Drug company Moderna says its combined flu and Covid vaccine, which targets the two diseases in a single shot, has passed a vital part of final-stage scientific checks.

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At an assisted living facility in New York State, a small crowd had gathered at the dining room entrance at lunchtime, waiting for the doors to open. As a researcher observed, one woman, growing tired and frustrated, asked the man in front of her to move; he didn’t appear to hear.“Come on, let’s get going!” she shouted — and pushed her walker into him.In Salisbury, Md., a woman awoke in the darkness to find another resident in her bedroom in an assisted living complex. Her daughter, Rebecca Addy-Twaits, suspected that her 87-year-old mother, who had dementia and could become confused, was hallucinating about the encounter.But the man, who lived down the hall, returned half a dozen times, sometimes during Ms. Addy-Twaits’s visits. He never menaced or harmed her mother, but “she’s entitled to her privacy,” Ms. Addy-Twaits said. She reported the incidents to administrators.In long-term care facilities, residents sometimes yell at or threaten one other, lob insults, invade fellow residents’ personal or living space, rummage through others’ possessions and take them. They can swat or kick or push.Or worse. Eilon Caspi, a gerontologist at the University of Connecticut, has searched news coverage and coroners’ reports and identified 105 resident deaths in long-term care facilities over 30 years that resulted from incidents involving other residents.The actual number is higher, he said, because such deaths don’t always receive news media attention or are not reported in detail to the authorities.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.

4 hours agoBBC/Emma LynchAm I the hunter or the hunted?

New eye-tracking research has shown that simply looking at natural elements during urban walks can offer significant mental health benefits.
The study, by Bangor University and Technion- Israel Institute of Technology, published in the scientific journal People and Nature, involved city-dwellers, and showed how paying visual attention to greenery, rather than human-made structures, can alleviate anxiety and enhance restorative feelings.
The 117 urban residents who took part in the study, were guided on a 45-minute urban walk, while wearing eye-tracking glasses. They were instructed to focus their gaze on trees, plants, lawns and flowers, man-made structures or a mix of both. This unique methodology revealed that a participants’ focus on nature was associated with improvements in various mental health metrics, including anxiety levels and feelings of restorativeness.
Dr Whitney Fleming, a lecturer in Human Geography at Bangor University explained the findings, saying,
“We found that the individuals who were guided to direct their gaze more frequently at green elements reported a significant reduction in anxiety, with trees showing the most substantial positive effect.”
The study highlights a strong link between observing green elements, especially trees, and an increase in perceived restorativeness, suggesting that even brief interactions with nature can provide mental health benefits.”
Urban Design Implications
These insights offer valuable guidance for urban planners and architects, suggesting that integrating more natural features into city landscapes can play a crucial role in enhancing the mental well-being of residents. “The Nature Gaze” study supports the idea of urban environments that promote engagement with nature, highlighting a simple yet effective strategy for improving urban mental health.

Northwestern University researchers have developed a new antioxidant biomaterial that someday could provide much-needed relief to people living with chronic pancreatitis.
The study will be published on June 7 in the journal Science Advances.
Before surgeons remove the pancreas from patients with severe, painful chronic pancreatitis, they first harvest insulin-producing tissue clusters, called islets, and transplant them into the vasculature of the liver. The goal of the transplant is to preserve a patient’s ability to control their own blood-glucose levels without insulin injections.
Unfortunately, the process inadvertently destroys 50-80% of islets, and one-third of patients become diabetic after surgery. Three years post-surgery, 70% of patients require insulin injections, which are accompanied by a list of side effects, including weight gain, hypoglycemia and fatigue.
In the new study, researchers transplanted islets from the pancreas to the omentum — the large, flat, fatty tissue that covers the intestines — instead of the liver. And, to create a healthier microenvironment for the islets, the researchers adhered the islets to the omentum with an inherently antioxidant and anti-inflammatory biomaterial, which rapidly transforms from a liquid to a gel when exposed to body temperature.
In studies with mouse and non-human primates, the gel successfully prevented oxidative stress and inflammatory reactions, significantly improving survival and preserving function of transplanted islets. It marks the first time a synthetic antioxidant gel has been used to preserve function of transplanted islets.
“Although islet transplantation has improved over the years, long-term outcomes remain poor,” said Northwestern’s Guillermo A. Ameer, who led the study. “There is clearly a need for alternative solutions. We have engineered a cutting-edge synthetic material that provides a supportive microenvironment for islet function. When tested in animals, we were successful. It kept islet function maximized and restored normal blood sugar levels. We also report a reduction in units of insulin that animals required.”
“With this new approach, we hope that patients will no longer have to choose between living with the physical pain of chronic pancreatitis or the complications of diabetes,” added Jacqueline Burke, a research assistant professor of biomedical engineering at Northwestern and the paper’s first author.

An expert in regenerative engineering, Ameer is the Daniel Hale Williams Professor of Biomedical Engineering at Northwestern’s McCormick School of Engineering, a Professor of Surgery at Northwestern University Feinberg School of Medicine and founding director of the Center for Advanced Regenerative Engineering.
‘Compromised quality of life’
For patients living without a pancreas, side effects such as managing blood-sugar levels can be a lifelong struggle. By secreting insulin in response to glucose, islets help the body maintain glycemic control. Without functioning islets, people must closely monitor their blood-sugar levels and frequently inject insulin.
“Living without functional islets places a great burden on patients,” Burke said. “They must learn to count carbs, dose insulin at the appropriate time and continuously monitor blood glucose. This consumes much of their time and mental energy. Even with great care, exogeneous insulin therapy is not as effective as islets for maintaining glucose control. Patients with out-of-range blood glucose will develop complications, such as blindness and amputation. Our goal is for this biomaterial to preserve the islets, so patients can live a normal life — a life without diabetes.”
“It’s a compromised quality of life,” Ameer said. “Instead of multiple insulin injections, we would love to collect and preserve as many islets as possible.”
But, unfortunately, the current standard of care for preserving islets often leads to poor outcomes. After the surgery to remove the pancreas, surgeons isolate islets from the pancreas and transplant them to the liver through portal vein infusion. This intraportal perfusion procedure has several common complications. Islets in direct contact with blood flow undergo an inflammatory response, more than half of the islets die, and transplanted islets can cause dangerous clots in the liver. For those reasons, physicians and researchers have been searching for an alternate transplantation site.

In previous clinical studies, researchers transplanted islets to the omentum instead of the liver in order to bypass issues with clotting. To secure the islets on the omentum, physicians used plasma from the patients’ own blood to form a biologic gel. While the omentum appeared to work better than the liver as a transplantation site, several issues, including clots and inflammation, remained.
“There’s been significant interest in the research and medical communities to find an alternate islet transplantation site,” Ameer said. “The results from the omentum study were encouraging, but outcomes were varied. We believe that’s because the use of the patients’ blood and the added components required to create the biologic gel can affect reproducibility among patients.”
A citrate solution
To protect the islets and improve outcomes, Ameer turned to the citrate-based biomaterials platform with inherent antioxidant properties developed in his laboratory. Used in products approved by U.S. Food and Drug Administration for musculoskeletal surgeries, citrate-based biomaterials have demonstrated the ability to control the body’s inflammatory responses. Ameer set out to investigate whether a version of these biomaterials with biodegradable and temperature-responsive phase-changing properties would provide a superior alternative to a biologic gel obtained from blood.
In cell cultures, both mouse and human islets stored within the citrate-based gel maintained viability much longer than islets in other solutions. When exposed to glucose, the islets secreted insulin, demonstrating normal functionality. Moving beyond cell cultures, Ameer’s team tested the gel in small and large animal models. Liquid at room temperature, the material turns into a gel at body temperature, so it’s simple to apply and easily stays in place.
In the animal studies, the gel effectively secured the islets onto the omentum of the animals. Compared to the current methods, more islets survived, and, over time, the animals restored normal blood glucose levels. According to Ameer, the success is partially due to the new material’s biocompatibility and antioxidant nature.
“Islets are very sensitive to oxygen,” Ameer said. “They are affected by both too little oxygen and too much oxygen. The material’s innate antioxidant properties protect the cells. Plasma from your own blood doesn’t offer the same level of protection.”
Integrating into tissues
After about three months, the body resorbed 80-90% of the biocompatible gel. But, at that point, it was no longer needed.
“What was fascinating is that the islets regenerated blood vessels,” Ameer said. “The body generated a network of new blood vessels to reconnect the islets with the body. That is a major breakthrough because the blood vessels keep the islets alive and healthy. Meanwhile, our gel is simply resorbed into the surrounding tissue, leaving little evidence behind.”
Next, Ameer aims to test his hydrogel in animal models over a longer period of time. He said the new hydrogel also could be used for various cell replacement therapies, including stem cell-derived beta cells for treating diabetes.
The study, “Phase-changing citrate macromolecule combats oxidative pancreatic islet damage, enables islet engraftment and function in the omentum,” was supported by the U.S. Department of Defense and the National Science Foundation.

In a clinical trial conducted by Stanford Medicine investigators and their colleagues, a 15-day course of Paxlovid — an antiviral drug combination targeting SARS-CoV-2, the virus that causes COVID-19 — proved safe as an extended-duration treatment but didn’t lessen select symptoms of the syndrome known as long COVID: the persistence, or reappearance, of COVID-related symptoms three months or more after an initial COVID-19 infection.
The findings are described in a paper to be published June 7 in JAMA Internal Medicine.
Paxlovid is a highly effective antiviral agent licensed for treatment of acute COVID-19. It’s approved by the Food and Drug Administration for the treatment of adults who are newly infected with SARS-CoV-2, have mild or moderate COVID symptoms, and are at high risk of complications because of age or various predisposing conditions. A five-day Paxlovid regimen has been shown to reduce recipients’ likelihood of hospitalization and death by more than 85%.
While the Stanford trial did not show that Paxlovid reduced long COVID symptoms, it did show that taking the drug for more than two weeks was safe.
“We’ve demonstrated the overall safety of a 15-day course of Paxlovid — that’s three times as long as it’s being taken for acute COVID,” said Linda Geng, MD, PhD, clinical associate professor of primary care and population health, who was one of the trial’s two co-principal investigators.
Geng is the paper’s lead author. Its senior author is the trial’s other co-principal investigator, Upinder Singh, MD, professor and chief of infectious disease and geographic medicine and of microbiology and immunology.
Desperate people
“While there are now improved therapies and treatment practices for acute COVID, there’s nothing FDA-approved for long COVID, people continue to suffer and the numbers keep piling up,” Geng said.

An estimated 10% to 20% of SARS-CoV-2-infected people — tens of millions in the United States alone — develop long COVID. That estimate is fuzzy, because the definition of long COVID is ambiguous. More than 200 separate symptoms have been ascribed to the syndrome. These symptoms are often shared by other conditions, making a definitive diagnosis hard to pin down. It may well be that long COVID is a collection of different diseases set in motion by acute COVID but with different underlying mechanisms and effects and accordingly distinct methods required to alleviate them.
Indeed, numerous causes of long COVID have been posited. Among them are virus-induced changes in our resident gut bacteria; residual inflammatory overdrive; COVID-spurred autoimmunity; and the reawakening of other infectious viruses that have woven themselves into our genomes and remained dormant, only to emerge when our SARS-CoV-2-preoccupied or exhausted immune systems let their guard down.
The randomized, controlled, double-blinded phase 2 trial, known as STOP-PASC, is the first such test of Paxlovid treatment for long COVID. (STOP stands for Selective Trial of Paxlovid. PASC is an acronym for Post-Acute Sequelae of COVID, medical scientists’ formal name for long COVID.) The trial was designed to explore the so-called viral-reservoir hypothesis of long COVID: the possibility that while initial symptoms may have abated and measured viral counts gone to zero, the virus or viral debris persists in deep tissues, hiding out and perhaps replicating slowly there.
“Some studies suggest that viral particles and molecular debris could be responsible for some long-COVID sufferers’ ongoing symptoms,” Singh said. “We figured if that’s the case, maybe treating them with Paxlovid could relieve some of these symptoms.”
There are anecdotal reports of Paxlovid providing relief for long-COVID symptoms. “We’ve observed long-COVID patients who’ve improved after taking Paxlovid for new infections,” said Geng, who co-directs Stanford’s long-COVID clinic.
The trial
Between November 2022 and September 2023, Geng, Singh and their colleagues enrolled and followed 155 trial participants who’d tested positive for SARS-CoV-2. All but two had been vaccinated. Demographically, they broadly reflected the San Francisco Bay Area’s ethnic distribution. Their median age was 43; about two-thirds were between 34 and 54 years old.

On average, participants had been initially infected more than 16 months before enrolling in the trial. Yet, each participant reported moderate to severe cases of at least two out of six common “core” long-COVID symptoms: fatigue, brain fog, shortness of breath, body aches, and cardiovascular or gastrointestinal symptoms.
Half of the study participants were randomized to a 15-day course of Paxlovid; the others received a placebo along with low dosages of one of the two separate drugs that, combined, constitute Paxlovid. Both of these drugs are antiviral agents, but only one of the two, nirmatrelvir, has been found effective against SARS-CoV-2. The other drug, ritonavir, has no direct efficacy against this virus, but it ties up some of the same liver-resident enzymes that break down nirmatrelvir, boosting nirmatrelvir’s effective concentration in the body.
Because ritonavir can cause an easily recognized side effect — a metallic taste in the mouth — the investigators added it to the placebo formulation so placebo recipients wouldn’t be able to distinguish it from the active drug, and vice versa.
Partway through the study, the data was submitted to an independent group for preliminary analysis. On determining that safety appeared to pose no problem but no benefit was yet evident, the researchers continued the trial but stopped recruiting new participants.
At 10 weeks, the prespecified time point for the final comparison, there was no statistically significant difference between the two groups in the study’s primary endpoint: a reduction in the severity of the six core symptoms. Nor was there any detectable divergence between the two groups in numerous secondary outcomes such as seated and standing blood pressure and heart rates, and performance on the one-minute “sit and stand” test (subjects are asked to sit in a chair, stand up and sit down again repeatedly as fast as they can for a minute).
The 15-day drug regimen was, however, safe. There was one serious, possibly trial-related adverse event (hepatitis) among the placebo recipients, while the three cases of serious adverse events experienced by Paxlovid recipients (blood loss anemia, forearm fracture and melanoma) were judged to be unrelated to the drug treatment.
“One reasonable implication of our results is that Paxlovid can be given safely for a longer period of time,” Singh said, “for example, in instances where a newly infected patient is immunocompromised.”
The challenge of being first
The apparent absence of a clinical response in the recent trial doesn’t rule out the possibility that Paxlovid might be found to reduce long-COVID symptoms in some people, Singh said, remarking that too many questions remain unanswered: “Should we have tested patients with symptoms present after only seven or eight months instead of 16 or 17? Should we have treated them for a longer time? Were we even testing the right patients? Maybe only some symptoms will be responsive to antiviral treatment.”
If long COVID is not a single entity, the required treatment could differ among people exhibiting different clusters of symptoms.
Even routine testing of participants for the initial or post-treatment presence of cryptic SARS-CoV-2 — which by definition would be tucked away out of reach of the immune system and, perhaps, simple blood tests — was a nonstarter, Singh said, because simple, noninvasive, cheap tests are nonexistent.
Intriguingly, on average both the intervention- as well as placebo-arm participants’ overall symptoms improved over the course of the study. That could be good news, indicating that long-COVID symptoms generally subside with time. On the other hand, there’s the possibility of a placebo effect: The extra attention and concern from nurses, doctors and other health-provider types, as well as the hope of relief from the drug, may nudge placebo recipients to sense subjective improvement — or even to experience objective improvement — in their condition.
Plus, the absence of validated objective biomarkers made it tough to tell if one person’s reported improvement was bigger than another person’s.
Results from a number of chemical tests, immunological tests and wearables measurements taken throughout the trial may help the Stanford Medicine team find out whether some people benefited considerably more than others from Paxlovid and, if so, how they might be distinguished in advance of treatment or enrollment in a new trial.
“We hope to report on our analyses of these measurements in four to six months,” Singh said. The results may inform other clinical trials, now underway or in planning stages, of Paxlovid and other drugs’ capacity to counter long-COVID symptoms. These trials are sponsored by the National Institutes of Health as well as by Pfizer, Inc., Paxlovid’s developer, manufacturer and marketer.
Researchers from Kaiser Permanente North California and Pfizer contributed to the work.
The trial was funded by Pfizer.

By studying mutations in yeast and human cells, Johns Hopkins Medicine scientists say they have found that biochemical bonds between fats and proteins in the mitochondrion, the cell’s powerhouse, play a crucial role in how our cells produce energy.
The study results, published June 5 in The EMBO Journal, shed new light, researchers say, on the way the altered mitochondrial membranes found in people with metabolic diseases such as Barth syndrome, a rare genetic disorder that weakens the heart, fail to enable cellular power production.
Metabolism is a set of biochemical reactions central to making energy to fuel life and to getting rid of substances a body no longer needs. Metabolic diseases include forms of high cholesterol that run in families. Approximately one in three adults have some form of a metabolic syndrome, according to the National Heart, Lung, and Blood Institute.
Building on previous research, the Johns Hopkins scientists sought to better understand the interaction of two components in the mitochondrial membrane: cardiolipin, a fatty compound, or lipid, and proteins that transport the building blocks of adenosine triphosphate, or ATP, an energy molecule made by the mitochondria that fuels cell metabolism.
“Down the line, a better understanding of protein-lipid interactions could help researchers find new therapeutic targets for a wide range of metabolic diseases, including Barth syndrome,” says senior author Steven Claypool, Ph.D., professor of physiology at the Johns Hopkins University School of Medicine.
He says previous studies suggested it’s likely that protein-lipid interactions in mitochondrial membranes play an important role in regulating mitochondria’s powerhouse activities.
The researchers conducted their experiments in samples of yeast with mutations, or alterations, in a mitochondrial membrane protein called AAC and samples of human cells that modeled a person with a mutation of the protein ANT1 who was diagnosed with metabolic disease, symptoms of which include weakness in the heart and skeletal muscles, exercise intolerance and hyperlactatemia, or elevated lactate levels in the blood.

The protein in yeast, AAC, is the equivalent of ANT in humans, Claypool says.
Looking at three areas where cardiolipin binds to the AAC proteins in yeast, Claypool and his colleagues found that when they introduced mutations into AAC2 to disrupt these interactions, cardiolipin could no longer bond to the protein, which weakened its structure and lowered its function.
Similarly, in the cell model of the person with mutations in ANT1, the protein’s structure was weakened, limiting its ability to transport ATP across the mitochondrial membrane.
“These findings indicate that when the interaction between cardiolipin and proteins break down, the entire process that makes mitochondria our powerhouse is disrupted,” says first author Nanami Senoo, Ph.D., a postdoctoral fellow in Claypool’s lab.
Claypool says few studies have detailed individual protein-lipid interactions, and many more experiments will be needed to “understand the full complement of mechanisms and roles that these interactions have in the membrane.”
Mitochondrial membranes contain a lot of proteins, many of which associate with lipids.
“This discovery opens up new possibilities for understanding the complexities of how our cells produce energy,” Claypool says. “In the future, we plan to explore how other protein-lipid interactions contribute to energy production.”
Other scientists who contributed to the study are Matthew G. Baile, Oluwaseun B. Ogunbona, James A. Saba, Teona Munteanu, Yllka Valdez, Kevin Whited and Macie S. Sheridan of Johns Hopkins; Dinesh K. Chinthapalli, Bodhisattwa Saha, Abraham O. Oluwole, Dror Chorev and Carol V. Robinson of University of Oxford; Vinaya K. Golla, Nathan N. Alder and Eric R. May of University of Connecticut.
Funding for this study was provided by the National Institutes of Health (R01HL108882, R01HL165729, R35GM119762, T32GM007445 and T32GM136577), the American Heart Association, the Uehara Memorial Foundation, the Barth Syndrome Foundation and the Royal Society Newton International Fellowship.

Where there’s smoke, there’s not necessarily fire.
Wildfire smoke, sometimes drifting from hundreds of miles away, touched nearly every lake in North America for at least one day per year from 2019 to 2021, according to a study from the University of California, Davis.
Even more significantly, the study, published in the journal Global Change Biology, found that 89% of the lakes in North America experienced smoke for more than 30 days during each of those three years of intense wildfire activity.
“That was surprising, even to us,” said lead author Mary Jade Farruggia, a Ph.D. candidate in the UC Davis Graduate Group in Ecology and the Department of Environmental Science and Policy. “With this study, we quantified for the first time the scope of the smoke problem. We show that it’s not just a widespread problem, but one that is long-lasting in a lot of places.”
Introducing the ‘lake-smoke day’
The study introduces a concept the authors call the “lake-smoke day” to serve as a metric for monitoring smoke prevalence at lakes. It refers to the number of days a lake is exposed to smoke in any given fire season.
A lake-smoke day metric could help establish a baseline to better understand the extent and intensity of events such as 2023’s persistent blanket of wildfire smoke from Canada that reached the Northeastern United States and crossed the Atlantic Ocean to Western Europe.

The authors established the metric using a hazard mapping product from the National Oceanic and Atmospheric Association that quantifies smoke density based on a combination of satellite imagery and ground-based measurements. They also analyzed databases of about 1.3 million North American lakes larger than 25 acres to learn the prevalence and duration of exposure.
“Smoke is widespread, and smoke is pervasive,” said senior author Steven Sadro, a UC Davis limnologist and associate professor in the Department of Environmental Science and Policy. “We knew that by looking out the window and looking at satellite images we see almost every summer. Now we’re starting to quantify it.”
The science of smoke
While wildfire has been a consistent and even healthy presence on the landscape for millions of years, the frequency and severity of catastrophic wildfires in recent years is novel compared to previous decades. For that reason, the impacts of smoke on natural systems are understudied.
This study is part of a growing, broader effort to examine how smoke affects lake environments. The authors worked with the Global Lakes Ecological Observatory Network, or GLEON, to create a working group to share, understand and communicate these impacts.
They reviewed the known and theoretical impacts of smoke on lakes, such as how smoke can change the amount and composition of solar radiation that reaches lakes. Smoke and ash also can alter the deposition of carbon, nutrients or toxic compounds. Yet these impacts tend to be lake-specific and highly variable.
“We just don’t know yet how smoke affects food webs, lake ecology or what the future of these systems will be if there’s an increase in lake-smoke days,” said Farruggia. “I think quantifying the scope of the problem is really the first step. We’re pointing out that this is something we need to manage for across the globe, and not just areas affected by wildfire.”
Funded primarily through the National Science Foundation, the authors emphasize the research was a “massive team effort.” Its 22 authors span disciplines ranging from chemistry and atmospheric science to geography and ecology.