Critics are not trolls, milord: Faceless and nameless troll writes open letter to Chief Justice of India – OpIndia

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Dear Chief Justice of India,

On behalf of all faceless nameless social media trolls, I am writing this letter. Before I start ranting, please let me explain what trolls mean and why they choose to remain faceless and nameless. Trolls are the ones who criticise powerful people, politicians, law makers, bureaucrats, journalist celebrities, intellectuals, civil society, businessmen, Judiciary and Courts too.

So, you must be thinking why are we called trolls not critics? Because we criticise people who dont like to be criticised. For example, elite journalists, if we question them, they will see it as an attack on journalism, they themselves want power to question everyone but they dont like to be questioned back because they are sitting on their self-assumed pedestal of being the 4thpillar of Democracy. So they started calling us troll and once they started naming social media critics as troll, all others joined them in calling us troll. We kind of like this name so we are happily accepting it.

Why do we choose to be nameless and faceless? Nothing is hidden from you milord, you are very well aware how powerful people react when you take them to the place they are not comfortable in and expose them. They can go after our jobs, our family and sometime, send goons to beat us up. And there is also a benefit of being nameless and faceless that powerful people will have to reply on topic only and they cant use religion, caste or race to divert the topic.

Who are abusive trolls? Trolls mostly use humour, sarcasm, satire or meme to criticise but it is backed with facts not abuses. Anyone, including me, using abuses is giving bad name to trolls and must avoid it and it also makes it easy for powerful people to take action. Not only trolls but anyone who is abusing should be dealt with laws, be it a Rajya Sabha MP calling an actress haramkhor or an actor abusing journalist. But such abusive trolls are few in number.

Milord, coming to the point, recently you asked central agencies to take action against trolls who are questioning judges on social media. Had this statement come from any politician or journalist, we would have seen as badge of honour but this statement coming from lordship has hurt us badly. We look upon you as our chief defender of freedom of expression. To paraphrase Justice Gautam Patel, there is no such things as too much dissent. Justice Chandrachud advices us to stand up and be dissenters. And while protecting rights of dissenters, Delhi Court said if you dont agree with the author, dont read the book. There are thousands of instances when Judiciary stood up for dissenters and freedom of expression.

As I had mentioned earlier, we are called trolls by people who dont like to be criticised, with due respect to your chair, judiciary has joined that league when you asked central agencies to take action against social media trolls. We are taught that everyone has right to criticise anyone and no one is above law, even the law makers and law implementer. It should not be a crime to criticise any court order or any judge at his/her personal capacity. People should be bound to follow court order no matter if they like it or not, but criticising that order should not be crime.

Coming to attack on the judiciary, Its not trolls who are hurting judiciary, its news publishers and media who portray court order as per their wish. They can turn a court order towards any direction as per their need. They use oral remarks of judges as headlines of article, which might be completely different from the order of that case. Nothing is harming judiciary more than fake news. And I am really sorry to say this but courts always protect those fake news peddlers in the name of freedom of press and dissent. Instead of going after trolls, milords should have asked law makers to frame laws against fake news peddlers. I am not against freedom of press, but freedom comes with a price and here that price is one and only TRUTH. Freedom of press must not be confused with freedom to lie.

Milord, I am too young to tell this, but in my opinion, serving judges should refrain for putting their opinion and off-the-cuff remarks, as suggested by supreme court. Once a judge has an opinion, his/her chances of being unbiased gets reduced and it can also influence the decision. Judges are supposed to be unbiased and no opinion is unbiased.

Concluding this letter with an expectation that courts will protect freedom of expression of trolls who are already targeted by many powerful chairs. And in future, if anyone will attack on freedom of expression of trolls, courts will take Suo moto to defend trolls and idea of India.

If you find this letter offensive, please accept my apologies. I am now off to the nearest communal mandir to pray that I get away with just one rupee fine like Prashant Bhushan, who attacked the judiciary far more uncharitably than any of us trolls do.

Yours obediently,Nameless, faceless but not shameless troll.

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Critics are not trolls, milord: Faceless and nameless troll writes open letter to Chief Justice of India - OpIndia

‘A Time Outside This Time’ is a searing reflection of a world riddled by fake news – Telegraph India

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Told in curious and simple prose, this novel is wildly reminiscent of a contemplative Douglas Adams pondering over an Orwellian present

A wonderfully honest read of recent time would be Amitava Kumars A Time Outside This Time (Aleph; Rs 699). Told in curious and simple prose, this novel is wildly reminiscent of a contemplative Douglas Adams pondering over an Orwellian present. Kumar is a Guggenheim fellow and a professor of English at Vassar College with books like Writing Badly is Easy and The Lovers in his oeuvre.

In this book, Satya is an Indian writer based in New York, enjoying a residency for artists in Italy. His wife Vani and daughter Piya await his return home as he narrates and is mesmerised by the web of fake news building around the world at break-neck speed. Caught between Trump and Modi, his resilient pursuit of social norms as defined in a post-truth world results in him building a plotline for his book. As the thin line between truth and lie starts to vanish, it soon becomes barely discernible from fiction.

Lamenting about the state of affairs and the media narratives which could well be fictional stories, there is incredulity accompanying his keen observations. He draws parallels between the world outside and the novel that begins to gently take shape in his mind. Commenting on the state of affairs, Satya wonders if the leaders of the country just like him cannot imagine a time outside this time. He writes:

The most popular stories on Snopes.com:

Did Eleven U.S. Marines Give Their Lives This Week? [False]

Did a Principal Ban Candy Canes Because They Are Shaped Like Js for Jesus? [True]

Did a Brain-Eating Amoeba Kill a Woman Who Rinsed Her Sinuses with Tap Water? [True]

Did Miley Cyrus Tell Fans to Worship Satan if They Want to Be Rich and Famous? [False]

Did Jon Voight Urge Americans to Fight for Donald Trump? [True]

The list is fairly ridiculous. It reveals the low stakes in the battle for truth in our culture.

Kumars novel comes with a wry sense of humour and readers are compelled to start wondering with Satya and question their own memory-making process. Satya decides that to make sense of the copious notes he had taken since Trump came to presidency to his days at the residency with the novel corona virus beginning to rear its fangs around the world he must go far back into his childhood. With a matter-of-fact style of storytelling, Satya remembers his childhood fraught with communal violence and thinks I was trying to remember the earliest lies I was told about others and the stories I had invented about myself. In a seamless manner, Kumars own story becomes Satyas story as he recounts his time as an author in New York.

There are little stories that make up this gigantically ambitious novel spanning across various parts of the world. There is Khalid Farooq whose tale moved Satya to provide financial help that was never returned. Instead what emerged were a few lies. There is an English professor Ghosh in Siliguri who thought of Hamlet on the death of a peasant leader. There is Vishal Kishore, a police officer in Calcutta who paves the way for the authors research into someone named Avinash. And there is Gautam Sikdar, a popular TV journalist who was once married to his wife Vani. Through these various little stories, Kumar throws light upon different aspects of life and the presence of lies in those very spheres.

There is anecdotal history, the bizarre nature of data and dubious scientific research strewn across the book that has an undulating narrative. However, if for a second you feel yourself slipping away, you remember that there is some part of a loose thread that remains to be tied and you carry on. Pick up a copy to feel seen as familiar events around the world build into a narrative that is unique and personal to you. The gorgeous yellow cover, designed by the author himself, will lead you right to it.

Photo: Imrul Islam

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'A Time Outside This Time' is a searing reflection of a world riddled by fake news - Telegraph India

Former ‘RHONY’ star Heather Thomson says show’s storylines are ‘staged,’ ‘fake’ – Fox News

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Former "Real Housewives of New York" star Heather Thomson called out the show for creating "staged" and "faked" storylines.

Thomson criticized the show while talking to a New York Post photographer outside the high-end Japanese restaurant BondST in New York City.

Heather Thomson criticized "The Real Housewives of New York" in a recent interview. (Charles Sykes/Bravo/NBCU Photo Bank via Getty Images)

The reality TV star specifically called Sonja Morgan's engagement to Harry Dubin during season 12 "fake." Dubin proposed to Morgan while Luann de Lesseps was crying over her breakup with Jacques Azoulay.

"It was completely staged and totally fake," Thomson told the outlet. "It was a ring that Ramona was wearing. And she took it off and gave it to Harry to pretend that it was his it was oneupmanship."

RHOBH STAR KYLE RICHARDS SAYS DORIT KEMSLEY IS NOT SO GREAT AFTER HOME INVASION: PTSD, FOR SURE

"The authenticityismissing," she said. "The women were self-producing, and many storylines were forced and contrived."

Thomson originally left "RHONY" in 2015, but has since made appearances on the reality TV show.

Thomson did defend the women who decide to join the "Real Housewives" franchise and instead laid the blame on the "machine."

Thomson accused the show of creating "staged" and "fake" storylines. (Charles Sykes/Bravo/NBCU Photo Bank via Getty Images)

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"Generally speaking, the women that join the show are not self-absorbed, catty, horrible people. Theyre birds in gilded cages. They go in there with the right intention, but then you get sucked into this system of what the viewers want," Thomson said. "These women are part of a machine that has awarded them and fed them for outrageous behavior. Its a career. Its their check. And they dont have other jobs outside of it. And so you become a product of the environment of what the fan is looking for.

"Lets be honest: Watching women behaving well and doing great things for each other doesnt make must-see TV."

Thomson officially left the show in 2015 but has made appearances since. (Jared Siskin/Patrick McMullan via Getty Images)

CLICK HERE TO GET THE FOX NEWS APP

She also blamed the audience.

"You cant really talk about the people without talking about the system," Thomson said. "Everybody has culpability in this the viewers, the network, the women on the show. Were all complicit."

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Former 'RHONY' star Heather Thomson says show's storylines are 'staged,' 'fake' - Fox News

Natural selection has been acting on hundreds of human genes in the last 3,000 years – Livescience.com

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Natural selection, the evolutionary process that guides which traits become more common in a population, has been acting on us for the past 3,000 years, right up to the modern day, new research suggests.

And it seems to be acting in surprising ways on complex traits encoded by multiple genes, such as those tied to intelligence, mental illness and even cancer.

In natural selection, genes that confer some sort of survival or reproductive advantage get passed down and persist in a population, while those that lead to lower survival or fewer offspring become less common. There's no question that natural selection shaped the evolution of humans in our more distant past. But the impact of natural selection in the recent past is a much more controversial question.

The new research suggests that natural selection is indeed an important factor in modern times, though the methods used in the study have led to missteps before, said John Novembre, a computational biologist at the University of Chicago who was not involved in the new research. This means the findings should not be taken as the final word in modern-day natural selection.

Related: How would Earth be different if modern humans never existed?

The new study focuses on traits that emerge from a combination of multiple gene variants, such as intelligence and skin pigmentation. The complex genetics of these traits makes unraveling the action of individual genes difficult. To find these subtle effects, researchers conduct genome-wide association studies (GWAS), in which they scan for genetic markers across the entire genome to find short genetic sequences that are more common in certain traits than in others.

These results can be challenging to interpret even comparing people at a single point in time. Newer studies up the ante by looking not only for genes associated with complex traits, but also for signs of natural selection on these traits. In essence, genes that become more common over time are under positive selection: They're beneficial in some way and are thus likely to be passed down. Genes that become less common with time are under negative selection. They're somehow harmful to survival or reproduction, and thus are less likely to be passed down.

"There is quite a lot of controversy about whether GWAS is ready for this type of application," Novembre told Live Science.

In their study, published Nov. 15 in the journal Nature Human Behaviour, the researchers found a total of 755 traits showing signs of selection in the last 2,000 to 3,000 years.

For the modern samples, the researchers used data from people of European ancestry in the U.K. BioBank, a repository of genetic and health data from 500,000 participants. To look deeper into history, the researchers also used three datasets of ancient human DNA from the pre-Neolithic, Neolithic and after the advent of agriculture in the Near East, comprising a total of 512 individuals. The researchers looked in three timeframes: The modern era, the past 2,000 to 3,000 years, and up to about 100,000 years ago. The oldest data is the most unreliable, said study leader Guan Nin Ling, a professor in the school of biomedical engineering at Shanghai Jiao Tong University.

While the researchers had detailed health and lifestyle information from the U.K. BioBank, they had only partial genetics to go on for the older samples, and no direct information about things like how many children a person had or what they ate. Thus, they used the genes themselves to infer traits. If a gene known to be involved in height increased in frequency over time, the researchers took that as a signal that height might have been under positive natural selection.

The traits that seemed to be under selection ranged from skin traits such as "ease of tanning" to various body measurements. Somewhat surprisingly, genes associated with some seemingly undesirable traits increased in prevalence over time, including genes associated with conditions like skin cancer, inflammatory bowel disease and anorexia nervosa. This suggests that some of these disorders arise as side effects of genes that are beneficial for other reasons, the researchers suggested.

"If one variant elevates the risk of one disease but decreases the risk of another, natural selection would have little power to eliminate this variant," Lin told Live Science.

Ling and his colleagues were most interested in the question of why disorders with complex genetics, such as schizophrenia or attention deficit hyperactivity disorder (ADHD), persist despite natural selection.

But GWAS can be a tricky tool for trying to unravel natural selection, Novembre told Live Science. One of the biggest problems is something called "stratification." Differences between two populations can appear genetic, when they are actually environmental. Because GWAS can't show that a gene causes a trait, only that they're associated, the results can get weird, fast. To use a classic example from a 1994 paper, chopstick skills are clearly not a gift of DNA: They're a matter of practice from a young age. But a GWAS study in a diverse population like San Francisco might very easily turn up evidence of genes associated with chopstick skills simply by revealing genes that are more common in East Asian populations than in European populations.

This mistake has actually happened. In the last decade, a number of papers came out claiming that height-conferring gene variants are more prevalent in Northern Europe than in Southern Europe and that natural selection was pushing Northern Europeans to become taller, on average, according to research published in 2012 in the journal Nature Genetics.

But it turned out the impact of these genetic variants was overestimated, Novembre said. When looking at those same genetic variants in less diverse populations (a strategy for reducing the stratification problem), the evidence for natural selection vanished. The study had been picking up on so-far-unknown environmental differences between northern and southern Europeans and mistaking them for something purely genetic. Researchers had to completely rethink the results and are still uncertain about whether natural selection has anything to do with height differences across Europe, according to a 2019 paper in the journal eLife.

The use of data from people of only European ancestry helps limit the stratification problem, Novembre said. But there are still opportunities for the stratification problem to arise, he warned.

Among the hundreds of traits the researchers found might be under natural selection, a few stood out. When focusing on modern-day data, the researchers found that higher IQ was associated with having more sexual partners but fewer children. Meanwhile, ADHD and schizophrenia were both associated with having more sexual partners. These two conditions are examples of traits that might be a challenge in daily life, yet improve mating success, Lin told Live Science.

When looking back over more than 100,000 years of human history, the researchers found that traits having to do with skin tone and body measurements were the most common to show selection pressure. These included things like facial measurements, height and torso length. For example, genes associated with face shape and size were apparently under natural selection over the past 100,000 years, the researchers found, which might have to do with changes to the jaw and skull associated with diet and brain growth.

Looking back as far as 3,000 years ago, the researchers found that inflammatory bowel disease seemed to be favored by natural selection. This could be an example of a trait that is helpful in one context and harmful in another, Lin said.

"We hypothesize that in ancient times with poor hygiene conditions, a highly activated immune system in the intestine would protect us from infection," he wrote in an email to Live Science. "However, a highly activated immune system in modern society only causes our intestine to attack itself."

But it can be very hard to show why a particular trait relates to evolutionary success. To use height as an example, being tall might benefit reproduction by making someone more appealing to potential sexual partners. Or maybe height is just a side effect of an efficient metabolism, which improves survival rates, and that increased likelihood of surviving to reproductive age could lead to the genes getting passed down to the next generation. If genes tend to vary together and many do natural selection could be acting on a totally different trait than the one that seems most intuitive. For example, Novembre said, the variants that made skin tanning easier, which showed up as highly selected in the new research, are likely related to a lot of other traits, like rates of skin cancer, freckling and hair color. It's hard to know what path, exactly, leads to someone reaching reproductive age, attracting a fertile mate, and having lots of babies, and which genes are just lucky hangers-ons in that process.

Making matters more complicated, there are times when the genetics of a trait may be completely swamped by the environment. Something like this could theoretically happen with human intelligence. IQ is partially hereditary, so if it's true that higher-IQ people do have fewer children, that would arguably push the collective IQ of the population downward over time. But if the environment became more conducive to brain development better nutrition, reductions in lead or other pollutants the population might well become brighter.

"Just because the apparent genetic basis for something is changing doesn't mean the population has even been evolving in that direction," Novembre said.

One approach to nailing down natural selection would combine large-scale GWAS with studies on the genomes of single families, Novembre said. Family members, especially siblings, usually grow up in fairly similar environments, so it's easier to tell when genes are affecting any given trait. These family studies could be used to ground-truth claims from large GWAS samples, teasing out which genes still show impacts when you remove as much of the environment as possible from the equation.

Lin and his colleagues plan to conduct family studies to learn more about the genetics of complex conditions like schizophrenia. They're also working to quantify genetic variants that can give rise to both beneficial and harmful effects simultaneously, he said. The findings of the new study are a starting point, Lin said, and a reminder that natural selection is still a force in human biology.

"It is simply not true that humans have stopped evolving by natural selection, even given our capacity to change the environment towards facilitating and reducing physical tasks, minimizing the energetic costs to get better food, and better health care system," Lin said.

Originally published on Live Science

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Natural selection has been acting on hundreds of human genes in the last 3,000 years - Livescience.com

Heart attacks struck Sek Kathiresan’s family. He’s devoted his life to stopping them. – BioPharma Dive

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Sekar Kathiresan was driving home when his cell phone rang. The voice on the other end belonged to his father. It was the evening of Sept. 12, 2012, his father's 65th birthday. But that wasn't why he was calling.

"Senthil collapsed at home," Kathiresan's father said. "He's in the hospital."

Senthil, Kathiresan's older brother, was a seemingly healthy 42-year-old, training for a race. But that night he returned from a run dizzy and sweating profusely. He called 911, then had a seizure as paramedics arrived.

Senthil had had a heart attack; his brain starved of oxygen for minutes. He died a little over a week later.

His death devastated Kathiresan, an immigrant from India who spent his early childhood overseas with his brother, waiting for the day they'd join their parents in the U.S. "We relied on each other," Kathiresan said. Both had thrived in the U.S. They were married the same year and each had young children.

This story might be familiar to the millions of people and families affected by heart disease, the world's leading cause of death. But it's more than that for Kathiresan, who, when Senthil died, was a cardiologist and emerging as one of the field's leading geneticists.

"It really shook Sek. It shook all of us," said David Altshuler, the former Broad Institute of MIT and Harvard geneticist, a Vertex Pharmaceuticals executive and mentor to Kathiresan. "It was a tragic irony."

Kathiresan channeled his despair into motivation. He rose to the top of his profession, making discoveries that changed the way people think about heart disease. He launched a startup with an exceptionally ambitious aim to prevent heart attacks, for life, with a single treatment. Nearly a decade after his brother's death, the startup, called Verve Therapeutics, could soon test that treatment in people.

"I tried to turn that negative energy into Verve," Kathiresan said, "to make sure what happened to Senthil doesn't happen to others."

The road ahead is daunting still. Kathiresan is an academic-turned-CEO on a personal mission, not a seasoned biotech executive. His company is attempting a scientific moonshot, relying on cutting-edge, but unproven, gene editing technology to develop a one-time medicine for one of the most prevalent diseases. In doing so, he will have to prove the world needs what is essentially a longer-lasting version of cholesterol-lowering drugs that are already available.

"It's a pretty high bar to say gene editing has an important role to play here," said Richard Lifton, the president of Rockefeller University and a geneticist known for research into heart disease.

"But the flip side of that," he added, is a drug "that could last, potentially, a lifetime."

Kathiresan was only four years old when his world upended.

Kathiresan's father, an aspiring engineer, had received a full scholarship at the University of Pittsburgh, thousands of miles away from the tiny southern India village of Viramathi he, his wife and three children called home. He dreamed of coming to the U.S. and pursuing a higher education, but couldn't afford to bring the whole family, Kathiresan said. So, in 1975, he left for the U.S. with his wife, baby daughter Davi and about $40. Sek and Senthil stayed in India.

Kathiresan remembers a sense of loss, a "yearning." He didn't see his parents or hear their voices for five years. There were no phones in the house the brothers shared with their grandparents, nor at the boarding school they attended. They communicated through letters sent across the ocean. "I'm not sure I would have had the courage to leave my kids behind," he said, reflecting on his father's decision.

But the plan worked. Kathiresan's father earned a Ph.D. and saved enough money to bring his sons to the U.S.

Kathiresan vividly remembers the flight from Mumbai to New York. The brothers, who had never seen a plane before, were awestruck. They flew by themselves, with an attendant as their guardian. Picked up at the airport by their father, their first meal in the U.S. was at McDonald's, where Kathiresan had french fries for the first time. He devoured them and asked for more.

"We can't afford another one," his father told him.

The Kathiresan family in 1975. Sek is second from left. Courtesy of Sekar Kathiresan

Senthil and Sek Kathiresan, aged 10 and 9, in India in 1980, just before leaving for the U.S. Courtesy of Sekar Kathiresan

The Kathiresan family soon moved into a house outside of Pittsburgh. The brothers, who spent half their childhood in a town with no running water, would live the other half in a middle-class and predominantly White U.S. suburb, an upbringing each wrestled with.

Growing up, Kathiresan was one of the few people of color in his school. Though he made fast friends, he wasn't comfortable, caught between his two worlds: weekly prayers at a nearby Hindu temple and weekend football games at school. His mother pushed him and Senthil to remember their heritage, anxious they would become "too American."

While Kathiresan dated and met his wife in college, Senthil had an arranged marriage. "We respected each other's approach," he said. "Some immigrants want to jump right in and be all in," and others "want to keep as much of their home culture as possible."

Kathiresan majored in history and even flirted with a career in finance before finding medicine, which he said "offered a sense of purpose and a mission."

His choice of profession was also personal, even before Senthil's death. Kathiresan's uncle, a physician, had died of a heart attack. So had his grandmother. His father had a heart attack at 54. Each time Kathiresan was more certain he'd become a cardiologist.

He embraced the grueling hours and sleepless nights that came with residency training at Massachusetts General Hospital, undeterred even when accidentally stuck by a needle that had been in the neck of an HIV patient. "I saw my whole life flash in front of me," he recalled, yet, after initially panicking, he took antiviral drugs and went back to the hospital.

"It comes with the territory," he said. "You're teaching, you're trying to help, but there's risk, you know?"

Kathiresan wasn't satisfied being a doctor, though. He wanted to understand why the people closest to him were getting sick and learn how to do something about it.

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David Altshuler recalls sitting in his office at MGH one morning in 2000 when he heard a knock on the door.

Altshuler was already well on his way to being recognized as one of the world's top geneticists. His academic lab would soon co-lead three large genetic research studies the 1,000 Genome Project, the SNP Consortium and the International HapMap Project and he would become one of the founding members of the Broad Institute.

Kathiresan, then a young cardiology fellow, sought him out and burst into his office.

"I want to figure out what causes people to have premature heart attacks," Kathiresan exclaimed, according to Altshuler.

Dressed in scrubs, Kathiresan looked exhausted, having gone to Altshuler's office straight from an overnight shift at the hospital. Altshuler can still recall the big, dark circles under Kathiresan's eyes.

Many people can talk a good game. But Sek is the real deal. He reminds us of why we do what we do.

David Altshuler, chief scientific officer of Vertex Pharmaceuticals

"How are you going to do that?" he asked.

Kathiresan laid out a plan to discover what puts people at risk for heart attacks. Then he'd figure out which risk factors were actually important, before finding a way to intervene before health problems began.

"I need to learn genetics," Kathiresan told Altshuler. "That's why I'm here."

Altshuler was impressed. "He was personally compelling," he said, "and obviously incredibly motivated." When Kathiresan finished his doctoral training three years later, he went to work for Altshuler at the newly founded Broad Institute.

Kathiresan (front row, third from left) during his time as chief resident in internal medicine at Massachusetts General Hospital. Source: Sekar Kathiresan

The experience was a crash course in genetics. Altshuler pushed Kathiresan to answer scientific questions that mattered, not just the ones he could solve. He taught Kathiresan how to manage and develop talent, skills he'd call on in the future. "He had an immeasurable influence on me," Kathiresan said.

Over the next decade, the two wrote grants together and teamed up on studies aimed at identifying genetic markers for heart attacks. They became good friends and confidants. Along the way, Kathiresan emerged as "the leading person in the world studying the genetics of coronary artery disease, certainly of his generation," Altshuler said.

"Many people can talk a good game," Altshuler said. "But Sek is the real deal. He reminds us of why we do what we do."

A research lab is like a small company. There's money to raise, a budget to manage. A team to put together, mold and motivate. Careers to foster and a vision to rally a team around. Kathiresan got that chance in 2008, when he started a lab at MGH and the Broad to search for genetic clues into the underpinnings of heart disease.

As a first-time lab leader, Kathiresan had to convince people to believe in him. One of the first was Kiran Musunuru, a young heart doctor doing a fellowship at Johns Hopkins University.

At the time, Musunuru was disillusioned with cardiology. There were plenty of ways to treat heart disease, he said, but not enough tools to prevent it. Musunuru thought genetic research was the key and desperately wanted to be a part of the building "wave" of studies. That led him to Kathiresan's lab at MGH.

Kathiresan didn't have experience. His lab was brand new and his future there wasn't secure. But Musunuru felt a kinship with him. "In the same way that I was, he was all in," he said. "You've got to take some risks, right?"

Kiran Musunuru, professor of cardiovascular medicine and genetics at UPenn Source: American Heart Association

What followed was a prolific partnership. Musunuru became Kathiresan's mentee, one of his first post-doctorate students, and eventually, the head of his own lab at the University of Pennsylvania and a Verve co-founder. They were willing to put in "insane amounts of time" to finish work and publish papers as quickly as possible, according to Musunuru. Conditioned by working long hospital shifts, they'd each wake up before dawn, texting and calling one another.

The two partnered on a number of important research papers, looking into, among other things, the genetic basis of cholesterol and a protective gene known as ANGPTL3 that would become a top therapeutic target of drugmakers including, years later, Verve.

In the meantime, Kathiresan's lab turned into a training ground for dozens of other young scientists. By the time he stepped away, Kathiresan taught more than 60, many of whom are now faculty members. And he had discredited a long-held belief about heart disease.

For many years, Ethan Weiss, a cardiologist at the University of California, San Francisco, told his patients to exercise so their levels of "good cholesterol" would increase. He wasn't alone. Doctors were taught in medical school that high levels of high-density lipoprotein, or HDL, were associated with fewer heart attacks. Conventional wisdom was "you wanted to do everything you could to get your HDL up," Weiss said.

But researchers didn't know much about HDL and its relationship to fats in the blood called triglycerides, which were also linked to heart disease. High HDL, for example, was associated with low triglycerides and vice versa. "The question has been, which of these is the dominant one? Which one carries risks?" said Lifton, of Rockefeller. "It's been very hard to disentangle."

Researchers and drugmakers were nonetheless convinced HDL was the key, and that medicines that raised it would prevent heart attacks. Years of research led to drugs, known as CETP inhibitors, that could boost HDL. Several were thrust into large clinical trials early last decade, poised to become the next big thing in heart medicine.

"But correlation," Kathiresan said, "does not mean causation."

He basically changed a paradigm that we had clung to forever.

Ethan Weiss, cardiologist at the University of California, San Francisco

In 2012, Kathiresan's lab at MGH made a startling discovery: Good cholesterol isn't so good after all. By studying the genes of more than 100,000 people, they separated the effects of triglyceride levels from HDL. They found people with more HDL weren't safer from heart attacks.

HDL appeared to be a mirage, its link to heart disease perhaps conflated with other factors. Drugs that raise it likely wouldn't protect people from heart attacks, the team wrote in a paper published in The Lancet in May 2012.

The news stunned cardiologists. "He basically changed a paradigm that we had clung to forever," said Weiss, who now tells patients to ignore HDL levels because "it doesn't seem to matter."

The findings rippled across the pharmaceutical industry. One by one, CETP inhibitors from Roche, Amgen, Merck & Co. and Eli Lilly failed in clinical trials or were dropped by their developers. The class was largely shelved, along with a long-running hypothesis.

"It was a beautiful demonstration of using large-scale genomics to address a clinically vexing and important problem," Lifton said.

Just a few months after the paper's publication, Kathiresan's brother died of a premature heart attack.

Kathiresan took time off work and reexamined his own health. He went for heart tests, committed to being more active and dropped weight hed put on in college but hadn't lost.

"You mourn," Kathiresan said, and then "focus on the things you have control over."

So Kathiresan kept going. He and his labmates found more genes associated with either risk of early heart attacks or protection against them, confirming research by others in the process. They used a trove of genetic data from the U.K. to develop a diagnostic test that can identify higher risks of coronary artery disease, diabetes and other conditions in seemingly healthy people. "He decided, 'I will redouble myself to this effort,'" Altshuler said. "That took courage."

David Altshuler, Vertex's chief scientific officer Source: Vertex Pharmaceuticals

By 2018, they'd amassed a body of work so impactful that Kathiresan received the same Curt Stern award an honor given to pioneering human geneticists by the American Society of Human Genetics that Altshuler previously won.

In his acceptance speech, Kathiresan recalled the journey that took him from a small town in India to an awards stage in San Diego.

He then showed an ambulance report from the 911 call a 42-year-old made before he suffered a heart attack. He shared the man's electrocardiogram, his cholesterol and triglyceride levels and troubling family history. He explained how he died. He went through all the work he and his team had done to understand why the same thing happens to millions of other people.

The patient was his brother, he explained. New drugs were needed to avert the same tragedy in others, he said, and that was something he was working on. A high-profile competition he had recently lost gave him an opportunity.

Kathiresan, accepting the Curt Stern award from the American Society of Human Genetics on Oct. 18, 2018. Source: American Society of Human Genetics, via YouTube

In January 2016, the American Heart Association, the British drugmaker AstraZeneca and Google's life sciences arm Verily came up with an idea for a competition. Called "One Brave Idea," they promised a $75 million award and partnership opportunities to a researcher with the best idea to cure heart disease.

"What we're seeing is this growing epidemic of cardiovascular disease worldwide," said AHA CEO Nancy Brown, in a video describing the competition, "and we know that we need a new answer."

The AHA received 349 applications from research teams in 22 different countries. Kathiresan submitted one of them. Musunuru, then at UPenn, wrote another.

Unknown to one another, both pitched the same idea: a single shot of a gene editing drug that could drive down "bad cholesterol," or LDL, as low as possible for as long as possible.

Kathiresan cowrote an application with Anthony Philippakis, another Altshuler trainee who worked with the venture firm GV; and Feng Zhang, also of the Broad and one of the leaders of CRISPR gene editing research. Musunuru's team included UPenn gene therapy pioneer James Wilson.

The proposals were "eerily similar," Musunuru said. "Almost interchangeable."

Neither even made it to the competition's final round. The award went to a group of researchers led by Calum MacRae, chief of cardiovascular medicine at Brigham and Women's Hospital, who won for a genomics project meant to detail the biological changes that occur when heart disease begins.

The loss still bothers both of them. "I was bitterly disappointed," Kathiresan said. Musunuru calls it a "big, lost opportunity for the AHA."

Musunuru turned his attention back to research. Kathiresan decided to change careers.

Academia and the drug industry are closely linked. Academic researchers, after all, often make the discoveries that companies turn into medicines.

But that doesn't make it easy to leave the research bench for an industry job. The switch involves learning an entirely new language. Kathiresan, for example, had never heard the term "CMC," which is industry parlance for the process and regulation of drug manufacturing.

Jumping from academia to biotech can also mean giving up a secure position for a role in a company that, history would suggest, is likely to fail. Scientific glory isn't the only goal for a biotech, either: it has to eventually make money.

Kathiresan said he didn't have the "antipathy to the for-profit model that some people have." Previously, he had been focused on research, turning down industry job offers along the way. But his perspective changed after Altshuler left the Broad Institute in 2015 for a job as Vertex's top scientist. That "opened my eyes to the fact that there's a much larger world out there, and ways to have impact," he said.

So after losing the One Brave Idea competition, Kathiresan turned to Philippakis. It was a role reversal, of sorts: Kathiresan had advised Philippakis throughout medical school and after. "I really consider him a mentor in my life," Philippakis said.

Now it was Kathiresan who needed help. Philippakis cowrote the AHA application, he said, to help figure out how to build a company around the one-shot project. And Philippakis, who was well-versed in the biotech business because of his role with GV, could teach Kathiresan how to make that happen.

For almost two years, they gathered a small group every Friday to go through all the steps and potential roadblocks ahead. They tried to convince themselves "that this was actually doable," Philippakis said. They discussed how and where they'd get the intellectual property. The type of gene editing medicines they'd make. The business plan. How to raise the money and which firms to contact. Who the founders would be.

They came up with the name Endcadia Therapeutics a nod to ending coronary artery disease and prepared a pitch for GV.

Krishna Yeshwant is a venture capitalist who has worked with GV since its inception more than a decade ago. Over that time he's invested in dozens of healthcare startups. He's been asked to back plenty more.

Yeshwant has heard plenty of stories like the one Kathiresan told. Different versions of how "this family member of mine, this boyfriend or girlfriend, came down with this condition and I've devoted my life to it," he said. An emotional pitch only goes so far, though. And venture capitalists don't often invest in heart drugs because of how expensive they are to develop and test. In recent years, they've taken a back seat to promising new cancer and rare disease medicines.

But Yeshwant, who had joined Kathiresan and Philippakis for many of those Friday morning meetings, thought they were on to something. The treatment they envisioned, if successful, could change "how society works," he said, and Kathiresan was devoted to seeing it through. The plan they'd laid out was realistic as well: First they would prove the drug could work in a rare, inherited heart disease, a faster and less expensive clinical development path. Then they would go bigger and broader.

"It's aspirational," Yeshwant said, "but there was a nice on-road to it."

Krishna Yeshwant, managing partner at GV Source: GV

The others agreed. The startup became the first drugmaker GV better known for forming digital health companies ever incubated. The firm led a $59 million financing that closed in August 2018 and was announced the following year.

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Heart attacks struck Sek Kathiresan's family. He's devoted his life to stopping them. - BioPharma Dive

Animal Genetics Market Worth ($7,705.23 Mn by 2027) by (6.3% CAGR) with Impact of Coronavirus Outbreak and Global Analysis & Forecast by The…

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Growth of Animal Genetics Market is attributed to rise in production of porcine and increase in pork consumption across the globe. The same segment is likely to register highest CAGR in the global animal genetics market during the forecast period.

PUNE, India, Nov. 25, 2021 /PRNewswire/ -- According to The Insight Partners study on "Animal Genetics Market to 2027 Global Analysis and Forecast by Animal Genetic Material, Genetic Material and Service" the animal genetics market was valued at US$ 4,778.67 million in 2019 and is projected to reach US$ 7,705.23 million by 2027; it is expected to grow at a CAGR of 6.3% during 20192027. The growth of the market is attributed to the growing preference for animal derived proteins supplements and food products and rising adoption of progressive genetic practices such as artificial insemination (AI) and embryo transfer. However, limited number of skilled professionals in veterinary research and stringent government regulations for animal genetics is expected to hinder the market growth.

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The North American region holds the largest market share of this market and is expected to grow in forecasted years. The growth in North America is characterized by the presence of new market players, various product launches and increasing government initiatives.

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Likewise, Mexico is likely to offer attractive business opportunities for livestock genetics. Over the last decades, Mexico's beef, pork, and dairy productions have undergone valuable developments. Mexican generators in the expanding livestock intensive systems are frequently using modern genetic improvement technologies such as artificial insemination and embryo transfers.

In North America, the US is the largest market for animal genetics market. Livestock groups provide consumers with different products and services, including meat, milk, eggs, fiber, and draught power. The genetic variation within livestock communities produces the raw material for evolving through natural selection in answer to changing conditions and human-managed genetic improvement plans. As per the Food and Agriculture Organization (FAO), animal genetics is one of the livestock development support. It is a wide field, ranging from characterization to conservation to genetic development. According to the National Institute of Food and Agriculture (NIFA), there have been dramatic improvements in animal production yields and efficiencies. Therefore, the ever-increasing demand for dietary protein in the United States has been observed. These demands are achieved by one the best Animal breeding is one strategy by which these improvements may be performed. NIFA, with the help of scientists from universities and research organizations and food animal industries, provides national leadership and funding opportunities to conduct basic, applied, and integrated research to increase knowledge of animal genetics and genomics.

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The COVID-19 outbreak has disturbed various trades and businesses across the world. The incidence of corona virus or COVID 19 has not yet been registered the animals. Also, there is no evidence that companion animals are the prime source of the spreading epidemic in humans. However, various studies have been conducted to check the spread of disease from animals to humans. In many cases, zoonotic diseases were found in humans due to interaction with animals. Therefore, government bodies are taking more precautions and safety measures to prevent the spread of corona virus in the animals. The measures are widely carried out for companion animals as they frequently come in contact with their owners. Also, it is essential to report the cases to a veterinary authority. For instance, in the region, to report the cases of detection of COVID-19 is done to OIE through WAHIS, in accordance with the OIE Terrestrial Animal Health Code as an emerging disease.

The OIE is actively working by providing assistance to research for their on-going research and other implications of COVID-19 for animal health and veterinary public health. The assistance is also providing risk assessment, risk management, and risk communication. Also, the OIE has put in place an Incident Coordination System to coordinate these activities. In addition, OIE is also working with the Wildlife Working Group and other partners to develop a long-term work program. The aims are to provide better understandings, dynamics, and risks around wildlife trade and consumption. Also, it aims to develop strategies to reduce the risk of future spillover events.

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Additionally, various product and service launches have been initiated, which is helping the US market to grow. For instance, The Veterinary Genetics Laboratory (VGL) at the UC Davis School of Veterinary Medicine has launched an updated and advanced website along with several new tests for veterinary community. As the VGL is one of the foremost genetic testing laboratories in the world, the new site and tests will bring yet another level of global impact to the top-ranked veterinary school. Thus, the consistent support for combating addiction in the country undertaken by various organizations likely to augment the growth of animal genetics market during the forecast years.

The Asia Pacific region is expected to be the fastest-growing region among all other regions. The growth of the market in the region is majorly due to countries like China, India and Japan, which drives the major consumption of animal derived products. Moreover, growing preference for animal derived proteins supplements and food products, and rising adoption of progressive genetic practices such as artificial insemination (AI) and embryo transfer are also likely to contribute to market growth. On the other hand, significant investment by government in various breeding programs is supporting the growth of market. For instance, the central and local governments have invested more than RMB 5 billion to build breeding or multiplier farms and conservation farms for breed improvement programs and the building of centers for testing the quality of breeding stock, semen, and embryos.

Based on product, the animal genetics market is segmented poultry, porcine, bovine, canine, and others. The porcine segment accounted for more than 35.84% of the market share in 2019. In terms of genetic material, the animal genetics market is segmented into semen, and embryo. The embryo segment held the largest share of the market in 2019. In terms of service, the animal genetics market is segmented into DNA typing, genetic trait tests, genetic disease tests, and others.The DNA typing segment held the largest share of the market in 2019.

Rising Adoption of Progressive Genetic Practices Such as Artificial Insemination (AI) and Embryo Transfer in Animal Genetics Market:

Growing focus on developing superior animal breeds using genetic engineering to obtain high reproduction rates for large-scale production of modified breeds is expected to drive animal genetics market during the forecast period. Animal genetics emphasizes the inheritance and genetic variations in wild and domestic animals. This science is used at a commercial level for services such as testing genetic disorders, screening genetic traits, and typing DNA. For identifying genetic hybridizations, animal genetics uses various genetic practices, such as artificial insemination, embryo transfer, and cytological studies. Moreover, artificial insemination (AI) can reduce various risks involved in animal breeding and disease transmission. It is found that female offspring cattle born through artificial insemination yield more milk than normal offspring. Additionally, the use of antibiotic-containing semen extensors is effective in preventing bacterial infectious diseases. Therefore, the entire AI process is considered hygienic than natural mating.

The market players are focusing on partnerships, collaboration, and acquisitions to develop genetically modified breeds and maintain their market share. For instance, in August 2020, Cogent and AB Europe collaborated to launch a novel sexed semen service for sheep producers in the UK. In May 2018, Recombinetics entered into partnership agreement with SEMEX for the implementation of a precision breeding program, which is expected to improve animal health and well-being through hornless dairy cattle genetics. According to the Brazilian Association of Artificial Insemination, the number of commercialized doses of semen increased from 7 million in 2003 to ~14 million in 2017. Thus, rising adoption of genetic practices will support the market growth in coming years.

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Market: Segmental Overview

In terms of product, porcine segment is anticipated to register the highest CAGR during the forecast period. Growing production of porcine and increase in pork consumption is likely to favor the growth of the market. Pork is the most consumed meat across the globe. In the US, pork production generates $23.4 billion output per year. Additionally, 26% that is around 2.2 million metric tons of pork and its products are exported to other countries. Despite of the challenges such as tariffs, labor and disease risks, the pork industry in US is still growing with around 66,000 sows in 2019. Also, developments by the major pork producers in the country is likely to grow the pork production industry. For instance, in 2017, 123-year-old Clemens Food Group partnered with 12 independent hog farmers to establish a new packing plant in Michigan. Thus, growing pork production industry is likely to favor market growth. In terms of genetic material, the animal genetics market is segmented into semen, and embryo. The embryo segment held the largest share of the market in 2019. In terms of service, the animal genetics market is segmented into DNA typing, genetic trait tests, genetic disease tests, and others.The DNA typing segment held the largest share of the market in 2019.

Animal Genetics Market: Competition Landscape and Key Developments

Neogen Corporation, Genus, Groupe Grimaud, Topigs Norsvin, Zoetis Services Llc, Hendrix Genetics Bv, Envigo, Vetgen, Animal Genetics Inc, Alta Genetics Inc. and among others are among the key companies operating in the animal genetics market. These players are focusing on the expansion and diversification of their market presence and the acquisition of a new customer base, thereby tapping prevailing business opportunities.

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In September 2020, Genus Plc and Tropic Bioscience entered into collaboration. Tropic Biosciences the pioneering agricultural-biotechnology company entered into collaboration with Genus in order to explore the application of Tropic's Gene Editing induced Gene Silencing (GEiGS) technology in porcine and bovine genetics.

In July 2020, Topigs Norsvin entered into strategic partnership with Acuity swine genetics company. This partnership will provide the opportunity for joint collaboration and expansion of technical expertise, commercial product testing and supply chain infrastructure in animal genetics market across the North America region.

In April 2020, Zoetis Animal Genetics and Angus Australia have entered into a strategic partnership that will aid Australian Angus breed stock and commercial breeders an additional benefit from genomic, or DNA-based technology. Zoetis have made a considerable investment in the expansion of the Angus genomic reference population through the provision of genotyping services and sponsorship.

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Amgen To Present At The 2021 Evercore ISI Healthcare Conference – Yahoo Finance

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THOUSAND OAKS, Calif., Nov. 24, 2021 /PRNewswire/ -- Amgen (NASDAQ:AMGN) will present at the 2021 Evercore ISI Healthcare Conference at 5:10 p.m. ET on Tuesday, Nov. 30, 2021. Rob Lenz, M.D., Ph.D., senior vice president of Global Development at Amgen will present at the conference. Live audio of the conference call will be broadcast over the internet simultaneously and will be available to members of the news media, investors and the general public.

The webcast, as with other selected presentations regarding developments in Amgen's business given at certain investor and medical conferences, can be accessed on Amgen's website, http://www.amgen.com, under Investors. Information regarding presentation times, webcast availability and webcast links are noted on Amgen's Investor Relations Events Calendar. The webcast will be archived and available for replay for at least 90 days after the event.

About Amgen Amgen is committed to unlocking the potential of biology for patients suffering from serious illnesses by discovering, developing, manufacturing and delivering innovative human therapeutics. This approach begins by using tools like advanced human genetics to unravel the complexities of disease and understand the fundamentals of human biology.

Amgen focuses on areas of high unmet medical need and leverages its expertise to strive for solutions that improve health outcomes and dramatically improve people's lives. A biotechnology pioneer since 1980, Amgen has grown to be one of the world's leading independent biotechnology companies, has reached millions of patients around the world and is developing a pipeline of medicines with breakaway potential.

For more information, visit http://www.amgen.com and follow us on http://www.twitter.com/amgen.

CONTACT: Amgen, Thousand Oaks Megan Fox, 805-447-1423 (media)Trish Rowland, 805-447-5631 (media)Arvind Sood, 805-447-1060 (investors)

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Exercise may lower inflammation by increasing endocannabinoids – Medical News Today

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Cannabis exerts its effects on the body by binding to cannabinoid receptors. These cannabinoid receptors also bind to endogenous cannabinoids that the body makes, called endocannabinoids.

Endocannabinoids are involved in the modulation of numerous biological processes, including metabolism, pain, inflammation, and transmission of information in the brain. The release of endocannabinoids, along with opioids, is also responsible for the feeling of euphoria that people generally experience after an intense workout.

A new study has shown that daily physical exercise is effective in lowering the levels of inflammation-related markers. Moreover, the study suggests that the endocannabinoid system may interact with gut microorganisms to produce such a reduction in inflammatory markers.

Researchers at the University of Nottingham led the research, which appears in the journal Gut Microbes.

Endocannabinoids bind to cannabinoid receptors present in the brain, peripheral nervous system, and immune system. The enteric nervous system, which controls the gut, also expresses cannabinoid receptors.

The dysregulation of the endocannabinoid system is associated with obesity and metabolic disorders.

Microorganisms present in the gut, which people collectively refer to as the gut microbiota, also have a significant influence on metabolism. Changes in the composition of these microorganisms, including reduced diversity of gut microorganisms, are associated with obesity and other metabolic disorders.

Studies suggest that the endocannabinoid system interacts with the gut microbiota to influence metabolism and energy homeostasis.

For instance, gut microbiota composition can influence endocannabinoid and cannabinoid receptor levels in the intestine. Specifically, changes in gut microbiome composition in obesity occur alongside lower endocannabinoid levels.

Obesity and other metabolic disorders are also associated with chronic, low grade inflammation. Both endocannabinoids and gut microbiota are involved in the modulation of inflammation, including in the aforementioned conditions.

Certain gut bacteria species can break down dietary fiber to produce short-chain fatty acids. These short-chain fatty acids have a link with lower inflammation and may exert protective effects against obesity.

Similarly, the endocannabinoid system can limit inflammation, and changes in the endocannabinoid system are observed in irritable bowel syndrome (IBS) and obesity.

Scientists do not fully understand whether the short-chain fatty acids that gut microorganisms produce can interact with the endocannabinoid system to produce anti-inflammatory effects.

The present study reports that the endocannabinoid system may mediate, in part, the anti-inflammatory effects of short-chain fatty acids that the gut microbiota produces, and vice versa.

Exercise is associated with an increase in endocannabinoid levels and long-term anti-inflammatory effects. The researchers used a 6-week exercise intervention to investigate further the association between endocannabinoids, inflammation, and short-chain fatty acids produced by gut microorganisms.

The researchers found that physical exercise was associated with lower inflammation, which higher short-chain fatty acid and endocannabinoid levels accompanied.

The studys first author, Dr. Amrita Vijay, a research associate at the University of Nottingham, told Medical News Today:

The findings from the current study highlight that simple lifestyle interventions such as exercise can modulate endocannabinoids, and this is a timely discovery, especially in the time when there is increasing interest around the use of cannabidiol and other related supplements in reducing levels of inflammation.

The present study involved two cohorts. The first cohort consisted of 78 adults who were aged over 45 years, living with knee arthritis, and residing in a community setting.

The researchers examined the relationship between the endocannabinoid system, gut microbiota, and inflammation in this cohort at baseline. They then confirmed these results in a second cohort consisting of 35 individuals over 18 years of age.

The researchers also assessed the effects of a 6-week exercise intervention tailored to people with osteoarthritis on the relationship between the endocannabinoid system, inflammation, and gut microbiota in the first cohort. To do this, they divided the participants into a treatment group, consisting of 38 participants, and a control group, involving 40 individuals.

The researchers used blood samples from the participants to evaluate the serum levels of endocannabinoids, short-chain fatty acids, and inflammatory markers. The inflammatory markers included cytokines, a class of immune proteins that have either pro-inflammatory or anti-inflammatory effects.

The team used stool samples and conducted DNA sequencing to assess the abundance of various gut microbiota species.

Before the onset of the exercise intervention in the first cohort, the researchers found that endocannabinoid levels had a positive correlation with gut microbial diversity, short-chain fatty acids levels, and levels of gut microbiota species that produce these short-chain fatty acids.

In contrast, higher endocannabinoid levels were associated with lower levels of Collinsella, a gut bacteria genus that is linked with increased inflammation.

Consistent with these results, endocannabinoid levels were positively correlated with anti-inflammatory cytokines levels but had a negative relationship with pro-inflammatory cytokine levels. These results from the first cohort were similar to those that the team obtained from the second cohort.

The researchers then estimated the contribution of endocannabinoids to mediating the anti-inflammatory effects of short-chain fatty acids. They used a statistical method called mediation analysis, which can help estimate the extent to which a third factor plays a role in mediating the relationship between two variables.

They found that endocannabinoids mediated roughly one-third of the effects of short-chain fatty acids on inflammatory markers. This suggests that other biological factors or pathways, in addition to the endocannabinoid system, may play a role in mediating the anti-inflammatory effects of short-chain fatty acids that the gut microbiome produces.

Likewise, the researchers investigated the extent to which short-chain fatty acids mediated the effects of endocannabinoids on inflammation. They estimated that short-chain fatty acids mediated about half of these effects.

However, the authors caution that such estimates, which they obtained using mediation analysis, do not imply causality.

Next, the researchers examined how the 6-week exercise intervention affected the association between endocannabinoids levels on one hand and short-chain fatty acid levels, gut microbiome composition, and inflammatory markers on the other.

They found that endocannabinoid and short-chain fatty acid levels increased in the exercise group but did not show any changes in the control group. At the same time, there was a decline in the level of pro-inflammatory cytokines in the participants in the exercise group.

Changes in the levels of the endocannabinoid anandamide correlated with the short-chain fatty acid butyrate after 6 weeks across the two groups. Moreover, the researcher found a positive correlation between the changes in endocannabinoid levels and the increase in the abundance of short-chain fatty acid-producing bacteria.

On the other hand, changes in endocannabinoid levels were negatively correlated with the changes in the abundance of bacteria and cytokines associated with pro-inflammatory effects.

Lastly, the endocannabinoid levels were positively associated with the expression levels of the genes for the short-chain fatty acid receptor FFAR2 and the cannabinoid receptor CNR2.

The short-chain fatty acid receptor is associated with a lower risk of obesity, whereas CNR2 is associated with anti-inflammatory effects.

These results suggest that the anti-inflammatory effects resulting from physical exercise could potentially involve an interaction between endocannabinoids and short-chain fatty acids.

Highlighting the studys salience, Dr. Vijay said, The findings are novel, as we may have found a key link between how substances produced by gut microbes interact with the substances produced by our own bodies, which tell us how physical exercise reduces inflammation.

The authors note that their findings are observational and do not establish causation. Furthermore, Dr. Vijay added, The exercise intervention we carried out was performed in individuals with painful knee osteoarthritis and may not be directly relevant to other groups.

It would be interesting to test if different forms of exercise have different effects on our bodies in relation to the levels of these substances being produced and thereby influencing inflammation. It is also important to consider the effect of diet on these relationships.

Dr. Vijay

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Exercise may lower inflammation by increasing endocannabinoids - Medical News Today

How experts have deployed data to tackle Covid-19 and plan for future pandemics – The Scotsman

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It involves understanding human behaviour, addressing inequalities, optimising our communications. It brings in public health and how that interacts with animal health, and then there is the economics lurking behind that. In parallel, there is a whole gamut of aspects to do with education.

Whitelaw says that Scotland, and specifically the University of Edinburgh, is ideally positioned to take advantage of the One Health agenda because of its expertise in human and animal health and in data.

He adds: Edinburgh has a joint medical and vet medical college, a leading science and engineering college and the wonderful humanities, arts and social sciences in the third college. It is not individually that we can address One Health, it is by bringing all these together, by intertwining roles and ideas, that we will achieve success, or do One Health data better.

But how has the One Health approach of collaboration and data sharing between scientists, health practitioners and the wider academic community helped shape our efforts to understand and tackle the coronavirus pandemic? And, building on the achievements already made, how better prepared are we for another global virus outbreak?

Dr Sam Lycett, a genetics expert at the University of Edinburgh, uses phylodynamics to study the spread of viruses. She says: This technique makes use of the now large collections of virus genome sequence data and the fact that these viruses accumulate mutations over time.

She uses this information to look at who infected whom either at an individual level or group level, such as a city or region. Going deeper than this we can also estimate predictive factors for why we see the transmission patterns. Is it just distance, known host movement patterns or a change in environmental conditions?

During the coronavirus pandemic, the amount of available data has been huge, Lycett says. In this current pandemic, there has been a massive global and UK-specific Sars-CoV-2 sequencing effort for people there are almost four million genomes now, with almost one million just in the UK and close to 100,000 just for Scotland.

This is a really good surveillance sample roughly, we are sequencing one in five or six positive cases. We use this sequence data to calculate how individual lineages and mutations are being generated, imported, and growing and declining, in Scotland.

Dr Kenny Baillie, a senior clinical research fellow at the Roslin Institute, says viral sequence data is now converging with clinical and biological data from humans and being used to find treatments for Covid-19.

The Roslin Institute is leading the most powerful study of human genetics of Covid more powerful in terms of discovery power than all of the other genetics studies in the world put together, says Baillie. Most recently, we have reported25 genetic associations with critical illness in Covid, many of which lead us to promising therapeutic avenues.

Discoveries reported after only five months of Covid being in the UK included two genes which have led directly to treatments being included in large-scale clinical trials.

In the future, Baillie wants to be able to look at treatments even more quickly than the five months which was achieved in the pandemic. We can move towards doing this in real time there is a convergence between animal and human science which means the same statistical techniques are used for both livestock and human genetics. With computing power and the human resource that is being deployed, we can move towards close to real-time host and viral genetic studies.

The study of zoonotic pathogens those that can move from animal to a human is at the heart of discovering the way coronavirus spreads, both locally and globally.

Virologist Christine Tait-Burkard, a research fellow at the Roslin Institute, has been working on coronaviruses for more than 12 years. She says: Coronaviruses have an inherent potential for cross-species transmission as one of the properties they have is that they can swap large parts of their genome relatively easily, and that is a bit reminiscent of the most known zoonotic virus, the influenza virus.

International data accumulation and sharing has helped build understanding of coronavirus. Tait-Burkard says this includes looking at treatments for other diseases, such as cardiac conditions and cancer, which can help develop help with coronavirus we can harness that and also tackle coronavirus.

And she says the drugs needed should be taken as early as possible, not when a patient has had to be hospitalised. We really need a pill that people can take at home when they get the first symptoms.

Tait-Burkards work with international colleagues includes looking at the livestock, the wildlife and the human coronaviruses and finding the commonalities, taking all the data together so that we can get drugs that are there for any future pandemic.

We need to leverage lessons from Covid, says Professor Ross Fitzgerald, personal chair of molecular bacteriology at the University of Edinburgh. His work focuses on antimicrobial resistance (AMR), described as a slow pandemic and a huge public health threat, with estimates suggesting hundreds of thousands of deaths occur worldwide due to infections caused by resistant bacteria. This is a major health crisis that has taken a back seat since the pandemic, he says, warning that effective antibiotics could run out.

A lot of the work to find a solution to AMR surrounds data, says Fitzgerald faster diagnostics, more sequence information and real time surveillance of humans, animals and the environment on a global scale.

And he adds that the work on coronavirus can now help tackle AMR. We need to unite academia, industry, government and policy-makers so we are all working together, communicating the data effectively to address the impact of AMR.

Fitzgerald is concerned there is not sufficient volume of data to address AMR at the moment. We need more data, but to get the value from it we need to have really good descriptive information it is high-quality data that we need.

And he is a strong advocate of developing artificial intelligence and machine learning to harness that data. We know that it will allow us to track the emergence and spread of resistance and pathogens.

Professor Lisa Boden, chair of population medicine and veterinary public health policy at the University of Edinburgh, says that from a One Health perspective, there have been issues surrounding the way coronavirus has been dealt with.

She says: Covid-19 has really made visible different types of vulnerabilities in our institutions, our governance and our legal structures, and those are really due to entrenched health, social, racial, political and economic inequalities at different scales, at a local and international level.

Boden says there has been a lack of complete data particular for people living on the edges of society and those people who are living in communities which might be remote, rural and geographically isolated.

To change this, she advocates a non-linear approach which looks at both the causes of inequality as well as at a disease itself, using multi-sectoral datasets.

But with the experience of a vast amount of data collection, use and sharing surrounding the pandemic, some believe future outbreaks could look a lot different.

Lycett says: We will be able to predict and quantify the risk of having a pandemic. Whether we will be able to predict the exact time and place of the event itself is very variable. But certainly to predict risky areas and risky situations, it is possible.

Tait-Burkard agrees, saying: It is probably not all that easy to predict when the transmission is going to happen but what we can learn from this pandemic is to be better prepared. And we now have the facilities in place to do that preparedness, we will have to make sure there is money available to maintain these facilities.

This article first appeared in The Scotsmans Life Sciences 2021 supplement. A digital version can be found here.

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How experts have deployed data to tackle Covid-19 and plan for future pandemics - The Scotsman

Studies Reveal Designs of Nucleus and DNA – Discovery Institute

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Image credit: Miroslaw Miras, via Pixabay.

You may have heard that all the DNA in your body, if stretched out, could reach to the Sun and back more than 70 times. What is even more amazing is that all this DNA occupies only a tiny fraction of the space within your body it is packed away inside the tiny nucleus of each cell. Furthermore, the DNA is not merely packed away and sitting idly; rather, it is a dynamic molecule taking part in several active processes including gene expression and cell division. Three new scientific papers have been published in recent weeks that reveal exquisite patterns of design in the DNA and nucleus in which it is housed.

The human genome is organized in 23 pairs of chromosomes. Most of the pairs are of similar length, but in the final 23rd pair, the first chromosome designated X is much longer than the second chromosome designated Y. That is not the only unique characteristic of the 23rd pair. These so-called sex chromosomes differ between the genders. While males have both an X and Y chromosome, females have two X chromosomes. As if to avoid a double dose of X chromosome genes, females inactivate one of their two X chromosomes during embryonic development. As for which of the two X chromosomes is inactivated, this appears to be done randomly in each cell. This means that females, unlike males, have two different functional genomes operating in their bodies, making for a fascinating twist to female genetics. That is, in some cells of the female, the first X chromosome is active whereas in the remainder of the cells the other X chromosome is active. A classic example is the colorful calico cat whose two X chromosomes code for two different colors.

Exactly how the developing female embryo inactivates one of the X chromosomes has not been well understood. What has been clear is that the story involves a region on the X chromosome itself, and information in that region that codes for a long RNA molecule, known as Xist. The name Xist stands forX-inactive specific transcript, a direct reference to its function of inactivating the X chromosome. But a genetic region that, ultimately, causes the inactivation of the entire chromosome must be handled very carefully. It is present on all X chromosomes but causes inactivation not of the single male X chromosome, and not of one of the two female X chromosomes. Importantly it causes inactivation only of the other female X chromosome.

In addition to the fact that Xist must be very carefully controlled, new research1is shedding light on how this single molecule can produce such a significant result. While it seemed that a very large number of Xist molecules must be required to inactivate the much larger X chromosome, the researchers studied mouse embryonic stem cells and found that only about one hundred Xists are required. The Xists, operating in pairs, recruit a large number of proteins. The result is about 50 complexes, each consisting of two Xists and an army of proteins, spaced along the X chromosome. Some of the proteins twist and condense the overall chromosome, compressing it so that most of the genes are close to one of the 50 complexes. Other proteins act to silence those nearby genes, thus essentially inactivating the entire X chromosome. Obviously, there are many important, coordinated, steps in this inactivation process, allowing for a small number of Xists to manage this big job. As the papers lead author remarked, It was kind of shocking to us that from just 50 sites, Xist manages to silence a thousand genes.2

X chromosome inactivation is not the only function that RNA molecules perform in the nucleus. They also, for example, help to maintain the overall three-dimensional structure of the various macromolecules in the nucleus, including the DNA. This is important because otherwise in the crowded nucleus, molecules can inadvertently chemically bond, or link, to one another. DNA crosslinking, for example, can result from environmental toxins and radiation. Such crosslinking, whether between DNA or other molecules, can cause cell death and is the goal in some chemotherapies. But crosslinking also is proving to be a valuable research tool. As another new paper reports,3crosslinking is now being used, along with several other complicated steps, to map out the three-dimensional structure of the DNA, various RNAs, and many proteins, within the nucleus. Simply put, the general idea is to link together molecules that are in close proximity. The cell is then broken down into clusters of linked molecules which can be identified and mapped out to reconstruct the structures within the nucleus.

The researchers found the certain RNA molecules serve to recruit and organize other RNA and protein molecules. Those recruited RNA and protein molecules, which otherwise would randomly move about, then serve important regulatory roles in accessing and processing the DNAs genetic information. The researchers also found that several high-concentration territories are formed within the nucleus, where these molecules cluster and function. As the paper explains, the organizing RNA molecules recruit diffusible RNA and protein regulators into precise 3D structures. What we are seeing is a much more detailed, elegant, and exacting picture of the nucleus than textbooks have ever envisioned.

The problem of organizing and maintaining the molecular structures within the nucleus becomes even more intriguing when one considers cellular division. When a cell divides, producing two daughter cells, the precise 3D nucleus structure discussed above must somehow be reestablished in the new cells. Certain proteins have been known to be important in this process, and another new study4has now identified a single protein that is particularly important in this cell division process. The protein, called lamin C, is, according to the paper, uniquely required for large-scale chromosome organization, and global 3D genome organization in the daughter cells.

During the process lamin C is phosphorylated, meaning a phosphoryl group is attached by special proteins. The phosphoryl group is removed when lamin C is done with its job, which is just one part of a larger, more complex process. As the lead researcher explained, There is this exquisite choreography of the different lamin proteins and DNA to get things just as they should be.5

Beyond this exquisite choreography, the crucial role of lamin C highlights another hallmark of design; namely, the teleology implicit when a part is required for its own production. Because lamin C, a protein, is produced by cellular protein synthesis. That is a process that begins with the genome in the nucleus, which is maintained by lamin C. In other words, lamin C is required for the production of lamin C.

These three studies of the structures within the cells nucleus continue to reveal a natural world that gives evidence design in many different ways.

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Studies Reveal Designs of Nucleus and DNA - Discovery Institute

What are the Trollocs in The Wheel of Time? Creatures origin explored – HITC

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**Warning Spoilers ahead**

Sacrifice the mince pies this Christmas for a slice of Amazons The Wheel of Time. Up ahead, we explore the big bad enemies, the Trollocs, and where the creatures came from.

The Wheel of Time follows Rosamund Pikes wizard, Moiraine, who journeys across the lands in order to pinpoint who the reincarnation of the Dragon is and oversee their destiny to navigate the fate of the world.

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Trollocs are a species of Shadowspawn (creatures formed by the Dark One) created during the Age of Legends.

These creatures are known to have made up a large portion of the Dark Ones army and are a cross between humans and animal stock similar to Orcs.

Trollocs are able to communicate with the local tongue, however, their primitive side decreases their intelligence across the board, and therefore, they require supervision on the battlefield.

Similar to J. R. R. Tolkiens Uruk Hai, the antagonist during the War of the Shadow in The Wheel of Time, the Dark One, was hellbent on creating super soldiers for his army.

Using the skills of the Forsaken Aginor, human genetics were mixed with intelligent and sturdy animals, such as boars and eagles, to produce an advanced breed.

While early creations of the Trollocs were looked on as a failed experiment, the offspring of this new species eventually resulted in the birth of more sentient Trollocs known as the Myrddraal.

The Trollocs were introduced during the three-episode premiere of The Wheel of Time when Moiraine and Lan were ambushed.

Using a combination of Moiraines magical abilities and Lans swordsmanship to mitigate the Trollocs ambush, a telekinetic lightning storm was then produced.

The Trollocs arrival at the Two Rivers foreshadows a much larger threat looming and fans will have to wait and see the full force of the Dark One later on in season 1.

In other news, Release date for JoJos Bizarre Adventure Stone Ocean explained

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What are the Trollocs in The Wheel of Time? Creatures origin explored - HITC

Lost Women of Science, Episode 4: Breakfast in the Snow – Scientific American

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From the COVID vaccine to pulsars to computer programming, women are at the source of many scientific discoveries, inventions and innovations that shape our lives. But in the stories weve come to accept about those breakthroughs, women are too often left out.

Each season at Lost Women of Science, well look at one woman and her scientific accomplishment: who she was, how she livedand what she found out. Katie Hafner, a longtime reporter for the New York Times, explains the science behind each womans work and explores the historical context in which she lived.

Our first season, The Pathologist in the Basement, is all about Dorothy Andersen, a physician and pathologist who solved a medical mystery when she identified and defined cystic fibrosis in 1938. A passionate outdoorswoman, a rugged individualist and a bit of an enigma, Andersen changed the way we understand acute lung and gastrointestinal problems in young children.

This podcast is distributed byPRXand published in partnership withScientific American.

Episode Transcript

FRANCIS COLLINS: [singing a capella] Dare to dream, dare to dream, all our brothers and sisters breathing free. Unafraid, our hopes unswayed, till the story of CF is history.

KATIE HAFNER: Im Katie Hafner and this is Lost Women of Science, a podcast in which we unearth stories of female scientists who didnt receive the recognition they deserved. We devote each season to the life and work of one woman. Were revisiting the historical record, one extraordinary scientist at a time.

This is the final episode of our first season, The Pathologist in the Basement. Weve been telling the story of Dr. Dorothy Andersen, a physician who was the first to identify the disease cystic fibrosis in the 1930s.

This episode is divided into two parts. One of those parts is linked to that voice you just heard singing. It belongs to Dr. Francis Collins, the outgoing director of the NIH. Dr. Collins is one of the geneticists who isolated the cystic fibrosis gene in 1989. In this episode, well explore advances in CF treatment. And well also explore Dorothy Andersens legacy, starting at the end of her life.

The last living keeper of that legacy is Dr. Celia Ores, a pediatrician mentored by Dr. Andersen in the early 1960s.

CELIA ORES: Can you put this down and we go and pick up Dr. Andersen and put her here on the table?

SOPHIE MCNULTY: Oh, the photo. Yeah. Yeah, let's go. Let's go find the photo.

MICHELLE ORES: I have it here, mom.

SOPHIE MCNULTY: Michelle has them.

CELIA ORES: Oh, okay.

MICHELLE ORES: I have the two photos. I have the one of Dorothy. And the one of you in Switzerland in medical school.

KATIE HAFNER: Were back in the New York apartment of Celia Ores.

Dr. Ores is now in her nineties. Shes holding a black-and-white photograph of Dr. Andersen close to her chest, as she talks to Sophie McNulty, our associate producer.

CELIA ORES: When I came to the United States, she was the only one who treated me really, really well.

KATIE HAFNER: Dorothy Andersen took Celia Ores under her wing, passing on what she had learned about cystic fibrosis, and in turn, Dr. Ores dedicated a large part of her career to patients with the disease.

CELIA ORES: Every little bit of cystic fibrosis that I know is what she told me. She told me everything.

If I had some issues with a patient that I don't fully understand, I went to her and told her that I don't know what I can do next for this patient.

KATIE HAFNER: But she couldnt help everyone. In the 1960s, cystic fibrosis patients rarely lived past their mid-teens.

But the story of cystic fibrosis takes a turn for the better.

And thats the heart of this episode: we believe Celia Ores is the only living person who actually knew Dorothy Andersen well, and in holding that photograph, shes holding Dr. Andersens legacy tight. In this episode, we want to tell you about that legacyand the progress that grew from her lifes work.

KATIE HAFNER: When she was working in the 1940s and 50s, Dorothy Andersen was driven to get the word out about what shed learned about cystic fibrosis. She went on lecture circuits, giving talks up and down the East Coast. When she was on vacation one summer in Europe -- or what she joked was a busmans holidayshe agreed to speak at medical schools and hospitals.

UNKNOWN: Dr. Andersen?

DOROTHY ANDERSEN: If you place a child with the celiac syndrome on a diet designed for celiac disease, you will find that most children with any form of failure to thrive will improve in weight somewhat.

KAITE HAFNER: It occurred to me while putting this season together that I didnt have a clue what Dr. Andersens spoken voice sounded like. But I was lying in bed one night, reading Scott Bairds biography of Dr. Andersen, and I noticed that he mentioned this, just in passing:

Her voice (from a professional recording in the late 1950s) was soft and musical.

I wrote to Scott immediately, and asked if he had the recording. He sent back an excerpt from a recording in which Dorothy Andersen and a few other physicians discuss the syndrome known as failure to thrive. Thats a catch-all term that was used to describe children who werent growing or gaining weight as quickly as they should.

UNKNOWN: Dr. Andersen, wed now like to hear what you have to say about the celiac syndrome, which includes cystic fibrosis and a variety of other conditions, some labeled as celiac disease.

DOROTHY ANDERSEN: The three characteristics of the celiac traid are failure to thrive, the passage of large, undigested stools, and an enlarged abdomen. The two most common diseases in this group are cystic fibrosis of the pancreas and gluten-induced celiac disease. Its fairly easy nowadays to sort out the cystic fibrosis cases from the rest by means of the sweat test.

KATIE HAFNER: Hearing her voice was a revelation. It was like hearing about someone for months then finally meeting them.

But despite all the work Dr. Andersen had done, at the end of the day, CF was still deadly and the stories of the patients were incredibly sadfor the families, of course, but also for the doctors.

CELIA ORES: Well, you go home and cried. It was very, very difficult for me to adjust to it. Because I would see young children that I tried to save from dying. And I didn't always succeed.

KATIE HAFNER: As a pediatrician in the 1960s, Celia Ores did all she could to extend the life of her patients. As did Dorothy Andersen.

CELIA ORES: It was a function to maintain the patient as best you can, as long as you can. And that's exactly what we were doing.

DORIS TULCIN: I knew Dorothy Anderson because she diagnosed my daughter who has cystic fibrosis.

KATIE HAFNER: Thats Doris Tulcin. You met her in episode one. Mrs. Tulcin took her daughter Ann to see Dr. Andersen in 1953, and she helped start the Cystic Fibrosis Foundation in the 1950s.

DORIS TULCIN: And I know that if she were alive today, she would be amazed at the journey that we've gone on for over 65 years.

KATIE HAFNER: Sadly, Dorothy Andersens own health took a nosedive in the early 1960s.

CELIA ORES: Every evening around four o'clock we would have some meeting. And there was five or six doctors, and some of the doctors she liked she would invite. So she would make some tea and we would talk about subjects such and such.

And one day she said in the evening, what are we going to talk about tonight? And the doctor, a male doctor, said, why don't we talk about Dorothys smoking? She said, You know, I like you very much. I think you're a very good doctor and you're a very nice human being, but if you behave like this, I will ask you not to come to our meetings.

[Sophie laughs]

SOPHIE MCNULTY: She was very tough?

CELIA ORES: Well, she didn't want to leave the smoking,

KATIE HAFNER: Research was starting to show that smoking was deadly.

AUDIO CLIP: The committee has reached the overall judgment that cigarette smoking is a health hazard of sufficient importance to the United States to warrant remedial action.

KATIE HAFNER: But many people in the 1950s and 60seven doctors, including Dorothy Andersenwere in denial. She was a lifelong chainsmoker. Almost everyone we spoke to about her mentioned itand this was all the more surprising since she spent so much of her professional life examining lungs that had become incapable of exchanging air.

Smoking eventually killed her.

Sophie McNulty: Do you remember the last time you saw her?

CELIA ORES: Yes. Uh, she was in a room alone and there was a sign, no, no entry, but she called me and I went to her to her to see her.

KATIE HAFNER: Dr. Andersen had always worked to protect Dr. Ores in an environment that was less than friendly to women.

CELIA ORES: And she said that she wanted to apologize to me that she didn't do more for me than she should have.

I told her that I lived under Hitler, I lived under Stalin, and I think I'll be able to survive the people in this unit. If I don't get as much in money or fame, that doesn't bother me.

It was very difficult because the women were considered for nothing.

KATIE HAFNER: Dorothy Hansine Andersen died on March 3, 1963. The cause was lung cancer. She was buried in Chicago alongside her parents.

SOPHIE MCNULTY: After she died, how did your work change?

CELIA ORES: I felt lonely in the hospital. I continued to take care of the children just as much as I did before, but it was... I didn't have anyone to discuss with the things that I discussed with her.

She was my guide. I could come to her and say, you know, such and such, that such and such, you know, I just felt comfortable when she was there.

KATIE HAFNER: After Dr. Andersens death, her farm in the Kittatinny mountains in New Jerseythe farm on which Dorothy Andersen built her cabin with her own hands, the farm where she invited colleagues and friends and put them to work chopping wood, and laying brick for the fireplace, the farm Celia Ores would visit with her childrenshe left that to close friends. Today, that land is a nature preserve.

Dorothy Andersen left her personal papers to Bessie Coombs Haskell.

Wait. Who?? We couldnt find much documentation of this friendship, except the brief mention of the bequest. But, according to people we called, Bessie was a friend of Dorothy Andersenor Andy as she was known to Bessie. Bessie Coombs Haskell ran a camp in St. George, Maine called the The Blueberry Cove Campand used to be a dancer in New Yorkbut we couldnt find much more than that.

Just what was the what, where, when and how of their friendship? What made Bessie Coombs Haskell so important in Dorothy Andersens life that she left her papers to this person, and not, say, to one of her friends in New Jersey, or to Celia Ores, or to another colleague at Columbia? It just goes to show you (and us) that there are many things we will never know about Dorothy Andersens life.

As far as we can tell, Bessie Coombs Haskell kept Dr. Andersens papers until she died. After that, its anybodys guess. We contacted the library in the small town of St. George on the coast of Maine, as well as the local museum and historical society. They had nothing. We did find Bessies grandson, who told us he was pretty sure he threw the papers away after his grandmother died.

At the end of the day, a legacy comes down to the stories people tell us, yes, but also to the things left behind. What gets kept and what gets thrown away. Its haphazard. Boxes get tossed in the trash. This is nobodys fault, but still, its profoundly disappointing.

Its profoundly disappointing because its not like Dorothy Andersen died in a previous millennium, in which case the lack of archival material would be totally understandable. But in the scheme of things, she died relatively recently.

So, one of the lessons I take from our dive into the life of Dorothy Andersen is this: if youre clearing out the basement or attic of a relative whos died, open the boxes. Dont throw out your grandmothers papers, because you just never know.

Coming up, the second part of this episode: Cystic fibrosis in the decades since Dorothy Andersens death. Im Katie Hafner and this is Lost Women of Science.

[AD BREAK]

KATIE HAFNER: Im Katie Hafner and this is Lost Women of Science: The Pathologist in the Basement.

Given all weve just said you might think the story ends with Dorothy Andersens death in 1963. But it doesnt. Her work has pioneered almost a century of science and discovery. To this day, Dorothy Andersens foundational research in cystic fibrosis continues to be built on. In the years since she died, the prognosis for CF patients has just gotten better and better and better.

Dr. William Skach is the outgoing chief scientific officer at the Cystic Fibrosis foundation. Hes been working on this disease for more than 30 years.

BILL SKACH: Well, in the 50s, the therapies were really incredibly simple and supportive.

It was recognized that the mucus in the lung was thick and couldn't be coughed out. So hydrating that mucus became one of the key goals. And, and patients used to sleep in mist tents because they thought that the breathing in the, the mist would then soften those secretions, which didn't really work very well.

Another problem at that time was antimicrobials, antibiotics, for, for the infections because the people with CF frequently got lung infections and that's really what caused most of the damage to the lungs, which was progressive, and, and eventually led to lung failure.

KATIE HAFNER: Parents were the lynchpin of the CF community. In the 1950s, with Doris Tulcin and a handful of others leading the way, parents banded together to form the Cystic Fibrosis Foundation. Today, the CF Foundation has a fund totaling more than $4.5 billion, which is about the same as the endowment of NYU.

BILL SKACH: And I will say that from its very beginning, it was really a collaborative effort with the community, with the scientists, with the physicians, to try to understand the disease better and to really work with the technology and the science at the time to take all of our understanding about the disease and turn it into therapies.

KATIE HAFNER: And it was during this period in the 50s, when Dr. Andersen was still at the forefront, that the focus was firmly on treating symptomsmaking CF patients as comfortable and functional as possible. But, as Dr. Skach points out:

BILL SKACH: With symptomatic therapy, you could only go so far. If you didn't really know what caused the disease, you couldn't really attack the basic root cause and reverse it. And so we got fairly good at treating the symptoms, but not good enough.

KATIE HAFNER: Children were still dying. The life expectancy had slowly been increasing over the years, but it was still devastatingly low.

For instance, in the 1980s, cystic fibrosis patients still werent expected to live much past their teens. Heres Brian OSullivan, the pediatric pulmonologist youve already met. Hes been working with CF patients for more than three decades.

BRIAN OSULLIVAN: And I do remember one family where the teenage girl was, was very sick, had been in the hospital for over two weeks, getting IV antibiotics, and and she had continued to deteriorate, um, and her parents knew she was dying and, and the parents actually came up to me and asked me to give their child permission to die, because they couldn't do it, but they knew she was hanging on just for them.

And so they left the room, I held her hand and told her that she had done everything she could do. She'd put up a great fight, but that she wasn't getting better.

And, uh, shortly thereafter she died, um, and her parents thanked me. Um, and that kind of experience doesn't leave you.

KATIE HAFNER: Around this time, scientists began redoubling their efforts in basic research, much of it funded by the Cystic Fibrosis foundation.

This takes us back to Francis Collinsthe outgoing director of the NIH. Back in the late 1980s, as a geneticist, he led a research team at the University of Michigan that was furiously searching for the CF gene, along with Lap-Chee Tsui, at the University of Toronto.

FRANCIS COLLINS: Lap-Chee and I met at a genetics conference in 1987. And it was clear we were all really struggling, trying to find what was quite literally, in my view, a needle in the haystack and the haystack was really big and the needle was hard to find. And we sat in the sun and talked about what each of our labs was doing as far as our approaches and realized that our approaches were not the same. They were actually beautifully complementary and we kind of decided on the spot and much credit to Lap-Chee, that he was willing to take this leap as well, that we would just merge our labs and we would stop competing. And we would basically become one family of researchers between Toronto and Ann Arbor.

And what seemed like it might be an unsolvable problem got solved in just about two years.

JANE GROGAN: Can you describe the moment when you and, and/or you and the team knew that you had the cystic fibrosis gene or the gene that causes cystic fibrosis?

KATIE HAFNER: Thats Jane Grogan, our scientist-in-residence. Shes an immunologist by training and currently running research in cell and gene therapy at GraphiteBio in San Francisco.

FRANCIS COLLINS: At the time I remember, uh, we were at a meeting. He and I were at Yale. It was one of those human genetics meetings and, uh, he had set up a fax machine in his room. We were all staying in the dorms at Yale, which were, shall we say a little austere.

And we had a very long day. And at the end of the day, he and I went to his room where the fax machine was. And there was all this paper on the floor. That's the way we communicated back then, there was no email.

JANE GROGAN: Some of us sending furious messages, right?

FRANCIS COLLINS: Yes! Cause it was that day's data. And so we pull the papers up off the floor and we began to look at the evidence that this three base pair deletion in a previously unknown gene correlated with cystic fibrosis and that as we looked through the data, it got better and better.

And that was it. That was it for me. That was a rainy night in May, 1989 in New Haven.

And I was like, over the moon, excited.

KATIE HAFNER: This discovery was a big big dealit was on the cover of the journal Science, and it was all over the popular press too. Now that the gene abnormality had been identified, it seemed that a cure for CF was just around the corner.

KATIE HAFNER: And the discovery of the gene has led to all kinds of things, right?

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Lost Women of Science, Episode 4: Breakfast in the Snow - Scientific American

Treatment in Texas: For families of kids with rare diseases, its a full-time job to advocate for, raise millions for research – KXAN.com

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AUSTIN (KXAN) How far would you go to save your childs life? Thats a question some parents have to ask themselves after learning their child has been diagnosed with a rare disease.

While each rare disease only impacts a small portion of the population, thousands of them exist. KXAN found many Texas parents are forced to quit their jobs and become full-time advocates for their kids after diagnosis. Funding research for potential treatments costs millions of dollars.

Here are some of those families.

Five-year-old Simon could probably hold his own against just about anyone in a game of Horse. Its something you would see go viral on social media, the little guy can sink baskets on his Little Tikes hoop for hours.

Simon loves basketball. His mom says hes been that way since he was 2 years old.

While his shooting is beyond impressive, its actually the happy dance he does when hes made a particularly impressive shot that might be more fun to watch. Its hard not to match Simons energy when youre in a room with him especially when hes sinking baskets one after another.

But this isnt what Simons life is going to look like much longer without treatment.

Simon has Sanfilippo Syndrome, a rare disease that his mom, Alina Gorniak, describes as Alzheimers in children. As the disease progresses, Simon will lose his ability to speak, care for himself, he wont be able to run or jump or shoot a basketball, hell suffer from seizures and by his teens, Simon will likely die.

I just cried and cried and cried, Gorniak said sitting on the floor with Simon in her lap, remembering the night she learned Simon had Sanfilippo. And then I woke up in the morning thinking okay, what do we do next?

The answer to that question was to fight, and parents like her have to if they want to see the needle move on potential treatments or cures for rare diseases. Because a rare disease, as the name indicates, impacts so few people proportionally, biotechnology companies dont generally initiate or fund the research.

Thats where the parents come in.

We have vulnerably opened our world up to the rest of the world in hopes of finding a cure for Simon and other kids with Sanfilippo Syndrome, Gorniak said.

Even though rare diseases are well, rare Simons family is far from alone. Maxwells family is going through a very similar process, trying to raise money for research that could potentially save their sons life.

Maxwell has a disease that doesnt even have a formal name, referred to by the gene SLC6A1. The disease causes developmental disabilities, a movement disorder and eventually debilitating epilepsy. Doctors told Maxwells parents that nothing could be done.

They said give him the best life you can, we have no idea what the future holds, youre going to become the expert in this disease,' Maxwells mom, Amber Freed, said.

Freed quit her job and started calling around to scientists and research groups hoping for a better answer. She found that UT Southwestern in Dallas was willing to develop a gene therapy that could potentially help Maxwell, and other kids with the same disease.

The catch, again, was money. Freed now works around the clock trying to raise enough of it to keep the research from being tabled.

By far the greatest challenge for me has been balancing motherhood while trying to help Maxwell. Its finding a balance between fighting for him and being with him, Freed said.

For these two families, its a full-time job seeking out groups and trials that could help their children. At the end of the day, Freed described her sons disease as one that fell into the too rare to care category.

Doctors are only going to see a couple of these cases in their lifetime, scientists dont work on them often and biotechs dont work on diseases that dont effect many people because its not profitable, Freed said.

UT Southwestern is where Maxwells family turned. Just this month, UT Southwestern was named a rare disease center for excellence by the National Organization for Rare Disorders (NORD). That designation is designed to help expand access, and advance care and research for rare disease patients in the United States, a news release said.

But to get her son connected to UT Southwestern, Freed says she had to send a researcher Uber Eats snacks with messages from Maxwell every day. Finally, she found he was going to be at a conference and just showed up.

Sat down right next to him in a row with no people in it and he turned to me and said hi, Amber,' Freed said. It was either going to be a beautiful team or he was going to file for a restraining order, and Im very happy to report that it has become a beautiful team.

Meanwhile, the Croke family turned to the Cure Sanfilippo Foundation. Glenn ONeill, the president of the foundation, also has a child with the syndrome Simon has. Like these families, he and his wife work full-time seeking out a cure.

Oftentimes its left to these parent foundations and organizations to make the difference, ONeill said.

The general rule of thumb is that to fund basic research, you need $100,000. To move that to a preclinical research stage, you need $1 million. To fund a phase one clinical trial youll need about $10 million and to get an approved treatment all the way through the FDA approval process costs between $50 and $100 million, ONeill told KXAN.

Were not going to sit back and do nothing, ONeill said. Were going to try and fund that early research so that it actually de-risks the research so biotechs are more interested because some of that early research has been done.

The National Organization for Rare Disorders puts out a report card every year, breaking down how all 50 states stack up when it comes to supporting people with rare diseases.

In their most recent report, published in January of 2021, Texas failed in three of the seven ranked categories. The state passed, or was given an A for three others.

You can read the report here:

There are more than 7,000 identified rare diseases, according to the National Institutes of Health (NIH). Roughly 95% of those diseases have no treatment.

Dr. Brendan Lee, professor and chairman of the department of molecular and human genetics at the Baylor College of Medicine, and the main investigator for the Undiagnosed Diseases Network, says theres just not enough research available to look into each and every rare disease.

There are so many rare diseases, and while theres enormous research that goes on in this country, in the world, and obviously the U.S. has been the leader in the world in investing in research and technology innovation, there still isnt enough research to account for every rare disease, Lee said.

The Undiagnosed Diseases Network works to help patients identify undiagnosed rare diseases and connects hospitals and researchers in an attempt to spread awareness and get people to solutions faster.

Patients often bounce around getting all different types of tests and they dont point to a known association, a label, Lee said. Thats where we and this network come together.

For more information about the UDN and the application process, visit the networks website.

Both of these Texas families need your help donating, and sharing their story.

The Freed family is working to raise $1 million to benefit SLC6A1 Connect, which is advocating for research to help find a treatment and cure for kids like Maxwell. To donate visit their GoFundMe here.

Gorniak and her husband working to raise $1 million for the Cure Sanfilippo Foundation, which is doing research that could help kids like Simon. A fundraiser for the Cure Sanfilippo Foundation through Simons family can be found on GoFundMe.

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Treatment in Texas: For families of kids with rare diseases, its a full-time job to advocate for, raise millions for research - KXAN.com

I write while my children steal cars and rob houses: the awful human cost of racist stereotypes – The Guardian

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As I write this article, my children are stealing cars and robbing houses, I suppose. I am an Indigenous father so, doesnt that tell you everything you need to know about me as a parent, and about my childrens capacity to understand right from wrong?

I know you sense the sarcasm in this. Well, a great, great majority of Australians would. But there is a certain type of person I am implicating here. The type who have an ignorance so deeply ingrained, that it is a wonder they havent wandered off into the dark recesses of our colonial history and followed each other off the edge of a cliff. Shouldnt they be extinct?

An article celebrating an infamous Bill Leak cartoon the one which depicts an Indigenous father unable to remember his childs name sparked me to respond to those with this mindset. I suggest you dont bother reading any of these articles dont give them the benefit of a click. But I will summarise: A journalist, hiding behind a rotting faade of caring about Indigenous children, argued that the statistics of Indigenous over-representation in prisons are caused by Indigenous parents [who] routinely abandon their responsibilities and do little to instil in their children respect for our laws and the property of others. According to this privileged white man, While [Indigenous parents] march up and down the street waving flags, their children are stealing cars, robbing houses and being hauled off to the watch-house.

The harm that racist comments and cartoons cause is never felt by those who make them. It is not white males, nor their children, who are creepily shadowed by security as they shop. They dont feel the suspicious glances that a First Nations father feels when he hugs his child, as if he is not a protector of the child, but as if the child needs protection from him. They would never have felt that thick and heavy fear that we feel, when we imagine what may well happen to our children should they step into the path of a cop who has nodded in agreement at a cartoon in a major paper, and believes that all Black kids, thanks to all Black parents, carry a greater criminal intent in our DNA.

Racist stereotypes have an awful human cost.

The fact that Indigenous people die around eight years younger than other Australians says more about how little regard our political system has for my people, than it does about our genetics. And the fact that Indigenous people are proportionately the most incarcerated people on the planet says more about our powerlessness as a people to hold the nations law and policymakers to account, than it does about my childrens capacity to understand right from wrong.

It really is as the Uluru Statement so eloquently and powerfully says:

Proportionately, we are the most incarcerated people on the planet. We are not an innately criminal people. Our children are aliened from their families at unprecedented rates. This cannot be because we have no love for them. And our youth languish in detention in obscene numbers. They should be our hope for the future. These dimensions of our crisis tell plainly the structural nature of our problem. This is the torment of our powerlessness.

And how can you argue with that, unless you believe we are less than human unless you are racist?

I had to think hard about if I bite back by writing this article. Why give the likes of Leak and others any attention, I wondered. Should I ignore it and focus on the positives rather than the negatives?

I concluded there should be a response. The stereotype must be defeated; not so much by changing the ignoramus mind, but by changing the country so the ignoramus is forced closer to that cliff.

And so it is to the pen, the ink, the keyboard we go, more and more Indigenous writers who are fighting fire with fire. We are the authors of who we are. Not old white men.

This is one of the reasons 12 First Nations men wrote a book with me, Dear Son Letters and reflections from First Nations fathers and sons. We wrote it, partly in response to publications like Bill Leaks racist cartoon, but also because of the awful legacies of the Northern Territory Intervention, and the crap we were taught about our First Nations forefathers in school that our forefathers were savages while the white students forefathers were our discoverers and saviours. Dear Son celebrates Indigenous fatherhood through letters and poems. We express love for ourselves and our families in a beautiful act of defiance.

The key factor is that contrary to claims of failed responsibility by Indigenous parents, we in fact are calling for greater responsibility. We march the streets and fly our flags, we protest because we love our children. We are calling to change this country for the better we want a referendum for a constitutionally enshrined Indigenous voice, so we may hold parliament accountable for failing to meet their responsibility to keep all Australians equally safe.

Thomas Mayor is a Kaurareg Aboriginal and Kalkalgal, Erubamle Torres Strait Islander. He is the Indigenous officer of the Maritime Union of Australia and the author of Dear Son Letters and reflections from First Nations fathers and sons. He tweets @tommayor11

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I write while my children steal cars and rob houses: the awful human cost of racist stereotypes - The Guardian

Europe has learned nothing from Brexit – POLITICO.eu

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Dr. Eoin Drea is senior research officer at the Wilfried Martens Centre for European Studies.

It remains remarkable that for such a seismic event, Brexit continues to be most noticeable by its absence in the formulation of future European Union strategy. From the Conference on the Future of Europe to European Commission President Ursula von der Leyens state of the union address, Brexit, Britain and the future of the Anglo-EU relationship struggle to elicit a single reference or positive soundbite.

This in itself is a remarkable achievement given Britains unique role in the EU landscape. A European economic giant and a 47-year veteran of (mostly positive) EU policymaking is now deemed less relevant than Brussels unspecified vision for connected Global Gateway.

It is almost as if as in many a Parisians dreams Britain never really existed at all.

Alas, as the first anniversary of Brexit approaches, its clear that the EU has learned every wrong lesson from the divorce. Riled by the deliberately provocative actions of successive British governments since 2016, the EU has been unable to separate the U.K.s bark from its bite and the danger this poses is swiftly growing.

Consider how the EUs current approach to discussing Britain is based entirely on a strategy of moving past Brexit.

This is an approach that has been strengthened by the pandemic, which has allowed the EU to subsume Brexit within a broader reimagining of a more relevant, more assertive, more global union.

Europe, in its own mind, has bigger fish to fry.

But while moving past Brexit may make the EU feel better about being jilted by one of its biggest members, it is a woefully short-sighted approach to understanding Brexits potential consequences for its own long-term development.

Another weakness in the EUs approach to understanding Brexit is that it has obsessively focused on Brexiteer misrepresentations of Europe.

This its not me, its you approach has constructed a narrative that views Brexit as a wholly disfigured British issue. Feeding into lazy tropes of British detachment, this blueprint has trapped the EU in easy tales of British exceptionalism.

No real attempt has been made to place the U.K.s engagement in Europe in the specific context of the European integration process. Brexit was never just a wholly British affair. It was also shaped by the strategic choices made in Brussels over several decades.

The final EU miscalculation when it comes to Britain may be its most damaging. Brussels is continuing to underestimate the U.Ks strategic importance and refusing to acknowledge or even contemplate the political risks of an even mildly successful Britain.

The EUs focus on the grinding technical details of protecting the single market due to Britains annoying but highly effective diversionary focus on Northern Ireland has resulted in Brussels misjudging the medium-term risks of Britain as a strategic competitor.

But that risk is real.

The coming years will bring a stabilization of Britains internal politics and a refocusing of the countrys economic priorities in areas where it has existing strengths. Finance, education, security and defense, Fintech and AI are just some of those areas that could lead to a stable, and relatively dynamic, economic framework for the country.

And for all the talk of the economic costs of Brexit and COVID-19, Britains economic outlook in terms of public debt, economic growth and unemployment remain considerably better than most other major European economies, with the exception of Germany.

Britain isnt Italy, no matter how much the EU might wish it so.

Britains return to growth will be complemented by London doubling down on its strategic partnerships with the United States and the other English-speaking economies of the Anglosphere.

Although completely derided in the EU, Britains relationship with the U.S. remains the underpinning of its post-EU identity. This is a relationship whose strategic importance has been masked by Brusselss perceptions of British weakness.

For Westminster, it is irrelevant whether Britain is viewed as Washingtons most important partner Londons preferred choice or as a vassal of the U.S., in the words of Clment Beaune, Frances minister of state for European affairs.

Even subjugation brings the benefits of proximity, relevance and inclusion in Washingtons wider geopolitical strategies. These are benefits lacking in other EU member countries relationships with the Anglosphere, as evidenced by the recent controversy over Australian submarines and the AUKUS defense pact.

Its clear that the EU needs to adopt a new strategy toward Britain. All the hard talk in Schuman coffee shops in Brussels of punishing or going hard on Britain if the Northern Ireland Protocols Article 16 is invoked is ridiculous. Europe missed its chance to impose its economic power on Westminster during the Brexit negotiations.

What recent British actions have really shown is that beyond the political theatrics, Prime Minister Boris Johnsons plan is simply to keep the Brexit fires burning at home through a constant feed of mutual Anglo-EU antagonism. An EU overreaction to British goading is the ultimate aim.

So, rather than succumbing to every little British provocation, Europe needs to take the long view and claim the high ground. Brussels should shrug off British threats with a smile, talk the language of strategic partnership through gritted teeth and understand that Brexit doesnt start and end with the Irish border and angry French fishermen.

Theres a much bigger game at play.

Because Britain wont always be a political disaster. Soon it will be a serious economic threat.

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Europe has learned nothing from Brexit - POLITICO.eu

Ask a Brexit economic expert anything about the current situation between the UK and the EU – The Independent

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The Brexit heat is still firmly lodged on the government as negotiations and discussions around next steps continue.

Only this week it emerged that before Brexit Britains chief Brexit negotiator warned that leaving the single market and customs union would cost 1,500 per person.

Lord Frost is now among the hardest of Brexiteers in the government arguing this week that the UK needs to ditch a European-style economy entirely.

Meanwhile, Frenchfishermenhave said they plan to blockade the channel tunnel in protest at Britains refusal to issue them with work licences.

The running dispute over the post-Brexit fishing rights is expected to boil over on Friday and cause even more disruption to UK supply chains.

The channel tunnel is a vital artery and carried vast volumes of freight and passenger traffic between the continent and the UK.

Not only that but in a week when 27 people died while trying to cross the English Channel, it is also clear that Britain leaving the EUs sphere of cooperation has made it harder to police Britains sea border, not easier.

So where does all this leave when it comes to the Brexit deal and what is likely to happen next?

To answer some of your latest Brexit questions we have got a Brexit economics expert on hand.

Victoria Hewson is the Institute of Economic Affairs Head of Regulatory Affairs and Research Associate. She will be on hand to answer your Brexit questions in the comments section below on Friday, 26 November, between 1-2pm.

Victoria is a lawyer and practiced for 12 years in the fields of technology and financial services, before joining the Legatum Institute Special Trade Commission to focus on trade and regulatory policy.

She has published work on the implications and opportunities of Brexit in financial services and movement of goods and the issues in connection with the Irish border. Before entering the legal profession Victoria worked for Procter & Gamble in the UK and Germany.

Register to submit your question in the comments box under this article. If youre not already a member, click sign up in the comments section to leave your question.

Dont worry if you cant see your question they will be hidden until Victoria joins the conversation to answer them.

Then join us live on this page from 1-2pm as Victoria tackles as many of your travel queries as she can within an hour.

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Ask a Brexit economic expert anything about the current situation between the UK and the EU - The Independent

‘Tear up the ENTIRE deal!’ Boris urged to strike back in Brexit row if EU refuses to cave – Daily Express

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The UK's Brexit minister Lord Frost has continued to insist the Northern Ireland Protocol is not working, and has called for large parts of the mechanism to be completely overhauled. He has continued to demand the removal of the European Court of Justice (ECJ) from the deal, which would effectively act as a referee between the two sides in any future disputes. The EU has flat-out rejected this and so far several rounds of talks between London and Brussels have failed to make any significant breakthrough.

This has led Lord Frost to warn the UK could trigger Article 16 of the Protocol, which could see the deal significantly overhauled or completely torn apart.

But Brussels has said it will retaliate, sparking fears of a potentially destructive trade war that would send tensions between the two sides soaring.

Ben Harris-Quinney, chairman of the Bow Group think tank, believes the EU is gradually "softening" its stance in talks, a move the UK should move to embrace.

However, he warned if progress can't be made in the negotiations soon and the EU won't move from its position, "it is better to scrap the entire deal".

Mr Harris-Quinney told Express.co.uk: "The EU remains unwilling to make significant concessions on goods and use of the ECJ as final court of arbitration.

"The EU began by formally refusing to renegotiate the Northern Irish Protocol, but we are now effectively in a renegotiation, so there is a genuine softening and that should be embraced.

"The UK was the party to begin the renegotiation, and there is no point entering into that process and not solving the problem.

"We need to resolve the issue now and if the EU are unwilling to budge then it is better to scrap the entire deal than to continue a circumstance that clearly is not working, creating only further discord and uncertainty."

READ MORE:France rushes to its Caribbean islands as fury surges over pandemic

The politics expert has urged the UK to trigger Article 16 and "force a conclusion" if the EU continues its hard-line stance on key issues such as checks on goods and the role of the ECJ.

But he also fears the EU could once again gain the upper hand while there also being a risk Britain has not fully prepared for the chaotic fallout triggering Article 16 could inflict.

Mr Harris-Quinney added: "If the EU is not willing to budge on key issues like goods checks and ECJ arbitration, the Government should trigger Article 16 and force a conclusion, rather than allowing the status quo and negotiations to carry on indefinitely.

"The Government has however taken a naive approach thus far, there is a danger of being out-manoeuvred by the EU again, and there is a risk that they have not adequately prepared or positioned themselves for the potential fallout of triggering Article 16."

DON'T MISSBoris risks losing US ally: ministers don't understand Irish feeling[REPORT]Brexiteer hits out at bloc as he urges Macron to listen to Boris[COMMENTS]Macron's hatred of Britain will keep migrants coming says PAUL BALDWIN[OPINION]

On Friday, Lord Frost warned a "significant" gap remains between the UK and the EU after crunch talks aimed at resolving the Protocol issues once again ended in stalemate.

The Brexit minister repeated a threat to use Article 16 of the protocol to override some of the rules he negotiated because of the impact on Northern Ireland.

Lord Frost said in a statement: "We would still like to find a negotiated solution.

"But the gap between our positions is still significant and we are ready to use Article 16 to protect the Belfast (Good Friday) Agreement if other solutions cannot be found."

Following the talks with his UK counterpart, European Commission vice president Maros Sefcovic said a "decisive push" is required to get a medicines deal over the line.

The pair will hold further talks on possible changes to the Northern Ireland Protocol in Brussels this week.

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'Tear up the ENTIRE deal!' Boris urged to strike back in Brexit row if EU refuses to cave - Daily Express

Our Brexit deal is the reason Channel crossings are out of control – The Independent

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One of the biggest issues concerning the government is what to do about asylum seekers crossing the English Channel. About 8,460 made the crossing in 2020, but more than 23,000 have done so this year. The government has undoubtedly been taken by surprise and didnt anticipate such a major spike in crossings.

These journeys are perilous. Last Wednesday saw the deadliest tragedy yet, as 27 drowned while making the crossing, including several children.

In response, former government ministers have accused the home secretary Priti Patel of making it up as she goes along, as she seems to have neither a workable plan to reduce numbers nor any explanation for why crossings are at record levels on her watch.

So far, the ideas offered are nonsense, unlawful, or both. One idea was to process all asylum seekers in Albania at an estimated cost of 100k each. However, the Albanian ambassador said this would never happen as its against international law. Earlier, there had been talk of suggestions that processing might happen elsewhere, for instance in Gibraltar or Rwanda, but the government said the reports were groundless speculation.

A second idea is to push refugees back, putting those in sinking rafts, including women and children, in grave danger. This has been branded inhumane and unconscionable by Labour, but it is also a breach of the Merchant Shipping (Safety of Navigation) Regulations 2020, which require the rescue of those in distress at sea.

For her part, Patel has spent most of her energy pointing fingers rather than solving problems. She has blamed open borders, even though there have been post-Covid restrictions in place; and the French authorities for not doing more, even though the UK was reportedly in arrears with regard to financially supporting such efforts. No doubt more can and should be done on the French coast.

Yet none of this explains why now; why so many more people are crossing the English Channel since 2019 than ever before. It is not because the water is warmer, or the waves less rough; its not that there is less Channel traffic, or that better rafts are being used. The one big thing that has happened, and that may play a key role in explaining the increase, is the prime ministers Brexit deal.

The relevant problem with Brexit is that, in exiting the European Union, the UK left what was arguably one of the most popular immigration policies among the British public: the Dublin III Regulation. This is an EU agreement among member states that if anyone sets foot in another EU country first, they can be returned to that country. Under the Dublin Regulation, anyone found leaving French shores to come to England could be returned as per this agreement.

The issue now is that leaving the European Union has meant leaving the Dublin Regulation. The government was repeatedly asked by Labour during the Brexit negotiations whether the Dublin Regulation membership would be part of any deal; in essence, the government either forgot or did not take it seriously, leaving any mention of it out of the final deal and nothing to replace it.

This matters, because the regulatory change will have been noticed. It means that, since the prime ministers oven-ready deal was accepted despite having no provision for dealing with Dublin Regulation cases, anyone travelling post-Brexit to Britain will arrive without the rule in place that means they can be returned to another country in the EU. What is worse is that the government has failed to create any extradition treaties to address this matter, and so faces extra hurdles in trying to enforce returns. This has contributed to the UKs enforced returns being at a record low.

So, despite the tough-sounding rhetoric of processing individuals abroad, which other countries have rejected or resisted on the grounds that it is unlawful, the government has no grip on how this situation came into being in the first place.

Now, those who make the crossing know it will be difficult to return them to France. Plus, with the Home Office taking longer and longer to process and assess applications, arrivals also know they will be unlikely to be going anywhere soon, and will be able to reside in the UK for months or even years as their applications are slowly considered.

It was a clear failure of Brexit talks to omit the inclusion of the Dublin Regulation or some other alternative in its place, just as it is a failure of caseload management that the Home Office is understaffed and under-resourced.

Frankly, if Patel is looking for someone to blame, she should look in the mirror when standing next to the prime minister. Their shortsighted handling of negotiations has led us to where we are today. They did not take back control, but gave it up in a rush. Until they learn lessons and correct their oversight, things may get much worse for them.

Thom Brooks is a professor of law and government at Durham University

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Our Brexit deal is the reason Channel crossings are out of control - The Independent

Only 18 per cent of Britons think Brexit is going well, poll finds – The Independent

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Fewer than one in five people in Great Britain believe Brexit has been a success, a YouGov poll has found.

Meanwhile, 52 per cent of respondents think that things have gone badly since the transition period ended 11 months ago.

The percentage of Britons dissatisfied with the effects of the divorce hovered around 40 per cent at the start of the year. However, this figure has shot up in recent months, following the petrol crisis in September, which was sparked by a shortage of HGV drivers.

The latest numbers are likely to make grim reading for a government that continues to suggest Brexit is in the best interest of the country.

The electorate now thinks Brexit is the largest single issue facing the UK, according to an Ipsos Mori survey carried out last month.

Some 28 per cent of people viewed it as the most pressing concern, slightly more than those who thought the pandemic should be the governments main focus.

In September, it was the other way around, with 37 per cent of voters deciding Covid-19 was the nations most urgent problem and 20 per cent thinking it was Brexit.

The increased concern over Brexit came around the same time that Richard Hughes, the chairman of the Office for Budget Responsibility (OBR) warned that the decision to leave the bloc would reduce our long run GDP by around 4 per cent.

By comparison, Mr Hughes, speaking after the Budget was announced on 27 October, estimated that the impact of the pandemic would lower the countrys GDP by roughly another 2 per cent.

Other Brexit headaches include the UKs ongoing fishing dispute with France, which flared up again on Friday, as French fishermen blocked ports and the Channel Tunnel over a disagreement about operating licences.

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Only 18 per cent of Britons think Brexit is going well, poll finds - The Independent

Northern Ireland is huge in TV, but post-Brexit reality is far less glitzy – The Guardian

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Bars are full, restaurants are turning away customers who dont have reservations and, judging by the people laden with bags, the Christmas shopping season is already under way. Belfast has known plenty of crises down the decades but this doesnt feel like one of them.

Instead, on a Thursday evening in November, Northern Irelands capital has the air of any other big provincial UK city, with a thriving hospitality sector and plenty of money changing hands. Were it not for the accents, it could be Leeds or Manchester.

But as with Leeds and Manchester, scars are visible just a short walk from the city centre, and in Belfast these result not just from the impact of industrial decline but from the Troubles, too. The Berlin Wall may have come down; the peace wall separating the Falls and Shankill roads has not.

Brexit has added a new level of complexity to the highly charged politics of Northern Ireland. The protocol agreed by London and Brussels prevented a hard border being created between Northern Ireland and the Republic of Ireland by putting a barrier between Northern Ireland and the rest of the UK in the Irish Sea.

If the plan was to make the peace process more secure, it didnt work. Unionist politicians say strict interpretation of the protocol by the EU has made the agreement unworkable, and Brexit minister Lord Frost has for weeks been threatening to invoke article 16, which puts an emergency brake on the Northern Ireland chapter of the UK-EU deal. That could trigger a full-blown trade war, which would be devastating for businesses already feeling the impact of the extra trade friction.

Archie Norman, chairman of Marks & Spencer, says: At the moment things are not too bad. We do have border constraints but they are deal-able-with. Things are a lot better than they are in the Republic of Ireland or in continental Europe, where weve announced a restructuring of our food operations.

Norman insists there isnt a food safety problem. Our food standards are higher than those in continental Europe. The sensible thing would be to agree to product equivalence, where we would agree not to drop standards. If we were planning any variations, we would notify the EU and they could then decide what to do about it.

In the grand scale of things the economic issue is so trivial. Northern Ireland has a similar population to Hertfordshire. Of course it matters hugely politically, but there is no hazard to anyone from produce from the rest of the UK arriving there. We are at risk of going to war over nothing.

Northern Ireland secretary Brandon Lewis wants a deal that gives exporters the best of both worlds access to the EU single market and the UK internal market.

The conditions are met to trigger article 16, he said, but we dont want to use it. We would much rather come to an agreement with the EU. Thats achievable with a different implementation process.

Lewis says the public discourse over Northern Ireland focuses on Brexit and the Troubles, and it is hard to cut through that so businesses and individuals see the opportunities that exist. Everyone wants to talk about the protocol and the legacy of the past. There is a different story going on.

One part of that story is the boom in Northern Irelands film and TV industry catalysed by Game of Thrones. What began with some modest pump-priming in 2010 led to eight blockbuster series and acted as a magnet for other productions. We invested heavily in the pilot. We took a risk and it paid off, said Richard Williams, chief executive of Northern Ireland Screen.

GoT blazed a trail: after it came, among others, Line of Duty, Derry Girls, Dalgleish, a new mini-series based on Henry Fieldings novel Tom Jones, and The Northman, a new Viking revenge film starring Nicole Kidman. Belfast now has three film studios, and Williams says the success of the industry is a shining example of what was meant to happen post the Good Friday agreement.

PAC group a manufacturing firm in north Belfast that comes up with solutions to engineering problems may lack the stardust of a new Kidman movie, but in its way it is emblematic of the Northern Ireland economy: small (45 employees) but growing fast post-lockdown, and now running into supply constraints.

Darren Leslie, the companys business development director and one of its founders, said: Things are starting to bounce back. Everybody is busy. Nobody can get people. Workload is going through the roof. We are having trouble finding the right people and keeping them.

More than any other part of the UK, Northern Ireland is a land of contrasts. It has by far the highest share of public sector employment, yet Queens Belfast boasts the most spin-offs of any university, and over the past 25 years public-private partnership has helped build an impressive cybersecurity cluster. It is the poorest region and the happiest.

John Turner, professor of finance at Queens, said Northern Ireland had an abundance of social capital that may explain high happiness levels. People have come through the Troubles and can deal with adversity. Maybe it has made people a bit more resilient.

Graham Brownlow of Queens Universitys management school said Northern Ireland had three sets of economic problems. First, it shared in the problems of the UK economic model and was entwined in that. Second, the UKs weaknesses such as poor productivity and low investment in R&D, were magnified in Northern Ireland. Finally, it had its own unique problems: the protocol, the shared border, and the fact that the Good Friday agreement didnt really take account of the need to run for economic reconstruction alongside political reconciliation.

A lot of people suggest solutions that dont deal with all the sets of problems. Theyll suggest a silver-bullet solution such as having the same low rate of corporation tax as the republic but there isnt one, Brownlow says.

The Troubles held the economy back, leading to weaker investment and trade. Public spending plugged the gap, and has been rebadged since the Good Friday agreement to form part of the peace dividend. But political instability has been holding back the economy since partition in 1921, and in the early 1960s the Treasury pressed for closure of the shipbuilders Harland and Wolff as part of an economic restructuring.

The close links between politicians and businesspeople foster cronyism. The education system remains largely fractured along Catholic-Protestant lines. Northern Ireland has the largest proportion of Neets young people not in employment, education or training in the UK. Small businesses tend to stay small.

Owen Reidy, assistant general secretary at the Irish Congress of Trade Unions, also complained of a lack of a long-term strategy, and of squabbling local politicians possibily over-estimating their importance: This is a little place on the fringes of Europe. There is too much emphasis on looking south, looking east or looking across the Atlantic.

Some look to daddy in London; some look to mummy in Dublin. But mummy and daddy are not that interested any more.

Ever since Milton Friedman coined the phrase, economists have been arguing about the merits of helicopter money drops of free cash designed to encourage consumers to spend. Northern Ireland is putting the theory to test.

Taking its lead from a scheme tried in Jersey last year, every adult in the country has been given a Mastercard loaded with 100 that they have to spend before mid-December. In an attempt to support local businesses and encourage high street footfall, the money cant be spent online.

Gordon Lyons, Northern Irelands minister of the economy, says if every adult spends up to the 100 limit, there will be a 140m boost to the economy. We wanted to give businesses an immediate shot in the arm and we are at the peak of the scheme right now.

Lyons is hoping for an even bigger boost thanks to a multiplier effect from, say, someone buying a new washing machine and needing to hire a plumber to fit it. Mastercard says there was a discernible multiplier effect in Jersey.

Even so, some say the money from the UK governments Covid recovery fund might have been used more effectively. Peter Bryson of Save the Children in Northern Ireland said helicopter money would be better spent on topping up the incomes of those on universal credit or child payments to the one in four Northern Irish children living in poverty.

SDLP politician Matthew OToole asked: Is this the right time for a stimulus? People are going to be using it on Black Friday and it is hard to see it having an added stimulus.

He thinks it a fascinating economic experiment, though. People will be doing PhDs on it for years.

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Northern Ireland is huge in TV, but post-Brexit reality is far less glitzy - The Guardian