Publisher Health

Just about everyone knows that exercise is good for you. Some people can even rattle off reasons it keeps your muscles and joints strong, and how it fights off certain diseases. But how many people can tell you the story of why and how physical activity was built into human biology?
A team of evolutionary biologists and biomedical researchers from Harvard are taking a run at it (sometimes literally) in a new study published in PNAS. The work lays out evolutionary and biomedical evidence showing that humans, who evolved to live many decades after they stopped reproducing, also evolved to be relatively active in their later years.
The researchers say that physical activity later in life shifts energy away from processes that can compromise health and toward mechanisms in the body that extend it. They hypothesize that humans evolved to remain physically active as they age — and in doing so to allocate energy to physiological processes that slow the body’s gradual deterioration over the years. This guards against chronic illnesses such as cardiovascular disease, type 2 diabetes, and even some cancers.
“It’s a widespread idea in Western societies that as we get older, it’s normal to slow down, do less, and retire,” said Harvard evolutionary biologist?Daniel E. Lieberman, the paper’s lead author. “Our message is the reverse: As we get older, it becomes even more important to stay physically active.”
The research team, which includes Aaron Baggish and I-Min Lee from Harvard Medical School, believes the paper is the first detailed evolutionary explanation for why lack of physical activity as humans age increases disease risk and reduces longevity.
Baggish, 47, who also serves as team cardiologist for the New England Patriots and U.S. Soccer, and Lieberman, 57, are longtime running buddies and often discussed the ideas that went into the paper during 5-to-10-mile morning runs.

Scientists at Scripps Research in Florida have created a collection of new pain-relieving compounds that, like morphine and other drugs, provide relief via activation of opioid receptors, but without inducing many dangerous and unwanted side-effects that have driven opioid-related overdose and deaths.
Writing Nov. 22 in the journal the Proceedings of the National Academy of Sciences, biochemist Laura Bohn, PhD, and colleagues describe a compound called SR-17018, which activates the same pain-relieving receptor as opioid drugs including morphine, oxycodone and fentanyl; however it binds to opioid receptors in a different way from those drugs, leaving the opioid receptor open and available to the body’s own natural pain-relieving substances, apparently augmenting pain relief. In a study published earlier this year (Pantouli et al., 2021, Neuropharmacolgy), the group showed that the compound performed particularly well in mouse studies of chemotherapy-induced neuropathic pain, the scientists write.
In the current report, the authors have made strides in understanding why these drugs seem so different.
“We demonstrate that these compounds bind to a different site on the receptor than a typical opioid. Because of that, they seem to leave the receptor on and yet still receptive to endogenous opioids,” says Bohn, who chairs the Scripps Research Department of Molecular Medicine in Jupiter, Florida. “In neuropathy pain, we show they are far superior to morphine and oxycodone; moreover, SR-17018 does not decrease breathing.”
The authors also described a related compound that, being more potent, induces respiratory suppression, but at higher doses than are needed to relieve pain. Importantly for safety, this compound, SR-14968, proved responsive to overdose rescue medication naloxone, when given at doses high enough to suppress breathing.
Perhaps most importantly for people with severe chronic pain, SR-17018 showed an ability to provide sustained pain relief over time without development of tolerance, the problem of reduced efficacy over time that requires increased doses, increasing danger of overdose.

Every day, cytologists around the world use optical microscopes to analyze and classify samples of bone marrow cells thousands of times. This method to diagnose blood diseases was established more than 150 years ago, but it suffers from being very complex. Looking for rare but diagnostically important cells is both a laborious and time-consuming task. Artificial intelligence has the potential to boost this method — however it needs a large amount of high-quality data to train an AI algorithm.
Largest open-source database for bone marrow cell images
The Helmholtz Munich researchers developed the largest open access database on microscopic images of bone marrow cells to date. The database consists of more than 170,000 single-cell images from over 900 patients with various blood diseases. It is the result of a collaboration from Helmholtz Munich with the LMU University Hospital Munich, the MLL Munich Leukemia Lab (one of the largest diagnostic providers in this field worldwide) and Fraunhofer Institute for Integrated Circuits.
Using the database to boost artificial intelligence
“On top of our database, we have developed a neural network that outperforms previous machine learning algorithms for cell classification in terms of accuracy, but also in terms of generalizability,” says Christian Matek, lead author of the new study. The deep neural network is a machine learning concept specifically designed to process images. “The analysis of bone marrow cells has not yet been performed with such advanced neural networks,” Christian Matek explains, “which is also due to the fact that high-quality, public datasets have not been available until now.”
The researchers aim to further expand their bone marrow cell database to capture a broader range of findings and to prospectively validate their model. “The database and the model are freely available for research and training purposes — to educate professionals or as a reference for further AI-based approaches e.g. in blood cancer diagnostics,” says study leader Carsten Marr.
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After studying the effectiveness of varying layers of masks in stopping respiratory droplets from escaping face masks, a team of international researchers has now turned their attention to modeling what happens to droplets when they come in contact with wet masks. Their results show that damp masks are still effective at stopping these droplets from escaping the mask and being atomized into smaller, easier-to-spread aerosolized particles.
This study only investigated the effects of wet masks on droplet penetration; the researchers note that people should follow public health guidance to change their mask if it is wet, since wet masks are harder to breathe through, less efficient at filtering inhaled air, and can vent more around the edge of the mask than dry masks.
“While the efficacies of various dry face masks have been explored, a comprehensive investigation of wet masks is lacking. Yet, users wear masks for long periods of time, and during this time the mask matrix becomes wet due to respiratory droplets released from breathing, coughing, sneezing etc,” wrote the team of engineers from the University of California San Diego, Indian Institute of Science, and University of Toronto. The researchers presented their findings on Nov. 21 at the American Physical Society’s 74th Annual Meeting of the APS Division of Fluid Dynamics. The same paper will be published in Physical Review Fluids on Dec. 7.
They found that, perhaps counterintuitively, wet masks actually make it more difficult for these respiratory droplets to penetrate and escape the mask, splintering into smaller, aerosolized particles; research has shown that these smaller particles are more likely to spread the SARS-CoV-2 virus by lingering in the air longer than the larger droplets that fall to the ground. In modeling the physics behind why this happens, they discovered that two very different mechanisms are present for hydrophobic masks like common surgical masks, versus hydrophilic masks like the cloth varieties.
To study exactly how wetness impacts droplet penetration, the researchers generated mock respiratory droplets using a syringe pump, which slowly pushed liquid through a needle and onto one of three types of mask materials: a surgical mask, and two cloth masks of different thicknesses. The researchers recorded what happened as the droplets hit the mask using a high-speed camera capturing the impact at 4,000 frames per second, and continued to study it as the mask became damp.
They found that droplets from a cough or sneeze have to be traveling at a higher velocity to be pushed through a mask when wet, compared to when it’s dry. On hydrophobic masks with low absorptivity,like surgical masks, the respiratory droplets form small beads on the mask’s surface, providing additional resistance for the impacted droplets against possible penetration.
The hydrophilic cloth masks do not exhibit this beading; instead, the cloth absorbs the liquid, with the wetted area spreading as the mask absorbs more volume. The porous matrix of these cloth masks become filled with liquid, and the droplets are therefore required to displace a larger volume of liquid to penetrate the mask. Due to this additional resistance, penetration is weaker.
“In summary, we showed that wet masks are capable of restricting ballistic respiratory droplets better than dry masks,” said Sombuddha Bagchi, first author of the paper and a mechanical engineering PhD student at the Jacobs School of Engineering at UC San Diego.
“However, we also need to pay attention to side leakage and breathability of wet masks, which were not investigated in our study,” added Abhishek Saha, a co-author and professor of Mechanical and Aerospace Engineering at UC San Diego.
The team of engineers — which also includes Professors Swetaprovo Chaudhuri from University of Toronto, and Saptarshi Basu of the Indian Institute of Science — were well-versed in this type of experiment and analysis, though they were used to studying the aerodynamics and physics of droplets for applications including propulsion systems, combustion, or thermal sprays. They turned their attention to respiratory droplet physics last year when the COVID-19 pandemic started, and since then, have been studying the transport of these respiratory droplets and their roles in transmission of Covid-19 type diseases.
In March 2021, this same team published a paper in Science Advances detailing the effectiveness of dry masks of one, two, and three layers in stopping respiratory droplets from penetrating the mask. Using a similar methodology to this wet mask experiment, they showed that three-layered surgical masks are most effective at stopping large droplets from a cough or sneeze from getting atomized into smaller droplets. These large cough droplets can penetrate through the single- and double-layer masks and atomize to much smaller droplets, which is particularly crucial since these smaller aerosol droplets are able to linger in the air for longer periods of time.

Poor sleep in the over 50s is linked to more negative perceptions of ageing, which in turn can impact physical, mental and cognitive health, new research has revealed.
A study led by the University of Exeter and found that people who rated their sleep the worst also felt older, and perceived their own physical and mental ageing more negatively.
Lead author Serena Sabatini, of the University of Exeter, said: “As we age, we all experience both positive and negative changes in many areas of our lives. However, some people perceive more negative changes than others. As we know that having a negative perception of ageing can be detrimental to future physical health, mental health, and cognitive health, an open question in ageing research is to understand what makes people more negative about ageing. Our research suggests that poor sleepers feel older, and have a more negative perception of their ageing. We need to study this further – one explanation could be that a more negative outlook influences both. However, it could be a sign that addressing sleep difficulties could promote a better perception of ageing, which could have other health benefits.”
Researchers surveyed 4,482 people aged 50 and over who are part of the PROTECT study. Run by the University of Exeter and the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King’s College London, and funded by the National Institute for Health Research (NIHR) Maudsley Biomedical Research Centre, PROTECT is an innovative online study in which participants take regular cognitive tests and complete lifestyle questionnaires. The study aims to understand what helps people stay cognitively healthy in later life.
The research team noticed that many PROTECT participants were commenting on their relationship with sleep as part of standard questionnaires within the study. Comments included: “How I feel fluctuates widely depending on my sleep. I feel great if I get six hours so about half the time I feel younger and half the time I feel older!”
Another comment read: “I have chronic pain problems and get very little sleep which impacts on my life quite a lot.”
As a result of such comments, the team decided to conduct a questionnaire looking specifically at sleep. In the research, published in Behavioral Sleep Medicine, participants were asked whether they had experienced a list of negative age-related changes, such as poorer memory, less energy, increased dependence on the help of others, decreased motivation, and having to limit their activities. They also rated their quality of sleep. The participants completed both questionnaires twice, one year apart.
Professor Clive Ballard, of the University of Exeter, said: “This research is an important part of the growing body of evidence about the crucial role of sleep in healthy ageing. We now need more people to sign up to PROTECT, to help us understand this further. We’ve got some exciting trials ahead on how to optimise sleep in some particularly vulnerable groups, such as people with dementia in care homes.”
The paper is entitles ‘Cross-Sectional and Longitudinal Associations between Subjective Sleep Difficulties and Self- Perceptions of Aging’, published in Behavioral Sleep Medicine. The research is the result of a PhD funded by the Australian National Health and Medical Research Council Centre for Research Excellence in Cognitive Health.
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Identical twins share the same DNA, but one twin can suffer from type 2 diabetes while the other twin does not develop the disease. A study led by Lund University in Sweden has now discovered that there are differences in gene activity in twins where only one sibling had developed the disease. The researchers’ discovery could contribute to the development of new treatment methods.
“Identical twins have the same genetic background, sex and age, and they are therefore interesting to study for researchers seeking to understand the mechanisms behind diseases. We found an epigenetic change in twins with type 2 diabetes which provides us with new clues to the disease,” says Emma Nilsson, researcher in epigenetics and diabetes at Lund University, and one of the principal authors behind the study.
For the study, 14 pairs of twins from Sweden and Denmark were recruited. Among the sibling pairs, one of the identical twins had developed type 2 diabetes. The average age of the participants was 68 years and the twins who had developed diabetes had a somewhat higher BMI compared to their sibling.
Epigenetic changes occur through DNA methylation, among other things, a chemical process that controls the function of the genes. The process is affected by various environmental factors, such as diet, exercise and stress. The researchers analysed DNA methylation and microRNA in fat biopsies from the pairs of twins to increase their knowledge about why only one twin had developed type 2 diabetes. MicroRNA regulates the production of proteins in the cells.
The researchers’ analyses showed that a gene responsible for producing a specific microRNA, microRNA-30, was less active in the twins with type 2 diabetes. This led to them having lower levels of microRNA-30 in their fatty tissue than their sibling. The same pattern was present in the control group, which consisted of 28 people with type 2 diabetes and 28 people without the disease. The participants in the control group were not biologically related to one another.
“We were able to confirm our results in individuals with no twin siblings and this proves that our results are relevant to all people and not only to identical twins,” says Emma Nilsson.
The researchers also conducted experiments in which they reduced the amount of microRNA-30 in cultured fat cells, to see how it affected the cells’ ability to take up glucose.
In type 2 diabetes, the body becomes worse at processing blood sugar. This is partly due to the cells having become less sensitive to insulin. Insulin resistance causes an increase in blood sugar levels. The researchers’ experiment showed that cells with a smaller amount of microRNA-30 also had a reduced ability to take up glucose.
“We see the same pattern in people with type 2 diabetes. The study is an importance piece of the puzzle in our work to understand the mechanisms behind type 2 diabetes. The more pieces of the puzzle we find, the better the new drugs we can develop,” says Emma Nilsson.
Increased knowledge about the mechanisms behind the disease could lead to more effective treatment of type 2 diabetes. Many patients experience side-effects, or find it difficult to achieve good control of their blood sugar with the drugs currently available. The researchers plan to follow up on their findings in forthcoming studies.
“Our study could be a step on the way to new treatment options in which microRNA is used as an active substance in drugs to treat patients with type 2 diabetes. Clinical studies are already underway in which microRNA is being tested as a drug against cancer, for example,” concludes Emma Nilsson.
The study, which is published in the journal Diabetes, was conducted in collaboration between researchers from Lund University, Sahlgrenska University Hospital in Sweden and Steno Diabetes Centre in Denmark.
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A research team at the University of Washington has developed a wearable device to detect and reverse an opioid overdose. The device, worn on the stomach like an insulin pump, senses when a person stops breathing and moving, and injects naloxone, a lifesaving antidote that can restore respiration.
The results demonstrate the proof-of-concept of a wearable naloxone injector system, according to the paper published Nov. 22 in Scientific Reports.
“The opioid epidemic has become worse during the pandemic and has continued to be a major public health crisis,” said lead author Justin Chan, a UW doctoral student in the Paul G. Allen School of Computer Science & Engineering. “We have created algorithms that run on a wearable injector to detect when the wearer stops breathing and automatically inject naloxone.”
Co-author Jacob Sunshine, an associate professor of anesthesiology and pain medicine at the UW School of Medicine, said one of the unique aspects of opioid overdoses is that naloxone, a benign drug, is highly effective and can save lives if it can be administered in a timely fashion.
The UW team is looking to make these devices widely available, which would first require approval by the U.S. Food and Drug Administration. The FDA is currently working to accelerate efforts to address this critical public health problem and has recently published special guidance on emergency-use injectors.
In a multiyear collaboration, the UW investigators worked on the prototype with West Pharmaceutical Services of Exton, Penn, which developed a wearable subcutaneous injector that safely administers medications.

Accurately assessing the exposure of a population to a particular virus is difficult because the tools for doing so do not account for the fact that many viruses comprise multiple circulating strains, or the fact that people can be vaccinated or naturally immune, among other factors. Using influenza as a model, a team of researchers led by Penn State has developed a new technique that overcomes many of these roadblocks, and they say the tool may be useful for better assessments of exposure to a variety of viruses, including the ones that cause COVID-19 and pneumonia.
“Without an accurate picture of a population’s exposure to a particular virus, we cannot effectively plan and implement public health interventions,” said Maciej Boni, associate professor of biology who led the study.
In their study, which appeared on Nov. 18 in the journal Nature Communications, the researchers specifically investigated the attack rate for human influenza A virus in a tropical setting, which comprises two subtypes — H3N2 and H1N1 — and multiple strains.
According to Boni, an attack rate is an estimate of how many people have been infected with a particular disease, regardless of whether they had symptoms or whether they were tested or not.
“Accurately estimating the attack rate of a virus sounds like something epidemiologists should be able to do quite easily,” he said, “but there are at least four major complications. First, you need to pre-plan collections of blood samples, otherwise there’s no way to get a snapshot of who in the population right now has antibodies and who doesn’t. Second, when testing for antibodies, you cannot always differentiate someone who was infected from someone who was vaccinated. Third, antibodies wane, so you may not be able to tell if someone was infected if their antibody levels are low now. Finally, many pathogens circulate as groups of strains or groups of variants, and there may be no laboratory assay to test for general exposure to any of these variants.”
The team, which included researchers from Vietnam and the Netherlands, created a new method that resolves many of these problems and presents accurate general-population, attack-rate estimates for influenza A virus. To conduct their study, the researchers used a dataset of 24,402 general-population serum — or blood plasma — samples collected in central and southern Vietnam between 2009 to 2015 and assayed the samples for antibodies to eleven different strains of human influenza A, including the 1918 pandemic ‘Spanish Flu’ strain and the 2009 ‘swine flu’ pandemic virus strain, which are within the H1N1 subtype. Next, they used this large set of antibody measurements to derive a ‘composite antibody measurement’ across both subtypes of influenza and across all the different strains.

Volcanic gases are helping researchers track large-scale movements in Earth’s deep interior.Woods Hole Oceanographic Institution (WHOI) scientists, together with a group of international collaborators, have discovered anomalous geochemical compositions beneath Panama.
This interdisciplinary team used helium isotopes and other geochemical data from fluids and rocks to show that volcanic material is sourced from the Galapagos plume, over 900 miles (1500 km) away. The findings of this study, “High 3He/4He in central Panama reveals a distal connection to the Galápagos plume,” were published today in the journal Proceedings of the National Academy of Sciences.
“The lateral transport of plume material represents an understudied mechanism that scatters enriched geochemical signatures in mantle domains far from plumes,” said David Bekaert, postdoctoral scholar at WHOI, and lead author of the paper.
“We can compare volcanic systems to the body of a living organism; when the organism bleeds, it’s kind of like magma bleeding out of the Earth. And you can measure the composition of that magma, just like you can measure a blood type. In this study, we measured an unexpected volcanic gas composition, sort of like when a human has a rare blood type. In the case of the Earth, we then try to explain where it came from in terms of deep geological processes.”
The team showed that relatively hot material originating from Earth’s deep interior travels laterally through the shallow mantle, similar to wind blowing at Earth’s surface. Chemical observations were combined with geophysical imaging of Earth’s deep interior to pinpoint the source and direction of this so-called “mantle wind.”
Typically, material cannot easily pass through a subduction zone, where the edge of a tectonic plate, called a “slab,” acts as a barrier. However, the region beneath Panama is unusual in that there appears to be a “slab window” that allows this mantle wind to blow through. Overall, this study tells us that, even after billions of years of evolution, our planet remains a dynamic system marked by large-scale movements of solid material, miles beneath our feet.
“Exotic volcanic chemical features have previously been documented in Central America. We use these chemical characteristics as indicators for large geological processes. In this case, our findings help explain why plume-derived volcanic material shows up in central Panama, even though there are no active volcanoes there,” added Bekaert.
“Our work suggests that small bits of deep mantle material were carried by ‘mantle wind’ blowing through the window in the subduction zone. Broadly speaking, this informs us about the nature and extent of large-scale mixing processes that contribute to the heterogeneous, or diversified, nature of the solid Earth” said Peter Barry, assistant scientist at WHOI and senior author of the paper.
Many of the study’s samples were collected over the past 15 years, but only in light of the insights from other disciplines of geoscience — such as geophysics and lava studies — did the message from helium isotopes become clear.
The geochemical composition of Earth’s interior is highly diverse. It has been well established that rising plumes of superheated rock in Earth’s mantle are the main channels for transporting geochemically enriched material deep underground, but the extent to which lateral flow processes disperse mantle material far from vertical plumes, remains widely unknown. The finding of lateral transport of deep, exotic material across the Earth’s interior could have far-reaching implications for scientist’s understanding of the chemical evolution of our planet over geological time.

Infections with the novel coronavirus and vaccination lead to strong antibody responses against SARS-CoV-2. Immune responses to other human coronaviruses, which mostly only cause harmless colds, also provide some protection against SARS-CoV-2. This cross-reactive immune response is an important piece of the puzzle of how to achieve comprehensive coronavirus immunity, researchers at the University of Zurich have shown.
The population’s immunity to SARS-CoV-2, achieved either through infection or vaccination, is crucial to overcome the COVID-19 pandemic. A team of researchers led by the University of Zurich (UZH) has now discovered another component that contributes to SARS-CoV-2 immunity — previous antibody responses to other, harmless coronaviruses. “People who have had strong immune responses to other human coronaviruses also have some protection against SARS-CoV-2 infection,” says Alexandra Trkola, head of the Institute of Medical Virology at UZH.
In their study, the researchers used a specially developed assay to analyze antibody levels against four other human coronaviruses in 825 serum samples taken before SARS-CoV-2 emerged. They also examined 389 samples from donors infected with SARS-CoV-2. Combining these analyses with computer-based models enabled the team to precisely predict how well the antibodies would bind to and neutralize invading viruses.
Cross-reactivity reduces severity of infection
The researchers were able to demonstrate that people who caught SARS-CoV-2 had lower levels of antibodies against coronaviruses that cause common colds compared to uninfected people. In addition, people with high levels of antibodies against harmless coronaviruses were less likely to have been hospitalized after catching SARS-CoV-2. “Our study shows that a strong antibody response to human coronaviruses increases the level of antibodies against SARS-CoV-2. So someone who has gained immunity to harmless coronaviruses is therefore also better protected against severe SARS-CoV-2 infections,” says Trkola. This type of immune response is referred to as cross-reactivity, and it also occurs with T cell responses, the additional line of the immune system in the defense against infections.
People are only fully protected against SARS-CoV-2 shortly after they have recovered from an infection or have received an effective vaccination. This is when antibody levels against the virus are still very high. As these levels drop over time, infection is no longer prevented, but the immunological memory quickly reactivates the body’s defenses, the production of antibodies as well as the T cell defense. “Of course, immune responses targeting SARS-CoV-2 that are mounted by the memory cells are far more effective than cross-reactive responses. But even though the protection isn’t absolute, cross-reactive immune responses shorten the infection and reduce its severity. And this is exactly what is also achieved through vaccination, just much, much more efficiently,” says Trkola.
Towards comprehensive protection against coronaviruses
It is not yet known whether this cross-reactivity also works in the opposite direction. Whether immunity to SARS-CoV-2 — achieved through vaccination, for example — also offers protection against other human coronaviruses still needs to be elucidated. “If SARS-CoV-2 immunity also offers some degree of protection from infection with other coronaviruses, we would be a significant step closer to achieving comprehensive protection against other coronaviruses, including any new variants,” the virologist explains. This idea is also supported by the fact that cross-reactive protection is not only based on antibodies, but very likely also on T cells.
Funding
The study was funded through the Pandemic Fund of the University of Zurich, the Swiss Red Cross, the University Hospital Zurich, the Swiss National Science Foundation and Gilead.
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