chinese men are much more likely to smoke than women, which can lead to a weaker immune system.

In fact China has the largest population of smokers in the world - accounting for nearly a third of the world's smokers - but just two per cent of them are women.

Meanwhile, in the UK 16.5 per cent of men - around 3.9 million - and 13 per cent of women - around 3.2 million - reported being current smokers.

Chinese men also have higher rates of high blood pressure, Type 2 diabetes and chronic obstructive pulmonary disease than women.

All of these conditions can increase the risk of complications following infection of coronavirus.

Then new strain of deadly coronavirus doesn't discriminate and can infect anyone of any age.However, it's older adults - aged 60 and upwards - who are more likely to get seriously ill from it - with the scientists discoveringthat those who died from Covid-19 had amedian age of 65.8 years.

Medics say it's because our immune systems weaken with age, meaning an older person's body is less able to fight Covid-19.

Dr Sarah Jarvis, GP and Clinical Director of Patient Access, told The Sun: "We know that as you get older, your immune system becomes less efficient thats why older people are at higher risk of serious complications of coronavirus infection.

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"If your immune system isnt strong, its more likely that the virus can multiply deep inside your lung, causing inflammation and scarring.

"Your immune system will try and fight it off, and will often destroy healthy lung tissue in the process.

"This makes you more prone to get secondary infections like pneumococcal pneumonia."

In fact, evidence from China, where the deadly virus originated, shows one in seven of those over 80 known to have contracted coronavirus have died.

Those who died from Covid-19 in the study mostly had underlying chronic conditions, such as heart problems or diabetes.

The greatest number of deaths in our cohort were in males over 50 with noncommunicable chronic diseases, the researchers said.

We hope that this study conveys the seriousness of Covid-19 and emphasizss the risk groups of males over 50 with chronic comorbid conditions, including hypertension (high blood pressure), coronary heart disease, and diabetes, they added.

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In fact, another study recently revealed that your risk of dying from coronavirus is 80 per cent higher if you have just one underlying health issue.

For those with two pre-existing conditions or more, the chances of being admitted to intensive care are even higher, experts warned.

Some of the chronic conditions said to heighten the risk among patients are asthma, cancer, cystic fibrosis, chronic obstructive pulmonary disease (COPD), diabetes and HIV and AIDS.

People who are obese or seriously overweightfall into the high risk category for coronavirus.

This is because being overweight or obese can weaken the bodys immune system which could make people more likely to catch coronavirus and makes it harder for the body to fight the bug.

The NHS has said people with a BMI of 40 or above have a greater risk of developing complications if they catch the virus.

More than 60 per cent of patients in intensive care with the virus were overweight or classed as morbidly obese, arecent NHS survey found.

Those who were overweight, with a BMI of 25 to 40, made up 64 per cent of the 194 coronavirus patients who were in ICU at the time, while seven per cent were classed as obese with a BMI over 40.

BMI is a measure of whether youre a healthy weight for your height, you can calculate yours on the NHS website.

In the past, studies have shown overweight and obese people are at greater risk of serious complications or death from infections, like flu.

The extra weight on obese people's diaphragms puts pressure on lungs and makes it harder to breathe, starving them of oxygen.

Clogged up arteries can also make it harder for blood carrying immune cells to circulate and travel to fight infection around the body.

In terms of other potentially relevant information, the research team found that 81.2 per cent of those who died from Covid-19 in the study had very low eosinophil counts on admission to the hospital."

This is a type of white blood cells, which are specialised immune cells that help fight infection.

The medics suggested that having abnormally low levels of eosinophils a condition known as eosinophilopenia may correlate with a greater risk of severe outcomes in people who have contracted Covid-19.

While the scientists hope that their current findings may help other doctors better understand and prepare for fighting coronavirus, the researchers nevertheless urge other experts to keep on recording all possible information about people receiving care for this new illness.

Our study, which investigated patients from Wuhan, China, who died in the early phases of this pandemic, identified certain characteristics, the researchers said.

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"Yet as the disease has spread to other regions, the observations from these areas may be the same, or different.

They added: Genetics may play a role in the response to the infection, and the course of the pandemic may change as the virus mutates, as well.

"Since this is a new pandemic that is constantly shifting, we think the medical community needs to keep an open mind as more and more studies are conducted.

We pay for your stories and videos! Do you have a story or video for The Scottish Sun? Email us at scoop@thesun.co.uk or call 0141 420 5300

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The 5 factors people who die of coronavirus have in common - The Scottish Sun

Why Young People Should Not Take AAS

Adapted from the r/steroids Wiki

Nandrolone has been reported to induce psychiatric side effects such as aggression and depression. Adolescence represents an extremely sensitive neurodevelopmental period to influence by detrimental effects.

Side Effects of Drugs Annual (2015)

AAS use by teenagers is a primary concern because of the potential side effects where remodeling of the brain and behavioral maturation occurs.

Journal of Behavioral Processes (2015)

Until you're around the age of 25, your brain and endocrine system are still developing. This should be obvious as you are still going through the end of puberty, getting acne, etc. During this time period, supplementing with exogenous hormones is extremely dangerous.

Taking anything before you are completely finished with puberty can have negative side effects. While you are maturing, your brain, organs, and cells are consistently gauging the overall development of your body. When you introduce a foreign substance, you risk your bodys ability to truly judge how far along your maturation is, resulting in the possibility of premature shutdown or stunting your growth and development processes.

Natural Blast

Your body is already pumping out blast levels of testosterone as part of the natural course of late adolescence. It's the highest that it's ever going to be in your lifetime.

Why prematurely shut that down and ruin a great thing? You're essentially on free steroids right now. Don't take that opportunity for granted and abort your own physiological development by injecting additional variables that short-circuit the whole equation.

Sides

There's a serious potential for long-term side effects. People oft-say I've stopped growing, so it's okay. No: it's not okay. The rest of you hasn't finished developing yet. There are many other potential side effects besides simply your growth plates. Here are a few.

Brain Function, Memory, Alzheimers Disease

It's well known that hormones play a role in the development of cognitive brain function. Your neuroendocrine system is still developing until the age of 25. Adding external hormones when your brain is still developing can stunt normal development and maturation.

Many steroids are neurotoxic.

They lead to depression, memory loss and learning difficulties.

They cause longstanding dysfunction in brain reward systems.

They give rise to the accumulation of amyloid plaques, which leads to Alzheimers.

Do you really want to add these variables to a still-growing and developing brain? How can you know many years down the road there won't be even more problems?

Cancer, Liver, Kidney Disease

You hear all the time teenagers say Well my friends it and they got big and nothing happened to them. Really? How do you know? Have they been to a doctor and had their liver and kidney values checked? Just because a person looks okay on the outside, doesn't mean that they don't already host serious problems on the inside. If treated improperly or in an untimely manner, liver and kidney damage can prove to be fatal.

Premature Closing of Growth Plates

This one is the most known about. Even if you think you've stopped growing, there still is a potential for height increase over time. Scientists have found that growth plates don't fuse completely in some cases until individuals are past 22. Don't be deterred just because you haven't grown taller in awhile. You grow out as well as up. Do you want broader shoulders, or do you want to stay stuck with what you've got now?

Impotence

Your neuroendocrine system is still developing. Supplementing with hormones while you are still growing can potentially cause permanent impotence and fertility issues in teenagers. When you add testosterone, estrogen and a wealth of other synthetic androgens to your body it can cause problems with your normal testicular growth and function. Remember, some of these effects are more than just temporary.

Gyno, or Bitch Tits

Androgen usage in teens increases the risk of gyno. Gyno has already been known to happen naturally in many teenagers because of fluctuating hormones. When you add more hormones to the mix, you dramatically increase the problems. Remember once you have gyno, it's very hard to get rid of. Unless you take the proper precautions up front, you'll have to resort to surgery and go under the knife.

Hair Loss, Acne, Prostate Dysfunction

All of these can be accelerated and aggravated with exogenous androgen use.

Have you seen a 20-year old already going bald?

What about permanent scarring from severe cystic acne?

How about being unable to use the bathroom due to the excruciating pain involved in the process? It's not pretty.

Don't think it can't happen to you.

References

A few references.

Trenbolone neurotoxicity:

Deca, or Nandrolone, is eleven times more damaging to blood vessels than Testosterone. It causes longstanding changes in the brain reward system, affects learning and memory, and induces genetic damage across multiple organ systems.

Nandrolone impaired spatial learning and memory, and this effect was not rescued by exercise. The harmful effects of ND and other AAS on learning and memory should be taken into account when athletes decide to use AAS for performance or body image improvement.

Adapted from the r/steroids Wiki

Originally posted here:
[Discussion] Dealing with shitty male genetics. : steroids

A team of researchers from eight institutions in China and the U.S. has offered a fresh insight into why 85 patients died of multiple organ failure after suffering severe COVID-19.

All individuals whose data the team studied received care at either the Hanan Hospital or the Wuhan Union Hospital between January 9 and February 15, 2020.

The researchers came from the Chinese Peoples Liberation Army General Hospital in Beijing, and the University of California Davis and six other institutions.

Their study uncovered a series of factors that the majority of these patients shared.

The study has been published by the American Journal of Respiratory and Critical Care Medicine.

The majority were older malesThe research team was able to access and analyze the deceased patients medical histories, including whether they had any underlying, chronic conditions.

The researchers were also able to find out what symptoms the patients experienced once they had contracted the virus and access information from laboratory tests and CT scans.

They also accessed information about the medical treatment they received while in the hospitals.

They found that 72.9% of those who died with COVID-19 were male, with a median age of 65.8 years and underlying chronic conditions, such as heart problems or diabetes.

The greatest number of deaths in our cohort were in males over 50 with noncommunicable chronic diseases, the investigators note.

They found that 72.9% of those who died with COVID-19 were male, with a median age of 65.8 years and underlying chronic conditions, such as heart problems or diabetes. The greatest number of deaths in our cohort were in males over 50 with noncommunicable chronic diseases, the investigators note.

We hope that this study conveys the seriousness of COVID-19 and emphasises the risk groups of males over 50 with chronic comorbid conditions, including hypertension (high blood pressure), coronary heart disease, and diabetes, they have commented.

The team also notes that, among the 85 patients whose records it analyzed, the most common COVID-19 symptoms were fever, shortness of breath, and fatigue.

Some important observationsIn terms of other potentially relevant information, the research team found that 81.2% of the study individuals had very low eosinophil [a type of white blood cells, which are specialized immune cells that help fight infection] counts on admission.

Among the complications that the patients experienced while hospitalised with COVID-19, some of the most common were respiratory failure, shock, acute respiratory distress syndrome, and cardiac arrhythmia, or irregular heartbeat.

As part of their treatment, the majority received antibiotics, antivirals, and glucocorticoids, and some received intravenous immunoglobulins (also known as antibodies), or interferon alpha-2b, which is also a stimulant for the immune response.

Yet, the researchers note, the effectiveness of medications, such as antivirals or immunosuppressive agents, against COVID-19 is not completely known.

Based on their observations, the authors indicate that treatments, including combinations of antimicrobial drugs, did not appear to have much of a positive effect.

Perhaps our most significant observation is that while respiratory symptoms may not develop until a week after presentation, once they do there can be a rapid decline, as indicated by the short duration between time of admission and death (6.35 days on average) in our study, they write.

They also suggest that having abnormally low levels of eosinophils a condition known as eosinophilopenia may correlate with a greater risk of severe outcomes in people who have contracted SARS-CoV-2.

While they hope that their current findings may help other doctors better understand and prepare for fighting COVID-19, the researchers nevertheless urge the global scientific community to keep on recording all possible information about people receiving care for this new illness.

Our study, which investigated patients from Wuhan, China, who died in the early phases of this pandemic, identified certain characteristics, the researchers say, yet as the disease has spread to other regions, the observations from these areas may be the same, or different.

They continue: Genetics may play a role in the response to the infection, and the course of the pandemic may change as the virus mutates, as well.

Since this is a new pandemic that is constantly shifting, we think the medical community needs to keep an open mind as more and more studies are conducted.

*Originally published by Medical News Today

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Insight: What those dying of COVID-19 have in common - P.M. News

In recent reports, it has been said that the coronavirus takes a higher toll on menwith some experts warning that being male may be a risk factor for COVID-19, as much older age is.

In fact, a scientist who studies sex difference in viral infections at Johns Hopkins Bloomberg School of Public Health, Sabra Klein told the New York Times: Being male is as much a risk factor for the coronavirus as being old. People need to be aware that there is this pattern. Just like being old means youre at higher risk, so does being male. Its a risk factor.

She also said the vulnerability could be biological or behavioural, adding that women have more robust immune systems than men.

But a new study from the Centers for Disease Control and Prevention (CDC) is suggesting it may have more to do with biology than lifestyle. In particular, it may even have to do with genetics.

Male COVID-19 patients are more common than females, study finds. | Image source: iStock

In CDCs Morbidity and Mortality Weekly Report published on Monday (6 April), it is found that there is a higher prevalence of COVID-19 in males across every pediatric age groupincluding newborns and infants.

Specifically, in the study of over 2,500 childrenaged 0 to 18with COVID-19, some 57 percent were male, suggesting that biological factors could make men more susceptible to the virus.

Based on the study, among the cases in children, the median age was 11 years, with nearly one-third of reported pediatric cases of cases involving teens between the ages of 15 and 17.

Among pediatric cases for which sex was known, 57 percent occurred in malesmuch higher in percentage compared to adult cases, in which 53 percent occurred in males.

The study also found that most of the children reported symptoms of cough or fever, only 5.7 percent were hospitalized.

These data support previous findings that children with COVID-19 might not have reported fever or cough as often as do adults, the report said.

Children who were hospitalised reported at least one underlying health condition, with most common being chronic lung diseases (such as asthma), cardiovascular diseases.

Meanwhile, in Singapore, a quick check on the summary of made available since the beginning of April shows that among the 21 reported pediatric patients who tested positive for COVID-19, 16 are male. Furthermore, based on this online dashboard, among the 49 pediatric cases reported here as of 11 April, 29 are male.

Still, it is noted that the research is still in its preliminary stages and that the authors are working with limited information. It is noted that the research did not suggest that parents should now be more concerned about their male childrenmore than their female childrengetting severely ill from COVID-19. Experts said it is no reason for parents of boys to panic, and for parents of girls to think they are immune to the virus.

24 hour clinics in singapore, Male COVID-19

Image source: iStock

They also reiterated that the risk for children remains very low. In fact, though there have been multiple reports from all over the world about coronavirus-related death in children recently, only 0.1 percent of the children infected died.

Story continues

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COVID-19: Young Boys At Higher Risk Of Infection and Severe Illness From Coronavirus, Says Study - Yahoo Singapore News

Marisa Thompson, Southwest Yard and Garden Published 3:12 a.m. MT April 12, 2020

Small fruit are developing at the base of the female flower (bottom left), but not on the male flower (top left). Pollen from the stamens in the center of the open male flower (top right) can be translocated to the stigma in the center of the open female flower (bottom right) by pollinating insects or by humans.(Photo: Abrahami, Wikimedia Commons)

Question: I would love to be able to grow both zucchini and watermelon this year, but I am hesitant because of problems with cross-pollination in the past. Any tips?

Seed to Supper online course participant, somewhere in New Mexico

Answer: First of all, for readers who dont already know about New Mexico State University'sSeed to Supper program through ICAN (Ideas for Cooking & Nutrition), this is a free, online, self-paced beginning gardening course that was first developed by the Oregon State University Extension Service and modified by our own NMSU Food Systems Specialist Sally Cassady to be web-based and New Mexico-oriented (https://ican.nmsu.edu/seedtosupper.html).

It sounds like the problems youve had in the past with zucchinis and watermelons may have been more about fruit set issues which could include pollination problems than cross-pollination. Cross-pollination can only occur within plants of the same species. The old gardening tip dont plant cucumbers next to squash or melons because theyll cross-pollinate and form bad fruit isnt true. NMSU Extension Vegetable Specialist Stephanie Walker confirmed: As long as the cucurbits are different species, its very unlikely theyll cross-pollinate. Zucchini is Cucurbita pepo and watermelons are Citrullus lanatus, so they wont cross-pollinate to produce viable seed.

Marisa Y. Thompson(Photo: Courtesy)

Plants in the cucurbit (gourd) family include melons, pumpkins, squashand cucumbers. Each of those different cucurbits includes plants of different species and genera (plural of genus). Remember, the scientific names of plants consist of two parts: the genus and the species. So musk melons scientific or botanical name is Cucumis melo, with Cucumis as the genus and melo as the species. Cucumber is Cucumis sativus, so even though musk melons and cucumbers are in the same genus (Cucumis), they are not the same species and wont be likely to cross-pollinate. Even if they did cross-pollinate, the evidence would not be visible in this years crop. If you saved seed from cross-pollinated fruit and grew it next year, you might get something cool and yummy, although its more likely to be undesirable. Pumpkins with green bumps could be the result of seeds that were saved from normal pumpkins crossed with green-warted gourds.

Its not just that plants from different species arent likely to cross-pollinate based on their genetics. Amanda Skidmore, NMSU Extension integrated pest management specialist for urban and small farms, explains that our pollinators are picky too: Interestingly, different pollinators will visit each plant because of the flower shape and inflorescence. For example, squash bees will visit zucchini, but not watermelon.Skidmore encourages gardeners to take some time to watch and see what different pollinators are visiting the two plants. There will be some overlap (honey bees, bumble bees), but some cool differences too.

For information, check out our NMSU Extension Guide collection for vegetables. Related titles include Starting Plants Early Outdoors, Spices and Herbs for the Home Garden, Home Vegetable Gardening in New Mexico and Growing Zones, Recommended Crop Varieties, and Planting and Harvesting Information for Home Vegetable Gardens in New Mexico.

As retired NMSU Extension Horticulture Specialist Curtis Smith explained in a 2008 column, cucurbits have separate male and female flowers on the same plant. You can recognize the male flowers because they do not have a small fruit behind them (more on this later). They produce the pollen needed to form the fruit, but they do not produce the fruit. The female flower, on the other hand, has a small fruit behind the flower even before it opens. The female flower cannot produce the pollen needed to cause the fruit to develop and is dependent upon insect (or human) pollinators to transport the pollen from the male flower. The male flowers begin forming before the female flowers form. So, it is possible to have cucurbits blooming, but not producing fruit. The time between the first development of male flowers and the female flowers depends on plant variety and environmental conditions. Your problem may just be that the female blossoms have not formed yet. They should be forming soon. However, if you see the female flowers on your cucurbit plants, but they are not "setting" fruit, then the problem may be that you do not have pollinators.

Smith also offers tips on how to pollinate your cucurbit flowers yourself: Each morning, collect pollen from the stamens in the center of the male flowers and then transfer that pollen to the stigma in the center of the female flowers. Use a small, soft-bristled paintbrush to do this. If you are successful, you should see small fruit forming within a few days. Leave some female flowers unpollinated (by you), so you can watch for the return of the natural pollinators to relieve you of the early morning effort of pollination.

A few years ago, I wasnt convinced that Id be able to tell the difference between male and female flowers on a squash plant. That is, until I looked closer. Both flower types are huge and bright orange-yellow, but if you look just behind the flowers, youll know when you find a female versus a male because theres a swollen fruit structure developing at the base of female flowers. In some cucurbits, that baby fruit will be more rounded, and in others more like a small pickle.

For gardening information, including decades of archived Southwest Yard & Garden columns, visit the NMSU Extension Horticulture page (http://desertblooms.nmsu.edu/), follow us on social media (@NMDesertBlooms), or contact your County Extension office (https://aces.nmsu.edu/county).

Marisa Thompson, PhD, is the Extension Horticulture Specialist for New Mexico State University and is based at the Agricultural Science Center at Los Lunas.

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Exploring the gourd family of cucumbers, squashes and melons - Las Cruces Sun-News

What are the genetics of male pattern baldness? originally appeared on Quora: the knowledge sharing network where compelling questions are answered by people with unique insights.

Answer by Adriana Heguy, Director of the NYUMC Genome Technology Center and Professor of Pathology, on Quora:

Unfortunately the genetics of androgenetic alopecia (male-pattern baldness) is not really well understood. The more complex the biology behind a phenomenon is, the more difficult is going to be to find all the genetic factors. Regulation of hair growth in mammals is extremely complicated and poorly understood, in spite of this subject being a very active area of research. Hair is very important to mammalianthermoregulation thus it makes sense for its biology to be very complex.

It is clear that male-pattern baldness is a highly heritable condition [1], although there is also some evidence for the involvement of epigenetic factors [2]. There are a few genes implicated in androgenetic alopecia from different studies [3]. Unsurprisingly, the androgen receptor (AR) gene is one of them, as it is well known that the condition is dependent on testosterone (an androgen). The androgen receptor is on the X chromosome, which is why some people propagate the myth that male-pattern baldness comes from the mother's side of the family (a male inherits the X chromosome from mom, the Y chromosome from dad). But it is not the only gene involved, or even the main gene involved. There are genes in basically all chromosomes that have been implicated in androgenetic alopecia, and this is what makes it so difficult to unravel, as we would have to examine the overall contribution that each gene variant (single nucleotide polymorphism, or SNP) play in hair loss, and also how these genes interact with each other and the environment to result in the phenotype.

Position of genes implicated in male pattern hair loss, from [4].

Some of these genes code for transcription factors or histone deacetylases. TheWnt pathway appears to be involved. Even though we know a fair amount about transcription factors, the Wnt pathway, etc., this still does not tell us much about what's actually going on in androgenetic alopecia and why the hair follicles shrink and die. The hope is that identifying these genes will provide targets for therapeutic intervention. But so far, we are still far from a definitive "cure" for androgenetic alopecia.

If there is any consolation for men (or at least, heterosexual men) distressed about hair loss, if it was a phenotype that was repulsive to females, the gene variants would have been weeded out a long time ago, by sexual selection. Many of us find bald heads very manly and attractive.

Footnotes

[1] Genetic basis of male pattern baldness.

[2] Eleven pairs of Japanese male twins suggest the role of epigenetic differences in androgenetic alopecia.

[3]Hunting the genes in male-pattern alopecia: how important are they, how close are we and what will they tell us?

[4] Hunting the genes in male-pattern alopecia: how important are they, how close are we and what will they tell us?

This question originally appeared on Quora. Ask a question, get a great answer. Learn from experts and access insider knowledge. You can follow Quora on Twitter, Facebook, and Google+. More questions:

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The Unpredictable Genetics Of Male-Pattern Baldness

Nearing COVID-19s fatality peak means having a larger pool of severe cases to draw correlates from.

A new study published in The American Journal of Respiratory and Critical Care Medicine has successfully identified several clinical similar sites linking fatal reactions to SARS-Cov-2 infection.

The global death toll from COVID-19 virus exceeds 21000. The risk factors for death were attributed to advanced age and comorbidities, but havent been accurately defined, the authors wrote in the new paper. Medical records of 85 fatal cases of COVID-19 between January 9 and February 15, 2020, were collected. The information recorded included medical history, exposure history, comorbidities, symptoms, laboratory findings, CT scans, and clinical management.

The researchers were not only able to determine the underlying factors that lead to acute COVID-19 symptoms, but they were also able to link onset symptoms with critical outcomes.

According to the data, the majority of COVID-19 deaths occur as a result of multiple organ failure. Patients on ventilators do not receive enough oxygen in their bloodstream to sustain vital biological functions or combat accompanying effects of prolonged illness like inflammation, pneumonia and acute respiratory distress syndrome (ARDS). Between 30% and 40% of patients who experience ARDS do not survive

The median age of the patients involved in the new study who succumbed to COVID-19 was 65.8 years old and 72.9% were male. The common symptoms in cases that went on to become fatal were fever, shortness of breath, fatigue, and dyspnea (labored breathing).

Early onset of shortness of breath may be used as an observational symptom for COVID-19 exacerbations. Eosinophilopenia may indicate a poor prognosis. The combination of antimicrobial drugs did not offer considerable benefit to the outcome of this group of patients, the report continued.

Symptoms were not the only instructive element of case severity. Hypertension, diabetes and coronary heart disease were the most common comorbidities in the cases analyzed.

Eighty-one percent of patients who had low white blood cell counts at admission developed fatal cases of COVID-19. Complications associated with these predictors included respiratory failure, shock, ARDS, and arrhythmia.

Antibiotics were administered the most often for patients under intensive care, followed by antiviral therapeutics and glucocorticoid treatments.

As the disease has spread to other regions, the observations from these areas may be the same, or different. Genetics may play a role in the response to the infection, and the course of the pandemic may change as the virus mutates as well, the authors conclude. Since this is a new pandemic that is constantly shifting, we think the medical community needs to keep an open mind as more and more studies are conducted.

Danish researchers from Aarhus University collaborated with scientists from the University of Siena for an independent study premised by the high COVID-19 mortality rates in Italy.

The researchers compellingly establish a correlation between air pollution and coronavirus-related deaths in two regions of Northern Italy: Lombardy and Emilia Romagna.

These areas evidence a mortality rate of 12%, which is considerably higher than any other impacted community (16,000 coronavirus deaths as of April 7th).

Lombardy and Emilia Romagna rank among the most heavily air-polluted areas in all of Europe. After reviewing air data collected by the NASA satellite Aura and comparing it with the European Environment Agencys Air Quality Index, Lombardy and Emilia Romagna ranked as one of the most heavily air-polluted areas in the entire continent of Europe.

It stands to reason that turbulent air has a hand to play considering SARS-Cov-2 targets lung cells and damages the hairlike projections that keep our airways clear of mucus and debris.

The authors are quick to point out that the findings published in the journal Environmental Pollution do not wholly account for the disproportionately high mortality rates observed in the regions studied, but they should not be counted outbecause at this stage nothing should be counted out.

There are several factors affecting the course of patients illness, and all over the world, were finding links and explanations of what is important. Its very important to stress that our results are not a counter-argument to the findings already made. At the moment, all new knowledge is valuable for science and the authorities, and I consider our work as a supplement to the pool of knowledge about the factors that are important for the course of patients illness, says environmental scientist Dario Caro in a release.

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Everything you need to know about fatal cases of COVID-19 - Ladders

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About six to 10 days after viral exposure,the body begins to develop antibodies that bind and react specifically to the proteins found on SARS-CoV-2. The first antibody produced is called immunoglobulin m (IgM), which is short-lived and only stays in the bloodstream for a few weeks. The immune system refines the antibodies and just a few days later will start producing immunoglobulins G (IgG) and A (IgA), which are much more specific. IgG stays in the blood and can confer immunity for months, years, or a lifetime, depending on the disease its protecting against.

In someone who has survived infection with covid-19, the blood should, presumably, possess these antibodies, which will then protect against subsequent infection by the SARS-CoV-2 virus. Knowing whether someone is immune (and eligible for potential future certification) hinges onserological testing,drawing blood to look for signs of these antibodies. Get a positive test and, in theory, that person is now safe to walk the street again and get the economy moving. Simple.

Except its not. There are some serious problems with trying to use the tests to determine immunity status. For example, we still know very little about what human immunity to the disease looks like, how long it lasts,whether an immune response prevents reinfection, and whether you might still be contagious even after symptoms have dissipated and youve developed IgG antibodies. Immune responses vary greatly between patients, and we still dont know why. Genetics could play a role.

Weve only known about this virus for four months, says Donald Thea, a professor of global health at Boston University. Theres a real paucity of data out there."

SARS-CoV-1, the virus that causes SARS and whose genome is about 76% similar to that of SARS-CoV-2, seems toelicit an immunity that lasts up to three years. Other coronaviruses that cause the common cold seem to elicit a far shorter immunity, although the data on that is limitedperhaps, says Thea, because there has been far less urgency to study them in such detail. Its too early to tell right now where SARS-CoV-2 will fall in that time range.

Even without that data, dozens of groups in the US and around the world are developing covid-19 tests for antibodies. Many of these are rapid tests that can be taken at the point of care or even at home, and deliver results in just a matter of minutes. One US company, Scanwell Health, has licensed a covid-19 antibody test from the Chinese company Innovita that can look for SARS-CoV-2 IgM and IgG antibodies through just a finger-prick blood sample and give results in 13 minutes.

There are two key criteria we look for when were evaluating the accuracy of an antibody test. One is sensitivity, the ability to detect what its supposed to detect (in this case antibodies). The other is specificity, the ability to detect the particular antibodies it is looking for. Scanwells chief medical officer, Jack Jeng, says clinical trials in China showed that the Innovita testachieved 87.3% sensitivity and 100% specificity(these results are unpublished). That means it will not target the wrong kind of antibodies and wont deliver any false positives (people incorrectly deemed immune), but it will not be able to tag any antibodies in 12.7% of all the samples it analyzesthose samples would come up as false negatives (people incorrectly deemed not immune).

By comparison, Cellex, which is the first company to get a rapid covid-19 antibody test approved by the FDA, has a sensitivity of 93.8% and a specificity of 95.6%. Others are also trumpeting their own tests vital stats. Jacky Zhang, chairman and CEO of Beroni Group, says his companys antibody test has a sensitivity of 88.57%, for example. Allan Barbieri of Biomerica says his companys test is over 90% sensitive. The Mayo Clinic is making available its own covid-19 serological test to look for IgG antibodies, which Elitza Theel, the clinics director of clinical microbiology, says has 95% specificity.

The specificity and sensitivity rates work a bit like opposing dials. Increased sensitivity can reduce specificity by a bit, because the test is better able to react withanyantibodies in the sample, even ones you arent trying to look for. Increasing specificity can lower sensitivity, because the slightest differences in the molecular structure of the antibodies (which is normal) could prevent the test from finding those targets.

It really depends on what your purpose is, says Robert Garry, a virologist at Tulane University. Sensitivity and specificity rates of 95% or higher, he says, are considered a high benchmark, but those numbers are difficult to hit; 90% is considered clinically useful, and 80 to 85% is epidemiologically useful. Higher rates are difficult to achieve for home testing kits.

But the truth is, a test that is 95% accurate isnt much use at all. Even the smallest errors can blow up over a large population. Lets say coronavirus has infected 5% of the population. If you test a million people at random, you ought to find 50,000 positive results and 950,000 negative results. But if the test is 95% sensitive and specific, it test will correctly identify only 47,500 positive results and 902,500 negative results. That leaves 50,000 people who have a false result. Thats 2,500 people who are actually positiveimmunebut are not getting an immunity passport and must stay home. Thats bad enough. But even worse is that a whopping 47,500 people who are actually negativenot immunecould incorrectly test positive. Half of the 95,000 people who are told they are immune and free to go about their business might never have been infected yet.

Because we dont know what the real infection rate is1%, 3%, 5%, etc.we dont know how to truly predict what proportion of the immunity passports would be issued incorrectly. The lower the infection rate, the more devastating the effects of the antibody tests inaccuracies.The higher the infection rate, the more confident we can be that a positive result is real.

And people with false positive results would unwittingly be walking hazards who could become infected and spread the virus, whether they developed symptoms or not. A certification system would have to test people repeatedly for several weeks before they could be issued a passport to return to workand even then, this would only reduce the risk, not eliminate it outright.

As mentioned, cross-reactivity with other antibodies, especially ones that target other coronaviruses, is another concern. There are six different coronaviruses known to infect humans, says Thea. And its entirely possible if you got a garden-variety coronavirus infection in November, and you did not get covid-19, you could still test positive for the SARS-CoV-2 antibodies.

Lee Gehrke, a virologist and biotechnology researcher at Harvard and MIT, whose company E25Bio is also developing serological tests for covid-19, raises another issue. It's not yet immediately clear, he says, that the antibodies these tests pick up are neutralizing. In other words, the antibodies detected in the test may not necessarily actagainstthe virus to stop it and protect the bodythey simply react to it, probably to tag the pathogen for destruction by other parts of the immune system.

Gehrke says he favors starting with a smaller-scale, in-depth study of serum samples from confirmed patients that defines more closely what the neutralizing antibodies are. This would be an arduous trial, but I think it would be much more reassuring to have this done in the US before we take serological testing to massive scale, he says.

Alan Wells, the medical director of clinical laboratories at the University of Pittsburgh Medical Center, raises a similar point. He says that some patients who survive infection and are immune may simply not generate the antibodies youre looking for. Or they may generate them at low levels that do not actually confer immunity,as some Chinese researchers claim to have found.

I would shudder to use IgM and IgG testing to figure out whos immune and whos not, says Wells. These tests are not ready for that.

Even if the technology is more accurate, it might still simply be too early to start certifying immunity just to open up the economy. Chris Murray from the University of Washingtons Institute for Health Metrics and Evaluationtold NPRhis groups models predict that come June, at least 95% of the US will still be susceptible to the virus, leaving them vulnerable to infection by the time a possible second wave comes around in the winter. Granting immunity passports to less than 5% of the workforce may not be all that worthwhile.

Theel says that instead of being used to issue individual immunity passports, serology tests could be deployed en masse, over a long period of time, to see ifherd immunity has set inlifting or easing restrictions wholesale after 60 to 70% of a communitys population tests positive for immunity. There are a few case studies that hold promise. San Miguel County in Colorado has partnered with biotech company United Biomedical in an attempt to serologically test everyone in the county. The community is small and isolated, and therefore easier to test comprehensively. Iceland has been doing the same thing across the country.

This would require a massively organized effort to pull off well in highly populated areas, and its not clear whether the decentralized American health-care system could do it. But its probably worth thinking about if we hope to reopen whole economies, and not just give a few individuals a get-out-of-jail-free card.

Not everyone is so skeptical about using serological testing on a case-by-case basis. Thea thinks the data right now suggests SARS-CoV-2 should behave like its close cousin SARS-CoV-1, resulting in an immunity that lasts for a maybe a couple of years. With that in mind, its not unreasonable to identify individuals who are immune from reinfection, he says. We can have our cake and eat it too. We can begin to repopulate the workforcemost importantly the health-care workers. For instance, in hard-hit cities like New York that are suffering from a shortage of health-care workers, a serological test could help nurses and doctors figure out who might be immune, and therefore better equipped to work in the ICU or conduct procedures that put them at a high risk of exposure to the virus, until a vaccine comes along.

And at the very least, serological testing is potentially useful because many covid-19 cases present, at most, only mild symptoms that dont require any kind of medical intervention. About 18% of infected passengers on theDiamond Princesscruise shipshowed no symptoms whatsoever, suggesting there may be a huge number of asymptomatic cases. These people almost certainly arent being tested (CDC guidelines for covid-19 testing specifically exclude those without symptoms). But their bodies are still producing antibodies that should be detectable long after the infection is cleared. If they develop immunity to covid-19 thats provable, then in theory, they could freely leave the house once again.

For now, however, there are too many problems and unknowns to use antibody testing to decide who gets an immunity passport and who doesnt. Countries now considering it might find out they will either have to accept enormous risks or simply sit tight for longer than initially hoped.

Correction: The initial version of the story incorrectly stated: "The higher the infection rate, the more devastating the effects of the antibody tests inaccuracies." A higher infection would actually produce more confident antibody test results. We regret the error.

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Why its too early to start giving out immunity passports - MIT Technology Review

Rare congenital condition

XX male syndrome, also known as De la Chapelle syndrome, is a rare congenital intersex condition where an individual with a 46 XX karyotype (otherwise associated with females) has phenotypically male characteristics that can vary among cases.[2] In 90 percent of these individuals, the syndrome is caused by the Y chromosome's SRY gene, which triggers male reproductive development, being included in the crossing over of genetic information that takes place between the pseudoautosomal regions of the X and Y chromosomes during meiosis in the father.[2][3] When the X with the SRY gene combines with a normal X from the mother during fertilization, the result is an XX male. Less common are SRY-negative XX males, which can be caused by a mutation in anautosomalor X chromosomal gene.[2] The masculinization of XX males is variable.

This syndrome is diagnosed through various detection methods and occurs in approximately 1:20,000 newborn males, making it much less common thanKlinefelter syndrome.[2][4][5] Treatment is medically unnecessary, although some individuals choose to undergo treatments to make them appear more male or female.[1][6]

The appearance of XX males can fall into one of three categories: 1) males that have normal internal and external genitalia, 2) males with external ambiguities, and 3) males that have both internal and external genital ambiguities (true hermaphrodites).[7] External genital ambiguities can include hypospadias, micropenis, and clitoromegaly.[7] Typically, the appearance of XX males differs from that of an XY male in that they are smaller in height and weight.[2] Most XX males have smalltestes,are sterile, and have an increase in maldescended testicles compared to XY males.[2][8] Some XX male individuals have decreased amounts of body hair and decreased libido.[8] Individuals with this condition sometimes have feminine characteristics, with varying degrees ofgynecomastiabut with no intra-abdominalMllerian tissue.[8] According to research at theUniversity of Oklahoma health science centers, despite XX males exhibiting feminine characteristics, their behaviours are usually representative of masculinity in their culture.[9]

The degree to which individuals with XX male syndrome develop the male phenotype is variable, even among SRY-positive individuals.[10] A completely male phenotype usually develops in the presence of the SRY gene but, in some cases, the presence of the SRY gene can result in internal and/or external genitalia ambiguities.[10] Normal XX females undergo X inactivation during which one copy of the X chromosome is silenced. It is thought that X inactivation in XX males may account for the genital ambiguities and incomplete masculinization seen in SRY-positive XX males.[11][10] The X chromosome with the SRY gene is preferentially chosen to be the active X chromosome 90% of the time, which explains complete male phenotype being observed often in SRY-positive XX males.[11][10] In the remaining 10%, X inactivation spreads to include a portion of the SRY gene, resulting in incomplete masculinization.[11][10]

Masculinization of SRY-negative XX males is dependent upon which genes have mutations and at what point in development these mutations occur.[12]

Males typically have one X chromosome and one Y chromosome in eachdiploidcell of their bodies. Females typically have two X chromosomes. XX males that are SRY-positive have two X chromosomes, with one of them containing genetic material from the Y chromosome, making them phenotypically male but genetically female.[2]

The SRY gene plays an important role in sex determination by initiating testicular development. In most XX males the SRY gene is present. The tip of the Y chromosome contains the SRY gene and, during recombination, a translocation occurs in which the SRY gene on the Y chromosome is moved to become part of an X chromosome.[7][13] The presence of the translocated SRY gene leads to an XX embryo developing male characteristics.

In 10% of cases, an XX male does not have the SRY gene, causing variations in their levels of masculinity.[2] The exact cause of this condition is unknown but it has been proposed that mutations in the SOX9 gene may contribute to this syndrome since SOX9 plays a role in testes differentiation during development.[14][12] Another proposed cause is mutations to the DAX1 gene which encodes a nuclear hormone receptor.[15][16] DAX1 represses masculinizing genes, therefore, if there is a loss of function of DAX1 then testes can develop in an XX individual.[16] Mutations in SF1 and WNT4 genes are also being studied in connection with SRY-negative XX male syndrome.[16]

Hypothesis that XX occurs in males because of the interaction of the testis-determining portion of the Y chromosome and part of the X chromosome, called the Xg gene, is generally supported by various data.[17] The frequency of the Xg phenotype in XX males is closer to normal males' frequency than normal females' frequency.[17] There have been at least four cases where XX males have inherited the Xg allele from their father, and at least nine cases where XX males did not inherit the allele from their father.[17]

In cases where the individual is being evaluated for ambiguous genitalia, such as a small phallus, hypospadias, or labioscrotal folds, exploratory surgery may be used to determine if male and/or female internal genitalia is present.[18]

A standard karyotype can be completed to cytogenetically determine that an individual with a partial or complete male phenotype has a XX genotype.[7][18]

FISH analysis determines the presence or absence of the SRY gene.[10]

Localization of the SRY gene can by determined using fluorescent in situ hybridization.[2]

Indicators include two testes which have not descended the inguinal canal, although this is seen in a minority of XX males, and the absence of Mllerian tissue.[8] External indicators include decreased body weight and small testes.[2]

As of 2010, only 200 cases have been reported it is estimated that 1 of every 20,000 to 30,000 males has a 46,XX karyotype.[19][20]

XX males are sterile due to no sperm content and there is currently no treatment to address this infertility.[21] Genital ambiguities, while not necessary to treat for medical reasons, can be treated through the use of hormonal therapy, surgery, or both. Since XX male syndrome is variable in its presentation, the specifics of treatment varies widely as well. In some cases gonadal surgery can be performed to remove partial or whole female genitalia. This may be followed by plastic and reconstructive surgery to make the individual appear more externally male.[22] Conversely, the individual may wish to become more feminine and feminizing genitoplasty can be performed to make the ambiguous genitalia appear more female.[23] Hormonal therapy may also aid in making an individual appear more male or female.[22][23]

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XX male syndrome - Wikipedia

Androgen insensitivity syndrome is a condition that affects sexual development before birth and during puberty. People with this condition are genetically male, with one X chromosome and one Y chromosome in each cell. Because their bodies are unable to respond to certain male sex hormones (called androgens), they may have mostly female external sex characteristics or signs of both male and female sexual development.

Complete androgen insensitivity syndrome occurs when the body cannot use androgens at all. People with this form of the condition have the external sex characteristics of females, but do not have a uterus and therefore do not menstruate and are unable to conceive a child (infertile). They are typically raised as females and have a female gender identity. Affected individuals have male internal sex organs (testes) that are undescended, which means they are abnormally located in the pelvis or abdomen. Undescended testes have a small chance of becoming cancerous later in life if they are not surgically removed. People with complete androgen insensitivity syndrome also have sparse or absent hair in the pubic area and under the arms.

The partial and mild forms of androgen insensitivity syndrome result when the body's tissues are partially sensitive to the effects of androgens. People with partial androgen insensitivity (also called Reifenstein syndrome) can have genitalia that look typically female, genitalia that have both male and female characteristics, or genitalia that look typically male. They may be raised as males or as females and may have a male or a female gender identity. People with mild androgen insensitivity are born with male sex characteristics, but they are often infertile and tend to experience breast enlargement at puberty.

Continue reading here:
Androgen insensitivity syndrome - Genetics Home Reference ...

As the novel coronavirus cuts its relentless swath across the globe, doctors have identified one grim constant: COVID-19 has men, more than women, in its sights.

In Italy, men account for at least 70 percent of all coronavirus deaths. While South Korea has seen more confirmed COVID-19 cases in female patients than in males, a higher percentage of men have been felled by it. Here in New York City, more men than women are testing positive for coronavirus, with 55 percent of all cases. They also are dying of it at even higher rates. As of Friday, 1,159 men in the five boroughs had been killed by COVID-19 62 percent of the citys 1,867 deaths.

The phenomenon has stumped medical experts. In their rush to make sense of the data, many are pointing fingers at men and their behavior. Some speculate that higher male smoking rates leave them vulnerable to the respiratory infection. Others guess that men are blowing off social-distancing guidelines, or are neglecting to wash their hands.

I find that so offensive, genetic researcher Sharon Moalem, MD, told The Post. Talk about blaming the victim.

Sure, there are some behaviors that might affect the number of infections, he said. But why should poor hand-washing lead to death for a patient whos already in intensive care? Its ridiculous.

In fact, the coronavirus bulls-eye on men is consistent across age groups, regardless of underlying risk factors.

What we are actually seeing is that males do not do well once infected, Moalem said. So it comes down to genetics. There is a genetic component to this illness.

As a clinical researcher studying genetic disease, Moalem spent years working with patients at both ends of the human life span from babies in the neonatal intensive care unit to seniors grappling with Alzheimers. In both groups he noticed that his female patients were more resilient than males, better at fighting off infections and recovering from injuries.

The hardest thing a human being can do is surpass the age of 110, he noted. And 95 percent of those supercentenarians are women. Meanwhile, around the world, more girls than boys make it to their first birthdays.

That brought Moalem to a startling conclusion contradicting centuries worth of conventional wisdom: Men, not women, are the weaker sex.

In The Better Half (Farrar, Straus and Giroux), out Tuesday, Moalem explains that from the time they are still in the womb to their final breaths, womens immune systems outperform those of men an inherent advantage that lengthens their lives and improves their overall health.

And when it comes to outwitting COVID-19, Moalem says, womens genes provide an even bigger edge.

With this virus, there is immense risk simply due to the fact of being male.

Its not just that females have a stronger immune system to fight this infection, he said. Its that their genes give them a better defense at the cellular level.

Every human, male and female, carries a set of 46 chromosomes in our cells. One of those 23 chromosome pairs determines a humans biological sex. A mans cells contain an X chromosome inherited from his mother and a Y chromosome provided by his father. A womans cells carry two X chromosomes one from each of her parents.

The genes within our chromosomes contain the code that builds our bodies. The Y chromosome, with only about 70 genes, is a specialist that fashions the male reproductive system. But the X chromosome, with nearly 1,000 genes, does much more.

The X chromosome has the genes that go into making the brain and the immune system, the two crucial things you need to survive as a human being, Moalem said.

Both of a females X chromosomes are present in all her cells. But within each cell, only one of the Xs calls the shots. Half of a womans cells are dominated by the X chromosome that came from her mother, half by the X contributed by her father.

That genetic diversity is really valuable, Moalem explained. One of the immune systems most important weapons is the ability to recognize a virus. Well, genes on the X chromosome are involved in viral recognition. Right away, women have two different populations of immune cells that are best at spotting invaders.

Meanwhile, maybe the other X has a gene thats very good at identifying and killing infected cells, he said. So womens immune cells function like a tactical unit. They specialize, then they interact and cooperate to fight the invaders.

Men, with their single X chromosome, have a far less nimble immunological army at their command.

As a man, I dont have all those options, Moalem said. I can only hope that my one X has the genes that can recognize the virus and can kill it, too.

It gets worse for men in the age of COVID-19: The new coronavirus takes direct aim at their single-X vulnerability.

What we researchers are seeing right now is the way this coronavirus gets into our lung cells, Moalem said. It has a key: a spike protein we think it uses to break in. And the lock it picks to enter is called ACE2 an enzyme attached to the outer surface of the cell membrane.

The gene that makes ACE2 is on the X chromosome, he continued. So if the coronavirus has the right key, it can unlock every one of a males lung cells. But females have two Xs so half of their lung cells use one ACE2 lock, and the other half use a slightly different ACE2 lock. The chance that the virus has the perfect key to unlock both of them is not great. So thats another enormous advantage for females.

The virus lock-picking action damages the ACE2 so badly that it can no longer perform one of its crucial functions: preventing the buildup of fluid in the lungs during the infection.

Its the lungs filling up with fluid that happens in COVID-19 that can lead to the breathing difficulties experienced by so many, Moalem said. The severest lung injury were seeing with this infection is not likely to occur unless all your locks get picked. In females, the virus cant usually get into enough of their cells to do that amount of damage and that may be the reason why were seeing so many men dying.

If that idea is correct, he said, we should expect more tragedies like that of the Fusco family of New Jersey, who lost four closely related members 73-year-old matriarch Grace Fusco, two of her sons, and a daughter to the coronavirus last month.

We will likely see siblings or families that are particularly susceptible to this virus, because their cells share the same lock that the coronavirus is picking, Moalem said. We will see young people succumbing very quickly, very likely because they were born with a genetic version of the ACE2 lock that the coronavirus easily picks.

And yet he sees reason to hope as research laboratories around the world home in on ACE2 to thwart the coronavirus attack.

In that effort we can learn from the superimmunity of females, he said.

Moalems own lab was in the midst of investigating new antibiotics when the crisis hit.

We quickly switched our research efforts to find out if we can repurpose a drug that already exists, he said. There are a lot of drugs available, drugs whose safety profile we know, that could be used. Im hopeful we can find something already in the toolkit that will be effective.

Until then, he said, understanding the genetic risk factors of COVID-19 should spur us to safeguard those who are most in danger.

We should be shielding all our seniors, but we should actually be protecting our male elders most of all, he said. With this virus, there is immense risk simply due to the fact of being male.

The homogenous chromosomes benefit other animals too.

Human females are not the only ones that benefit from the double-X advantage. Across the animal kingdom, in all kinds of creatures whose sex is determined by their chromosomes, researchers are learning that the sex that has the doubled chromosome is almost always the one that lives longer.

Essentially Im proposing a new biological law, genetic researcher Sharon Moalem told The Post. The sex that gets two of same chromosomes will have an immense genetic advantage.

Moalem calls it the Law of Homogameity (same-gene).

In a study published just last month, researchers from Australias University of New South Wales found new evidence to support his thesis. Biologists analyzed life-span data on 229 different animal species mammals, birds, insects, fish, spiders, and more.

We found that across that broad range of species, the heterogametic sex does tend to die earlier than the homogametic sex, and its 17.6 percent earlier on average, lead researcher Zoe Xirocostas said.

It isnt always the female of a species that gets the edge. Birds, some reptiles and butterflies dont have the X and Y chromosomes that humans and other mammals share. Instead, they have whats called a ZW sex-determination system. Female birds cells contain Z and W chromosomes; males get the double-Z.

Just as Moalem suspected, its the males in those animal species that gain the longevity edge.

Across the animal kingdom, these creatures benefit from a double chromosome hit

See the rest here:
Why women are better than men at beating the coronavirus - New York Post

Male infertility is a heterogeneous condition of largely unknown etiology that affects at least 7% of men worldwide. Classical genetic approaches and emerging next-generation sequencing studies support genetic variants as a frequent cause of male infertility. Meanwhile, the barriers to transmission of this disease mean that most individual genetic cases will be rare, but because of the large percentage of the genome required for spermatogenesis, the number of distinct causal mutations is potentially large. Identifying bona fide causes of male infertility thus requires advanced filtering techniques to select for high-probability candidates, including the ability to test causality in animal models. The mouse remains the gold standard for defining the genotype-phenotype connection in male fertility. Here, we present a best practice guide consisting of (a) major points to consider when interpreting next-generation sequencing data performed on infertile men, and, (b) a systematic strategy to categorize infertility types and how they relate to human male infertility. Phenotyping infertility in mice can involve investigating the function of multiple cell types across the testis and epididymis, as well as sperm function. These findings will feed into the diagnosis and treatment of male infertility as well as male health broadly.

PubMed

Excerpt from:
A framework for high-resolution phenotyping of candidate male infertility mutants: from human to mouse. - Physician's Weekly

Written by Oscar Holland, CNNHong Kong

Despite his father having an "m-shaped" hairline, Alex Han from northeast China never thought he'd experience hair loss in his 20s.

"I was prepping my masters entrance examinations and there was a lot of pressure, so I probably didn't sleep very well," Han said in a phone interview. "At that time, (my receding hairline) was under control, but after three years in Beijing getting my masters, I moved to Germany for PHD study ... and not only me, but other Asian students there, had a problem with hair loss."

Commuters crowd the subway in Beijing in July 2008. China has traditionally had some of the world's lowest rates of baldness, though changes to people's lifestyles are contributing to an increase in hair loss. Credit: Guang Niu/Getty Images

Han opted to travel to Thailand for the transplant, which sees thousands of hair follicles grafted from other parts of the body -- such as the chest, or back of the neck -- onto the head. The eight- to 10-hour procedure cost him around $9,000, though he found clinics in China quoting "a sixth of that." The transplant may take months to take effect, though Han expressed hope that he will "see the results and see my hair return to normal in the next two or three months," adding, "then I'll behave as if nothing has happened."

Navigating stigmas

Han's fears mirror those experienced by men with receding hairlines around the world, namely the impact on his confidence, professional prospects and first impressions. "Hairstyles, for me, are critically important for men's first impressions," he said.

But losing your hair may be especially difficult in countries where it's less common. The male beauty standards in East Asian popular culture -- from Korean K-pop to Hong Kong's movie industry -- often favor big hair and boyish looks. "In Asian cultures the younger generation really like idols like (Chinese pop band) TFBoys," Han said, adding that standards for white or black men are often different.

"Whenever there is a precedent, people tend to feel (more confident) to follow," he said in an email interview.

A man looks at a robotic hair transplant machine at the China International Import Expo in Shanghai in 2019. Credit: China News Service/Visual China Group/Getty Images

Chinese American entrepreneur Saul Trejo, who has lived in various cities around Asia since 2011, began losing his hair while studying in Beijing. The 30-year-old said he "definitely noticed" the lower proportion of bald men in the city, compared to the US, and "it probably bothered me, but I tried to not let it." He also found that people were more comfortable than those in the West to pass comment -- even if in an entirely observational way.

"People will tell you straight out," he said in a phone interview from Taipei, recounting instances when his loss of hair was casually pointed out to him. "Normally when they're saying it they're not trying to be mean, they're just commenting, so I can't be mad. But you remember.

"I tried to shave my head, but I didn't think it was suitable for my head and body shape," he added, naming Dwayne "The Rock" Johnson and actor Jason Statham as non-Asians who can pull off the look. "I think Asian people, including myself, tend to be a little slimmer, so if I had to choose between bald and slim versus bald and athletic, or even muscular, then I think it looks better with the more size you have."

In 2018, Trejo underwent a hair transplant in Bangkok, where he was based at the time. While it took almost a year to see the final results, Trejo said his new hairline is "a major blessing," that "massively improved my dating life." Before-and-after images shared with CNN show a remarkable amount of hair restoration at the top and sides of his head.

Chinese American Saul Trejo, pictured before and after undergoing a hair transplant in Thailand. Credit: Saul Trejo

The doctor behind Trejo's procedure, Damkerng Pathomvanich, is a leading researcher into hair loss. He said that the number of hair transplant clinics in Asia is "skyrocketing," and that business among Chinese patients at his clinic is "booming."

Alternative approaches

A judge examines finalists at a 1957 baldness competition in Japan, where rates of hair loss have historically been among the world's lowest. Credit: Keystone Features/Hulton Archive/Getty Images

In Korea, meanwhile, houttuynia cordata -- also known as fish mint, or chameleon plant -- can be brewed into a black liquid that is applied to the scalp, according to the journalist, David Ko, who received some from his concerned mother-in-law.

"I used it like a shampoo whenever I washed my hair," he said. "After wetting my hair, I poured a handful of the plant-steeped water on my scalp, finger-massaged my scalp for about one minute, then rinsed it off with fresh water.

"But as time went by without seeing any clear sign of improvement, I got so tired of the remedy that I dumped more of (it) on my hair each time to finish the jar faster and get the practice over with." He then tried other suggested home remedies. "My wife also nudged me to sprinkle some sea salts over my scalp instead of the plant water, and one of my co-workers told me her balding father benefitted from eating lots of black sesame seeds as a snack."

Related video: Beauty is protest for young North Korean women

While New York dermatologist Norman Orentreich is widely known as the father of hair transplants, Japanese doctor Shoji Okuda is believed to have performed the very first procedure in 1937 (though the breakout of World War II meant that his research was largely overlooked). With baldness on the rise in Asia, it's perhaps no surprise that the continent's scientists -- Japan's and South Korea's in particular -- are again leading some of the field's most promising research.

Like 'a triad'

But, still, Asia poses unique challenges for receding men. Undergoing the scalp tattoo procedure requires patients to permanently sport a shaved-head look, which, as the Korean study suggested, may be "stereotyped in Asian cultures as (being like) a gangster or criminal." According to Ko, however, such labels are a thing of the past.

"Back in the day, when young males shaved their heads, seniors would mildly chide them with a totally unproven and absurd hypothesis," he said, suggesting that elders once saw a skinhead as a sign that someone was a rebel, or had "a problem with society."

"Nowadays (these attitudes) almost never exist, but it is still true people look at bald males with a certain awe."

A model with a shaved head walks the runway at China Fashion Week in 2017. The rise of street style may be helping popularize the skinhead look. Credit: Visual China Group / Getty Images

Eric But of Synergy Model Management, which has offices in Hong Kong and Guangzhou, said that clients are still often looking for Asian models to be "cute (with) long hair -- that Korean drama, perfect boyfriend kind of look." But while he distinguishes between shaved and bald heads, the modeling agent said that the rise of street fashion is gradually normalizing the skinhead look in Asia.

"For our parents' generation, a skinhead in Asia is kind of like a gangster -- if you want to be a triad, or if you go to prison, you have to shave your head," he said over the phone. "But now, for people born in the '90s or later, they see having a skinhead as a streetwear trend. And streetwear is massive in Asia."

Even in the home of coiffed K-pop, visibility may be growing gradually. Ko cited restaurateur Hong Seok-cheon (below), rapper Gill and actor Kim Kwang-kyu as examples of a slowly-growing number of high-profile bald celebrities in South Korea.

"It would be more helpful if there were more Koreans with hair loss --- if there were more cases (people) could look up to and think they are not alone out there."

Top image: Chinese artist Fang Lijun pictured with one of his paintings, which since the 1990s have often featured bald-headed protagonists. The artist uses the hairless figures as symbols of disillusionment and rebellion in modern China.

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With hair loss on the rise, Asia's men grapple with what it means to be bald - CNN

For weeks, infectious disease experts have been investigating why the coronavirus is proving particularly devastating to males, with early theories from China suggesting that higher rates of smoking among men may be to blame. But a new study from the Centers for Disease Control and Prevention (CDC) is suggesting it may have more to do with biology specifically, genetics than lifestyle.

The research, released on Monday in the CDCs Morbidity and Mortality Weekly Report, found a higher prevalence of COVID-19 in males across every pediatric age group including infants. Fifty-seven percent of the more than 2,572 pediatric cases of COVID-19 studied (out of 149,750 cases overall) were found in males, ranging in age from newborns to 18.

To be clear, the research did not suggest that parents should now be concerned about their male children or female children getting seriously ill from COVID-19. The risk for children remains very low.

Most of the children reported symptoms of cough or fever, but only a small fraction (five percent) were hospitalized, bolstering reports that kids often develop a mild case of the virus. Those hospitalized were far more likely to report underlying health conditions than those who werent, including asthma, chronic lung disease and cardiovascular disease. Only 0.1 percent of the children infected died.

The median age of the more than 2,500 children with COVID-19 was 11, with over a third of cases involving teens between the ages of 15 and 17. But the most striking statistic for the researchers was that 57 percent of cases occurred among males an even higher number than the adult group, in which 53 percent of the cases involved males. The researchers conclude that the higher rate of boys testing positive in every pediatric age groupsuggests that biologic factors might play a role in any differences in COVID-19 susceptibility by sex.

So what exactly may be driving the higher incidence in young boys, and should parents take this as a concern? GregoryA.Poland,MD, an infectious diseases expertandheadofthe Mayo Clinic's Vaccine ResearchGroup, tells Yahoo Lifestyle that the study is no reason to panic, and shouldnt be taken as a roadmap for parents with boys. Instead, Poland helps unpack what the new research can teach us.

Poland says the concept that females are less susceptible to disease is a generalizable phenomenon beyond just infectious diseases (such as COVID-19). In fact, women also tolerate starvation and dehydration and survive longer than men do in austere environments, Poland tells Yahoo Lifestyle. So there does appear to be a sex advantage on the side of females that males don't have, meaning a better immune response.

Although the gender disparity may lead to theories about hormones, Poland says studies like this one are the reason researchers dont consider hormones to be the source. These are children who are absent the kind of hormonal levels or differences that we would see post-pubertal, Poland says, adding that the disparity in infection is one seen in post-menopausal women, too. That doesn't mean there couldn't be some still fine hormonal differences. But it leads to the idea that while hormones are important, it's again just one factor in this complex web that still needs to be teased apart.

Its still unclear to experts exactly why women respond better to certain diseases and harsh environments, but Poland says that genes may inform the answer. We don't fundamentally understand this... but what we do know is that females depending on the virus will tend to activate or suppress different genes than males do when their cells are exposed to these viruses, says Poland. So we think a strong driver of this is going to be just genetic, not just hormonal.

There is no evidence that females may be better equipped to fight disease due to evolution, but Poland says the idea has been floated. We don't have any evidence but people always postulate ... the idea has been in general: Is it this way for the primary reason of propagation of the species? he says. You need women to have children. You can have a lot of children with a few men, but you can only have them one by one with women.

An immunologist at the Heinrich Pette Institute in Hamburg, Germany, Marcus Atlfeld, raised another theory in a Scientific American piece from 2016 suggesting that women might have evolved a particularly fast and strong immune response to protect developing fetuses and newborn babies. Poland says that, in the absence of evidence, it may not be possible to form a conclusion.

Poland says males facing disease at higher rates than women is something currently being studied through the lens of vaccines. When you give males versus females of any age a vaccine, females almost always respond better than males, Poland says. He says that it shows females, even when faced with a small viral load of an inactivated disease, are often able to respond better than males something seen with vaccines against smallpox, measles and influenza.

Women responding more efficiently to disease may be beneficial in the midst of a coronavirus pandemic, but Poland says it has a negative side, too a higher likelihood that the immune system will overreact. This supercharged immune system has a negative side to it, says Poland. And that is women have higher rates of autoimmune diseases diseases where their own immune system attacks their own body. (According to the National Institutes of Health, roughly eight percent of the population has an autoimmune disease; 78 percent of them are women).

Like the authors of the CDC study, who note many limitations of the research, Poland says the study doesnt necessarily mean that more young boys are getting the virus. Instead, it could be showing that they do not have the same quality of immune response that girls do. There could be a lot of girls out there who had it but had zero symptoms, says Poland. So she may not even go and be tested to know that she has COVID-19. The boy is more likely to have symptoms [and] that may drive testing.

For that reason and many others, Poland says the new research should not be a reason for parents of boys to panic, nor for parents of girls to consider them immune. I would not want this to give false reassurance to a parent because yes, there were girls that got sick, Poland tells Yahoo Lifestyle. There were girls that had severe illness. So I would put it in the category of, that's interesting. More research needs to be done. But for me as a parent, I put whatever appropriate layers of protection around my children, regardless of their gender.

For the latest coronavirus news and updates, follow along at https://news.yahoo.com/coronavirus. According to experts, people over 60 and those who are immunocompromised continue to be the most at risk. If you have questions, please reference the CDC and WHOs resource guides.

See more here:
CDC: Coronavirus is more prevalent in young boys than girls - Yahoo Lifestyle

In April 1980, almost exactly forty years ago, the journal Nature published a pair of highly influential articles on the topic of what has become known as junk or selfish DNA. Both reflected the key concept of The Selfish Gene, the highly influential 1976 book by Richard Dawkins, namely, that organisms are merely DNAs way of making more DNA. The first was authored by W. Ford Doolittle and Carmen Sapienza and titled Selfish genes, the phenotype paradigm and genome evolution.1 The second was authored by Leslie Orgel and Francis Crick and titled Selfish DNA: the ultimate parasite.2 Together they posited an easy-to-grasp way to conceive of excess nucleotides along chromosomes repetitive sequences in general and transposable elements in particular. In short, it was proposed that most such DNA elements neither had nor have (developmental) effects or functions (in general) in the shaping of an organisms traits (its phenotype). And because they have no phenotypic expression (as Doolittle and Sapienza put it) or little or no effect on the phenotype (as Orgel and Crick put it), the only role that can be ascribed to them is that of replicative survival.

But there are two problems with this outlook, one empirical and one formal. That which is empirical involves the organization of (eukaryotic) chromosomes, whereas that which is formal involves how to define effect, expression, and function when it comes to repetitive DNA sequences of any type. And so to narrow our focus on these problems, let us give some thought to the Y chromosome of Drosophila melanogaster, that engaging fly which is the bond-servant of genetics, as it is replete with a junk and selfish typography. Note that I will only be briefly touching on the first problem in this piece.

Now the Y chromosome of this species is approximately 40,000,000 bases in length, and that is significant for it makes up around 20 percent of the male haploid DNA content.3-4 While it is essential for male fertility, it has but few protein-coding regions and these are interrupted by or surrounded by vast tracks of (often degenerated) transposable elements, tandemly arranged runs of satellite units (such as AACAC, AATAG, AATAT, and so forth), a block of ribosomal-RNA genes, and various other sequence families.5 In addition, its various components are densely compacted in somatic-cell nuclei, and this heterochromatin is supposedly inert until around the stage the primary spermatocytes are formed. I hasten to mention also that its composition of DNA varies from strain to strain of D. melanogaster, even though its protein-coding sequences are stable throughout.6 What all of this seems to suggest, then, is that the bulk of this chromosome may have no phenotypic expression or little or no effect on the phenotype in males of this species.

Recall, however, that I said that there are two problems with this outlook, one of which is empirical. Concerning that, let us note that by the mid 1950s it was well-established that introducing a Y chromosome into a female D. melanogaster (by the feats of fruit-fly genetics) leads to a broad range of phenotypic effects, as does increasing the copies or dosage of a Y chromosome in a male of the same.7 Not only that, but with the sixty-plus years that have elapsed, we are much closer to understanding how such phenotypic effects due to junk or selfish DNA sequences take place. For one thing, it is now clear that different Y-chromosome sequence variants can differentially alter the expression of hundreds of genes in the somatic cells of male flies.8-10 For another, the characters that are affected are those of interest to the population geneticist including such things as male reproductive traits. Then again, many of the genes so modulated by the Y chromosome in this Drosophila species are positioned in so-called repressed chromatin domains.11

Apropos is an in-press work by Emily Brown, Alison Nguyen, and Doris Bachtrog that tests a hypothesis to explain such Y-chromosomal-based phenotypic effects.12 Some have suggested that long stretches of repetitive elements on that chromosome (which again is millions of bases long) can serve as a sink that titrates out heterochromatic proteins, thereby depleting the latter in other domains of a nucleus.13 Congruent with this hypothesis, Brown and colleagues showed that a consequence of introducing a Y chromosome into a female, or by decreasing or increasing the copies or dosage of a Y chromosome in a male line, is a widespread redistribution in nuclei of histone markers that are specific for heterochromatin, but not for those that are specific for active euchromatin. This means that the Y-sequences do make their absence or presence and (if present) quantities known in morphogenesis. What is more, the balance of chromatin domains in female versus male flies is likely to be en masse modulated by such parameters.

We can thus rephrase what Doolittle and Sapienza or Orgel and Crick asserted back in 1980 in this manner: Seemingly excess nucleotides do have phenotypic expressions be they ever so indirect, which is to say that they do have major effects on the phenotype. It thus looks like there is a why to the fly Y, though it does not fit the axioms with which the junk DNA advocates beset us. Yet we should note that such a possibility was never actually excluded, for as Doolittle and Sapienza claimed: We do not deny thatrepetitive and unique-sequence DNAs not coding for protein in eukaryotes may have roles of immediate phenotypic benefit to the organism.2

Photo: Drosophila melanogaster, an engaging fly, bySanjay Acharya / CC BY-SA.

Excerpt from:
The Why of the Fly Y: Reflections on Junk DNA - Discovery Institute

An elderly woman wears a mask as a precautionary measure against covid-19, as people take their ... [+] daily exercise in Battersea Park in London on March 28, 2020, as life in Britain continues during the nationwide lockdown to combat the novel coronavirus pandemic. - The two men leading Britain's fight against the coronavirus -- Prime Minister Boris Johnson and his Health Secretary Matt Hancock -- both announced Friday they had tested positive for COVID-19, as infection rates accelerated and daily death rate rose sharply. (Photo by Tolga AKMEN / AFP) (Photo by TOLGA AKMEN/AFP via Getty Images)

According to a recent Reuters/Ipsos poll, 54% of women said they were very concerned about Coronavirus. For men, this number was only 45%.

And thats just the beginning. The poll also reported men to be less likely to wash their hands and use hand sanitizers frequently, less committed to avoiding public gatherings, less supportive of the closing of public schools, and more likely to believe people were unnecessarily panicked about COVID-19.

Clearly, men are more cavalier in their assessment of the risk posed by COVID-19. But is this reflective of some underlying wisdom or calculated cost-benefit analysis, or is it another case of male stubbornness? Research in gender psychology suggests that there may be truth to both of these ideas. They are discussed below.

Stereotypes abound regarding the stubbornness of men. Men are less likely to stop and ask for directions when they are lost. They are less likely to take the advice of others. They are more likely to engage in risky behaviors.

And, where theres smoke, theres fire. Research has found men to be significantly less likely to seek out professional help to address mental or physical health problems. Mens reluctance to visit a doctor may be one of the reasons why they tend to die younger than women and why they have a higher mortality rate for 14 out of the 15 most common causes of death.

Even more damning is the finding that men are more likely to refer others to seek out health-related help; they just tend not to take their own advice.

Why is this the case? Part of it has to do with societal expectations. In cultures around the world, men are expected to be strong, dominant, confident, and unemotional. This begins early in their socialization, when boys are taught that real men dont show emotion or ask for help. Over time, this leads to the development of behaviors that negatively impact their health for example, increased substance use, fighting, and risky sexual behaviors.

It may also have to do with underlying male personality traits. Research has found men to be less agreeable than women, and less extroverted. Women also tend to be more cooperative in social and economic situations. Whether or not these trait differences are due to socialization pressures or genetics is an open debate. The most likely answer is that both factors are at play.

In the case of COVID-19, these traits may explain why men are generally less concerned about the disease. In the face of threat, they are expected to exhibit an air of invincibility; it is a trait promoted by culture and society as much as it may be hardwired into their personality.

Theres also evidence to suggest that men are better than women at tapping into their rational mind. For instance, a recent study published in the Journal of Behavioral and Experimental Economics examined gender differences on three brain teasers used to measure a persons ability to engage in reflective, systematic, and non-intuitive thinking. In case you are curious, the questions are listed below and the answers can be found at the end of the article.

If youve reviewed the answers, youll see how these questions assess a persons ability to forgo intuitive yet incorrect responses in favor of correct answers that require a deeper level of thinking.

The researchers examined over 44,000 responses to these questions from 21 different countries. They found clear evidence of a male advantage. They write, We find that: (i) males perform better in every single question, (ii) females are more likely to answer none of the questions correctly, and (iii) males are more likely to answer all three questions correctly. Importantly, gender differences persist even when we control for test characteristics (for example, monetary incentives, computerized, student samples, positioning of the experiment, etc.).

Again, whether there is a genetic component to this difference, or whether it is based solely on environmental factors, is an open debate (and a controversial one). It does, however, suggest that men might be better equipped to size up the COVID-19 risk for what it is: a threat that, in most cases, is still exceptionally remote.

There is a third factor at play, and that has to do with the finding that men might be less equipped to fight off the disease in the event they are exposed to it. This was discussed in a recent New York Times opinion piece, written by Dr. Sharon Moelem. He states, The disproportionate toll this virus is taking on males isnt an anomaly. When it comes to survival, men are the weaker sex. If true, perhaps this tips the scale in favor of the stubbornness hypothesis.

Brain teaser answers:

Excerpt from:
Men Are Less Concerned About COVID-19 Than Women. Is This Due To Reason Or Stubbornness? - Forbes

As citizens of developed nations continue to live longer and longer, dementia cases will begin to appear more frequently.

One in 14 Americans over the age of 65 will experience cognitive decline, and nearly one in six will endure the same at some point in their eighties. Despite the prevalence of the disease, there is a lot we still dont know about its pathology.

Advanced stages of dementia typically follow a series of muted symptoms patients might mistake for less serious conditions, like stress or sleep deprivation. In fact, according to a new study conducted by researchers from Duke University, many of us evidence one of the premiere red flags associated with the illness almost every day.

There has been a misperception that financial difficulty may occur only in the late stages of dementia, but this can happen early, and the changes can be subtle, explained senior author P. Murali Doraiswamy, MBBS, a professor of psychiatry and geriatrics at Duke University, in a media release.

The new paper, published in The Journal of Prevention of Alzheimers Disease, examines the cross-sectional relationship between dementia and financial management skills in the elderly. The strength of the reports findings highlights how limited the diagnostic scope has been up until very recently.

The researchers began with a longitudinal study of 243 adults between the ages 55 and 90 from the Alzheimers Disease Neuroimaging Initiative.

The study pool contained a heterogeneous mix of cognitively healthy adults, adults with mild memory impairment and adults who had been previously diagnosed with Alzheimers disease before recruitment.

After coupling financial literacy tests with brain scans that measured levels of protein buildup of beta-amyloid plaque, the researchers were able to establish a punitive correlation between the two.

On balance, even healthy adults showcased a drop in financial skills as they age, but after controlling for relevant variables the data yielded a direct relationship between increased amyloid plaques (a common predictor of degenerative disease) and a decreased ability to comprehend basic financial concepts, successfully calculated values and effectively balance an account.

Using a multicenter study sample, we document that financial capacity is impaired in the prodromal and mild stages of AD and that such impairments are, in part, associated with the extent of cortical -amyloid deposition. In normal aging, -amyloid deposition is associated with slowing of financial tasks. These data confirm and extend prior research highlighting the utility of financial capacity assessments in at-risk samples, the authors wrote in the report.

These outcomes were consistent among male and female participants.

As covered in a previously published Ladders article, the protein-plaque buildup is a biological inevitability that is not in and of itself instructive of onset cognitive decline. This rule also applies to many of the symptoms mentioned above. Any and each warrant concern when genetics and severity are applied.

Plaque buildup in adults who go on to develop dementia occurs aggressively, as do the pathological substrates associated with it. The problem is diagnosis is more often than not informed by reduced memory capabilityan important feature of cognitive illness but by no means the only reliable one.

Older adults hold a disproportionate share of wealth in most countries and an estimated $18 trillion in the U.S. alone, Doraiswamy continues. Little is known about which brain circuits underlie the loss of financial skills in dementia. Given the rise in dementia cases over the coming decades and their vulnerability to financial scams, this is an area of high priority for research.

Link:
This very common issue could be an early sign of dementia - Ladders

Helen PilcherBloomsbury Sigma2020384 pp.Purchase this item now

Hailing from rare wild mutants, the golden gnu, an uncharacteristically fawn-colored wildebeest, was for the past decade at the center of a speculation bubble in the African trophy-hunting business. Owners of wildlife preserves banked on hunters being willing to part with large sums for the privilege of shooting these beasts, and breeding stock changed hands for up to US$500,000 per animal. The speculators were wrong. The price people were prepared to pay was nowhere near what ranchers had hoped. Prices plummeted and reserve owners were left with herds of worthless mutant wildlife.

This is one of many tales Helen Pilcher tells in Life Changing, the central theme of which is how humans are, more deeply and pervasively than ever before, changing nature. She interprets her brief broadly, loosely weaving together intentional as well as accidental changes, (self-)domestication, conventional breeding, genetic modification (including CRISPR-Cas9), cloning, de-extinction, sterile male and kamikaze-gene techniques, hybridization, contemporary evolution, assisted evolution, conservation genetics, and rewilding.

Pilcher presents these stories in a pleasant, chatty style, garnished with funny asides. Part of the book consists of retellings of stories from other recent books on this topic (13). Still, it covers some new ground and makes for exciting reading, especially when Pilcher gives firsthand accounts of, for example, a captive breeding program for the endangered kkp parrot in New Zealand or an assisted evolution facility for coral at Londons Horniman Museum.

Pilcher tends to skirt around the more challenging parts of her subjects, such as the evolutionary biology of how species have adapted, and continue to adapt, to humans. When her examples involve her own academic field (cellular biology), however, she is on more secure footing. Her tale of the world of horse-cloning techniques and their implications, for instance, is fascinating.

Around 10 years ago, Argentinian polo champion Adolfo Cambiaso produced no fewer than six copies of his favorite mare, Cuartetera. In polo, players can change to fresh horses throughout the game, meaning that Cambiaso can ride multiple clones in a single match.

Toward the end of the book, Pilcher surveys her portfolio of human-induced changes in the worlds species and ponders what their impact will be on ecosystems of the future. She reminds readers of Darwins words that natural selection is immeasurably superior to mans feeble efforts and that there is hubris in thinking that we can fix the environment using technology.

Her chapter on rewilding shows how new ecosystems will appear, as if by magic, if we stop interfering with nature. The Knepp estate in England, for example, where feral pigs play their original role as a keystone species, is now a mosaic of habitats where rare species, once characteristic of the English half-open forest landscape, abound.

Pilcher waxes lyrical about successful attempts to save biodiversity by micromanaging species genetic makeup, as has been done to prevent inbreeding in the precariously small Kkp population. Unfortunately, the vertebrate component of biodiversity is negligible compared with the huge numbers of nonvertebrate organisms that make up the bulk of the food web. To this point, when the remaining wild Kkps entered the captive breeding program, they were dewormed, which probably drove to extinction Stringopotaenia psittacea, the kkps unique tapeworm species. For all its technological prowess, the net biodiversity benefit of the Kkp Recovery Program is probably exactly zero.

While the ultimate impact of intentional modification of species should not be oversold, the unintentional impact of our actions on the worlds ecosystems might be even vaster than Pilcher dares imagine. Forecasting these changes will be impossible, and only time will tell how those ecosystems will look and function.

References and notes1. L. A. Dugatkin, L. Trut, How to Tame a Fox (and Build a Dog) (Univ. of Chicago Press, 2017).2. T. Kornfeldt, The Re-Origin of Species (Scribe, 2018).3. K. van Grouw, Unnatural Selection (Princeton Univ. Press, 2018).

The reviewer is at the Naturalis Biodiversity Center, Darwinweg 2, 2333 CR Leiden, Netherlands.

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Through actions big and small, intentional and unintentional, we are reshaping life on Earth - Science Magazine

Fukami M, Shozu M, Ogata T. Molecular bases and phenotypic determinants of aromatase excess syndrome. Int J Endocrinol. 2012;2012:584807. doi: 10.1155/2012/584807. Epub 2012 Jan 26.

Fukami M, Shozu M, Soneda S, Kato F, Inagaki A, Takagi H, Hanaki K, Kanzaki S, Ohyama K, Sano T, Nishigaki T, Yokoya S, Binder G, Horikawa R, Ogata T. Aromatase excess syndrome: identification of cryptic duplications and deletions leading to gain of function of CYP19A1 and assessment of phenotypic determinants. J Clin Endocrinol Metab. 2011 Jun;96(6):E1035-43. doi: 10.1210/jc.2011-0145. Epub 2011 Apr 6.

Fukami M, Tsuchiya T, Vollbach H, Brown KA, Abe S, Ohtsu S, Wabitsch M, Burger H, Simpson ER, Umezawa A, Shihara D, Nakabayashi K, Bulun SE, Shozu M, Ogata T. Genomic basis of aromatase excess syndrome: recombination- and replication-mediated rearrangements leading to CYP19A1 overexpression. J Clin Endocrinol Metab. 2013 Dec;98(12):E2013-21. doi: 10.1210/jc.2013-2520. Epub 2013 Sep 24.

Shihara D, Miyado M, Nakabayashi K, Shozu M, Ogata T, Nagasaki K, Fukami M. Aromatase excess syndrome in a family with upstream deletion of CYP19A1. Clin Endocrinol (Oxf). 2014 Aug;81(2):314-6. doi: 10.1111/cen.12329. Epub 2013 Oct 18.

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Aromatase excess syndrome - Genetics Home Reference - NIH

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In being released into a South Taranaki river, whio Tipunakore, Trev and Tui made history.

It was a low key event for three juvenile whio blue ducks released to the Kapuni Stream recently - the first release of whio ona South Taranaki river in Egmont National Park.

A previous event with Te Korowai o Ngruahine, Supporting Today's At Risk Teenagers (START) Taranaki, and whio support groupswas cancelled due to Covid-19 risk.

Two male and one female whio were bred at Ng Manu Nature Reserve in Waikanae and taken to a 'hardening' facility at the Tongariro Trout Centre where thebirds provided new genetics to the current population.

The birds join a record number of whio ducklings found by Department of Conservation rangers on eight regularly surveyed rivers.

READ MORE:Whio population boosted by release of three more ducks on Mt Taranaki

The upcoming five yearly whio census scheduled in 2020would determine if overall numbers have increased since 2015.

There are now estimated to be more than 80 whio in the national park.

The released whio - Tipunakore, Trev and Tui - are named after two Taranaki START students now working with the Taranaki Mounga Project, and a supporter of the programme.

Taranaki Mounga project manager Sean Zieltjes saidTrev, one of the students, hadworked with the project for nearly a year.

He wasstokeda whio is named after him, Zieltjes said.

"Trev worked incredibly hard to help protect these taonga.

"Hebuilt over 300 DOC200 stoat traps in his neighbour's carport, and also helped to cut the tracks were these traps are all active on the southern side of the maunga.

"Thanks to Trevhe's protecting whio and giving them the best chance to thrive."

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Juvenile whio ducks take to the water for first time on a South Taranaki river - Stuff.co.nz

Newswise Women undergoing radiotherapy for many cancers are more likely than men to be cured, but the side effects are more brutal, according to one of Australias most experienced radiation oncology medical physicists.

University of South Australia (UniSA) Professor of Medical Radiation, Eva Bezak, says women are generally more sensitive to radiation than men, but this is not considered in international guidelines for radiation dosages.

Current guidelines are generally based on a persons height, weight or BMI, and radiobiological responses of the general population.

In a paper published in Critical Reviews in Oncology/Hematology, Professor Bezak and her colleagues Louis de Courcy from University College Dublin and Professor Loredana Marcu from the University of Oradea in Romania highlight the need for gender to be taken into account when administering radiation.

It is clear that gender plays a role in the occurrence and response to therapy of many diseases, Professor Bezak says.

For example, it is already well established that men are more susceptible to head, neck and blood cancers and women are more prone to auto immune diseases as well as developing osteoporosis.

Scientists also know that individual responses to radiotherapy are up to 80 per cent determined by genetics.

So, where do we start with gendered medicine?

The next step is to ensure that we use both male and female mice even in our pre-clinical testing so we can get a better understanding of how gender influences treatment outcomes.

It is also important to collect data retrospectively so we can compare the radiotherapy outcomes for men and women who were prescribed radiotherapy for the same cancer.

It is a double-edged coin for men, too. Because they are more radio-resistant than women, their healthy tissues are better protected when receiving radiotherapy with fewer side effects, but their long-term survival rates are shorter.

The differences in radiation responses are highlighted by two major events in history: the Chernobyl nuclear reaction disaster in 1986 and the atomic bombings of Hiroshima and Nagasaki in 1945.

Professor Bezak says following Hiroshima and Nagasaki, the incidence of cancer in Japan was much higher in women (58 per cent) compared to men (35 per cent).

Likewise, after the Chernobyl nuclear accident, millions fewer girls were born to irradiated men and women were at greater risk of endocrine imbalance, thyroid cancer and brain tumours.

The one area that does appear to give women some protection against radiation is the female hormone oestrogen, which has a neuroprotective effect during head irradiation.

As healthcare becomes progressively more tailored to the individual, gender is a factor that can no longer be disregarded. It needs to be taken into account as an independent prognostic factor, Prof Bezak says.

A video explaining the differences in radiation outcomes between men and women can be viewed at https://youtu.be/BtDniRA7DMs

Notes for editors

Gender-dependent radiotherapy: the next step in personalised medicine? is published in Critical Reviews in Oncology/Hematology. The other contributing authors are Louis de Courcy from University College, Dublin, and Professor Loredana G. Marcu from the University of Oradea.

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The pros and cons of radiotherapy: will it work for you? - Newswise

TORONTO , March 31, 2020 /CNW/ - The Gairdner Foundation is pleased to announce the 2020 Canada Gairdner Award laureates, recognizing some of the world's most significant biomedical research and discoveries. During these challenging times, we believe it is important to celebrate scientists and innovators from around the world and commend them for their tireless efforts to conduct research that impacts human health.

2020 Canada Gairdner International AwardThe five 2020 Canada Gairdner International Award laureates are recognized for seminal discoveries or contributions to biomedical science:

Dr. Masatoshi Takeichi Senior Visiting Scientist, RIKEN Center for Biosystems Dynamics Research, Kobe, Japan ; Professor Emeritus, Kyoto University , Kyoto, Japan

Dr. Rolf Kemler Emeritus Member and Director, Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany

Awarded "For their discovery, characterization and biology of cadherins and associated proteins in animal cell adhesion and signalling."

Dr. Takeichi

The Work: The animal body is made up of numerous cells. Dr. Takeichi was investigatinghow animal cells stick together to form tissues and organs, and identified a key protein which he named 'cadherin'.Cadherin is present on the surface of a cell and binds to the same cadherin protein on the surface of another cell through like-like interaction, thereby binding the cells together. Without cadherin, cell to cell adhesion becomes weakened and leads to the disorganization of tissues. Dr. Takeichi found that there are multiple kinds of cadherin within the body, each of which are made by different cell types, such as epithelial and neuronal cells. Cells with the same cadherins tend to cluster together, explaining the mechanism of how different cells are sorted out and organized to form functional organs.

Further studies by Dr. Takeichi's group showed that cadherin function is supported by a number of cytoplasmic proteins, includingcatenins, and their cooperation is essential for shaping of tissues. His studies also revealed that the cadherin-dependent adhesion mechanism is involved in synaptic connections between neurons, which are important for brain wiring.

Dr. Kemler

The Work: Dr. Kemler, using an immunological approach, developed antibodies directed against surface antigens of early mouse embryos. These antibodies were shown to prevent compaction of the mouse embryo and interfered with subsequent development. Both Dr. Kemler and Dr. Takeichi went on to clone and sequence the gene encoding E-cadherin and demonstrate that it was governing homophilic cell adhesion.

Dr. Kemler also discovered the other proteins that interact with the cadherins, especially the catenins, to generate the machinery involved in animal cell-to-cell adhesion. This provided the first evidence of their importance in normal development and diseases such as cancer. It has been discovered that cadherins and catenins are correlated to the formation and growth of some cancers and how tumors continue to grow. Beta catenin is linked to cell adhesion through interaction with cadherins but is also a key component of the Wnt signalling pathway that is involved in normal development and cancer. There are approximately 100 types of cadherins, known as the cadherin superfamily.

Dr. Takeichi

The Impact: The discovery of cadherins, which are found in all multicellular animalspecies, has allowed us to interpret how multicellular systems are generated and regulated. Loss of cadherin function has been implicated as the cause of certain cancers, as well as in invasiveness of many cancers. Mutations in special types of cadherin result in neurological disorders, such as epilepsy and hearing loss. The knowledge of cadherin function is expected to contribute to the development of effective treatments against such diseases.

Dr. Kemler

The Impact: Human tumors are often of epithelial origin. Given the role of E-cadherin for the integrity of an epithelial cell layer, the protein can be considered as a suppressor of tumor growth. The research on the cadherin superfamily has had great impact on fields as diverse as developmental biology, cell biology, oncology, immunology and neuroscience. Mutations in cadherins/catenins are frequently found in tumors. Various screens are being used to identify small molecules that might restore cell adhesion as a potential cancer therapy.

Dr. Roel Nusse Professor & Chair, Department of Developmental Biology; Member, Institute for StemCell Biology andRegenerativeMedicine, Stanford University , School of Medicine. Virginia and Daniel K. Ludwig Professor of Cancer Research. Investigator, Howard Hughes Medical Institute

Awarded"For pioneering work on the Wnt signaling pathway and its importance in development, cancer and stem cells"

The Work: Dr. Nusse's research has elucidated the mechanism and role of Wnt signaling, one of the most important signaling systems in development. There is now abundant evidence that Wnt signaling is active in cancer and in control of proliferation versus differentiation of adult stem cells, making the Wnt pathway one of the paradigms for the fundamental connections between normal development and cancer.

Among Dr. Nusse's contributions is the original discovery of the first Wnt gene (together with Harold Varmus) as an oncogene in mouse breast cancer. Afterwards Dr. Nusse identified the Drosophila Wnt homolog as a key developmental gene, Wingless. This led to the general realization of the remarkable links between normal development and cancer, now one of the main themes in cancer research. Using Drosophila genetics, he established the function of beta-catenin as a mediator of Wnt signaling and the Frizzleds as Wnt receptors (with Jeremy Nathans ), thereby establishing core elements of what is now called the Wnt pathway. A major later accomplishment of his group was the first successful purification of active Wnt proteins, showing that they are lipid-modified and act as stem cell growth factors.

The Impact: Wnt signaling is implicated in the growth of human embryos and the maintenance of tissues. Consequently, elucidating the Wnt pathway is leading to deeper insights into degenerative diseases and the development of new therapeutics. The widespread role of Wnt signaling in cancer is significant for the treatment of the disease as well. Isolating active Wnt proteins has led to the use of Wnts by researchers world-wide as stem cell growth factors and the expansion of stem cells into organ-like structures (organoids).

Dr. Mina J. Bissell Distinguished Senior Scientist, Biological Systems and Engineering Division, Lawrence Berkeley National Laboratory; Faculty; Graduate Groups in Comparative Biochemistry, Endocrinology, Molecular Toxicology and Bioengineering, University of California Berkeley , Berkeley, CA , USA

Awarded "For characterizing "Dynamic Reciprocity" and the significant role that extracellular matrix (ECM) signaling and microenvironment play in gene regulation in normal and malignant cells, revolutionizing the fields of oncology and tissue homeostasis."

The Work: Dr. Mina Bissell's career has been driven by challenging established paradigms in cellular and developmental biology. Through her research, Dr. Bissell showed that tissue architecture plays a dominant role in determining cell and tissue phenotype and proposed the model of 'dynamic reciprocity' (DR) between the extracellular matrix (ECM) and chromatin within the cell nucleus. Dynamic reciprocity refers to the ongoing, bidirectional interaction between cells and their microenvironment. She demonstrated that the ECM could regulate gene expression just as gene expression could regulate ECM, and that these two phenomena could occur concurrently in normal or diseased tissue.

She also developed 3D culture systems to study the interaction of the microenvironment and tissue organization and growth, using the mammary gland as a model.

The Impact:Dr. Bissell's model of dynamic reciprocity has been proven and thoroughly established since its proposal three decades ago and the implications have permeated every area of cell and cancer biology, with significant implications for current and future therapies. Dr. Bissell's work has generated a fundamental and translationally crucial paradigm shift in our understanding of both normal and malignant tissues.

Her findings have had profound implications for cancer therapy by demonstrating that tumor cells can be influenced by their environment and are not just the product of their genetic mutations. For example, cells from the mammary glands grown in two-dimensional tissue cultures rapidly lose their identity, but once placed in proper three-dimensional microenvironments, they regain mammary form and function. This work presages the current excitement about generation of 3D tissue organoids and demonstrates Dr. Bissell's creative and innovative approach to science.

Dr. Elaine Fuchs Howard Hughes Medical Institute Investigator and Rebecca C. Lancefield Professor and Head of the Robin Chemers Neustein Laboratory of Mammalian Cell Biology and Cell Biology; The Rockefeller University , New York, NY , USA

Awarded"For her studies elucidating the role of tissue stem cells in homeostasis, wound repair, inflammation and cancer."

The Work: Dr. Fuchs has used skin to study how the tissues of our body are able to replace dying cells and repair wounds. The skin must replenish itself constantly to protect against dehydration and harmful microbes. In her research, Fuchs showed that this is accomplished by a resident population of adult stem cells that continually generates a shell of indestructible cells that cover our body surface.

In her early research, Fuchs identified the proteins---keratinsthat produce the iron framework of the skin's building blocks, and showed that mutations in keratins are responsible for a group of blistering diseases in humans. In her later work, Fuchs identified the signals that prompt skin stem cells to make tissue and when to stop. In studying these processes, Fuchs learned that cancers hijack the fundamental mechanisms that tissue stem cells use to repair wounds. Her team pursued this parallel and isolated and characterized the malignant stem cells that are responsible for propagating a type of cancer called "squamous cell carcinoma." In her most recent work, she showed that these cells can be resistant to chemotherapies and immunotherapies and lead to tumor relapse.

The Impact: All tissues of our body must be able to replace dying cells and repair local wounds. Skin is particularly adept at performing these tasks. The identification and characterization of the resident skin stem cells that make and replenish the epidermis, sweat glands and hair provide important insights into this fountain of youth process and hold promise for regenerative medicine and aging. In normal tissues, the self-renewing ability of stem cells to proliferate is held in check by local inhibitory signals coming from the stem cells' neighbours. In injury, stimulatory signals mobilize the stem cells to proliferate and repair the wound. In aging, these normal balancing cues are tipped in favour of quiescence. In inflammatory disorders, stem cells become hyperactivated. In cancers, the wound mechanisms to mobilize stem cells are hijacked, leading to uncontrolled tissue growth. Understanding the basic mechanisms controlling stem cells in their native tissue is providing new strategies for searching out refractory tumor cells in cancer and for restoring normalcy in inflammatory conditions.

2020 John Dirks Canada Gairdner Global Health AwardThe 2020 John Dirks Canada Gairdner Global Health Award laureate is recognized for outstanding achievements in global health research:

Professor Salim S. Abdool Karim Director of CAPRISA (Centre for the AIDS Program of Research in South Africa), the CAPRISA Professor in Global Health at Columbia University , New York and Pro Vice-Chancellor (Research) at the University of KwaZulu-Natal, Durban, South Africa

Professor Quarraisha Abdool KarimAssociate Scientific Director of CAPRISA, Professor in Clinical Epidemiology, Columbia University , New York and Professor in Public Health at the Nelson Mandela Medical School and Pro Vice-Chancellor (African Health) at the University of KwaZulu-Natal, Durban, South Africa

Awarded"For their discovery that antiretrovirals prevent sexual transmission of HIV, which laid the foundations for pre-exposure prophylaxis (PrEP), the HIV prevention strategy that is contributing to the reduction of HIV infection in Africa and around the world."

The Work: UNAIDS estimates that 37 million people were living with HIV and 1.8 million people acquired HIV in 2017. In Africa, which has over two thirds of all people with HIV, adolescent girls and young women have the highest rates of new HIV infections. ABC (Abstinence, Be faithful, and use Condoms) prevention messages have had little impact - due to gender power imbalances, young women are often unable to successfully negotiate condom use, insist on mutual monogamy, or convince their male partners to have an HIV test.

In responding to this crisis, Salim and Quarraisha Abdool Karim started investigating new HIV prevention technologies for women about 30 years ago. After two unsuccessful decades, their perseverance paid off when they provided proof-of-concept that antiretrovirals prevent sexually acquired HIV infection in women. Their ground-breaking CAPRISA 004 trial showed that tenofovir gel prevents both HIV infection and genital herpes. The finding was ranked inthe "Top 10 Scientific Breakthroughs of 2010" by the journal, Science. The finding was heralded by UNAIDS and the World Health Organization (WHO) as one of the most significant scientific breakthroughs in AIDS and provided the first evidence for what is today known as HIV pre-exposure prophylaxis (PrEP).

The Abdool Karims have also elucidated the evolving nature of the HIV epidemic in Africa , characterising the key social, behavioural and biological risk factors responsible for the disproportionately high HIV burden in young women. Their identification of the "Cycle of HIV Transmission", where teenage girls acquire HIV from men about 10 years older on average, has shaped UNAIDS policies on HIV prevention in Africa .

The impact: CAPRISA 004 and several clinical trials of oral tenofovir led tothe WHO recommending a daily tenofovir-containing pill for PrEP as a standard HIV prevention tool for all those at high risk a few years later. Several African countries are among the 68 countries across all continents that are currently making PrEP available for HIV prevention. The research undertaken in Africa by this South African couple has played a key role in shaping the local and global response to the HIV epidemic.

2020 Canada Gairdner Wightman AwardThe 2020 Canada Gairdner Wightman Award laureate is a Canadian scientist recognized for outstanding leadership in medicine and medical science throughout their career:

Dr. Guy Rouleau Director of the Montreal Neurological Institute-Hospital (The Neuro); Professor & Chair of the Department of Neurology and Neurosurgery, McGill University ; Director of the Department of Neuroscience, McGill University Health Center

Awarded "For identifying and elucidating the genetic architecture of neurological and psychiatric diseases, including ALS, autism and schizophrenia, and his leadership in the field of Open Science."

The Work: Dr. Rouleau has identified over 20 genetic risk factors predisposing to a range of brain disorders, both neurological and psychiatric, involving either neurodevelopmental processes or degenerative events. He has defined a novel disease mechanism for diseases related to repeat expansions that are at play in some of the most severe neurodegenerative conditions. He has significantly contributed to the understanding of the role of de novo variants in autism and schizophrenia. In addition, he has made important advances for various neuropathies, in particular for amyotrophic lateral sclerosis (ALS) where he was involved in the identification of the most prevalent genetic risk factors -which in turn are now the core of innumerable ALS studies worldwide.

Dr. Rouleau has also played a pioneering role in the practice of Open Science (OS), transforming the Montreal Neurological Institute-Hospital (The Neuro) into the first OS institution in the world. The Neuro now uses OS principles to transform research and careand accelerate the development of new treatments for patients through Open Access, Open Data, Open Biobanking, Open Early Drug Discovery and non-restrictive intellectual property.

The Impact: The identification of genetic risk factors has a number of significant consequences. First, allowing for more accurate genetic counselling, which reduces the burden of disease to affected individuals, parents and society. A revealing case is Andermann syndrome, a severe neurodevelopmental and neurodegenerative condition that was once relatively common in the Saguenay-Lac-St-Jean region of Quebec . Now this disease has almost disappeared from that population. Second, identifying the causative gene allows the development of treatments. For instance, his earlier work on a form of ALS linked to the superoxide dismutase-1 gene (SOD1) opened up studies which are now the focal point of phase 2 clinical studies showing great promise.

Byactingasalivinglabforthelast coupleofyears,TheNeuroisspearheading the practice of OpenScience (OS).TheNeurois alsoengagingstakeholdersacross Canadawiththegoal of formalizinganational OSallianceforthe neurosciences.Dr.Rouleau'sworkinOScontributesfundamentallytothetransformationoftheveryecosystemofsciencebystimulatingnewthinkingandfosteringcommunitiesofsharing.InspiredbyTheNeuro'svision,theglobalsciencecommunityisreflecting oncurrentresearchconventionsandcollaborativeprojects,andthemomentumforOSisgainingafootholdinorganizationsandinstitutionsinallcornersoftheearth.

About the Gairdner Foundation:

The Gairdner Foundation was established in 1957 by Toronto stockbroker, James Gairdner to award annual prizes to scientists whose discoveries have had major impact on scientific progress and on human health. Since 1959 when the first awards were granted, 387scientists have received a Canada Gairdner Award and 92 to date have gone on to receive the Nobel Prize.The Canada Gairdner Awards promote a stronger culture of research and innovation across the country through our Outreach Programs including lectures and research symposia. The programs bring current and past laureates to a minimum of 15 universities across Canada to speak with faculty, trainees and high school students to inspire the next generation of researchers. Annual research symposia and public lectures are organized across Canada to provide Canadians access to leading science through Gairdner's convening power.

http://www.gairdner.org

SOURCE Gairdner Foundation

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2020 Canada Gairdner Awards Recognize World-renowned Scientists for Transformative Contributions to Research That Impact Human Health - Yahoo Finance