Publisher Health

This year marks the 100th anniversary of the discovery of insulin, a scientific breakthrough that transformed Type 1 diabetes, once known as juvenile diabetes or insulin-dependent diabetes, from a terminal disease into a manageable condition.
Today, Type 2 diabetes is 24 times more prevalent than Type 1. The rise in rates of obesity and incidence of Type 2 diabetes are related and require new approaches, according to University of Arizona researchers, who believe the liver may hold the key to innovative new treatments.
“All current therapeutics for Type 2 diabetes primarily aim to decrease blood glucose. So, they are treating a symptom, much like treating the flu by decreasing the fever,” said Benjamin Renquist, an associate professor in the UArizona College of Agriculture and Life Sciences and BIO5 Institute member. “We need another breakthrough.”
In two newly published papers in Cell Reports, Renquist, along with researchers from Washington University in St. Louis, the University of Pennsylvania and Northwestern University, outline a new target for Type 2 diabetes treatment.
Renquist, whose research lab aims to address obesity-related diseases, has spent the last nine years working to better understand the correlation between obesity, fatty liver disease and diabetes, particularly how the liver affects insulin sensitivity.
“Obesity is known to be a cause of Type 2 diabetes and, for a long time, we have known that the amount of fat in the liver increases with obesity,” Renquist said. “As fat increases in the liver, the incidence of diabetes increases.”
This suggested that fat in the liver might be causing Type 2 Diabetes, but how fat in the liver could cause the body to become resistant to insulin or cause the pancreas to over-secrete insulin remained a mystery, Renquist said.

When 16-year-old Liliana Jackson caught Coronavirus she thought it would only last a week or two. But months later she was experiencing repeated flare-ups including skin rashes, nerve pain, chest cramps and severe fatigue.But her and her mother Gail, who live in the East Midlands in the UK, felt let down by doctors who they say at first, didn’t take them seriously.While the majority of children and young people are not severely affected by Covid, some do experience continuing symptoms. NHS England says it’s setting up specialist long Covid services for young people as part of a £100 million expansion of care for those with the condition.Video produced by Jasmin Souesi, Trystan Young and Daniel South.

Los Angeles County and the W.H.O. warned that even immunized people should wear masks indoors. Some scientists agreed, but urged a localized approach.Throughout the pandemic, masks have ranked among the most contentious public health measures in the United States, symbolizing a bitter partisan divide over the role of government and individual liberties.Now, with a new variant of the coronavirus rapidly spreading across the globe, masks are again the focus of conflicting views, and fears, about the course of pandemic and the restrictions required to manage it.The renewed concerns follow the wildfire growth of the Delta variant, a highly infectious form of the virus first detected in India and later identified in at least 85 countries. It now accounts for one in five infections in the United States.In May, federal health officials said that fully vaccinated people no longer needed to mask up, even indoors. The advice signified a sea change in American life, setting the stage for a national reopening that continues to gain momentum.But that was before the spread of the Delta variant. Worried by a global surge in cases, the World Health Organization last week reiterated its longstanding recommendation that everyone — including the inoculated — wear masks to stem the spread of the virus.On Monday, health officials in Los Angeles County followed suit, recommending that “everyone, regardless of vaccination status, wear masks indoors in public places as a precautionary measure.”Barbara Ferrer, the county’s public health director, said the new recommendation was needed because of upticks in infections, a rise in cases due to the worrisome Delta variant, and persistently high numbers of unvaccinated residents, particularly children, Black and Latino residents and essential workers.Roughly half of Los Angeles County residents are fully vaccinated, and about 60 percent have had at least one dose. While the number of positive tests is still below 1 percent in the county, the rate has been inching up, Dr. Ferrer added, and there has been a rise in the number of reinfections among residents who were infected before and did not get vaccinated.To the extent that Los Angeles County has managed to control the pandemic, it has been because of a multilayered strategy that combined vaccinations with health restrictions aimed at curbing new infections, Dr. Ferrer said. Natural immunity among those already infected has also kept transmission low, she noted, but it is not clear how long natural immunity will last.“We don’t want to return to lockdown or more disruptive mandates here,” Dr. Ferrer said. “We want to stay on the path we’re on right now, which is keeping community transmission really low.”A Covid-19 memorial wall in London, where infections with the Delta variant are rising fast. Andy Rain/EPA, via ShutterstockHealth officials in Chicago and New York City said on Tuesday that they had no plans to revisit mask requirements. Officials at the Centers for Disease Control and Prevention declined to comment, but have not signaled any intention to revise or re-examine masking recommendations for those who are fully vaccinated.“When the C.D.C. made the recommendation to quit masking, it didn’t anticipate being in a situation where we might need to recommend masking again,” said Angela Rasmussen, a research scientist at the Vaccine and Infectious Disease Organization at the University of Saskatchewan in Canada.“Nobody’s going to want to do it. People are understandably accusing them of moving the goalposts.”But the Delta variant’s trajectory outside the United States suggests that concerns are likely to intensify.Countries in the Asia-Pacific region are now reimposing restrictions and stay-at-home orders as the variant drives new surges. Four Australian cites have reimposed lockdowns, and on Monday, the Malaysian government said nationwide stay-at-home orders would be extended indefinitely.Even Israel — which has one of the highest vaccination rates in the world and is aggressively immunizing younger adolescents and teenagers who qualify — has reinstated masking requirements in public indoor spaces and at large public gatherings outdoors, after hundreds of new Covid-19 cases were detected in recent days, including among people who had received both doses of the Pfizer-BioNTech vaccine.This is not the first time the world has been consumed by a more contagious variant of the coronavirus. The Alpha variant walloped Britain and brought the rest of Europe to a standstill earlier this year. In the United States, Alpha quickly became the dominant variant by late March, but the rapid pace of vaccination blunted its spread, sparing the nation a big surge in infections.But Delta is thought to be even more fearsome. Much of what is known about the variant is based on its spread in India and Britain, but early evidence indicates that it is perhaps twice as contagious as the original virus and at least 20 percent more contagious than Alpha.In many Indian states and European nations, Delta quickly outpaced Alpha to become the dominant version of the virus. It is on track to do the same in the United States.Among the variant’s many mutations are some that may help the virus partly dodge the immune system. Several studies have shown that while the current vaccines are effective against Delta, they are slightly less so than against most other variants. For individuals who have received only one dose of a two-dose regimen, protection against the variant is significantly reduced, compared with efficacy against other forms of the virus.A drive-through vaccination site in North Sumatra, Indonesia, on Tuesday.Dedi Sinuhaji/EPA, via ShutterstockThe W.H.O.’s rationale for maintaining masking is that while immunization is highly effective at preventing severe illness and death, the degree to which vaccines prevent mild or asymptomatic infections is unknown. (Officials at the C.D.C. disagree, saying the risk is minimal.)The W.H.O. maintains that vaccinated people should wear masks in crowded, close and poorly ventilated areas, and should continue with other preventive measures, like social distancing.“What we’re saying is: ‘Once you’ve been fully vaccinated, continue to play it safe, because you could end up as part of a transmission chain. You may not actually be fully protected,’” Dr. Bruce Aylward, a senior adviser to the W.H.O., said at a news briefing last week.Even countries with relatively high vaccination rates have seen an increase in infections driven by the Delta variant. Britain, where some two-thirds of the population have received at least one dose of the Pfizer-BioNTech or AstraZeneca vaccine and just under half have received two doses, is nonetheless grappling with a sharp rise in infections from the variant.It is not certain what course the Delta variant will take in the United States. Coronavirus infections have been plunging for months, as have hospitalizations and deaths. But Dr. Anthony S. Fauci, the nation’s top infectious disease doctor, has called the variant “the greatest threat” to eliminating the virus in the United States.In May, when C.D.C. officials lifted masking recommendations, they cited research showing that fully vaccinated people were unlikely to become infected with the virus, even with asymptomatic infections.But the variant’s talent for even partial immune evasion makes researchers nervous, as it suggests that fully vaccinated people may sometimes pick up asymptomatic infections and unknowingly spread the virus to others even if they never become ill.The Delta variant can infect vaccinated people, although its ability to do so is very limited, said Bill Hanage, an epidemiologist at the Harvard T.H. Chan School of Public Health. “If you are in a place where cases are climbing, wearing a mask indoors in crowded public spaces is a way to keep yourself from contributing to the spread of Delta,” he said.Other scientists stop short of recommending that fully vaccinated people always wear masks indoors, but some now suggest that this may be appropriate depending on local circumstances — for example, wherever the virus is circulating in high numbers, or vaccination rates are very low.“Masking in public enclosed spaces needs to continue even after vaccination, until we can get everyone vaccinated or a new vaccine that is more effective against Delta transmission,” said Dr. Ravindra Gupta, a virologist at the University of Cambridge in the United Kingdom.Even now, roughly half of Americans are not vaccinated, and a wide swath of the country remains vulnerable to outbreaks of the virus and its variants. Vaccines for children under age 12 are not likely to be authorized until the fall, at the earliest.Streets in Sydney, Australia, emptied after a two-week lockdown to contain an outbreak of the Delta variant.Saeed Khan/Agence France-Presse — Getty ImagesIn Saskatchewan, Canada, reopening has proceeded in stages that are tied to population vaccination rates and the percentage of people in certain age brackets who have been vaccinated.The province is moving to Step 3 of re-entry on July 11, but may maintain indoor masking requirements and restrictions on the size of gatherings, said Dr. Rasmussen, of the University of Saskatchewan. The strategy “makes a lot more sense than just saying, ‘If you’re fully vaccinated, go ahead and take off your mask,’” she said.Yet some scientists fear it will be nearly impossible to reimpose mask mandates and other precautions, even in places where it may be a good idea to do so.“It’s difficult to walk that back,” said David Michaels, an epidemiologist and professor at the George Washington School of Public Health, referring to the C.D.C. advice. Yet with the rise of the Delta variant, it also is “extremely dangerous to continue the cultural norm of no one wearing a mask.”Dr. Ezekiel Emanuel, vice president for global initiative at the University of Pennsylvania, said the arrival of the variant should prompt a rethinking of mask mandates.He still wears a mask indoors in public places like grocery stores, and even on crowded city sidewalks. “We don’t know the long-term consequences of even a mild infection,” he said, referring to so-called long Covid. “Is a little more insurance from wearing a mask worth it? Yes.”Sipping coffee outside the Whole Foods Market in downtown Los Angeles on Tuesday morning, Monroe Harmon, 60, said he thought a step back toward masking requirements for everyone might be a good idea.“There’s so many people suggesting that they just want their lives back,” said Mr. Harmon, who works for a security company. “I think you kind of roll the dice when you decide, ‘I want my life back, I’m not going to wear the mask, I’m not going to distance.’”Jill Cowan and Ana Facio-Krajcer contributed reporting from Los Angeles.

The oldest strain of Yersinia pestis — the bacteria behind the plague that caused the Black Death, which may have killed as much as half of Europe’s population in the 1300s — has been found in the remains of a 5,000-year-old hunter-gatherer. A genetic analysis publishing June 29 in the journal Cell Reports reveals that this ancient strain was likely less contagious and not as deadly as its medieval version.
“What’s most astonishing is that we can push back the appearance of Y. pestis 2,000 years farther than previously published studies suggested,” says senior author Ben Krause-Kyora, head of the aDNA Laboratory at the University of Kiel in Germany. “It seems that we are really close to the origin of the bacteria.”
The plague-carrying hunter-gatherer was a 20- to 30-year old man called “RV 2039.” He was one of two people whose skeletons were excavated in the late 1800s in a region called Rinnukalns in present-day Latvia. Soon after, the remains of both vanished until 2011, when they reappeared as part of German anthropologist Rudolph Virchow’s collection. After this re-discovery, two more burials were uncovered from the site for a total of four specimens, likely from the same group of hunter-fisher-gatherers.
Krause-Kyora and his team used samples from the teeth and bone of all four hunter-gatherers to sequence their genomes and then tested them for bacterial and viral pathogens. They were surprised to find evidence of Y. pestis in RV 2039 — and after reconstructing the bacteria’s genome and comparing it to other ancient strains, the researchers determined that the Y. pestis RV 2039 carried was indeed the oldest strain ever discovered. It was likely part of a lineage that emerged about 7,000 years ago, only a few hundred years after Y. pestis split from its predecessor, Yersinia pseudotuberculosis.
“What’s so surprising is that we see already in this early strain more or less the complete genetic set of Y. pestis, and only a few genes are lacking. But even a small shift in genetic settings can have a dramatic influence on virulence,” says Krause-Kyora.
In particular, this ancient strain lacked one crucial thing: the gene that first let fleas act as vectors to spread the plague. This gene was responsible for efficient transmission of the bacterium to human hosts, which resulted in the growth of the infamously grotesque pus-filled buboes in the sick associated with the medieval bubonic plague. Flea-based transmission also required the death of the human host, which means that the appearance of the gene could have driven the evolution of a deadlier disease.
From RV 2039, it likely took more than a thousand years for Y. pestis to acquire all the mutations needed for flea-based transmission. And it’s not clear to what extent RV 2039 experienced the effects of the plague at all.
Y. pestis was found in his bloodstream, meaning he most likely died from the bacterial infection — although, the researchers think the course of the disease might have been fairly slow. They observed that he had a high number of bacteria in his bloodstream at his time of death, and in previous rodent studies, a high bacterial load of Y. pestis has been associated with less aggressive infections. Additionally, the people he was buried near were not infected and RV 2039 was carefully buried in his grave, which the authors say also makes a highly contagious respiratory version of the plague less likely.
Instead, this 5,000-year-old strain likely was transmitted directly via a bite from an infected rodent and probably didn’t spread beyond the infected person. “Isolated cases of transmission from animals to people could explain the different social environments where these ancient diseased humans are discovered. We see it in societies that are herders in the steppe, hunter-gatherers who are fishing, and in farmer communities — totally different social settings but always spontaneous occurrence of Y. pestis cases,” says Krause-Kyora.
These conclusions — that the early form of Y. pestis likely was a slow-moving disease and wasn’t very transmissible — challenge many theories about the development of human civilization in Europe and Asia. For example, some historians have suggested that infectious diseases like Y. pestis evolved mostly in megacities of over 10,000 people near the Black Sea. However, 5,000 years ago — the age of RV 2039’s strain — was long before the formation of large cities. Instead, agriculture was just beginning to appear in Central Europe, and populations were much sparser.
This timeline, plus the less contagious and deadly nature of this early Y. pestis strain, also contradicts the hypothesis that Y. pestis led to the large population declines in Western Europe at the end of the Neolithic Age.
The authors say that examining the history of Y. pestis could also potentially shed light on human genomic history. “Different pathogens and the human genome have always evolved together. We know Y. pestis most likely killed half of the European population in a short time frame, so it should have a big impact on the human genome,” says Krause-Kyora. “But even before that, we see major turnover in our immune genes at the end of the Neolithic Age, and it could be that we were seeing a significant change in the pathogen landscape at that time as well.”
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Materials provided by Cell Press. Note: Content may be edited for style and length.

Langerhans cell histiocytosis (LCH) is a rare cancer involving dendritic cells, a type of white blood cell that usually helps defend against infections. The current standard of care for LCH, chemotherapy, cures fewer than half of patients.
“Our research team focuses on identifying the causes of LCH so that we can develop better therapies for patients,” said Dr. Rikhia Chakraborty, assistant professor of pediatrics — hematology and oncology at Baylor College of Medicine.
Most cells in LCH lesions are not abnormal dendritic cells but other invading immune cells, such as T cells, that are recruited to sites of disease. The contribution of T cells and other immune cells to LCH disease is not known. Chakraborty and her team at the Texas Children’s Cancer Center Histiocytosis Program characterized the types of immune cells in LCH lesions and the activity of those cells.
“We wanted to understand the composition of the immune microenvironment in LCH and why the accessory immune cells are present,” Chakraborty said. “Are they trying to help and can’t? Or are they influenced by diseased dendritic cells to aggravate the situation?”
Understanding the immune microenvironment in LCH
There are two broad categories of T cells: one that battles and kills, called the cytotoxic T cells, and another that assists in keeping the immune system in check, called regulatory T cells. In a study published in the journal Blood, Chakraborty’s team found that both cytotoxic and regulatory T cells are present in increased numbers in LCH lesions. However, the cytotoxic T cells are paralyzed — a state called “exhaustion” — and are ineffective in preventing LCH lesion formation.

Fireworks are synonymous in the United States with the celebration of Independence Day and other special events, but the colorful displays have caused a growing risk to public safety in recent years, according to a study by environmental health researchers at the University of California, Irvine.
Relying on real-time air quality measurements crowdsourced from a network of more than 750 automated sensors distributed throughout California, scientists from UCI’s Program in Public Health found that short-term, extremely high-particulate-matter air pollution from the widespread use of fireworks spiked during the periods of late June through early July in 2019 and 2020.
The increase was most pronounced in Southern California counties where fireworks regulations are less strict than in northern parts of the state and where the illegal use of do-it-yourself pyrotechnics is also more prevalent. This and other findings are the subject of a study published recently in the International Journal of Environmental Research and Public Health.
“You may have seen discussions on social media lately about people worrying for their pets on nights when the skies are filled with exploding fireworks, but we’ve found that there is a real threat to human well-being too,” said co-author Jun Wu, UCI professor of public health. “And like many other environmental justice issues, we find the worst impacts among residents of low-income communities.”
Aerial explosions cause the release of fine particles less than 2.5 micrometers in diameter. Airborne particulate matter of this size is hazardous because when inhaled, it can be absorbed by the lungs and passed to other tissues inside the body. Fireworks get their distinct colors from compounds containing barium, copper, magnesium, potassium and strontium. As rockets burst in the sky, they release these chemicals, trace redox-active metals and water-soluble ions, which inevitably fall on those below.
“These fine particles are known to cause a wide range of adverse health effects, including premature mortality, respiratory and cardiovascular diseases, adverse pregnancy outcomes, and neurological diseases,” Wu said.
The UCI team used data accumulated via a statewide network of PurpleAir sensors, low-cost devices deployed in households. Utilizing this method, the researchers built a high-resolution map tracking levels of airborne particulate matter less than 2.5 micrometers in diameter before, during and after Fourth of July fireworks during the study period.
“The PurpleAir network includes sensors that monitor air continuously, which offers advantages over the traditional monitoring installations that are often positioned away from residential areas and take intermittent measurements that may miss peak days such as the Fourth of July,” said lead author Amirhosein Mousavi, a postdoctoral scholar in UCI’s Program in Public Health. “By taking data from a large, distributed sensor network that’s always collecting data in neighborhoods where people from various socioeconomic profiles live, we were able to get a much clearer characterization of the health risks posed by do-it-yourself fireworks.”
The team found that among all 58 California counties, Los Angeles County experienced the highest daily PM2.5 levels around the Fourth of July holiday in both 2019 and 2020. They believe this was the result of larger numbers of individuals shooting off their own rockets in neighborhoods where they lived, as well as the nature of L.A.’s topography, which has long been known to facilitate the buildup of air pollution.
In addition, researchers believe they detected a COVID-19 effect in their data. PM2.5 concentrations on July 4 and 5 in 2020 were, on average, 50 percent higher than in 2019, likely due to the increased use of household-level fireworks during the pandemic lockdowns.
The team also learned that peak fireworks pollution was two times higher in communities with lower socioeconomic status, larger minority-group populations and higher asthma rates.
“This work highlights the important role that policy and enforcement can play in reducing fireworks-related air pollution and protecting public health,” Wu said. “As there is a patchwork of different restrictions and regulations regarding fireworks in our state, it’s clear that a more coordinated approach would help people breathe easier during times of celebration.”

Combining structural biology and computation, a Duke-led team of researchers has identified how multiple mutations on the SARS-CoV-2 spike protein independently create variants that are more transmissible and potentially resistant to antibodies.
By acquiring mutations on the spike protein, one such variant gained the ability to leap from humans to minks and back to humans. Other variants — including Alpha, which first appeared in the United Kingdom, Beta, which appeared in South Africa, and Gamma, first identified in Brazil — independently developed spike mutations that enhanced their ability to spread rapidly in human populations and resist some antibodies.
The researchers published their findings in Science.
“The spike on the surface of the virus helps SARS-CoV-2 enter into host cells,” said senior author Priyamvada Acharya, Ph.D., director of the Division of Structural Biology at the Duke Human Vaccine Institute.
“Changes on the spike protein determine transmissibility of the virus — how far and quickly it spreads,” Acharya said. “Some variations of the SARS-CoV-2 spike are occurring at different times and different places throughout the world, but have similar results, and it’s important to understand the mechanics of these spike mutations as we work to fight this pandemic.”
Acharya and colleagues — including first author Sophie Gobeil, Ph.D., and co-corresponding author Rory Henderson, Ph.D., — developed structural models to identify changes in the virus’s spike protein. Cryo-electron microscopy allowed atomic level visualization, while binding assays enabled the team to create mimics of the live virus that directly correlated with its function in host cells. From there, the team used computational analysis to build models that showed the structural mechanisms at work.
“By building a skeleton of the spike, we could see how the spike is moving, and how this movement changes with mutations,” Henderson said. “The different variant spikes are not moving the same way, but they accomplish the same task. “The different variant spikes are not moving the same way, but they accomplish the same task. The variants first appearing in South Africa and Brazil use one mechanism, while the UK and the mink variants use another mechanism.”
All the variants showed increased ability to bind to the host, notably via the ACE2 receptor. The changes also created viruses that were less susceptible to antibodies, raising concerns that continued accumulation of spike mutations may reduce the efficiency of current vaccines.
Gobeil said the research illuminated the complexity of the virus: “It’s amazing how many different ways the virus comes up with to be more infectious and invasive,” she said. “Nature is clever.”
In addition to Gobeil, Acharya and Henderson, study authors include Katarzyna Janowska, Shana McDowell, Katayoun Mansouri, Robert Parks, Victoria Stalls, Megan F. Kopp, Kartik Manne, Dapeng Li, Kevin Wiehe, Kevin O. Saunders, Robert J. Edwards, Bette Korber and Barton F. Haynes.
The study received support from the National Institutes of Health (R01 AI145687, AI142596) and the State of North Carolina through the CARES Act.

Mayo Clinic researchers are taking a close look at rare cases of inflammation of the heart muscle, or myocarditis, in young men who developed symptoms shortly after receiving the second dose of the Moderna or Pfizer messenger RNA (mRNA) COVID-19 vaccines. Several recent studies suggest that health care professionals should watch for hypersensitivity myocarditis as a rare adverse reaction to being vaccinated for COVID-19. However, researchers stress that this awareness should not diminish overall confidence in vaccination during the current pandemic.
While reports of post-vaccine myocarditis in some areas are higher than baseline, the imminent and greater risk for heart damage and death continues to be from becoming infected with COVID-19. Up to 60% of people who are seriously ill with COVID-19 experience injury to their heart, and nearly 1% of fit athletes who had a mild COVID-19 infection show myocarditis on an MRI.
A retrospective case series published in JAMA Cardiology studied 23 men in the U.S. military who were hospitalized with myocarditis symptoms within four days of receiving the second dose of a messenger RNA COVID-19 vaccine. Three of the patients previously had been infected with COVID-19, and their symptoms started after the first dose of the vaccine. The cases occurred between January and April. Sixteen had received the Moderna vaccine and seven had received the Pfizer vaccine. For context, it is important to note that the military administered more than 2.8 million doses of messenger RNA COVID-19 vaccines during that time.
All 23 military patients had symptoms of severe chest pain and significantly elevated cardiac troponin levels, which is a protein marker used to measure heart damage. Each patient rapidly recovered, which, combined with the timing and symptoms, supports the diagnosis of hypersensitivity myocarditis. This unusual type of myocarditis is usually related to a drug allergy, but it has been researched in relation to the smallpox vaccine.
“Hypersensitivity myocarditis following vaccination is rare, with the exception of smallpox vaccine. The risk of myocarditis after receiving mRNA vaccine is far less than the risk of myocarditis following actual COVID-19 infection,” says Leslie Cooper, M.D., chair of the Department of Cardiology at Mayo Clinic in Florida. Dr. Cooper is senior author of the study, which was conducted with U.S. military medical centers.
Another observational case study recorded details of eight men between the ages of 21 and 56 who were hospitalized with chest pain and diagnosed with myocarditis by laboratory and cardiac MRI. The patients developed symptoms, starting with a fever, within two to four days of receiving their second dose of a COVID-19 vaccine. One patient who had previously recovered from COVID-19 had symptoms after the first dose. All eight patients in the study recovered from the effects of myocarditis and no longer had chest pain. The findings, co-authored by Dr. Cooper with researchers from Mayo Clinic and other medical institutions in the U.S. and Italy, are published in Circulation.
“People of all ages should choose to get a COVID-19 vaccine because the risks are extremely low compared to the benefits. Additionally, the growing body of research shows that vaccine-associated myocarditis resolves quickly in almost all cases,” says Dr. Cooper.
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Materials provided by Mayo Clinic. Original written by Terri Malloy. Note: Content may be edited for style and length.

Using real-time deformability cytometry, researchers at the Max-Planck-Zentrum für Physik und Medizin in Erlangen were able to show for the first time: Covid-19 significantly changes the size and stiffness of red and white blood cells — sometimes over months. These results may help to explain why some affected people continue to complain of symptoms long after an infection (long Covid).
Shortness of breath, fatigue and headaches: some patients still struggle with the long-term effects of a severe infection by the SARS-CoV-2 coronavirus after six months or more. This post Covid-19 syndrome, also called long covid, is still not properly understood. What is clear is that — during the course of the disease — often blood circulation is impaired, dangerous vascular occlusions can occur and oxygen transport in is limited. These are all phenomena in which the blood cells and their physical properties play a key role.
To investigate this aspect, a team of scientists led by Markéta Kubánková, Jochen Guck, and Martin Kräter from the Max-Planck-Zentrum für Physik und Medizin, the Max Planck Institute for the Science of Light (MPL), the Friedrich Alexander University Erlangen-Nuremberg and the German Centre for Immunotherapy measured the mechanical states of red and white blood cells. “We were able to detect clear and long-lasting changes in the cells — both during an acute infection and even afterwards,” reports Professor Guck, currently managing director of MPL. The research group has now published their results in Biophysical Journal.
To analyse the blood cells, they used a self-developed method called real-time deformability cytometry (RT-DC), which has recently been recognized with the prestigious Medical Valley Award. In this method, the researchers send the blood cells through a narrow channel at high speed. In the process, the leukocytes and erythrocytes are stretched. A high-speed camera records each of them through a microscope, and custom software determines which cell types are present, and how big and deformed they are. Up to 1000 blood cells can be analysed per second. The advantage of the method: It is fast and the cells do not have to be labelled in a laborious procedure.
The method could help as an early warning system to detect future pandemics by unknown viruses
The biophysicists from Erlangen examined more than four million blood cells from 17 patients acutely ill with Covid-19, from 14 people who had recovered and 24 healthy people as a comparison group. They found that, for example, the size and deformability of the red blood cells of patients with the disease deviated strongly from those of healthy people. This indicates damage to these cells and could explain the increased risk of vascular occlusion and embolisms in the lungs. In addition, the oxygen supply, which is one of the main tasks of the erythrocytes, may be impaired in infected persons. Lymphocytes (one type of white blood cell responsible for the acquired immune defense) were in turn significantly softer in Covid-19 patients, which typically indicates a strong immune reaction. The researchers made similar observations for neutrophil granulocytes, another group of white blood cells involved in the innate immune response. These cells even remained drastically altered seven months after the acute infection.
“We suspect that the cytoskeleton of immune cells, which is largely responsible for cell function, has changed,” explains Markéta Kubánková, first author of the research article. In her view, real-time deformability cytometry has the potential to be used routinely in the diagnosis of Covid-19 — and even to serve as an early warning system against future pandemics caused by as yet unknown viruses.
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Materials provided by Max-Planck-Gesellschaft. Note: Content may be edited for style and length.

A recent proof-of-concept study finds that a low-cost training program can reduce hazardous driving in older adults. Researchers hope the finding will lead to the training becoming more widely available.
“On-road training and simulator training programs have been successful at reducing car accidents involving older drivers — with benefits lasting for years after the training,” says Jing Yuan, first author of the study and a Ph.D. student at North Carolina State University. “However, many older adults are unlikely to have access to these training programs or technologies.”
“We developed a training program, called Drive Aware, that would be accessible to anyone who has a computer,” says Jing Feng, corresponding author of the study and a professor of psychology at NC State. “Specifically, Drive Aware is a cognitive training program for older adults to help them accurately detect road hazards. The goal of our recent study was to determine the extent to which Drive Aware influences driving behaviors when trainees actually get behind the wheel.”
To test Drive Aware, the researchers enlisted 27 adults, ages 65 and older. All of the study participants took a baseline driving test in a driving simulator. Nine of the study participants were then placed in the “active training” group. The active training group received two interactive Drive Aware training sessions, about a week apart. Nine other study participants were placed in a “passive training” group. This group watched video of other people receiving the Drive Aware training sessions. This took place twice, with sessions about a week apart. The remaining nine study participants served as the control group and received no training. All 27 study participants then took a second driving test in the driving simulator.
The researchers found that study participants who were part of the active training group had 25% fewer “unsafe incidents” after the training. Unsafe incidents included accidents with other vehicles, pedestrians, running off the road, etc. There was no statistically significant change in the number of unsafe incidents for study participants in the passive training group or the control group.
“In short, we found that older adults were less likely to have an accident in the driving simulator after receiving the Drive Aware training,” Yuan says.
“This testing was done with a fairly modest number of study participants,” Feng says. “If we can secure the funding, we’d like to scale up our testing to more clearly establish how effective this training is at reducing accidents among older drivers. If the results are as good as they look right now, we’d want to find ways to share the training program as broadly as possible. Not many people can afford one-on-one on-the-road training, or training that involves high-end driving simulators. But we think a lot of people would be able to access Drive Aware, and it has the potential to save a lot of lives.”
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Materials provided by North Carolina State University. Original written by Matt Shipman. Note: Content may be edited for style and length.