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The World Health Organization (WHO) today welcomed the announcement by Pfizer Inc. that it will extend its donation of the antibiotic Zithromax (azithromycin) for trachoma elimination until 2030, building on the companys 23-year commitment to fight the worlds leading infectious cause of blindness.

Caused by repeated bacterial infection of the eyes, trachoma blinds the poorest people in the world. WHO recommends a four-part strategy to eliminate trachoma as a public health problem. This strategy takes the acronym SAFE, representing: surgery for advanced disease, antibiotics to clear infection, and facial cleanliness and environmental improvement (particularly increased access to water and sanitation) to reduce transmission. Pfizers Zithromax donation is a critical part of SAFE, and is managed by the International Trachoma Initiative at the Task Force for Global Health, Decatur (GA), USA, an organization in official relations with WHO.

Continuing the donation programme will bring relief to millions of people around the world who are affected by this preventable neglected tropical disease, said Dr Ren Minghui, WHOs Assistant Director-General for Universal Health Coverage/Communicable and Noncommunicable Diseases. WHO is very grateful for Pfizers ongoing commitment to helping prevent trachomatous blindness.

Caroline Roan, Senior Vice-President Global Health & Patient Impact, Pfizer Inc., commented, Trachoma is a debilitating disease that should no longer wreak havoc on peoples lives and livelihoods. We are proud to support our longstanding trachoma partners working tirelessly towards elimination and improving lives worldwide.

Between 2002 and 2021, due to a combination of SAFE strategy implementation, improved living conditions and better data, the estimated number of people living in trachoma-endemic areas worldwide fell 91% from 1517 million to 136 million. But over the past 2 years, the coronavirus disease (COVID-19) pandemic has limited the activity of programmes against neglected tropical diseases in many countries. Community-based work, such as antibiotic mass drug administration for trachoma, has been particularly adversely affected.

In the road map for neglected tropical diseases 20212030, endorsed by the World Health Assembly in November 2020, trachoma is targeted for global elimination as a public health problem by 2030. To date, 13 countries (Cambodia, China, the Islamic Republic of Iran, the Lao Peoples Democratic Republic, the Gambia, Ghana, Mexico, Morocco, Myanmar, Nepal, Oman, Saudi Arabia and Togo) have been validated as having achieved this milestone.

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Trachoma elimination: millions more to benefit from donated azithromycin - World Health Organization

A new strain of super gonorrhoea has been reported after an Austrian man had unprotected sex with a Cambodian sex worker.

What makes this strain so worrying is that it is resistant to most antibiotics commonly used to treat the infection, scientists have warned.

Adding to this risk, experts have cited that if multidrug-resistant strains of gonorrhoea keep spreading, many cases of the STD might become untreatable.

This was highlighted in a study published recently in the medical journal Eurosurveillance, part of the European Centre for Disease Prevention and Control.

The disease is caused by the bacterium called Neisseria gonorrhoeae.

The infection is spread by unprotected vaginal, oral and anal sex.

Lead author of the report, Dr Sonja Pleininger of the Austrian Agency for Health and Food Safety, said such a strain poses a major global public health threat.

If such strains manage to establish a sustained transmission, many gonorrhoea cases might become untreatable, she added.

The unidentified Austrian man in his 50s complained of unusual symptoms five days after his sexual encounter.

His symptoms reported included pain while peeing and a discharge coming out of his penis.

The man was initially treated with azithromycin and ceftriaxone.

Two weeks later, his symptoms resolved, but a penile swab showed he still had gonorrhoea.

Tests showed his "super" bug was still immune to treatment.

Typical symptoms of gonorrhoea include a thick green or yellow discharge from the vagina or penis, pain when peeing and, in women, bleeding between periods, warns the NHS.

The national health body added: But around one in 10 infected men and almost half of infected women do not experience any symptoms.

The bacteria that cause gonorrhoea are mainly found in discharge from the penis and in vaginal fluid.

In women, it can lead to pelvic inflammatory disease, which could cause problems with fertility and future pregnancy.

It may also increase the risk of ectopic pregnancy, a medical emergency.

Gonorrhoea can also increase the risk of transmitting or acquiring HIV.

According to Dr Teodara Wi, World Health Organisations (WHO) medical officer specialising in STIs, other serious risks of super gonorrhoea include:

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Dangers of super gonorrhoea from infertility to blindness as global warning issued - Daily Star

Jen Patja Howell shared an episode of the Lawfare Podcast in which Benjamin Wittes Wittes sat down on Twitter Spaces with Roger Parloff, Quinta Jurecic, and Molly Reynolds to discuss day four of the Jan. 6 committee hearings:

She alsoshared an episode of the Lawfare Podcast in which Wittes talked with Jurecic, Parloff, and Katie Benner of the New York Times about day five of the Jan. 6 select committee hearings:

Pollard shared a livestream of day four of the Jan. 6 select committee hearings. He also shared a livestream of day five of the Jan. 6 select committee hearings.

Elena Kagan shared an episode of Lawfare No Bull which features audio from the fourth public hearing held by the Jan. 6 select committee:

Bob Bauer argued that presidents seeking reelection can pose unique challenges to democratic elections in situations in which their desire to win can lead to disastrous results.

Daniel Richman discussed the role that the doctrine of willful blindness might have in proving Trumps criminal liability if a case were brought against the former president for his role in the Jan. 6 Capitol attack.

David Priess shared an episode of Chatter in which Shane Harris sat down with Tim Naftali to discuss the legacy of Watergate in light of the Jan. 6 Capitol attack:

Howell shared an episode of the Lawfare Podcast from the November 2020 archives in which Evelyn Douek and Jurecic sat down with Alex Stamos to discuss the state of election security and the difficulty of countering false election claims:

Robert Chesney and Steve Vladeck shared an episode of the National Security Law Podcast in which they discussed the latest Jan. 6 conspiracy indictment, the Navarro contempt of Congress charge, the lawsuits challenging the Texas and Florida social media content-moderation laws, and more:

Stewart Baker shared an episode of the Cyberlaw Podcast in which he sat down with Amy Gajda to discuss her book, Seek and Hide: The Tangled History of the Right to Privacy:

Baker shared another episode of the Cyberlaw Podcast in which he sat down with Matthew Heiman, Scott Shapiro, and Nick Weaver to discuss the bipartisan effort to transform the Committee on Foreign Investment in the United States, cryptocurrency firms on the verge of collapse, TikTok, and more:

Herb Lin discussed the functional trade-offs in baked-in cybersecurity in product management.

Susan Landau argued that the EU proposal on combating child sexual abuse material online could present national security problems and relies on technology that does not exist yet.

Steve Bunnell reviewed James E. Bakers The Centaurs Dilemma: National Security Law for the Coming AI Revolution (Brookings Institution, 2020).

Howell shared an episode of the Lawfare Podcast in which Wittes sat down with Asfandyar Mir and Daniel Byman to discuss the current position of al-Qaeda in the world:

Howell also shared an episode of Rational Security in which Alan Rozenshtein, Jurecic, and Scott R. Anderson sat down to discuss the extradition of Julian Assange, Chinese access to TikTok customer data, and Googles potentially sentient LaMDA artificial intelligence program:

Jordan Schneider shared an episode of ChinaTalk in which he sat down with Weijian Shan to discuss Shans personal story of exile during the Cultural Revolution and his view on Chinas economic transformation:

Anoush Baghdassarian analyzed recent cases from the International Court of Justice that Armenia and Azerbaijan each brought against one other for alleged violations of the International Convention on the Elimination of All Forms of Racial Discrimination.

Max Johnston and Bryce Klehm shared the final episode of Allies, which they discuss the uncertain long-term legal status of Mahnaz, a former member of the Afghan militarys Female Tactical Platoon, and other Afghans who are on parole after coming to the U.S. during the U.S.s withdrawal from Afghanistan:

Matthew Tokson discussed what a recent ruling from the First Circuit means for Fourth Amendment cases concerning the use of telephone pole cameras for surveillance purposes.

Kyleanne Hunter discussed the potential impacts that overturning Roe v. Wade would have on women in uniform.

And Hyemin Han and Katherine Pompilio shared an application for the fall 2022 Lawfare internship.

And that was the week that was.

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The Week That Was: All of Lawfare in One Post - Lawfare - Lawfare

How the illusion of a post-queer society let actor Rebel Wilson down.

Its been nearly two weeks since we heard the Sydney Morning Herald had a hand in making the actor Rebel Wilson reveal she was dating another woman.But as the news cycle swiftly barrels on, there are questions that continue to linger.

Namely, how could reporter Andrew Hornery and editor Bevan Shields who are both gay not understand that threatening to reveal a celebritys first same-sex relationship is an inherently harmful idea? How could they have been so blind?

Thats the theme that kept sticking out to me: sustained, wilful blindness. Blindness to the fact that we continue to inhabit a culture where queer people are marginalised, regardless of how many legal gains may have been made.

As both Hornery and Shields pushed out their articles over the weekend, at first furiously agreeing with each other before conceding that some harm may have been done, there was a common through-line: Both went out of their way to use non-gendered language. Rebel was simply in a new relationship; Ramona Agruma was her new partner, they were simply trying to break the news of this celebrity romance.

Both men seemed desperate to ignore the elephant in the room Rebel Wilson, an actress who most people know as straight, was in a same-sex relationship. And Hornerys email, regardless of what he intended, threatened to out her.

I couldnt help but be reminded of the problem of colour-blindness; the people who insist they dont see race, a narrative captured in the platitude, theres only one race, the human race. Its this same spirit that permeated the Sydney Morning Heralds recent festival of cluelessness, but this time, it wasnt colour blindness, but its LGBTIQ analogue: queer blindfolding.

In the way that colour-blindness perpetuates racism by denying the existence of white privilege, queer blindfolding is the process of perpetuating homophobia by not acknowledging it exists. The concept was coined by US researchers Richard Shin and Lance Smith, who define it as well-intentioned heterosexual identifying individuals that results in the disappearing of queer identities. And while straight people probably thinks that theyre doing a good thing by ignoring a persons sexuality were all just people, are we not? the narrative comes with pernicious consequences.

Namely, adopting the ideology of queer blindfolding can result in minimising or even denying the marginalisation that is experienced by those who identify as queer. And in my opinion, it is this wilfully blind way of looking at the world that has contributed to the Sydney Morning Heraldunknowingly threatening Wilson with an ultimatum.

Both Andrew Hornery and Bevan Shields used language that indicated that they were fans of this school of thought. Consider the following turns of phrase: [We] asked Wilson if she wished to comment about her new partner, wrote Bevan Shields in his initial supportive response to Andrew Hornerys first article. We would have asked the same questions had Wilsons new partner been a man.

Similarly, in Hornerys (now deleted) initial article, he was at a loss as to why a woman who previously used to brag about her handsome ex-boyfriend wouldnt do the same with her same girlfriend. Of course, who anyone dates is their business, but Wilson happily fed such prurient interest when she had a hunky boyfriend on her arm, he adds.

Here, both Shields and Hornery are taking the bizarre stance that when youre a woman, having a girlfriend is equally as socially acceptable as having a boyfriend.

And that, in a nutshell, is clear blindfolding: wilfully ignoring the heterosexism that we swim in every day.

While Shin and Smith point out that heterosexual attitudes toward LGBTIQ folks are generally improving, were not exactly in some post-gay utopia. Heterosexuality is obviously the dominant sexual orientation in our culture. Take, for example, the fact that most love stories in our culture involve cis-gendered men and cis-gendered women; the fact that we assume people are straight by default; and that a fear of abuse still means that many queer people hide their sexuality at work.

Or the teacher who was sacked because of their sexuality in 2021, or the constant targeting of trans peopleduring the lead-up to the federal election. Or the current horrendous discourse around trans participation in elite swimming. Just the simple fact that straight people dont need to come out tells you that straight people and queer people are obviously not on a level playing field.

And yet, we get Hornery coming out with the astonishing take that thanks to decades of battling for equality sexual orientation is no longer something to be hidden, even in Hollywood, adding that same-sex marriage is legal in many parts of the world, as though Wilson, by not publicly coming out to the entire world right away, is being overly dramatic or creating a problem that isnt there.

They are. Both reporter Andrew Hornery and editor Bevan Shields identify as gay men. But while Shin and Smith say that its heterosexual identifying people who are prone to queer blindfolding, queer folks arent immune to taking on the same.

In particular, studies have found its not uncommon for gay men who are white, cis-gendered, and affluent to use queer blindfolding as a narrative strategy. Those who inhabit other marginalised identities, though queer women of colour, for example tend to consider their queerness within the context of a matrix of domination. As such, people like Shields and Hornery may not realise that queerness in other bodies unlike theirs has different implications.

Thats where the importance ofintersectionality comes in a concept that describes the way that systems of inequality based on gender, race, ethnicity, sexual orientation, gender identity, disability, class and other forms of discrimination intersect to create unique dynamics and effects. While Rebel is white, she deals with the added marginalisation of being a woman plus, shes dealt with fatphobia in the past.

The reason that Hornery and Shields went so wrong with Rebel Wilson is simple: they assumed that homophobia was an artefact of the past. In doing so, they ended up causing harm to a person who, like everyone, has a right to come out on her own terms.

Weve heard little from Rebel Wilson herself about the situation, but she wrote on Twitter that it was a very hard situation and she was trying to handle it with grace. But she never should have had to deal with this in the first place, with grace or otherwise.

Perhaps the current trend of epistemic deference has something to do with this: the idea that people who inhabit the same marginalised identities have each others back. But like white supremacy, which no longer needs white people for it to function, weve seen that homophobia, too it no longer requires straight folks to thrive.

Reena Gupta is Junkees culture writer. Follow her on Twitter.

Photo Credit: Future Publishing, Getty Images

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How The SMH Got That Rebel Wilson Story So Wrong - Junkee

On June 23, 1972, President Richard Nixon signed the Education Amendments of 1972 into law. Title IX of those amendments, which spanned sections 1681-1688, covered key protections for students in education programs: discrimination based on sex or blindness.

Fifty years later, that protection has become popularly known as Title IX: No person in the United States shall, on the basis of sex, be excluded from participation in, be denied the benefits of, or be subjected to discrimination under any education program or activity receiving Federal financial assistance.

Its a law that youve certainly heard referenced most often when talking about womens college sports but how did it come to be? What does it actually cover? And what does its future look like? Heres what you need to know about Title IX.

Title IX was a follow-up to the Civil Rights Act of 1964, which was enacted to end discrimination based on race, color, religion, sex or national origin in regard to employment and public accommodation. But when it came to the college classroom, significant gaps remained.

Eight years after that landmark 1964 Act, the Title IX portion of the 1972 amendments sought to expand those protections by focusing on educational funding.

Today, I am signing into law the Education Amendments of 1972, President Nixon said. This legislation includes comprehensive higher education provisions, authority for a new effort to revitalize our educational research effort and authority to provide financial assistance to school districts to meet special problems incident to desegregation.

Before Nixon signed the 1972 amendments, the college sports landscape was dominated by men. The NCAA was founded in 1906 to govern college football before gradually growing as a discussion group and rules committee for a plethora of sports.

By 1972, 200,000 athletes were competing in college sports. Just 30,000 of them were women.

Athletic scholarships were virtually nonexistent for women and no national championships were held for womens teams. According to the History Channel, just 2 percent of college athletic budgets went toward women athletes.

Off the field, women were discriminated against in the classroom as well. Many universities barred women from attending while many others offered male-only classes, which ranged from criminal justice to wood shop.

NCAA data from 2016 shows the gender disparity in college athletes has shrunk dramatically in the 50 years since Title IXs inception. Of the 486,859 athletes who participated in college sports, 211,886 were women. Additionally, women received 45 percent of the total athletic scholarship dollars at DI schools in 2016.

The law has also done far more than increase the size of the scholarship slice. The historic 1980 Alexander v. Yale case was the first to use Title IX in charges of sexual harassment against an educational institution. Title IX has also been credited with helping increase the number of women who pursue higher education.

And from 2010 to 2016, the Obama administration expanded the protection of Title IX to protect transgender students from gender discrimination.

However, Title IX advocates argue there is still significant progress to be made. While the participation gap has narrowed, data shows the opportunity gap remains. Despite Title IXs intention for women to receive opportunities proportionate to the schools enrollment, a report from the Womens Sports Foundation found that 86 percent of colleges are offering a disproportionate number of athletic opportunities to men compared to their enrollment. They argue that this resulted in 60,000 missed opportunities for women athletes.

We should absolutely celebrate the fact that girls participation in high school sports is nearly 12 times higher than it was when Title IX was passed, but we cannot rest on it, WSF founder Billie Jean King said. The mere existence of Title IX does not ensure equal opportunities unless it is enforced for everyone, particularly among girls and women of color, those with disabilities and the LGBTQ+ community where the gap is consistently the widest.

While the answer may be clear that Title IX was effective for most of its initial intentions, many have debated in recent years if our structure of collegiate athletics has outgrown the now-50-year-old law. Some have proposed that the future of college sports may need a revamped Title IX to scale with the ever-changing landscape of the industry.

One such change has been the recent opportunity for college athletes to profit off their name, image and likeness (NIL). Some have argued that NIL legislation and Title IX protections are on a collision course that the 1972 law never could have imagined.

The stakes are high; the potential for making money is huge. Here is the issue: As soon as a university, its employees, or its booster clubs play any role in helping athletes earn money or make deals, the school is necessarily providing a benefit to them, attorneys Arthur Bryant and Cary Joshi wrote for Sportico. And Title IX requires that male and female athletes be treated equally. If the university arranges or offers deals for men and not women, or vice versa, it has trouble under the law.

However, while changes like NIL will continue to shift the college sports world every few years, the now-50-year-old law has proven to provide much-needed protections for who will be impacted by those changes. Regardless of what the next 50 years bring, no one can deny that Title IX has left an undeniable imprint on the college sports landscape, for the betterment of millions of women athletes.

(Top photo: Andrew Wevers / USA TODAY Sports)

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Fifty years of Title IX: What is it, what does it cover and do we still need it? - The Athletic

It's Brad Pitts world and were all just living in it!

The superstar actor and producer, 58, recently opened up about life, art and everything in between in a new interview with GQ, during which he explained how hes been pretty much hiding out in his Los Angeles home for much of the pandemic and how hes used that time to quit smoking and drinking altogether.

While chewing a nicotine mint, Pitt explained that he quit smoking cigarettes during the pandemic after realizing he didn't have it in him to simply "cut back."

I dont have that ability to do just one or two a day, he explained. Its not in my makeup. Im all in. And Im going to drive into the ground. Ive lost my privileges.

The actor went on to explain that after his ex, Angelina Jolie, filed for divorce in 2016, he got sober and spent a year and a half attending Alcoholics Anonymous though, given his star status, has had to make adjustments for the sake of maintaining his privacy.

I had a really cool mens group here that was really private and selective, so it was safe, he said. Because Id seen things of other people who had been recorded while they were spilling their guts, and thats just atrocious to me.

Pitt shares six kids with Jolie: Maddox, 20; Pax, 18; Zahara, 17; Shiloh, 16; and twins Vivienne, and Knox, 13. Jolie had adopted Maddox and Zahara before her relationship with Pitt (he later adopted them both as well).

Still, while he cherishes old memories of smoking a cigarette in the morning, with the coffee just delicious," he also knows his body cant handle it the same way others can, like, say, the British painter David Hockney. Hes still chaining, the hard-core English way. It looks great, Pitt says of Hockney. I dont think I have that. Im just at that age when nothing good comes from it.

The actor also spoke candidly about his struggle to remember new people and to recognize their faces, which has been a hindrance his entire adult life especially at parties.

Pitt believes he may suffer from prosopagnosia, an inability to recognize peoples faces (otherwise known as face blindness). Though he wants to remember the people he meets and hes ashamed he cant above all, he fears the condition has led people to assume hes remote or aloof or self-absorbed.

Nobody believes me! he said.

As for finding solace, the actor says he always finds it in art and music. "Im one of those creatures that speaks through art. I just want to always make. If Im not making, Im dying in some way."

Music fills me with so much joy," he continued. "I think joys been a newer discovery, later in life. I was always moving with the currents, drifting in a way, and onto the next. I think I spent years with a low-grade depression, and its not until coming to terms with that, trying to embrace all sides of self the beauty and the ugly that Ive been able to catch those moments of joy.

Continued here:
Why Brad Pitt quit smoking and drinking altogether during the pandemic - BusinessGhana

Express News Service

HYDERABAD: The recent spell of rain has brought respite after months of scorching heat. But these rains bring about a rise in humidity, meaning, higher chances of eye infection.Our eyes are one of the most sensitive yet ignored parts of our body. And unfortunately, the rainy season can make us susceptible to eye infections. Explaining why, Dr Deepthi, consultant ophthalmologist and retina specialist at Care Hospitals, HITEC City, says, The moisture content in the air creates a favourable condition for bacteria, viruses and other germs to grow and multiply, especially in your eyes.

The doctor names conjunctivitis as one of the most common eye infections during the monsoon. Some of the common symptoms of conjunctivitis include redness of the eye, swelling, yellow sticky discharge from the eyes, and itching, associated with pain. Fortunately, it is an easily treatable eye problem. Proper eye care should become a priority during monsoons to help protect from infections like conjunctivitis, dry eyes and corneal ulcers which can lead to blindness. Commonly known as pink eye, the infection can be easily spread from one person to another by touch, she informs.

Other common eye infections during the monsoon include keratitis and trachoma. This infection of the cornea caused by injury to the eyes, due to routine of contact lenses. If left unattended, the infection can even lead to blindness, the Dr Deepthi warns.

Trachoma is a bacterial infection responsible for blindness in almost 1.9 million people across the globe! This irreversible blindness can be caused through direct touch or towels and flies that have come in contact with the eyes or nose of an infected person. So it calls for more care than one might think, the doctor shares.

Dr Aparna Saripalli, general physician, Ankura Hospital, Boduppal, says, Kids should avoid touching or rubbing the eyes. Infections spread faster commonly touched items.

Keep infectionsat bay:

Dr Swapna, ophthalmologist, Care Hospitals, Nampally

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Watch your eye - The New Indian Express

A Hamilton artist wants you to forget about the no touching rule. The Scales That Fall From Our Eyes at Centre [3] goes against the formalities of an art gallery and invites visitors to experience it through touch and sound.

Olivia Brouwer, 27, is a partially blind artist aiming to bring accessible art to the visually impaired community. With abstract visuals and Braille language exhibits, Brouwer addresses her disability with tactile paintings and challenges the idea that art does not need to be touched in order to be felt.

I am partially blind in one eye and so I wanted to discuss that in my work and become more confident in myself by doing that, said Brouwer.

The exhibit brings a series of conversations with Brouwers friends Tim Peters, Eric Bourgeois and Jesse Hannigan about the meaning of blindness and colour blindness in their lives while raising awareness of the inclusivity and accessibility needed for the visually impaired.

I interviewed each of them individually, questioning how they would describe their perception of the world through the lens of their experience of blindness in a positive light, but also allowing them to express challenges associated with their form of blindness, said Brouwer.

Each conversation is translated into Braille and painted on a tactile canvas with acrylic paint. Visitors can also listen to the interviews with headphones activated by touching a conduit paint on the wall.

This is the first time Im showing work that is tactile. It will be interesting to see how people respond to it just as we come out of the pandemic. People can grab some gloves available to touch the pieces if theyre not comfortable, said Brouwer.

Inspired and influenced by Christianity, The Scales That Fall From Our Eyes visuals portray Brouwers interpretation of the Biblical story of Saul. He was a Jewish leader who persecuted Christians, and became blind for three days because of that. When he realized what he was doing wrong, the blindness spell fell like scales from his eyes.

According to Brouwer, the story of Saul represents the change that takes place when prejudiced barriers are removed, contributing to justice and inclusivity for minorities.

I like this kind of metaphor for realizing whats wrong in the world and releasing those scales and bringing clarity to what we need to change. Justice needs to happen, accessibility needs to be implemented not just to art galleries, she said.

Even though she brought her Christian faith to the exhibits title and concept, there was a moment of hesitancy throughout the creation process due to fear of negative feedback.

It was a bit confusing for me, so I stepped away from it for a while. I have a hard time bringing it into my art because I didnt want it to be evangelical, Brouwer said. I think the story of Saul will come into my work in the future. Theres a lot of stories in the Bible that talk about blindness and healing, but I think its more about how everybody sees what needs to change, what accessibility there is.

In March 2020, Brouwer was selected to participate in a three month long Emerging Artist Residency at Centre [3] which has extended until this year because of the pandemic. During the residency, Brouwer started a CONTACT kit which introduces Braille decoding to sighted viewers with the goal of bringing awareness to visually impaired folks.

The kit contains a tactile painting, an embossed booklet, interactive Braille pieces to read and decode, and a Braille translation of the English text describing the instructions and meaning of the project. The idea of the kit kind of kick started the work that Im doing now. How can we give voices to these minority groups? With the pandemic, blind people are very limited to touching things.

Brouwer, a Bachelor of Fine Arts at the University of Toronto and Sheridan College grew up in a creative family filled with illustrators and woodworkers who gave her space and incentive to follow a career in the arts. However, the artist struggled to understand who she was as an artist and accept her disability.

In high school, I was always self-conscious about it. In university, I was trying to figure out what I wanted to say and who I was as an artist. I think being partially blind is part of who I am. Its important for me to put that into my artwork, especially because art is mostly visual, said Brouwer.

The Scales That Fall From Our Eyes will run until July 2 at Centre [3], a not-for-profit, charitable artist-run centre on 173 James St N.

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Olivia Brouwer's art is for everyone to see and touch - Hamilton Spectator

The recent outbreak of monkeypox virus has called into question the capabilities of these kinds large DNA viruses to evolve, adapt and change their biology.

Compared with small RNA viruses such as coronavirus, monkeypox virus and other large DNA viruses are thought to evolve slowly. Yet theres clear evidence that this really isnt a hindrance to these viruses. In fact, they can adapt to new environments like us.

Although most infections remain mild, monkeypox can be a serious life-threatening disease, resulting in sepsis, encephalitis (brain inflammation) and blindness. The most common symptoms are rash and skin lesions, alongside flu-like symptoms and swollen lymph nodes.

Cumulative monkeypox cases in current outbreak

Monkeypox virus naturally infects wild rodents, such as squirrels and rats, in west and central Africa but it can jump species into humans and other animals. However, once it has jumped to humans, it cannot keep transmission going and eventually outbreaks die out. This is probably because monkeypox has not adapted itself to its new environment of humans, as spillback into wild rodents from infected humans is unlikely.

Monkeypox is closely related to the viruses that caused smallpox (variola viruses) and the virus that we use to vaccinate and eradicate smallpox (vaccinia virus). This group of viruses, referred to as poxviruses, are a kind of large DNA virus, meaning that their genome is composed of a chemical known as DNA, like our genome. (Coronavirus and related viruses use a cousin molecule called RNA.)

Other DNA viruses are the large DNA viruses adenoviruses and herpesviruses, but also small ones like papillomaviruses and parvoviruses. The viral genomes composed of either DNA or RNA essentially are the instructions to make new viruses, infect us and cause disease. Changes to the instructions can change virus biology.

As we have seen with SARS-CoV-2 and its variants, viruses can change how they behave with regards to spreading, disease severity and vaccine sensitivity. This is because of changes accumulating in the virus genome. Virus replication generates diversity in its genome, which can be acted on by evolutionary forces such as natural selection, to increase in frequency and maybe even out-compete older versions.

Evolutionary changes can occur when the virus encounters a new environment that it is not fully adapted to. Although all viruses can evolve rapidly due to their vast population sizes and rapid generation times, RNA viruses are thought to be masters of evolution because they have high mutation rates due to their small size, and many often lack error-correcting ability meaning more mutations occur every time they replicate.

Poxviruses have some characteristics that make them more generalist, including stable infectious particles, giving them more chances to infect. They use very common molecules on your cells to gain entry and infect, unlike SARS-CoV-2 which needs the specific ACE2 protein to gain entry to our cells.

Large DNA viruses such as monkeypox also contain lots of genes that target and manipulate different parts of the immune system.

However, theres clear evidence that improvements can be made, because, in humans, monkeypox transmission is relatively inefficient, with long incubation periods.

In general, large DNA viruses such as monkeypox are no different from other viruses, and their mutability is the basis for our ability to track and trace monkeypox outbreaks. They make mistakes and errors accumulate, which can be used as fuel for evolution and biological changes. Theres even evidence from the recent monkeypox outbreak that the host cell is directly mutating the virus genome.

Studies focusing on related poxviruses like the vaccinia virus have even uncovered new tricks they can use, which include rapidly amplifying the number of genes they use to attack our immune system. They could even borrow some of our own genes to help them infect us.

We cant predict the trajectory that monkeypox evolution will take, so we must take the threat of this virus adapting to its new hosts (humans) seriously. And we need to use all the public health tools at our disposal to halt the current outbreak in all countries including those where it is endemic.

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Monkeypox may not mutate as fast as coronaviruses, but that doesn't mean it can't adapt to its new hosts - The Conversation

Signature Theatre

Timothy McClimon, interim executive director for the past six months, will continue in the role permanently.

Before joining the Off-Broadway nonprofit theater, he was president of the American Express Foundation and senior vice president of corporate social responsibility at the American Express Company from 2006 until 2021.

Jason Menzo has been promoted from president and chief operating officer to CEO of the $181 million foundation. He succeeds Ben Yerxa, who has led the foundation since 2017 and will now become CEO of Opus Genetics.

In addition, Russell Kelley has been promoted to managing director of the Retinal Degeneration Fund, the foundations venture arm. Most recently he was the funds senior vice president of investments and alliances.

Gary Ginstling, executive director of the National Symphony Orchestra, will start as its executive director on November 1. He will then become president and CEO of the New York performing-arts group on June 30, 2023.

Ginstling will replace Deborah Borda, who will remain with the orchestra as executive adviser to the president and Board of Directors, beginning next summer.

Tom Cotter, director of emergency response and preparedness at Project HOPE, has been appointed executive director of Healthcare Ready.

Marisa Rohn will be the next president of the Sisters of Charity Foundation of Canton. Most recently she was vice president of advancement, human resources, and partnerships at Stark State College and executive director of the Stark State College Foundation.

Renee Archawski is now managing director of development at Caring for Friends. Most recently she was managing director of development and interim executive director of Teach for America Metro Atlanta, and a development coach for the education organizations national team.

Selena Deckelmann will become chief product and technology officer at the Wikimedia Foundation on August 1. She is currently senior vice president at Mozilla, where she oversees its Firefox web browser.

Paul Dien, head of strategic partnerships for Good and Upworthy, has joined the Grammy Museum as vice president of advancement and partnerships.

Anupa Fabian, evaluation manager at Catholic Charities Brooklyn and Queens, is joining the Mother Cabrini Health Foundation as its first chief evaluation and learning officer. She succeeds Daniel Frascella, who was promoted from managing director for programs and grants to chief programs and grants officer.

Anedra Kerr, a senior consulting associate at the Morten Group, will now serve as vice president of development at the Jeremiah Program.

Otis Kollie has joined the Global Fund for Children as a program specialist for Africa and Asia. Previously he was assistant project coordinator at Lifewater Liberia.

Judy Nagai has joined the University of Hawaii Foundation as senior executive director of campaign planning. She most recently worked at the University of the Pacific as associate vice president for development.

Brian Siegel, senior vice president of global arts and culture at Bank of America, has been promoted to global arts and heritage executive.

Oren Etzioni, founding CEO of the Allen Institute for AI, will step down on September 30 after leading the artificial-intelligence group for nine years. He will become technical director of the AI2 Incubator.

Send an email to people@philanthropy.com.

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Former American Express Foundation President Takes Helm of Signature Theatre - The Chronicle of Philanthropy

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Faltering or falling energy consumption, particularly electricity, is not an indication of a healthy economy

Since 2007, something historically unprecedented has been happening in most Western economies energy consumption is in a nosedive.

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U.K. energy use has fallen by 30 per cent to quantities not seen since the 1950s, while the rest of Europe has regressed 30 years to 1990s levels. The U.S. is following suit. Whereas total energy consumption had been flatlining, it then fell 13 per cent by 2020, approaching levels not seen since the mid-1990s. A subsequent post-covid increase gives one hope but may not reverse the trend.. This downward spiral also holds for electricity usage, the very index of a modern society, with the U.K. dropping over the past decade to levels last seen in the 1970s. The Canadian case is less dramatic but still concerning: both total energy and electricity consumption have flatlined over this period, and since 2018 have begun to decline.

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Faltering or falling energy consumption, particularly electricity, is not an indication of a healthy economy. You might think otherwise its evidence of increased efficiency, right? For some individual consumers, in the short run, potentially, yes. For society as a whole, in the longer run, emphatically not. As a rule, gains in efficiency will increase demand for the now cheaper goods or services, or save energy for another purpose, so total consumption rises. Savings from LEDs, for example, will first be translated into more lighting. (Who knew a lit driveway looked so pretty?) And when that demand becomes satisfied it will be spent on vacations, better health care, and education, and further out in the economic system on roads or defence. Like cash, energy is never left on the table, and given its availability, there is no limit to possible improvements in human well-being. Put simply, efficiency fuels welfare-enhancing consumption.

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Energy demand is falling because of environmental policies, including subsidies to modern renewables such as wind and solar. As distasteful as this might sound, it is nonetheless true. So far, both the U.S. and Canada are relatively minor players, the U.S. having spent a mere US$125 billion between 2008-2018, and while Canadian national totals are lower, the province of Ontario alone is reported to have spent about US$30 billion in the period 2006 to 2014. But the EU, where the biggest energy collapse is observed, has spent a staggering US$800 billion since 2008, a total that has been increasing at $US70 billion a year. And the U.K., a country of 65 million people, is shelling out well over US$10 billion every year.

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The intention of these subsidies was to reduce costs, but the gamble has not paid off nor will it so long as Mother Nature and her laws of physics are at the table. Wind and solar remain stubbornly expensive for consumers in spite of a blizzard of misinformation and propaganda claiming otherwise.

How did we get here? The answer lies in our intuitive understanding of energy itself. The human mind contains programs enabling us to reason about survival-dependent concepts mating, food, co-operation. The physics of energy is not such a concept. Without science we lack the lens to focus effectively on energy, leaving us more or less energy-blind. Energy is a strange concept in the strict scientific sense it isnt a substance, such as coal or oil, but instead an abstract property of all substances, namely the capacity to cause change in the world, to do work.

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Moreover, energy varies in quality, not just quantity. To support complex society a fuel must be of high quality, that is, structured so that it has the potential to do a lot of work. In thermodynamics, this is referred to as a fuels degree of disorder or entropy. Greater disorder equals greater entropy equals less work. But our energy-blindness, the inability to easily grasp thermodynamic principles, means that we must rely on physics to see and what it reveals is that fossil fuels and uranium are highly ordered and rich in their potential to do work, making them cheap, while wind and solar are the reverse.

In fact, to render wind and solar functional requires much additional work and resources, both often supplied by fossils. Transforming renewables into useable grid electricity relies on turbines and photovoltaic panels, themselves complex and expensive states of matter, to say nothing of the management costs of buffering the electricity system against their variability.

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The sunshine and wind might be free, but their extraction, conversion, and delivery to market are not. If you are concerned about carbon dioxide emissions, as we are, then it is critical to acknowledge our energy-blindness and follow the physics: fossil fuels are the necessary bridge to a nuclear-based, low-carbon future. The optics of wind and solar are superficially attractive but their promise of a green, low-carbon nirvana is empty. But dont blame us, blame Mother Nature.

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At stake are the creation and maintenance of wealth. The availability of high-quality energy created the tools and technologies that make human lives healthier, longer, and more fulfilling. Mortality rates, particularly for children, are extraordinarily low by historical standards. Many people in the world today, not just the richest, have temperature control in their homes, low levels of pathogens in their food supplies, transport essentially at will, phones, and access to vast information-storage systems. These highly improbable states exist only by virtue of the work done by energy-dense fuels such as fossils and nuclear.

By spending heavily on wind and solar, world leaders are degrading the quality and productivity of national energy supplies, causing rising costs and falling consumption. The causal linkage is on display across the West. This will damage not just the ability to create new wealth, but also to maintain a complex, pleasant and secure environment in which to live and raise our families, and this damage is already happening.

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Before you dismiss us as Chicken Littles screaming that the sky is falling (though we are and it is), we grant that the world currently looks far from dystopian. Countries where energy consumption is plummeting dont feel much pain yet. And there is a good reason for that. One country is increasing its energy use, propping up Western consumption with exports and giving us a false sense of well-being. That country is, of course, China.

Since the West began its energy starvation diet, Chinese energy consumption has increased by over 50 per cent and its electricity consumption has increased by 200 per cent, overtaking the U.S. by a large margin. China, unlike the EU, U.K. and U.S., is still 90 per cent reliant on fossil fuels and nuclear. Whats more, only some of the immense wealth these fuels are generating is being exported. What is China doing with the rest? Time will tell.

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But right now, as a matter of urgency, we must reverse the decline in Western energy quality and consumption by ending impoverishing renewable subsidies and clearing the path for fossil fuels and nuclear. Toying with low-density, thermodynamically incompetent renewables is an indulgence we cannot afford. With the Chinese economy on an energetically sound footing and those in the West not, the world has turned upside down. The economic consequences of this reversal are serious, the security implications terrifying. Our energy blindness is both costly and dangerous.

JohnConstable is energy director of the Global Warming Policy Foundation in London and author of its forthcomingstudyEuropesGreen Experiment: A costly failure in unilateral climate policy.Debra Lieberman is a professor of psychology at the University of Miami and author ofObjection: Disgust, Morality, and the Law(OUP, 2018).

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Junk Science Week: Net-Zero Edition John Constable & Debra Lieberman: The energy of nations and the creation of wealth - Financial Post

A spoon of saffron derived from the flower of Crocus sativus. Photo: Salonik Saffron/Wikimedia Commons, CC BY-SA 4.0

Saffron, the worlds most expensive spice, is extracted from the flowers of the saffron crocus, Crocus sativus. It has been grown for thousands of years in the Mediterranean region. But when and where was saffron first domesticated by our ancestors? In a review in Frontiers in Plant Science, researchers conclude that lines of evidence from ancient art and genetics converge on the same region.

Both ancient artworks and genetics point to Bronze Age Greece, in approximately 1700 BC or earlier, as the origin of saffrons domestication, said Ludwig Mann, one of the leading authors and a PhD student at Technische Universitt Dresden, Germany.

The genus Crocus, with approximately 250 species, ranges from South and Central Europe and North Africa to Western China. Unlike domesticated saffron, these species reproduce sexually in the wild. The first known use by humans of wild crocuses was as pigment for cave paintings, approximately 50,000 years ago in todays Iraq. Ancient texts from Sumer, Assyria and Babylonia also describe the use of wild crocuses in medicine and dye.

Asexually propagated by humans

In contrast, domesticated saffron doesnt grow in the wild, and can only be propagated asexually with human help, by dividing its underground corms stem-like storage organs. The process was first described by the Greek philosopher Theophrastus in the fourth to third century BC.

Today, domesticated saffron is grown around the globe, for use in cooking and perfumes and as a yellow dye. Between 15,000 and 16,000 flowers, requiring between 370 and 470 person-hours to collect, yield a single kilo, worth between $1,300 and $10,000.

Finding out where and when saffron was first domesticated isnt straightforward: the species is difficult to study genetically, because it has three copies of every chromosome instead of the usual two, and a large genome containing a high percentage of difficult-to-sequence repetitive DNA, said leading author Seyyedeh-Sanam Kazemi-Shahandashti, a PhD student at the Institute of Bio- and Geosciences of the Forschungszentrum Jlich, Germany.

As there are no ancient crocus remains preserved from ancient times, we here revisit ancient artworks that depict saffron-like plants. We expected that these could point us to specific regions.

Two independent lines of evidence

The authors argue that artworks from the Minoan civilization of ancient Greece are likely the oldest to depict domesticated saffron. For example, the dense patches of crocus flowers on the fresco The Saffron Gatherers from the island of Santorini (approximately 1600 BC) suggest cultivation. Another fresco on the same island, The Adorants, shows flowers with long, dark-red stigmas which overtop dark violet petals, typical of domesticated saffron.

Flowers with these traits are also depicted on ceramics and cloth from Bronze Age Greece, and symbolically rendered in the ideogram for saffron in the ancient Linear B script. In Egypt, tombs from the 15th and 14th centuries BC depict how ambassadors from Crete brought tribute in the form of textiles dyed with saffron.

An origin in Bronze Age Greece agrees with results from genetic studies from 2019, which showed that C. cartwrightianus, which only occurs in mainland Greece and Crete, is saffrons closest wild relative.

The authors believe that the modern saffron crocus with its three genomes arose naturally from the wild, either exclusively from C. cartwrightianus or from hybrids between C. cartwrightianus and another crocus species. The saffron crocus would then have been retained by the Bronze Age Greeks because of its superior qualities as a spice.

The authors will continue to trace saffrons properties, said final author Tony Heitkam, leader of the plant genomics group at Technische Universitt Dresden: Around the globe today, all saffron crocuses are effectively clones dating back to saffrons emergence in ancient Greece. Nevertheless, despite sharing the same genome, saffron can have different properties depending on the region. We have started to investigate the molecular causes, in particular so-called epigenetic differences, for this regional variation.

This article was first published on the Frontiers news blog.

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Ancient Art and Genetics Reveal Origin of World's Most Expensive Spice - The Wire Science

SALT LAKE CITY, June 23, 2022 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc., (NASDAQ: MYGN), a leader in genetic testing and precision medicine, today announced a partnership with Epic, the industry leading healthcare software company, to integrate Myriads full line of genetic tests with Epics expansive network of 600,000 physicians and more than 250 million patients.

The integration creates a seamless, end-to-end workflow solution for healthcare providers to order Myriad tests and review results directly within their everyday Epic platform without additional steps or manual ordering processes. Epic enables a secure exchange of information between healthcare institutions that care for patients.

With the ability to review pertinent health information, order tests, and receive results natively in Epic, providers will have the critical genetic insights and related information they need to drive better health outcomes and improve the patient experience. Patients will also be able to easily access their Myriad test results and other health information directly within their EHR portal.

Simplifying the process of genetic testing by making it more accessible and interoperable with electronic health records is a key component of our mission to advance health and well-being for all, said Paul J. Diaz, president and CEO, Myriad Genetics. Our collaboration with Epic reflects our strategy to partner with other healthcare industry leaders so we can advance precision medicine together. Increasing access to genetic insights and integrating our tests into Epics vast network of healthcare systems represents a significant step forward to better serve patients and healthcare providers.

As part of its transformation and growth plan, Myriad is focusing on new customer-centric, tech-enabled tools to make the genetic testing process easier for patients and clinicians. With the recent launch of Myriads Precise Oncology Solutions, providers can now place a single order for multiple Myriad tests and receive timely results through a unified online portal. Now, through the partnership with Epic, Myriad is expanding efforts to help physicians and health systems gain access to genetic testing faster and conveniently within the platform they use every day.

Genetic testing and precision medicine save lives, said Alan Hutchison, vice president of Population Health at Epic. Through this relationship, were bringing genetic insights to the point of care at scale, giving providers and patients the information they need to make more timely, informed decisions.

Myriads integration with Epic is expected to go live later this year.

About Myriad Genetics Myriad Genetics is a leading genetic testing and precision medicine company dedicated to advancing health and well-being for all. Myriad develops and commercializes genetic tests that help assess the risk of developing disease or disease progression and guide treatment decisions across medical specialties where genetic insights can significantly improve patient care and lower healthcare costs. Fast Company named Myriad among the Worlds Most Innovative Companies for 2022. For more information, visit http://www.myriad.com.

Myriad, the Myriad logo, BRACAnalysis, BRACAnalysis CDx, Colaris, Colaris AP, MyRisk, Myriad MyRisk, MyRisk Hereditary Cancer, MyChoice CDx, Prequel, Prequel with Amplify, Amplify, Foresight, Precise, FirstGene, Health.Illuminated., RiskScore, Prolaris, GeneSight, and EndoPredict are trademarks or registered trademarks of Myriad Genetics, Inc. 2022 Myriad Genetics, Inc. All rights reserved.

Safe Harbor StatementThis press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, including statements relating to the integration of the companys genetic tests with Epics network of physicians and patients and the expected timing of the integration; the companys growth plan to scale customer-centric, tech-enabled commercial capabilities with 600+ EHR integrations this year; the anticipated benefits of the integration, including that the integration will create an end-to-end workflow solution for healthcare providers to order Myriad tests and review results directly with their everyday Epic workflows, provide providers with critical genetic insights and related information they need to drive better health outcomes and improve the patient experience, and allow patients to easily access their Myriad test results directly from their EHR portal; and the companys strategic imperatives under the caption About Myriad Genetics. These forward-looking statements are managements present expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those described in the forward-looking statements. These risks include, but are not limited to: uncertainties associated with COVID-19, including its possible effects on the companys operations and the demand for its products and services and the companys ability to efficiently and flexibly manage its business; the risk that sales and profit margins of the companys existing molecular diagnostic tests may decline or that the company may not be able to operate its business on a profitable basis; risks related to the companys ability to generate sufficient revenue from its existing product portfolio or in launching and commercializing new tests; risks related to changes in governmental or private insurers coverage and reimbursement levels for the companys tests or the companys ability to obtain reimbursement for its new tests at comparable levels to its existing tests; risks related to increased competition and the development of new competing tests and services; the risk that the company may be unable to develop or achieve commercial success for additional molecular diagnostic tests in a timely manner, or at all; the risk that the company may not successfully develop new markets for its molecular diagnostic tests, including the companys ability to successfully generate revenue outside the United States; the risk that licenses to the technology underlying the companys molecular diagnostic tests and any future tests are terminated or cannot be maintained on satisfactory terms; risks related to delays or other problems with operating and constructing the companys laboratory testing facilities; risks related to public concern over genetic testing in general or the companys tests in particular; risks related to regulatory requirements or enforcement in the United States and foreign countries and changes in the structure of the healthcare system or healthcare payment systems; risks related to the companys ability to obtain new corporate collaborations or licenses and acquire or develop new technologies or businesses on satisfactory terms, if at all; risks related to the companys ability to successfully integrate and derive benefits from any technologies or businesses that it licenses, acquires or develops; risks related to the companys projections about the potential market opportunity for the companys current and future products; the risk that the company or its licensors may be unable to protect or that third parties will infringe the proprietary technologies underlying the companys tests; the risk of patent-infringement claims or challenges to the validity of the companys patents; risks related to changes in intellectual property laws covering the companys molecular diagnostic tests, or patents or enforcement, in the United States and foreign countries; risks related to security breaches, loss of data and other disruptions, including from cyberattacks; risks of new, changing and competitive technologies and regulations in the United States and internationally; the risk that the company may be unable to comply with financial operating covenants under the companys credit or lending agreements; risks related to the material weakness related to general information technology controls, including the impact thereof and the companys remediation plan, and its ability to achieve and maintain effective disclosure controls and procedures and internal control over financial reporting; risks related to current and future lawsuits, including product or professional liability claims; and other factors discussed under the heading Risk Factors contained in Item 1A of the companys Annual Report on Form 10-K filed with the Securities and Exchange Commission on February 25, 2022, as well as any updates to those risk factors filed from time to time in the companys Quarterly Reports on Form 10-Q or Current Reports on Form 8-K. The reported number of physicians and patients in Epics network were provided by Epic.

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Myriad Genetics Teams Up with Epic to Make Genetic Testing Accessible to More Patients with Electronic Health Record (EHR) Integration - GlobeNewswire

Obesity is a health condition which involves accumulation of a large amount of fat. Unlike what we think, Obesity is not just a cosmetic condition. It, in fact, involves and increases the risk of a lot of other disorders such as heart disease, diabetes, high blood pressure and even certain types of cancers. Obesity is caused by a range of factors it usually involves eating a lot of calories and not burning enough of them which causes the fat to accumulate. Genetics is also one of the causes of obesity. Speaking to HT Lifestyle, Yash Vardhan Swami, Nutritionist, Health and Fitness Expert said, To gain weight we need to eat more calories than we burn (over time) and to lose weight, we need to eat lesser calories. To control this equation, we can eat more or fewer calories, or we can burn more or fewer calories. We can also do a bit of both.

Yash Vardhan Swami further added that this formula applies to everyone irrespective of the genetic makeup that they are a part of. Can our genes make it harder to lose weight? Certain gene variants can make it easier for us to gain weight by making it easier for us to eat more calories than what we burn over time which would lead to weight gain by increasing drive to eat (hunger and cravings) or reducing drive to move/burn calories (in simple terms, making us lazier).

ALSO READ: Health tips for adolescents: 5 problems due to obesity, ways to lose weight

The nutritionist further referred to the presence of the FTO Gene also known as the obesity gene, FTO gene is Fat Mass and Obesity Associated Gene which raises the risk of obesity. Referring to the part played by the FTO gene, the expert added, If you have one copy of gene (one parent), there would be a difference of 1.5kgs only (on an average). If you have two copies of the gene (both parents), there would be a difference of 3kgs only (on an average). So, if we are up to 3kgs up, we can blame our genetics. If it's more, genetics are not to be blamed. The expert recommended regular exercise which can reduce and slash the effect of the FTO gene and can prevent obesity.

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Obesity and genetics: Expert shares insights - Hindustan Times

Its a quirk of history that the foundations of modern biology and as a consequence, some of the worst atrocities of the 20th century should rely so heavily on peas. Cast your mind back to school biology, and Gregor Mendel, whose 200th birthday we mark next month. Though Mendel is invariably described as a friar, his formidable legacy is not in Augustinian theology, but in the mainstream science of genetics.

In the middle of the 19th century, Mendel (whose real name was Johann Gregor was his Augustinian appellation) bred more than 28,000 pea plants, crossing tall with short, wrinkly seeds with smooth, and purple flowers with white. What he found in that forest of pea plants was that these traits segregated in the offspring, and did not blend, but re-emerged in predictable ratios. What Mendel had discovered were the rules of inheritance. Characteristics were inherited in discrete units what we now call genes and the way these units flowed through pedigrees followed neat mathematical patterns.

These rules are taught in every secondary school as a core part of how we understand fundamental biology genes, DNA and evolution. We also teach this history, for it is a good story. Mendels work, published in 1866, was being done at the same time as Darwin was carving out his greatest idea. But this genius Moravian friar was ignored until both men were dead, only to be rediscovered at the beginning of the new century, which resolved Darwinian evolution with Mendelian genetics, midwifing the modern era of biology.

But theres a lesser-known story that shaped the course of the 20th century in a different way. The origins of genetics are inextricably wedded to eugenics. Since Plato suggested the pairing of high-quality parents, and Plutarch described Spartan infanticide, the principles of population control have been in place, probably in all cultures. But in the time of Victorian industrialisation, with an ever-expanding working class, and in the wake of Darwinian evolution, Darwins half-cousin, Francis Galton, added a scientific and statistical sheen to the deliberate sculpting of society, and he named it eugenics. It was a political ideology that co-opted the very new and immature science of evolution, and came to be one of the defining and most deadly ideas of the 20th century.

The UK came within a whisker of having involuntary sterilisation of undesirables as legislation, something that Churchill robustly campaigned for in his years in the Asquith government, but which the MP Josiah Wedgwood successfully resisted. In the US though, eugenics policies were enacted from 1907 and over most of the next century in 31 states, an estimated 80,000 people were sterilised by the state in the name of purification.

American eugenics was faithfully married to Mendels laws though Mendel himself had nothing to do with these policies. Led by Charles Davenport a biologist and Galton devotee the Eugenics Record Office in Cold Spring Harbor, New York, set out in 1910 to promote a racist, ableist ideology, and to harvest the pedigrees of Americans. With this data, Davenport figured, they could establish the inheritance of traits both desirable and defective, and thus purify the American people. Thus they could fight the imagined threat of great replacement theory facing white America: undesirable people, with their unruly fecundity, will spread inferior genes, and the ruling classes will be erased.

Pedigrees were a major part of the US eugenics movement, and Davenport had feverishly latched on to Mendelian inheritance to explain all manner of human foibles: alcoholism, criminality, feeblemindedness (and, weirdly, a tendency to seafaring). Heredity, he wrote in 1910, stands as the one great hope of the human race; its saviour from imbecility, poverty, disease, immorality, and like all of the enthusiastic eugenicists, he attributed the inheritance of these complex traits to genes nature over nurture. It is from Davenport that we have the first genetic studies of Huntingtons disease, which strictly obeys a Mendelian inheritance, and of eye colour, which, despite what we still teach in schools, does not.

One particular tale from this era stands out. The psychologist Henry Goddard had been studying a girl with the pseudonym Deborah Kallikak in his New Jersey clinic since she was eight. He described her as a high-grade feeble-minded person, the moron, the delinquent, the kind of girl or woman that fills our reformatories. In order to trace the origin of her troubles, Goddard produced a detailed pedigree of the Kallikaks. He identified as the founder of this bloodline Martin Kallikak, who stopped off en route home from the war of independence to his genteel Quaker wife to impregnate a feeble-minded but attractive barmaid, with whom he had no further contact.

In Goddards influential 1912 book, The Kallikak Family: A Study in the Heredity of Feeble-Mindedness, he traced a perfect pattern of Mendelian inheritance for traits good and bad. The legitimate family was eminently successful, whereas his bastard progeny produced a clan of criminals and disabled defectives, eventually concluding with Deborah. With this, Goddard concluded that the feeble-mindedness of the Kallikaks was encoded in a gene, a single unit of defective inheritance passed down from generation to generation, just like in Mendels peas.

A contemporary geneticist will frown at this, for multiple reasons. The first is the terminology feeble-minded, which was a vague, pseudopsychiatric bucket diagnosis that we presume included a wide range of todays clinical conditions. We might also reject his Mendelian conclusion on the grounds that complex psychiatric disorders rarely have a single genetic root, and are always profoundly influenced by the environment. The presence of a particular gene will not determine the outcome of a trait, though it may well contribute to the probability of it.

This is a modern understanding of the extreme complexity of the human genome, probably the richest dataset in the known universe. But a meticulous contemporary analysis is not even required in the case of the Kallikaks, because the barmaid never existed.

Martin Kallikaks legitimate family was indeed packed with celebrated achievers men of medicine, the law and the clergy. But Goddard had invented the illegitimate branch, by misidentifying an unrelated man called John Wolverton as Kallikaks bastard son, and dreaming up his barmaid mother. There were people with disabilities among Wolvertons descendants, but the photos in Goddards book show some of the children with facial characteristics that are associated with foetal alcohol syndrome, a condition that is entirely determined not by genetic inheritance, but by exposure to high levels of alcohol in utero. Despite the family tree being completely false, this case study remained in psychology textbooks until the 1950s as a model of human inheritance, and a justification for enforced sterilisation. The Kallikaks had become the founding myth of American eugenics.

The German eugenics movement had also begun at the beginning of the 20th century, and grown steadily through the years of the Weimar Republic. By the time of the rise of the Third Reich, principles such as Lebensunwertes Leben life unworthy of life were a core part of the national eugenics ideology for purifying the Nordic stock of German people. One of the first pieces of legislation to be passed after Hitler seized power in 1933 was the Law for the Prevention of Genetically Diseased Offspring, which required sterilisation of people with schizophrenia, deafness, blindness, epilepsy, Huntingtons disease, and other conditions that were deemed clearly genetic. As with the Americans tenacious but fallacious grip on heredity, most of these conditions are not straightforwardly Mendelian, and in one case where it is Huntingtons the disease takes effect after reproductive age. Sterilisation had no effect on its inheritance.

The development of the Nazis eugenics programmes was supported intellectually and financially by the American eugenicists, erroneously obsessed as they were with finding single Mendelian genes for complex traits, and plotting them on pedigrees. In 1935, a short propaganda film called Das Erbe (The Inheritance) was released in Germany. In it, a young scientist observes a couple of stag beetles rutting. Confused, she consults her professor, who sits her down to explain the Darwinian struggles for life and shows her a film of a cat hunting a bird, cocks sparring. Suddenly she gets it, and exclaims, to roars of laughter: Animals pursue their own racial policies!

The muddled propaganda is clear: nature purges the weak, and so must we.

The film then shows a pedigree of a hunting dog, just the type that you might get from the Kennel Club today. And then, up comes an animation of the family tree of the Kallikaks, on one side Erbgesunde Frau and on the other, Erbkranke Frau genetically healthy and hereditarily defective women. On the diseased side, the positions of all of the miscreants and deviants pulse to show the flow of undesirable people through the generations, as the voiceover explains. Das Erbe was a film to promote public acceptance of the Nazi eugenics laws, and what follows the entirely fictional Kallikak family tree is its asserted legacy: shock images of seriously disabled people in sanatoriums, followed by healthy marching Nazis, and a message from Hitler: He who is physically and mentally not healthy and worthy, may not perpetuate his suffering in the body of his child. Approximately 400,000 people were sterilised under this policy. A scientific lie had become a pillar of genocide in just 20 years.

Science has and will always be politicised. People turn to the authority of science to justify their ideologies. Today, we see the same pattern, but with new genetics. After the supermarket shootings in Buffalo in May, there was heated discussion in genetics communities, as the murderer had cited specific academic work in his deranged manifesto, legitimate papers on the genetics of intelligence and the genetic basis of Jewish ancestry, coupled with the persistent pseudoscience of the great replacement.

Science strives to be apolitical, to rise above the grubby worlds of politics and the psychological biases that we are encumbered with. But all new scientific discoveries exist within the culture into which they are born, and are always susceptible to abuse. This does not mean we should shrug and accept that our scientific endeavours are imperfect and can be bastardised with nefarious purpose, nor does it mean we should censor academic research.

But we should know our own history. We teach a version of genetics that is easily simplified to the point of being wrong. The laws in biology have a somewhat tricksy tendency to be beset by qualifications, complexities and caveats. Biology is inherently messy, and evolution preserves what works, not what is simple. In the simplicity of Mendels peas is a science which is easily co-opted, and marshalled into a racist, fascist ideology, as it was in the US, in Nazi Germany and in dozens of other countries. To know our history is to inoculate ourselves against it being repeated.

This article was amended on 20 June 2022. The mass shooting in Buffalo, US, in May 2022 was at a supermarket, not a school as an earlier version said.

Control: The Dark History and Troubling Present of Eugenics by Adam Rutherford is published by Weidenfeld & Nicolson (12.99). To support the Guardian and Observer order your copy at guardianbookshop.com. Delivery charges may apply

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Where science meets fiction: the dark history of eugenics - The Guardian

Researchers at Boston University on Thursday announced a breakthrough discovery about a gene associated with the risk of Alzheimer's disease.This risk is tied to the APOE4 gene, which destroys brain cells if a person carries the gene. It puts them at higher risk for developing the disease, although inheriting the gene doesn't necessarily mean one will develop the disease, according to the NIH. The APOE3 gene is the most common and isn't known to affect Alzheimer's risk.Although the link between the gene and the disease is well established, the mechanism responsible for the underlying risk in brain cells has been unclear in research until the recent discovery, according to researchers from the BU School of Medicine.Alzheimer's is a progressive neurodegenerative disorder and is the most common cause of dementia. It affects more than 5.8 million individuals in the United States.In the recent finding, two important aspects of the gene were discovered the human genetic background associated with the gene is unique to APOE 4 patients and the genetic defects are unique to human cells.Our study demonstrated what the APOE4 gene does and which brain cells get affected the most in humans by comparing human and mouse models. These are important findings as we can find therapeutics if we understand how and where this risk gene is destroying our brain," said assistant professor in the BU School of Medicine Julia TCW.Researchers used three models to investigate the effects of the gene on brain cells, human-induced pluripotent stem cells, post-mortem human brains and experimental models.It is also known that the gene carries a risk for Parkinson's disease and rare genetic diseases.

Researchers at Boston University on Thursday announced a breakthrough discovery about a gene associated with the risk of Alzheimer's disease.

This risk is tied to the APOE4 gene, which destroys brain cells if a person carries the gene. It puts them at higher risk for developing the disease, although inheriting the gene doesn't necessarily mean one will develop the disease, according to the NIH. The APOE3 gene is the most common and isn't known to affect Alzheimer's risk.

Although the link between the gene and the disease is well established, the mechanism responsible for the underlying risk in brain cells has been unclear in research until the recent discovery, according to researchers from the BU School of Medicine.

Alzheimer's is a progressive neurodegenerative disorder and is the most common cause of dementia. It affects more than 5.8 million individuals in the United States.

In the recent finding, two important aspects of the gene were discovered the human genetic background associated with the gene is unique to APOE 4 patients and the genetic defects are unique to human cells.

Our study demonstrated what the APOE4 gene does and which brain cells get affected the most in humans by comparing human and mouse models. These are important findings as we can find therapeutics if we understand how and where this risk gene is destroying our brain," said assistant professor in the BU School of Medicine Julia TCW.

Researchers used three models to investigate the effects of the gene on brain cells, human-induced pluripotent stem cells, post-mortem human brains and experimental models.

It is also known that the gene carries a risk for Parkinson's disease and rare genetic diseases.

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Researchers discover genetic variants that increase Alzheimer's risk - WCVB Boston

This article is sponsored by BASE10 Genetics. This article is based on a Q&A discussion that took place during the Clinical Conference, with Dr. Phil Jacobson, Senior Medical Director at Base10 Genetics. The Q&A took place on May 5, 2022. The discussion has been edited for length and clarity.

Skilled Nursing News: Im here with Dr. Phil Jacobson whos the senior medical director of the company. Hell share with you a little bit about himself and what they do.

Dr. Phil Jacobson: BASE10 provides data-driven technology platforms and software solutions to help improve patient care, as well as reduce costs and reduce the time burden for staff. I have an extensive background in academic and clinical practice in managing respiratory viruses, as well as with quality improvement, including designing sepsis alert tools and things that use technology to enhance patient care.

What is clinical decision support and how has it evolved?

Historically, clinical decision support I think of as clinical pathways or clinical protocols for specific disease entities, which can standardize care, and those pathways when theyre instituted correctly, they resulted in improved outcomes, as well as considerable cost savings. What weve done at BASE10 is develop some of these pathways in a way that uses consensus-based guidelines from authoritative entities such as AMDA, CDC, Infectious Diseases Society of America, and American Thoracic Society.

They come from the best experts in the world with these consensus ways of diagnosing and managing these things. Im going to focus my comments today mostly on the infectious disease management aspect of this. Now, the way its evolved though, its gone beyond just saying to the providers and the nurses, heres a pathway, heres an algorithm, figure out how your patient fits into this.

Now, what weve been able to do at BASE10 is create software that actually reads the electronic chart and uses pertinent data from the patient, and pinpoints the area of the algorithm which is specific for that patient, so that you get very pointed recommendations about diagnosis and management from the software that we provide.

What pathways and tools have worked in the long-term care settings, and are they widely used?

Pathways are used throughout hospitals and some long-term care facilities. Theres some very interesting recent literature on pathways, most notably the one from the University of Missouri investigators. They developed the Missouri Health Quality Initiative. What these investigators did was they looked at 11 facilities in the St. Louis area, and they instituted clinical pathways for specific entities such as bacterial pneumonia, urinary tract infection, and influenza.

What they did was they planted nurse practitioners every day in each of those facilities, in addition to instituting these clinical pathways. Then what they found was that by using the clinical pathways and the nurse practitioners, they were able to get earlier detection and earlier treatment for these infectious disease entities, thereby reducing the severity of illness, and ultimately, considerably reducing hospitalizations over a six-year period. They demonstrated a considerable reduction in hospitalizations with improved care, early detection, and a savings of approximately $35 million.

Now, the issue becomes how do you implement this at scale, having a practitioner on site every single day in this environment that may not be so simple? The next best thing we think is to have this technology answer, the software that can actually read the patient chart and have the pertinent data available to providers who are offsite so that they can better manage the patients without being physically present. We think that that could be something thats really important.

Theres another very important study done out of Ontario, Canada. This one didnt involve nurse practitioners, but it involved 22 facilities looking specifically at the management of bacterial pneumonia to see if they could prevent hospitalizations by using clinical pathways. The clinical pathway they used was one where they instituted antibiotics IV fluids, pulse oximetry, and supplemental oxygen, if necessary. Half the patients were on the clinical pathway track and the other half just went about with standard operating procedures.

In some cases, they used standing orders to empower the nursing staff to just institute the pathway when the diagnosis was made, or the providers would be saying, okay, we got the diagnosis, go ahead and institute the pathway without giving specific explanations of what to do. What they found was once again they were able to get earlier detection, and earlier treatment of bacterial pneumonia, and they had marked improvement over the controls in terms of hospitalization rate for the pathway group so obviously improved care, but so much so also that they saved on average $1,000 per patient per diagnosis of pneumonia. Once again, another demonstration of how pathways or protocols can enhance, and this one didnt even use the technology that I was talking about or the software reading the chart.

What are the implications of clinical decision support on quality and medication management which is something we hear in the nurse space all the time right now?

The three basic things that this can accomplish are improved care, cost savings, and time savings for the staff. All things that Ive heard throughout the theme of todays activities. In terms of the pathways themselves and keeping up to date with consensus guidelines, thats one of the things that were doing. Were taking the experts in the fields from all those authoritative entities. Were able to give the best possible practice of these pathways and keep them up to date.

Now, some things are static but if you think about the pandemic how much has changed in terms of what the recommendations are, the monoclonal antibodies arent working very well, etc. Were able to stay up to date about what the treatment guidelines are and what the diagnostic guidelines are from these entities.

In addition to that, it allows for these disparate points of data from the patient specifically to be captured in a way thats useful for the management of the patient. Instead of the providers and the nurses scrounging around the chart, looking for data such as allergies or previous infection or renal function, or things that are really important, the software is able to provide this in a nutshell right in front of the face and provide recommendations associated with it.

Our software even uses data from antibiograms so that you can know what the resistance patterns are within the particular facilities. Up until this time, Ive been emphasizing early detection and early diagnosis to prevent hospitalizations, to get better treatment, to have decreased severity of illness, but a very important aspect of infection management is preventing overdiagnosis and overtreatment, and theres a strong public health initiative about antibiotic stewardship.

We dont want to overuse antibiotics. What happens when we use antibiotics too much? For one thing, antibiotics have side effects just like any other drug. If you think about long-term care residents, there are already potentially a lot of other drugs, and the potential for drug-drug interactions which are adversarial is considerable. Thats one place where its a problem.

The use of antibiotics can create an environment thats ripe for an infection called Clostridium difficile to thrive. Clostridium difficile can cause severe gastroenteritis which can be life-threatening, and in fact, does kill many patients every year. Maybe the most common and worst of all, the problems associated with the overuse of antibiotics is a multiple of drug resistance. The more we use antibiotics, the more pathogens evolve, so that they become resistant. When true infections occur, these antibiotics arent available to us to use, to treat these infections. This is a major public health problem in which thousands and thousands of people die every year because of multiple drug resistance.

For these reasons, we have to find a way with technology to pinpoint, to thread the needle of catching infections early, and get them treated while preventing overdiagnosis and overtreatment for all of these reasons.

Can you tell me what the cost benefits are? What cost benefits can be seen by implementing a successful clinical decision support system?

There are direct and indirect cost benefits, and the direct cost benefits are things like prevention of hospitalization, getting less severe ailments, and on the other side of that, prescribing too many drugs and too many lab tests are also very costly. There are some very direct, measurable cost benefits associated with using appropriate infectious disease management, and threading that needle as I mentioned about not underdiagnosing but not overdiagnosing. Then there are a number of indirect costs associated with it.

If you think about the time that a nurse spends just administering the drug seems fairly simple, but what does a nurse have to do? They have to find the drug wherever its stored, whether its a refrigerator or some compartment closet. They have to get that open. They have to use a scanning tool. They have to check the right drug, the right patient, and the right dose.

They have to come and administer the drug. If its an oral drug, they may have to bring some water. Then, of course, theres making sure the patients able to take the drug plus the charting that goes along with it.

Every seemingly simple task has a lot of micro-tasks associated with it and is time-consuming. If you think about the scheduled drug, well, that can really throw off workflows. These are the types of indirect time-related costs that could be associated with this problem. We estimated at BASE10 that just for infectious disease management alone, we believe that up to 75% based on CDC reports and other people that about 75% of antibiotics prescribed, are inappropriate or overused. Thats a lot, and so just having this antibiotic stewardship can be something really important.

In addition to that, we estimate that savings, with appropriate infectious disease management direct costs of that facility of about 100 residents, could save about $80,000 per year just by getting this right, and from indirect cost and time, about 80 hours per year per 100-bed facility. We could see that theres a lot of different things that could be done to save time and to save money.

Another thing that BASE10 does to help facilities is reporting. Were talking about infectious diseases right now. Theres a lot of responsibility for state and government reporting. As many of you know during the pandemic, COVID reporting was a major burden on facilities, very time-consuming, and very difficult. Fifty-seven percent of facilities incurred citations for inappropriate or underreporting of COVID, and these citations come with hefty fines, and weve instituted a way with our technology to offer the service and take on the burden of reporting.

Additionally, the clients have been extremely pleased with the amount of time that was saved from the staff not being burdened with this. In short, I think that weve heard a lot about lobbying and doing things with the government, but we at BASE10 are focusing on creative solutions to how to take better care of the patients, how to do it at lower costs, and how to do it with reducing the burden of time thats obviously on the shorthanded facilities.

BASE10 Genetics brings hope to the lives of vulnerable patients by helping them access the latest in precision medicine technologies through our disease management platform. To learn more, visit http://www.base10genetics.com.

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Clinical Conference: A Discussion with BASE10 Genetics - Skilled Nursing News

Fathers Day is celebrated on different days in various places around the world, but most of them honor their dads on the third Sunday in June. Somehow it is always so difficult to come up with an idea of what could be the best present to show our love to our dads as they rarely need anything, and actually, nothing seems good enough to express our gratitude.

But what it takes is just a little bit of creativity. This woman on TikTok decided that she could recreate some of her dads photos from his youth and make a cute video for him, showing how similar they actually look.

More info: TikTok

Image credits: lakynthrifts

TikToker lakynbowman, also known as Lakyn Bowman, is a 26-year-old woman from West Tennessee who has a business of transforming her thrift finds into home decor to promote sustainability.

She is also quite busy creating content on social media, especially on TikTok, where she shares her thrift finds for her home, her business and also shows what outfits can be composed of second-hand clothing.

Image credits: lakynthrifts

Image credits: lakynthrifts

Bored Panda has already talked about one of her videos that went viral with 8.8 million views a few months ago. In that video, Lakyn decided to recreate her grandmothers photos from when she was young as a gift for her birthday.

She wanted to surprise her grandma and did her hair and makeup exactly like in the pictures. The granddaughter also found some clothes that looked very similar and posed in the same way as her grandma did. If you would like to read more, you can follow this link.

Image credits: lakynbowman

This time we are looking at her latest photo recreation video that she dedicated to her dad in honor of Fathers Day. She again found similar-looking clothes and manipulated her hair to look like she had a short bob like her dad when he was a kid. She nailed the poses and the comparison shots are proof that these two people are definitely family.

Lakyn herself confessed in the text overlay in the video that she was a bit freaked out looking at her dads old photos and seeing how much the two of them look alike, and its fascinating to observe with the naked eye how genes work.

Image credits: lakynbowman

Image credits: lakynbowman

While seeing photos side by side is very satisfying, the best part about this gift was the dads reaction. Lakyn posted a video of her dad watching the montage for the first time and it made the dad quite emotional as he couldnt stop smiling.

The man recognized his jersey and his coat, praising his daughter for doing such a good job. Actually, he was so impressed that he wanted to see the video a couple of more times.

You can hear Lakyn asking her dad which of the recreations he liked the most and his answer was I like all of them! But he was especially happy about the one in which she was wearing a red jacket because it was the actual jacket he wore in that photo.

The dad also revealed a little bit of more context to the photo in which he was wearing a blue shirt. Apparently, he was a cheerleader for a while because he wasnt allowed to play more than 2 basketball games on a weekend, so he asked if he could participate in the game as a cheerleader.

Image credits: lakynbowman

Image credits: lakynbowman

The dad said that he remembered all of the photos and you could see the nostalgia in his eyes reminiscing about the times he did sports. He also said that he really misses his dark hair, as now it has silver strands in it.

He noticed that Lakyn even has his eyebags and they both agreed that Lakyn is definitely her fathers kid. Lakyn confessed that she was really excited to do this because couldnt grasp how her face could be so similar to her dads.

Image credits: lakynbowman

Image credits: lakynbowman

Before surprising her dad with the video, Lakyn did one for her mom on Mothers Day as well. Lakyn isnt so sure that she has any physical similarities with her mom, but she has heard from some people that they do. With the power of makeup, clothes, poses and filters, it would be hard to think that the two women are strangers.

Moms reaction was as wholesome as the dads. She loved the result and told Lakyn that the swing picture in the park was actually taken by her, even though she didnt remember that because she was so little.

Image credits: lakynbowman

Its quite impressive how children can grow up looking so similar to their parents and even though its easily explained by science, its mesmerizing nonetheless.

Have you ever looked at your parents pictures from their youth and were surprised to discover you now look like them? Do you see the similarities between Lakyn and her dad in these pictures? Let us know in the comments!

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Genetics Really Said Copy And Paste: People Are Amazed At How Similar This Woman Looks To Her Dad In These 5 Recreation Photos - Bored Panda

Varicose veins are a very common manifestation of chronic venous disease, affecting over 30% of the population in Western countries. In America, chronic venous disease affects over 11 million men and 22 million women aged 4080 years old. Left untreated it can escalate to multiple health complications including leg ulcers and ultimately amputations. A new international study by Oxford researchers published on 2 June 2022 in Nature Communications establishes for the first time, a critical genetic risk score to predict the likelihood of patients suffering with varicose veins to require surgery, as well as pointing the way towards potential new therapies.

In a vasttwo-stage genome-wide association study of varicose veins in 401,656 individuals from UK Biobank, and replication in 408,969 individuals from 23andMe, Oxford researchers identified 49 genetic variants that increase the risk of varicose veins. They highlighted pathways including problems with the connective tissues of the body, and the immune system as key players in varicose vein pathology.

This study was an interdisciplinary collaborative effort across the Medical Sciences Division at the University of Oxford. Researchers from theNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, theNuffield Department of Surgical Sciencesand theNuffield Department of Women's & Reproductive Healthworked withan Americancommercial, direct to consumer genotyping company called23andMeto explore which people were moresusceptible to developingVaricose veins.

Lead authorProfessor Dominic Furnisscommented: 'The inclusion of surgeons in the research team was vital as they enabled the identification of patients whose disease was more severe, and they had therefore had surgery. This lead to the discovery of49 genetic variants at 46 areas into the genome thatpredisposes to Varicose veins. This breakthroughgreatly improves our team's knowledge of the biology of Varicose veins, and it will be the foundation of further research into the biology and potentially new treatment'.

Co-authorProfessor Krina Zondervansaid: 'This large study brings together a great deal of new evidence of the genetics underlying varicose veins, a condition that is highly prevalent in women and in pregnancy. It opens up exciting new avenues for the development of new future treatments.'

Reference:Ahmed WUR, Kleeman S, Ng M, et al. Genome-wide association analysis and replication in 810,625 individuals with varicose veins. Nat Commun. 2022;13(1):3065. doi: 10.1038/s41467-022-30765-y

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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49 Genetic Variants That Increase the Risk of Varicose Veins Identified - Technology Networks

Different structures were detected between the Brazilian and US genetic bases

Principal component analysis (PCA) revealed that most Brazilian cultivars (red circle) were grouped with a subgroup of US cultivars (green circle). Most of them belonged to MG VI, VII, VIII and IX (Fig.1A). Based on the Evanno criterion (Fig.1B), the structure results based on four groups (K=4) showed a high K value (312.35), but the upper-most level of the structure was in two groups (K=2; K=1885.43).

Population structure analysis between Brazilian and US germplasms. (A) Principal component analysis of Brazilian and US soybean cultivars based on SNPs markers; (B) Delta K as a function of the number of groups (K); (C) assignment coefficients of individual cultivars (bar plots) considering K=2; and (D) considering K=4.

Considering K=2 (Fig.1C), the Brazilian cultivars jointly presented an assignment to the Q1 group (green) equal to 86.7% which was much higher than that observed for the US cultivars (43.9%). Considering K=4 (Fig.1D), the Brazilian cultivars jointly presented an assignment to the Q2 group (red) of only 4.7% while the US cultivars jointly presented an assignment to the Q2 group of 27.4%. The Q1 group (green) has a lower assignment in Brazilian cultivars than US accessions (11.1%, and 30.1%, respectively). These results demonstrate that the set of Brazilian cultivars has a narrower genetic base compared to US cultivars.

When we compared the cultivars between maturity groups, we observed a clear differentiation between early and late groups. The highest genetic distances (0.4158) observed were between MG 000 and MG VIII-IX cultivars (Supplementary Table S1).

To examine the influence of maturity groups on population structure, we analyzed the average assignment coefficients (K=4) of Brazilian and US cultivars for each maturity group (Supplementary Figure S1). Brazilian cultivars from maturity group V presented Q1, Q2, Q3, and Q4 equal to 30.4%, 1.9%, 32.1, and 32.0%, respectively; US cultivars from this same maturity group (V) presented means of Q1, Q2, Q3, and Q4 equal to 9.2%, 8.2%, 65.1%, and 17.6%, respectively. This result indicates that, although belonging to the same maturity group, the Brazilian group V cultivars present considerably different allelic frequencies than the US cultivar group V cultivars, especially for Q3 and Q4. US cultivars belonging to earlier maturity groups (00, 0, I, and II) had significantly higher mean assignment coefficient to Q2 group (red) compared to other later maturity groups (V=8.2%, VI=8.1%, VIII=5.0%, and IX=13.6%). In the case of Brazilian cultivars, the average assignment coefficients for Q2 were much lower (V=1.9%, VI=4.2%, VII=5.6%, VIII=4.9% and IX=4.9%). These results demonstrate an important allelic pool that distinguishes early to late genetic materials present in Q2.

In general, the Brazilian germplasm showed few differences between maturity groups (Supplementary Table S1 and Fig.2A). This was also observed when we generated a population structure analysis exclusively with these cultivars (Fig.2C). In contrast, the US germplasm showed a high variation of genetic distance when we analyzed their maturity groups (Supplementary Table S1) with a clear clustering of cultivars (Fig.2B), which is more obvious when we observed their exclusive population structure analysis (Fig.2D). The results show that early cultivars tend to be genetically distant from late cultivars in the US. The maturity groups from the southern-breeding program of the US (V, VI, VII, VIII, and IX) tend to be less genetically divergent versus northern groups (00, 0, I, II, III, and IV). This agrees with previous studies indicating distinct Northern and Southern genetic pools in the US6. There is a low divergence among US soybean cultivars from maturity groups higher than V (Fig.2B). In contrast, cultivars from MG 00 and 0 were more genetically distant from cultivars of MG III and IV while maturity groups I-II were an intermediate group. The population structure analysis showed a high influence of Q2 in cultivars with MG 00-II. For cultivars in MG III and IV, we observed an increase of Q1. Finally, there is a high influence of Q3 in cultivars with maturity groups higher than V, which agrees with the genetic distance data.

Population structure analysis of Brazilian and US cultivars according to their maturity groups. Principal component analysis (PCA) within Brazilian (A) and US (B) germplasms for each maturity groups; population structure of the Brazilian (C) and the US (D) genetic basis arranged according to their maturity groups.

The results demonstrate that both genetic bases had few increases in genetic distance among modern genetic materials (releases after 2000) when compared to cultivars from the 1950s to 1970s (Supplementary Table S2). According to the IBS genetic distance mean, the Brazilian genetic base was more diverse over the decades compared to US germplasm especially when we compared cultivars released before the 1970s and released after the 2000s (Supplementary Table S2).

Average assignment coefficients (Q1, Q2, Q3, and Q4) from genetic structure results were calculated for both germplasm pools. All accessions were sorted according to their origin and decade of release (Fig.3). We observed high genomic modifications over the decades in the Brazilian germplasm. Modern genetic materials (20002010) had Q1, Q2, Q3, and Q4 values of 36.8%, 2.3%, 31.7%, and 26.0%, respectively, while old accessions (1950-1960s) had means of Q1, Q2, Q3, and Q4 equal to 1.6%, 6.6%, 7.0%, and 84.7%, respectively. A high decrease was observed for Q4 starting in the 1990s whereas Q1 and Q3 highly increased during the same period. For the US genetic base, we observed an increase of Q3 and a decrease of Q2 over time. Old cultivars (19501970) had Q1, Q2, Q3, and Q4 values of 36.0%, 33.7%, 12.3%, and 18.1%, respectively, while modern cultivars (20002010) had Q1, Q2, Q3, and Q4 of 24.3%, 17.5%, 40.3%, and 17.8%, respectively.

Mean assignment coefficients of the Brazilian and US cultivars belonging to the different decades of release (1950 to 2010) to STRUCTURE groups (Q1, Q2, Q3, and Q4) considering K=4.

Modification during the 1990s became more evident upon analysis of the PCA and genetic structure results of the Brazilian genetic base considering the decades of release (Fig.4A and C). We observed an increase in the influence of the Q2 in modern genetic materials (20002010) when we compared the results to old genetic materials (19501970). In contrast, the US genetic base showed few variations over time according to the average of genetic distance (Supplementary Table S2), PCA, and the exclusive population structure analysis (Fig.4B and D). These results suggest a large influence of new alleles in the Brazilian germplasm after the 1990s.

Population structure of Brazilian and US cultivars according to their decade of release. Principal component analysis (PCA) within Brazilian (A) and US (B) germplasm for each decade; population structure of the Brazilian (C) and the US (D) genetic bases arranged according to their decade of release.

Seventy-two SNPs with FST0.4 between Brazilian and US cultivars were identified (Supplementary Table S3). These SNPs are located on chromosomes 1, 4, 6, 7, 9, 10, 12, 16, 18, and 19 (Supplementary Figure S2). Twenty-six 100-Kbp genomic regions with a high degree of diversification between Brazilian and US genetic bases were also found (Table 1). The results for Tajimas D showed that these regions had balancing events that maintained the diversity of their bases. Two regions on chromosome 6 (47.3 47.4 Mbp and 47.347.4 Mbp) and another on chromosome 16 (31.1031.20 Mbp) had few variations in Brazilian accessions (Supplementary Table S4). In contrast, the allele distribution for most of the SNPs present in these genomic regions in US germplasm was higher compared to Brazilian germplasm. An opposite scenario was observed for the other three regions located on chromosomes 7 (6.30 6.40 Mbp), 16 (30.70 30.80), and 19 (3.00 3.10) (Supplementary Table S4). The allele variance was higher in the Brazilian genetic base than US germplasm for these three intervals.

Six SNPs located close to maturity loci E1 (Chr06: 20,207,077 to 20,207,940bp)14, E2 (Chr10: 45,294,735 to 45,316,121bp)15, and FT2a (Chr16: 31,109,999 to 31,114,963)16 had a large influence on the differentiation of the Brazilian and US genetic bases (Fig.5). For the SNPs ss715607350 (Chr10: 44,224,500), ss715607351 (Chr10: 44,231,253), and ss715624321 (Chr16: 30,708,368), we found that the alternative allele was barely present in US germplasm whereas the Brazilian genetic base had an equal distribution between reference and alternative alleles. When we examined the SNPs ss715624371 (Chr16: 31,134,540) and ss715624379 (Chr16: 31,181,902), the frequency of the alternative allele remains low in the US germplasm. However, the alternative alleles of these two SNPs were present in more than 78% of the Brazilian accessions in contrast to the previous three SNPs. Finally, the alternative allele for SNPs ss715593836 (Chr06: 20,019,602) and ss715593843 (Chr06: 20,353,073) were extremely rare in Brazilian germplasm with only 2% of the accessions carrying them. In contrast, the US germplasm had an equal distribution of reference and alternative alleles in their accessions. However, all accessions with the alternative alleles belonged to MGs lower than VI with less than five cultivars in MG V.

The allele frequency distribution for SNPs close to loci (A) E1 (chromosome 6), (B) E2 (chromosome 10), and (C) FT2a (chromosome 16) in Brazilian and US germplasms.

Ten SNPs were identified related to the genes modifier mutations present in Brazilian and US germplasm; these were distributed on chromosomes 4, 6, 10, 12, 16, and 19 (Supplementary Table S5). These SNPs had differing allele frequencies and could distinguish both genetic bases. Six modifications had a clear influence on the maturity of the accessions whereas two of these had a large influence in some decades of breeding (Supplementary Figure S3). The SNP ss715593833 had a similar haplotype as two SNPs described as close to the E1 loci (ss715593836 and ss715593843) due to the linkage disequilibrium (LD) among them. At the end of this chromosome, we also observed another three relevant SNPs in LD: ss715594746, ss715594787, and ss715594990. In the US germplasm, we observed a decrease in the alternative allele in accessions with MG values lower than IV. We detected other relevant modifications on chromosome 12 for SNPs ss715613204 and ss715613207. Both SNPs had a minor allele frequency higher than 0.35 in Brazilian germplasm with an increase in the alternative allele in cultivars with MGs higher than VII. In contrast, alternative alleles for both SNPs were extremely rare in the US germplasm except for accessions with MG higher than VII.

There were 312 genomic regions that differentiate northern (00 IV MG) and southern (V IX MG) cultivar groups (Supplementary Table S6), which included the Dt1 locus. We compared the SNPs observed in the genomic region close to the Dt1 gene (Chr19: 45.2045.30 Mbp) with the growth habit phenotype data available for 284 lines at the USDA website (www.ars-grin.gov). The phenotypic data suggests that these SNPs are associated with growth habit. Moreover, our diversity analysis demonstrated a putative selective sweep for the Dt1 gene in the northern germplasm, which has the dominant loci fixed for Dt1; the southern lines tend to be more diverse compared to the northern US cultivars (Supplementary Table S7). In contrast, other genomic regions have lower nucleotide diversity in southern accessions compared to the northern accessions. An important disease resistance gene cluster was observed on chromosome 13 bearing four loci: Rsv1, Rpv1, Rpg1, and Rps317,18,19,20. In this interval, we observed two genomic regions (29.70 29.80 Mbp and 31.90 32.00 Mbp) under putative selective sweeps in the southern germplasm (Supplementary Table S8).

Besides these regions, 1,401 SNPs with FST values higher than 0.40 between northern and southern US cultivars were also identified (Supplementary Table S9). In addition, there were 23 SNPs with FST values higher than 0.70 spread on chromosomes 1, 3, 6, and 19. Seven of them were located close to another important soybean locus: E1 (involved in soybean maturity control) (Supplementary Table S10). These SNPs clearly differentiate northern and southern US cultivars with the reference allele fixed in northern genetic materials, and the alternative alleles in southern accessions. Gene modification in US germplasm was also detected in our study. One hundred twenty-six SNPs were identified in FST analysis modifying 125 genes (Supplementary Table S11).

Finally, we detected 1,557 SNPs with FST values higher than 0.40 between super-early cultivars (00 0 MG) and early cultivars (III IV MG) (Supplementary Table S12). Seventeen SNPs had FST values higher than 0.70 spread on chromosomes 4, 7, 8, and 10. The SNPs identified on chromosome 10 were close to the E2 locus. We also detected 168 SNPs associated with modifications in 164 genes (Supplementary Table S13).

We observed two SNPs with large differences in allelic frequencies in the Brazilian germplasm (Supplementary Figure S4). On chromosome 4, SNP ss715588874 (50,545,890bp) had a decrease of the allele A in cultivars released after 2000 with only nine of the 45 Brazilian cultivars with this allele. A similar situation was observed on chromosome 19 for ss715633722 (3,180,152bp) with half of the modern accessions having the presence of allele C. Both SNPs had similar distribution according to their decades in the US genetic base with a large influence of reference alleles.

There were 126 genomic regions spread on almost all soybean chromosomes in Brazilian cultivars. The only exception was chromosome 20 (Supplementary Table S14). Our analysis between cultivars released before and after 1996 identified 30 putative regions under breeding sweep events. Thirteen regions had a decrease in diversity in modern genetic cultivars according to Tajimas D and results. Two genomic regions observed were close to important disease resistance loci: one on chromosome 13 (30.30 30.40 Mbp) close to the resistance gene cluster (with Rsv1, Rpv1, Rpg1, and Rps3)17,18,19,20 and another on chromosome 14 (1.70 1.80 Mbp) with a southern stem canker resistance loci21,22. In contrast, thirty-one genomic regions had an increase in diversity in modern cultivars, which suggested putative introgression events in these accessions. Two genomic regions were observed, on chromosome 2 (40.90 40.10 Mbp) and 9 (40.3040.40 Mbp). Thesewere previously reported to have an association with ureide content and iron nutrient content, respectively23,24.

Besides these regions, there were also 409 SNPs with FST values higher than 0.40, distributed across all soybean chromosomes. There were 73 SNPs with FST values higher than 0.70 (Supplementary Table S15). Some of these SNPs were also reported to be associated with important soybean traits such as plant height, seed mass, water use efficiency, nutrient content, and ureide content23,24,25,26,27.

We also identified gene modifications with a high impact on the Brazilian genetic base when we compared cultivars according to their decade of release. Of the 409 SNPs identified in FST analysis, we observed 40 SNPs causing modifications in 39 soybean genes (Supplementary Table S16). Three SNPs with FST values higher than 0.70 were associated with non-synonymous modifications: ss715588896 (Glyma.04G239600 a snoaL-like polyketide cyclase), ss715607653 (Glyma.10g051900 a gene with a methyltransferase domain), and ss715632020 (Glyma.18G256700 a PQQ enzyme repeat).

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Genetic relationships and genome selection signatures between soybean cultivars from Brazil and United States after decades of breeding | Scientific...