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A blood test that can accurately detect when someone has not slept for 24 hours has been developed by experts at Monash University, in Australia, and the University of Birmingham, in the UK.
This level of sleep deprivation increases the risk of serious injury or fatality in safety critical situations.
Published in Science Advances, the biomarker used a combination of markers found in the blood of healthy volunteers. Together, these markers accurately predicted when the study volunteers had been awake for more than 24 hours under controlled laboratory conditions.
The biomarker detected whether individuals had been awake for 24 hours with a 99.2 percent probability of being correct, when compared to their own well-rested sample. When a single sample was considered without the well-rested comparison (similar to a diagnostic blood test), it dropped to 89.1 per cent, which was still very high.
With about 20 per cent of road accidents worldwide caused by sleep deprivation, researchers hope the discovery may inform future tests to quickly and simply identify sleep deprived drivers. The biomarker could also be developed for other situations where sleep deprivation may lead to catastrophic consequences, such as in safety-critical workplaces.
Senior author Professor Clare Anderson led the research while she was with the Monash University School of Psychological Sciences and Turner Institute for Brain and Mental Health. She is now Professor of Sleep and Circadian Science at the University of Birmingham in the UK.
“This is a really exciting discovery for sleep scientists, and could be transformative to the future management of health and safety relating to insufficient sleep,” Professor Anderson said. “While more work is required, this is a promising first step.

“There is strong evidence that less than five hours’ sleep is associated with unsafe driving, but driving after 24 hours awake, which is what we detected here, would be at least comparable to more than double the Australian legal limit of alcohol performance wise.”
The test may be also ideal for future forensic use but further validation is required.
First author Dr Katy Jeppe, from the Monash Proteomics and Metabolomics Platform, previously from the School of Psychological Sciences, said it was difficult to say how soon the test could be developed for post-accident use.
“Next steps would be to test it in a less controlled environment and maybe under forensic conditions, particularly if it was to be used as evidence for crashes involving drivers falling asleep,” Dr Jeppe said.
“Given it’s blood, the test is more limited in a roadside context, but future work could examine whether our metabolites, and therefore the biomarker, are evident in saliva or breath.”
This sleep deprivation biomarker is based on 24 hours or more awake, but can detect down to 18 hours awake. A biomarker for limited sleep over the previous night could be developed but more research is required to combine the time since sleep with the amount of sleep in the predictions.

“Much further work would be needed if laws were to change and a sleep deprivation test introduced on the road or in workplaces,” Dr Jeppe said. “This would include further validation of biomarkers, as well as establishing safe levels of sleep to prevent and recover from impairment, not to mention the extensive legal process.”
“A biomarker for limited sleep over the previous night could be developed, and others have made progress in this respect (Depner et al.).”
Sleep deprivation can have fatal consequences for other safety-critical occupations. Major catastrophes including the Chernobyl nuclear reactor meltdown and the Challenger space shuttle Disaster* are thought to be caused, in part, by human error associated with fatigue.
“Objective tests that identify individuals who present as a risk to themselves or others are urgently needed in situations where the cost of a mistake is fatal,” Professor Anderson said.
“Alcohol testing was a game changer for reducing road crashes and associated serious injuries and fatalities, and it is possible that we can achieve the same with fatigue. But much work is still required to meet this goal.”
This research was conducted in association with the Cooperative Research Centre for Alertness, Safety and Productivity.

Federal regulators said that the Jool Baby swings should not have been marketed as sleep products because they have an incline angle that is not safe.Jool Baby, a brand of children’s products, has recalled about 63,000 infant swings that were sold at Walmart stores and online because they posed a suffocation risk, federal safety regulators said.The U.S. Consumer Product Safety Commission said on Thursday that the Jool Baby Nova Baby Infant Swing that was marketed, intended or designed for infant sleep posed a suffocation risk because it had an incline angle greater than 10 degrees.The product was in violation of the commission’s Infant Sleep Products Regulation and the Safe Sleep for Babies Act, the agency said.A study cited in the federal regulation of infant sleep products found that infants who slept in products with a 20-degree incline were exposed to increased demand on the abdominal muscles, which could lead to fatigue and suffocation. The same study determined that an incline of 10 degrees or below does not significantly affect infant motion or muscle activity.The recall notice affects infant swings that were manufactured from June 2022 through September 2023.Those swings are gray and measure about 28 inches long, 19 inches wide and 24 inches high. They have a round aluminum base with music buttons on the front, a metal seat frame, a cloth seat with restraints and a headrest, and a canopy with hanging toys, such as moons, clouds and stars.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.

She helped introduce free breakfasts and lunches for schoolchildren and open pantries and soup kitchens for the poor.Kathy Goldman, who devoted her career as a civic leader to establishing food banks, pantries and free breakfast and lunch programs in public schools to sustain low-income New Yorkers, died on March 5 in Brooklyn. She was 92.The cause of death, in a hospital, was congestive heart failure, her daughter, Julie Goldman, said.Ms. Goldman was determined to confront the collective indifference that she felt had contributed to the Holocaust. Over five decades she worked with many collaborators to successfully lobby for federal subsidies like food stamps and nutrition assistance for women, children and infants; create partnerships between corporate providers of provisions and local communities; and expand the mandate of anti-hunger programs to include help with housing, health care, education and other needs.In 1980, she founded the Community Food Resource Center, a food pantry, as a buffer against stricter eligibility requirements for welfare. Three years later she helped organize what is now the Food Bank for New York City, which served scores of soup kitchens and food pantries around the city from the Hunts Point market in the Bronx. She was the center’s executive director until she retired in 2003.A Food Bank of New York City truck delivers food to the Community Kitchen of West Harlem in 2009.Neilson Barnard/Getty ImagesIn 1984 she started the Community Kitchen of West Harlem, an innovative program that not only offered food, but also helped the hungry with other needs, including housing and health care. After renovations to the dining area, “when a 10-year-old boy exclaimed, ‘It’s just like McDonald’s!’ Goldman ‘considered it the greatest compliment of all time coming from a kid,’” Lana Dee Povitz wrote in “Stirrings: How Activist New Yorkers Ignited a Movement for Food Justice” (2019).In the early 1990s, she persuaded the city to open school cafeterias in Chinatown and Harlem in the evenings to serve dinners to older adults.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 Missouri hospital said the amputations involved mostly fingers and toes after a game in January when temperatures were below zero.Several fans of the Kansas City Chiefs who attended a playoff game on a bitterly cold January day in Missouri suffered frostbite that required amputations, according to the hospital that treated them.Twelve people — including some football fans who were at Arrowhead Stadium on Jan. 13 — had to undergo amputations involving mostly fingers and toes, the hospital, Research Medical Center in Kansas City, said in a statement on Saturday.The center said it treated dozens of patients who experienced frostbite during an 11-day cold snap. Not all of the patients who had amputations attended the Chiefs game. Some were people who worked outdoors in the extreme cold, the hospital said.The exact number of fans who attended the game who had amputations was unclear. The hospital said there was some overlap among the fans and those who had also worked outdoors.The hospital also noted that symptoms of frostbite can develop slowly, and that many of the frostbite patients it treated could not identify when their injuries occurred — when their pain, numbness and other symptoms began.The hospital said it was a record number of frostbite patients since the burn center opened 11 years ago.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.

At SXSW, a documentary traces the arc of plastics in our lives, and highlights evolving research of the potential harm of its presence in our bodies.It’s been more than five decades since Dustin Hoffman’s character in “The Graduate” was offered a kernel of wisdom about the path to prosperity.“Plastics,” he’s told by Mr. McGuire, the starched corporate executive who offers the advice. “There’s a great future in plastics.”Plastics have indeed been a game changer for humanity, and the enormous range of cheap, durable plastic goods, from food containers and PVC pipes to polyester clothing and single-use medical products, have inarguably improved life.The problem, as nearly everyone knows, is that plastics are forever and very little of it has been recycled. The U.N. has estimated that most of the 400 million metric tons churned out annually — a doubling of production since 2000 — will remain on Earth in some form as they are broken down into teeny specks by sunlight, wind and the sea.Roughly 20 years ago, Richard Thompson, a marine biologist, first discovered a worrisome accumulation of small plastic particles in ocean habitats and coined the word “microplastics.” Since then, scientists have been finding these fragments everywhere, from remote mountain peaks and the Arctic to the ocean seafloor.In the decade that followed, scientists began to discover microplastics embedded in a wide range of living creatures, including in the seafood we eat. More recently, microplastics have been found inside the human body: in our lungs, our blood, our feces and in breast milk.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.

Published28 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, PHSOBy Smitha MundasadHealth reporter Cancer patients could be at risk due to overstretched and “exhausted” health staff in a “system at breaking point”, England’s NHS ombudsman has warned. Rob Behrens’ office carried out 1,019 investigations related to cancer between April 2020 and December 2023 – with 185 upheld or partly upheld. Issues included delays in diagnosis, treatment and pain management. The Department of Health and Social Care said record numbers of people had been treated in the last two years.Meanwhile recent analysis by the BBC revealed cancer waiting times in England last year were the worst on record. Mr Behrens, the parliamentary and health service ombudsman who investigates unresolved complaints against NHS England, said everyone deserves safe and effective care. He added: “But patient safety will always be at risk in environments that are understaffed and where staff are exhausted and under unsustainable pressure.”He called for concerted and sustained government action to ensure NHS leaders could prioritise the safety of patients. “A key part of this is investing in the workforce, for today and for the long term, including providing full funding for the long-term workforce plan,” he added.Problems investigated by his team included concerns about poor communication, end-of-life care and how complaints were handled.Most were about lung cancer, followed by breast cancer and colorectal cancer – some of the most common cancers in the UK. Image source, PrHOOne investigation involved the death of Mrs Sandra Eastwood, whose rare cancer was not diagnosed for nearly a year, after scans were not interpreted correctly. The delay meant she missed out on the chance of very effective treatment that could have prolonged her life, according to the report. Mrs Eastwood, who lived in York, died in 2022, with a rare digestive system cancer called gastrointestinal stromal tumour. In June 2020 she went to hospital with abdominal pain. CT scans showed a mass which medics put down to a blood clot caused by medication she was taking for a unrelated heart valve replacement.The following May her symptoms worsened and she returned to hospital and was diagnosed with GIST. The report found that if Mrs Eastwood had been diagnosed earlier and scans interpreted correctly, the cancer might not have spread and she may have been eligible for surgery. John, her husband of 54 years, said: “Sandra was wonderful. I worked away a lot when our two children were young and she did absolutely everything for them. She loved baking, making jams and chutneys, and travelling.The 79-year-old continued: “I feel absolutely disgusted with the care she received from the hospital. They didn’t investigate the scan results and just put it down to Warfarin [her medication] straight away. “It seemed like the medical teams did not communicate with each other and everything felt very disjointed. They left her in agony for months before she died.”The whole experience was very distressing, which is why I went to the ombudsman. I didn’t want this to happen to anybody else.”A spokesperson for York and Scarborough Teaching Hospitals NHS Foundation Trust said it “fully accepts” the ombudsman’s findings and apologised for the distress caused to Mrs Eastwood and her family.The spokesperson added that the trust has made a number of improvements and agreed to change its practice following the case.Mr Behrens said: “What happened to Mrs Eastwood was unacceptable and her family’s grief will no doubt have been compounded by knowing that mistakes were made in her care.”Her case also shows, in the most tragic of ways, that while some progress has been made on my recommendations to improve imaging services, it is not enough and more must be done.”Government must act now to prioritise this issue and protect more patients from harm.”The Department of Health said: “The NHS has seen and treated record numbers of cancer patients over the last two years and cancer is being diagnosed at an earlier stage, more often, with survival rates improving across almost all types.”We have invested £2.3bn into speeding up diagnosis and launched 154 community diagnostic centres across England.”The NHS long-term workforce plan will boost the number of healthcare workers diagnosing and treating cancer, doubling the number of medical school and adult nurse training places.”More on this storyCancer waiting times in 2023 worst on recordPublished8 FebruaryNHS struggling to provide safe cancer care, say doctorsPublished8 June 2023Key cancer waiting target set to be missed in EnglandPublished7 March 2023Related Internet LinksPHSOThe BBC is not responsible for the content of external sites.

A physician, scientist and academic, he brought together experts across disciplines to focus on the economic, political and social causes of poor health, not just the biological factors.Howard H. Hiatt, a physician, scientist and academic who reshaped the field of public health, steering it away from the narrow study of infectious diseases toward big-picture issues of fiscal and societal accountability in medicine, died on Saturday at his home in Cambridge, Mass. He was 98.His son Jonathan Hiatt said the cause was pulmonary hypertension.Harvard Public Health, a magazine published by the Harvard School of Public Health, where Dr. Hiatt was dean for 12 years, wrote in 2013 that Dr. Hiatt “made public health the conscience of medicine.”Early in his seven-decade career, Dr. Hiatt worked in Paris with future Nobel Prize winners on the discovery of messenger RNA, a key element of cellular biology. He later visited the White House to urge President Ronald Reagan to end the nuclear arms buildup of the era, which Dr. Hiatt called “the final epidemic.”A Harvard-trained physician who held leadership posts at some of the country’s most prestigious hospitals, Dr. Hiatt was an outspoken critic of the inequities in American health care. He accused American medicine of having a bias toward expensive, high-tech treatments while excluding millions of people from basic care.In a 1987 book, “America’s Health in the Balance: Choice or Chance?,” he argued for government-run universal health insurance, modeled on aspects of the systems in Britain, Canada and China. “I am particularly anxious to reach those who are so callous as to accept the prospect of two-class medicine in America,” he told The Toronto Star.At the Harvard School of Public Health (now the Harvard T.H. Chan School of Public Health), where Dr. Hiatt was dean from 1972 to 1984, he brought experts together across disciplines, including biostatistics and health management, to focus on the economic, political and social causes of poor health, not just the biological factors.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.

Hospitals, doctors and clinics expressed frustration that they will have to wait even longer for reimbursements after hackers paralyzed the largest U.S. billing clearinghouse.More than two weeks after a cyberattack, financially strapped doctors, hospitals and medical providers on Friday sharply criticized UnitedHealth Group’s latest estimate that it would take weeks longer to fully restore a digital network that funnels hundreds of millions of dollars in insurance payments every day.UnitedHealth said that it would be at least two weeks more to test and establish a steady flow of payments for bills that have mounted since hackers effectively shut down Change Healthcare, the nation’s largest billing and payment clearinghouse, on Feb. 21.But desperate providers that have been borrowing money to cover expenses and employee payrolls expressed skepticism at that estimate, worrying that it could be months before the logjam of claims and payments cleared up.“We have nearly a three-week gap in cash flow,” said Brad Larsen, a psychologist and founder of Portland Mental Health & Wellness in Oregon, adding that the group had received only about 10 percent of its expected insurance payments. He said the practice had to borrow $300,000 to meet its first of two payrolls for the month. “It’s not good.”In an apparent move to mollify some providers who had expressed disappointment at United’s earlier remedy of a loan program that offered stopgap payments of as little as $20 a week, the parent company agreed to issue advances. United announced that its insurer, the largest in the United States, would begin advancing payments to hospitals and doctors based on amounts billed before the cyberattack.And given that three of every patient records in the country goes through Change, the cyberattack affected not only United’s clients but also those of many other insurers. That led UnitedHealth’s executive to recommend that they also offer advances. “To me, that is the quickest way to get money in the hands of providers,” Dirk McMahon, United’s president and chief operating officer, said in an interview. .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.

The COVID-19 virus can persist in the blood and tissue of patients for more than a year after the acute phase of the illness has ended, according to new research from UC San Francisco that offers potential clues to why some people develop long COVID.
The scientists found pieces of SARS-CoV-2, referred to as COVID antigens, lingering in the blood up to 14 months after infection and for more than two years in tissue samples from people who had COVID.
“These two studies provide some of the strongest evidence so far that COVID antigens can persist in some people, even though we think they have normal immune responses,” said Michael Peluso, MD, an infectious disease researcher in the UCSF School of Medicine, who led both studies.
The findings were presented at the Conference on Retroviruses and Opportunistic Infections (CROI), which was held March 3 to 6, 2024, in Denver.
Evidence of long-term infection
Early in the pandemic, COVID-19 was thought to be a transient illness. But a growing number of patients, even those who had previously been healthy, continued having symptoms, such as, brain fog, digestive problems and vascular issues, for months or even years.
The researchers looked at blood samples from 171 people who had been infected with COVID. Using an ultra-sensitive test for the COVID “spike” protein, which helps the virus break into human cells, the scientists found the virus was still present up to 14 months later in some people.

Among those who were hospitalized for COVID, the likelihood of detecting the COVID antigens was about twice as high as it was for those who were not. It was also higher for those who reported being sicker, but were not hospitalized.
“As a clinician, these associations convince me that we are on to something, because it makes sense that someone who had been sicker with COVID would have more antigen that can stick around,” Peluso said.
Virus persists up to two years in tissue
Since the virus is believed to persist in the tissue reservoirs, the scientists turned to UCSF’s Long COVID Tissue Bank, which contains samples donated by patients with and without long COVID.
They detected portions of viral RNA for up to two years after infection, although there was no evidence that the person had become reinfected. They found it in the connective tissue where immune cells are located, suggesting that the viral fragments were causing the immune system to attack. In some of the samples, the researchers found that the virus could be active.
Peluso said more research is needed to determine whether the persistence of these fragments drives long COVID and such associated risks as heart attack and stroke.

But, based on these findings, Peluso’s team at UCSF is involved in multiple clinical trials that are testing whether monoclonal antibodies or antiviral drugs can remove the virus and improve the health of people with long COVID.
“There is a lot more work to be done, but I feel like we are making progress in really understanding the long-term consequences of this infection,” Peluso said.
Authors: Additional UCSF co-authors include Sarah Goldberg, MAS, Brian H. LaFranchi, Scott Lu, MD, Thomas Dalhuisen, MS, Badri Viswanathan, Ma Somsouk, MD, MAS, J.D. Kelly, MD, Steven G. Deeks, MD, Zoltan Laszik, MD, PhD, Jeffrey Martin, MD, MPH, and Timothy J. Henrich, MD.
Funding: The studies were supported by funding from the PolyBio Research Foundation to support UCSF’s Long-Term Impact of Infection with Novel Coronavirus (LIINC) Clinical Core and a Merck Investigator Studies Program Grant. The National Institute of Health’s National Institute of Allergy and Infectious Diseases also provided funding (3R01AI1411003-03S1, R01AI158013 and K23AI134327, K23AI157875 and K24AI145806). Additional support came from the Zuckerberg San Francisco General Hospital Department of Medicine and Division of HIV, Infectious Diseases and Global Medicine.

University of Pittsburgh researchers have uncovered blood-based markers linked with healthy and rapid aging, allowing them to predict a person’s biological age — how fast a person’s cells and organs age regardless of their birthdate.
The new research, published in Aging Cell, points to pathways and compounds that may underlie biological age, shedding light on why people age differently and suggesting novel targets for interventions that could slow aging and promote healthspan, the length of time a person is healthy.
“Age is more than just a number,” said senior author Aditi Gurkar, Ph.D., assistant professor of geriatric medicine at Pitt’s School of Medicine and member of the Aging Institute, a joint venture of Pitt and UPMC. “Imagine two people aged 65: One rides a bike to work and goes skiing on the weekends, and the other can’t climb a flight of stairs. They have the same chronological age, but very different biological ages. Why do these two people age differently? This question drives my research.”
Towards answering this question, Gurkar and her team compared 196 older adults who they classified as healthy or rapid agers by how easily they completed simple walking challenges. Because walking ability is a holistic measure of cardiovascular fitness, physical strength and neurological health, other studies have shown that it’s the single best predictor of hospitalization, disability, functional decline and death in older adults.
Healthy agers were 75 years or older and could ascend a flight of stairs or walk for 15 minutes without resting, and the rapid agers, who were 65 to 75 years old, had to rest during these challenges.
According to Gurkar, this study is unique because the rapid agers were chronologically younger than the healthy agers, allowing the researchers to home in on markers of biological — not chronological — aging, unlike other studies that have compared young adults with older people.
To define a molecular fingerprint of biological aging in blood samples from participants, they performed metabolomics — an analysis of metabolites, molecules that are produced by chemical pathways in the body — with blood samples from the two groups.

“Other studies have looked at genetics to measure biological aging, but genes are very static: the genes you’re born with are the genes you die with,” said Gurkar. “We chose to look at metabolites because they are dynamic: They change in real time to reflect our current health and how we feel, and we have the power to influence them through our lifestyles, diet and environment.”
Healthy and rapid agers showed clear differences in their metabolomes, indicating that metabolites in the blood could reflect biological age.
Gurkar and her team next identified 25 metabolites that they termed the Healthy Aging Metabolic (HAM) Index. They found that the HAM Index was better than other commonly used aging metrics — including the frailty index, gait speed and the Montreal Cognitive Assessment test — at distinguishing healthy and rapid agers.
To validate their new index, the researchers analyzed a separate cohort of older adults from a Wisconsin-based study. The HAM index correctly predicted whether individuals could walk outside for 10 minutes without stopping with accuracy of about 68%.
“We took a very different cohort of people from a different geographical region, and we saw the same metabolites were associated with biological aging,” said Gurkar. “This gives us confidence that the HAM Index can truly predict who is a healthy ager versus a rapid ager.”
Using an artificial intelligence model that can predict potential drivers of biological traits, the team identified three main metabolites that were most likely to promote healthy aging or drive rapid aging. In future research, they plan to delve into how these metabolites and molecular pathways that produce them contribute to biological aging and explore interventions that could slow this process.

Gurkar is also planning more research to evaluate how the metabolome of younger people shifts over time. Eventually, she hopes to develop a blood test that could estimate biological age in young adults or predict those who might go on to develop diseases of aging.
“While it’s great that we can predict biological aging in older adults, what would be even more exciting is a blood test that, for example, can tell someone who’s 35 that they have a biological age more like a 45-year-old,” Gurkar said. “That person could then think about changing aspects of their lifestyle early — whether that’s improving their sleep, diet or exercise regime — to hopefully reverse their biological age.”
“Today, in medicine, we tend to wait for a problem to occur before we treat it,” she added. “But aging doesn’t work that way — it’s about prevention. I think the future of medicine is going to be about knowing early on how someone is aging and developing personalized interventions to delay disease and extend healthspan.”
Other authors on the study were Shruthi Hamsanathan, Ph.D., Tamil Anthonymuthu, Ph.D., Denise Prosser, Anna Lokshin, Ph.D., Susan L. Greenspan, M.D., Neil M. Resnick, M.D., Subashan Perera, Ph.D., and Satoshi Okawa, Ph.D., all of Pitt or UPMC; and Giri Narasimhan, Ph.D., of Florida International University.
This research was supported in part by the Pittsburgh Claude D. Pepper Older Americans Independence Center (P30 AG024827). The Gurkar Lab is supported through the National Institutes of Health (R00 AG049126, R01HL161106, U54AG075931, P30CA047904, R01AG054047 and RF1AG054047), the National Academy of Medicine Catalyst grant, AFAR/Hevolution and the R.K. Mellon Foundation.