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Instead of requiring personalized gene edits for each patient, the new approach could create a standardized method to use for many diseases.Gene-editing therapies offer great hope for treating rare diseases, but they face big hurdles: the tremendous time and resources involved in devising a treatment that might only apply to a small number of patients.A study published on Wednesday outlines a new approach that could make the process more efficient and less costly. Writing in the journal Nature, researchers presented a path toward a gene-editing strategy that could eventually be standardized for many different rare diseases, instead of personalized edits for each one.“We are purposefully forgoing what is the most obvious way to treat a patient — fix their individual mutation back to the normal sequence,” said the study’s senior author, David R. Liu, a biologist at the Broad Institute and Harvard, who has pioneered several gene-editing advances.Instead, he said, the idea is a “disease-agnostic” strategy: developing a technique that “could treat many more patients regardless of what mutation they have.”There are more than 7,000 rare genetic diseases, conditions defined in the United States as affecting fewer than 200,000 people. Together, these diseases afflict about 30 million Americans and about 400 million people worldwide.While the new approach is years away from potential use, it might ultimately apply to “a significant fraction” of those patients, conservatively about 10 percent, said Dr. Richard P. Lifton, the president of the Rockefeller University and head of its laboratory of human genetics and genomics.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.

Some psychologists and parents argued that it risked glamorizing the condition, but one performer described the experience as empowering: “Onstage, I can be who I really am.”When a Swiss theater invited people with eating disorders to be involved in a play about Joan of Arc this fall, it caused a furor. Some therapists and parents of girls with anorexia criticized the move as “ethically reprehensible” and said it could jeopardize performers’ health.So when Janine Rickenbach, who has had anorexia for decades, took the Theater Basel stage last week in the premiere, she knew that some audience members were judging her appearance as much as her performance.Yet during the two-hour show, Rickenbach, 44, appeared unfazed. At one point, wearing a camisole top that revealed her arms and neck, she stared impassively at the audience while delivering a monologue that seemed to address the outcry.“What are you thinking right now?” she said: “Are you thinking, ‘Oh my God…’” Was that “because I look the way I look?” she asked, “Or because I’m standing here on this stage? Because my struggle is visible?”Theater makers have long depicted health struggles onstage, including the realities of living with H.I.V. and cancer, but the debate around this production, titled “Jeanne Dark” and running through May 22, has shown that ethical questions remain about how various conditions are portrayed theatrically — and who gets to shape those depictions.Ulrike Schmidt, a specialist in eating disorders at King’s College, London, said in an email that anybody depicting mental health onstage needed to consider the potential for stigmatization, perpetuating stereotypes or “inappropriate glamorization”We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

A research team at the Federal University of ABC (UFABC) in Brazil has created a new chemical compound that may offer a promising way to treat Alzheimer’s disease. Their work involved a combination of computer-based modeling (in silico), laboratory tests with cell cultures (in vitro), and experiments in animals (in vivo). After obtaining encouraging early results, the scientists are now looking to collaborate with pharmaceutical companies to move toward clinical trials.
The compounds, developed with support from FAPESP, are easy to produce and are thought to work by breaking down beta-amyloid plaques that build up in the brains of people with Alzheimer’s disease. These plaques form when amyloid peptide fragments accumulate between neurons, triggering inflammation and interfering with communication between brain cells.
Targeting Copper to Break Down Beta-Amyloid Plaques
A study published in ACS Chemical Neuroscience reports that the compounds function as copper chelators. By binding to excess copper found within beta-amyloid plaques, the molecules help degrade these toxic structures and lessen symptoms associated with the disease. Tests in rats showed that the compound reduced memory impairments, improved spatial awareness, and enhanced learning ability. Biochemical analysis also revealed a reversal in the pattern of beta-amyloid plaques.
“About a decade ago, international studies began to point to the influence of copper ions as an aggregator of beta-amyloid plaques. It was discovered that genetic mutations and changes in enzymes that act in the transport of copper in cells could lead to the accumulation of the element in the brain, favoring the aggregation of these plaques. Thus, the regulation of copper homeostasis [balance] has become one of the focuses for the treatment of Alzheimer’s,” explains Giselle Cerchiaro, a professor at the Center for Natural and Human Sciences at UFABC who coordinated the study.
Designing Molecules That Reach the Brain
Using this understanding, the research team created molecules that can cross the blood-brain barrier and remove copper from beta-amyloid plaques. Ten candidate molecules were developed, and three advanced to testing in rats with induced Alzheimer’s disease. One compound showed particularly strong results for both effectiveness and safety.

This work formed the basis of the doctoral thesis of FAPESP scholarship recipient Mariana L. M. Camargo, the master’s thesis of Giovana Bertazzo, and the undergraduate research project of Augusto Farias. A team led by Kleber Thiago de Oliveira at the Federal University of São Carlos (UFSCar) contributed by synthesizing one of the compounds included in the study.
Improvements in Brain Health and Behavior
In experiments with rats, the compound lowered neuroinflammation and oxidative stress and restored copper balance in the hippocampus, the brain region responsible for memory processing. Treated animals also demonstrated better performance in tasks requiring spatial navigation.
Beyond these behavioral improvements, the compound proved non-toxic in both hippocampal cell cultures and the animals themselves, whose vital signs were closely followed throughout the experiments. Computer models confirmed that the compound can cross the blood-brain barrier and reach the areas most affected by Alzheimer’s-related damage.
A Potentially Affordable New Direction for Alzheimer’s Care
Alzheimer’s disease is a complex and multifaceted neurodegenerative condition with no cure and no clearly defined cause. While an estimated 50 million people worldwide are affected, current treatment options are limited and often provide only partial symptom relief or rely on costly therapies such as monoclonal antibodies.
The findings from UFABC have already resulted in a patent application, and the team hopes to secure industry partnerships to begin clinical trials in humans. “It’s an extremely simple, safe, and effective molecule. The compound we’ve developed is much less expensive than available drugs. Therefore, even if it only works for part of the population, since Alzheimer’s disease has multiple causes, it’d represent a huge advance over current options,” Cerchiaro celebrates.

Every moment, the bone marrow generates millions of fresh blood and immune cells. This nonstop renewal depends on a carefully balanced relationship between hematopoietic stem cells (HSCs), supportive stromal cells, and a network of immune signals.
Over the years, this balance becomes vulnerable. Aging, chronic inflammation, or somatic mutations can disrupt communication among these cell groups, reducing normal stem-cell renewal and allowing mutated HSCs to expand unnoticed. This process leads to clonal hematopoiesis of indeterminate potential (CHIP), which appears in about 10 to 20% of adults over 60 and nearly 30% of those over 80.
Although people with CHIP typically have no symptoms, the condition increases the risk of blood cancers by tenfold and doubles the likelihood of cardiovascular disease and early death. Myelodysplastic syndrome (MDS), a related disorder involving clonal HSCs, causes inefficient blood-cell production and gradual failure of the bone marrow. It affects up to 20 in every 100,000 adults over 70, and around 30% of cases advance to acute myeloid leukemia (AML), an aggressive and often fatal cancer.
Despite the seriousness of these disorders, the contribution of the bone marrow microenvironment to their development has remained unclear.
Mapping Hidden Changes in the Bone Marrow Microenvironment
To better understand how mutated HSC clones gain dominance, an international research team co-led by Judith Zaugg from EMBL and University of Basel and Borhane Guezguez from UMC Mainz carried out an extensive molecular and spatial analysis of human bone marrow. The samples came from the BoHemE cohort study in collaboration with Uwe Platzbecker at the National Center for Tumor Diseases (NCT) Dresden.
Using single-cell RNA sequencing, biopsy imaging, proteomics, and co-culture models, the researchers created a detailed map of the bone marrow microenvironment in healthy donors (including those with CHIP) and in patients with MDS. Their analysis revealed an unexpected cellular shift that begins long before clinical signs appear. The team found that a population of inflammatory stromal cells gradually replaces the usual mesenchymal stromal cells (MSC) that support stem-cell function.

“I was surprised to observe such pronounced remodeling of the bone marrow microenvironment already in individuals with CHIP, although the underlying cause-and-effect relationships remain unclear,” said Zaugg, co-senior author, EMBL Group Leader, and Professor at Basel University.
Unlike healthy stromal cells, these inflammatory MSCs (iMSC) produce large amounts of interferon-induced cytokines and chemokines. These molecules attract and activate interferon-responsive T cells, which then intensify the inflammatory activity. This creates a feed-forward loop that maintains chronic inflammation, disrupts normal blood formation, and contributes to vascular changes in the marrow.
Identifying What Drives Bone Marrow Inflammation
Interestingly, the researchers did not find signs that mutated hematopoietic cells in MDS directly trigger this inflammatory response. They were able to separate mutated from non-mutated cells using SpliceUp, a computational method developed by co-lead author and EMBL alumnus Maksim Kholmatov in collaboration with Pedro Moura and Eva Hellström-Lindberg from Karolinska Institute. SpliceUp identifies mutated cells in single-cell datasets by detecting abnormal RNA-splicing patterns. In MDS, the inflammatory network within the microenvironment becomes dominant and replaces much of the marrow’s normal regenerative structure.
“Another striking observation was that MDS stem cells couldn’t trigger stromal cells to produce CXCL12, an important signal that triggers blood cells to settle in the bone marrow. This failure may help explain why the bone marrow stops working properly,” said Karin Prummel, co-lead author and EMBL postdoc.
“It was quite surprising to see the lack of a direct inflammatory effect that we could attribute to the mutant cells,” said Maksim Kholmatov, co-lead author and EMBL alumnus. “However, when viewed in the context of changes in the T cell and stromal compartments, it underlines the importance of the bone marrow microenvironment in shaping disease progression.”
Inflammation as an Early Driver of Blood Disease

These findings indicate that inflammation plays a central role in the earliest phases of disease and highlight the bone marrow microenvironment (also called the bone marrow niche) as a key therapeutic focus. By directing attention to the ecosystem that supports mutated stem cells rather than the mutated cells alone, the research points to new opportunities for early treatment and prevention.
Anti-inflammatory drugs or therapies that adjust interferon signaling may help preserve marrow function in older adults with CHIP. Combining targeted treatments with therapies that act on the microenvironment could slow or prevent the transition from CHIP to MDS or AML. The specific molecular features of iMSCs and interferon-responsive T cells may also serve as early biomarkers for people at elevated risk.
“Our findings reveal that the bone marrow microenvironment actively shapes the earliest stages of malignant evolution,” said Guezguez, Principal Investigator in the Department of Hematology at UMC Mainz and co-senior author. “As advances in molecular profiling allow us to detect pre-leukemic states years before clinical onset, understanding how stromal and immune cells interact provides a foundation for preventive therapies that intercept disease progression before leukemia develops.”
Inflammaging and the Wider Impact on Age-Related Disease
Beyond blood disorders, the results contribute to a broader understanding of ‘inflammaging’, the low-level, chronic inflammation that supports many age-related conditions, including cancer and cardiovascular and metabolic disease. The bone marrow, once considered only a site of blood production, now appears to be both affected by and responsible for systemic inflammatory aging. By showing how interactions between immune and stromal cells drive these changes, the study offers a model for exploring inflammatory remodeling in other myeloid malignancies and advanced leukemia.
“It will be crucial to study these processes over time; our current findings are based on cross-sectional data,” Zaugg said. “This has important implications for therapies that replace malignant cells but leave the bone marrow niche intact, such as blood stem cell transplantation. We are now investigating to what extent the niche retains a ‘memory’ of disease, which could shape how it responds to new, healthy stem cells.”
The work appears alongside a complementary study examining the MDS bone marrow microenvironment, also published in Nature Communications and led by Marc Raaijmakers from Erasmus MC Cancer Institute in Rotterdam. Together, the two studies offer a more complete view of inflammatory remodeling during the early phases of bone marrow disease.
The research involved collaborators from UMC Mainz, University of Basel, University Hospital Dresden, Karolinska Institute Sweden, The Jackson Laboratory USA, Sorbonne University, France, and DKTK partner institutions, including DKFZ and NCT Dresden. Funding came from the DKTK-CHOICE programme, the ERC grant EpiNicheAML to Judith Zaugg, the MCSA-funded ITN ENHPATHY, EMBO, Swiss National Foundation, and the José Carreras Leukämie-Stiftung.

Polycystic kidney disease (PKD) is an inherited disorder in which clusters of fluid-filled cysts gradually develop within the kidneys. As these cysts enlarge and multiply, they damage the surrounding tissue and limit the organs’ ability to function. Many people with advanced PKD eventually require dialysis. There is currently no cure.
Researchers at UC Santa Barbara are exploring a new therapeutic direction that aims to reach and disrupt the uncontrolled expansion of these cysts by using carefully designed monoclonal antibodies — lab-made proteins commonly used in immunotherapy.
“The cysts just keep growing endlessly,” said UCSB biologist Thomas Weimbs, senior author of the study published in Cell Reports Medicine. “And we want to stop them. So we need to get a drug into these cysts that will make them stop.”
This work received partial support from the National Institutes of Health and the U.S. Department of Defense.
Why Current Treatments Fall Short
Interrupting a runaway process There are several small-molecule drugs that show potential for slowing cyst expansion. However, according to Weimbs, the only approved drug that offers some benefit also brings significant side effects and toxicity to nearby kidney tissue. Therapeutic antibodies grown in the lab can be more selective, but the form most commonly produced today, immunoglobulin G (IgG), is too large to enter the cysts.
“They’re very successful for cancer therapy,” Weimbs said. “But IgG antibodies never cross the cell layers and they can never make it inside the cysts.” This limitation is crucial, he added, because the interior of each cyst — essentially a sealed chamber lined with epithelial cells — is the location where disease-driving activity occurs.

“Many of the cyst-lining cells actually make growth factors and they secrete them into the cyst fluid,” he explained. “And these growth factors then bind back to the same cells or to neighboring cells and continue to stimulate themselves and each other. It’s like a never-ending scheme in which the cells just keep activating themselves and other cells in there. Our premise was that if you block either the growth factor or the receptor for the growth factor, you should be able to stop this constant activation of the cells.”
A New Antibody Designed to Enter Kidney Cysts
Enter dimeric immunoglobulin A (dIgA), a monoclonal antibody that can cross epithelial membranes. In nature, dIgA is produced as part of the immune system and is released into tears, saliva and mucus as an early defense against pathogens. In a 2015 paper, Weimbs and colleagues proposed that by binding to polymeric immunoglobulin receptors on epithelial cells, dIgA could move in a one-way direction through the membrane and into kidney cysts, allowing it to reach specific receptors involved in the growth cycle.
The new study builds on that earlier hypothesis and demonstrates that this strategy can work by targeting a key driver of cyst development, the cell mesenchymal-epithelial transition (cMET) receptor.
Testing a Cyst-Penetrating Antibody
The research team first modified the antibody by altering the IgG DNA sequence to “give it a different backbone” that converted it into a dIgA antibody. They then verified that the redesigned protein could recognize the intended receptor and proceeded to test it in mouse models. The antibody successfully entered the cysts and remained there.

“The next question was, could it actually block that particular growth factor receptor,” Weimbs said. Their findings showed that activity of the cMET receptor decreased, which reduced the signals that encourage cell growth. In addition, the paper reports that the treatment triggered a “dramatic onset of apoptosis (cell death) in cyst epithelial cells, but not in healthy renal tissue” without any noticeable harmful effects.
Looking Ahead to Future Applications
Because the work is still in the preclinical stage, Weimbs emphasized that it will be some time before this approach can be adapted for human treatment. The researchers now face several challenges, including finding partners interested in PKD therapies, accessing technology needed to generate more antibody variants, and identifying additional biological targets that may be suitable for similar strategies.
“In the literature there are dozens of growth factors that have been shown to be active in these cyst fluids,” Weimbs said. “So it would be a good idea to compare blocking of several different growth factors and several receptors, maybe side-by-side to see which is the most effective, and see if we can achieve slowing or reversal of the disease with any one of them. We can also combine different antibodies against different receptors at the same time. That would be the next step.”
Research in this paper was also conducted by Margaret F. Schimmel (lead author), Bryan C. Bourgeois, Alison K. Spindt, Sage A. Patel, Tiffany Chin, Gavin E. Cornick and Yuqi Lu at UCSB.

28 minutes agoShareSavePhilippa RoxbyHealth reporterShareSaveGetty ImagesAction is needed now to reduce ultra-processed food (UPF) in diets worldwide because of their threat to health, say international experts in a global review of research.They say the way we eat is changing – with a move away from fresh, whole foods to cheap, highly-processed meals – which is increasing our risk of a range of chronic diseases, including obesity and depression.Writing in The Lancet, the researchers say governments need “to step up” and introduce warnings and higher taxes on UPF products, to help fund access to more nutritious foods.However some scientists say this review can not prove that UPFs directly cause health harms and more research and trials are needed to show that.Ultra-processed foods are defined as containing more than five ingredients which you would not find at home in your kitchen cupboard, such as emulsifiers, preservatives, additives, dyes and sweeteners. Examples of UPFs include sausages, crisps, pastries, biscuits, instant soups, fizzy drinks, ice cream and supermarket bread. Surveys indicate these industrially-manufactured foods are on the rise in diets around the world, worsening the quality of what we eat with too much sugar and unhealthy fats and a lack of fibre and protein.This review of evidence on the impact of UPFs on health, carried out by 43 global experts and based on 104 long-term studies, suggests these foods are linked to a greater risk of 12 health conditions.These include type 2 diabetes, cardiovascular disease, kidney disease, depression and dying prematurely from any cause.Review author Prof Carlos Monteiro, from the University of Sao Paulo in Brazil, who set up the Nova classification system for categorising food, said the growing consumption of ultra-processed foods “is reshaping diets worldwide, displacing fresh and minimally processed foods and meals”.”This change in what people eat is fuelled by powerful global corporations who generate huge profits by prioritising ultra-processed products, supported by extensive marketing and political lobbying to stop effective public health policies to support healthy eating,” he added.Co-author Dr Phillip Baker, from the University of Sydney, said the answer was “a strong global public health response – like the coordinated efforts to challenge the tobacco industry”.The review acknowledges a lack of clinical trials showing exactly how UPFs damage health – but says that should not delay action to protect people worldwide from potential health harms.Some scientists have commented that it is difficult to untangle the effects of UPFs in people’s diets from other factors in people’s lives, such as lifestyle, behaviour and wealth.Critics of the Nova classification system say it relies too much on the level of processing in foods, and not on how nutritious that particular food is. For example, wholegrain bread, breakfast cereals, low-fat yoghurts, baby formula milk and fish fingers all count as ultra-processed but have lots of good in them.Prof Kevin McConway, emeritus professor of applied statistics at the Open University, said: “A study like this can find a correlation, but it can’t be certain about cause and effect.”He said there was still “room for doubt and for clarification from further research”.”It seems to me likely that at least some UPFs could cause increases in the risk of some chronic diseases. But this certainly doesn’t establish that all UPFs increase disease risk.”It is still not clear what it is about ultra-processed foods that could be causing or contributing to diseases.Prof Jules Griffin, from the University of Aberdeen, said there were some positive sides to food processing, and more research to understand how it influences our health was “urgently needed”.The Food and Drink Federation says UPFs can form part of a balanced diet, like frozen peas and wholemeal bread.”Companies have been making a series of changes over many years to make the food and drink we all buy healthier, in line with government guidelines,” says Kate Halliwell, chief scientific officer at the Food and Drink Federation, which represents industry.The amount of sugar and salt in products on sale in shops and supermarkets has gone down by a third since 2015, she added.Current UK government advice on diet is to eat more fruit, vegetables and fibre, and cut back on sugar, fat and salt.

24 minutes agoShareSaveMarie-Louise ConnollyHealth correspondent, BBC News NIShareSaveBBCA County Antrim GP has said she is “hugely concerned” for women who need breast cancer treatment in Northern Ireland after three patients in her surgery received late cancer diagnoses.The patients are among 32 women in the Notting Hill Medical Practice, based in the Northern Trust, who were red-flagged within a five-month period this year.The three women, who have asked for their identities to be protected, had to wait more than eight weeks to be seen by a consultant, while nine others are still waiting, one for more than 10 weeks.Dr Jilly O’Hagan told BBC News NI the wait is “traumatic”.One of the women said she has been in limbo for months and “just wants the cancer out”.She said that after being told there were more than 80,000 women in front of her on the waiting list, she paid for a private diagnosis which confirmed she had stage two breast cancer.The woman said she is “furious” about the delay and is feeling the strain mentally and physically.Dr O’Hagan said such failings are not happening in England, Scotland and Wales and asked why women in Northern Ireland should be getting a “substandard service”.”The new regional breast cancer service is not functioning – there is a bottleneck, they are not meeting the targets for women who are red-flagged,” Dr O’Hagan said. “It never used to be like this, it’s not working.” Red-flag referralA red-flag referral means a GP believes the patient should be treated as a high priority for suspected cancer based on specific clinical symptoms outlined in the Northern Ireland Cancer Network (NICaN). These referrals are the highest priority for waiting lists, and patients should ideally be seen by a specialist within two weeks.After a diagnosis, there is a 62-day target for treatment to start.Between April to June 2025, about 840 patients (67%) waited longer than 62 days to start treatment for cancer following an urgent GP referral for suspected cancer.Getty ImagesA woman in the Southern Trust area who has stage four breast cancer said all the “faffing around between various health trusts and hospitals” delayed her diagnosis.In her early 40s, she said she is an “emotional wreck” after being told different outcomes between different health trusts.”My care has been inadequate, not joined up and impersonal,” she said.In June, the woman first felt what she described as like a “pull” under her armpit.It was two weeks before she could get an appointment with her GP who on examination felt a “pea-sized” lump and red-flagged her in early July.With a history of breast cancer in the family, the woman had received two previous annual mammograms both of which had been clear. After she was red-flagged, there was confusion as she received communication between Craigavon Area Hospital and then was referred to the Ulster Hospital, in a different health trust.The mother of three considered seeking private treatment in Northern Ireland or the Republic of Ireland.The pea-sized lump had got larger, and her breast was red and swollen.Almost 10 weeks after that initial GP appointment, she was diagnosed with stage four cancer in August and began chemotherapy at the end of October.”It’s been horrific and my family and I are emotional wrecks,” she said.Her experience prompted her to write to the health minister.’UK’s worst cancer waiting times’Naser Turabi, from Cancer Research UK, said Northern Ireland’s cancer waiting times are the worst in the UK.Too many patients are waiting too long for treatment, particularly for cancers like lung, gynaecological and blood that can often be quite aggressive, Mr Turabi told BBC News NI.”It’s a matter of patient safety and survival with around 70% of patients missing the target every month, that represents thousands of people whose treatment is being delayed and they are potentially coming to harm.” Research shows that getting treatment quickly is crucial with every four-week delay reducing patient survival by an average of 10%.In August, BBC News NI reported that some patients who have been red-flagged for breast cancer assessments are waiting up to 10 weeks to be seen.The target set by Northern Ireland’s devolved Department of Health, which oversees five health and social care trusts, is 14 days.’Appalling statistic’PacemakerThe chair of Stormont’s health committee, Sinn Féin’s Philip McGuigan, said women were being let down.”In the three months prior to June of this year almost 2,000 patients were seen by breast cancer specialists following urgent referral for breast cancer,” he said.”Only 129 of those patients were seen within 14 days of their urgent referrals”So the examples of Dr O’Hagan’s practice are unfortunately far too common across the north and it is totally unacceptable.”Another member of the committee, the DUP’s Diane Dodds said that the new regional cancer service “does not seem to be actually set up in a way that makes it efficient and makes women be seen much, much earlier”.She said it was not just patients with breast cancer who were being failed: “In the quarter up to June 2025, 840 patients – two third of all patients diagnosed with cancer – waited longer that 62 days to start treatment.”That, across all the tumour sites, all of the cancer issues, is an appalling statistic.”‘Heightened patient anxiety’In a statement the Department of Health said: “The implementation of the single regional waiting list for breast assessment was introduced in May to address regional inequity for people accessing breast assessment. “However current core capacity of the breast assessment service is insufficient to meet ongoing demand. “For this reason, £5m has been allocated through the Elective Care Framework to address this capacity shortfall.”Health Minister Mike Nesbitt said he recognised that “delays in access to breast assessment will heighten patient anxiety” and welcomed that, in recent weeks, women have waited about seven weeks to be seen. “While this is still too long, I anticipate that this will continue to reduce,” he added.Waiting list money ‘diverted’According to the Department of Health, since April 2025, more than 122,600 red-flag or time-critical patients have been seen or treated, with plans to reach about 226,700 by the end of the year. “Outpatient waits over four years are down 29% – that’s 29,500 patients – and treatment waits down 41% – that’s 8,300 patients,” a spokesperson said.Earlier this year, £215m was set aside to tackle hospital waiting lists. But on Tuesday the Health Minister, Mike Nesbitt, confirmed that a third of that money has since been diverted to deal with the Department of Health’s (DoH) massive deficit.During a debate on cancer waiting times in the assembly, the minister said more than £70m had been used to help tackle budget difficulties.The DoH had faced a deficit of £600m and has been reducing that figure through efficiencies.Nesbitt told assembly members there had been some improvements on hospital waiting lists, but acknowledged there was more still to be done.

4 hours agoShareSaveNikki FoxEast of England health correspondentShareSaveORTHOPAEDIC ACADEMYLawyers representing more than 50 people treated by a surgeon being investigated over allegations of botched operations have written to Health Secretary Wes Streeting calling for a public inquiry.The patients were children when they were operated on by Kuldeep Stohr, and theirs are among 800 cases being reviewed by Cambridge University Hospitals NHS Foundation Trust (CUH) over concerns they fell “below expected standards”.They include Amy, 16, who suffered “severe physical harm”. She said: “I feel like my youth has been taken, but not just my youth, my life.”The Department of Health and Social Care (DoH) said a national review would look at how complex orthopaedic surgery was overseen.JAMIE NIBLOCK/BBCThe patients are demanding to know how the surgeon was able to practise unchecked, despite warnings almost a decade earlier.Amy, from Bury St Edmunds, Suffolk, was one of the first to receive the findings of an independent assessment into her treatment.Conducted by a panel of external clinicians, chaired by Andrew Kennedy KC, it said the care “did not meet the standards they would expect”.It raised concerns that surgeries were carried out on Amy’s knees when she was nine, and her legs were still growing.JAMIE NIBLOCK/BBCFamily photoShe was born with Russell-Silver Syndrome, a rare growth disorder, and her left leg was 3cm (1.2in) longer than her right.In 2018, Ms Stohr said surgery was necessary.But the assessment said metal plates inserted into her longer leg to stop it growing were too big, causing pain and requiring replacement.”I wouldn’t wish that pain on anyone. It was pretty traumatising,” said Amy.”I was in a healing process, month after month, and my friends would say ‘Do you want to go out?’ and I would say ‘I can’t, I’m in pain’. “I missed out on so many great opportunities because my physical health was down.”Hudgell Solicitors with permission from Amy’s familyAmy’s right leg was then allowed to grow too much and ended up 3cm longer than her left.”I remember crying and breaking down in the back of the car, because I had so believed it was over,” said Amy,The family was informed Amy required further leg-lengthening surgery or could develop spinal issues.She was first operated on by Ms Stohr, two-and-a-half-years after a colleague first raised concerns about her practice in 2015.JAMIE NIBLOCK/BBC”It’s the fact Addenbrooke’s had opportunities to address concerns by colleagues, but nothing ever came of it, and children, including Amy, may not have suffered” said Amy’s mother, Sharon.”Eight years and four procedures later, Amy can walk, but she suffers from pain, and because of the leg length discrepancy, she places extra pressure on her hip.”Sadly, she has suffered physically and psychologically. She has been diagnosed with post-traumatic stress disorder.”Amy said: “My main question is ‘Why me?’.”I feel like my youth has been taken, but not just my youth, my life. There’s been a lot of times where I’ve had to cut things short or go home because I’m in pain.”Roland Sinker, chief executive of CUH, said he was “deeply sorry for the harm” Amy had experienced and the impact “on her and her family”.He added: “I am saddened that this happened while Amy was under our care. It should not have happened, and we are working to implement improvements to ensure something like this cannot happen again.”An independent report into opportunities missed to identify harm caused to Ms Stohr’s patients was published last month by investigations company Verita and found an external review in 2016 was not acted upon.The author of that earlier review, Robert Hill, a senior paediatric orthopaedic surgeon, said the trust demonstrated “little, if any, insight into the issues confronting them”.Ms Stohr operated on hundreds more patients, until she was suspended in February 2025.Mr Sinker said: “Last month we published an action plan to address the findings of the independent investigation into the missed opportunities to have identified and addressed concerns sooner.”In this plan we detail how we are improving clinical governance, better managing and supporting doctors, and encouraging a more open culture where concerns are raised and escalated sooner.”‘Deeply distressing’Maria Repanos of Hudgell Solicitors, representing Amy and her mother, said: “The findings of the review into Amy’s case are deeply concerning and highlight extremely serious shortcomings.”A wide-scale public health matter of such gravity requires the full public scrutiny at a statutory inquiry.”A DOH spokesperson said: “Our sympathies are with Amy and all families affected by this deeply distressing situation”They said the Verita report had already made “several recommendations”, adding: “We expect the trust to deliver every recommendation and provide strong support for families. Independent bodies will oversee this to ensure lessons are learned and that this can never happen again.”The DOH said a further independent clinical review should report next year and that NHS England was reviewing governance around high-complexity, low-volume orthopaedic and spinal surgery services.Ms Stohr, through her lawyers, did not respond to the BBC’s questions about Amy’s case, but had previously said: “I always strive to provide the highest standards of care to all my patients.”I am cooperating fully with the trust investigation, and it would not be appropriate to comment further at this time.”CUH said patients and families concerned about their care could call a freephone helpline on 0808 175 6331.More on this storyRelated internet links

A research team at the University of California, Riverside has found that routine exposure to microplastics — tiny pieces released from packaging, fabrics, and common consumer plastics — may speed up the formation of atherosclerosis, the artery-narrowing condition associated with heart attacks and strokes. The effect appeared only in male mice, offering new insight into how microplastics may influence cardiovascular health in people.
“Our findings fit into a broader pattern seen in cardiovascular research, where males and females often respond differently,” said lead researcher Changcheng Zhou, a professor of biomedical sciences in the UCR School of Medicine. “Although the precise mechanism isn’t yet known, factors like sex chromosomes and hormones, particularly the protective effects of estrogen, may play a role.”
Microplastics Found Throughout the Environment and the Body
Microplastics are found widely in the modern environment, including in food, drinking water, and the air. They have also been detected inside the human body. Recent clinical studies have identified microplastics in atherosclerotic plaques and associated higher concentrations with elevated cardiovascular risk, although it was not clear whether these particles directly cause arterial injury.
“It’s nearly impossible to avoid microplastics completely,” Zhou said. “Still, the best strategy is to reduce exposure by limiting plastic use in food and water containers, reducing single-use plastics, and avoiding highly-processed foods. There are currently no effective ways to remove microplastics from the body, so minimizing exposure and maintaining overall cardiovascular health — through diet, exercise, and managing risk factors — remains essential.”
Study Design Using a Heart Disease Mouse Model
In their paper published in Environment International, Zhou and colleagues describe their use of LDLR-deficient mice, a common model for examining atherosclerosis. Both male and female mice were placed on a low-fat, low-cholesterol diet similar to what a lean and healthy person might eat.

The team then administered microplastics daily (10 milligrams per kilogram of body weight) for nine weeks. This amount reflects levels that could realistically be encountered through contaminated food and water.
Microplastics Intensify Plaque Formation in Male Mice
The results showed a sharp increase in atherosclerosis, but only in males. Male mice exposed to microplastics developed 63% more plaque in the aortic root, the segment of the aorta connected to the heart, and 624% more plaque in the brachiocephalic artery, a major vessel branching from the aorta in the upper chest. Female mice exposed to the same conditions did not show significant plaque progression.
The researchers confirmed that microplastics did not cause weight gain or increased cholesterol in either sex. The mice stayed lean, and their lipid profiles remained unchanged, indicating that traditional risk factors such as obesity or high cholesterol did not explain the heightened arterial damage.
Disruption of Artery-Lining Cells
The study also showed that microplastics interfered with the function and makeup of cells lining the arteries. Using single-cell RNA sequencing, which identifies gene activity in individual cells, the researchers observed that microplastics altered several cell types involved in atherosclerosis. Endothelial cells — the cells that form the inner lining of blood vessels and help regulate inflammation and circulation — were affected the most.

“We found endothelial cells were the most affected by microplastic exposure,” Zhou said. “Since endothelial cells are the first to encounter circulating microplastics, their dysfunction can initiate inflammation and plaque formation.”
Microplastics Enter Arterial Plaques and Alter Gene Activity
Fluorescent microplastics used in the study were found inside plaques and concentrated within the endothelial layer, consistent with reports from human samples that have revealed microplastics in arterial lesions.
Another key observation was that microplastics activated harmful gene pathways in endothelial cells from both mice and humans. This included genes associated with pro-atherogenic (plaque-promoting) activity, suggesting that microplastics trigger similar biological responses across species.
“Our study provides some of the strongest evidence so far that microplastics may directly contribute to cardiovascular disease, not just correlate with it,” Zhou said. “The surprising sex-specific effect — harming males but not females — could help researchers uncover protective factors or mechanisms that differ between men and women.”
Future Research on Sex Differences and Microplastic Types
Zhou and his team emphasize that more work is needed to determine why males appear more susceptible. The group plans to investigate whether humans show similar patterns.
“We would like to investigate how different types or sizes of microplastics affect vascular cells,” Zhou said. “We will also look into the molecular mechanisms behind endothelial dysfunction and explore how microplastics affect male and female arteries differently. As microplastic pollution continues to rise worldwide, understanding its impacts on human health — including heart disease — is becoming more urgent than ever.”
Zhou conducted the study with collaborators from UCR, Boston Children’s Hospital and Harvard Medical School in Massachusetts, and the University of New Mexico Health Sciences.
The work received partial support from the National Institutes of Health.
The title of the paper is “Microplastic exposure elicits sex-specific atherosclerosis development in lean low-density lipoprotein receptor-deficient mice.”

New studies are revealing how medications that act on the glucagon-like peptide-1 (GLP-1) system influence brain networks tied to nausea, thirst, and reward-driven behaviors. GLP-1 drugs include commonly used treatments such as semaglutide (Ozempic, Wegovy), liraglutide (Victoza, Saxenda), and tirzepatide (Mounjaro, Zepbound). These findings will be featured at Neuroscience 2025, the Society for Neuroscience’s annual meeting and the largest global event for new research in brain science and health.
Medications that work through the GLP-1 system are widely prescribed for type 2 diabetes and obesity. They imitate a natural hormone released in the digestive tract after eating and signal the brain to reduce hunger. Although these drugs are effective, up to 40% of people taking them experience side effects such as nausea and vomiting, which often lead to stopping treatment. Scientists are now examining whether the helpful actions of GLP-1 medications can be separated from the uncomfortable ones, and whether these drugs might have additional therapeutic applications.
Key New Findings Across Brain and Behavior
Today’s new findings show that:
Combining low doses of the drug tirzepatide, a “dual agonist” that works, in part, by activating GLP-1 receptors, with the hormone oxytocin results in weight loss without gastrointestinal side effects in obese rats. (James E. Blevins, University of Washington)
Nerve cells in the area postrema — the brain’s vomit center — are important for both weight loss and nausea in response to GLP-1 drugs in mice. (Warren Yacawych, University of Michigan)
In mice, activation of GLP-1 receptors on cells in the central amygdala activates a newly identified brain circuit that suppresses signals driving pleasure-based eating. (Ali D. Güler, University of Virginia)
GLP-1 receptor agonists suppress thirst as well as appetite, and a region in the forebrain of rats called the median preoptic area appears to be involved in this effect. (Derek Daniels, University at Buffalo)

“Research demonstrates an effect of these medications on the brain beyond treating diabetes and obesity, via mechanisms that are still not fully understood,” says Lorenzo Leggio, MD, PhD, a physician-scientist and clinical director of the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health. “GLP-1 therapies appear to have multiple synergistic effects that may be useful for treating chronic diseases with overlapping neural mechanisms, including binge eating disorders and addictive disorders.”
This research was funded by national agencies including the National Institutes of Health (NIH), the Department of Veterans Affairs (VA), and private organizations. The authors are solely responsible for the content, which does not necessarily represent the views of NIH or VA. Media credentials are required for full in-person and online access to Neuroscience 2025.
Highlights From the GLP-1 Press Conference GLP-1 medications effectively treat type 2 diabetes and obesity by curbing hunger, but these drugs often cause gastrointestinal side effects like nausea and vomiting, as well as decreases in other motivated behaviors like thirst. Working with rodent models, research demonstrates that GLP-1 drugs affect reward processing in the brain, and ongoing efforts are working to reduce the gastrointestinal side effects of these drugs.Oxytocin May Enhance Tirzepatide’s Weight-Loss Benefits
James E. Blevins, Abstract PSTR033.02 Tirzepatide (TZP; Mounjaro®) is a dual GLP-1 receptor (GLP-1R)/glucose-dependent insulinotropic polypeptide receptor (GIPR) agonist approved for obesity and type 2 diabetes, but it can also lead to nausea, vomiting, and loss of muscle mass. Oxytocin, a hormone known for its role in social behavior, can reduce bodyweight without causing nausea or vomiting. In this study, obese rats were treated with low doses of TZP combined with oxytocin. Researchers monitored changes in bodyweight and kaolin intake — a soft clay animals consume when nauseated — over 28 days. Oxytocin and low-dose TZP each produced a 6-7% reduction in bodyweight when used alone, but the combination nearly doubled the effect to 11%. Food intake and body fat mass decreased without an increase in kaolin consumption, indicating the absence of gastrointestinal discomfort. These findings suggest that pairing oxytocin with lower doses of TZP may promote weight loss while minimizing unpleasant side effects.Pinpointing the Brain Region Responsible for Both Nausea and Weight Loss
Warren Yacawych, Abstract PSTR083.12 GLP-1 receptor agonists reduce hunger and support weight loss through actions in the brain. However, they also frequently cause nausea and vomiting. To understand how these effects are controlled, researchers examined two key brain areas: the nucleus tractus solitarius (NTS) — involved in satiety — and the area postrema — involved in vomiting. Although NTS cells containing GLP-1 receptors naturally help regulate bodyweight, directly targeting this region with GLP-1 receptor agonists did not lead to weight loss. In contrast, targeting the area postrema — the brain’s vomit center — produced both weight loss and nausea. The results indicate that the area postrema is central to both the beneficial and unpleasant effects of GLP-1 receptor agonists. Separating appetite suppression from nausea will be a major focus for improving these medications.

A Newly Identified Brain Circuit That Dampens Reward-Driven Eating
Ali D. Güler, Abstract PSTR151.06 GLP-1 receptor agonists can reduce appetite and bodyweight, but the precise neural pathways behind these effects are still being mapped. Using genetically engineered mice, researchers demonstrated that GLP-1 drugs influence two major brain systems: one that regulates hunger and another that reduces cravings for highly “rewarding” foods. The team studied GLP-1 receptor-expressing cells in the central amygdala. When activated, these cells lowered food intake. They send signals to the ventral tegmental area, which is important for dopamine responses to “rewarding” stimuli. Activation of these central amygdala neurons lowered dopamine activity in this reward circuit, revealing a pathway that connects the amygdala, brainstem, and midbrain. This circuit appears relevant to pleasure-based eating, binge eating, addiction, and other conditions involving reward-related behaviors.How GLP-1 Drugs Influence Thirst and Hydration Signals
Derek Daniels, Abstract PSTR083.03 GLP-1 receptor agonists decrease thirst in addition to reducing food intake. Brattleboro rats, a specific laboratory strain, are especially sensitive to this thirst-suppressing effect. Researchers observed that brain regions involved in thirst — including the nucleus of the solitary tract and the median preoptic area — showed significant changes in GLP-1 receptor expression after thirsty Brattleboro rats were rehydrated. These results offer insight into why GLP-1 drugs affect thirst and may guide the development of medications that maintain metabolic benefits without altering hydration behaviors.