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Who can assess and diagnose cardiac function best after reading an echocardiogram: artificial intelligence (AI) or a sonographer?
According to Cedars-Sinai investigators and their research published today in the peer-reviewed journal Nature, AI proved superior in assessing and diagnosing cardiac function when compared with echocardiogram assessments made by sonographers.
The findings are based on a first-of-its-kind, blinded, randomized clinical trial of AI in cardiology led by investigators in the Smidt Heart Institute and the Division of Artificial Intelligence in Medicine at Cedars-Sinai.
“The results have immediate implications for patients undergoing cardiac function imaging as well as broader implications for the field of cardiac imaging,” said cardiologist David Ouyang, MD, principal investigator of the clinical trial and senior author of the study. “This trial offers rigorous evidence that utilizing AI in this novel way can improve the quality and effectiveness of echocardiogram imaging for many patients.”
Investigators are confident that this technology will be found beneficial when deployed across the clinical system at Cedars-Sinai and health systems nationwide.
“This successful clinical trial sets a superb precedent for how novel clinical AI algorithms can be discovered and tested within health systems, increasing the likelihood of seamless deployment for improved patient care,” said Sumeet Chugh, MD, director of the Division of Artificial Intelligence in Medicine and the Pauline and Harold Price Chair in Cardiac Electrophysiology Research.

In 2020, researchers at the Smidt Heart Institute and Stanford University developed one of the first AI technologies to assess cardiac function, specifically, left ventricular ejection fraction — the key heart measurement used in diagnosing cardiac function. Their research also was published in Nature.
Building on those findings, the new study assessed whether AI was more accurate in evaluating 3,495 transthoracic echocardiogram studies by comparing initial assessment by AI or by a sonographer — also known as an ultrasound technician.
Among the findings: Cardiologists more frequently agreed with the AI initial assessment and made corrections to only 16.8% of the initial assessments made by AI. Cardiologists made corrections to 27.2% of the initial assessments made by the sonographers. The physicians were unable to tell which assessments were made by AI and which were made by sonographers. The AI assistance saved cardiologists and sonographers time.”We asked our cardiologists to guess if the preliminary interpretation was performed by AI or by a sonographer, and it turns out that they couldn’t tell the difference,” said Ouyang. “This speaks to the strong performance of the AI algorithm as well as the seamless integration into clinical software. We believe these are all good signs for future AI trial research in the field.”
The hope, Ouyang says, is to save clinicians time and minimize the more tedious parts of the cardiac imaging workflow. The cardiologist, however, remains the final expert adjudicator of the AI model output.
The clinical trial and subsequent published research also shed light on the opportunity for regulatory approvals.
“This work raises the bar for artificial intelligence technologies being considered for regulatory approval, as the Food and Drug Administration has previously approved artificial intelligence tools without data from prospective clinical trials,” said Susan Cheng, MD, MPH, director of the Institute for Research on Healthy Aging in the Department of Cardiology at the Smidt Heart Institute and co-senior author of the study. “We believe this level of evidence offers clinicians extra assurance as health systems work to adopt artificial intelligence more broadly as part of efforts to increase efficiency and quality overall.”

Water in California’s Central Valley contains enough manganese to cause cognitive disabilities and motor control issues in children, and Parkinson’s-like symptoms in adults.
A naturally occurring metal, manganese is found in water supplies throughout the world. It is regulated as a primary contaminant in many Southeast Asian countries where the climate causes it to leach into groundwater. However, in the U.S. it is regulated only as a secondary contaminant, meaning no maximum level is enforced.
A new UC Riverside-led study shows that, among Central Valley communities, the highest concentrations of manganese are in private, untreated well water systems. However, the researchers also found it in public water systems at higher concentrations than what studies have shown can have adverse health effects.
The study, published in the journal Environmental Science & Technology, not only measured levels of manganese in Central Valley water supplies, but also mapped the highest concentration areas according to annual income levels.
Overall, the research team estimates nearly half of all domestic well water users in the Central Valley live in disadvantaged communities, as defined by annual income. Within this population, nearly 89% have a high likelihood of accessing water that is highly contaminated with manganese.
“It is a relatively small number of people, compared to the total population of the state, who are getting the tainted water. But for them, the health risks are high,” said Samantha Ying, UCR soil scientist and principal study investigator. “These people are particularly concentrated in disadvantaged communities, so if they wanted to monitor and treat the water, they would have a hard time doing so,” Ying said.

Point-of-use treatment options range from oxidation and precipitation filters to water softeners, chlorination, and reverse osmosis systems. But devices for monitoring water quality can cost up to $400 annually, and treatments for manganese-tainted water are just as expensive.
“It is possible to purchase filters for manganese, but a lot of people cannot afford them. We are hoping people in these communities can be subsidized to buy treatment options,” Ying said.
Previously, the research team found that manganese-contaminated groundwater tends to occur in relatively shallow depths, compared to arsenic. They wondered if digging deeper wells would avoid the manganese contamination. Unfortunately, that strategy is unlikely to be effective.
“Using existing groundwater model predictions of manganese concentrations at deeper depths did not change the number of wells likely to be contaminated,” Ying said.
The conditions that cause arsenic and manganese to leach are similar, so they tend to show up in groundwater in tandem. Arsenic has long been regulated as a primary contaminant in the U.S. “Wells are labeled unsafe if they contain arsenic, but not if they contain manganese,” Ying said. “Thus, the number of wells considered safe may be greatly overestimated.”
Furthermore, the researchers used a benchmark of 300 parts per billion of manganese to assess water quality. This is a level of manganese contamination that some studies have associated with neurological development issues, particularly for fetuses and infants during early growth periods. It is likely though that adverse effects can occur at lower levels.
“New studies from Canada, where manganese is now a primary contaminant, show there may be effects at 100 parts per billion,” Ying said. “We were being conservative at 300.”
This study focused on the Central Valley in part because the conditions that cause manganese to move from aquifer materials into water are so prevalent there. It is likely that drinking water from wells in other parts of the state is similarly tainted. Over 1.3 million Californians rely on unmonitored private wells.
“The population being exposed is much bigger than we might think. There are a lot of communities statewide drinking from private wells,” Ying said.

Published4 hours agoShareclose panelShare pageCopy linkAbout sharingImage source, Getty ImagesBy Philippa RoxbyHealth reporterA virus carried by ticks, which is common in many parts of the world, is now present in the UK and health officials are reminding the public how to avoid bites from the tiny bugs.They say the risk of tick-borne encephalitis is very low – only one person is confirmed to have been infected in England so far, last year.But the tick species which carries the virus is widespread in the UK.Most people do not develop symptoms but swelling to the brain is possible.The UK Health Security Agency has recommended changes to testing in hospital so that any new cases can be picked up quickly.Enhanced surveillance for the virus is now being carried out in England and Scotland, where there is one probable case of tick-borne encephalitis.Health officials are also testing for the presence of the virus in blood samples of people with no symptoms in parts of Yorkshire, where the confirmed case was infected.Feed on bloodTicks are small, spider-like creatures that feed on the blood of animals and people. They tend to be found in dense woodland or moorland and feed on deer.While feeding, they can transmit viruses and infections that cause disease, with the most common being Lyme disease – a bacterial infection which can be treated with antibiotics.Getting tick-borne encephalitis (TBE) from a tick is much less likely. Dr Meera Chand, deputy director at the UK Health Security Agency, said it was “very uncommon in the UK” and the risk to the general population was “very low”. But she said the public should take steps to avoid being bitten by ticks when outdoors in moorlands and woodlands, and remember to check for ticks and remove them promptly.How to avoid ticks:walk on clearly marked paths to avoid brushing against vegetationcover your skin while walking outdoors and tuck trousers into sockswear light-coloured clothes so ticks can be spotted and brushed offuse insect repellents such as DEETcheck your clothes and body regularly for ticks, and your children and pets as welladults are usually bitten on the legs, while children are usually bitten on the head or neckHow to remove ticks safely:remove them as soon as possibleuse a pair of fine-tipped tweezers or a tick removal toolgrasp the tick as close to the skin as possiblepull upwards slowly and firmly, as mouthparts left in the skin can cause infectionclean the bite area with antibacterial wash/soap and water, and monitor it for several weeks for any changescontact your GP promptly if you begin to feel unwell with flu-like symptoms or develop a spreading circular red rashImage source, Getty ImagesTicks infected with TBE virus have been found in a small number of areas in England, including Hampshire, Dorset and Norfolk, and, on rare occasions, people nearby may have been infected – but until now, no cases were confirmed.In research being presented at the European Congress of Clinical Microbiology and Infectious Diseases next week, scientists report that TBE cases are on the rise in Europe with some 3,800 reported in 2020.They speculate that infected ticks may have been brought into the UK by migratory birds because of climate change.Health officials say anyone who becomes unwell after a tick bite should see a GP. More serious symptoms to look out for include severe headache, stiff neck, unexplained seizure, sudden confusion and weakness in arms and legs.Related Internet LinksTick-borne encephalitis- epidemiology, diagnosis and prevention – GOV.UKLyme disease – NHSThe BBC is not responsible for the content of external sites.

Federal regulators plan to authorize an additional dose for seniors and immunocompromised people in the coming weeks, ahead of the introduction of a newly formulated booster later in the year.WASHINGTON — The Food and Drug Administration plans to allow older and immunocompromised Americans to get a second updated coronavirus booster shot in the near future, an acknowledgment of the virus’s continuing risks to vulnerable people whose immunity might be sagging months after a previous inoculation.Federal regulators are expected to authorize the additional dose in the next few weeks, according to people familiar with the agency’s planning. Those 65 and older would be able to receive the vaccine free of charge at least four months after their previous updated shot. Those with immune deficiencies would also be eligible.Regulators are expected to authorize the additional dose without explicitly recommending it for those groups, a stance that emphasizes the discretion of patients and their health providers. Dr. Rochelle P. Walensky, the director of the Centers for Disease Control and Prevention, is expected to sign off on the decision — a customary step in the regulatory process.Michael Felberbaum, an F.D.A. spokesman, said in a statement that the agency was monitoring data on the virus and would “base any decision on additional updated boosters upon those data.”The decision reflects the Biden administration’s ongoing concerns about the durability of protection against the virus for those Americans most at risk, even as the pandemic’s threat to younger, healthier Americans has receded. About 1,600 deaths from Covid-19 were reported for the week ending March 29, according to the most recent federal data. Those who are dying from Covid-19 are overwhelmingly 65 and older.Looking to blunt the effects of a potential winter Covid surge, the F.D.A. authorized the retooled booster shots, which are aimed at Omicron subvariants, at the end of August. But only about 55 million Americans — less than 17 percent of the population — have received an updated booster, according to the C.D.C. Among those 65 and older, 42 percent have received one of the shots.The Washington Post earlier reported the coming authorization.The Biden administration is planning to roll out another reformulated booster late in the summer or early in the fall, a schedule that would align with the annual flu vaccine. In the coming months, regulators plan to select the version of the virus they want to target with that retooled booster.In the meantime, a second booster for some groups would be in line with a proposal that regulators made at a January meeting of an independent group of vaccine advisers, at which the panel discussed offering vulnerable Americans more than one annual coronavirus shot.At that meeting, federal health officials pointed to research that showed the reformulated boosters were still working to protect Americans against newer versions of the virus that circulated deeper into the winter.The Biden administration has a substantial stockpile of the updated booster shots, and many of those doses could end up going to waste once a new booster is rolled out later this year. Federal health officials purchased more than 170 million doses of the updated shots last year. A senior Department of Health and Human Services official said recently that the administration was considering donating some of the vaccine.

The review found that the methodology of many previous studies was flawed and that risk of myriad health problems increased significantly after less than two drinks a day for women and after three for men.For decades, scientific studies suggested moderate drinking was better for most people’s health than not drinking at all, and could even help them live longer.A new analysis of more than 40 years of research has concluded that many of those studies were flawed and that the opposite is true.The review found that the risks of dying prematurely increase significantly for women once they drink 25 grams of alcohol a day, which is less than two standard cocktails containing 1.5 ounces of distilled spirits, two 12-ounce beers or two 5-ounce glasses of wine. The risks to men increase significantly at 45 grams of alcohol a day, or just over three drinks.The new report, which analyzed more than 100 studies of almost five million adults, was not designed to develop drinking recommendations, but to correct for methodological problems that plagued many of the older observational studies. Those reports consistently found that moderate drinkers were less likely to die of all causes, including those not related to alcohol consumption.Most of those studies were observational, meaning they could identify links or associations but they could be misleading and did not prove cause and effect. Scientists said that the older studies failed to recognize that light and moderate drinkers had myriad other healthy habits and advantages, and that the abstainers used as a comparison group often included former drinkers who had given up alcohol after developing health problems.“When you compare this unhealthy group to those who go on drinking, it makes the current drinkers look more healthy and like they have lower mortality,” said Tim Stockwell, a scientist with the Canadian Institute for Substance Use Research who was one of the authors of the new report, which was published in JAMA Network Open last week.Once Dr. Stockwell and his colleagues corrected for these errors and others, he said, “Lo and behold, the supposed health benefits of drinking shrink dramatically, and become non-statistically significant.”Dr. Stockwell said that the comparisons of moderate drinkers with non-drinkers were flawed for numerous reasons. People who abstain completely from alcohol are a minority, and those who aren’t teetotalers for religious reasons are more likely to have chronic health problems, to have a disability or to be from lower income backgrounds.Moderate drinkers tend to be moderate in all ways. They tend to be wealthier, are more likely to exercise and to eat a healthy diet, and are less likely to be overweight. They even have better teeth, scientists say.“They have a lot of things going for them that protect their health, that have nothing to do with their alcohol use,” Dr. Stockwell said.The idea that moderate drinking may be beneficial dates back to 1924, when a Johns Hopkins biologist named Raymond Pearl published a graph with a J-shaped curve, the low point in the middle representing the moderate drinkers, who had the lowest rates of mortality from all causes.The high point in the J represented the well-known risks of heavy alcohol consumption, such as liver disease and car crashes. The hook on the left represented abstainers.In more recent decades, wine — and particularly red wine — developed a reputation for having health benefits after news stories highlighted its high concentration of a protective antioxidant called resveratrol, which is also found in blueberries and cranberries.But the moderate alcohol hypothesis has come under increasing criticism over the years as the alcohol industry’s role in funding research has come to light, and newer studies have found that even moderate consumption of alcohol — including red wine — may contribute to cancers of the breast, esophagus and head and neck, high blood pressure and a serious heart arrhythmia called atrial fibrillation.In January, Canada issued new guidelines warning that no amount of alcohol consumption is healthy, and urged people to cut drinking as much as possible. The new guidance, issued by the Canadian Centre on Substance Use and Addiction, was a stark departure from its 2011 guidelines, which recommended women limit themselves to no more than 10 standard drinks a week and men no more than 15.Now the Canadian agency says that consuming even two standard drinks a week is associated with health risks, and seven or more weekly drinks carry a high level of risk.Current U.S. dietary guidelines are nowhere near as strict, recommending men limit themselves to two drinks or less a day and women to one or less.But guidelines about alcohol consumption issued by numerous health organizations have been amended to include the proviso that people should not drink alcohol for the express purpose of improving their health.That caveat was repeated by a scientist with the Distilled Spirits Council, though she took issue with the findings of the new report.Amanda Berger, vice president for science and health with the Distilled Spirits Council, said the new analysis still “suggests that those who drink in moderation live longer than those who do not,” but added, “no one should drink alcohol to obtain potential health benefits and some individuals should not drink at all.”The new analysis shows, however, that those who drink moderately have no statistically significant advantage in longevity compared with those who are lifelong abstainers, the study’s authors said.

Each year about 1.5 million people in the U.S. survive a traumatic brain injury due to a fall, car accident, or a sports injury, which can cause immediate and long-term disability.
University of Maryland School of Medicine (UMSOM) researchers wanted to better understand what happens in the brain during injury, so they conducted a study in mice to determine how different types of brain cells in mice react to severe trauma. In a new study published in the January issue of Autophagy, they found that after traumatic brain injury, the brain’s immune system cells’ internal recycling function slowed dramatically, allowing waste products to build up and interfere with recovery from injury.
The researchers also found that treating mice that had traumatic brain injury with a drug to promote cellular recycling improved the mice’s ability to recover from injury and solve a water maze, a measure of memory function in mice.
“Many drugs and potential solutions have been proposed to treat traumatic brain injury, but none have ever worked in practice,” said lead researcher Marta Lipinski, PhD, Associate Professor of Anesthesiology and Anatomy & Neurobiology at UMSOM and a member of the Shock, Trauma, and Anesthesiology Research (STAR) Center at the University of Maryland Medical Center (UMMC). “It could be that designing drugs for patients that promote this cellular recycling might reverse or prevent damage from traumatic brain injury as we saw in our animal studies. We are continuing to learn more about the molecular and cell biology mechanisms in trauma, so we can use a more guided approach for developing solutions.”
The body’s cells regularly recycle their own worn-out or damaged parts that accrue through normal wear and tear, infection, or injury in a process known as autophagy. Most cells in the brain use that process for cleaning up their own waste and recycling it on a smaller scale. In a previous study, Dr. Lipinski’s group showed that traumatic brain injury reduced the ability of neurons — the cells that send electrical impulses — to recycle their own damaged parts, which then led to these neurons dying off. However, some cells in the brain can perform greater feats of recycling, such as the resident immune cells in the brain known as microglia, which can engulf, digest, and recycle entire damaged or dead cells in the tissue.
After a traumatic brain injury, white blood cells — normally excluded by the blood-brain barrier — can also get into the brain and work alongside the microglia cells to eat and remove damaged cells. For this new study, Dr. Lipinski’s team focused on the immune cells — microglia and white blood cells — in the brain after traumatic brain injury and found that, like the neurons, their recycling function was also suppressed.
“Dr. Lipinski’s discovery of the recycling function suppression in both neurons and immune cells demonstrates how important it is for neuroscientists to fully understand the complex system involved in a traumatic brain injury,” said Dean Mark Gladwin, MD, who is Vice President for Medical Affairs at the University of Maryland, Baltimore, and the John Z. and Akiko K. Bowers Distinguished Professor at UMSOM. “Developing effective drugs for traumatic brain injury treatment requires a deeper understanding of these cell-to-cell interactions and what impact each cell type has on the brain’s ecosystem.”
To demonstrate the full impact of the recycling process on traumatic brain injury and recovery, Dr. Lipinski and her team blocked one of the essential proteins needed to carry out the immune cell’s recycling function in the brains of mice with a brain injury. These mice experienced an even greater suppression of their cell recycling processes, resulting in more inflammation in their brain. They even performed worse, as measured by their ability to solve the water maze, than the mice with only brain injury. These findings suggested that the recycling function of the immune cells in the brain is essential for recovery after brain trauma. Conversely, boosting it may possibly lessen the impact of the trauma.
To test that, the researchers used a drug, rapamycin (normally used as a cancer drug or to prevent organ rejection), to promote cellular recycling in the brains of mice who had traumatic brain injury. The researchers found that with the treatment, the mice had lower levels of inflammation in the brain and these mice did better in navigating the water maze.
“The drug we used in our study blocks a set of proteins that are important for regenerating the body’s cells, so it cannot be used for extended time periods,” said Dr. Lipinski. “We need to continue this line of research to identify the exact mechanism of how autophagy protects against neurological damage in order to find more targeted drugs that increase this process without targeting the vital proteins needed by the brain to regenerate.”
This study was funded by grants from the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (NINDS) (R01NS094527, R01NS091218, R01NS115876).

Animals, like humans, appear to be troubled by a Linda problem.
The famous “Linda problem” was designed by psychologists to illustrate how people fall prey to what is known as the conjunction fallacy: the incorrect reasoning that if two events sometimes occur in conjunction, they are more likely to occur together than either event is to occur alone.
Now, for the first time, UCLA psychology researchers have shown that this type of logical error isn’t the sole province of humans — surprisingly, rats seem to make the same mistakes. Their study is published in the journal Psychonomic Bulletin and Review.
“The classical research has all been done with humans, so the usual explanation for the effect attributes it to a departure from rationality distinct to humans,” said Valeria González, a postdoctoral psychology researcher at UCLA and first author of the study. “Our work shows that maybe there is a more general mechanism shared between humans and rats.”
If rats do, as the research findings suggests, succumb to the conjunction fallacy, they could potentially serve as good research models for studying psychopathological conditions characterized by false beliefs or the perception of nonexistent events, like schizophrenia and certain anxiety disorders, the authors said.
But back to Linda. In the 1980s, Nobel laureate Daniel Kahneman and his colleague Amos Tvesrky showed that in a variety of scenarios, humans tend to believe, irrationally, that the intersection of two events is more probable than a single event. They asked participants to answer a question based on the following scenario.

Linda is 31 years old, single, outspoken and very bright. She majored in philosophy. As a student, she was deeply concerned with issues of discrimination and social justice and also participated in anti-nuclear demonstrations.
Which is more probable? Linda is a bank teller. Linda is a bank teller and is active in the feminist movement.The great majority of participants chose No. 2, although logically it is less probable than Linda being a bank teller alone. After all, No. 1 would not preclude Linda from also being an active feminist, but given the description of Linda, No. 2 may be easier for respondents to imagine.
The Linda problem and numerous similar studies seem to indicate that humans estimate the likelihood of an event using mental shortcuts, assessing how similar the event is to a model they already have in their minds. The formation of these models, known as representativeness heuristics, relies on a combination of memory, imagination and reasoning universal in humans but thought to be rare or nonexistent in other animals.
Sound, light and the conjunction fallacy in rats
Some have argued that the conjunction fallacy, rather than being a true logical error, may hinge on language, particularly people’s uncertainty about the meaning of words like “likely” and “probability.” Others have pointed out that Linda’s detailed backstory might have biased respondents. But previous research has suggested that humans also are prone to conjunction fallacies when performing physical tasks.

To determine whether the fallacy necessarily involves language and whether it is unique to humans, González engaged rats in a physical, not social, task. With psychology professor Aaron Blaisdell, she designed two experiments that required the rats to judge the likelihood of just a sound being present or both a light and sound being present in order to receive a food reward.
Rats were trained in two scenarios: Tone + light = reward. In the first, they received sugar pellets if they pressed a lever when a tone played and a steady light was on; they received no food if they pressed they lever when the tone played but the light was off. Noise alone = reward. In the second scenario, they received pellets if they pressed a lever while a white noise played and a flashing light was off; they received nothing if they pressed the lever when the noise played and the flashing light was on.The researchers then played the different sounds, a tone or white noise, while the light bulb was unobscured but turned off. The rats reacted accordingly, tending to avoid pressing the lever in response to the tone and pressing it in response to the white noise.
But when researchers obscured the light bulb with a piece of metal and played the sounds, the rats were forced predict whether it was on or off in hopes of receiving the food reward. Interestingly, the rats were much more likely to predict that the obscured light was on. This was true regardless of whether the light had previously signaled the presence or absence of food when accompanying the sound.
The tendency to overestimate the likelihood that both sound and light were present, even if it meant no reward, demonstrates that, like humans, rats can show a conjunction fallacy, the authors said.
“Until now, researchers said this is unique to human cognition only because we haven’t looked for it in animals,” Blaisdell said. “If humans and other animals consider alternative states of the world during ambiguous situations to help decision-making, we might expect systematic biases such as the conjunction fallacy to show a broader distribution in the animal kingdom.”

Published11 hours agoShareclose panelShare pageCopy linkAbout sharingImage source, Poole FamilyBy Andre Rhoden-PaulBBC NewsA pensioner with Alzheimer’s faces being split from her family and deported to the UK from Sweden, after nearly two decades in the country.Sweden has ordered British-born Kathleen Poole, 74, to leave after her application to remain in the country post-Brexit was not accepted, her family told the BBC. They said it was “disgraceful” Sweden wants to deport the grandmother.The Swedish government said authorities are in contact with the family.Mrs Poole – who moved from Macclesfield, Cheshire, nearly two decades ago to Sweden to be closer to her family – is currently bedbound and receives round-the-clock care in a home where she has been living for the last 10 years. The grandmother-of-four’s family was told in September 2022 she would be deported, despite making her application for Swedish residence status before the December 2021 deadline brought about by the EU-UK Withdrawal Agreement. Her family said her application was rejected because she did not have a valid British passport – which they said she did not need as she could not travel due to her poor health – and despite sick notes from doctors.Speaking to the BBC, daughter-in-law Angelica said: “I sent six doctors’ notes. I sent personal letters explaining the situation and it wasn’t good enough. “In the end they said ‘sorry’ you have to leave the country.”Then they wanted us to book her a flight to the UK, which we refused. So now the British embassy are having to look for accommodation and the police are on their backs. “I think it’s disgraceful really how you can deport somebody who is sick and take her from her family. She’s one of the nicest people you will ever meet.”The family are now hoping a sick note from a doctor, who has visited Mrs Poole in person at her care home, will persuade the Swedish Migration Agency to reopen the case. But in the meantime, Angelica said her children remain worried sick that the grandmother may be sent away from them. “It’s not human to split somebody bedridden from her family,” Angelica added. “All this is due to Brexit. The way I see it she’s lived here for 19 years this year.”Image source, Poole FamilyMP Hilary Benn, former Brexit Select Committee chair, has urged the UK foreign secretary, James Cleverly, to intervene in the case. He said: “The continuing threat by the Swedish authorities to deport this frail elderly woman is heartless and inexplicable. “It is also in clear breach of the EU/UK Withdrawal Agreement which promised to protect citizens’ rights.”The follow-on legislation from Brexit, which ended freedom of movement, allowed EU citizens resident in Britain to apply to permanently live in the UK. Some EU nations also opted for this system to allow Britons to remain resident in their country. David Milstead, part of the British in Sweden campaign group, told the BBC he was disappointed but not surprised by Mrs Poole’s case and that the UK and European Commission needed to look at the wider issue in the Scandinavian nation. He said: “Sweden’s approach to implementing the Withdrawal Agreement has led to a lot of long-standing residents being forced out of their homes. “Sweden has issued more deportation notices to UK nationals during 2021-2022 than any other EU country. “This is in spite of the Withdrawal Agreement containing protections that should ensure that people like Mrs Poole get to stay. These protections clearly aren’t working.”Sweden has expelled 1,100 British nationals since Brexit, according to the Guardian, which first reported Mrs Poole’s case. Jane Golding, chair of the British in Europe group and a Berlin-based lawyer, has written to the European Commission about Mrs Poole and said she understands they are following up the case with Swedish authorities. She told the BBC: “The problem that Kathleen Poole’s family has come up against is that the UK and some EU countries including Sweden, decided to go for a system where citizens had to reapply for their status post-Brexit.”We warned that it would be vulnerable and elderly people who would suffer as a result. People like Kathleen Poole – someone who has lived in another country for years and whose residence now depends on a successful application and is not capable of making the application herself.”Each EU country implements the Withdrawal Agreement nationally and there are differences in approach. That is why guidance across the EU on cases involving the vulnerable and elderly who have problems applying would help.”In a statement, Sweden’s Minister of Migration Maria Malmer Stenergard said: “Decisions related to residence applications are applied directly by the Swedish state agencies and courts in line with the EU-UK Withdrawal Agreement. “As laid down in the constitution, the Swedish government is not permitted to interfere in or comment on individual decisions taken by these independent state bodies. “With regard to the case in question, I have been informed that the Swedish Migration Agency is in contact with the family concerning additional information.”A UK Foreign Office spokesperson said: “We are supporting a British woman and her family in Sweden.”ASKING FOR IT?: Emily Atack explores why she is sexually harassed online on a daily basis A MOTHER’S LOVE FOR HER DAUGHTER: Daisy May Cooper stars in brand new comedy-drama Rain Dogs

A landmark discovery linking iron regulation to a rare blood cancer has led to clinical trials of a potential new treatment for patients with the incurable disease.
The study focused on polycythemia vera (PV), a blood disorder causing excessive red blood cells, and found that restricting iron access to the bone marrow could reduce the production of red blood cells in this disease.
The research, led by WEHI in collaboration with the University of Melbourne, the Peter MacCallum Cancer Centre (Australia) and the University of Cambridge and Silence Therapeutics (UK), has led to new clinical trials of a drug that has the potential to control iron regulation in patients with PV.
At a glance Researchers discover new way to potentially treat polycythemia vera (PV), a rare form of blood cancer characterised by too many red blood cells. Study found raising hepcidin, a hormone that regulates how your body uses iron, reduces the production of red blood cells and complications from the disease in pre-clinical models. Recruitment for clinical trials based on this landmark research has begun, investigating the effect of a drug that has the potential to control iron regulation in patients with PV.An estimated 250 Australians are diagnosed with polycythemia vera (PV) each year. PV is a chronic disease and there currently is no cure.
Without treatment, PV can be life-threatening as an overproduction of red blood cells causes thicker blood, elevating a patient’s risk of developing blood clots and cardiovascular conditions like heart attacks and stroke.

The cancer is currently treated with venesection, where about 500mL of blood is taken from a patient multiple times a month, to rapidly reduce their red cell count and blood thickness.
The new study, published in Blood, provides a promising new treatment avenue that could see the often painful and disruptive blood draws replaced with a simple injection every few months.
First author, Dr Cavan Bennett, said discovering that restricting iron access to the bone marrow could reduce the disease severity of PV was a gamechanger.
“Through our pre-clinical studies, we found the hormone hepcidin, which is the master regulator of iron availability, is critical for controlling red blood cell production in models of this disease,” Dr Bennett said.
“The more hepcidin you have in the body, the more you restrict iron access to the bone marrow.

“This iron restriction is critical to preventing an excess of blood cell production and this is what is crucial to alleviate the severity of the disease in PV patients.”
Patients with PV often develop iron deficiency when treated with venesection, but they are also advised against taking iron supplements as this would further accelerate the production of red blood cells in their body.
Dr Bennett said targeting hepcidin could also help combat the iron deficiency symptoms faced by PV patients.
“This approach restricts iron access only to the bone marrow, without depleting iron from other organs, such as the liver,” he said.
Silencing power
The research is being translated into Phase 1/2 clinical trials taking place across Australia, Malaysia and the United States.
The trials will use SLN124, a new drug developed by London-based Silence Therapeutics, in hopes of controlling hepcidin expression in PV patients for the first time.
Senior author and Head of WEHI’s Population Health and Immunity Division, Professor Sant-Rayn Pasricha, said the trials involved PV patients receiving an injection every few weeks, in hopes of replacing their need for regular venesections.
“A treatment option like this would simplify long-term therapy for this disease for patients and the health care system,” Professor Pasricha said.
SLN124 is a gene silencing therapy that works by inhibiting a gene responsible for hepcidin regulation in the liver. The clinical trials will investigate the effect of temporarily ‘silencing’ this geneto increase production of hepcidin by the liver, which is expected to reduce disease severity.
“We recognised the opportunity to adapt an emerging clinical therapeutic initially designed for other hematological diseases such as b-thalassemia and apply it to polycythemia vera.
“To go from a concept to a clinical trial in less than four years is quite astounding.
“Our work has laid the essential foundation needed to hopefully transform patient care options for people with PV and provides unique insight that could lead to better understanding the disease.”
Recruitment for the clinical trials has begun.
Landmark genome study
The study also uncovered a genetic link between a disorder that causes excess iron accumulation (hemochromatosis) and PV, made possible through WEHI’s analysis of extensive population genetics databases including the UK Biobank.
The research team was able to leverage this data to conduct a genome-wide association study that analysed data from 440 PV patients to further examine the role of iron in the blood cancer.
Professor Melanie Bahlo, laboratory head in WEHI’s Population Health and Immunity Division, said having access to the UK Biobank was key to these discoveries.
Analysis of a second dataset, the Finnish FinnGen Biobank, confirmed the findings — highlighting the power of these databases to help formulate and test novel biological hypotheses.
“We were the first research team to use the UK Biobank to solely focus on PV samples, which led us to this powerful and novel insight about iron status and PV,” she said.
“This saw us further discovering that the genetic mutations which cause hemochromatosis are one of the strongest risk-factors for diagnosis of PV — an insight that will help the research field better understand this rare disease.”
Dr Victoria Jackson, a postdoc in Professor Bahlo’s lab, performed the genetic analysis using a method called genome-wide association study.
The research conducted at WEHI was funded by the National Health and Medical Research Council (NHMRC).

Being overweight may be physically changing the environment within people’s joints, as new research suggests that obesity is promoting pro-inflammatory conditions which worsen arthritis.
In a new study published in Clinical and Translational Medicine today, researchers from the University of Birmingham have found that specific cells in the joint lining tissue (synovium) of patients with osteoarthritis are being changed due to factors associated with obesity.
Previous research has shown that fat tissue that has been metabolically altered by obesity releases proteins called cytokines and adipokines, which are known to promote inflammation around the body. The newly published study funded by Versus Arthritis observed that in cells taken from biopsies of arthritic joints, obesity also changes the environment within the joint itself, leaving cells in the joint vulnerable to being ‘turned’ into those that promote inflammation.
Dr Susanne Wijesinghe from the Institute of Inflammation and Ageing at the University of Birmingham said: “We have seen that obesity can promote the kind of destructive inflammation in joints that goes far beyond what we might expect to see from wear and tear alone, even in non weight-bearing joints such as the hands.
“Obesity is creating an environment in the body, which is negatively affecting cells called synovial fibroblasts, which are stem cells involved in regulating the lubricating fluid of the joints. The effect is that these cells get recoded into those that promote inflammation within the fluid around the joints. Then, like bad apples in a barrel, they begin to affect the whole joint, increasing secretion of chemicals such as CHI3L1 which degrade the joint and increase the progression of osteoarthritis.”
Hips don’t lie — weight isn’t driving factor in load-bearing joints
Weight wasn’t determined to be the driving factor for impacting the joint cells leading to greater inflammation, the research found.

The team of researchers used biopsy information from a range of joints including both weight-bearing joints such as hips and knees as well as the hands to determine whether the additional physical strain on joints associated with obesity was driving pro-inflammatory cytokines. The results found that there were independent impacts of obesity on load bearing and non-load bearing joints, and that among the 16 patients with BMI of over 30, weight alone didn’t account for the molecular changes in those joints.
Simon Jones, Professor in Musculoskeletal Ageing in the Institute of Inflammation and Ageing at the University of Birmingham said: “This research helps us to both design better studies that more accurately understand the different conditions that affect patients with osteoarthritis, and it also better guides the way we develop drugs for the condition in the future.
“Potential targets and ways of delivering drugs can now be specifically considered for patients who do and don’t have metabolic changes driven by obesity. In addition, if we treat osteoarthritis patients with obesity as a clinical sub-group we can also see whether specific therapies that address the metabolic element driving the disease can halt that underlying risk.”
Zoe Chivers, Director of Services and Influencing at the charity Versus Arthritis said: “This study provides further evidence that osteoarthritis (OA) is not just inevitable ‘wear and tear,’ but the result of complex and diverse biochemical changes in the joint.
“The research reveals that obesity can lead to a change in the cells in the joint lining to make them more inflammatory, and that these changes occur not only in load bearing joints such as the knee and hips, but also in non-load bearing joints such as the hand.
“These findings greatly enhance our understanding of what can cause osteoarthritis, bringing us closer to discovering more effective treatments in the future.”