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The researchers also incorporated Artificial Intelligence tools, including machine learning, to analyze biomarker patterns. These methods allowed them to accurately differentiate Long COVID patients from healthy individuals and to pinpoint the most informative biomarker combinations. Such insights could support more precise diagnostics and future personalized treatments. small, unusual clusters of blood clotting proteins that circulate in the bloodstream. The term became widely used in 2021 after Prof Resia Pretorius of Stellenbosch University’s Department of Physiological Sciences reported finding these abnormal protein clumps in blood samples from COVID-19 patients. Their potential involvement in COVID-related clotting problems drew significant attention as the pandemic unfolded.What are neutrophil extracellular traps (NETs)?Dr. Alain Thierry and his group at the Montpellier Cancer Institute (IRCM) at INSERM in Montpellier were among the first to highlight the importance of NETs in COVID-19. NETs form when neutrophils release their DNA through a process called NETosis, creating thread-like structures filled with harmful enzymes that can quickly trap and neutralize invading microbes.Although NETs help defend against infection, producing too many of them can be harmful. Excess NET formation has been linked to serious inflammatory and clotting conditions, including severe infections, autoimmune diseases, cancer, diabetes, and arthritis. Dr. Thierry notes that ongoing overproduction of NETs, driven by cycles of inflammation and clot formation, may worsen disease severity.In light of this, the teams led by Prof Pretorius and Dr. Thierry worked together to examine whether microclots and NETs interact in patients with Long COVID.Key findingsUsing imaging flow cytometry and fluorescence microscopy, the researchers conducted detailed measurements of microclots and NETs in the plasma of individuals with Long COVID and compared the results to healthy controls. They also quantified NETs by assessing proteic markers and circulating DNA.They reported several major observations: Biomarkers linked to both microclots and NETs were significantly elevated in Long COVID patients. Patients showed not only an increased number of microclots but also larger microclots. Most notably, the team identified a structural relationship between microclots and NETs. This association appeared in all samples but was far more substantial in people with Long COVID.”This finding suggests the existence of underlying physiological interactions between microclots and NETs that, when dysregulated, may become pathogenic,” explains Dr. Thierry.
The researchers also incorporated Artificial Intelligence tools, including machine learning, to analyze biomarker patterns. These methods allowed them to accurately differentiate Long COVID patients from healthy individuals and to pinpoint the most informative biomarker combinations. Such insights could support more precise diagnostics and future personalized treatments.Prof Pretorius emphasizes that the study reveals a buildup of microclots in the plasma of Long COVID patients, likely supported by excessive NET activity: “This interaction could render microclots more resistant to fibrinolysis, promoting their persistence in circulation and contributing to chronic microvascular complications,” she explains.By clarifying how NETs may stabilize microclots, the study contributes valuable information about the biological processes involved in Long COVID. The findings also highlight potential therapeutic approaches aimed at reducing harmful clotting and inflammation.In addition, the work advances the search for new biomarkers that could help diagnose and manage Long COVID. As the authors note, “The combination of advanced imaging techniques and machine learning confers methodological robustness and contributes significantly to the ongoing scientific discourse on post-viral syndromes.”
In patients with Long COVID, a new study has revealed structural association between circulating microclots and neutrophil extracellular traps (NETs).
This finding suggests the existence of underlying physiological interactions between microclots and NETS that, when dysregulated, may become pathogenic.
What are microclots?
The term microclots, recently adopted in the scientific literature, refers to abnormal clumps of blood clotting proteins circulating in a patient’s blood stream. The concept was introduced in 2021 by Prof. Resia Pretorius from Stellenbosch University’s Department of Physiological Sciences, when they found the abnormal presence of such microclots in the blood samples of COVID-19 patients. This discovery generated widespread attention during the pandemic due to its potential role in COVID-related coagulopathies.
What are neutrophil extracellular traps (NETs)?
Dr. Alain Thierry’s team at the Montpellier Cancer Institute (IRCM) at INSERM in Montpellier, was among the first to identify the critical role of NETs in the pathogenesis of COVID-19. NETs are produced through a specialised form of innate immune response known as NETosis, whereby neutrophils expel their DNA to form filamentous structures embedded with cytotoxic enzymes capable of rapidly trapping and neutralizing pathogens.

However, excessive NETs formation can become detrimental, contributing to a wide range of inflammatory and thrombotic diseases, including severe infections, autoimmune disorders, cancer, diabetes, and arthritis.
According to Dr. Thierry, it may be that persistent overproduction of NETs, fueled by self-perpetuating inflammatory and thrombotic loops, exacerbates disease severity.
In a collaborative effort, the teams of Prof. Pretorius and Dr. Thierry investigated the potential interaction between microclots and NETs in the context of Long COVID.
Key findings
Using imaging flow cytometry and fluorescence microscopy, they performed a quantitative and structural analysis of microclots and NETs in the plasma of Long COVID patients, compared to healthy controls. NETs were also quantified by analyzing NETs proteic markers and circulating DNA. They observed a significant increase in biomarkers associated with both microclots and NETs in patient samples. Microclots were not only more abundant but also larger in size among patients. Most importantly, they discovered a previously unreported structural association between microclots and NETs, observed in all subjects but markedly more pronounced in Long COVID patients.”This finding suggests the existence of underlying physiological interactions between microclots and NETs that, when dysregulated, may become pathogenic,” explains Dr. Thierry.

Furthermore, the integration of Artificial Intelligence tools, such as machine learning, into the biomarker analysis enabled them to distinguish Long COVID patients from healthy individuals with high accuracy. The algorithms identified the most predictive biomarker combinations, enhancing diagnostic reliability and paving the way for personalized medicine approaches.
According to Prof. Pretorius, the results reveal a significant accumulation of microclots in the plasma of Long COVID patients, likely driven and stabilized by excessive NETs production: “This interaction could render microclots more resistant to fibrinolysis, promoting their persistence in circulation and contributing to chronic microvascular complications,” she explains.
By identifying the mechanistic role of NETs in microclot stabilization, this study provides new insight into the pathophysiology of Long COVID. These findings support the development of targeted therapeutic strategies aimed at modulating thrombo-inflammatory responses.
Finally, the study paves the way for the development of novel biomarkers for diagnosis and management: “The combination of advanced imaging techniques and machine learning confers methodological robustness and contributes significantly to the ongoing scientific discourse on post-viral syndromes,” they conclude.

A commonly used, low-cost medication for gout may help lower the chances of heart attacks and strokes in people with cardiovascular disease, according to a new Cochrane review.
Researchers evaluated the impact of taking small doses of colchicine, a standard gout treatment, and reported no rise in serious side effects.
Cardiovascular disease is often linked to long-term, low-level inflammation that increases the likelihood of repeat events such as heart attacks and strokes. Because colchicine reduces inflammation, it has emerged as a potentially useful option for people living with heart disease.
A promising effect on cardiovascular risk
The review assessed 12 randomized controlled trials that followed nearly 23,000 individuals with a history of heart disease, heart attack or stroke. Participants took colchicine for at least six months, usually at doses of 0.5 mg once or twice daily. About 80% of those enrolled were male (~80%), and their average age ranged from 57 to 74 years. Half received colchicine, while the rest were given either a placebo or no added medication on top of their typical care.
People taking low-dose colchicine experienced fewer heart attacks and strokes overall. For every 1,000 individuals treated, 9 heart attacks and 8 strokes were avoided compared with those who did not receive the drug. No serious adverse events were seen, although mild and short-lived stomach or digestive discomfort was more common among colchicine users.
“Among 200 people with cardiovascular disease — where we would normally expect around seven heart attacks and four strokes — using low-dose colchicine could prevent about two of each,” says Dr. Ramin Ebrahimi, co-lead author from the University Medicine Greifswald, Germany. “Reductions like this can make a real difference for patients who live with ongoing, lifelong cardiovascular risk.”
A new use for a long-established medicine

Since cardiovascular diseases remain the leading cause of death worldwide, colchicine offers a potentially affordable and widely available strategy for preventing additional heart problems in high-risk patients.
“These results come from publicly funded trials repurposing a very old, low-cost drug for an entirely new use,” says Lars Hemkens, senior author from the University of Bern, Switzerland. “It shows the power of academic research to reveal treatment opportunities that traditional drug development often overlooks.”
Questions still remain about whether colchicine influences overall mortality or reduces the need for procedures such as coronary revascularization. The trials also did not determine whether the drug improves quality of life or shortens hospital stays. The authors emphasize that more research is required to address these gaps.

Just nowShareSaveJames GallagherHealth and science correspondentShareSaveNye familyScientists have discovered why type 1 diabetes is more severe and aggressive when it develops in young children.Type 1 is caused by the immune system attacking cells in the pancreas that control blood sugar levels.The research team showed the pancreas was still developing in childhood, particularly under the age of seven, making it far more vulnerable to damage.They say newly developed drugs could buy patients time for the pancreas to mature, delaying the disease.Type 1 diabetes affects around 400,000 people in the UK.Gracie, age eight from Merseyside, became suddenly ill on Halloween in 2018. It started as a slight cold, but rapidly escalated.”She went from being a very happy one-year-old, who would go to nursery and dance and sing, to almost dying in less than 48 hours,” says dad Gareth.”The diagnosis remains the worst part of our life.Suddenly everything we took for granted was 10-20 times harder,” he says.Nye familyThe Nye family had to adapt quickly – keeping on top of everything Gracie had to eat or drink, checking blood sugar levels and giving the hormone insulin to tell her body to absorb the sugar in her blood.Gracie now has a glucose monitor and an insulin pump and is “bossing diabetes”, says her dad.”Gracie’s a superstar,” he adds.But why children diagnosed young like Gracie, especially those under the age of seven, have a more aggressive disease than those diagnosed in their teenage years or later, has remained a mystery. The study, published in the journal Science Advances, shows it is down to the development of the beta cells living in the pancreas.These are the cells that release the hormone insulin when sugar levels rise in the blood after we eat. Researchers at the University of Exeter studied pancreas samples from 250 donors, allowing them to see how the beta cells formed normally as people got older, and in type 1 diabetes. Diabetes UKEarlier in life these beta cells were shown to exist as small clusters or as individual cells, but as we age they grow in number and mature into larger groups known as Islets of Langerhans.The study was able to see what happened after the immune system turned against a patient’s own beta cells.Beta cells in small clusters were picked off and destroyed so they never had the chance to mature. Those in larger islets were still attacked, but were more durable allowing patients to still produce low levels of insulin which reduced the severity of their disease.”I think this is a really significant finding for type 1 diabetes – this research really sheds light on why the disease is more aggressive in children,” Dr Sarah Richardson, from the University of Exeter, told the BBC.She said “the future is much brighter” for children being diagnosed with type 1 now. This includes the possibility of screening healthy children for the disease and of new immunotherapy drugs to delay it.The UK has licensed teplizumab – an immunotherapy that can stop the immune system attacking beta cells and may be able to give them time to mature – although it is not available on the NHS. “Because we have new drugs for the treatment of type 1 diabetes in children, we hope that these will be able to prevent or delay the onset in those young people,” said Dr Richardson.Missing piece of the puzzleThe research was part of the Type 1 Diabetes Grand Challenge organised by the Steve Morgan Foundation, Diabetes UK, and Breakthrough T1D. Rachel Connor, director of research partnerships at Breakthrough T1D, said: “This study gives us a missing piece of the puzzle, explaining why type 1 diabetes progresses so much faster in children than in adults.”Dr Elizabeth Robertson, director of research and clinical at Diabetes UK, said: “Uncovering why type 1 diabetes is so aggressive in young children opens the door to developing new immunotherapies aimed at slowing or stopping the immune attack, potentially giving children more precious years without insulin therapy and, one day, preventing the need for it entirely.”

21 minutes agoShareSaveMichael Buchanan,Social affairs correspondent and Adam Eley,BBC NewsShareSaveFamily handoutDozens of patients were put at risk after two of the UK’s leading transplant centres continued fitting a heart device – despite knowing of concerns it had a higher mortality rate than its rival product.Concerns were raised by the NHS about the device in 2018. Of the patients who were subsequently fitted with the mechanical pump, half went on to die within three years.The mother of Greg Marshall – one of the patients who received the device after concerns were known and who subsequently died – told us she was “disgusted and appalled”.The BBC has also learned that leading cardiologists at both hospitals were paid consultants for the device’s manufacturer. The hospitals were aware of this.Both hospitals – the Freeman in Newcastle and Harefield in London – continued to use the pump for years, and questioned the reliability of the data flagged by the NHS. The pump’s manufacturer, Medtronic, eventually withdrew it on safety grounds.Patients with a weakened heart, who may be waiting for a transplant or deemed not suitable for one, can be offered a machine called an LVAD, a Left Ventricular Assist Device. It helps the heart pump blood around the body and, for many patients, this is their only chance of survival until a transplant becomes available.The device is implanted into the heart, with an external wire coming out of the body – usually at the abdomen – that connects to a controller and external batteries.LVADs have been life-savers for decades and, for a number of years, hospitals had a choice of two devices – the HeartWare HVAD, sold by the Irish-American company Medtronic, and the Heartmate III, sold by US manufacturer Abbott.MedtronicIn October 2018, NHS Blood and Transplant (NHSBT), which oversees transplants in the UK, conducted a preliminary audit comparing how the two pumps had performed. A more detailed analysis followed in April 2019.The results were stark. Of the 119 patients who had received the Medtronic device, 45% – or 54 patients – had died within two years. In contrast, just 15% – 15 out of 97 patients – who were given the Abbott pump had died over the same period. Similarly, the number of complications – such as strokes or needing a new pump – were significantly higher for the Medtronic device. The audit said there were “no significant differences” between the types of patients who received each device.One of the UK’s six transplant centres, the Royal Papworth Hospital in Cambridge, did not wait for the NHS analysis. It had picked up on the growing international concerns and had stopped using the Medtronic device in February 2018 “after considering the results of two randomised controlled trials”, as their clinicians “considered the Heartmate III as superior”.However, Harefield Hospital continued to solely use the Medtronic device until early 2021, shortly after the manufacturer had issued a safety notice. The Freeman Hospital continued until June 2021, when the manufacturer withdrew it from sale “in the interest of patient safety”.The regulator, the Medicines and Healthcare products Regulatory Agency (MHRA), continued to approve the device for use after the 2019 analysis, though it had not been informed by the NHS of the data’s existence.Throughout this time, patients fitted with the Medtronic device continued to die at a higher rate than those with the Abbott device. Between October 2018, when the first set of NHS data was produced, and June 2021, when Medtronic discontinued its pump, the mortality rate of the Medtronic device was two-and-a-half times higher than the Abbott device, figures released under the Freedom of Information Act show.Forty-nine percent of those who received the Medtronic device (39 of 80 patients) in that time died within three years. By comparison, 19% of recipients of the Abbott device (20 of 106 patients) died during the same timeframe.Family handoutMedtronic decided to withdraw the device in June 2021 after growing evidence that its pump had a higher frequency of strokes and deaths compared with other devices. It also cited a specific malfunction where pumps would experience a delay or fail to restart after they were stopped.Greg Marshall was one of the patients fitted with the Medtronic device, unaware of the studies about its effectiveness compared with the rival product. A fit and healthy young man, he had ambitions of joining the Royal Marines but he suffered acute heart failure in 2019.”It was a massive shock to us all,” his mother Tessa Marshall remembers.By June of that year, Greg was offered the Medtronic device by the Freeman Hospital, several months after the first set of NHS data was known about.His family say they were not presented with the long-term risks associated with the device, though an existing patient was brought in to tell them of its benefits.Greg agreed to the surgery, but a significant complication in theatre – which the family say was never fully explained to them – led to a stroke. Greg lost movement down the left-hand side of his body, and his speech was significantly impaired.Over time, his health slowly began to recover, but a year later, in July 2020, the heart device suddenly stopped working. When he tried to restart it, it failed to switch back on.”The pump was not pumping, and he just slowly went blue,” Tessa says.Greg was rushed to hospital, but the device could not be fixed. He was told he could have it removed, but, terrified of having another stroke, he refused the surgery.The broken device remained inside him, switched off, as his heart continued to function for a further three years, during which time he was on a transplant waiting list.In September 2023, while in hospital, he unexpectedly went into cardiac arrest. By the time Tessa had reached the Freeman, Greg had died aged 26.His family, devastated by his loss, say they want answers.  ”We said ‘Look, Greg, this is the only option you’ve got, you have got to go with it,'” said Tessa. “I kick myself now, for not doing any more research.” Three patients may have died of this failure, the NHS Trust in Newcastle told the Department of Health and Social Care in a letter seen by the BBC.The trust has since told the BBC the issue of the device failing to restart in patients first came to light in December 2020 – five months after Greg encountered the issue – when Medtronic published a safety notice.ISHLTHospital documents show Greg’s responsible health professional was Prof Stephan Schueler, who until recently was head of the Freeman’s cardiothoracic department. Described by a former colleague as “king of the castle” in the transplant unit, Prof Schueler had a decade-long relationship with the manufacturer of the Medtronic device, public records show.Greg’s family say he did not declare to them his financial relationship with the heart device’s manufacturer, despite such a disclosure being a requirement of the doctor’s regulator, the General Medical Council (GMC).In a statement to the BBC, Prof Schueler said that “there was never a financial incentive nor any salary arrangements with Medtronic for me or anybody else in our team to choose one device over the other”. He did not respond to a direct question about what he had told Greg Marshall about his relationship with Medtronic but said that he “always worked within GMC standards for good medical practice” and that consenting patients for a procedure was “carried out by a whole team of specialised colleagues”.It is common for clinicians to work as consultants for medical manufacturer and pharmaceutical companies. Such arrangements are recognised as being mutually beneficial and can lead to better outcomes for patients, though there are rules around what medics need to declare to patients.The Freeman said in a statement to the BBC that it offered its “sincere condolences” to Greg’s family and it was investigating his case.It said that, although it was “aware” of the NHS data in April 2019, it felt its scientific value was not reliable, and pointed out that it was not accepted in any national or international scientific publication. It said there were other publications at that time which indicated “excellent outcomes” for the Medtronic device.Robbie Burns, a patient representative with NHS Blood and Transplant, obtained many of the documents relating to the hospitals’ continued use of the Medtronic device. He believes there should be an external investigation into how it was allowed to happen.”It was entirely preventable,” he said.”If I had been in the position of receiving this [Medtronic] device, and looked back at the data, I would be going, ‘Why on earth did you do this?'”Prof Schueler said the Medtronic device had several benefits, including being more suitable for children and small adults. He said the decision to continue using the pump was taken after internal discussions had considered all the risk and benefits carefully.Another doctor, André Simon, the director of heart and lung transplantation and ventricular assist devices at Harefield Hospital, had a similarly long-standing relationship with HeartWare and Medtronic, going back to 2014.The man who replaced him at the hospital on the edge of west London, Dr John Dunning, told the BBC that Harefield had continued to use the Medtronic device as “it was the preference” of his predecessor.Dr Simon, who no longer works at the hospital, did not respond to the BBC’s questions. In its statement, the Harefield said it was “aware” of his work for Medtronic and that this had been declared in multiple papers. The hospital added that he was one of a number of senior people “involved” in choosing which devices were used, and that “the continued use of the [Medtronic device] had collective support of clinicians at Harefield” until the manufacturer issued a safety notice in early 2021.In separate statements to the BBC, both the Freeman and Harefield hospitals said their decisions to continue using the Medtronic device were based on “complex clinical decisions” and stressed that there were “no clear grounds” at the time to believe the Medtronic device was significantly inferior to the Abbott device.Harefield said it commissioned an external review of its services in 2019 from the then-chair of the NHSBT’s Cardiothoracic Advisory Group, and this made no comment on its selection of devices.

Owen Collumb was paralyzed in 1993, when he was 21 years old. A tire on his motorbike blew out and he fell into a ravine, breaking a single bone in his spine. When he recovered, he couldn’t move his legs and could control only the biceps in his arms, meaning that he could lift his hands but, to put them down, he had to twist his shoulders and let gravity unbend his elbows.He spent years in an assisted living home before petitioning to move to his own place in Dublin, with the help of home aides. Living alone was liberating; he could choose what he ate and when he woke in the morning. He began working multiple jobs for foundations and advocating for people with disabilities. One of his assistants, Sylwia Filipiek, a Polish immigrant to Ireland, had been employed at a printing factory. She had no experience with home care and struggled to help Mr. Collumb into his wheelchair at first. But, over the years, they learned how to work together, and grew close.In the summer of 2024, Mr. Collumb and Ms. Filipiek flew to Bath, England, to train for the Cybathlon, an international competition run every four years to encourage the development of assistive technologies. The competition, hosted in Switzerland by the university ETH Zurich, consists of eight races for teams and their pilots (which is what the primary competitors, with varying disabilities, are called), each targeting different innovations, such as arm prostheses, leg prostheses and vision assistance.Each race consists of remote tasks that are supposed to simulate everyday life for the pilots: walking across a room, picking up a grocery bag, throwing a ball. One of Cybathlon’s founders, Roland Sigrist, compared it to Formula 1. Teams are encouraged to develop prototypes toward the ultimate goal of “the independence of people with disabilities,” but the competition is straightforward and real, with all its accompaniments: nerves, heartbreak, glory. The pilots are the ones that put themselves on the line. “They’re the masters of the technology, and not the other way around,” Mr. Sigrist said.Mr. Collumb, who is now 54, has participated in the Cybathlon since its first iteration, in 2016, as a pilot in the competition’s most abstract category: brain-computer interfaces. Imagine staring at a cursor at the center of your computer and willing it to move to the right. A brain-computer interface, which allows humans to control computers with just their minds, can turn that willing into action. As someone who lacks almost all ability to move his body, a brain-computer interface could allow Mr. Collumb to play video games, use the internet and direct his wheelchair himself.With artificial intelligence increasing the accessibility and sophistication of technological progress, the integration of organic and robot life is now a matter of degree. How tightly should we embrace these new tools? Will they make life better in the end? Can they change our idea of what people are capable of? The Cybathlon and its participants distill these questions into something concrete. “This isn’t showing your disabilities, it’s showing what you can do,” Mr. Collumb said. “You may be in a wheelchair, you may not be able to move, but you can compete.”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.

12 minutes agoShareSaveNick TriggleHealth correspondentShareSaveGetty ImagesThe doctors’ union, the British Medical Association (BMA), is acting “like a cartel” and threatening the future of the NHS, the health secretary says.Wes Streeting attacked the doctors’ union ahead of the 13th strike by resident doctors in their long-running dispute in England, which is due to begin on Friday.Speaking at the NHS Providers conference in Manchester, Streeting said the BMA was holding the public and the government to ransom with their actions. He also criticised its objection to higher taxes for the wealthy as a way to invest more in public services.The BMA has been approached for comment.In his speech, the health secretary said the BMA union was lobbying against higher taxes to try to protect pensions and consultants, the most senior doctors in the NHS, who earned an average of £127,500 last year.The five-day walkout of resident doctors – who used to be called junior doctors – begins at 07:00GMT on Friday. It comes after talks between the government and the BMA broke down last week.The government offered the union a deal to cover the cost of exam fees and expanding training places more quickly than planned, but it was rejected by the BMA which said pay needed to be addressed.Streeting has maintained he would not negotiate on pay after resident doctors had received pay rises totalling nearly 30% in the past three years.But the BMA has argued that, despite the pay rises, resident doctors’ pay is still a fifth lower than it was in 2008, once inflation is taken into account.’Untold misery to patients’Streeting was applauded by the audience of NHS managers after making what is arguably his strongest attack on the BMA to date.He said: “I just urge them to think about a few things. “The first is, I’m responsible for 1.5 million people in the NHS, not just resident doctors, many of whom have not had a pay rise anything like what resident doctors have had, and many of whom, at the height of their career earnings, will never earn as much as the lowest paid doctor.”The second thing I’d say is that this strike action causes untold misery and disruption to patients who could do without it,” the health secretary said.”Thirdly, it is always true, and especially during winter, it puts untold pressure on other NHS staff who are picking up the pieces for the damage and disruption that resident doctors and the BMA are inflicting on the service.”I think the leadership of the BMA need to really consider whether, at this time, with green shoots of recovery, they want to set the system back, because there isn’t a more pro-doctor, pro-NHS, health secretary or government waiting in the wings.”‘Reprehensible’The health secretary then went on to criticise the union for opposing higher taxes on the wealthy, which he said was an option for improving public finances and investing in the NHS.”Let me tell you, when we ask some of the wealthier to pay more, some of the most effective lobbyists against paying higher tax are the BMA consultants committee and the BMA pensions committee.”So what they effectively do is say, ‘we want other people to pay the higher salaries for doctors’.”It’s time for the BMA to get real. We’re not going to be held to ransom. We are going to plow on regardless,” Streeting said.”And I think it’s become increasingly clear that the BMA is no longer a professional voice for doctors.”They are increasingly behaving in cartel-like behaviour, and they threaten not just the recovery of the NHS under this government. “They threaten the future of the NHS full stop. And I think that is a morally reprehensible position to be in.”

Liver disease most often develops due to one of three major causes: excessive alcohol use, the buildup of fat in the liver associated with obesity, diabetes, and high cholesterol, or viral infections such as hepatitis B and C.
Researchers from Keck Medicine of USC have identified another potential cause of liver damage. A new study published in Liver International links tetrachloroethylene (PCE), a chemical widely used in dry cleaning and found in household products like adhesive glues, spot removers, and stainless steel polish, to serious liver harm.
According to the findings, exposure to PCE can triple the risk of significant liver fibrosis, a condition where scar tissue builds up in the liver. Over time, this scarring can progress to liver cancer, liver failure, or even death. The study also revealed a clear dose-response relationship: the greater the exposure to PCE, the higher the likelihood of developing liver fibrosis.
“This study, the first to examine the association between PCE levels in humans and significant liver fibrosis, underscores the underreported role environmental factors may play in liver health,” said Brian P. Lee, MD, MAS, a hepatologist and liver transplant specialist with Keck Medicine and lead author of the study. “The findings suggest that exposure to PCE may be the reason why one person develops liver disease while someone with the exact same health and demographic profile does not.”
Everyday Exposure to PCE
PCE is a man-made, colorless liquid widely used to remove grease in industrial and household settings, including dry cleaning. People are often exposed to the chemical through the air when it slowly evaporates from recently dry-cleaned clothes. It can also enter drinking water when spills or improper disposal contaminate soil and groundwater.
The International Agency for Research on Cancer classifies PCE as a probable carcinogen. Previous studies have connected it to bladder cancer, multiple myeloma, and non-Hodgkin lymphoma. Dr. Lee noted that other research has also linked PCE exposure to liver cancer.

Because of these health concerns, the U.S. Environmental Protection Agency has initiated a 10-year phaseout of PCE in dry cleaning and placed restrictions on its use in other industries. Still, the chemical persists in certain products and remains unregulated in some countries.
Study Findings: Greater Exposure, Greater Risk
Lee and his colleagues analyzed data from the National Health and Nutrition Examination Survey (NHANES), a large, nationally representative study of U.S. adults. They examined blood samples from participants aged 20 and older collected between 2017 and 2020 and found that about 7% of people had detectable levels of PCE.
Those with measurable PCE exposure were three times more likely to have significant liver fibrosis compared to those without exposure, regardless of age, sex, race, or education level.
Interestingly, higher-income individuals appeared more likely to have detectable PCE in their blood, possibly due to greater use of dry-cleaning services. However, workers in dry-cleaning facilities may face the highest risk because of long-term, direct contact with the chemical.
For every one nanogram per milliliter increase in PCE in the bloodstream (a nanogram equals one-billionth of a gram), the likelihood of significant liver fibrosis rose fivefold.

A Hidden Explanation for Unexplained Liver Disease
The researchers found that traditional risk factors like alcohol consumption and fat accumulation in the liver did not appear to influence fibrosis when PCE was present. “Patients will ask, how can I have liver disease if I don’t drink and I don’t have any of the health conditions typically associated with liver disease, and the answer may be PCE exposure,” said Lee.
Dr. Lee emphasized that PCE may be just one of several environmental toxins contributing to liver disease. “No doubt there are other toxins in our environment besides PCE that are dangerous to the liver,” he said.
He also hopes the findings will lead to earlier detection and better outcomes for those affected. “We hope our research will help both the public and physicians understand the connection between PCE exposure and significant liver fibrosis,” Lee said. “If more people with PCE exposure are screened for liver fibrosis, the disease can be caught earlier and patients may have a better chance of recovering their liver function,” said Lee.

Weight-loss drugs Ozempic and Mounjaro deliver impressive heart protection for people with type 2 diabetes. Large real-world study finds new GLP-1 drugs help protect the heart in people with cardiovascular risk. Clear evidence shows these medications support heart health beyond their weight-loss effects. Semaglutide (Ozempic) and tirzepatide (Mounjaro) offer similar levels of heart protection, with only small differences in results.GLP-1 Drugs Linked to Better Heart Health
Injectable medications used for weight loss may also lower the risk of major cardiovascular problems in people with type 2 diabetes. Researchers from the Technical University of Munich (TUM) and Harvard Medical School reached this conclusion after analyzing insurance claims data. Their findings show that semaglutide and tirzepatide (sold as Ozempic and Mounjaro) can reduce the risk of serious heart-related events by as much as 18 percent.
The research, published in Nature Medicine, drew on a vast collection of data from U.S. health insurance records. “Those data are collected in routine clinical care and can be used for research. They allow us to answer a broad range of relevant questions efficiently. Importantly, we are studying patients who reflect everyday clinical practice — unlike the highly selected participants typically enrolled in randomized trials,” explains Dr. Nils Krüger, the study’s lead author and a physician at the Department of Cardiovascular Diseases at the TUM University Hospital German Heart Center.
Heart Protection Beyond Weight Loss
The results clearly indicate that these newer diabetes treatments help protect the heart in people with elevated cardiovascular risk. Compared with sitagliptin, a diabetes medication known to provide no measurable heart benefits, semaglutide cut the risk of stroke and heart attack by 18 percent. Tirzepatide lowered the combined risk of stroke, heart attack, and death by 13 percent compared with dulaglutide, an older GLP-1 drug already in use.
“Both substances have a cardioprotective effect. Our data show that the benefits emerge from early on, indicating that the effect goes beyond weight loss alone,” says Dr. Krüger. However, researchers note that the biological mechanisms behind this protective effect remain uncertain.

Because semaglutide and tirzepatide are relatively new, studies directly examining their cardiovascular effects have been limited, especially those comparing the two drugs head-to-head. The research team from TUM, Harvard Medical School, and Brigham and Women’s Hospital aimed to fill this knowledge gap to guide better treatment decisions for patients at risk of heart disease.
Comparing Ozempic and Mounjaro
“According to the manufacturers’ claims, each one suggests its own product is more effective than the competitor’s at reducing cardiovascular risk,” says Prof. Heribert Schunkert, Director of the Department of Cardiovascular Diseases at TUM University Hospital. “Our study, however, shows only small differences in heart outcomes between tirzepatide and semaglutide in the risk groups we analyzed.”
Dr. Krüger adds: “We hope our findings will provide clarity to physicians about how these new medications perform in clinical practice. Our transparent study design is also intended to support open scientific discussion about whether and how modern GLP-1 drugs should become part of the standard therapeutic repertoire in cardiovascular medicine.”
Recently, Dr. Krüger’s team was able to show that treatment with semaglutide or tirzepatide can reduce health risks for people with heart failure with preserved ejection fraction by over 40 percent. The study has been published in the journal JAMA (PMID: 40886075).
This work was funded by the National Institutes of Health (R01-HL141505, R01-AR080194) and the German Heart Foundation (S/02/24, SRF-HF/24, RWE/11/25).

Heart disease remains the world’s top killer, claiming more lives each year than any other condition. Scientists are uncovering how gut microbes may influence coronary artery disease (CAD), one of the most common and serious forms of heart disease. A research team in Seoul has identified 15 specific bacterial species connected to CAD, offering new insight into how the gut and heart interact. Their analysis reveals several biological pathways tied to disease severity, including heightened inflammation and disruptions in metabolism that may worsen heart health.Cardiovascular diseases claim nearly 20 million lives each year, making them the leading cause of death worldwide. While genetics and lifestyle factors clearly affect a person’s heart health, scientists are discovering that microorganisms living in the gut may also have an important influence. These microbes appear to be deeply involved in the development of coronary artery disease (CAD), though their exact roles have long been unclear.Recent research suggests that the gut microbiome may promote CAD through a variety of biological pathways, influencing inflammation and metabolism in ways that impact the arteries. However, which specific bacteria are responsible — and how they contribute to disease progression — has remained uncertain.
Mapping Microbes in Coronary Artery Disease
Researchers in Seoul are beginning to unravel this mystery. Writing in mSystems, a team led by Han-Na Kim, Ph.D., at the Samsung Advanced Institute for Health Sciences and Technology at Sungkyunkwan University, examined how gut microbes interact with the cardiovascular system. “We’ve gone beyond identifying ‘which bacteria live there’ to uncovering what they actually do in the heart-gut connection,” Kim explained.
The team analyzed fecal samples from 14 people with CAD and compared them to samples from 28 healthy participants using metagenomic sequencing, a powerful technique that identifies all the DNA within a sample. This approach allowed them to reconstruct the genetic makeup of individual microbes. From this analysis, the researchers identified 15 bacterial species linked to CAD and mapped the pathways that connect these microbes to the severity of the disease.
Inflammation, Imbalance, and Microbial Shifts
According to Kim, “Our high-resolution metagenomic map shows a dramatic functional shift toward inflammation and metabolic imbalance, a loss of protective short-chain fatty acid producers, such as Faecalibacterium prausnitzii, and an overactivation of pathways, such as the urea cycle, linked to disease severity.”

The findings suggest that the gut ecosystem in people with CAD undergoes significant changes that promote inflammation and disrupt normal metabolic processes. These shifts may help explain why the gut microbiome plays such a strong role in cardiovascular disease.
When “Good” Bacteria Turn Harmful
Surprisingly, the study also showed that bacteria typically seen as beneficial can sometimes become harmful. Microbes such as Akkermansia muciniphila and F. prausnitzii, often considered “friendly” species, appear to act differently depending on whether they come from a healthy or a diseased gut. This dual nature, Kim noted, highlights how context can transform even protective microbes into contributors to disease.
The results also revealed how complex it is to link specific bacteria to disease outcomes. Earlier research had reported that certain species within the family Lachnospiraceae decrease in people with CAD. Yet Kim’s team found that other Lachnospiraceae species actually increase in abundance. “Lachnospiraceae may be the Dr. Jekyll and Mr. Hyde of the gut,” Kim said. Some types appear beneficial, while others may worsen disease. “The big unanswered question now is which strains are the healers, and which are the troublemakers.”
Toward Precision Microbial Medicine
The researchers plan to combine microbial data with genetic and metabolic information to better understand how gut microbes influence heart disease at a mechanistic level. Their long-term goal is to develop precision-based treatments that use microbial insights to prevent cardiovascular disease before it begins.
Kim emphasized that prevention is the most promising approach to lowering the global impact of heart disease. Potential strategies could include microbial therapies — such as stool-based diagnostic screening — or dietary interventions designed to restore beneficial bacteria or inhibit harmful pathways.
By uncovering the specific bacterial species and biological mechanisms involved, scientists are moving closer to using the gut microbiome as a powerful tool for maintaining heart health.

A new study from the University of California San Diego suggests that glucagon-like peptide-1 (GLP-1) receptor agonists, a class of medications originally developed for type 2 diabetes, may have benefits that extend far beyond blood sugar and weight management. These drugs, which include semaglutide (sold as Ozempic and Wegovy) and tirzepatide (known as Mounjaro), are already well known for helping people lose weight and manage metabolic conditions. Now, researchers have discovered that they might also be linked to better survival outcomes in colon cancer patients.
The study analyzed medical records from more than 6,800 people diagnosed with colon cancer across University of California Health facilities. Patients who were taking GLP-1 medications were less than half as likely to die within five years compared to those not using the drugs (15.5% versus 37.1%). This striking difference points to a potentially powerful new use for drugs that are already transforming diabetes and obesity treatment.
The research was led by Raphael Cuomo, Ph.D., an associate professor in the Department of Anesthesiology at UC San Diego School of Medicine and a member of the UC San Diego Moores Cancer Center. His team used the University of California Health Data Warehouse to review outcomes across the state’s academic medical centers.
After accounting for important factors such as age, body mass index (BMI), cancer severity, and other health conditions, the team found that people taking GLP-1 drugs still had a significantly lower risk of death. This consistency suggests the protective benefit of GLP-1 therapy may be independent of other medical or lifestyle variables.
Why GLP-1 Drugs Might Protect Against Cancer
The benefit appeared strongest in patients with obesity (BMI over 35). This finding hints that GLP-1 drugs may help offset some of the inflammation and metabolic stress that can make cancer harder to treat.
Scientists are exploring several possible explanations for this effect. GLP-1 receptor agonists are known to lower inflammation throughout the body, enhance insulin sensitivity, and promote weight loss — all factors that can influence cancer growth and progression. Experimental studies in laboratories also indicate that GLP-1 drugs may directly inhibit the growth of tumor cells, encourage cancer cell death, and alter the surrounding environment within tumors to make them less supportive of disease spread.

However, researchers caution that it is still unclear whether the lower death rate seen in this study reflects a direct anti-cancer action or an indirect result of improved overall metabolic health.
Next Steps: Clinical Trials Needed
Dr. Cuomo emphasized that the findings are observational, meaning they do not yet prove that GLP-1 drugs directly improve cancer outcomes. These results highlight an urgent need for clinical trials to test whether GLP-1 medications can actually enhance cancer survival, particularly among patients with obesity-related cancers.
The study was published in Cancer Investigation on November 11, 2025.