Published36 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, Skyle CurtisBy Philippa Roxby, Tara Mewawalla, Osob Elmi and Victoria ParkBBC News Hundreds of women have contacted BBC News with their stories of experiencing trauma during childbirth – from their pain at not being believed, to being left bleeding and alone after their baby was born.It follows a report,

The word “failure” is rampant in medicine. Hearts, livers, lungs, and kidneys all “fail,” which simply means they cease to do their job. But the failures that patients tend to remember are the ones that seem to indict not an organ but an entire person. Just ask anyone who has been told that they have “failed” vaginal delivery (meaning that labor was slow or the cervix didn’t dilate) or “failed” chemotherapy (meaning that the tumor didn’t respond to treatment).Worst among these phrases, many doctors say, is a common diagnosis for both infants and older adults: “failure to thrive.”In pediatrics, the term refers to infants who struggle to hit key milestones in size, weight and cognitive development. When Dr. Deborah Frank, a retired pediatrician, was in medical school in the 1970s, the diagnosis meant one of two things: “Either you had major congenital heart disease or cystic fibrosis, or you had a bad mother,” she said. “Or maybe you had both.”If the term sounds slightly accusatory, that’s because it is. It arose from the idea that struggling infants were ailing not because of any underlying disease or lack of nutrients but because of poor parenting.The first known appearance of “failure to thrive” was in the 1933 edition of a medical textbook, “The Diseases of Infancy and Childhood.” An explanation for the condition came near the end of World War II, when René Spitz, an Austrian psychoanalyst, observed that infants in a Mexican orphanage tended to be listless, scrawny and slow to develop.This concerning syndrome, Spitz surmised, resulted from a lack of “maternal affection, maternal care and maternal love.” Pediatrics took the idea and ran with it​ — “in the fine old tradition of mother-blaming,” Dr. Frank said. (A similar psychoanalytic idea that became popular around this time was “refrigerator mother theory,” which posited, incorrectly, that autism was caused by “cold mothering.”)We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Published6 minutes agoShareclose panelShare pageCopy linkAbout sharingBy Jim ReedBBC PanoramaAll Sam Rushby can remember about his family are fleeting memories of hospital corridors and waiting rooms.In 1994, at just two years old, he lost his mum to Aids. His dad died with the condition a year later at Liverpool Royal Infirmary.His sister had also been infected with HIV, then a new and untreatable virus, and had died.”My family was literally torn apart and ripped away from me,” he tells BBC Panorama in his first-ever interview.”It just feels like they’ve been disposed of and that’s the end of it now.”Image source, Family photoSam’s father Gary was one of more than 1,200 people infected with HIV as part of the infected blood scandal, most after being given a drug made from US blood plasma in the late 1970s and 1980s.A long-running public inquiry into what has been called the worst treatment disaster in NHS history is preparing to report its findings.One of the key areas it is examining is whether the authorities were too slow to act at the time.Now, BBC Panorama has seen evidence that the British Embassy in Washington warned the UK government about the risk of Aids from contaminated blood in the early 1980s.An embassy official wrote a five-page memo to a senior figure at the Department of Health after meeting a member of the US Aids taskforce. The warning – one of several – came a decade before Sam was born. Infected Blood: Time for AnswersJim Reed meets the families of some of the children with bleeding disorders who were infected with HIV, to discuss their campaign for justice and what they hope for from the inquiry.Watch on BBC One at 20:00 BST on 13 May or on BBC iPlayer (UK Only) It wasn’t until he was in his teens that Sam, now 32, started to learn the truth.His father Gary was born with haemophilia, a genetic condition that damages the blood’s ability to clot. It almost always affects men, although women carry the haemophilia gene and can pass it on.In the late 1970s, Gary started on a new treatment meant to radically improve his life.Factor VIII was marketed as a wonder drug. Patients could simply take a bottle of the white powder from the fridge, mix it with distilled water and inject themselves.The bleeding would stop and, for the first time ever, haemophiliacs could live a more normal life.But those patients would later learn that entire batches of the new treatment had been contaminated with HIV and hepatitis C.About two-thirds of those infected with HIV in the 1980s developed Aids and died before modern antiretroviral drugs became available.Sam struggled to comprehend the truth about what happened to his family when he was finally told by his grandparents.”I didn’t believe it, I couldn’t believe it,” he says. “I just can’t get over, why did it have to happen?”In the early 1980s, the UK could not keep up with demand for Factor VIII, which was made by pooling – or mixing – the blood plasma of thousands of individual donors.Instead the treatment was shipped from the US.In the UK, blood donations have always been voluntary, but in the US, drug companies were allowed to pay cash for plasma.High risk groups, from prisoners to drug users, had a clear financial incentive to give blood and potentially lie about their medical history.Evidence uncovered by campaigners and seen by the ongoing public inquiry into the wider contaminated blood scandal shows that, as the risk from Aids started to become known, a series of clear warnings were sent to the UK government.In May 1983, Dr Spence Galbraith, the director of the UK’s Communicable Disease Surveillance Centre, wrote to Dr Ian Field, the senior principal medical officer at the Department of Health, urging that all US blood products should be withdrawn from use until the risk of Aids was “clarified”.The letter from the British embassy in Washington – which Panorama has now seen – was also sent to Dr Field, just a month later on 28 June 1983.In it, an embassy official describes a meeting with a representative from the US Centers for Disease Control’s Aids taskforce.The transmission of HIV in blood was discussed, he writes. Haemophiliacs were “most at risk” from the “dubious habits” of some paid American blood donors, and the mixing of thousands of those donations to make Factor VIII.The Tainted Blood group, which represents hundreds of survivors and their families, says the letter shows a “staggering level of awareness and detail” about the dangers.But this – and other – warnings were not acted on. NHS patients continued to be given untreated Factor VIII imported from the US until at least 1985.Many of those involved in decisions in the 1980s are no longer alive, including Dr Ian Field.In 1983, knowledge of HIV and Aids was still emerging.At the time, a Department of Health official described the call to withdraw American Factor VIII as premature and said it did not take into account the risks to haemophiliacs of removing a major source of their treatment.Image source, Family photoSam says his dad didn’t know he had been infected with HIV for many years.Gary unwittingly passed the virus on to his wife Lesley. She later gave birth to a daughter, Abbey, who was born HIV+ and died at just four months old.Lesley did become pregnant again and in 1992 Sam arrived, this time testing negative for HIV.But just two years later, Lesley died of an Aids-related illness, followed just a year later by her husband.”The sad thing is, I have literally no memories of them, just a handful of pictures,” says Sam. “It’s that constant gutting feeling of sadness, of wondering what growing up would have been like.”Sam was brought up by his grandparents, who initially told him his mum and dad had died of cancer and a stroke.He only started to learn what really happened in his early teens, although the stigma surrounding Aids meant he kept the details secret as, he says, “teenagers could be mean”.”I’ve always suffered with anxiety and depression. If you lose your mum and dad at such a young age, it’s going to make you anxious,” he says.”But then, in later life, I found out why and that just compounded the agony.”What is the infected blood scandal and will victims get compensation?Hundreds infected with hepatitis C without knowing it, BBC findsChildren were used as ‘guinea pigs’ in clinical trialsSam is one of hundreds of children to have lost parents to the scandal. To date, none have received government compensation.In total, more than 30,000 NHS patients were infected with HIV and hepatitis C between 1970 and 1991 through contaminated blood products such as Factor VIII and IX – or blood transfusions after surgery, treatment or childbirth.In other countries – from France to Japan – investigations into the medical disaster were completed many years ago. In some cases, criminal charges were brought against doctors, politicians and other officials.In the UK, campaigners say the scandal has never had the same level of attention.A private inquiry in 2009, funded entirely by donations, lacked any real powers, while a separate Scottish investigation in 2015 was branded a “whitewash” by victims and their families.In 2017, following political pressure, then-Prime Minister Theresa May ordered a UK-wide public inquiry.Led by the former high court judge, Sir Brian Langstaff, it had the power to compel witnesses to give evidence under oath and order the release of documents.After a series of delays, his final report is now due on 20 May.Image source, Family photoResearch for the inquiry has found that 380 of the 1,250 patients with bleeding disorders infected with HIV were children at the time.Many families also had to deal with the stigma of what was then an untreatable disease.Sarah-Jane’s younger brother Colt was infected with HIV and died, aged 10, in 1992. She says the family, from Plymouth, had to move house three times to try to escape abuse from people in the local area.”We were shunned, we were talked about. Colt didn’t have any friends because nobody wanted to play with him,” she says.”Friends and neighbours became distant, afraid and accusing.”In September 1985, a primary school in Hampshire made national news headlines when the parents of a young haemophiliac told teachers he had tested HIV+.Other families pulled their children out of class, and didn’t allow them back until Aids specialists had been sent in to properly explain the risks.Image source, Family photoThe boy at the centre of the media storm was aged just nine and was anonymous at the time. But he can now be named as 48-year-old Peter Adlam.”I just remember, I didn’t want to get caught by the cameras outside the school gates,” he tells BBC Panorama in his first-ever interview. “I’d try to blend in with the other kids as much as I could. As a child you should think you’re indestructible and going to live forever and I was becoming very aware that I wouldn’t.”Peter went on to develop serious health problems linked to HIV including three episodes of pneumonia in 1996. At one point, his parents were told he may only have weeks to live.New HIV drugs arrived in time to save his life, although he has still had to deal with multiple health problems to this day.”Up until that point, I hadn’t thought I’d see the year 2000. So it was very bleak and there wasn’t a lot of hope,” he says.”I saw other people my age living their lives and I wasn’t able to. I haven’t had a career, I haven’t travelled. I can’t imagine what my life would be like if I hadn’t been infected.”In August 2022, the government agreed to make the first-ever interim compensation payments of £100,000 to about 4,000 survivors of the scandal or their bereaved partners.Ministers have indicated they are planning to extend that to the parents and children of those infected, including Sam Rushby, and to also set up a final compensation scheme.But no firm timetable has yet been put in place to make the payments, with the total cost likely to run to billions of pounds.The government told Panorama in a statement: “This was an appalling tragedy that never should have happened. We are clear that justice needs to be done, and swiftly. “This includes establishing a new body to deliver an Infected Blood Compensation Scheme, it will have all the funding needed to deliver compensation once they have identified the victims and assessed claims.”We will continue to listen carefully to the community as we address this dreadful scandal.”You can follow Jim on X.More on this storyWhat is the infected blood scandal and how many people died?Published1 MayChildren used as ‘guinea pigs’ in clinical trialsPublished18 AprilHundreds infected with hepatitis C without knowing it, BBC findsPublished3 days ago

Richard Slayman received the historic procedure in March. The hospital said it had “no indication” his death was related to the transplant.Richard “Rick” Slayman, who made history at age 62 as the first person to receive a kidney from a genetically modified pig, has died about two months after the procedure.Massachusetts General Hospital, where Mr. Slayman had the operation, said in a statement on Saturday that its transplant team was “deeply saddened” at his death. The hospital said it had “no indication that it was the result of his recent transplant.”Mr. Slayman, who was Black, had end-stage kidney disease, a condition that affects more than 800,000 people in the United States, according to the federal government, with disproportionately higher rates among Black people.Surgeons performing the world’s first kidney transplant from a genetically modified pig into a living human in March.Michelle Rose/Massachusetts General Hospital, via Agence France-Presse — Getty ImagesThere are far too few kidneys available for donation. Nearly 90,000 people are on the national waiting list for a kidney.Mr. Slayman, a supervisor for the state transportation department from Weymouth, Mass., had received a human kidney in 2018. When it began to fail in 2023 and he developed congestive heart failure, his doctors suggested he try one from a modified pig.“I saw it not only as a way to help me, but a way to provide hope for the thousands of people who need a transplant to survive,” he said in a hospital news release in March.His surgery, which lasted four hours, was a medical milestone. For decades, proponents of so-called xenotransplantation have proposed replacing ailing human organs with those from animals. The main problem with the approach is the human immune system, which rejects animal tissue as foreign, often leading to serious complications.Recent advances in genetic engineering have allowed researchers to tweak the genes of the animal organs to make them more compatible with their recipients.The pig kidney that was transplanted into Mr. Slayman was engineered by eGenesis, a biotech company based in Cambridge, Mass. Scientists there removed three genes and added seven others to improve compatibility. The company also inactivated retroviruses that pigs carry and could be harmful to humans.“Mr. Slayman was a true pioneer,” eGenesis said in a statement on social media on Saturday. “His courage has helped to forge a path forward for current and future patients suffering from kidney failure.”Mr. Slayman was discharged from the hospital two weeks after his surgery, with “one of the cleanest bills of health I’ve had in a long time,” he said at the time.In a statement published by the hospital, Mr. Slayman’s family said he was kind, quick-witted and “fiercely dedicated to his family, friends and co-workers.” They said they had taken great comfort in knowing that his case had inspired so many people.“Millions of people worldwide have come to know Rick’s story,” they said in the statement. “We felt — and still feel — comforted by the optimism he provided patients desperately waiting for a transplant.”

Half a century ago, one of the hottest questions in science was whether humans could teach animals to talk. Scientists tried using sign language to converse with apes and trained parrots to deploy growing English vocabularies.The work quickly attracted media attention — and controversy. The research lacked rigor, critics argued, and what seemed like animal communication could simply have been wishful thinking, with researchers unconsciously cuing their animals to respond in certain ways.In the late 1970s and early 1980s, the research fell out of favor. “The whole field completely disintegrated,” said Irene Pepperberg, a comparative cognition researcher at Boston University, who became known for her work with an African gray parrot named Alex.Today, advances in technology and a growing appreciation for the sophistication of animal minds have renewed interest in finding ways to bridge the species divide. Pet owners are teaching their dogs to press “talking buttons” and zoos are training their apes to use touch screens.In a cautious new paper, a team of scientists outlines a framework for evaluating whether such tools might give animals new ways to express themselves. The research is designed “to rise above some of the things that have been controversial in the past,” said Jennifer Cunha, a visiting research associate at Indiana University.The paper, which is being presented at a science conference on Tuesday, focuses on Ms. Cunha’s parrot, an 11-year-old Goffin’s cockatoo named Ellie. Since 2019, Ms. Cunha has been teaching Ellie to use an interactive “speech board,” a tablet-based app that contains more than 200 illustrated icons, corresponding to words and phrases including “sunflower seeds,” “happy” and “I feel hot.” When Ellie presses on an icon with her tongue, a computerized voice speaks the word or phrase aloud.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

A bioethicist, she pioneered bedside methods for helping patients, their families and doctors deal with anguishing life-or-death decisions in a high-tech age.Nancy Neveloff Dubler, a medical ethicist who pioneered using mediation at hospital bedsides to navigate the complex dynamics among headstrong doctors, anguished family members and patients in their last days, died on April 14 at her home on the Upper West Side of Manhattan. She was 82.The cause was heart and lung disease, her family said.A Harvard-educated lawyer who won her college student presidency by campaigning to dissolve the student government, Ms. Dubler was a revolutionary figure in health care who sought, in her words, to “level the playing field” and “amplify nonmedical voices” in knotty medical situations, especially when deciding next steps for the sickest of patients.In 1978, Ms. Dubler founded the Bioethics Consultation Service at Montefiore Medical Center in the Bronx. Among the first such teams in the country, the service employed lawyers, bioethicists and even philosophers who, like doctors on call, carried pagers alerting them to emergency ethical issues.Modern medical technology, Ms. Dubler wrote in her 1992 book, “lets us take a body with a massive brain hemorrhage, hook it up to a machine, and keep it nominally ‘alive,’ functioning organs on a bed, without hope of recovery.”Harmony Books/Crown Publishers“My colleagues and I spend most of our time working with doctors, nurses, and social workers,” Ms. Dubler wrote with her co-author, David Nimmons, in “Ethics On Call: A Medical Ethicist Shows How to Take Charge of Life-or-death Choices” (1992). “We start where they get stuck, in the web of rights and responsibilities that ensnares all patients and caregivers.”Bioethics consultants emerged as a medical subspecialty following groundbreaking advances in technology, pharmaceuticals and surgical techniques.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Published4 hours agoShareclose panelShare pageCopy linkAbout sharingBy Shiona McCallumTechnology reporterA new device to help reduce the time cancer patients spend in hospital has been given regulatory approval. The Liberty allows patients to take blood tests – and upload the results – at home, and without supervision.Its users say it allows them to cut down on draining hospital visits, while clinicians suggest it could boost NHS productivity.After being trialled at the Christie, in Manchester, the device will now be deployed at 12 NHS sites. However, Cancer Research UK says it has so far only been trialled on a small number of people. More work is needed before we know whether it can be used more widely in cancer care, the charity says.Being treated for cancer involves a battery of blood tests, as medical staff monitor multiple health indicators such as haemoglobin levels and total white blood cell count.Lynn Thompson, who has faced both ovarian and bowel cancer since 2017 – and was one of the trial patients – said being able to do some of those tests at home was a great relief.”I just fell in love with the machine to be really honest with you. It was so simple to follow and to use,” the 52-year-old said.She said it enabled her to be no longer so tied to a fixed schedule of hospital visits, which she found physically and mentally exhausting – especially given her fear of needles.”By the time I would go into the blood room to the chair, I would probably faint, and that has a knock-on effect – it made me feel really poorly all day. “The machine took all that away, it’s a simple finger prick that doesn’t hurt. It’s a small amount of blood and then it’s hidden away – there’s no stress or anxiety.”The device, the size of a small printer, can feed blood sample analysis directly back to hospital teams.Sacha Howell, a senior lecturer in medical oncology at the University of Manchester, said the shift to blood testing from the confines of hospital to the comfort of patients’ homes was not only more convenient for patients but could also mean savings for the NHS. Recently, The Christie – one of the largest cancer treatment centres of its type in Europe – has positioned phlebotomy units around the region in what’s known as “bloods closer to home.””But it still means we have to staff those units, in order for the patients to be able to have the blood tests,” said Dr Howell. “If the patients were able to simply do them themselves at home, that would result in significant efficiencies.”Trials conducted at The Christie have yielded promising results, though the patient numbers are low.There have been 22 patients like Lynn participating in a home study, complemented by regulatory approval trials involving 470 patients. Cancer Research said those low numbers meant some caution was needed.”It is very early days” for this tech “and further research is needed” it said in a statement.”The regulatory approval does not give indications of effectiveness or clinical utility at this stage – those questions would need to be addressed in future clinical trials of the device before it could be used more widely,” it added.The boss of the company which makes it, Entia, is upbeat though about what he says is the world’s first ever blood count analyser that patients can use in their own home. “By providing insights into patients’ health status, the device empowers healthcare professionals to pre-emptively address complications, reducing hospitalizations and treatment interruptions,” Dr Toby Basey-Fisher said.More on this storyCoppaFeel! founder Kris Hallenga dies aged 38Published4 days agoNHS AI test spots tiny cancers missed by doctorsPublished21 March

Although you may not appreciate them, or have even heard of them, throughout your body, countless microscopic machines called spliceosomes are hard at work. As you sit and read, they are faithfully and rapidly putting back together the broken information in your genes by removing sequences called “introns” so that your messenger RNAs can make the correct proteins needed by your cells.
Introns are perhaps one of our genome’s biggest mysteries. They are DNA sequences that interrupt the sensible protein-coding information in your genes, and need to be “spliced out.” The human genome has hundreds of thousands of introns, about 7 or 8 per gene, and each is removed by a specialized RNA protein complex called the “spliceosome” that cuts out all the introns and splices together the remaining coding sequences, called exons. How this system of broken genes and the spliceosome evolved in our genomes is not known.
Over his long career, Manny Ares, UC Santa Cruz distinguished professor of molecular, cellular, and developmental biology, has made it his mission to learn as much about RNA splicing as he can.
“I’m all about the spliceosome,” Ares said. “I just want to know everything the spliceosome does — even if I don’t know why it is doing it.”
In a new paper published in the journal Genes and Development, Ares reports on a surprising discovery about the spliceosome that could tell us more about the evolution of different species and the way cells have adapted to the strange problem of introns. The authors show that after the spliceosome is finished splicing the mRNA, it remains active and can engage in further reactions with the removed introns.
This discovery provides the strongest indication we have so far that spliceosomes could be able to reinsert an intron back into the genome in another location. This is an ability that spliceosomes were not previously believed to possess, but which is a common characteristic of “Group II introns,” distant cousins of the spliceosome that exist primarily in bacteria.
The spliceosome and Group II introns are believed to share a common ancestor that was responsible for spreading introns throughout the genome, but while Group II introns can splice themselves out of RNA and then directly back into DNA, the “spliceosomal introns” that are found in most higher-level organisms require the spliceosome for splicing and were not believed to be reinserted back into DNA. However, Ares’s lab’s finding indicates that the spliceosome might still be reinserting introns into the genome today. This is an intriguing possibility to consider because introns that are reintroduced into DNA add complexity to the genome, and understanding more about where these introns come from could help us to better understand how organisms continue to evolve.

Building on an interesting discovery
An organism’s genes are made of DNA, in which four bases, adenine (A), cytosine (C), guanine (G) and thymine (T) are ordered in sequences that code for biological instructions, like how to make specific proteins the body needs. Before these instructions can be read, the DNA gets copied into RNA by a process known as transcription, and then the introns in that RNA have to be removed before a ribosome can translate it into actual proteins.
The spliceosome removes introns using a two-step process that results in the intron RNA having one of its ends joined to its middle, forming a circle with a tail that looks like a cowboy’s “lariat,” or lasso. This appearance has led to them being named “lariat introns.” Recently, researchers at Brown University who were studying the locations of the joining sites in these lariats made an odd observation — some introns were actually circular instead of lariat shaped.
This observation immediately got Ares’s attention. Something seemed to be interacting with the lariat introns after they were removed from the RNA sequence to change their shape, and the spliceosome was his main suspect.
“I thought that was interesting because of this old, old idea about where introns came from,” Ares said. “There is a lot of evidence that the RNA parts of the spliceosome, the snRNAs, are closely related to Group II introns.”
Because the chemical mechanism for splicing is very similar between the spliceosomes and their distant cousins, the Group II introns, many researchers have theorized that when the process of self-splicing became too inefficient for Group II introns to reliably complete on their own, parts of these introns evolved to become the spliceosome. While Group II introns were able to insert themselves directly back into DNA, however, spliceosomal introns that required the help of spliceosomes were not thought to be inserted back into DNA.

“One of the questions that was sort of missing from this story in my mind was, is it possible that the modern spliceosome is still able to take a lariat intron and insert it somewhere in the genome?” Ares said. “Is it still capable of doing what the ancestor complex did?”
To begin to answer this question, Ares decided to investigate whether it was indeed the spliceosome that was making changes to the lariat introns to remove their tails. His lab slowed the splicing process in yeast cells, and discovered that after the spliceosome released the mRNA that it had finished splicing introns from, it hung onto intron lariats and reshaped them into true circles. The Ares lab was able to reanalyze published RNA sequencing data from human cells and found that human spliceosomes also had this ability.
“We are excited about this because while we don’t know what this circular RNA might do, the fact that the spliceosome is still active suggests it may be able to catalyze the insertion of the lariat intron back into the genome,” Ares said.
If the spliceosome is able to reinsert the intron into DNA, this would also add significant weight to the theory that spliceosomes and Group II introns shared a common ancestor long ago.
Testing a theory
Now that Ares and his lab have shown that the spliceosome has the catalytic ability to hypothetically place introns back into DNA like their ancestors did, the next step is for the researchers to create an artificial situation in which they “feed” a DNA strand to a spliceosome that is still attached to a lariat intron and see if they can actually get it to insert the intron somewhere, which would present “proof of concept” for this theory.
If the spliceosome is able to reinsert introns into the genome, it is likely to be a very infrequent event in humans, because the human spliceosomes are in incredibly high demand and therefore do not have much time to spend with removed introns. In other organisms where the spliceosome isn’t as busy, however, the reinsertion of introns may be more frequent. Ares is working closely with UCSC Biomolecular Engineering Professor Russ Corbett-Detig, who has recently led a systematic and exhaustive hunt for new introns in the available genomes of all intron-containing species that was published in the journal Proceedings of the National Academy of Sciences (PNAS) last year.
The paper in PNAS showed that intron “burst” events far back in evolutionary history likely introduced thousands of introns into a genome all at once. Ares and Corbett-Detig are now working to recreate a burst event artificially, which would give them insight into how genomes reacted when this happened.
Ares said that his cross-disciplinary partnership with Corbett-Detig has opened the doors for them to really dig into some of the biggest mysteries about introns that would probably be impossible for them to understand fully without their combined expertise.
“It is the best way to do things,” Ares said. “When you find someone who has the same kind of questions in mind but a different set of methods, perspectives, biases, and weird ideas, that gets more exciting. That makes you feel like you can break out and solve a problem like this, which is very complex.”

The payment system amounted to one of the most forceful actions taken so far by agriculture officials who have raced to keep up with the spread of the virus among dairy cows.The Biden administration said on Friday that it would compensate dairy farmers for cooperating with its efforts to limit the spread of the bird flu virus, part of a series of expansive measures aimed at containing an outbreak.The payment system amounted to one of the most forceful actions taken so far by agriculture officials who have raced to keep up with the spread of the virus among dairy cows. Farm owners have been reluctant to allow state and federal officials access to cows and workers exposed to or infected by the virus, and are fearful of the financial consequences of infected herds and contaminated milk.Under the so-called indemnity program, farms would receive up to $28,000 to protect workers and cover costs incurred treating and testing sick cows. Producers may also receive payments for lost milk production on farms with confirmed bird flu cases.Farm workers who agree to participate in government-led studies will also be compensated for their time.“We’re now moving into a phase of equipping producers to reduce the risk” of wider spread, Tom Vilsack, the agriculture secretary, said at a news briefing on Friday, acknowledging the difficulties of reaching farmers.The program was part of a broader federal push announced on Friday to increase spending on the bird flu response. The Centers for Disease Control and Prevention is planning to scale up testing capacity — a blind spot early in the coronavirus pandemic — and its assessment of bird flu vaccines, should they be needed.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Melanoma, an aggressive form of skin cancer that accounts for 75% of all skin-cancer-related deaths, is often detected later in people with darker skin complexions — and the consequences can be devastating, a Mayo Clinic study reveals.
While melanoma may be found less frequently in people with darker complexions than fair ones, this potentially serious form of cancer can strike anyone. The study, which consisted of 492,597 patients with melanoma, suggests that added vigilance in early screening is particularly needed for Black men, whose cancers are often found at later stages, leading to worse outcomes compared to white patients.
“We compared non-Hispanic Black patients to white patients and saw striking differences in how patients presented with the disease,” says surgical oncologist Tina Hieken, M.D., senior author of the study and a researcher at Mayo Clinic Comprehensive Cancer Center. “We saw more extremity melanoma, and more later-stage disease.”
Extremity melanoma refers to skin cancer that can develop on the arms, legs, hands and feet. Various factors, including social risk factors and biological components, could be at play, but further research is needed to help determine why these differences exist.
Revealing differences in sex-based immune response
The research found that Black female patients with melanoma fared better than Black male patients.
Men tended to be older at diagnosis and more likely to have cancer that had spread to their lymph nodes compared to women. This translated to worse survival rates. The researchers learned that Black men with stage 3 melanoma have only a 42% chance of surviving for five years, compared to 71% for Black women.

Most research on melanoma hasn’t focused on how race and sex affect outcomes and hasn’t looked at the influence of race and ethnicity across all groups. Dr. Hieken says the study highlights the need to understand these differences better, noting that this is the first large study to confirm that sex-based differences in melanoma outcomes exist within the non-Hispanic Black population.
“When we talk about later-stage melanoma patients who are female versus male in that non-Hispanic Black patient cohort who ended up doing worse, some biological things may be going on here that are interesting,” says Dr. Hieken.
One theory centers on variations in immune response.
“Several immune signals suggest that women may respond better to some immunotherapies than males,” says Dr. Hieken.
Identifying the need
Researchers note that more studies focused on melanoma in a broader range of people, including more Black participants in clinical trials, is key to bridging this knowledge gap and potentially identifying more effective treatments.

“We want to broaden and deepen our reach to better understand the disease that affects all patients,” says Dr. Hieken.
She underscores the role played by the Mayo Clinic Robert D. and Patricia E. Kern Center for the Science of Health Care Delivery in this study.
“What we’ve done with the Kern Center, with this study and others, is to identify the need,” says Dr. Hieken. “We have a rich, integrated, multidisciplinary clinical research practice in melanoma, and we want to address clinical needs and knowledge gaps relevant to our practice.”
A wake-up call in the battle against melanoma
Dr. Hieken notes that this study is a wake-up call for everyone battling to diagnose and cure melanoma, regardless of the patient’s sex or skin tone.
She emphasizes that healthcare professionals should carefully examine areas like palms, soles and under fingernails, where melanoma might be more challenging to spot on darker skin.
“We can incorporate screening for skin lesions or lesions under the nails into the visit for patients as part of their regular checkups,” says Dr. Hieken. “What we want to do is elevate care for our patients.”
The Mayo Clinic Robert D. and Patricia E. Kern Center for the Science of Health Care Delivery and Breast and Melanoma Surgical Oncology in the Department of Surgery supported this research.