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Published4 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, AFPBy Sharon Barbour and Natalie WrightBBC NewsWith an anonymous stem-cell donation, Marius Werner saved a British doctor’s life – and, the young German says, it may have saved him too, giving him purpose when he had felt suicidal.With a rare type of blood cancer, Dr Nick Embleton’s only hope was a bone-marrow transplant. And unable to find a match in the UK, the search was extended worldwide.Two years on, BBC News and charity Anthony Nolan help two “blood brothers” find each other for the first time. ‘Might die’For more than two decades, Nick has worked in Newcastle’s neonatal intensive-care unit, helping to save thousands of the world’s smallest patients.But in 2021, he needed a doctor himself.Walking down the hospital corridors, he says he “had no idea what was about to unfold”.”I was fully aware I might die, so I made a will,” he says.”I broke this news to my wife and my kids. “I felt saddest for my kids – I didn’t want them to grow up the rest of their lives without their dad.”Image source, BBC NewsA bone-marrow transplant replaces damaged blood cells with healthy ones – but the body automatically rejects them unless they match.Charlotte Hughes, from the Anthony Nolan charity, said: “We search the UK register first and hopefully find a match here. “If we are unable to, then Anthony Nolan search worldwide to find a match.”A match could come from anywhere.”‘Very overwhelmed’Both donor and patient must remain anonymous until the transplant is known to have worked As soon as he learned it had, after two years, Nick told BBC News he wanted to track down his donor.Working with Anthony Nolan, BBC News identified Marius, 24, of Chemniz, near Dresden, who had been on the donor register since his late teens. And he agreed to fly to the UK and meet Nick, at Maggie’s Newcastle cancer-support centre, at the Freeman Hospital, where he had his transplant.As the two men hug, Marius says: “I’m very overwhelmed – I’m shaking.”‘You’re welcome’Nick tells him: “The cancer cells have all gone. “When they check my blood, all of those blood cells belong to you. “I would be dead if it wasn’t for you. “I’ve got four children – they wouldn’t have their dad. “I mean I just really want to say, ‘Thank you.'”Lost for words, an emotional Marius manages: “You’re welcome.”And with tears now running down both their faces, Nick whispers to him: “Thank you so much.”‘Tears come’Later, Marius recalls learning the transplant had worked – and the patient survived.”After that information, only the tears come,” he says.”I was on the way to my work and I had to park my car and get out and need fresh air – tears came out.”Then, Marius reveals he had previously tried to kill himself and how – in a way – Nick had helped save him.”I struggled my whole life since I was 13 with mental issues,” he says.”It’s [been] hard for me to find my way in life – and my sense in life. “[Now,] I can say, ‘I did something right.'”And with the same blood running through their veins, the two strangers are now planning to remain in touch as “blood brothers”.Anyone affected by the issues in this report can find support from BBC Action Line.

Published39 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, Merope MillsBy Aurelia FosterHealth reporterHospitals in England will be offered funding from April to introduce “Martha’s rule”, the NHS has announced.The government has backed plans to roll out a system giving seriously ill patients easy access to a second opinion if their condition worsens.About two-thirds of hospitals – at least 100 – will initially be able to apply to participate in the scheme.It follows a campaign by the parents of Martha Mills, 13, who died of sepsis because her symptoms were missed.Martha’s mother, Merope, told BBC News the new system would save lives and mean her daughter had not died “in vain”.Ms Mills previously said she and her husband, Paul Laity, had been ignored when they had raised concern about Martha’s care and asked for her to be transferred to intensive care.Best of Today – Martha’s Rule: Challenging culture will make our hospitals safer – BBC SoundsFamilies’ observationsUnder the new scheme, acute hospital will receive government funding for posters and leaflets informing patients and their families they could directly ask a team of critical-care medics for a “rapid review” of treatment, NHS England said.Medics will also formally record families’ observations of a patient’s condition or behaviour. Hospital says second opinion phone line saves livesMs Mills said she was “pleased”, because patients and families had a “role to play”.”Sometimes, doctors are incredibly overstretched,” she told BBC R4’s Today programme.”And they cannot always spot the same changes in a patient that family and patients themselves can.”The new system would have saved Martha’s life, Ms Mills said.Image source, Merope MillsMartha was admitted to King’s College Hospital, south London, in 2021, after injuring her pancreas slipping on to the handlebars of her bike while cycling.She later developed sepsis – but with better care, could have survived, an inquest found.The hospital apologised for its mistakes.Ms Mills said: “We told three different consultants that we were worried about her and we were just told she would be fine and this was a normal infection she had.”And when I had my doubts, still, I had nowhere to go. There was no ripcord to pull. I just had to trust the doctors.”Patients already have the right to a second opinion if their condition deteriorates – but trusts currently operate different systems.Challenging doctors could be “difficult”, Ms Mills said. And without the new scheme, many patients and their families would not know how.NHS England chief executive Amanda Pritchard said: “NHS teams have been piloting ways to better identify and respond in these cases, over the last year, and the rollout of a national programme to give patients and families 24-7 access to a rapid clinical review will now help ensure that those experiencing acute deterioration can be identified and treated much more quickly. “While the need for escalation will hopefully only be needed in a small number of cases, I have no doubt that the introduction of Martha’s rule has the potential to save many lives in the future.”The scheme rollout would be evaluated over the next year and may be followed by further funding to include all acute hospitals, NHS England said.Proposals to adapt it for community hospitals and mental-health trusts are also being considered. More on this storySepsis death lessons still not learnt – ombudsmanPublished25 October 2023NHS to introduce Martha’s rule in hospitalsPublished14 September 2023Bereaved mother to press Barclay on Martha’s rulePublished12 September 2023Second opinion phone line saves lives – hospitalPublished5 September 2023Government to explore bringing in ‘Martha’s rule’Published4 September 2023Related Internet LinksDepartment of Health and Social CareNHS EnglandThe BBC is not responsible for the content of external sites.

Published44 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, Shaun Whitmore/BBCBy Lauren Woodhead, Paul Bradshaw & Alix HattenstoneBBC Local & BBC Shared Data UnitDisrepair in NHS buildings led to thousands of potentially-harmful incidents last year including critically-ill patients being moved when rainfall came through the ceiling.Sewage leaks, floods and failing equipment also featured in incident records obtained by the BBC under the Freedom of Information Act.Health chiefs called on the government to nearly double its capital spending.The government said “significant sums” had been invested to modernise the NHS.According to NHS data, the care of more than 2,600 acute hospital patients was disrupted last year by estates and infrastructure failure.The BBC asked 210 hospital trusts for examples, and a total of 86 trusts provided a response.Incidents included:Patients awaiting dialysis were sent home because of water supply issuesGreen algae growth in a hydrotherapy poolPower lost in an operating theatreSewage leaked into a waiting area for ophthalmologyParts of a ceiling collapsed in a clinical areaAn operating theatre reached 29C because of a broken air conditioning unitThe NHS Confederation, which represents trusts, has published a report setting out what health care leaders want the next government to prioritise. It has called on the government to increase capital spending on the health service from £7.7bn to £14.1bn. Matthew Taylor, its chief executive, said: “Put simply, a lack of capital funding can leave patients at risk.”Official data shows the total repairs backlog for the NHS was £11.6bn, a rise of 13.6% on the previous year.’A rat ran out’Image source, RebeccaRebecca, 28, and her six-year-old daughter Cleo often have to go to Queen Elizabeth Hospital in King’s Lynn. Cleo’s hypoglycaemia – a condition related to low blood sugar – means she sometimes has to stay overnight. Part of the Norfolk site was built using Reinforced Autoclaved Aerated Concrete (RAAC), a material which forced 100 schools to close last year.The hospital previously had to close operating theatres because of concerns the ceiling could collapse. All theatres are now back open and the RAAC work is complete.But Rebecca said staying in the children’s ward during the construction was worrying.”I want to put my whole trust in the hospital,” Rebecca said. “But when I’m in the children’s ward and there’s a massive beam that’s holding the roof up, it does make me worry. “That’s something you don’t want to worry about when you’re trying to worry about your child’s health.” Image source, RebeccaBut the roof was not Rebecca’s only concern. She said that in January 2023, she saw sewage leaking on hospital grounds. “You’ve got a sterile area and sewage coming out of a manhole cover,” she said. “There was building equipment leant up against the hospital wall and a rat ran out from under the building.”A trust spokesman said it worked immediately to clear the blockage.Director of estates and facilities Paul Brooks said his team was doing its utmost to keep disruption to a minimum.He said: “We appreciate it can be disconcerting for our patients and visitors when they see building work taking place.”Seriously-ill patients movedLaura – not her real name – works for Colchester Hospital, part of East Suffolk North Essex NHS Trust. She told the BBC heavy rain caused part of the ceiling on a critical care ward to swell and tiles to bulge.Laura said no one was hurt, but her colleagues had to move patients to a neighbouring part of the hospital while a clean-up was undertaken. “We’re talking patients on life support, multi-organ failure – and they all had to be moved over to the other side of the unit,” she said. Harlow: Urgent funding call to replace sewage leak hospitalPropped-up hospitals in the East of England to be rebuilt by 2030Inside the hospital deemed ‘not fit for purpose’Laura said it was the second time rainfall had come through the ceiling on the ward. She said black aspergillus mould was found, which can cause breathing difficulties. Nick Sammons, director of estates and facilities at East Suffolk and North Essex NHS Foundation Trust, said keeping patients safe was the trust’s “number one priority”. He said: “We took the highest level of precautions and actions possible. This included safely moving patients out of the affected area, deep cleaning and a full assessment of what happened. “We are also replacing part of the roof to prevent any future incidents.”Trust’s £25m annual repair billThe chief analyst for health think tank The King’s Fund, Siva Anandaciva, said the deteriorating condition of some NHS buildings should act as a “wake-up call” for the government.He said: “Despite pledges to build and refurbish NHS hospitals, the data clearly shows how some NHS facilities are simply not fit for the purpose of delivering modern health care.”

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Several hospital leaders said they were struggling to maintain ageing buildings, which “predate the NHS” at some sites. Imperial College in London had the largest high-risk repair backlog in 2022-23 at more than £392m. A high-risk repair “must be urgently addressed to prevent catastrophic failure or major disruption to clinical services”, according to NHS Providers.Eric Munroe, Imperial College’s director of estates and infrastructure, said: “Much of our estate pre-dates the NHS – some of our buildings are nearly 180 years old.” He said the trust spends £25m annually on the “highest risk maintenance issues” to keep it safe and operating. He added the only realistic way of properly addressing the maintenance backlog would be a full rebuild of St Mary’s Hospital in Paddington.All three of the trust’s main hospitals are included in the Government’s New Hospital Programme.Other trusts also highlighted the age of their buildings.Leeds Teaching Hospitals NHS Trust said large parts of its sites dated “as far back as Victorian times”, while Buckinghamshire Healthcare NHS Trust said it was “delivering 21st century healthcare in 20th century buildings”. It faces a £2m annual bill to maintain the tower at Wycombe Hospital, which contains its intensive care unit and operating theatres.A Department of Health and Social Care spokeswoman said the government had invested “significant sums to upgrade and modernise NHS buildings” including £4.2bn this financial year.She added: “Trusts are responsible for prioritising this funding to maintain and refurbish their premises, including the renewal and replacement of equipment.”Additional investment of over £20bn for the New Hospital Programme is expected, alongside nationally funded infrastructure improvements in mental health, urgent and emergency care and diagnostic capacity.Additional reporting: Paul Lynch, Jonathan Fagg and Alex Homer

The drug finasteride, also known as Propecia or Proscar, treats male pattern baldness and enlarged prostate in millions of men worldwide. But a new University of Illinois Urbana-Champaign study suggests the drug may also provide a surprising and life-saving benefit: lowering cholesterol and cutting the overall risk of cardiovascular disease.
The study, published in the Journal of Lipid Research, found significant correlations between finasteride use and lower cholesterol levels in men taking part in the National Health and Nutrition Examination Survey between 2009 and 2016. In mice taking high finasteride doses, the researchers found reductions in total plasma cholesterol, delayed atherosclerosis progression, lower inflammation in the liver, and related benefits.
“When we looked at the men taking finasteride in the survey, their cholesterol levels averaged 30 points lower than men not taking the drug. I thought we’d see the opposite pattern, so it was very interesting,” said lead study author Jaume Amengual, assistant professor in the Department of Food Science and Human Nutrition and the Division of Nutritional Sciences, both part of the College of Agricultural, Consumer and Environmental Sciences (ACES) at U. of I.
As exciting as the survey results were, they had their limitations. Of nearly 4,800 survey respondents meeting general health criteria for inclusion in the analysis, only 155, all men over 50, reported using finasteride. And the researchers couldn’t tell how much or how long men in the survey had taken the drug.
“This was not a clinical study in which you can control everything perfectly,” Amengual said. “It was more of an observation that led us to say, ‘Okay, now we’ve seen this in people. Let’s see what happens in mice.'”
But first, why would a hair loss and prostate drug affect cholesterol? Amengual studies atherosclerosis, the condition in which cholesterol plaques choke arteries, leading to stroke, heart attack, and other forms of cardiovascular disease. Because the disease is far more common in men than premenopausal women, scientists have long suspected the sex hormone testosterone is important in atherosclerosis, though its role isn’t entirely clear.
Finasteride works by blocking a protein found in hair follicles and the prostate gland that activates testosterone. The common thread, testosterone, was enough to pique Amengual’s interest.

“I was reading about this medication one day, and I started to notice that there were not many long-term studies of the implications of the drug. Initially, it was just my own curiosity, based on the fact that hormone levels are known to have an effect on atherosclerosis, hair loss, and prostate issues,” he said. “So, we decided to dig into it.”
After documenting the first-ever link, albeit observational, between finasteride and lower cholesterol in men, Amengual got doctoral student Donald Molina Chaves to see if the pattern held in mice.
Molina Chaves tested four levels of finasteride — 0, 10, 100, and 1000 milligrams per kilogram of food — in male mice genetically predisposed to atherosclerosis. The mice consumed the drug, along with a high-fat, high-cholesterol “Western” diet, for 12 weeks. After the experiment, Molina Chaves analyzed the levels of cholesterol and other lipids in the mice, along with evidence of atherosclerotic plaques. He also tested gene expression in the liver, looked at bile acid metabolism, and analyzed steroids, triglycerides, immune activity, and more.
“Mice that were given a high dose of finasteride showed lower cholesterol levels within the plasma as well as in the arteries,” Molina Chaves said. “There were also fewer lipids and inflammatory markers in the liver.”
Although the effects were only significant at the highest dose, a level Amengual calls outrageous for humans, he explains that mice metabolize finasteride differently than people.
“It’s an incredibly high level of the drug. But we use mice as a model, and they are extremely resistant to things that would kill any of us,” he said. “So it is not that crazy when you think about it that way.”
Humans take 1 milligram or 5 milligram doses of finasteride daily for hair loss and enlarged prostate, respectively. The fact that a clear pattern showed up in a survey of men likely taking one of these doses suggests the drug may be lowering cholesterol without the megadoses tested in mice.

The next step is for physicians to start tracking cholesterol in finasteride patients or conduct a clinical trial to verify the effect. Amengual says it may be especially important to understand how finasteride affects trans individuals.
“Over the past decade, doctors have started prescribing this drug for individuals transitioning either from male to female or female to male. In both cases, the hormonal changes can trigger hair loss,” he said. “The interesting thing is that transgender people are also at a higher risk of cardiovascular diseases. So this drug could have a potential beneficial effect to prevent cardiovascular disease not only in cis men, but also in transgender individuals.”
Finally, Amengual notes, like any medication, finasteride is not without risk. People should consult their doctors to learn more.

A team led by scientists at the Case Western Reserve University School of Medicine has identified a new therapeutic approach for combating neurodegenerative diseases, offering hope of improved treatments for Alzheimer’s disease, Parkinson’s disease, Vanishing White Matter disease and multiple sclerosis, among others.
Neurodegenerative diseases, which affect millions of people worldwide, occur when nerve cells in the brain or nervous system lose function over time and ultimately die, according to the National Institutes of Health. Alzheimer’s disease and Parkinson’s disease are the most common.
The research team’s new study, published online February 20 in the journal Nature Neuroscience, focused on astrocytes — the brain’s most abundant cells, which normally support healthy brain function. Growing evidence indicates astrocytes can switch to a harmful state that increases nerve-cell loss in neurodegenerative diseases.
The researchers created a new cellular technique to test thousands of possible medications for their ability to prevent these rogue astrocytes from forming.
“By harnessing the power of high-throughput drug-screening, we’ve identified a key protein regulator that, when inhibited, can prevent the formation of harmful astrocytes,” said Benjamin Clayton, lead author and National Multiple Sclerosis Society career transition fellow in the laboratory of Paul Tesar at the Case Western Reserve School of Medicine.
They found that blocking the activity of a particular protein, HDAC3, may prevent the development of dangerous astrocytes. The scientists discovered that by administering medications that specifically target HDAC3, they were able to prevent the development of dangerous astrocytes and significantly increase the survival of nerve cells in mouse models.
“This research establishes a platform for discovering therapies to control diseased astrocytes and highlights the therapeutic potential of regulating astrocyte states to treat neurodegenerative diseases,” said Tesar, the Dr. Donald and Ruth Weber Goodman Professor of Innovative Therapeutics and the study’s principal investigator.

Tesar, also director of the School of Medicine’s Institute for Glial Sciences, said more research needs to be done before patients might benefit from the promising approach. But, he said, their findings could lead to the creation of novel therapies that disarm harmful astrocytes and support neuroprotection — perhaps improving the lives of people with neurodegenerative illnesses in the future.
“Therapies for neurodegenerative disease typically target the nerve cells directly,” Tesar said, “but here we asked if fixing the damaging effects of astrocytes could provide therapeutic benefit. Our findings redefine the landscape of neurodegenerative disease treatment and open the door to a new era of astrocyte targeting medicines.”
The team included additional researchers from the Case Western Reserve School of Medicine, and from the George Washington School of Medicine, The Ohio State University and the University of Tampa.
The research was supported by grants from the National Institutes of Health, National Multiple Sclerosis Society and Hartwell Foundation, and philanthropic support by sTF5 Care and the R. Blane & Claudia Walter, Long, Goodman, Geller and Weidenthal families.

An enthusiastic response to food in early childhood may be linked to a higher likelihood of experiencing eating disorder symptoms in adolescence, according to a new study led by researchers at UCL and Erasmus University Rotterdam.
The study, published in The Lancet Child & Adolescent Health, looked at survey data from 3,670 young people in the UK and the Netherlands to investigate how appetite traits in early childhood might relate to the likelihood of developing eating disorder symptoms up to 10 years later.
The researchers found that a particularly high food responsiveness, defined as the urge to eat when you see, smell or taste palatable food, at the ages of four and five was linked to a higher likelihood of reporting a range of eating disorder symptoms at ages 12 to 14.
The team also found that a slower pace of eating and feeling full more quickly (high sensitivity to satiety) in early childhood may be protective against developing some eating disorder symptoms later.
Co-lead author Dr Ivonne Derks (UCL Institute of Epidemiology & Health Care) said: “Although our study cannot prove causality, our findings suggest food cue responsiveness may be one predisposing risk factor for the onset of eating disorder symptoms in adolescence.
“However, high responsiveness to food is also a normal and very common behaviour and should be seen as just one potential risk factor among many rather than something to cause parents worry.”
Higher food responsiveness was linked to a 16% to 47% increase in the odds of reporting eating disorder symptoms, including binge eating symptoms, uncontrolled eating, emotional eating, restrained eating and compensatory behaviours.

The 47% increase was found for binge eating symptoms (eating a very large amount of food and/or experiencing the feeling of loss of control over eating), meaning that adolescents whose parents rated them highest on food responsiveness were almost three times more likely to report binge eating symptoms compared to adolescents whose parents scored them lowest.
A 16% increase in odds was found for restrained eating, whereby a person restricts their intake of food to lose weight or avoid weight gain.
Just like food responsiveness, emotional overeating in early childhood was also linked with higher odds of engaging in compensatory behaviours, which are intended to avoid weight gain, such as skipping meals, fasting and excessive exercise.
In turn, some appetite traits seemed to be protective against developing eating disorder symptoms later. Higher satiety responsiveness — that is, feeling full more quickly after eating, and feeling full for longer — was linked to lower odds of uncontrolled eating (defined as the extent to which someone feels out of control and eats more than usual) and compensatory behaviours.
A slower pace of eating, meanwhile, was linked to lower odds of compensatory behaviours and restrained eating.
The researchers also found that appetite traits such as food fussiness, emotional undereating (eating less due to low mood), and enjoyment of food in early childhood were not linked to later eating disorder symptoms in adolescence.

For the study, the researchers looked at data from two separate longitudinal studies: Generation R, following children born in Rotterdam, the Netherlands, between 2002 and 2006, and Gemini, which follows twins born in England and Wales in 2007.
Appetite traits were assessed based on parents’ questionnaire responses when the children were aged four or five. Eating disorder symptoms were self-reported by the then adolescents themselves at ages 12 to 14, when eating disorder symptoms typically start to emerge.
About 10% of the adolescents reported binge eating symptoms, where people eat an unusual amount of food and/or experience the feeling of loss of control over eating. Next to that, 50% reported at least one behaviour to compensate their food intake or to avoid gaining weight, such as skipping a meal.
Co-senior author Dr Clare Llewellyn (UCL Institute of Epidemiology & Health Care) said: “While the role of appetite in the development of obesity has been studied for many decades, this is the first study to comprehensively examine the role of appetite traits in the development of eating disorder symptoms.
“Eating disorders can be harder to treat effectively once they develop and so it would be better to prevent them from occurring in the first place. Our work in identifying risk factors in early life aims to support the development of possible prevention strategies. These could, for instance, involve providing extra support to children at higher risk.”
Appetite traits indicate how we respond to food and the opportunity to eat, and the extent to which we want to eat more or less when experiencing negative emotions. They are divided into food approach appetitive traits (e.g. food responsiveness, enjoyment of food, emotional overeating) and food avoidance traits (e.g. satiety responsiveness, food fussiness, slowness in eating, emotional undereating).
Co-senior author Professor Pauline Jansen of Erasmus University Rotterdam said: “Overall, our findings suggest that developing and testing prevention strategies may be a worthwhile effort. Although appetite has a substantial genetic component, we also know that there are environmental influences that offer opportunities for behaviour change.”
The researchers indicate that a healthy food environment and responsive parental feeding strategies may help to lower the risk of developing eating disorders.
Co-lead author Dr Zeynep Nas (UCL Institute of Epidemiology & Health Care) explained: “A healthy food environment is an environment in which healthy foods are available and more prominent, salient and affordable than less healthy options. This also includes wider access to food such as what types of food outlets are available in our neighbourhood and what food we see on TV.
“Responsive feeding is about providing nutritious food at set mealtimes and snack times, and then allowing the child to decide what to eat and how much to eat (if anything at all) without pressuring them.”
In a separate paper, accepted for publication in the International Journal of Eating Disorders, a similar research team looked at the same two cohorts, Generation R and Gemini, to investigate how parental feeding practices in early childhood might affect likelihood of eating disorder symptoms in adolescence.
The researchers found that non-responsive feeding practices, such as putting pressure on children to eat or using food as a reward or to soothe emotions, were linked to a higher likelihood of specific eating disorder symptoms later. However, the associations were small and varied between the two cohorts, and the researchers said further replication studies were needed.
The research was supported by the mental health charity MQ Mental Health Research, Rosetrees Trust, and the Netherlands Organisation for Health Research and Development (ZonMw).

The researchers found that 670 nanometres (nm) of red light stimulated energy production within mitochondria, the tiny powerhouses within cells, leading to increased consumption of glucose. In particular, it led to a 27.7% reduction in blood glucose levels following glucose intake, and it reduced maximum glucose spiking by 7.5%.
While the study was conducted in healthy individuals, the non-invasive, non-pharmacological technique has the potential to have an impact on diabetes control after meals, as it can reduce damaging fluctuations of blood glucose in the body that contribute to ageing.
The study also highlights the significant long-term consequences for human health, including the potential dysregulation of blood sugars posed by lengthy exposure to blue light. Given the prominence of LED lighting and the fact that LEDs emit towards the blue end of the spectrum with very little red, the authors suggest that this may be a potential public health issue. The research has been published in the Journal of Biophotonics.
Mitochondria provide energy for vital cellular processes, using oxygen and glucose to produce the energy-rich nucleoside adenosine triphosphate (ATP). Previous research has established that long-wavelength light between approximately 650-900 nm (spanning the visible through to the near-infrared range) can increase mitochondrial production of ATP which reduces blood glucose and also improves health/lifespan in animals.
The authors Dr Michael Powner, Senior Lecturer in Neurobiology in the School of Health & Psychological Sciences at City, and Professor Glen Jeffery, Professor of Neuroscience in the UCL Institute of Ophthalmology, also say that this improvement in ATP production can cause signalling changes that are transmitted throughout the body.
They suggest that it may be mediating the abscopal effect, which refers to the phenomenon in cancer treatment where specific irradiation of a primary tumour can result in shrinkage of secondary tumours located in a different part of the body. Likewise, 670 nm light shone selectively on to the backs of mice in previous studies has been shown to result in improvements in ATP that improve symptoms in both a model of Parkinson’s disease and a model of diabetic retinopathy.
To explore the impact of 670 nm red light on blood glucose, the researchers recruited 30 healthy participants, who were then randomised into two groups: 15 in the 670 nm red light group, and 15 in the placebo (no light) group. They had no known metabolic conditions and were not taking medication.

Participants were then asked to do an oral glucose tolerance test and record their blood glucose levels every 15 minutes over the next two hours. People who received red light exposure 45 minutes prior to drinking glucose exhibited a reduced peak blood glucose level and reduced total blood glucose during the two hours.
Dr Powner, who was the lead author of the study, said:
“It is clear that light affects the way mitochondria function and this impacts our bodies at a cellular and physiological level. Our study has shown that we can use a single, 15-minute exposure to red light to reduce blood sugar levels after eating.
“While this has only been done in healthy individuals in this paper, it has the potential to impact diabetes control going forward, as it could help to reduce potentially damaging glucose spikes in the body after meals.”
Professor Jeffery said:
“Sunlight has a balance between red and blue, but we now live in a world where blue light is dominant because although we do not see it, LED lights are dominant in blue and have almost no red in them. This reduces mitochondrial function and ATP production. Hence our internal environments are red-starved. Long-term exposure to blue light is potentially toxic without red. Blue light on its own impacts badly on physiology and can drive disrupted blood sugars that may in the long run contribute to diabetes and undermine health spans.
“Pre-1990, we all had incandescent lighting which was OK because it had the balance of blue and red similar to sunlight, but there is a potential health span time bomb in the change to LEDs in an ageing population. This can partly be corrected by spending more time in sunlight.”
The research was sponsored by Sight Research UK.

Older people may be at greater risk of developing pancreatic cancer and have poorer prognoses because of age-related changes in cells in the pancreas called fibroblasts, according to research led by investigators from the Johns Hopkins Kimmel Cancer Center, the Johns Hopkins Bloomberg School of Public Health and the Bloomberg~Kimmel Institute for Cancer Immunotherapy.
The study, published online Feb. 8 in Cancer Research, provides clues as to why pancreatic cancer is more common and aggressive in older people. It may also help scientists develop new therapeutic approaches for this difficult-to-treat cancer. The study showed that aging alters fibroblasts in ways that enable them to promote pancreatic cancer tumor growth.
“Older fibroblasts release proteins that directly affect pancreatic cancer cells and ultimately lead to the growth and spread of pancreatic cancer tumors,” says the study’s lead author, Daniel Zabransky, M.D., Ph.D., assistant professor of oncology at the Johns Hopkins University School of Medicine. “The younger fibroblasts did not have these capabilities. We think this is a key reason why we see pancreatic cancer more commonly in older patients.”
Zabransky and his colleagues compared samples of pancreatic fibroblasts from patients older than 55 with pancreatic fibroblasts from patients younger than 35. They discovered that the cells from older patients behave very differently than younger ones. To find out why, they compared the proteins released by the younger and older cells and noted profound differences.
They determined that a critical change in older pancreatic fibroblasts is that they release more of a protein called growth/differentiation factor 15 (GDF-15). When the team treated young mice with pancreatic tumors with GDF-15, it caused the tumors to grow more rapidly, just as they do in older mice. Older mice that were genetically engineered to lack the gene encoding GDF-15 had reduced pancreatic tumor growth.
Experiments in human cells and mouse models revealed that GDF-15 activates the AKT signaling pathway in an age-dependent manner. The discovery was a surprise because the AKT pathway is typically not very active in mouse models of pancreatic cancer, Zabransky says. However, most studies look only at young mice. Experimental drugs already exist that inhibit the AKT pathway. When the team tested AKT-inhibiting drugs in mouse models of pancreatic cancer, they found the drugs reduced tumor growth in mice with aged fibroblasts. However, it had no effect in mice with young fibroblasts. Zabransky and his colleagues next plan to study age-related changes in other cells found in pancreatic cancer tumors, including immune cells, and their impact on pancreatic cancer.
Previous work by senior study author Ashani Weeraratna, Ph.D., co-chair of the Cancer Invasion and Metastasis Program and associate director for laboratory research for the Johns Hopkins Kimmel Cancer Center, demonstrated the importance of age-related changes in melanoma, a finding the team has now extended to pancreatic cancer. Weeraratna also is the E.V. McCollum Professor and chair of the Department of Biochemistry and Molecular Biology and a Bloomberg Distinguished Professor at the Johns Hopkins Bloomberg School of Public Health, and a professor of oncology at the Johns Hopkins University School of Medicine.

“We have very few treatment options for pancreatic cancer,” Weeraratna says. “Trying to understand how the aging microenvironment contributes to pancreatic cancer progression might open up new avenues for therapies.”
“Precision cancer therapy just got more complicated,” adds study co-author Elizabeth Jaffee, M.D., deputy director of the cancer center, co-director of the gastrointestinal cancers program, and the Dana and Albert “Cubby” Broccoli Professor of Oncology at Johns Hopkins. “This work by Dr. Zabransky and his team points out for the first time in pancreatic cancer that there are aging-specific signals in tumors that may need to be modulated to realize the potential of current and future treatments for this deadly disease.”
Zabransky says age-related changes may also be critical in other types of cancers. He noted scientists test most cancer drugs in young mice, and drugs that target age-specific cancerous changes may not work in these young mouse models. It also may be vital to examine the results of clinical trials of cancer drugs to see if the effects vary in different age groups, he says.
Other study co-authors were Yash Chhabra, Mitchell E. Fane, Emma Kartalia, James L. Leatherman, Laura Hu?ser, Jacquelyn W. Zimmerman, Todd D. Armstrong, Soren Charmsaz, Samantha Guinn, Sneha Pramod and Elizabeth D. Thompson of Johns Hopkins. Other authors were from the Fox Chase Cancer Center in Philadelphia; the German Cancer Research Center in Heidelberg, Germany; the University Medical Center Mannheim and Ruprecht-Karl University of Heidelberg in Mannheim, Germany; the Stanford School of Medicine in California; the University of Florida College of Medicine in Gainesville; and the National Institute on Aging in Baltimore.
The study was supported in part by the National Institutes of Health (grants T32 5T32CA009071, U01CA227550, P01CA114048, R01CA207935, K99CA263017, P01CA247886, P01CA114046, U01CA227550, and R01CA232256), a Conquer Cancer Foundation/ASCO Young Investigator Award, a MacMillan Pathway to Independence Award, the MD Anderson GI SPORE, the Maryland Cancer Moonshot Research Grant to the Johns Hopkins Medical Institutions (FY24), a Lustgarten Foundation Cancer Convergence Grant, and a Team Science Award from the Melanoma Research Alliance.
Zabransky and Zimmerman receive support from Roche and Genentech. Jaffee receives personal fees from Achilles, Dragon Fly, Parker Institute, Surge, Mestag, and Medical Group Home; grants from Lustgarten, Genentech, BMS, and Breakthrough Cancer; and other support from Abmeta and Adventris. Weeraratna serves on the board of Regain Therapeutics. These relationships are managed by The Johns Hopkins University in accordance with its conflict-of-interest policies.

Mounting evidence suggests that the secret to understanding human health and combating metabolic diseases lies hidden within the microscopic world of our gut bacteria. Recent research by scientists at the Boyce Thompson Institute (BTI) and Cornell University reveals that a specific fatty acid produced by gut bacteria directly influences fat metabolism in animals. This research is pivotal as it sheds light on the complex interplay between the diet, gut microbiota, and host metabolic health, offering insights that could open new avenues in our approach to managing metabolic disorders.
The researchers focused on certain gut bacteria that produce fatty acids with a special chemical structure, known as a cyclopropane ring, and showed that these can be converted into signals that turn on fat desaturation in the nematode C. elegans, a model organism often used to study human biology. Intriguingly, C. elegans itself produces a chemically similar fatty acid compound that regulates the same metabolic pathway as the bacterial cyclopropane fats.
“Our research suggests that the host organism may have acquired the ability to produce its own signaling molecule, mimicking bacterial biochemistry, through a gene obtained from bacteria — a process known as horizontal gene transfer,” shared Bennett Fox, a post-doctoral researcher at BTI and first author of the study.
The research, recently published in Nature Communications, showed that both the bacterial and endogenous fatty acids activate a host receptor that functions as a central regulator of overall fat metabolism. This direct link between microbiota metabolites and host lipid metabolism offers insight into how our bodies could harness beneficial gut bacteria to regulate vital processes like obesity and metabolic dysfunction.
“Microbiota-dependent metabolites regulate virtually every aspect of animal physiology, including development, metabolism, and immune responses. Despite the life-sustaining importance of these metabolites, many of their structures remain unknown,” noted Frank Schroeder, a professor at BTI and senior author of the study.
The fact that chemicals produced by bacteria can influence the metabolism of their host is a promising area of research. Further studies can investigate host-bacterial interactions to better understand — and potentially improve — metabolic health.
“The devil is in the details. As we gain clarity regarding the molecular mechanisms of fat metabolism and its regulation by specific diet-derived compounds, we step closer to harnessing this knowledge for better health outcomes in humans,” said Fox. “This research not only broadens our understanding of basic biological processes but also highlights potential pathways for future exploration in human health and disease management.”
Want to learn more? Dr. Fox has prepared an in-depth synopsis of the research paper, Evolutionarily related host and microbial pathways regulate fat desaturation in C. elegans, available here.
This research was supported in part by the National Institutes of Health and the Howard Hughes Medical Institute.

The findings are presented in a research paper authored by researchers from the Malawi-Liverpool Wellcome Programme published today (19 February 2024) in The Lancet Microbe.
Ciprofloxacin is the first-line drug for treating typhoid fever in many countries in Africa with a high disease burden, but the emergence of non-susceptibility poses a challenge to public health programmes. Through enhanced surveillance as part of vaccine evaluation, the researchers investigated the occurrence and potentialdeterminantsof ciprofloxacin non-susceptibility in Blantyre, Malawi.
The researchers identified an association between the proportion of Salmonella enterica serotype Typhi (S Typhi) with a drug-resistant mutation in the quinolone resistance-determining region (QRDR) and the number of ciprofloxacin prescriptions in the previous month. They used whole genome sequencing to identify that S Typhi isolates with mutations evolved locally from the endemic S Typhi population in Blantyre, Malawi,and were not the result of importations from other countries.
Dr Philip Ashton from the Malawi-Liverpool Wellcome Programme said: “The most plausible explanation for this is that the increase in antimicrobials caused the emergence of resistance. Better diagnostics and good vaccines for typhoid will be key to reducing antimicrobial usage, and preventing resistance emerging. Fortunately, an effective vaccine has been recently been rolled out across Malawi.
“Antimicrobial resistance is one of the biggest threats facing humanity in the 21st Century, and it will fall disproportionately on countries like Malawi. Currently, our understanding of antimicrobial resistance is based largely on data from high income countries, and that knowledge may not translate to lower income settings like Malawi. We urgently need more research on antimicrobial resistance in countries like Malawi to arm us with the understanding to tackle this deadly threat.”
The researchers conducted systematic surveillance of typhoid fever cases and antibiotic prescription in two health centres in Blantyre, Malawi, between 2016 and 2019, as part of the STRATAA and TyVAC studies. In addition, blood cultures were taken from eligible patients presenting at Queen Elizabeth Central Hospital, Blantyre as part of routine diagnosis.Between October 1, 2016, and August 31, 2019, of 177 typhoid fever cases confirmed by whole-genome sequencing, four (2%) were caused by S Typhi with QRDR mutations, compared with six (33%) of 18 cases between Sept 1, 2019, and Oct 31, 2019.
This increase was associated with a preceding spike in ciprofloxacin prescriptions. Every additional prescription of ciprofloxacin given to study participants in the preceding month was associated with a 4·2% increase in the relative risk of isolating S Typhi with a QRDR mutation.
This research was funded by Wellcome, The Bill & Melinda Gates Foundation, and the National Institute for Health and Care Research (UK).