Publisher Health

Professor Sir Jonathan Van-Tam has said he no longer wears a face covering as a matter of course. England’s former deputy chief medical officer told the BBC people “have got to learn to frame those risks for themselves” and that he would consider wearing a mask in certain circumstances. His comments come as Covid-19 cases continue to rise in the UK.

Recent studies in humans and mice have shown that late nights and early mornings may cause long lasting damage to your brain.The sleep debt collectors are coming. They want you to know that there is no such thing as forgiveness, only a shifting expectation of how and when you’re going to pay them back. You think of them as you lie in bed at night. How much will they ask for? Are you solvent? You fall asleep, then wake up in a cold sweat an hour later. You fall asleep, then wake up, drifting in and out of consciousness until morning.As most every human has discovered, a couple nights of bad sleep is often followed by grogginess, difficulty concentrating, irritability, mood swings and sleepiness. For years, it was thought that these effects, accompanied by cognitive impairments like lousy performances on short-term memory tests, could be primarily attributed to a chemical called adenosine, a neurotransmitter that inhibits electrical impulses in the brain. Spikes of adenosine had been consistently observed in sleep-deprived rats and humans.Adenosine levels can be quickly righted after a few nights of good sleep, however. This gave rise to a scientific consensus that sleep debt could be forgiven with a couple of quality snoozes — as reflected in casual statements like “I’ll catch up on sleep” or “I’ll be more awake tomorrow.”But a review article published recently in the journal Trends in Neurosciences contends that the folk concept of sleep as something that can be saved up and paid off is bunk. The review, which canvassed the last couple of decades of research on long term neural effects of sleep deprivation in both animals and humans, points to mounting evidence that getting too little sleep most likely leads to long-lasting brain damage and increased risk of neurodegenerative disorders like Alzheimer’s disease.“This is really, really important in setting the stage for what needs to be done in sleep health and sleep science,” said Mary Ellen Wells, a sleep scientist at the University of North Carolina, who did not contribute to the review.It has long been known that intense periods of sleep deprivation are bad for your health. Forced insomnia was used for centuries as punishment and torture. In the first experimental study of sleep deprivation, published in 1894 by the Russian scientist Maria Manasseina, puppies were forced to stay awake through constant stimulation; they died within five days. Examining their bodies afterward, Manasseina observed that “the brain was the site of predilection of the most severe and most irreparable changes.” Blood vessels had hemorrhaged and fatty membranes had degenerated. “The total absence of sleep is more fatal for the animals than the total absence of food,” Manasseina concluded.But there are many ways to not get enough sleep. You can go entirely without sleep for an extended period of time — what scientists call acute sleep deprivation. (In 1963, a high school student managed to stay awake for 264 hours.) You can consistently miss out on sleep — chronic sleep deprivation. You can lie awake, mind racing, or relax, watching television all night. Studies like Manasseina’s were seen as extreme to the point of being irrelevant to humans.Research continued, but “that was where it was sort of pigeonholed,” said Fabian Fernandez, a neuroscientist at the University of Arizona who did not contribute to the new review. “When are you ever going to keep an animal or human awake until they die?”Over the past couple of decades, however, the animal research on sleep deprivation has become more nuanced, precise and, possibly, applicable to humans, according to Dr. Sigrid Veasey, a neuroscientist at the University of Pennsylvania, and Zachary Zamore, a researcher in Dr. Veasey’s lab, the authors of the new review.After surveying past studies of sleep-deprived mice, many of which Dr. Veasey conducted, the researchers found that when the animals were kept awake for just a couple of hours more than usual each day, two key parts of the brain were notably affected: the locus coeruleus, which manages feelings of alertness and arousal, and the hippocampus, which plays an important role in memory formation and learning. These regions, which, in humans, are central to sustaining conscious experience, slowed down the animals’ production of antioxidants, which protect neurons from unstable molecules that are constantly being produced, like exhaust fumes, by functioning cells. When antioxidant levels are low, these molecules can build up and attack the brain from inside, breaking down proteins, fats and DNA.“Wakefulness in the brain, even under normal circumstances, incurs penalties,” Dr. Fernandez said. “But when you’re awake for too long, then the system gets overloaded. At some point, you can’t beat a dead horse. If you’re asking your cells to remain active for 30 percent more time each day, cells die.”In the brains of mice, sleep deprivation led to cell death after a few days of sleep restriction — a much lower threshold for brain damage than previously thought. It also caused inflammation in the prefrontal cortex and increased levels of tau and amyloid proteins, which have been linked to neurodegenerative diseases like Alzheimer’s and Parkinson’s, in the locus coeruleus and hippocampus.After a full year of regular sleep, the mice that previously had been sleep-deprived still suffered from neural damage and brain inflammation. To Dr. Veasey and Mr. Zamore, this suggested that the effects were long-lasting and perhaps permanent.Nevertheless, many scientists said that the new research should not be cause for panic. “It is possible that sleep deprivation damages rat and mouse brains, but that doesn’t mean that you should get stressed about not getting enough sleep,” said Jerome Siegel, a sleep scientist at the University of California, Los Angeles, who did not contribute to the review.Dr. Siegel noted that neural injury comes in degrees, and that the extent of sleep deprivation’s effect on the human brain is still largely unknown. He also expressed concern that undue worry about the long-term effects of sleep deprivation could lead people to try to sleep more, unnecessarily and with medication.“The simplest message is sleep deprivation is bad, but that doesn’t mean that sleep is monotonically good,” he said.There is currently no ethical way to measure the degree and kind of cell damage caused by sleep deprivation in the locus coeruleus and hippocampus of a living human. Instead, longitudinal studies published over the past 15 years have relied on behavioral changes and self-reported sleep data to link chronic bad sleep to dementia, depression, metabolic issues, cardiovascular disease, insufficient immune response and even lower grade-point averages. These experiments can be difficult to confirm, but, taken together with findings in animal models, they hint that there is some sort of long-term relationship between a lack of sleep and physical and cognitive damage.“Sleep loss can injure the brain, and if it happens in mice, and it has been shown to happen in other species, then it probably does happen in humans,” Dr. Veasey said. “It always begs the question: How much sleep loss would cause injuries? But looking at all of this literature together, of around one week of chronic sleep loss, it really does suggest that you injured the brain to some extent.”If a link can be drawn between mice and humans, it could change the way we think about sleep, which is typically in terms of sleepiness rather than neural damage. There is already a known gap between how people perceive their own cognitive capacities after sleep deprivation and how they actually perform on memory and reaction time tests. People can feel fine while their brains are in turmoil, and they can feel exhausted when their brains are fine. “Perception and reality of your sleep can be very, very different,” Dr. Wells said.That disconnect, in turn, “has actually hampered our asking the right questions,” Dr. Veasey added. Her hope is that people and scientists will come to understand sleep more fully. And then, informed, we’ll no doubt go into sleep debt anyway.

The agency ruled against the company’s application to stay on the market, a decisive blow to a once-popular vaping brand that appealed to teenagers.The Food and Drug Administration on Thursday ordered Juul to stop selling e-cigarettes on the U.S. market, a profoundly damaging blow to a once-popular company whose brand was blamed for the teenage vaping crisis.The order affects all of Juul’s products on the U.S. market, the overwhelming source of the company’s sales. Juul’s sleek vaping cartridges and sweet-flavored pods helped usher in an era of alternative nicotine products that were exceptionally attractive to young people. The company’s initial dominance invited intense scrutiny from antismoking groups and regulators who feared the products would do more harm to young people than good to cigarette smokers trying to quit.Although teenage vaping rates have declined during the coronavirus pandemic, public health experts and lawmakers continue to express concerns about the additive nicotine in some e-cigarettes that remain on the market, including brands like Puff Bar, whose fruity flavors appeal to young people.The F.D.A.’s decision did not deal with Juul’s relationship to youth vaping. Instead it was based on what the agency said was insufficient and conflicting data from the company about potentially harmful chemicals that could leach out of Juul’s e-liquid pods. There was not an imminent health threat to consumers, the F.D.A. said, but it did not have enough evidence to assess the potential risks.“Today’s action is further progress on the F.D.A.’s commitment to ensuring that all e-cigarette and electronic nicotine delivery system products currently being marketed to consumers meet our public health standards,” Dr. Robert M. Califf, the agency commissioner, said in a statement. And he acknowledged that many of the e-cigarette products had played a role in the rise in teenage vaping.The move by the F.D.A. is part of a wide-ranging effort to remake the rules for smoking and vaping products and to reduce illnesses and deaths caused by inhalable products containing highly addictive nicotine.On Tuesday, the agency announced plans to slash nicotine levels in traditional cigarettes as a way to discourage use of the most deadly of legal consumer products. In April, the F.D.A. said it would move toward a ban on menthol-flavored cigarettes.The F.D.A.’s action against Juul in particular is part of a newer regulatory mission for the agency, which must determine which electronic cigarettes currently for sale, or proposed for sale, will be allowed to permanently remain on shelves. It has already granted permission for other companies’ e-cigarettes to stay on the market.But it could take years before some of the agency’s new initiatives take effect — if they can withstand fierce resistance from the powerful tobacco lobby, antiregulatory groups and the vaping industry.Juul said it disagreed with the F.D.A.’s findings and planned to appeal. The company could seek a stay from the agency or from a court pending an appeal to the F.D.A. The company has not said which path it will seek but it will try to keep its products on the market during any proceedings.Read More on Smoking and VapingNicotine Levels: Aiming to reduce the toll of smoking, the Food and Drug Administration is planning to require tobacco companies to slash the amount of nicotine in cigarettes.Menthol Ban: The F.D.A. has also proposed a plan to ban sales of menthol cigarettes, a measure experts say may save hundreds of thousands of lives, especially among Black smokers.‘Smoking Is Back’: Cigarettes, still the No. 1 cause of preventable death in the United States, are making a comeback with a younger crowd.Vaping Loophole: A crackdown on flavored e-cigarettes was meant to curtail teenage vaping, but sales are rising due to synthetic nicotine.The Rise of Juul: A Times documentary traced the e-cigarette maker on its path from fledgling start-up to Silicon Valley juggernaut and, eventually, public health villain.“We intend to seek a stay,” Juul’s statement concluded, “and are exploring all of our options under the F.D.A.’s regulations and the law, including appealing the decision and engaging with our regulator.”Public health groups hailed the ruling.“The F.D.A.’s decision to remove all Juul products from the marketplace is both most welcomed and long overdue,” said Erika Sward, national assistant vice president of advocacy for the American Lung Association. “Juul’s campaign to target and hook kids on tobacco has gone on for far too long.”A statement from the American Vapor Manufacturers Association, an industry trade group, hinted at the fight ahead.“Measured in lives lost and potential destroyed, F.D.A.’s staggering indifference to ordinary Americans and their right to switch to the vastly safer alternative of vaping will surely rank as one of the greatest episodes of regulatory malpractice in American history,” Amanda Wheeler, the association’s president, said in a statement.Broadly, the F.D.A. is walking a fine line in remaking the landscape for nicotine products. It is trying to wean the public off traditional cigarettes while permitting less harmful vaping products that do not attract a new generation of users: The new devices must be appealing for smoking cessation but not so appealing that they lure young people en masse.The agency’s ruling against Juul capped a nearly two-year review of data that the company had submitted to try to win authorization to continue selling its tobacco and menthol-flavored products in the United States. Specifically, Juul sought approval for — and the F.D.A. rejected — a Juul vaping device and four different pods, including tobacco pods with nicotine concentrations of 3 percent and 5 percent and menthol-flavored pods with the same levels.“It’s clear that the company was given an opportunity to address questions and concerns related to safety, toxicology and potential genotoxicity, and for whatever reason the company was unable to meet its burden and that led to a negative marketing order,” said Mitch Zeller, a former director of the agency’s tobacco center who retired in April.He said Juul could submit an entirely new application for a revamped product — one that presumably addressed the agency’s concerns about the leaching of chemicals.The F.D.A. began an investigation into Juul’s marketing efforts four years ago. Before that time, Juul had advertised its product using attractive young models and flavors like cool cucumber and creme brulee that critics said attracted underage users.In April 2018, the F.D.A. announced a crackdown on the sale of such products, including Juul’s, to people under the age of 21.Use among young people had soared. In 2017, 19 percent of 12th graders, 16 percent of 10th graders and 8 percent of eighth graders reported vaping nicotine in the previous year, according to Monitoring the Future, an annual survey done for the National Institute on Drug Abuse.For its part, Juul routinely denied that it targeted young people, but it was pursued in lawsuits and by state attorneys general, with some cases resulting in millions of dollars in damages against the company. In one settlement in 2021, Juul agreed to pay $40 million to North Carolina, which represented various parties in the state who asserted the company had helped lure underage users to vaping. More than a dozen other states have lawsuits and investigations that are still pending.The news is somewhat less weighty for the industry now than it would have been in Juul’s heyday, given the company’s plummeting market share. Once the dominant player with 75 percent of the market, Juul now has a considerably smaller share of the market.But the news delivers a significant blow to Altria, formerly known as Philip Morris and the maker of Marlboro, which in December 2018 bought 35 percent of Juul for $12.8 billion.Altria made the investment to counteract slowing tobacco sales, while Juul looked to Altria as an ally to help it navigate increased regulatory scrutiny.Neither of those strategies appear to have worked out.Altria has written down the value of its investment in Juul by more than $11 billion, to $1.7 billion. Altria, which gets about 90 percent of its revenue from smokable products, saw revenue fall slightly last year. Its stock is down more than 40 percent over the past five years, and 20 percent just in the past month. Juul, for its part, saw its revenue fall to $1.3 billion in 2021, from $2 billion in 2019, with about 95 percent in U.S. sales.“We are disappointed with today’s decision and continue to believe that e-vapor can play an important role in harm reduction for adult smokers,” Altria said in a statement.At its peak, Juul had more than 4,000 employees. It now has slightly over 1,000, mostly in the United States, but with some in Canada, Britain and other countries.E-cigarettes have been sold on the U.S. market for more than a decade without formal F.D.A. authorization, because they did not fall under the agency’s regulatory purview for several years.In 2019, the F.D.A. issued a warning letter to Juul, saying that the company violated federal regulations because it had not received approval to promote and sell its products as a healthier option to smoking.The F.D.A. recently said it had so far rejected more than a million applications for products it considered more of a health risk than a benefit. In October, it authorized R.J. Reynolds to continue marketing Vuse. This was the first time the agency granted approval to a vaping product made by a big cigarette companyIn March, the agency authorized several tobacco-flavored products from Logic Technology Development, saying the company was able to show that its products were likely to help adults make the transition from traditional cigarettes while posing a low risk of attracting young, new users.Some tobacco control experts said the decision to ban Juul from the U.S. market could be counterproductive.Clifford Douglas, director of the University of Michigan Tobacco Research Network, said that many experts had come to see Juul and other e-cigarettes as valuable tools for helping adult smokers quit conventional cigarettes.“They are off ramps that can provide smokers an alternative to combustibles, which are responsible for virtually every death related to tobacco,” he said. “But now that off ramp is being narrowed and sort of paved over, which is putting millions of adult lives at stake. One hopes Juul can respond effectively to the request for more scientific analysis, make any product adjustments that may be called for, and again offer their products to adults in need.”Lauren Hirsch, Christina Jewett and Sheila Kaplan contributed reporting.

When diagnostic tests for the heart were first created, scientists at the time did not fully consider that no two bodies are the same, especially between the sexes.
According to University of Florida College of Nursing associate professor Jennifer Dungan, many of the current symptom profiles and lab tests for heart disease do not accurately reflect known differences in women’s heart disease. This oversight has led to increased gaps in health care equity.
“Because of this disparity, women are more likely than men to report heart disease symptoms that appear out of the norm, experience delayed treatment for heart disease and even have undiagnosed heart attacks,” Dungan said. “For reasons that remain uncertain, women can experience heart disease differently than men. This can lead to inequities for women that need to be addressed.”
Dungan said cardiac researchers believe that some of these differences in symptoms and outcomes may be due to genetic variation between men and women. She has identified a specific gene she believes may be responsible, named RAP1GAP2.
“RAP1GAP2 is a strong candidate for sex-linked effects on women’s heart disease outcomes,” Dungan said. “Certain DNA markers in this gene are thought to manage the activity of platelets, colorless blood cells that help our blood clot. This also presents a heart attack risk. An overactive gene could cause too many platelets to respond to the clot, which could block the flow of blood and oxygen to the heart muscle and lead to a heart attack.”
Since RAP1GAP2 was not linked to poor heart outcomes among men in her team’s study, she believes this gene may work differently in women. Her team included faculty from UF’s colleges of Medicine, Pharmacy, and Public Health and Health Professions. Their findings were recently published in American Heart Journal Plus.
Even less is known about such differences among races and ethnicities. Black women and some Hispanic women are at an even greater risk of poor heart disease outcomes, due to many factors that Dungan believes may include genetics.

A new study reveals important molecular information that could help scientists develop more effective treatment and prevention strategies for a difficult-to-treat form of melanoma skin cancer.
In this new report, The Ohio State University Comprehensive Cancer Center — Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC — James) researchers identify and describe key features of a gene mutation responsible for 15 to 20% of all melanomas.
Using a preclinical laboratory model, the team establishes that the frequency at which a specific NRAS gene mutation occurs in human melanoma is directly related to the ability of that gene mutation to initiate spontaneous melanoma formation.
“This means that properties of the mutant itself — rather than the ease at which that specific gene mutation occurs — is the cause of cancer formation,” said corresponding author Christin Burd who serves an associate professor of molecular genetics in The Ohio State University College of Arts and Sciences, Department of Molecular Genetics and a member of the OSUCCC — James Molecular Carcinogenesis and Chemoprevention Program.
“NRAS-mutant cancers are challenging to treat because effective therapies beyond immunotherapy don’t exist yet,” said Burd. “Each cancer type seems to prefer a specific ‘flavor’ of mutant NRAS, and it has not been clear why this is.”
The OSUCCC — James wanted to know what made the melanoma-promoting NRAS mutants different than those that promote other cancer types. Scientists say this knowledge could help investigators pinpoint the early events required for melanoma formation and develop treatments that prevent the disease.

Techniques used in weather forecasting can be repurposed to provide individuals with a personalized assessment of their risk of exposure to COVID-19 or other viruses, according to new research published by Caltech scientists.
The technique has the potential to be more effective and less intrusive than blanket lockdowns for combatting the spread of disease, says Tapio Schneider, the Theodore Y. Wu Professor of Environmental Science and Engineering; senior research scientist at JPL, which Caltech manages for NASA; and the lead author of a study on the new research that was published by PLOS Computational Biology on June 23.
“For this pandemic, it may be too late,” Schneider says, “but this is not going to be the last epidemic that we will face. This is useful for tracking other infectious diseases, too.”
In principle, the idea is simple: Weather forecasting models ingest a lot of data — for example, measurements of wind speed and direction, temperature, and humidity from local weather stations, in addition to satellite data. They use the data to assess what the current state of the atmosphere is, forecast the weather evolution into the future, and then repeat the cycle by blending the forecast atmospheric state with new data. In the same way, disease risk assessment also harnesses various types of available data to make an assessment about an individual’s risk of exposure to or infection with disease, forecasts the spread of disease across a network of human contacts using an epidemiological model, and then repeats the cycle by blending the forecast with new data. Such assessments might use the results of an institution’s surveillance testing, data from wearable sensors, self-reported symptoms and close contacts as recorded by smartphones, and municipalities’ disease-reporting dashboards.
The research presented in PLOS Computational Biology is proof of concept. However, its end result would be a smart phone app that would provide an individual with a frequently updated numerical assessment (i.e., a percentage) that reflects their likelihood of having been exposed to or infected with a particular infectious disease agent, such as COVID-19.
Such an app would be similar to existing COVID-19 exposure notification apps but more sophisticated and effective in its use of data, Schneider and his colleagues say. Those apps provide a binary exposure assessment (“yes, you have been exposed,” or, in the case of no exposure, radio silence); the new app described in the study would provide a more nuanced understanding of continually changing risks of exposure and infection as individuals come close to others and as data about infections is propagated across a continually evolving contact network.

Even as cases rise, genetic analysis suggests that the virus has been silently circulating in people since 2018.When the first monkeypox cases were identified in early May, European health officials were stumped. The virus was not known to spread easily among people, let alone infect dozens — and soon hundreds — of young men.The origins of the outbreak are now becoming clearer. Genetic analysis suggests that although the monkeypox virus is rapidly spreading in the open, it has been silently circulating in people for years.Health officials have already identified two versions of monkeypox among American patients, suggesting at least two separate chains of transmission. Researchers in several countries have found cases with no known source of infection, indicating undetected community spread. And one research team argued last month that monkeypox had already crossed a threshold into sustainable person-to-person transmission.The genetic information available so far indicated that, at some point in the last few years, the virus became better at spreading between people, said Trevor Bedford, an evolutionary biologist at the Fred Hutchinson Cancer Research Center in Seattle.“Genomic patterns would suggest this occurred around 2018,” Dr. Bedford said.If the virus has adapted to include people as hosts, monkeypox outbreaks could become more frequent and more difficult to contain. That carries the risk that monkeypox could spill over from infected people into animals — most likely rodents — in countries outside Africa, which has struggled with that problem for decades. The virus may persist in infected animals, sporadically triggering new infections in people.“We can also transmit this back to animals that can spread the disease within wildlife and back to humans,” said Sagan Friant, an anthropologist at Pennsylvania State University who has studied human-animal interactions in Nigeria for about 15 years.The longer it takes to contain the virus, the higher the odds that it will find a permanent new home in people or animals, Dr. Friant said.As of Wednesday, the United States had identified 156 cases in 23 states and the District of Columbia. The global toll has surpassed 3,400 confirmed cases, and another 3,500 cases are being evaluated, tripling the numbers from two weeks ago.In Africa, eight countries had reported more than 1,500 suspected cases and 72 deaths as of June 10, most of which were in the Democratic Republic of the Congo.Monkeypox is a large double-stranded DNA virus, about seven times as large as the coronavirus. DNA-based viruses can correct their own errors when they replicate their genetic material. They may collect just one or two mutations per year compared with 20 to 30 mutations for an RNA virus like the coronavirus.An electron microscope image of oval, mature monkeypox virions, left, and spherical, immature virions, right. The sample was obtained in 2003, when an outbreak in the United States infected 71 people.C.D.C., via Associated PressBut the monkeypox virus seems to have amassed an unexpectedly high number of mutations — nearly 50 compared to a version that circulated in 2018, according to preliminary analyses. Of the 47 mutations identified in one analysis, 42 carry the distinct signature of an enzyme called Apobec3. This enzyme, first discovered by researchers studying H.I.V., is a so-called host defense factor — an immune-system weapon that animals and people use to disarm viruses like monkeypox.The enzyme essentially forces viruses to make mistakes when they try to replicate, causing them to self-destruct. Mice carry just one version of this enzyme, while humans have seven. The rapid accumulation of mutations, characteristic of the enzyme since 2018, suggests that monkeypox may have switched to people as hosts around then, Dr. Bedford said.It is unclear how the mutations might change the virus. Of 48 mutations identified in Britain, 21 may affect how the disease spreads, its severity and how well it responds to a treatment called tecovirimat, according to the U.K. Health Security Agency.But because mutations introduced by the enzyme Apobec3 are meant to harm the virus, their quantity alone is not worrying, said Michael Malim, a virologist at King’s College London who discovered Apobec3 in 2002. The effect of the mutations is “more likely to be debilitating,” he said. Comparing the current version of the virus with samples from the past few years might help understand how it has evolved, but that information is scarce. Nigeria did not have the ability to sequence genetic material until 2017.Since then, scientists there have been analyzing the sequences from about 50 monkeypox cases, according to Dr. Ifedayo Adetifa, director of the Nigeria Center for Disease Control. But without the specialized equipment or expertise needed for rapid analysis, the scientists have not yet completed their work, he said.Although the researchers have fielded several requests for the data from outside Nigeria, Dr. Adetifa said they would wait to publish their work to prevent teams with more resources from outcompeting them and grabbing credit.What to Know About the Monkeypox VirusCard 1 of 5What is monkeypox?

Much research has been done on the effectiveness of masks to mitigate the spread of infectious diseases. However, standard infection models tend to focus only on disease states, overlooking the dynamics of a complex paradox: While masking reduces transmission rates and consequently disease prevalence, the reduction of disease inhibits mask-wearing — thereby promoting epidemic revival.
To investigate this bidirectional relationship, a team of researchers led by the University of Virginia*, developed a multi-contagion framework and intertwined a threshold model for mask-wearing behavior, or “social contagions,” with an epidemic model. The threshold model accounts for various behavioral mechanisms that influence mask-wearing, such as peer pressure, fear of infection, elite influence, and prosociality.
In their paper published in the Proceedings of the National Academy of Sciences, the researchers posit that the final epidemic size (or attack rate) of a disease exhibits a critical transition when populations assume the disease spreading is more infectious, triggering a sustained massive response of mask adoption which sharply decreases the final epidemic size.
The conundrum is that when disease rates are low, mask-wearing becomes an afterthought, and a less infectious disease could cause a higher attack rate than its more infectious counterparts.
Results highlight that without proper enforcement of masking, reduction in the disease transmission probability via other interventions — such as mass vaccination — may not be sufficient to reduce the final epidemic size. This was the case in a resurgence of COVID-19 cases in the United States after vaccinations when the number of new daily cases jumped by approximately an order of magnitude from early June 2021 to early September 2021.
“Interdisciplinary models are absolutely critical for helping refine our assumptions,” says Santa Fe Institute Fellow Stefani Crabtree (Utah State University), who contributed to the research. “The findings have helped me to not bow to peer pressure. I’m still masking at grocery stores and in crowded areas because, even though I am vaccinated, I know it will help.”
In their study, the researchers described mask-wearing as a “complex contagion” whose adoption requires multiple interactions and sources of reinforcement to produce the “contagion” and help model behavioral adoption (switching from masked to unmasked and vice versa). This is opposite to disease transmission for which a single contagion would be enough to transmit the disease.
While mandatory masking may be viewed as cumbersome and expensive, mathematical models incorporating individual adaptive human behavior during epidemics have shown the essential role of continuous reinforcement of masking in minimizing epidemics.
“An even larger issue to tackle is how polarized our society is,” says SFI External Professor Simon Levin (Princeton University), a co-author on the paper. “I have never in my lifetime seen individuals so divided over something I consider commonsense public health measures.”
*Authors include a prestigious international team of researchers from the University of Virginia; University of Amsterdam; Princeton University; Northeastern University; Utah State University; Santa Fe Institute; Stockholm School of Economics; and Cornell University.
Story Source:
Materials provided by Santa Fe Institute. Note: Content may be edited for style and length.

Spinal fusion — fusing two vertebrae together — can treat a wide variety of spinal disorders. Often, surgeons will use a cage to provide support where the disk once was between the vertebrae. But what if those cages could support the spine’s healing in more ways than one?
Researchers at the University of Pittsburgh Swanson School of Engineering are creating patient-specific 3D-printed smart metamaterial implants that double as sensors to monitor spinal healing. A paper detailing their work was recently published in the journal Advanced Functional Materials.
“Smart implants can provide real-time biofeedback and offer many therapeutic and diagnostic benefits,” said Amir Alavi, assistant professor of civil and environmental engineering, whose iSMaRT Lab led the research. “But it is very challenging to integrate bulky circuits or power sources into the small area of implants. The solution is to use the implant matrix as an active sensing and energy harvesting medium. That’s what we’ve been focused on.”
The Intelligent Structural Monitoring and Response Testing (iSMaRT) Lab has developed a new class of multifunctional mechanical metamaterials, which act as their own sensors, recording and relaying important information about the pressure and stresses on its structure. The so-called “meta-tribomaterials” a.k.a. self-aware metamaterials, generate their own power and can be used for a wide array of sensing and monitoring applications.
The material is designed such that under pressure, contact-electrification occurs between its conductive and dielectric microlayers, creating an electric charge that relays information about the condition of the material matrix. In addition, it naturally inherits the outstanding mechanical tunability of standard metamaterials. The power generated using its built-in triboelectric nanogenerator mechanism eliminates the need for a separate power source, and a tiny chip records data about the pressure on the cage, which is an important indicator of healing. The data can then be read noninvasively using a portable ultrasound scanner.
Not only is the proposed cage unique in its sensing capabilities, but it’s also made of a highly tunable material that can be customized to the patient’s needs.
“Spinal fusion cages are being widely used in spinal fusion surgeries, but they’re usually made of titanium or PEEK polymer materials (a semi-crystalline, high-performance engineering thermoplastic) with certain mechanical properties,” explained Alavi. “The stiffness of our metamaterial interbody cages can be readily tuned. The implant can be 3D-printed based on the patient’s specific anatomy before surgery, making it a much more natural fit.”
The team has successfully tested the device in human cadavers and are looking to move on to animal models next. Because the material itself is incredibly tunable and scalable, the smart sensor design could be adapted to many other medical applications in the future, like cardiovascular stents or components for knee or hip replacements.
“This is a first-of-its-kind implant that leverages advances in nanogenerators and metamaterial to build multifunctionality into the fabric of medical implants,” said Alavi. “This technological advancement is going to play a major part in the future of implantable devices.”
Story Source:
Materials provided by University of Pittsburgh. Original written by Maggie Lindenberg. Note: Content may be edited for style and length.

A new study focused on decoding the genetic chaos found in cancer cells will be on the cover of the June issue of the scientific journal Nature. This work reveals novel biomarkers with the potential to improve the development of precision therapies and treatment selection for the deadliest types of cancer.
Researchers at the Spanish National Cancer Research Centre (CNIO) and the Cancer Research UK Cambridge Institute have developed a method to understand the genetic chaos observed in the most lethal types of cancer. This information can be used to design more effective precision therapies as well as improve treatment selection for patients. The study will be published in Nature, one of the world’s leading scientific journals. The approach described in the paper detects patterns of large DNA alterations in tumor genomes that help make sense of the mutational processes underlying cancer development. A better understanding of the genomic identity of aggressive cancers can lead to improved treatment selection and the development of more effective therapies, which has been virtually impossible for these cancer types to date.
The research was jointy led by Geoff Macintyre, Head of the Computational Oncology Group at the CNIO, and Florian Markowetz, Senior Group Leader at the Cancer Research UK Cambridge Institute. CNIO researcher Barbara Hernando, and CRUK researcher Ruben Drews also took part in the study, along with scientists from British, Canadian, Belgian and German research centres.
The study investigated chromosomal instability — a distinctive feature of aggressive human cancers. Under normal conditions, a healthy cell will perfectly duplicate and divide, to form two identical daughter cells. Each daughter cell will contain the same number of chromosomes as their parent cell, with the exact same DNA sequence. In cancer cells, however, this duplication does not occur perfectly.
There are losses or gains of chromosome segments, and even entire chromosomes can be absent or present in more than usual numbers. This process, known as chromosomal instability, which generates genetic chaos, is observed more frequently in severe cancer types with high death rates. Increased levels of instability are associated with more advanced stages of disease, poor prognosis, metastasis and resistance to traditional therapy treatment.
Chromosomal instability is a highly complex biological process that is present in roughly 80% of all cancers. There are multiple causes of chromosomal instability and a variety of consequences, which has limited researchers understanding of the phenomenon to date. The study conducted by CNIO researchers unravels the complexity of chromosomal instability and allows for improved analysis of many different types of cancer. The study analysed the diversity and the extent of chromosomal instability across severe cancers. Moreover, it defined the biological causes of different types of chromosomal instability and how this relates to different tumour types.
Currently, the most advanced cancer treatments are based on the concept of precision medicine, which involves using genetic mutations to inform which therapy a patient should be treated with. Tumours with chromosomal instability exhibit many defective genes, not just a single mutation, which means there are too many potential options to target therapeutically. The study conducted by the CNIO researchers solves this problem by establishing a catalogue of chromosomal instability signatures that can be identified at the time of diagnosis. The information associated with each pattern includes potential responses to traditional cancer treatments and novel treatments. This means that the signatures can be useful as biomarkers for diagnosing aggressive cancers and selecting the most effective therapy for a patient. In the words of Macintyre, one of the senior members of the team, “Our biomarkers can predict the effectiveness of different therapies for a given tumour.” “To understand the genomic chaos seen in these deadly cancers, we developed an approach to quantify different types of chromosomal instability using a collection of 7880 tumours representing 33 cancer types,” he adds.
The team that carried out the study have also established a UK-based precision medicine start-up, Tailor Bio. The company has licensed a patent on the method described in the paper published in Nature, and obtained another patent based on previous work on the same subject. The team hope their findings will soon be translated to the clinic.