Archive for the ‘Female Genetics’ Category

Moles have a pretty tough life. They live underground, in the dark, burrowing through heavy dirt. And when faced with an enemy, there's nowhere to turn they have to fight.

In most mammals, females tend to be at a disadvantage when it comes to face-to-face combat, because they tend to be smallerand less aggressive than males.

But female moles have evolved a secret weapon: a hybrid organ made up of both ovarian and testicular tissue. This effectively makes them intersex, giving them an extra dose of testosterone to make them just as muscular and aggressive as male moles.

"As a consequence, basically the whole body of the female, they get masculinized," geneticist Daro Lupiez told Quirks & Quarks host Bob McDonald. "They become the body builders of nature."

Lupiez co-led a study to understand how the moles' genes facilitated this advantage, which was recently published in the journal Science.The research was part of a collaboration between the Max Planck Institute for Molecular Genetics and the Max Delbrck Center for Molecular Medicine in the Helmholtz Association in Germany.

The team worked with Iberian moles, commonly found in Spain and Portugal, however this intersex adaptation has been documented in at least six mole species.

"We know that intersexuality happens in species like humans, dogs or cats. But the difference actually in moles, it happens all the time, so all the females are intersexual. And this is really something unique among mammals,"said Lupiez.

To understand why this happens, the researchers completely sequenced the genome of the Iberian mole and sifted through their billions of genetic "letters" or nucleotides, looking for thoseresponsible for the change.They also comparedthe mole genometo several other animals, including humans. "I can really tell you that this is like looking for a needle in a haystack," said Lupiez.

They found that it wasn't the genes that had changed, but ratherthe regulatory elements, or instructions, associated with those genes, which gave the female moles this advantage.

"In moles, you have all the components there, but the only thing is that there have been new connections established," he said. "These new genes get completely different patterns of expression, and they start to make new functions which in this case is to help females develop as intersexual."

As a result of these different genetic instructions, the moles develop an organ made up of both ovarian and testicular tissue. This organ, called ovotestis, still functions as an ovary, but doesn't produce sperm. It does, however produce the same large amounts of testosterone as found in male moles.

This hormonal boost means that females and males are roughly the same size, equally muscular, and equally aggressive. Even their external genitalia looks alike, with the female's clitoris protruding much like the male's penis.

This boost of testosterone doesn't affect the molesfertility or reproductive abilities.

"What normally happens within mammals is that the males have these famous Y chromosomes and females do not. So this is exactly the same for moles," Lupiezsaid. "So from this perspective, you have two completely separate sexes."

He adds that this natural doping can make it very challenging for researchers in the fieldto figure out whether a mole is a male or a female.

"It took me quite a while of trying to really figure out when I had a female in front of me or a male," he said. "They are pretty tough ... they become pretty aggressive and pretty wild to handle. But you know, with time we learn how to handle them with care."

Produced and written by Amanda Buckiewicz.

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Female moles are intersex they have testicle-like tissue that helps them grow big and tough - CBC.ca

Humans come in all shapes and sizes, as well as in varying heights. These factors are primarily dictated by your genes. If you have taller-than-average parents, chances are youll be tall, too.

Your genes can also determine when youll experience growth spurts, which can sometimes make some people much taller than their peers at the same age.

Theres nothing inherently wrong with being tall. Many of the concerns with being taller than others derive from negative and very much outdated stereotypes.

In rare cases, there may be underlying medical issues that make some children grow taller than usual at a noticeably young age. Unless you have a medical concern, you should never try to stop yourself from growing taller.

Keep reading to learn more about how we grow and what determines how tall well be.

In short, there isnt a way you can limit how tall youll be unless theres an underlying medical issue at hand.

Concerns over being too tall primarily stemmed from psychosocial considerations that were prominent between the 1950s and 1990s.

In the United States, such concerns were often aimed at adolescent girls whose parents were concerned their daughters might become too tall and possibly not get married.

Such fears stemmed from the sexist idea that women werent supposed to be taller than men. These concerns were significant enough that some families opted for hormone treatments for their daughters via estrogen.

It was thought that estrogen therapy could help stop girls from growing taller. However, research shows that not only was estrogen not proven effective in preventing a tall stature, but many women also reported unpleasant side effects.

While attitudes surrounding marriage and the ideal partner have certainly evolved, there may be other areas of concern surrounding height that are medically relevant.

These include medical conditions that cause children to grow tall too quickly, such as Marfan syndrome and pituitary gland tumors.

Unless you have a legitimate medical concern, you should not try to stop growing taller.

On the flipside, some people are concerned that they might be shorter than average. These may be caused by medical conditions and are usually detected during childhood. Some of the causes include:

Treatment for a shorter than average stature depends on the underlying cause, and it must be evaluated before adulthood.

Human growth hormones may help increase height in children who have hormone deficiencies. Surgery may also be helpful in cases of achondroplasia.

Your genes are the primary factors that govern how tall youll be.

Such genetics can vary based on region and ethnicity, too. Chances are, if your parents are taller or shorter than average, then youll end up being around the same height.

However, there are also some gray areas to consider. For example, if you have one tall and one short parent, your own height may end up being somewhere in between.

Its also not out of the realm of possibilities to be an anomaly in your family, where you may be significantly taller or shorter than everyone else.

Childhood nutrition and overall health play other factors in determining your height. Developed countries have witnessed increasing heights in their populations thanks to better access to food and health care.

On the flipside, poor nutrition, inadequate health care, and premature birth can all contribute to a shorter than average stature.

As you age, hormones become crucial drivers of growth. Human growth hormones produced in the pituitary gland are the most influential, followed by sex hormones (estrogen, testosterone) and thyroid hormones.

A final consideration is your gender. Girls sometimes grow quicker than boys at the same age due to hitting puberty about 2 years earlier. However, boys tend to have larger growth spurts overall. This results in adult men being about 5 inches taller than adult women.

You should talk to a doctor if you have any concerns about your height. They can rule out the possibility of any underlying medical conditions. Theyll also likely offer reassurance about being taller.

Its also important to see your doctor for a physical every single year. If youre a parent, a pediatrician can determine where your child falls on a growth chart compared to other children their age.

Some children grow quicker (and end up being taller) than their peers, but this doesnt usually indicate a medical problem. Your doctor will let you know if your individual height and growth rate indicates any concerns.

Despite some social and cultural perceptions on height, theres nothing inherently wrong with being tall. To gauge how tall youll be, look to your parents own heights as a guide.

In rare cases, a medical condition might make you extremely taller than whats considered normal. Your doctor can help determine whether your taller-than-average height is of any concern.

Unless youre being treated for a medical condition that contributes to your tall stature, there isnt any treatment that stops you from achieving your full height. If concerns persist, talk to your doctor for advice.

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How to Stop Growing Taller and Why You Shouldn't - Healthline

by Matthew RosenbergDALTON: Sitting in the local Republican office most days is a lifelong conservative named Diane Putnam, who got her first taste of politics when Dwight D. Eisenhower was president and she was a little girl telling people that she liked Ike.

She still does. But these days, what really grabs Putnams attention is talk of a satanic criminal conspiracy hatched by a cabal of deep state child molesters who are seeking to take down President Donald Trump. In other words, she believes in QAnon. She insists she is just one of many.

The large majority of people, they understand about QAnon, Putnam, the Republican chairwoman of this small Georgia city, said in a recent interview.

Those that dont know, she added, they have not looked into really what its about.

Across the country, Republicans like Putnam long-standing party members who could hardly be described as fringe radicals are embracing QAnon. The followers of this online phenomenon believe that the Democratic establishment and much of the Republican elite are deeply corrupt, and that Trump was delivered to save America from both. Urged on by the president, whose espousal of conspiracy theories has only intensified in the waning weeks of his campaign, QAnon adherents are pushing such ideas into the conservative mainstream alongside more traditional issues like low taxes and limited government.

There was no acknowledgment of the real-world violence inspired by QAnon, which has prompted a preelection crackdown by social media networks, with YouTube last week becoming the latest platform to attempt to stop its spread. But dozens of recent interviews in Georgia and other parts of the country offered insights into the pull of a movement that has migrated far beyond the confines of the internet and, much like the Tea Party before it, plays to the sense of grievance on which Trumps political career was built.

People feel left out, said McKray Kyer, 24, the local Republicans vice chairman. QAnon, with its focus on criminal elites, helped them understand why. Its not about what were doing wrong its the swamp.

Kyer said he had looked into QAnon and was not sure what he believed. But many others interviewed said they believed in some or most of QAnon, and a significant portion of those who did not know the movements name were familiar with its themes, especially its talk of rampant child trafficking and devil worship among powerful elites.

Yet the movement is elastic, drawing on any number of well-worn tropes. Even people who explicitly dismissed QAnon as lunacy often volunteered similar conspiracy theories. There was talk of how the pandemic was an outright hoax or, at the very least, being wildly overblown. Many people repeated racist theories about former President Barack Obama or the anti-Semitic notion that financier George Soros controls the political system.

Its a real undercurrent in the party, said Jason Anavitarte, 42, a Republican running for the Georgia State Senate. Its QAnon; its other conspiracy theories. We hear them every day.

Or as Michael Conley, 42, a Trump supporter and QAnon adherent from Hagerstown, Maryland, put it: Everybodys talking about it.

Though there has been little public polling, there is growing anecdotal evidence that QAnon followers now make up a small but significant minority of Republicans. Adherents are running for Congress and flexing their political muscles at the state and local levels. The movements growth has picked up pace since the onset of the pandemic in March, and its potency is clear on social media before Facebook banned QAnon content earlier this month, there were thousands of dedicated Facebook groups with millions of members.

The phenomenon can be seen at Trump rallies, where people wearing QAnon shirts and hats are commonplace; at one recent rally in Las Vegas, the parents of a toddler in a QAnon shirt gamely posed for pictures with stranger after stranger. It was on display outside Walter Reed National Military Medical Center, where QAnon adherents gathered to support Trump after he was hospitalized with COVID-19. (Other QAnon adherents questioned whether the president had been hospitalized at all.)

Susan Cooper, 59, an insurance agent in nearby Calhoun, estimated that between 20% and 25% of her friends had bought into QAnon, though she had not. Others interviewed offered a similar assessment, and said it was a varied group young and old, male and female, poor and prosperous, urban and rural.

Its women that I talk to, Cooper said. These women are sharp ladies these women are women out of Atlanta, out of California, and friends of mine that are literally all over the country because of the company that I work with and they firmly believe this.

QAnon is spreading among evangelical Christians, too. The Biblical Recorder, a Southern Baptist newspaper in Cary, North Carolina, recently warned of its dangers. Christians should reject the movements fanatical and dangerous messages, wrote Seth Brown, the papers executive editor.

Many of the Republican Partys leaders and powerful donors are similarly concerned, as are a great many voters. Yet few high-profile Republicans have spoken out, demonstrating the thin line they are trying to walk between the moderate voters they need to win over and the members of their base who adore Trump.

Its a pro-Trump movement; QAnon is not of the Republican Party, said Dr. John Cowan, 45, a supporter of the president who ran in this years primary for a House seat representing northwest Georgia. It leaves no room between the president and Republican ideals and philosophy.

Cowan, a neurosurgeon, has seen up close the political impact of QAnon. He was trounced in the runoff by Marjorie Taylor Greene, 46, perhaps the most unabashed QAnon supporter running for Congress. She was caught on Facebook videos that surfaced earlier this year making offensive remarks about Black people, Jews and Muslims and openly courted the most extreme elements of the partys base during her primary campaign, presenting herself as the most loyal Trump supporter in the race.

Its corrupting the debate in the Republican Party, Cowan said of QAnon, because you cant separate yourself from the president in any way if you want to win.

It really is the religion of Trump devotees.

'God-tier genetics'The prophet of QAnon is Q, a purported government insider with a high-level security clearance who began posting cryptic messages in 2017 about the deep state trying to destroy the president. Followers pore over and interpret the postings known as Q drops and a core belief is that an apocalyptic showdown will smash the child-trafficking cabal and transform America. They call the transformation the Great Awakening.

At the center of the myth is Trump, often depicted as uniquely gifted with the abilities and fortitude needed to save America. The portrayal is taken straight out of his own playbook. From the moment he accepted the Republican nomination in 2016 and declared, I alone can fix it, to his claim earlier this month that catching the coronavirus was a blessing from God allowing him to stumble upon a miracle cure, the president has sought to present himself as a singular figure in history.

His most ardent supporters, especially QAnon believers, have amplified and further exaggerated his imagined powers. An entire cottage industry of online memes is devoted to photoshopping the president into famous great-man images, like the iconic painting of George Washington crossing the Delaware. It can now be found online with a grinning Trump pasted over the face of Americas first president.

At other times, Trump is treated as something close to divine. After the presidents coronavirus diagnosis, a prominent QAnon promoter, Brenden Dilley, told listeners of his radio show that Trump was blessed with god-tier genetics.

That same reverence was on display at Q Con Live!, a QAnon convention held in late August in Jacksonville, Florida. Much of the program was given over to extolling the accomplishments of Trump. The words glory and glorious came up often.

He has been gifted with abilities to do things that nobody else would even attempt or could actually accomplish, said David Martin, 58, a Navy veteran.

Martin, like most QAnon supporters, was certain the movement had the presidents support, a belief Trump and some of those around him appear to have encouraged well before his comments on Thursday night.

In August, the president described followers of QAnon several of whom have been charged with murder, domestic terrorism and planned kidnapping as people that love our country. His children and aides have shared social media posts related to the movement, their messaging becoming more explicit as Trumps poll numbers have dropped. His former national security adviser Michael Flynn a man seen in pro-Trump circles as a martyr unfairly persecuted in the Russia investigation posted a video this summer of himself taking what is known as the QAnon digital soldier oath.

The messages have been taken up by people like Bob Cox, 62, a retired construction worker who lives in Aragon, a small town about an hour outside Atlanta. He had little doubt that the political elite was rife with pedophiles, and he knew how he would handle them.

If people like that come in my neighborhood, I will shoot them, he said. I will absolutely do it.

But he was banking on Trump to take care of the problem first.

All this stuff is getting started through Soros, Cox added. He needs to be considered an enemy of the state, and Trump is on top of that. He knows.

QAnon countryThey began streaming into the Republican Party office in Dalton the self-described Carpet Capital of the World, a city of nearly 34,000 about 1.5 hours from Atlanta around dusk on a warm September day, husbands and wives, small groups of friends, young Republicans aspiring to careers in politics. They had come to see Marjorie Taylor Greene.

She is one of the more than dozen Republicans running for Congress who have signaled some degree of support for QAnon. Most are almost certain to be defeated in November, like Jo Rae Perkins, the long-shot Senate candidate in Oregon who posted a video in May declaring, I stand with Q and the team, and followed up in June with another video of herself taking the QAnon digital soldier oath. Others have a chance to win, including Lauren Boebert, who defeated a five-term Republican incumbent in a sprawling district in Colorado.

But it is Greene, alone among QAnon candidates, who is considered a near-lock to win a seat in Congress, and her campaign has turned Georgias 14th Congressional District into a ground zero of sorts for the transformation of QAnon into a political movement. She is, after all, the candidate who called QAnon a once-in-a-lifetime opportunity to take this global cabal of Satan-worshipping pedophiles out.

That might be a hindrance elsewhere, but not here. In this district, it can have benefits, said Kyer, the local party vice chairman.

Greenes district, which stretches from the northern exurbs of Atlanta all the way to the Tennessee border, is overwhelmingly white and Republican. Trump won upward of 70% of the vote in most parts of the district in 2016. Incomes in many areas are far below the national average, and railing against immigrants and foreign manufacturing plays well here. So does QAnon.

Were all aware of that pedophilia stuff, Kyer explained. But its also about how theyve the elites, that is been getting us into wars, just abusing power, taking advantage of the common middle-class people. It really hits home with a lot of people, whether they know all the details or not.

If Kyer was unsure about what he believed, others at the meeting were far more certain. Among those who subscribed to QAnon the crowd appeared to be split evenly between believers and nonbelievers many said they had learned about the movement from social media, and they ran the gamut from young digital natives to retirees who spent their days on Facebook, staying connected with old friends and being bombarded by disinformation.

Greta Hollis, 63, was typical. Though she had always considered herself a Republican, she said, politics had never much interested her. She saw Washington as a place where everyone was hustling to make a buck, not trying to help ordinary people. Then Trump ran for president, and said he was doing it to help people like her. She believed him.

She used to think greed was the driving force in politics. But how much money can somebody need? Hollis said. The more that greed and the money didnt make sense, I knew there had to be something else.

QAnon, she said, showed her what that was, and explained why Trump was facing so much resistance from Democrats and even some Republicans. All the pedophilia, all that kind of thing, the politics are so deep into that, I believe that, she said.

Then there were people like Putnam, the party chairwoman, who is in her 70s. She has served the local Republican Party in some capacity for most of the past 30 years. Her views, Putnam said, have evolved with the party, but she added, Ive always been a true conservative.

She acknowledged that meant something different back when she was a girl. There wouldnt be that much difference between Dwight Eisenhower and any of the Democrats, she said. And even going back to John Kennedy, even though he was a Democrat and everyone knew that he was more liberal than the conservative Republican, still his political policies were not so drastically different.

In her estimation, what changed was the proliferation of news sources on the internet peoples eyes began to be open to what was really happening and, most recently, Trumps decision to run for president.

Once he came down the escalator and announced his candidacy, people knew from the beginning he would be different, Putnam said. He couldnt be bought; he doesnt take his salary. So he cant be manipulated or controlled by financial contributions. Hes his own man.

She, too, was drawn to QAnon after seeing the resistance to Trump in Washington.

People know theres more going on than the public is aware of, she said. Donald Trump is trying to expose all of the corruption.

Greene, for her part, does her best to play it straight, now that she is in a general election, facing a somewhat broader ideological array of voters. Her stump speech makes no mention of QAnon or shadowy suspicions, and there is little hint of the unhinged conspiracy theorist that she was portrayed as by her opponents in the primary.

A political novice who declined an interview request, Greene knows how to work a crowd like a veteran. She cracks jokes and dispenses with any trappings of formality. Most important, she leaves little doubt where she stands on Trump.

After getting up to speak in Dalton, the first thing she did was push aside the lectern and replace it with a cardboard cutout of the president.

I just love this guy, she said.

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Republican voters are taking a radical internet conspiracy theory into the mainstream - Economic Times

The awarding of this year's Nobel Prize for Chemistry to Jennifer Doudna and Emmanuelle Charpentier has been heralded as an incredible step forward for women. For the first time, two female scientists have been honored for an accomplishment without being accompanied by a man.

Also being heralded is the incredible potential of Doudna and Charpentier's gene-editing technology, CRISPR. Announcing the award, the Secretary-General of the Swedish Royal Academy of Science gushed, "This year's prize is about rewriting the code of life."

Doudna has used similar language to describe CRISPR technology, stating "the genome would become as malleable as a piece of literary prose at the mercy of an editor's red pen." And, so far, congratulations and praise from fellow scientists includes predictions and speculations that CRISPR will offer humanity new potential to combat all sorts of illnesses and make the world a better place.

Not covered in all the press announcing the award is the danger that CRISPR poses to us all. Consider, for example, the incident in which a Chinese scientist used CRISPR to edit the genome of embryos before implantation, a move that drew international criticism and gave the world a glimpse of just how this whole thing could go very wrong, was barely mentioned, if at all.

CRISPR has been likened to a computer mouse or pair of genetic scissors. One researcher described, "You can just point it at a place in the genome and you can do anything you want at that spot." Of course, it's not quite that simple. Still, the statement reveals the kind of hubris behind the drive to make this technology available, with virtually no ethical guidelines in place.

There seems to be this assumption that, of course, scientists and researchers will "play nice" with the power CRISPR offers. History, of course, tells us that it's nearly impossible to resist the temptation to "play God" instead. And that never ends well.

Earlier this year, a team of researchers at the Francis Crick Institute in London used CRISPR to edit 18 donated human embryos, supposedly to study "the role of a particular gene in the earliest stages of human development." The Crick Institute team did everything by the book. Still, despite their best efforts, around half of the embryos contained what researchers called "major unintended edits." "Major unintended edits" is Newspeak for serious genetic damage, the kind of damage that can lead to birth defects or future medical issues, like cancer.

How did this happen when researchers were so careful to play by the rules? One genetics researcher put it this way: "You're affecting so much of the DNA around the gene you're trying to edit that you could be inadvertently affecting other genes and causing problems."

If these sorts of problems come with researchers playing by the rules and acting out of good intention, what might happen when research is driven by greed or is done in some unregulated environment? Seeing the results from the Crick Institute researchers prompted one molecular biologist to call for "a restraining order for all genome editors to stay the living daylights away from embryo editing."

Now, a few months later, the Nobel Prize committee has put its official stamp of approval on the technology and its promise to "rewrite the code of life." Absent regulations with real teeth, there will be no restraining order coming.

There's an ironic connection here to historic origins of the Nobel Prize. Alfred Nobel was the inventor of dynamite. He hoped and intended for his invention to be used for blasting rocks apart. Instead, it was used to blast people apart.

When Alfred's brother died, a French newspaper, mistakenly believing that it was Alfred who had died, proclaimed "The Merchant of Death Is Dead!" Appalled by the reputation his invention brought to him, Nobel established the Nobel Prizes, including the Nobel Peace Prize, hoping his legacy would be a better world instead of death and suffering.

By awarding the prize to the inventors of CRISPR, the committee is repeating Nobel's history and turning his intentions on their head. Like dynamite, whatever legitimate potential CRISPR holds will operate alongside of even greater potential for harm. And it's not regulated anywhere near the degree that dynamite is.

From BreakPoint, Oct. 12, 2020; reprinted by permission of the Colson Center, http://www.breakpoint.org.

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BreakPoint: Inventors of CRISPR win Nobel Prize, but should we 'rewrite the code of life'? - Chattanooga Times Free Press

Background

Observational studies have identified height as a strong risk factor for atrial fibrillation, but this finding may be limited by residual confounding. We aimed to examine genetic variation in height within the Mendelian randomization (MR) framework to determine whether height has a causal effect on risk of atrial fibrillation.

In summary-level analyses, MR was performed using summary statistics from genome-wide association studies of height (GIANT/UK Biobank; 693,529 individuals) and atrial fibrillation (AFGen; 65,446 cases and 522,744 controls), finding that each 1-SD increase in genetically predicted height increased the odds of atrial fibrillation (odds ratio [OR] 1.34; 95% CI 1.29 to 1.40; p = 5 10-42). This result remained consistent in sensitivity analyses with MR methods that make different assumptions about the presence of pleiotropy, and when accounting for the effects of traditional cardiovascular risk factors on atrial fibrillation. Individual-level phenome-wide association studies of height and a height genetic risk score were performed among 6,567 European-ancestry participants of the Penn Medicine Biobank (median age at enrollment 63 years, interquartile range 55-72; 38% female; recruitment 2008-2015), confirming prior observational associations between height and atrial fibrillation. Individual-level MR confirmed that each 1-SD increase in height increased the odds of atrial fibrillation, including adjustment for clinical and echocardiographic confounders (OR 1.89; 95% CI 1.50 to 2.40; p = 0.007). The main limitations of this study include potential bias from pleiotropic effects of genetic variants, and lack of generalizability of individual-level findings to non-European populations.

In this study, we observed evidence that height is likely a positive causal risk factor for atrial fibrillation. Further study is needed to determine whether risk prediction tools including height or anthropometric risk factors can be used to improve screening and primary prevention of atrial fibrillation, and whether biological pathways involved in height may offer new targets for treatment of atrial fibrillation.

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Genetics of Height and Risk of Atrial Fibrillation: A Mendelian Randomization Study - DocWire News

As its cultivation partner, Pink Haze tapped Clade9 Los Angeles, the 2019 recipient of the prestigious Cannabis Business Awards for Lifetime Achievement in Cultivation. Clade9 produces some of the most sought-after genetics and indoor flower popular among cannabis connoisseurs.

Founders of Pink Haze, Patty Roe and Summer Edwards, entered the cannabis industry in 2016 through a medical cannabis delivery platform, where the majority of patients were women. Roe and Edwards felt their clients deserved a higher-quality experience, in both products and community, so they changed focus from delivery to brand development and founded Pink Haze.

"I am thrilled to launch a product that celebrates and empowers women. Pink Haze is here to offer the women we love and support a product worthy of their time, standards, and money," said Patty Roe, CEO. "We don't want people to just buy a joint, we want people to celebrate the freedom and acceptance that we now have with cannabis and feel a part of something bigger."

Pink HazeFemale-owned and led luxury cannabis brand, Pink Haze, LLC, was founded by Patty Roe, whose diverse career took her from the securities industry, to Capitol Hill, to founding a successful multi-million dollar marketing firm. In 2016, she walked away and committed her future to cannabis and empowering women.

Co-founder Summer Edwards, is a lifestyle-branding expert and international award-winning photographer. Edwards built a successful photography business in Arizona and was named one of Phoenix's top photojournalist portrait photographers. Edwards was also a roller derby legend, playing for nearly ten years.

Founded in 2017, Pink Haze has launched their first round of funding, seeking $1.5 million utilizing convertible notes. Interested investors should contact Patty Roe.

Pink Sesh SocietyUnique among any other products in the market, Pink Haze is an important part of Pink Sesh Society, which Roe and Edwards founded early in the development of Pink Haze. What began as a casual monthly gathering of diverse Southern California women celebrating cannabis, rapidly became a life changing membership organization that now boasts 20,000 organic Instagram followers and a national following.

The unique relationship between Pink Sesh and Pink Haze promises to elevate Pink Haze's popularity in the market by elevating a woman's cannabis experience through community.

Pink Haze Instagram: https://www.instagram.com/thepinkhaze/

Pink Sesh Instagram: https://www.instagram.com/thepinksesh/

Pink Sesh TikTok: https://www.tiktok.com/@pinksesh?lang=en

SOURCE Pink Haze

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Women Rise Above with Launch of Pink Haze - PRNewswire

Most mammalian chromosomes dictate their sex-identity with X and Y chromosomes. XX is female, XY is male, including in humans. However, in nearly six species of moles, XX females have been found with a hybrid of ovaries and testes known as ovotestes.

The testes arent fully functional. They cannot produce any sperm but they can release very high levels of testosterone (male-associated hormone). As a result, these moles become excellent diggers which helps them with their underground life.

The puzzle for scientists is how these male reproductive tissues are being formed in female moles even without the Y-chromosome. The answer is probably to look at the regions which control the genes instead of the genes themselves. The study was published in journal Science.

The female Iberian mole can be considered as intersex, as it has both male and female reproductive tissue. However, she develops a vagina only during the mating season and has functional female organs.

With most animals, males fertilize the egg produced by a female. However, 1% of humans can be born intersex. Other species like snails, earthworms, slugs etc can be hermaphrodite i.e. fully developed male and female reproductive parts.

The mole, however, feels different from them all, she has a male-looking external genital with a clitoris that looks like a penis. And for the most part of her life, the vaginal canal has no opening. While the testosterone production low in mating season, it can be higher than XY males for the rest of the year in these intersex moles.

At a certain point, sexual development usually progresses in one direction or another, male or female, explained Daro Lupiez, Geneticist at Max Planck Institute. However, they want to study how the evolution of these animals modulates sexual behaviour. The team theorizes that the ovotestes suggest some other gene must be active in the females, one that is not found on Y chromosome. The gene responsible for producing male hormones is CYP17A1.

They observed that it was present three times in the female moles genome instead of one. The triplication appends additional regulatory sequences to the gene which ultimately leads to an increased production of male sex hormones in the ovotestes of female moles, especially more testosterone, explained Francisca Martinez. She is the lead author of the study from the Institute for Medical Genetics and Human Genetics in Berlin.

Studies like these are important to normalise the existence of intersex individuals, even in humans, who are generally pathologized.

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Female Moles Have 'Ovotestes' that Produce Testosterone That Make Them Excellent Diggers - News18

AVALONThe Catalina Island Conservancy has been working to expand the bison herd on the island.

Two pregnant female bison will arrive on the island in December and are expected to give birth in the spring. The new additions come from the Laramie Foothills Bison Conservation Herd and will integrate into Catalina Islands free-ranging bison herd of approximately 100.

The Conversancy said the new additions will supplement the genetic diversity of the current bison herd on Catalina Island with the valuable genetics of heritage bison.

The Laramie Foothills Bison Conservation Herd is managed by Colorado State University, the City of Fort Collins, Colorado, and Larimer County. The herd was established with nine adult females and one male calf in November 2015. It has now grown to over 100 bison, which has made it possible to share bison with tribal and conservation herds across the country.

According to the Conservancy, the bison have valuable genetics from the Yellowstone

National Park Herd and, thanks to science implemented at CSU by Assistant Professor Jennifer

Barfield and her team, the animals are also disease-free.

We look forward to watching our animals find a new home with the herd on Catalina Island, where they can contribute to the growth of a truly unique and iconic herd, Barfield, a reproductive physiologist, said in a released statement.

Bison have freely roamed Catalina Island since 1924 when 14 bison were brought to the Island for the filming of an adaptation of a Zane Grey novel, believed to be The Vanishing American. The Conservancy said bison have played a significant role in the cultural heritage of Catalina Island and will be roaming the island far into the future.

The unique opportunity to see American bison on Catalina Island brings wildlife lovers from around the world to learn about a species they might otherwise not have a chance to see roam, said Catalina Island Conservancy President & CEO Tony Budrovich. While here, they also learn about Catalinas endemic species, special Mediterranean climate and importance of conservation.

Those wishing to see bison on the island can do so through the Conservancys Eco Tour. The Conversancy reminds everyone that bison are wild animals and people should stay at least 125 feet away from bison at all times.

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New bison to join Catalina Island herd The Log - The Log Newspaper

ourtesy of Catalina Island Conservancy

Bison have played a significant role in the cultural heritage of Catalina Island for nearly 100 years and will be roaming Catalina Island far into the future. Catalina Island Conservancy is working with the Laramie Foothills Bison Conservation herd to bring two pregnant female bison to Catalina Island. The new additions will arrive in early December and supplement the genetic diversity of the current bison herd on Catalina Island with the valuable genetics of heritage bison.

The herd managed by Colorado State University, the city of Fort Collins, Colorado, and Larimer County was established with nine adult females and one male calf in November 2015. It has now grown to over 100 bison, which has made it possible to share bison with tribal and conservation herds across the country. The bison have valuable genetics from the Yellowstone National Park herd and, thanks to science implemented at CSU by Assistant Professor Jennifer Barfield and her team, the animals are also disease-free.

We are proud to continue our mission of collaborating with conservationists through this new partnership with Catalina Island Conservancy, said Barfield, a reproductive physiologist. We look forward to watching our animals find a new home with the herd on Catalina Island, where they can contribute to the growth of a truly unique and iconic herd.

Bison have freely roamed Catalina Island since 1924. Fourteen bison were brought to the island for the filming of an adaptation of a Zane Grey novel, believed to be The Vanishing American. There are currently approximately 100 bison on Catalina Island. The new animals will integrate into Catalina Islands free-ranging bison herd in December and are expected to give birth in the spring.

With goals of maintaining the health of the land and providing public benefit, Catalina Island Conservancy maintains its three-part mission of conservation, education and recreation. The bison population is a key example of this delicate balance, said Tony Budrovich, Conservancy president and CEO . The unique opportunity to see American bison on Catalina Island brings wildlife lovers from around the world to learn about a species they might otherwise not have a chance to see roam. While here, they also learn about Catalinas endemic species, special Mediterranean climate and importance of conservation.

With its location close to urban areas, Catalina provides a gateway to nature for a diverse population to experience and learn about wildlife and nature just steps away from home. The best way to view bison is through a Conservancy Eco Tour. Bison are wild animals. People should stay at least 125 feet away from bison at all times.

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More bison to join island herd - The Catalina Inslader

A 24-year-old patient diagnosed with Pompe disease, a genetic fatal disorder, delivered a healthy baby at the Amrita Hospital here.

Patients with this rare condition have muscle weakness and a spectrum of severe complications, and often require long term, specialised treatments and management through Enzyme Replacement Therapy (ERT).

Sheela Nampoothiri, head of paediatric genetics, Amrita Hospital, said the patient had undergone the entire cycle of pregnancy to deliver a healthy baby as she had been put on the life-saving ERT under an access programme around six years ago after she was diagnosed with juvenile onset of Pompe disease.

Dr. Sheela said that this case was a testimony that patients diagnosed with rare diseases such as Pompe could lead a near-normal life if they were put on life-saving treatment early. The new-born female child, which weighed 2.8 kg at birth, did not have the defective gene and was free of Pompe disease, she said. Radhamani K., head of obstetrics and gynaecology, said that the patient was on ERT throughout her 37- week pregnancy and would continue to be on treatment in the post-natal phase too.

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Woman with rare disease delivers healthy baby - The Hindu

Its this time of the year when those of us in northern temperate zones are spectators of a fascinating natural phenomenon the appearance of autumn leaf colors.

The leaves start to change colors as they age, or senesce. During this period a cluster of enzymes in the leaves start chewing up their green pigment, called chlorophyll. As the leaves become less green, their red, yellow, and orange pigments (known as anthocyanins and carotenes) begin to shine. However, exactly how chlorophyll breakdown works is still only partially understood.

While autumn leaves are a great example of chlorophyll breakdown, evergreen plants (those that remain green all year long), vegetables, and fruits also experience chlorophyll decay. However, this happens only under special conditions such when fruit ripen or when evergreen plants are deprived of nutrients and water.

Banana skin is one of the few fruits where chlorophyll degradation can be mapped under ultraviolet (UV) light. As bananas ripen, their skins lose their green color a sign of chlorophyll breakdown and form new pigments that fluoresce blue under the UV light. Scientists know that this new pigment, known as hypermodified fluorescent chlorophyll catabolite (hmFCC), is produced very briefly in most plants. Banana skins and grapevine leaves are known to produce hmFCCs for a longer period.

Recently scientists at Instituto de la Grasa, Spain analyzed devils ivy, an evergreen plant, in their quest to find signs of this fluorescent compound. They activated the aging process by starving the plant, and voila! Exposure to UV light produced the blue, fluorescent pigment hmFCC. The team also observed two other newly identified compounds that will provide more insights into the evergreen chlorophyll breakdown puzzle.

Although the actual benefit of producing this blue, fluorescent compound is still a mystery, scientists think that it could provide protection against radiation or function in communication between animals and plants.

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Working-class ants take the reins when the Indian jumping ant queen dies - Massive Science

publication date: Oct. 9, 2020

In a new clinical trial, City of Hope is investigating a treatment for cancer patients with COVID-19 by repurposing leflunomide, an anti-inflammatory drug for rheumatoid arthritis, which is inexpensive and has few serious side effects.

Patients treated for cancer in the past two years may also be eligible.

FDA has recently approved the start of a phase I trial. At a later date, a phase II randomized clinical trial may take place if the first trial finds leflunomide to be safe and tolerable for these patients. City of Hope plans to work with other local medical centers who are treating cancer patients for SARS-CoV-2, the virus that causes COVID-19, to enroll them in the trial.

There are currently few effective drugs against COVID-19, and our clinical trial targets a critical high-risk group cancer patients whose immune systems are already weak, Steven T. Rosen, City of Hope provost and chief scientific officer, and the Irell & Manella Cancer Center Directors Distinguished Chair and Morgan & Helen Chu Directors Chair of the Beckman Research Institute, said in a statement. Our hope is that leflunomide will eradicate COVID-19 in cancer patients, providing the medical community with an effective therapy against this devastating virus.

Sanjeet Dadwal, City of Hope chief of the Division of Infectious Diseases, is the principal investigator on the trial.

For the phase I trial, all patients will receive leflunomide and may also be able to simultaneously receive other standard of care treatments for COVID-19. They may receive remdesivir, an antiviral therapy. Patients with acute respiratory distress syndrome may receive the steroid, dexamethasone, and patients with complications of COVID-19 such as cytokine release syndrome, which can lead to multiple organ failure, can receive the antibody tocilizumab.

If the phase I trial is found to be a safe and tolerable treatment, then a phase II randomized, double-blind trial will open at a later date. About half the patients will receive leflunomide with standard of care therapies to treat COVID-19, and the other half will receive a placebo and standard of care drugs as well.

Leflunomide is an oral and generic anti-inflammatory drug approved by FDA to safely treat autoimmune diseases such as rheumatoid arthritis. The therapy has also been used in cancer patients with cytomegalovirus with tolerable side effects.

Laboratory experiments performed at City of Hope and Wuhan, China, indicate that leflunomide has high potential to shut down viral replication by preventing the synthesis of viral RNA, the genetic material. It also downregulates the expression of ACE 2, a receptor for COVID-19 cell entry. A small clinical trial using leflunomide in China also demonstrated the therapy has potential antiviral drug against COVID-19.

In a phase I clinical study, City of Hope treated patients with advanced multiple myeloma with leflunomide. The therapy stabilized their disease with tolerable side effects.

NCI has funded the trial with a P30 grant supplement for COVID-19 research projects. City of Hope is one of a few cancer centers that has received such funding during the pandemic.

City of Hope also received funding from private donors, including The Elias, Genevieve and Georgianna Atol Charitable Trust and The Norman and Sadie Lee Foundation.

Novel CAR T-cell lymphoma therapy developed at MCW advances to phase II study

A novel cancer therapy studied and developed at the Medical College of Wisconsin with promising clinical outcomes is leading to a larger phase II trial to improve on the current standard of care.

Results of phase I of the first-in-the-world double targeted CAR T-cell therapy clinical trial were published in Nature Medicine.

This is a novel, cell-based treatment against cancer targeting two proteins (antigens CD19 and CD20) on the surface of cancer cells. This CAR T-cell therapy trial began in October 2017 and resulted in safe and promising outcomes for patients with relapsed and refractory B cell non-Hodgkin lymphomas which are cancers of the immune system.

MCW researchers collected patient T cells and then used a specially engineered virus to augment their ability to identify and kill cancerous cells and effectively destroy the lymphoma. While phase I focused on safety and feasibility of the treatment, a multi-institutional phase II is being developed to determine the true efficacy and understand how the nuances of the treatment process can result in excellent outcomes for a larger subset of patients.

All patients in the clinical trial had failed prior treatments and their cancer had relapsed. Within 28 days of the CAR-T cell therapy, 82 percent responded positively. Six months later, more than half of the patients cancer remained in remission. A higher dose of the treatment correlated with a prolonged remission, a trend the researchers plan to study further in the trials second phase.

The new treatment genetically alters a persons own immune cells to target cancer cells in a unique and personalized fashion, a significant departure from more routine chemotherapy.

The cell product used for treatment was manufactured using the CliniMACS Prodigy device, which is part of an automated CAR T cell manufacturing platform developed by Miltenyi Biotec.

Housed at the Froedtert & MCW Clinical Cancer Center, the CliniMACS Prodigy device enabled the research team to conduct the CAR T-cell immunotherapy through a self-contained, desktop system, producing new cells ready to be infused back into a patients bloodstream within 14 days. With the device, the entire process was performed locally at Froedtert Hospital.

This research was made possible through philanthropic dollars raised by the Childrens Wisconsin Foundation and the MACC Fund and their support of the Cell Therapy Lab at MCW.

MD Anderson researchers identify characteristics of infused CAR T cells associated with efficacy and toxicity in large B-cell lymphoma

Researchers at MD Anderson Cancer Center have identified molecular and cellular characteristics of anti-CD19 CAR T cell infusion products associated with how patients with large B-cell lymphoma respond to treatment and develop side effects.

The research team also found that early changes in circulating tumor DNA one week after CAR T cell therapy may be predictive of treatment response in a particular patient. The paper was published online in Nature Medicine.

CAR T cell therapy is highly effective against LBCL, corresponding author Michael Green, associate professor of lymphoma and myeloma, said in a statement. However, we experience two main clinical challenges: achieving long-term remission and managing treatment-associated adverse events.

This study suggests that, within the first week of therapy, clinicians may be able to identify a subset of patients who may experience more poor outcomes or adverse treatment reactions, said Green. This would allow the care team to adjust therapy to improve efficacy or to act to mitigate toxicity.

For this study, researchers performed single-cell analysis on CAR T cells to study gene expression profiles in the infused cells. CAR T cells were collected from those remaining in infusion bags following treatment of 24 patients with LBCL. These genetic profiles were compared to treatment responses, determined at three months post-infusion by PET/CT scan.

When we look at the characteristics of the infused CAR T cells, we found that samples from patients who were less responsive to treatment had exhausted T cells, whereas those who experienced complete responses had T cells expressing memory signatures, co-corresponding author Sattva Neelapu, professor of lymphoma and myeloma, said in a statement. Additionally, one cellular signature of T cell exhaustion was more commonly found in patients who exhibited a poor molecular response, and poor molecular response is generally associated with less-positive, long-term outcomes.

Further, the researchers analyzed early molecular responses in the patients by monitoring changes in circulating tumor DNA from treatment to one week post-infusion. The magnitude of change in tumor-associated DNA corresponded with response, suggesting that patients who displayed an early molecular response were more likely to experience a clinical response to treatment.

When we examined the infusion product, we found that a cell population with characteristics similar to myeloid cells, with a monocyte-like transcriptional signature, was associated with development of high-grade neurotoxicity, Green said. Detecting these cells may subsequently lead us to identify patients who would be at higher risk of developing neurotoxicity, allowing us to provide prophylactic treatment with agents that target the specific cellular features.

Further examination may lead to insights into the types and attributes of the cells present within the CAR T infusion product.

This study also tells us that some rare and unexpected cells identified by single-cell analysis could be biologically important, said co-corresponding author Linghua Wang, assistant professor of Genomic Medicine. Going forward, we plan to functionally characterize these monocyte-like cells to better understand their specific biological mechanisms driving these clinical results.

These findings will help researchers develop clinical interventions that can block or target these cells. They also plan to validate the capacity of circulating tumor DNA to accurately predict patients long-term outcomes.

This research was supported in part by the B-cell Lymphoma Moon Shot, part of MD Andersons Moon Shots Program. With support from the Moon Shot and the Cancer Prevention & Research Institute of Texas, the research team plans to utilize PDX models of disease that relapsed following anti-CD19 CAR T cell therapy to preclinically test interventions that could lead to better treatment responses or to prevention of adverse side effects.

Other research support came from the Schweitzer Family Fund, NCI (P30 CA016672) and start-up research funds from MD Anderson. A full list of co-authors and their disclosures can be found here.

MD Anderson researchers: Cancer mutations accumulate in distinct regions based on structure of genome and mutational causes

A study from researchers at MD Anderson Cancer Center indicates that mutations found in cancers do not accumulate randomly, but are found in distinct patterns that vary based on the three-dimensional organization of the genome in the cell as well as the underlying factors causing the mutations.

Mutations caused by external factors, such as ultraviolet light or tobacco smoke, led to mutations in different regions than internal factors, such as defects in DNA damage repair or proofreading machinery. The findings, published in Nature Genetics, are important for understanding what factors may be driving mutations in a given cancer and may point to new therapeutic targets.

DNA is not randomly organized within the nucleus, and we found that this structure is strongly correlated with how cancer cells accumulate mutations, lead author Kadir Akdemir, instructor of genomic medicine, said in a statement. We know there are certain processes causing mutations in cancer cells, but we dont always understand the underlying causes. These findings should give us a clue as to how cancer accumulates mutations, and perhaps we can target and kill cancer cells by leveraging the mutations they accumulate.

Within the nucleus of the cell, DNA is packaged with proteins into chromatin, a highly organized and compacted structure that makes up our chromosomes. Within this structure, genes that are frequently used in the cells are organized together in active domains, which are more readily accessible. Those genes used less often are similarly organized together in inactive domains.

The researchers analyzed whether mutations are distributed more frequently in these active or inactive domains in cancer by studying publicly available whole-genome sequencing data of 3,000 paired samples of normal tissue and tumor tissue across 42 cancer types.

Across every cancer type studied, the inactive domains carried significantly more mutations than the active domains, suggesting that the accumulation of mutations is strongly correlated with the three-dimensional organization of the genome.

As a validation of these findings, the researchers looked specifically at the X chromosome in male and female patients. In females, one of their two X chromosomes is inactivated, so it is essentially itself an inactive domain. When comparing the X chromosome between sexes, females had more mutations than males with a marked distribution difference, largely driven by an abundance of mutations on the inactive chromosome.

Knowing that mutations can be caused by a variety of distinct processes, the researchers also investigated whether external environmental factors resulted in different mutation patterns compared to those caused by internal factors in the cell.

Interestingly, we found that different causes of mutations resulted in distinct accumulation patterns within the cell, senior author Andy Futreal, chair of genomic medicine, said in a statement. Extrinsic factors were associated with an enrichment of mutations in inactive domains, whereas intrinsic factors were correlated with enriched mutations in active domains. This provides us an important foundation going forward to understand the root of cancer mutations when we dont otherwise know the cause.

Knowing the causes and distributions of cancer-related mutations may open up potential therapeutic options, explained Akdemir, such as targeted therapies against a specific signaling pathway or combinations with immunotherapy.

For example, immunotherapy may be able to better recognize a cancer cell if more mutations are present. However, if mutations occur primarily in inactive domains, they would rarely be seen by the immune system. Therapeutic agents that restore activity to these domains, used in combination with immune checkpoint inhibitors, could stimulate a stronger anti-tumor immune response.

This research was supported by the Cancer Prevention & Research Institute of Texas (R1205), The Robert A. Welch Distinguished University Chair in Chemistry, and NIH (P50CA127001, DP5OD023071, Z1AES103266). A full list of authors and their disclosures can be found with the full paper here.

UCSD study: Personalized cancer therapy improves outcomes in advanced disease

Researchers at the University of California San Diego School of Medicine found that patients receiving care for advanced cancer at Moores Cancer Center at UC San Diego Health were more likely to survive or experience a longer period without their disease progressing if they received personalized cancer therapy.

The study was published in Nature Communications.

Led by Razelle Kurzrock, director of the Center for Personalized Cancer Therapy at Moores Cancer Center and senior author of the study, a multidisciplinary molecular tumor board was established to advise treating physicians on course of care using an individual patients molecular tumor makeup to design precision medicine strategies.

Patients who underwent a molecular tumor board-recommended therapy were better matched to genomic alterations in their cancer and had improved outcomes, Kurzrock said in a statement. The three-year survival for patients with the highest degree of matching and who received a personalized cancer therapy was approximately 55% compared to 25% in patients who received therapy that was unmatched or had low degrees of matching.

Of 429 patients evaluated by the molecular tumor board, 62% were matched to at least one drug. Twenty percent of patients matched to all recommended drugs, including combination therapies.

The tumor board acted in an advisory role and treating physicians chose not to use the boards recommended strategy in 38% of cases, opting instead for a standard therapy approach that might have been unmatched to the patients genetic alterations or had a low degree of matching. These patients experienced a lower progression-free survival and overall survival rates.

The use of next-generation sequencing allows for the identification of novel potential targets for patients with cancer to improve outcomes, but there are challenges to using this approach widely, said Shumei Kato, associate professor of medicine at UC San Diego School of Medicine and first author.

One of the hurdles is that every cancer patient appears to be carrying different molecular and genomic patterns despite having the same cancer type, Kato, a Moores Cancer Center medical oncologist specializing in rare and gastrointestinal cancers, said in a statement. This can be challenging since we are customizing therapy based on the unique genomic pattern patients have, and thus it is difficult to predict the response. In addition, this approach requires multidisciplinary expertise as well as access to drugs or clinical trials not always available in smaller practices.

At Moores Cancer Center, the molecular tumor board is composed of experts in basic, transitional and clinical research as well as bioinformatics, genetics, radiology, pathology and physicians in multiple specialties such as medical, surgical and radiation oncology.

This research was funded, in part, by NIH (P30 CA023100) and the Joan and Irwin Jacobs Fund.

Phase III CheckMate-816 trial: Opdivo + chemotherapy demonstrates improvement in pathologic CR in resectable NSCLC

The phase III CheckMate-816 trial met a primary endpoint of pathologic complete response in resectable non-small cell lung cancer.

In the trial, significantly more patients treated with Opdivo (nivolumab) plus chemotherapy before surgery showed no evidence of cancer cells in their resected tissue compared to those treated with chemotherapy alone. CheckMate-816 is the first and only phase III trial to demonstrate a benefit with an immune checkpoint inhibitor in combination with chemotherapy as a neoadjuvant treatment in non-metastatic NSCLC.

Opdivo is sponsored by Bristol Myers Squibb.

Patients in the experimental arm of the trial received up to three doses of Opdivo plus chemotherapy prior to surgery, a standard number of cycles of therapy in the neoadjuvant setting. The safety profile of Opdivo plus chemotherapy was consistent with previously reported studies in NSCLC.

Nivolumab has shown benefit as an adjuvant, or post-surgical, treatment option in other cancer types, and the positive results from CheckMate -816 speak to its potential in the neoadjuvant setting of resectable non-small cell lung cancer, Mark Awad, clinical director of Lowe Center for Thoracic Oncology at Dana-Farber Cancer Institute, said in a statement.

The CheckMate-816 trial is ongoing to assess the other primary endpoint of event-free survival, to which the company remains blinded, as well as key secondary endpoints.

In non-metastatic NSCLC, Bristol Myers Squibb and collaborators are exploring the use of immunotherapy in the neoadjuvant, adjuvant and peri-operative settings, as well as in association with chemoradiation. To date, Opdivo has shown improved efficacy in the neoadjuvant or adjuvant treatment of four tumor types: lung cancer, bladder cancer, esophageal/gastroesophageal junction cancer and melanoma.

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City of Hope leads novel clinical trial to treat cancer patients with COVID-19 - The Cancer Letter

Breeding the best in any type of livestock whether it be pedigree or commercial, sheep or cattle, requires a huge amount of determination, dedication and drive key features that come naturally to Laurencekirk-based Limousin breeder, Andrew Gammie and his wife Kathryn.

Passionate about the commercial, near dual purpose attributes of this beefy bovine, Andrew believes the Limousin is the breed for the future, when it can be finished in quicker period of time and to the desired weights demanded by the supermarkets with some of the highest killing out percentages.

Add to that the growing demand for young Limousin bull beef and he said producers are onto a winner when finishing such cattle not only bolsters end margins but also reduces greenhouse gas emissions.

Limousins are a great long-term option for the future because the females are so easy to keep and they produce fast growing calves that can either be sold for breeding or finishing, Andrew said.

An increasing number of butchers are now also looking for young bull beef too which is great for the breed as it adds another outlet. I can sell 13-14-month-old young bulls for 1400 at Carlisle and theyre all going for beef.

Andrew and Kathryn Gammie and young Finlay from Drumforber, Laurencekirk

It was Andrews grand-father George and father Jim Gammie, who established the Westpit pedigree Limousin herd at Drumforber in the early 1970s. At that time, the 480-acre unit was mostly home to 200 commercial cows, with an additional 1000 head of finishing cattle bought in every year for finishing off home-grown feeds.

It wasnt until Andrew returned home to farm in 2000 that he looked take the Limousin herd further.

Limousins have always appealed to me because we were brought up with them and because of their ease of management it doesnt cost anymore to keep a pedigree Limousin than a commercial cow, and breed the right ones, and the progeny can be worth so much more, he said.

Its a philosophy which is working a treat for team Gammie too as since Jim and Andrew bought 16 maiden heifers privately from Ian Nattress Greenwell herd in 2009, the Westpit herd has gone from strength to strength.

Most of these purchases were daughters of the French sires, Tanin and Vagabond, with one of the first bulls born, Westpit Fendt, selling for a colossal 15,500gns at Carlisle. He was bred from Greenwell Delight, which was served to Vagabond as a luckpenny before heading north to Drumforber.

It has nevertheless been the purchase of the 5800gns Brockhurst Holy, a Wilodge Vantastic daughter bought at Newark in 2015, that has bred the best to date for the herd.

Typical big stretchy cows and calves - just the type Andrew looks to breed

A daughter of the Grahams Samson show cow, Brockhurst Bolshoi, Holy has bred well in excess of 100,000 worth of bull sales. These include the 18,000gns Westpit Lowry sold at Carlisle to the Maraiscote herd; Westpit Nando, which was purchased privately by the Ronick herd for an undisclosed five-figure price and Westpit Omaha sold to Haltcliffe herd at last year's Royal Highland Show, again for an undisclosed sum.

Other notably bull sales from this top show winning female line include the two full brothers, Westpit Nevada and Westpit Nashville Dinmore Immense sons that sold at Carlisle in February 2019, for 14,000gns and 13,000gns. This years event also saw, Westpit Orlando, by Goldies Jackpot, sell for 12,000gns.

Ive always looked to breed big powerful easy fleshed square females, said Andrew who travelled down to Newark with his father specifically to buy Holy when she was bred from the show winning Brockhurst Bolshoi

I do like muscle but Im not a fan of double muscled females. I prefer to breed good big cows and then find a bull to suit them.

While foundation females from the Greenwell, Dinmore and Brockhurst herds have undoubtedly made their mark, the home-bred females now coming through, are also making their presence felt with Westpit Landlord, the first son of Jalex Itsallgood, a bull bought privately at the Highland Show, out of Westpit Finella, making 17,000gns in 2016.

Two years later, Westpit Macgregor, an AI son of Ampertaine Gigolo, bred from Westpit Florence realised 15,000gns and, at Carlisle in February, this year, Westpit Oklahoma, another by Itsallgood, out of Westpit Julie, made 13,000gns.

Westpit Julie one of the best breeding cows in the herd

Other top breeding bulls include Netherhall Double O Seven, purchased for 20,000gns which in turn has bred sons and daughters to 13,000gns and 10,000gns respectively.

Not afraid of modern technology either, Andrew has also exploited the herds genetic potential by introducing In-Vitro embryo Production (IVP), a cost effective and welfare friendly service from AB Europe.

This IVP process produces embryos from collected oocytes (unfertilised eggs) which are fertilised within a petri dish by selected semen, and subsequently cultured for seven days until fully developed embryos can be transferred or frozen.

A relatively new technique within the UK for producing embryos, it outcompetes MOET for its flexibility and multiple benefits to breeders and their donor animals, according to AB Europes vet Gavin Tait.

AB Europe currently offers two distinct IVP donor programmes dependent on the individual animal requirement and/or farmers preference, said Gavin.

The first programme is our non-stimulated system, where IVP donors are not subjected to any hormonal drugs or synchronisation prior to the collection of oocytes, which accordingly makes it the simpler, cheaper and less labour-intensive option.

The second is our stimulated system, which requires four injections prior to collection. Stimulation leads to a boost in oocyte quality on a given week sometimes it can improve number of oocytes too, however collection can only be done every fortnight and requires additional handling of the donor animal.

Jim and Andrew have seen huge success with the breeding system too.

Westpit Lioness, strength, depth, size, frame and femininity typical characteristics found in all the cattle

I could have continued to naturally expand the herd, however I became aware of In-Vitro embryo Production (IVP) as an alternative to MOET which has in fact put Westpit on the map, said Andrew.

IVP was preferred to MOET because no stimulation is required and the AB Europe team arrive on the farm to collect, whereas MOET requires multiple injections along with accompanying time, effort and cost.

Brockhurst Holy was the first female to undergo IVP, primarily as an insurance policy. We achieved 20 calves, including 18 bulls of which 16 sold to pedigree herds. Theyve also collected the silverware at both society shows and sales.

One of Holys IVP collections gave one heifer and four bulls which sold to average 12,000gns and they have secured both champion and reserve championships at 2019 Stars of the Future.

Last year AB Europe introduced IVP coasting featuring a programme with minimal stimulation. We achieved a better response in terms of embryos per collection, and it was much less invasive than MOET.

Andrew added: IVP and IVP coasting are enabling me to buy the best genetics I can. I select semen, anything from 50 to 1000 per straw to improve the herds genetic base selected for certain EBVs, according to accuracy, proven damline, breeding and showring success. One straw of semen can now cover up to five donors too.

AB Europe lines up an annual IVP programme with up to 10 cows; 2020 features five cows. Following collection, embryos are stored and implanted in commercial recipient cows and scheduled spring and autumn calving.

This years programme also features three, 12-month-old heifers. As long as they are cycling the process makes for a quicker turn around, speeding up genetic progress as well as spreading semen costs.

This year, we collected from one of Holys 12-month-old daughters, again as an insurance policy and a Sarkley heifer purchased from the Red Ladies sale of a similar age.

New to the herd from the Sarkley and Dinmore herds

Earlier this year we collected from 11 cows over two on-farm collections which resulted in 47 embryos. These fresh embryos went on to hold at around 70%, Andrew said, adding: If I have just one or two cows for collection, then Im finding its more cost effective to introduce them to AB Europes livery run by the companys vet, Gavin Tait on his farm in the Borders. It offers a safe and convenient environment. Communications are key for us farmers, and the team keeps us informed as to whats going on.

Its just as well too as with young Finlay fast approaching four years of age and Kathryn about to give birth to twins, Andrew is going to have his hands fuller than normal pretty soon. Add to that being elected on to the British Limousin Cattle Society Council as Scottish representative, and he's going to be busier than ever.

He does nevertheless have every confidence in the Limousin and the breeds potential to increase market share.

We have a fantastic product in the Limousin. What we need now is to get back to basics and create a level playing field for all members with increased communication to all members.

"With more promotion and support for all members, I am convinced the Limousin is the breed of the future, concluded Andrew.

Big, uniform, breedie cattle that are undoubtedly paying their way at Drumforber

Factfile

Farm business: Jim and Kate Gammie, son Andrew and his wife Kathryn

Livestock: 35 cow pedigree Westpit herd and 65 commercial breeding cows

Breeding policy: In-Vitro embryo Production (IVP) which has increased the genetic gain of the herd while also maximising potential sale returns.

Herd goal: Increase pedigree cow numbers at expense of commercial females with the introduction of Fleckviehs and Simmentals as recipient heifers.

Acreage: 100 acres grass and 380 acres spring barley

ONTHE spot

Biggest achievement? Establishing the herd, building it up to where it is today and selling bulls in to pedigree herds

Best investment? Brockhurst Holy a once in a lifetime cow

Where do you want to be in 2030? Hopefully building a successful business for the future generation and out of lockdown!

Best advice? Never stop learning and dont be afraid to ask questions

Biggest gripe? Kathryn says spending money!

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Andrew Gammie's Westpit Limousin herd makes its mark - The Scottish Farmer

Are you apprehensive about too much hair in your comb and shower, leading to a reduced hair volume and baldness? Does thinning of hair run in your family? Is hair loss a big concern for you? Is it messing with your confidence?

Then you are at the right spot. This article goes in-depth and discusses some key concepts linked to hair loss and technique to prevent it.

The Hair Growth Cycle

In order to achieve the desired hair length, some people either trim their hair regularly or leave them out to grow. Regardless, the hair growth cycle remains undisputed.

Your hair consists of a hair follicle and shaft. Present underneath the scalp, the hair follicle provides anchorage to the hair into the scalp. The hair shaft is the strand of hair made up of proteins. There are three phases of the hair growth cycle.

1. The Anagen Phase

The first phase is called the Anagen phase and corresponds to the growth period. During this phase, rapid cell division occurs in the hair follicles bulb, resulting in the growth of the hair strand. The hair length increases at the roots, with active growth for 2 to 7 years before the dormant period of the hair follicle is reached. During this period, the hair strand can lengthen from 18 to 30 inches long. The final length of the hair varies from individual to individual depending upon their genetic makeup, health, age, and other factors.

2. The Catagen Phase

The Catagen phase in the hair growth cycle is short and lasts for about 2 to 3 weeks. This is the transitional period during which the growth of hair stops, and it gets disconnected from the blood supply. This type of hair is called a club hair.

3. The Telogen Phase

The final stage of hair growth, the Telogen Phase, starts with a resting period and lasts for about 2 months. During this period, the club hair is in the resting phase, and new hair starts to grow beneath it.

Subsequently, the resting club hair falls out, letting the new hair strand to emerge from the scalp. This falling of hair is natural, usually doesnt get noticed, and thus shouldnt be alarming. The typical rate of hair shedding per day is 50 to 100 strands. Every hair strand undergoes the growth phase separately at different timings; thus, you wont notice hair loss in patches simultaneously.

What Is DHT?

Androgenic alopecia, also known as male or female pattern baldness, is a widespread cause behind male and female hair thinning. Although highly prevalent in women, it is more common in men. On average, around 30 million women and 50 million men in the U.S. suffer from this condition.

The phenomenon of alopecia is aggravated by the activity of sex hormones in the body, thereby called androgenic alopecia. One of the androgens responsible for this mechanism is Dihydrotestosterone (DHT), which brings about the development of male sex characteristics.

How Is DHT Produced In The Body?

DHT is produced in your body as a byproduct of the sex hormone, testosterone. 5-Reductase is the enzyme that breaks down about 10% of testosterone into DHT in tissues, including skin, prostate, liver, and hair follicles. While DHT results in body hair growth, it interestingly leads to loss of scalp hair faster and earlier in life. Consequently, blocking this androgen is what makes hair loss therapies effective in preventing hair fall.

How Does DHT Impact The Hair Follicles And Cause Miniaturization?

Researchhas shown that hair follicle miniaturization is the conversion of hair from terminal to vellus type. This process occurs at the follicular level when anagen to telogen ratio reduces, thereby increasing hair loss. It means that the anagen (growth) phases duration is reduced while the telogen phase is prolonged.

Male or female pattern hair loss occurs due to the shortening of the growth phase, which takes place with the miniaturization of the follicles. This signifies that hair cannot grow as long as it would have otherwise grown.

The anagen phase gradually narrows down so much that the new hair does not emerge from the scalp. Telogen hair type is poorly anchored in the scalp, allowing it to fall out easily.

The small-sized follicles lead to thinner hair shafts with each growth cycle. The hair eventually becomes vellus type soft and light hair type present on an infants body.

How Is DHT Blocked To Prevent Hair Loss?

Fortunately, the action of DHT can be blocked by compounds known as DHT blockers. DHT-blocking products include shampoos and oils containing DHT-blocking ingredients like biotin, saw palmetto, ketoconazole, etc. These agents decrease the production of the Alpha-5 Reductase enzyme, which then inhibits the formation of DHT. A combination of these active ingredients in shampoos and oils works by reducing the excess amount of DHT. Thus, it produces a favorable environment for hair growth.

Finasteride (generic name: Propecia) is also a proven DHT blocker. It is a prescription tablet that works well in preventing hair loss and receding hairlines. Finasteride binds to the 5-Reductase enzyme, leading to the inhibition of DHT production.

Using DHT-Blockers To Prevent Hair Loss

The phenomena of hair thinning in males and females occur due to numerous reasons, including underlying health conditions. However, genetics is the most significant factor in male and female pattern hair loss. DHT is another crucial player in causing male or female pattern baldness and must be blocked by using products containing proven DHT-blockers. For example, Hair Restoration Laboratories has a Hair Restore line of products that utilized what the company calls its DHT Halting Technology. Its lineup of shampoos, conditioner and serums contain a boatload of ingredients, such as saw palmetto, caffeine, green tea extract, pumpkin seed oil, and others that are clinically proven to help block DHT when applied topically. By helping to block DHT from attacking your hair follicles, male and female pattern hair loss can be prevented and your follicles can grow new and thicker hair.

In sum, if you wish to halt the progression of alopecia, you need to address and counter that adverse impact of DHT. If not kept in check, androgen alopecia will continue to progress and become worse with time.

References:

1. Ellis K. Hair growth cycle The 3 stages explained. The Hair Lab. (2018). https://www.growgorgeous.co.uk/blog/the-hair-lab/how-does-hair-grow/

2. Anonymous. (August 2020). Androgenetic alopecia. Genetics Home Reference. https://ghr.nlm.nih.gov/condition/androgenetic-alopecia

3. Jewell T. What You Need to Know About DHT and Hair Loss. (January 2019). Healthline. https://www.healthline.com/health/dht#purpose-and-function

4. Levy B. DHT and Male Hair Loss Explained. Hims. (September 2017). https://www.forhims.com/blog/dht-and-male-hair-loss-explained

5. Ravi A. The Best DHT Blockers & How They Can Combat Hair Loss. (July 2020). https://skinkraft.com/blogs/articles/what-is-dht

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Everything About Hair Loss & DHT - The Ritz Herald

Philip Patterson who is responsible for the day to day management of the herd with herdsman, Scott Cromwell, right

In recent years Philip Patterson has been responsible for the day to day running of the milking herd - he has always been keen to try new and innovative ways to manage the herd.

The 300 strong herd of Holsteins have been AI bred for the last four years using a mixture of proven and genomic sires from Genus ABS. Philip has taken the breeding policy a step further during the last 18 months, moving to a full Sexcel and beef strategy and employing a new herdsman to assist with the breeding of the cows, Scott Cromwell.

Sexcel is the name given to Genus ABSs proprietary technology for sexing bovine semen. This innovative technology does not subject the cells to the high pressures, electric currents and shear forces used to produce the sexed semen historically available to farmers. The result has been a superior sexed genetics product that has helped customers maximize their profitability in line with their individual economic herd goals.

Genus ABS have concentrated on developing a product with superior fertility. Data from UK RMS herds, based on 169,693 inseminations, has shown that the Relative Conception Rate (RCR) on maiden heifers is 92% and the improved performance from Sexcel is reaching as high as 94% in 3rd lactation cows. This data set has also shown that Sexcel has delivered up to a 92% skew rate, thats 92 female calves in every 100 born. So more pregnancies per service as well as more females per calving with Sexcel over any other sexed product.

Philip commented: I was keen to try Sexcel to minimise the number of low value Holstein bull calves using the very latest technology available. I started using it in February 2019 and have been extremely pleased with the results. The conception rates have been similar to what we were achieving with conventional semen.

Although the beef income will be important, the British Blue sires are selected to ensure that the cows calve down successfully and start milking well, so particular attention is paid to calving ease when selecting beef bulls.

Gareth Bell, Genus ABS, who works closely with Phillip said: We are aiming to create cows that are well balanced with a willingness to produce high volumes of milk. PLI is followed closely and with Genus having 20 of the top 30 PLI sires, there are lots of options when it comes to choosing sires that will leave more profit in the herd.

The Pattersons herd also uses Genus ABS to help with the day to day management of the herd, through the ABS Partner programme. Action lists are created on a weekly basis to aid with dry offs and also any fertility work carried out. These reports are then used by Scott to monitor the herds reproductive performance and highlight any areas that need attention.

The management reports have helped us become more structured in our approach to fertility. We can see the benefits of the improvements we have made, including increasing the herds overall conception rate and reducing the calving interval, said Scott.

For more information on Sexcel or other Genus ABS products please contact your local Genus ABS representative or the office on 028 38 334426.

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Sexcel The basis of a new plan! - Farming Life

Its this time of the year when those of us in northern temperate zones are spectators of a fascinating natural phenomenon the appearance of autumn leaf colors.

The leaves start to change colors as they age, or senesce. During this period a cluster of enzymes in the leaves start chewing up their green pigment, called chlorophyll. As the leaves become less green, their red, yellow, and orange pigments (known as anthocyanins and carotenes) begin to shine. However, exactly how chlorophyll breakdown works is still only partially understood.

While autumn leaves are a great example of chlorophyll breakdown, evergreen plants (those that remain green all year long), vegetables, and fruits also experience chlorophyll decay. However, this happens only under special conditions such when fruit ripen or when evergreen plants are deprived of nutrients and water.

Banana skin is one of the few fruits where chlorophyll degradation can be mapped under ultraviolet (UV) light. As bananas ripen, their skins lose their green color a sign of chlorophyll breakdown and form new pigments that fluoresce blue under the UV light. Scientists know that this new pigment, known as hypermodified fluorescent chlorophyll catabolite (hmFCC), is produced very briefly in most plants. Banana skins and grapevine leaves are known to produce hmFCCs for a longer period.

Recently scientists at Instituto de la Grasa, Spain analyzed devils ivy, an evergreen plant, in their quest to find signs of this fluorescent compound. They activated the aging process by starving the plant, and voila! Exposure to UV light produced the blue, fluorescent pigment hmFCC. The team also observed two other newly identified compounds that will provide more insights into the evergreen chlorophyll breakdown puzzle.

Although the actual benefit of producing this blue, fluorescent compound is still a mystery, scientists think that it could provide protection against radiation or function in communication between animals and plants.

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Scientists use 16 genes to distinguish between two types of lethal pancreatic cancer - Massive Science

Its one of the most important genes in biology: Sry, the gene that makes males male. Development of the sexes is a crucial step in sexual reproduction and is essential for the survival of almost all animal species.

Today in the journal Science, my international collaborators and I report the surprise discovery of an entirely new part of the Sry gene in mice a part we had no idea existed.

I co-discovered Sry in 1990. It is the gene on the Y (male) chromosome that leads to the development of male characteristics in mice, humans and most other mammals. Since then, Sry has been the subject of intense study worldwide because of its fundamental role in mammalian biology.

We have come to understand, in some detail, how Sry acts to trigger a cascade of gene activity that results in the formation of testes, instead of ovaries, in the embryo. Testes then stimulate the formation of other male characteristics.

But its clear we dont have all the answers just yet. Our results published today take us one step further in the right direction.

For 30 years, we have understood the Sry gene is made up of one exon, a segment of a gene used to code for amino acids, the building blocks of proteins. This can be compared to a computer file consisting of one contiguous block of data, on a hard disk.

Our newest research reveals theres actually a second exon in mouse Sry. This is like finding a whole new separate block of previously hidden data.

The mouse genome, like the human genome, has been extensively characterised due to the availability of advanced DNA sequencing and related technologies. Researchers commonly assume all the genes and all the parts of the genes have already been discovered.

But earlier this year, scientists in Japan uncovered what looked like a new piece of the Sry gene in mice. New sequencing approaches revealed what appeared to be two versions of Sry: a short, single-exon form and a longer, two-exon form. They called this two-exon version Sry-T.

They collaborated with my group at the University of Queensland and removed the new exon using CRISPR, a gene editing tool that lets researchers alter DNA precisely. Together we discovered this prevented Sry from functioning: XY mice (which would normally develop as males) developed as females instead.

Conversely, adding Sry-T to fertilised XX mouse eggs (which would normally develop as females) resulted in males.

On the left, an XY mouse lacking Sry-T that developed as female. On the right, an XX mouse carrying the Sry-T gene that developed as male. Makoto Tachibana, Osaka University, Author provided

Importantly, although human Sry does not have the added exon, our discovery may reveal new functions that might be shared between mouse and human Sry.

The DNA sequence of the new exon in Sry-T may point us towards discovering some of the genes and proteins that interact with Sry, something that has been elusive up till now.

And interactions we find in mice may also occur in humans. Studying what human Sry interacts with may help explain some cases of differences in human sex development, otherwise known as intersex development. This is a common but poorly understood group of mostly genetic conditions that arise in humans.

Intersex refers to people who are born with genetic, hormonal or physical sex characteristics that are not typically male or female. Shutterstock

Currently, we dont know the genetics behind a large proportion of intersex conditions. This is partly because we dont yet know all the genes involved in the human sex development pathway.

Scientifically, this discovery is a bit like discovering a new cell type in the body, or a new asteroid in the Kuiper belt. As with many scientific discoveries, it challenges what we thought we knew and raises many questions.

What is the function of the new exon in Sry-T?

Currently, we only have part of the answer. It turns out the first exon of Sry, the one we already knew about, contains instability sequences at its end. These are sequences that cause proteins to fray and degrade.

An important function of the newly discovered second exon is to mask the instability sequences, seal the end of the Sry protein and prevent it from degrading. In other words, this second exon is crucial to the development of male babies.

Whats more, this protection mechanism represents an unusual and intriguing evolutionary mechanism that has acted to help stop vulnerable Y-chromosome genes from literally falling apart.

But its early days yet. The challenge now is to understand whether there are more functions hidden within the newly discovered exon.

If so, this information may provide some of the missing links that have stood in the way of our full understanding of how Sry works at a molecular level and of how males and females come to be.

Peter Koopman, Professorial Research Fellow, The University of Queensland

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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We Discovered a Missing Gene Fragment Thats Shedding New Light on How Males Develop - Gizmodo Australia

Just as scientists are rapidly learning how SARS-CoV-2 affects humans, they are also quickly working to understand how it affects other animals. House cats, tigers, golden hamsters, and rhesus monkeys are all susceptible to SARS-CoV-2 infection. And while avian species such as duck and chicken are not, dogs, pigs, and ferrets have shown intermediate susceptibility.

The critical entry point for the virus into our cells is a protein called ACE2, which bonds withthe spike protein of SARS-CoV-2.Animals and humans both expressing ACE2 in their cells, so scientists have been wondering why different species have different SARS-CoV-2 susceptibility, and if it is possible to predict which animals might be at risk.

In a preprint posted on bioRxiv in July, researchers at Vanderbilt Universityapproached this question by comparing the amino acid sequence of ACE2 from different animal species. Amino acids are compounds that combine to form proteins. Inside cells, this amino acid chain folds into a three-dimensional shape. And as a result, some amino acids become hidden, and others exposed. Exposed ACE2 amino acids are of great interest because they determine whether SARS-CoV-2 can attach to the cell.

Using computer models, researchers identified amino acids in ACE2 that showed strong interactions with SARS-CoV-2. They observed that in non-susceptible animal species, these amino acids were often different, ultimately disrupting the attachment between the ACE2 protein and the spike protein of SARS-CoV-2. This allowed the researchers to make predictions about which animals species are possibly at risk of infection. They estimated that while horses and camels would be vulnerable to infection, cows, goats, and Malayan pangolins would present intermediate susceptibility.

In August, another preprint fromresearchers at Dalhousie University in Nova Scotiaexamined whether marine wildlife are susceptible to the virus. Using similar modeling methods, these researchers concluded that whales, dolphins, seals, and otters would be susceptible to SARS-CoV-2. They suggest that exposure could happen through contaminated sewage entering the sea.

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Lactose tolerance spread through Europe faster than previously thought - Massive Science

Just as scientists are rapidly learning how SARS-CoV-2 affects humans, they are also quickly working to understand how it affects other animals. House cats, tigers, golden hamsters, and rhesus monkeys are all susceptible to SARS-CoV-2 infection. And while avian species such as duck and chicken are not, dogs, pigs, and ferrets have shown intermediate susceptibility.

The critical entry point for the virus into our cells is a protein called ACE2, which bonds withthe spike protein of SARS-CoV-2.Animals and humans both expressing ACE2 in their cells, so scientists have been wondering why different species have different SARS-CoV-2 susceptibility, and if it is possible to predict which animals might be at risk.

In a preprint posted on bioRxiv in July, researchers at Vanderbilt Universityapproached this question by comparing the amino acid sequence of ACE2 from different animal species. Amino acids are compounds that combine to form proteins. Inside cells, this amino acid chain folds into a three-dimensional shape. And as a result, some amino acids become hidden, and others exposed. Exposed ACE2 amino acids are of great interest because they determine whether SARS-CoV-2 can attach to the cell.

Using computer models, researchers identified amino acids in ACE2 that showed strong interactions with SARS-CoV-2. They observed that in non-susceptible animal species, these amino acids were often different, ultimately disrupting the attachment between the ACE2 protein and the spike protein of SARS-CoV-2. This allowed the researchers to make predictions about which animals species are possibly at risk of infection. They estimated that while horses and camels would be vulnerable to infection, cows, goats, and Malayan pangolins would present intermediate susceptibility.

In August, another preprint fromresearchers at Dalhousie University in Nova Scotiaexamined whether marine wildlife are susceptible to the virus. Using similar modeling methods, these researchers concluded that whales, dolphins, seals, and otters would be susceptible to SARS-CoV-2. They suggest that exposure could happen through contaminated sewage entering the sea.

See original here:
DNA found in caterpillar guts points to what they are eating - Massive Science

Just as scientists are rapidly learning how SARS-CoV-2 affects humans, they are also quickly working to understand how it affects other animals. House cats, tigers, golden hamsters, and rhesus monkeys are all susceptible to SARS-CoV-2 infection. And while avian species such as duck and chicken are not, dogs, pigs, and ferrets have shown intermediate susceptibility.

The critical entry point for the virus into our cells is a protein called ACE2, which bonds withthe spike protein of SARS-CoV-2.Animals and humans both expressing ACE2 in their cells, so scientists have been wondering why different species have different SARS-CoV-2 susceptibility, and if it is possible to predict which animals might be at risk.

In a preprint posted on bioRxiv in July, researchers at Vanderbilt Universityapproached this question by comparing the amino acid sequence of ACE2 from different animal species. Amino acids are compounds that combine to form proteins. Inside cells, this amino acid chain folds into a three-dimensional shape. And as a result, some amino acids become hidden, and others exposed. Exposed ACE2 amino acids are of great interest because they determine whether SARS-CoV-2 can attach to the cell.

Using computer models, researchers identified amino acids in ACE2 that showed strong interactions with SARS-CoV-2. They observed that in non-susceptible animal species, these amino acids were often different, ultimately disrupting the attachment between the ACE2 protein and the spike protein of SARS-CoV-2. This allowed the researchers to make predictions about which animals species are possibly at risk of infection. They estimated that while horses and camels would be vulnerable to infection, cows, goats, and Malayan pangolins would present intermediate susceptibility.

In August, another preprint fromresearchers at Dalhousie University in Nova Scotiaexamined whether marine wildlife are susceptible to the virus. Using similar modeling methods, these researchers concluded that whales, dolphins, seals, and otters would be susceptible to SARS-CoV-2. They suggest that exposure could happen through contaminated sewage entering the sea.

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What is the COVID-19 polyclonal antibody treatment that President Trump took? - Massive Science

October 03, 2020

STATE COLLEGE, Penn. As Americans hunker down to weather the pandemic this winter at home, nearly every facet of life will remain upended to safeguard against the coronavirus.

Accuweathers team of long-range forecasters, led by Senior Meteorologist Paul Pastelok, released its annual predictions for the upcoming winter season this week. The team has been analyzing global weather patterns and various weather models to project what conditions will unfold across the lower 48 United States this winter, which arrives Dec. 21. Much of the time the setup will be driven by one key factor: La Nia.

La Nia is a phenomenon in which the surface water near the equator of the Pacific Ocean is cooler than normal, the opposite of El Nio when the water in the equatorial Pacific is in a warm phase. This change in the water temperature can have a major influence on the weather patterns all around the globe. According to NOAAs Climate Prediction Center, La Nia officially developed by early September and is forecast to continue through the winter months.

The ongoing La Nia is projected to bring weather conditions similar to what meteorologists expect across the country during a typical La Nia pattern, but there may be a few subtle differences, Pastelok said.

Southeast

The first part of the winter may be the coldest for the southeastern U.S., as a brief shot or two of cold air has the potential to rush down from the north all the way to the Gulf Coast.

Early cold may take a run at the eastern U.S. if snow lays in the Ohio Valley and parts of the Tennessee Valley in December, Pastelok said.

Atlanta, Huntsville, Alabama, Greenville, South Carolina, and Charlotte and Raleigh, North Carolina, could all be hit by a cold snap to kick off the season. Even Floridians may want to make sure to dig out heavier coats from the closet sooner rather than later.

There is a small chance for an early season frost in northern and central Florida perhaps impacting the citrus crop, Pastelok added.

Temperatures are projected to rebound as the season carries on, paving the way for much warmer conditions through the balance of the winter.

Near-record warmth [is predicted] at times in the Southeast, occasionally extending into the mid-Atlantic, Pastelok said.

This extended warmth will be good news for restaurants across the region that have added outdoor seating areas because of the coronavirus pandemic, and could perhaps allow them to utilize the extra space even during the winter months.

Restaurants that do have outdoor seating should still keep a close eye on the weather forecast, not just for temperatures, but also for disruptive storms, especially during the first few weeks of 2021.

Severe thunderstorms may occur more than usual from the central Gulf Coast to the Southeast in late January and February, Pastelok said.

Northeast, Midwest

The winter of 2019-2020 was tame across much of the northeastern U.S. with only a handful of Arctic outbreaks and very little snow to speak of along the Interstate 95 corridor and the upcoming winter could bring some echoes of last winter.

Another overall mild winter is possible for much of the eastern U.S., Pastelok said, referring to how temperatures will compare to the 30-year averages in many places. However, he expects near-normal snowfall across much of New England.

However, the entire season will not be mild all the way through. Instead, the season will be bookended by cold and snowy conditions with a pause in the wintry weather in the middle of the season.

The first waves of chilly Arctic air will set off rounds of lake-effect snow downwind of the Great Lakes and bring opportunities for snow in some of the bigger cities across the region heading into the holiday season.

There is a good chance for a white Christmas in Chicago, perhaps around 30-35% chance at this point, Pastelok said. For Pittsburgh, much of the lake-effect snow could fall north of the city and it may be tough to keep snow on the ground. But from this far out I give a 15-20% chance for a white Christmas in Pittsburgh, but, still, there is a chance.

Plains, Rocky Mountains

The central U.S. experienced a taste of winter as soon as autumn arrived. Meteorological fall began on the first day of September, and just one week later, a winter-like storm dove down across the Plains and northern Rockies, causing temperatures to tumble and delivering snow to the Rockies and some of the foothills.

The middle of the nation may go through some big swings in temperatures, [and] dry and active periods, Pastelok said. Periods of subzero cold can drive south down the Front Range of the Rockies, the central and western Plains.

Snow will be a prominent feature during these big swings, especially over the northern Rockies and into parts of Colorado, which will be beneficial for ski resorts across the region.

There is also the chance for some frequent snowfall in the northern Plains in parts of Nebraska, Iowa, North Dakota, South Dakota, and Minnesota.

Farther south, the chances for snow will be lower, including part of the southern Plains, the southern Rockies and westward into the Four Corners.

Meanwhile, the central Plains will be in the battleground zone, swinging from bitterly cold conditions to spells of milder weather and then back again in less than a weeks time.

West Coast

Autumn may feel shorter this year across the Pacific Northwest as wintry weather makes an early entrance across the region.

Mountain snow and stormy conditions may arrive in late fall for the Northwest, northern California and northern Rockies, Pastelok said.

Even the Interstate 5 corridor from Medford, Oregon, through Seattle will have several opportunities for accumulating snowfall, potentially even before 2020 draws to a close.

The waves of storms throughout the upcoming months will help to ease the drought conditions across the region, especially in Oregon where more than 60% of the state is in severe drought and over 30% is in an extreme drought.

More importantly, the early arrival of winter storms will spell the conclusion to a historic wildfire season that has charred millions of acres across Washington, Oregon and California.

However, after the flames have smoldered, heavy rains could pose an added danger in the burn scars left behind by the fires, especially in the mountainous terrain.

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RCC partners with Upswing to provide increased academic support services - The Robesonian

Oct 3rd 2020

IN 1981 PETER and Rosemary Grant, a husband-and-wife team of evolutionary biologists, spotted something odd on Daphne Major. Every year for the previous decade they had travelled from Princeton University to this island in the Galpagos, to study its three endemic tanager species, part of a group known colloquially as Darwins finches. On this occasion their eyes were drawn to an unusual male that sported dark feathers and sang a unique song. Genetic analysis later identified him as a large cactus finch, probably blown in from Espaola, another part of the archipelago that is over 100km away.

Intrigued, the Grants followed the castaway as he explored his new home. They watched him mate with a local female medium ground finch. That produced five fit, healthy offspring. Those offspring were also surprisingly sexually selective. A single male excepted, they and their descendants mated only among themselvesand they have continued to do so ever since.

Despite this heavy inbreeding, the hybrids (two of which are pictured above) have been successful. They have carved out a niche in which they use their size and their deep beaks to exploit the large woody fruits of the Jamaican feverplant, which grows locally. They have, to all intents and purposes, become another species of Darwin finch, of which 13 were previously recognised. Though they do not yet have a Latinised scientific name, they are known to all as the Big Bird lineage.

This story would once have been considered deeply implausible. Evolutions orthodox narrative does not suggest that hybridisation is how new animal species emerge. But, as genetic testing has proliferated, biologists have been confronted with an unexpected fact. Hybrids are not an evolutionary bug. They are a feature.

That knowledge is changing the way people think about evolution. The neat family trees envisaged by Charles Darwin in one of his early notebooks (see picture below) are turning into webs, and the primacy of mutation in generating the variation which natural selection then winnows is being challenged. The influx of genes accompanying hybridisation creates such variation tooand the harder people look, the more important that seems to get. Hybridisation also offers shortcuts on the long march to speciation that do not depend on natural selection at all. As the example of the Big Bird lineage shows, instead of taking millennia to emerge, a new species can appear almost overnight.

In truth, all this had already been recognised for simple organisms like bacteria. These exchange genes promiscuously between both more and less related individuals. But bacteria were unknown when Darwin came up with natural selection, and, ever since then, the subject of speciation has been dominated by examples drawn from animals and plants. To recognise that what is true for bacteria is also true for these multicellular organisms has profound implications, not least for how human beings understand their own origins. It seems appropriate, then, that the birds whose diversity helped inspire Darwin still have evolutionary tales to tell.

The conventional view of evolution is that mutations happen at random. Maladaptive ones are then eliminated by competitive pressure while adaptive ones proliferate. The result, over long periods of time and assisted by populations sometimes being split up by external circumstances, is change which eventually crystallises into new and separate species.

That process does leave the door open to hybrids. The genomes of closely related species may remain sufficiently similar to produce viable offspring. But these genes often fit together less well than those of parents from the same species. As a consequence, even viable hybrids are frequently infertile (think mules) and are also at higher risk of developmental and other types of illnesses. In fact, infertility in male hybrids is so common that it has a nameHaldanes rule. This sort of thing was enough to persuade most of Darwins 20th-century disciples that the need to avoid hybridisation was actually a driving force which caused natural selection to erect reproductive barriers between incipient species, and thus encouraged speciation.

There is, though, another way of looking at hybridisation. Mixing the traits of two parent species might actually leave their hybrid offspring better off. This is called hybrid vigour, or heterosis. The interplay of two species genes can even produce traits displayed by neither parent. This is known as transgressive segregation and the resulting hybrid may be surprisingly well adapted to a completely new niche, as was the case with the Big Birds.

Both the maleficent and beneficent effects of hybridisation are real. The question is, which wins out more often in practice? In plants, it is frequently the beneficent. This is a consequence of plants unusually malleable genetics. The nuclear genomes of complex organisms (animals, plants, fungi and single-celled organisms such as amoebae) are divided into bundles of DNA called chromosomes. Such organisms are generally either haploid or diploid, meaning that each cell nucleus contains either one or two copies of every chromosome. Human beings are diploid. They have 23 chromosomal pairs, for a total of 46 individual chromosomes. But there are exceptions. Plants, for instance, are frequently polyploidmeaning that each nucleus contains copies in greater multiples than two. To take one example, Californian coastal redwoods have six copies. Since redwood cell nuclei have 11 distinct types of chromosome, they host a total of 66 chromosomes altogether.

Sometimes, polyploidy is a result of an organisms genome spontaneously doubling. Often, though, it is a consequence of hybridisation, with the chromosomes of both parents ending up in a single nucleus. However it arises, polyploidy provides spare copies of genes for natural selection to work on while other versions of them continue with their original function. And if it is also the result of hybridisation, it brings the additional possibilities of heterosis and transgressive segregation.

On top of this, by changing an organisms chromosome count polyploidy has another pertinent effect. It creates an instant barrier to breeding with either parent species. That gives a new, incipient species a chance to establish itself without being reabsorbed into one of the parental populations. The results can be spectacular. Recent evidence suggests, for example, that hybridisation between two plant species in the distant past, followed by a simple doubling of the number of chromosomes in their offspring, may be responsible for much of the extraordinary diversity in flowering plants that is seen today.

Plants seem to be easy beneficiaries of hybridisation. For many animals, howeverand for mammals in particularextra chromosomes serve not to enhance things, but to disrupt them. Why, is not completely clear. Cell division in animals seems more easily confounded by superfluous chromosomes than it is in plants, so this may be a factor. Plants also have simpler cells, which are more able to accommodate extra chromosomes. Whatever the details, animal hybrids appear to feel the effects of genetic incompatibility far more acutely than do plants, and are therefore less able to benefit from heterosis. Evolutionary biologists therefore assumed for a long time that hybridisation played a negligible role in animal evolutionand there was little evidence to suggest otherwise.

Advances in DNA sequencing have changed that by letting people look under the bonnet of evolutionary history. This has uncovered a steady trickle of animals breathed into life entirely by hybrid speciation. They include some familiar names. The European bison, for instance, is the result of hybridisation, over 120,000 years ago, between two now extinct speciesthe ice-age steppe bison and the auroch. The latter were the wild antecedents of modern domestic cattle, and survived in Jaktorow Forest, in Poland, until 1627.

Something similar is true of the Atlantic Clymene dolphin. Genetic analysis has revealed that this cetacean, which roams the briny between west Africa, Brazil and the Gulf of Mexico, owes its existence to a hybridisation that happened between two globe-trotting others, the striped dolphin and the spinner dolphin.

At least one hybrid animal, moreover, traces its ancestry to three species. Genetic analysis shows that Artibeus schwartzi, a Caribbean fruit bat, is a result of hybridisation, within the past 30,000 years, of the Jamaican fruit bat (Artibeus jamaicensis), the South American flat-faced fruit-eating bat (Artibeus planirostris) and a third, as yet unidentified animal, which researchers speculate may now be extinct.

It also appears that, as in the case of flowering plants, hybridisation can fuel explosive radiations of novel animals. The best-known example is the case of the cichlids of Africas Great Lakesparticularly Lake Victoria, Lake Tanganyika and Lake Malawi. Great Lake cichlids are a group of thousands of closely related fish, famous for their panoply of shapes, sizes and colours (see picture). Each is adapted to a different depth and ecological niche.

Cichlids evolutionary history has long puzzled biologists. Lake Victoria, in particular, comes and goes with the climate. Its current instantiation is less than 15,000 years old. In evolutionary terms this is the blink of an eye, but in that time the lakes cichlids have diversified into more than 500 species.

The reason is hybridisation. Using genetic analysis to place Lake Victorias cichlids within the broader cichlid family tree, researchers have discovered that they descend from a tryst between two distinct parental lineages, one that swam in the Congo and the other in the Nile.

The value of being such a genetic mosaic is apparent from the history of one of the best-studied cichlid genes, which encodes a protein called long-wave-sensitive opsin that is found in the retina of the eye. This protein determines the eyes sensitivity to red light. That matters because red-light levels decline steeply in deeper water. Consequently, fish which live at different depths need eyes that are tuned differently from one another.

The cichlid lineage from the Congo had eyes which were optimised for clear, shallow water. Nile-lineage vision was more attuned to the deep and murky. Hybrids were able to chop and change these genetic variants to produce a range of sensitivities to light. This let them colonise the full depth of the water column in Lake Victoria as it developed. The new lake, for its part, offered the cichlids a host of empty ecological niches to fill. The result was a sudden and explosive process dubbed combinatorial speciation.

Elsewhere in the natural world, combinatorial speciation seems to have contributed to the striking diversity of Sporophila, a genus of 41 Neotropical songbirds, and of the munias, mannikins and silverbills of the genus Lonchura, a group of 31 estrildid finches that ranges across Africa and South-East Asia. Nor is it just in vertebrates that this phenomenon rears its head. Heliconius, a genus of 39 flamboyant New World butterflies, also owes its eye-catching diversity to combinatorial speciation.

These findings muddy Darwins concept of speciation as a slow and gradual process. Biologists now know that in the right circumstances, and with the help of hybridisation, new species can emerge and consolidate themselves in a mere handful of generations. That is an important amendment to evolutionary theory.

It is nevertheless true that, for animals, hybrid speciation in its full form remains rare. It requires an unlikely congruence of factors to keep a new hybrid population reproductively isolated from both parental species. The survival of the Galpagos Big Bird lineage, for example, involved physical isolation from one and strong sexual selection against the other.

More commonly, an incipient hybrid population is reabsorbed by one or both parental species before it can properly establish itself. The result is a percolation of genes from one species to another, rather than a full hybrid. This is called introgressive hybridisationor, simply, introgression. DNA analysis of a long list of closely related animals shows that this version of hybridisation is far more common than the full form. It may even be ubiquitous.

The North American grey wolf, for example, owes its gene for melanismthe deep black fur displayed by some wolvesto introgression from domesticated dogs brought 14,000 years ago from Asia by Americas first human settlers. In wolves that inhabit forests this gene has undergone strong positive selection, suggesting it is adaptive. The most obvious explanation is that melanism provides better camouflage in the stygian depths of North Americas woodlands. Alternatively, female wolves may simply prefer their males tall, dark and handsome.

Pantherathe genus to which most big cats belongis yet more impressive in the scope of its introgressive entanglement. It has five members: lions, tigers, leopards, snow leopards and jaguars. These have long been known to interbreed successfully in captivity, yielding crosses called ligers (lion x tiger), jaglions (jaguar x lion) and so on. But recent analysis shows that this has also happened in the wild. Researchers have identified at least six past introgressive episodes in the genus, with every member involved in at least one of them.

The most promiscuous of the five appears to be the lion. Gene variants have percolated between lions and tigers, lions and snow leopards, and lions and jaguars. There is also evidence that at least some of this gene flow has been adaptive. Three lion genes incorporated into jaguar genomes are known to have been strongly selected for. Two of these are involved in visionspecifically, they help guide the development of the optic nerve.

Genetic analysis also reveals a long history of hybridisation between polar bears and grizzlies, the largest of their brown bear cousins. It is not yet clear whether this has had adaptive valuebut it may soon have a chance to prove itself. As climate change warms the polar bears Arctic home, the species may have to adjust rapidly. A splash of grizzly, a group used to more temperate climes, might help that happen.

The best-studied case of introgression in animals is, though, closer to home than wolves, big cats and bears. It is looking back at you from the mirror. The most up-to-date evidence suggests that Homo sapiens arose more than 315,000 years ago from gene flow between a series of interlinked population groups spread across Africa. Whether these populations were different enough to be considered distinct species is still debated. In the grasslands of the African Pleistocene, however, these ancestral groups were not alone. Their world was interspersed with a menagerie of other hominins. And interspecies mating seems to have been rife.

Several members of this human menagerie appear to have descended from Homo heidelbergensis, a species that spread through eastern and southern Africa around 700,000 years ago before crossing the Middle East into Europe and Asia. This speciesa possible ancestor of the progenitor groups of Homo sapiensalso gave rise to at least two others, the Neanderthals (Homo neanderthalensis) and the Denisovans (Homo denisova). The former survived in Europe until 28,000 years ago, while the latter, an Asiatic group, lasted until roughly 50,000 years ago.

Other hominin species around at the time emerged directly from Homo erectus, a more primitive creature that was also the ancestor of Homo heidelbergensis and which, a million years beforehand, had blazed a similar transcontinental expansionary path to that of heidelbergensis. The local descendants of erectus were largely displaced by heidelbergensis when it arrived. But some holdouts survived in corners of the Old World that heidelbergensis never reached. These included the islands of Flores in Indonesia and Luzon in the Philippines. It was here that diminutive Homo floresiensis and Homo luzonensisthe island hobbitslasted, like the Denisovans, until 50,000 years ago. There were probably isolated descendants of even older cousins too. At least one is known, Homo naledi, which predated the emergence of Homo erectus and still roamed southern Africa around 230,000 years ago.

This grand hominin circus ultimately came to an abrupt end. The record in Africa is opaque. But in Europe, Asia and Oceania it is clear that the arrival of modern humans coincided with a great vanishing of local hominins. Whether through disease, competition for scarce resources or perhaps even genocide, a few thousand years of contact with Homo sapiens was enough to snuff out every other hominin species.

Even a few millennia, though, proved enough for Homo sapiens to get to know its cousins intimately. The record of these romantic entanglements remains in the DNA of almost everyone alive today. In 2010 a team led by Svante Pbo of the Max Planck Institutes campus in Leipzig published the first draft sequence of the Neanderthal genome. This led to the discovery that stretches of Neanderthal DNA constitute 1-4% of the modern human genome in all populations outside sub-Saharan Africa. That is consistent with a string of hybridising liaisons in Europe, the Middle East and Central Asia from around 65,000 years ago.

Neanderthal inheritance helped Homo sapiens adapt to the demands of the environments of these unfamiliar places. There seems to have been strong selection, for example, in favour of Neanderthal genes related to skin and hair growth. These include bnc 2, a gene linked to skin pigment and freckling that is still present in two-thirds of Europeans. There also appears to have been selection for Neanderthal-derived genes that deal with pathogens. Some govern the immune systems ability to detect bacterial infections. Others encode proteins which interact with viruses.

The Denisovans, and their contribution to Homo sapiens, were another of Dr Pbos discoveries. In 2009 one of his team sequenced DNA from a fossil finger bone excavated from Denisova cave in the Altai Mountains of Siberia. This bone turned out to belong to a previously unknown species that was then named after the cave it was found in. Physical specimens of this species remain rare. Examination of living people, however, reveals that stretches of Denisovan DNA make up 3-6% of the genome of contemporary Papuans, Aboriginal Australians and Melanesians. Many Chinese and Japanese also carry Denisovan DNA, albeit at lower rates.

As with Neanderthals, this inheritance has brought advantages. The Denisovan version of a gene called epas1 modulates production of red blood cells, which carry oxygen. This helps modern Tibetans to survive at high altitudes. Denisovan tbx 15 and wars 2 similarly help Inuit survive the harsh cold of the Arctic by regulating the amount of metabolic heat they produce.

That the Denisovans could lurk in modern human DNA yet leave so little fossil trace has caused geneticists to wonder what other ghosts they might find. The genomes of sub-Saharan Africans, in particular, reveal evidence of at least one further entanglement. In 2012 a genomic analysis of members of the Baka, Hadza and Sandawe, three groups of people of ancient lineage, suggested an archaic introgression. In 2016 a deeper analysis focused on the Baka pinpointed this to within the past 30,000 years. This February, a study of members of two other groups, the Yoruba and Mende, confirmed that between 2% and 19% of their genomes can be traced to an unidentified archaic species. Whether this is the same as the one which has contributed to the Baka, Hadza and Sandawe is unclear, but it appears to have diverged from the line leading directly to Homo sapiens not long before the Neanderthals and Denisovansan African Neanderthal, if you will.

The same genetic tools have revealed deeper ghosts, too. Denisovans show signs of hybridisation with a superarchaic lineageperhaps Homo erectus itself. This makes up 1% of the species genome. About 15% of this superarchaic inheritance has, in turn, been passed on to modern humans. There is even evidence of a minute genetic contribution to African populations by a similarly superarchaic relative.

To be human, then, is to be a multispecies mongrel. As the example of the big cats in particular shows, though, Homo sapiens is not, in this, an exception. Hybridisation, once seen as a spear-carrier in evolutions grand theatre, is rapidly becoming a star of the show. Meanwhile, Darwins idea of a simple, universal family tree is relegated to the wings.

In its place, some experts now prefer the idea of a tangled bush of interconnected branches. But this, too, is an imperfect comparison. A more fitting analogy is a frayed rope. Species are braided from individual strands. Where evolution proceeds in an orthodox Darwinian manner, braids unravel, strands split and new species result. But the rope does not fray neatly. Filaments of introgression criss-cross from braid to braid and, occasionally, two tangle to form a new braid altogether. This is a more complex conception of evolutionary history, but also a richer one. Few things in life are simplewhy should life itself be?

This article appeared in the Science & technology section of the print edition under the headline "Match and mix"

Link:
How hybrids have upturned evolutionary theory - The Economist

Rita Colwell in 2011. Photo: Chaman Sond/Wikimedia Commons, CC BY-SA 4.0.

From flipping through my brothers chemistry book, drawing chemical bonds on walls to doing lab experiments and getting a trinitrotoluene tattoo on my leg my love for chemistry is a famous fact among family and friends. Sadly, I gave up on that love quite early in my life when my father tried to get me to become a gynaecologist.

Anguished, I gravitated towards the social sciences instead, subsequently giving rise to my interest in science and feminism. I found here a sense of self-gratification, regret and hope in unravelling the lives of women scientists, their struggles and accomplishments.

When I started reading A Lab of Ones Own, dj vu crept in; I was reminded of books like Hypatias Heritage by Margaret Alic, various biographies of Rosalind Franklin, Barbara McClintock and other women scientists and of course stories about the likes of Anna Mani in India. Even though they lived through different times, cultures and contexts, gender-based discrimination was so common in their lives that it was both the norm and the normal.

Even today, this is true. However, as A Lab of Ones Own asks, how can we keep the wheels turning? After reading the book, it became clear to me that it is more than a biography of Rita Colwell the scientist, science administrator, policymaker and entrepreneur. The book, written by Colwell and Sharon Bertsch McGrayne, goes well beyond complaints and stories of victimhood.

A discussion of the broader concern and vision of Margaret Walsh Rossiter in the prologue resonated with me. Rossiter didnt want to stop with bringing more women into science; she wanted to bring everyone who had been excluded back women of any stripe, African American men, Latinos, other people of colour, immigrants, LGBTQ people, people with disabilities, or anyone else who doesnt fit the stereotype of the white male genius.

The book proper begins with Colwells recurring encounters with existing conventions, including the advice she received against studying science even though she had fared well in high school. I grew up in Bihar, and have met too many bright female students who simply couldnt pursue higher studies after high school due to socio-economic and cultural barriers. Science was male-dominated; my family encouraged my brothers to study engineering. And Colwells writing showed how, though the individual plots are different, the same tropes played out in the US as well.

Talented women in the US struggled to get fellowships and work opportunities despite strong academic performances. In almost all institutions of higher education, women were discriminated against, and denied their due. Ironically, anti-nepotism rules were used mostly against women.

Various feminist movements have highlighted similar cases in India. The #MeToo movement exposed among many, many issues the gender-insensitive character of practising science in India. In chapter after chapter, Colwell and McGrayne describe the stories of many women scientists who pursued science despite similar odds. Some were recognised for their contributions in their lifetime, others were only after they had died, and even others not at all.

Colwell studied bacteriology and genetics at Purdue University, Indiana, where she also battled against the deeply entrenched discriminatory practices. Together with my own experiences, I sense that discrimination in science is universal.

To avoid competing with established scholars in the field of marine bacteria, Colwell chose to work on Pseudomonas aeruginosa, a species thats usually found in water and the soil, and is known for its resistance to antibiotics.

When she presented her work at a workshop, Roger Stanier, a prominent scientist in that field, criticised and ridiculed her. Colwell recalled: I was not his student, not part of his laboratory, and I was intruding on his bacterium, about which he was clearly an expert. Would he have treated a male student the same way? Probably not. More likely, he would have been constructive in his criticism and actually helpful.

Colwell was offended. More significantly, she anticipated that Staniers continued criticism and ridicule could mothball her career, so she set about choosing a different bacterium to study eventually picking Vibrios.

The part of the natural universe that we are yet to explore with the scientific method is vast. But what we do study in this vastness is determined not only by curiosity or other benign forces. Our choices are also shaped by social considerations. I myself was dismayed by the twisted path that led Colwell to one species of bacteria instead of another. However, she also made seminal contributions to our knowledge of Vibrios.

As she wrote, A project that started in the crucible of despair turned into one of the best decisions I ever made. Now, fifty years later, that decision has kept me active in one of the hottest fields in the life sciences: microbiomes, the study of all the genetic material in all the microorganisms in a particular environment, whether it be the human gut, food, river water, or the ocean.

Only a woman of formidable courage, conviction and intellect could have spoken these words. And thanks to her work, we now have an advance-alert system to signal potential outbreaks of cholera, caused by the bacterium Vibrio cholerae, with huge implications for public health worldwide.

Science and government

The chapter on her research work at Georgetown University drew my attention as it reminded me of conversations with senior faculty members in Indian universities and technical institutions, during my PhD, who candidly shared how gender-biases intersect with the recruitment and promotion processes. Colwell recalls how the university, which first hired her, gave her the opportunities to grow and contribute but eventually declined to make her a full professor, despite all her accolades. She subsequently moved to the University of Maryland in 1972.

Her experiences there, as well as at the US National Science Foundation, where she became its first female director in 1998, show how she exemplified a blend of problem-solver and team-player, and her optimism and tactfulness.

As a science policy scholar, Im keenly aware of how policies influence Indias national innovation system. Reading of her work at the NSF in this regard was enlightening especially for showing how a single institution backed by political will can research ecosystems that are both sustainable and agile, to nurture innovation and entrepreneurship, particularly in emerging sciences and technologies.

Remarkably, Colwell and McGrayne dont portray Colwell as a victim of gender-biased science nor as an extraordinary warrior who demolished stereotypes. Instead, her story melds seamlessly with an ethos of scientific practice that has become coincident in the 21st century with fairness and equitability: of a scientist who valued team work, encouraged others to contribute and believed in conversations and dialogues irrespective of differences in viewpoints and perspectives.

Having said that, I wish I had come across a similar text for women who are interested in social sciences, to guide them with sources of opportunities and inspire them to pursue their dreams.

As a postdoctoral scholar working on issues in gender and science, technology and innovation, I found this book rewarding, enriching and amazing. In fact, I even felt a twinge of disappointment that there wasnt a similar book (from what I know) vis--vis the social sciences a book that told the story of a woman not as someone who made it big and challenged the system but as an exemplum of the need for and importance of perseverance and struggle.

Nimita Pandey is an STI Policy Fellow at the DST Centre for Policy Research, Indian Institute of Science, Bengaluru.

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In Rita Colwell's Memoirs, a Reminder That Discrimination in Science Is Universal - The Wire Science

Joints are the bodys hardworking hinges. When healthy, they connect your bones and give you the range of motion you need to carry out daily activities. Women, though, are particularly vulnerable to joint pain, stiffness and frustration. In fact, the Centers for Disease Control and Prevention predicts that by 2040, two-thirds of arthritis (joint inflammation) sufferers will be female.

Experts point to a number of explanations for the disparity between men and women in arthritis. For starters, obesity is a major risk factor for osteoarthritis, and weight gain triggered by menopause can place stress on joints. Plus, hormones make womens' ligaments more lax, so they offer less support for joints at certain points in the menstrual cycle. Some research suggests that the angle of womens hips to their knees could make women more prone to anterior cruciate ligament (ACL) injuriesanother factor in osteoarthritis.

Womens immune systems seem to be more robust than mens, says Iris Navarro-Millan, M.D., an assistant professor of medicine at Weill Cornell Medicine and Hospital for Special Surgery. But this disease-fighting superpower could put immune systems into overdrive, leading them to misguidedly attack joints. As a result, women are also much more likely to have autoimmune-related joint conditions such as rheumatoid arthritis and lupus.

Fortunately, theres much you can do to keep your hinges happy. Exercise and maintaining a healthy weight are key. Regular activity keeps joints nourished and lubricated and strengthens the muscles and tendons that keep them stable and protected, says Kathy Weber, M.D. an assistant professor of sports medicine at Rush University Medical Center. And every extra 10 pounds you carry increases the load on your weight-bearing joints by 40 pounds.

In addition to straining joints, obesity can cause metabolic changes that promote pain and inflammation. But you dont need to lose a lot to make a big difference: Dropping just five to 10% of your body weight can reduce knee pain and significantly improve function. Read on for what may be causing your pain and more ways to ease it.

Over 30 conditions could be the culprit, and they fall into two categories: mechanical wear and tear injuries and inflammatory disorders. Heres more about two of the most common.

Injury, years of use, genetics or inflammation can spur the breakdown of bone-protecting cartilage. Think of it as like potholes developing in a road, says Dr. Weber. In this setting, the lining of the joint, the synovium, can become inflamed as well.

Symptoms: OA can affect numerous joints, but they may not all flare up with symptoms at the same time. Hips, knees, the spine, the base of the thumb and small hand joints tend to be common OA sites for women. Tenderness and stiffness in affected areas may develop gradually.

Diagnosis: Your doctor will conduct a physical exam and take X-rays or other images. They may order blood work to rule out other conditions.

Treatment: Because damaged cartilage does not regrow on its own, surgery may be an option, but the goal of treatment is usually to reduce pain and restore function. Dr. Weber often starts by prescribing regular exercise or referring patients for physical therapy to strengthen muscles that support joints.

A physical therapist can create an individualized exercise plan to help you feel and function better. Medications such as nonsteroidal anti-inflammatories (NSAIDs) can relieve symptoms too. Steroids and other substances may be injected to ease discomfort at the site of a flare. Joint replacement is usually a last resort, and more conservative measures should be tried first.

The immune system attacks the joints, eventually causing permanent damage. The joint lining becomes inflamed and produces factors that destroy the cartilage and bone, explains Ellen Gravallese, M.D., president of the American College of Rheumatology. RA can run in families, but lifestyle factors can set it in motion. In fact, if you have a genetic predisposition and you smoke, it can increase the chances of developing RA by as much as 40 times.

Symptoms: One hallmark of RA, Dr. Gravallese says, is that your joints feel stiffest first thing in the morning or after prolonged inactivity, and then after an hour of activity and movement, they generally begin to loosen and feel less painful. (In contrast, OA pain typically gets worse with strenuous activity). RA often first appears in the small joints of the hands and feet. They may be swollen, warm and red and flare up on both sides of the body at the same time. RA symptoms can also include whole-body issues like fatigue.

Diagnosis: Episodes can come and go and early symptoms can be subtle, which means RA sufferers may not know they have it for months or even years. If you experience unexplained joint issues, be proactive. The earlier the treatment, the better the outcomeask for a referral for a rheumatologist. Doctors will start with a detailed history and a physical exam. Blood work can help detect markers of inflammation and disease.

Treatment: The goal is to halt inflammation to prevent further damage to joints. One option may be biologics, a class of drugs that can help downshift the immune system. If you continue to have active disease, you can consult with your doctor to try a different strategy.

Though common, this condition is still poorly understoodits sufferers, primarily female, may be wired to be especially sensitive to their bodies pain signals. Symptoms include pain all over the body, along with muscle aches and fatigue as well as brain fog. Fortunately, this chronic condition doesnt cause lasting damage to joints.

This infection is caused by bacteria transmitted through tick bites. If left untreated, Lyme disease can cause severe joint pain and swelling, particularly in the knees and other large joints.

Signs of this autoimmune condition include joint pain and swelling, fatigue and sometimes a butterfly-shaped facial rash. Nine out of 10 sufferers are women.

Its said that when it comes to joints, motion is lotion. So what exercise is best? Anything you enjoy enough to stick with. Even running, once thought to be a fast path to developing arthritis, has gotten the ok. In fact, a recent study found that serious runners were at no greater risk for knee arthritis. Keep these tips in mind:

Warming up for a few minutes readies the joint and the muscles around it to reduce the chance of injury, says Dr. Weber. Dont just stretch in place warm up dynamically, she says. Walk for a few minutes before you pick it up to a jog. If you are just starting an exercise routine, build up slowly in intensity and duration.

Variety in activity strengthens different muscle sets and reduces your chances of an overuse injury. An ideal joint-boosting routine combines 150 minutes a week of moderate aerobic exercise such as fast walking or biking with a couple of sessions of strength training such as with free weights or resistance bands. Yoga is also a great optionit increases your flexibility and gives a natural energy boost.

Proprioception is awareness of where your body is in space, which can help you prevent joint injuries. To improve your proprioception, try standing on one leg followed by the other for a minute each while you brush your teeth every day.

Long sessions hunched in front of a computer are a recipe for stiffness. Take regular breaks to keep joints lubricated. Try setting a timer on your phone as a reminder. Then, every 30 minutes, walk around (or even march in place) for a bit.

If you do develop a joint condition, theres no reason you have to cease all activity. Your doctor or physical therapist can suggest gentle exercises such as using an elliptical trainer, biking, tai chi or water aerobics.

Original post:
The Science of Joint Health - What Causes Pain and How to Ease It - GoodHousekeeping.com

For Jill M. Goldstein, PhD, sex matters.

A professor of psychiatry and medicine at Harvard Medical School, Goldstein is passionate about the need to develop initiatives focused on sex and gender differences in disorders of the heart and brain. Ask her why and she doesn't hedge.

"Every cell has a sex," she said. "Every cell in a woman's body is different from every cell in a man's body. So we want to raise the awareness that sex is an important factor in disease outcomes."

Women are twice as likely as men to present with major depressive disorder (MDD) and have twice the rate of co-occurrence of MDD and cardiovascular disease, a phenomenon associated with three to five times' greater risk for death from cardiovascular disease. Globally, approximately 2 of every 3 people diagnosed with Alzheimer's disease dementia are women.

In a recent viewpoint article published in JAMA Psychiatry, Goldstein along with colleagues Ana Langer, MD, and Jill Lesser, JD describe the need for researchers and clinicians to focus on these differences, particularly with respect to the co-occurrence of MDD, cardiovascular disease, and Alzheimer's disease. Doing so, the authors believe, could help stem the tide of what they call this "multimorbidity crisis."

For Goldstein, the quest for sex and gender equality in medicine goes back at least three decades, when she first realized that sex differences were rarely considered, either in the lab or the clinic. Since then, she has dedicated a considerable part of her career to elucidating the differences between men and women in a variety of disorders, including MDD and its comorbidity with cardiometabolic diseases, psychoses, and the risk for dementia. She has published more than 170 articles, chapters, and other original and peer-reviewed works in these areas.

Despite her efforts, substantial gaps and barriers remain, particularly with respect to these particular conditions. For example, most animal studies in neuroscience and cardiovascular disease still use an overwhelming proportion of male samples; few systematic clinical studies have examined sex differences in the brain and heart in MDD.In mixed-sex trials of cardiovascular disease, only one third of participants are women, and only 25% to 33% of such studies report outcomes by sex. Even fewer studies including those of Alzheimer's disease, which disproportionately affects women are designed on the basis of sex.

"Women have been historically neglected in terms of attention," Langer, professor of the practice of public health at the Harvard T. H. Chan School of Public Health, Boston, Massachusetts, told Medscape Medical News.

Equally troubling for the authors is the fact that researchers tend to examine each of these diseases independently at a single point in time, rather than as co-occurrences throughout life. This approach, they write, prevents a complete understanding of the shared effects of psychological, biological, social, and environmental factors across organs and tissues over an individual's lifetime.

People with both depression and cardiovascular disease have a three- to fivefold increased risk of death from heart disease.... And those people are primarily women.

"People with both depression and cardiovascular disease have a three- to fivefold increased risk of death from heart disease," Goldstein explained. "And those people are primarily women."

Not everyone agrees with Goldstein, including Lise Eliot, PhD, professor and acting discipline chair of neuroscience at Rosalind Franklin University of Medicine and Science in North Chicago, Illinois.

"I've been very unimpressed with studies of human brain-sex differences," Eliot told Medscape Medical News, "because one can find a brain-sex difference that fits with any gender stereotype, particularly when it comes to psychiatric disorders. But these are all disorders that have gender-difference ratios. The paradox is that sex differences are relatively trivial compared to other sources of variance, like environment and genetics."

Eliot went on to explain that gender has played a far more important role in medical outcomes than has sex. "There is a lot of gender bias built into our medical system that is, I think, the basis for a lot of these health disparities," she said. "Psychiatric diagnoses are infused with the gender stereotype. And yet, the drive is to get money to study biologic differences."

Although the current state of sex-based research in co-occurring disorders of the heart and brain has a long way to go, there are signs of improvement. Goldstein herself has been integral to these changes throughout her career, though her biggest impact may have come in 2017, when she founded the Innovation Center on Sex Differences in Medicine (ICON). The center which boasts world-renowned experts from a variety of fields seeks to change the way the world understands heart-brain disorders using sex and gender lenses.

"We really want to try to change how medicine thinks," she said.

ICON's mandate recently took on new significance when the center was designated as a National Institutes of Health (NIH) Specialized Center of Research Excellence on Sex Differences. The NIH grant will fund both basic science and clinical studies of the developmental origins of sex differences in depression and the dysregulation of cardiac function efforts, Goldstein hopes, that will ultimately open the door to the development of sex-dependent therapeutic strategies

"We have a number of projects that we're working on," Goldstein said. "For example, we're developing a clinical risk tool to help predict men and women in early mid-life who might be at risk for Alzheimer's disease later on. But the key is, we're developing it in a sex-dependent way."

Her coauthors are equally involved in similar undertakings. Langer currently serves as the director of the Women and Health Initiative at the Harvard T. H. Chan School of Public Health. In that role, she heads an organization that seeks female-driven solutions to women's healthcare needs around the globe. She also serves as the director of global policies and programs for ICON.

"We look at the effect of policies and programs on the health of women and try to come up with ways to identify modifying factors that would allow us to improve the health of women through the life course," Langer explained.

Lesser, on the other hand, is the president of WomenAgainstAlzheimer's, a group that seeks to find, fund, and implement a cure for Alzheimer's disease with respect to the way the disease affects women.

There are other signs of progress as well. In 1993, the National Institutes of Health Revitalization Act was enacted. Part of that legislation mandates that women and minorities who had been largely overlooked to that point need to be included in sufficient numbers in clinical research to receive NIH funding. The policy was amended to its current form in 2017.

Important advances have also been made in cardiovascular medicine, with women's cardiac health centers becoming more commonplace across the country. For Goldstein, these changes were an important first step in addressing the health differences between women and men. "Heart disease is the number one killer of women in the US," she explained. "Nevertheless, women were getting into treatment later because their symptoms were not the same as the typical male symptoms. And they were dying as a result."

Multidisciplinary efforts for enhancing knowledge around sex differences will require cooperation between academics, industry, advocacy, and policy. Pharmaceutical companies, in particular, can play a big role in this revolution, the authors stress.

"The way it stands, pharmaceutical companies do not incorporate sex into the design of their studies," Goldstein said. "They may do a post hoc analysis to separate their data by sex, but that's not the same as testing a sex effect.

"Nevertheless, I believe there are many molecules sitting in companies' libraries that actually may be more effective in one sex than the other but were thought to be ineffective because the original studies were not designed by sex to test such differences," she added.

Despite the complexity of revamping the way an entire industry delivers its products and services, Goldstein and her colleagues believe the field of psychiatry is positioned to play an important role in the change, particularly with respect to the multimorbidity of MDD, cardiovascular disease, and Alzheimer's disease. Of these disorders, MDD is often the first to emerge.

"It's very important to understand the shared early origins of these three diseases so we can target them and try to prevent them down the road," Goldstein said. "For example, if we know that sex differences in depression emerge just after puberty and we also know that these differences will place a person at a higher risk for cardiovascular disease later in life, why are we not targeting them earlier?"

The same holds true for Alzheimer's disease. "If we know that hypertension and depression are major independent risk factors for Alzheimer's disease, why are we not targeting them as soon as possible?" she added.

Richard S. Isaacson, MD, director of the Alzheimer's Prevention Clinic at Weill Cornell Medicine in New York City, agrees that this kind of precision medicine is desperately needed when it comes to preventing Alzheimer's disease. "I think we've made tremendous progress in our understanding of how cardiovascular disease and Alzheimer's disease are in some ways inextricably linked," he said. "And I think physicians really have to understand the two are intertwined quite a bit.

"Nevertheless, we have to realize that people may look similar on the outside, but there's a lot of biologic and genetic differences on the inside," he continued. "Precision health is the future of medicine, and that's absolutely the case for Alzheimer's and cardiovascular disease prevention."

Isaacson explained that this understanding has helped shape the way he approaches patients. "In the Alzheimer's Prevention Clinic, I feel like I'm one third neurologist, one third preventive cardiologist, and one third primary care doctor," he said. "And I really believe that, because our panels for Alzheimer's prevention are the same ones that are used by my cardiologist colleagues."

Jordan Smoller, MD, ScD, professor of psychiatry at Harvard Medical School, agrees, yet he recognizes that one specialty cannot tackle the issue of multimorbidity alone. The movement needs financial partners, as well as a pipeline of trained professionals from a variety of fields who prioritize these issues throughout their careers.

Research will also be key, he says, from basic science to translational studies. "Then we need to see if we can actually leverage basic biology and clinical research to develop therapies that account for sex differences," he said. "That's a vitally important area, because it hasn't really happened in any area of medicine to date."

...one silver lining of the COVID-19 outbreak is that it seems to have increased recognition of the associations between sex, gender, and disease outcomes.

According to Smoller, one silver lining of the COVID-19 outbreak is that it seems to have increased recognition of the associations between sex, gender, and disease outcomes. Yet he feels the change may also be due to a confluence of science and culture.

"Often in medicine there's a convergence of factors that really elevate certain questions to become priorities," he explained. "One of them is advances in the science that allow them to be studied in a more fruitful way.

"At a societal level, it's always been controversial to what extent sex and gender play a role," he added. "But it's an issue that has now gathered more interest among a broader field."

"I think the devil is in the details when it comes to cardiovascular health and Alzheimer's disease coexistence," Isaacson added. "There needs to be a deeper dive and more collaborative efforts between preventive cardiologists, neurologists, psychiatrists, and endocrinologists. And we really need to work together to push the needle forward to truly have an impact."

"Things feel very different now than when I first started doing this," said Goldstein. "I think the context is different, and there's even a hunger for this from the public. I think we have a better chance of success now than ever before"

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In Disorders of the Heart and Brain, Does Sex Matter? - Medscape