Publisher Health

Headlines proclaiming Covid lockdowns drastically reduced pollution were mostly referring to nitrogen dioxide, NO2, a reactive gas emitted from burning fuel. There had been less understanding of how lockdowns affected PM2.5, tiny particulate matter that can penetrate a person’s lungs, leading to a host of health problems, including increased risk for heart attack and cancer.
“PM2.5 is the leading global environmental determinant of longevity. It is a key pollutant of concern for health,” said Randall Martin, the Raymond R. Tucker Distinguished Professor in the Department of Energy, Environmental & Chemical Engineering in the McKelvey School of Engineering at Washington University in St. Louis.
New research from Martin’s lab, in collaboration with the Goddard Space Flight Center, California Institute of Technology and Dalhousie University in Nova Scotia, mapped PM2.5 levels across China, Europe and North America. Using satellite data, ground-based monitoring and an innovative computer modeling system, researchers found mostly slight changes in PM2.5 — with one exception.
The majority of changes they found were not driven by lockdown, but by the natural variability of meteorology. Their results were published June 23 in the journal Science Advances.
The meteorological effects that we experience everyday also affect PM2.5 variability, Martin said.
“The shorter time period, the more susceptible PM2.5 is to meteorology,” he said.

Researchers at the RIKEN Center for Brain Science and the RIKEN BioResource Research Center in Japan, along with collaborators at the State University of New York at Buffalo, have created a mouse model that allows the study of naturally occurring melatonin. Published in the Journal of Pineal Research, these first experiments using the new mice showed that natural melatonin was linked to a pre-hibernation state that allows mice to slow down their metabolism and survive when food is scarce, or temperatures are cold.
Melatonin is called “the hormone of darkness” because it’s released by the brain in the dark, which usually means at night. It tells the body when it’s dark outside so that the body can switch to ‘night mode’. Although other hormones are easily studied in the laboratory, it has been difficult to study how the body reacts to melatonin because laboratory mice don’t actually have any. To solve this problem, the researchers crossed laboratory mice with wild mice — which do produce melatonin — and bred new lab mice that can produce melatonin innately. This was a lot harder than it sounds and took over 10 mouse generations.
Once they had melatonin-producing lab mice, the researchers were able to study how the hormone affects entrainment — the alignment of the body clock with the outside world. Mice like to run on wheels regularly, and researchers can use this to measure entrainment after suddenly changing the light/dark cycle, which mimics sudden changes in times zones. Compared with regular lab mice, the mice with innate melatonin adapted their wheel running times faster to darkness starting six hours earlier, similar to ‘east-bound jet lag’.
The researchers were also able to resolve a debate about whether life span is affected by melatonin, which has been hard to study because of the missing melatonin in lab mice. “Now we finally have an answer: endogenous melatonin has no life-extending effects,” says Takaoka Kasahara, a senior author of the new study.
Despite many similarities, mice with innate melatonin differed from regular lab mice in several ways. The regular lab mice were heavier, had bigger reproductive organs, and were more successful at mating, producing more pups. On the other hand, melatonin-producing female mice were able to enter a state called daily torpor, a kind of low-power mode similar to hibernation that can last for a few hours a day. Daily torpor is a way for mice to deal with food scarcity and cold temperatures by conserving energy.
“There is an evolutionary advantage to producing melatonin, because it protects wild mice from losing weight when they can’t find enough food. Lab mice, however, are typically given unlimited food and live in warm cages,” Kasahara observes. “Our finding that mice lacking melatonin are more successful at reproducing can explain why lab mice lack melatonin. Over the years, by selecting for mice that reproduce the most pups, we might have also been inadvertently selecting for mice with lower and lower levels of melatonin.”
Having shown that melatonin can affect circadian rhythms, the specially bred melatonin-proficient mice will be valuable for studying the detailed molecular and neural mechanisms of melatonin signaling on the circadian clock and sleep, as well as the effects of melatonin on immunity and bone formation. These relationships have been suggested, but have not yet been closely examined.
Further research on melatonin’s relationship with daily torpor and hibernation is also important. Melatonin is necessary for seasonal reproduction in several animals, signaling the length of the night, which indicates the season. “This research could very well lead to a better understanding of seasonal affective disorder, or winter depression, in humans,” says Kasahara. “Indeed, one of the newest antidepressants, agomelatin, activates melatonin receptors.”
The study was authored by the following researchers: Chongyang Zhang, Shannon J. Clough, Ekue B. Adamah-Biassi, Michele H. Sveinsson, Anthony J Hutchinson, Ikuo Miura, tamio Furuse, Shigeharu Wakana, Yui K. Matsumoto, Kazuo Okanoya , Randall L. Hudson, Tadafumi Kato, Margarita L. Dubocovich , and Takaoki Kasahara
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National Institutes of Health scientists and their collaborators have identified an internal communication network in mammals that may regulate tissue repair and inflammation, providing new insights on how diseases such as obesity and inflammatory skin disorders develop. The new research is published in Cell.
The billions of organisms living on body surfaces such as the skin of mammals — collectively called microbiota — communicate with each other and the host immune system in a sophisticated network. According to the study, viruses integrated in the host genome, remnants of previous infections called endogenous retroviruses, can control how the host immune system and the microbiota interact, affecting tissue repair and antimicrobial defenses. Endogenous retroviruses can comprise up to 10% of all genes.
The newly discovered role of endogenous retroviruses adds to the scientific community’s understanding of certain diseases and inflammatory states and opens new research avenues. “Together, our results support the idea that mammals may have co-opted their endogenous viromes as a means to communicate with their microbiota, resulting in a multi-kingdom dialogue that controls both immunity and inflammation,” the authors state.
Scientists from NIH’s National Institute of Allergy and Infectious Diseases led the project with collaborators from the NIH Center for Human Immunology, the National Cancer Institute, Stanford University and Scripps Research in California, University of Pennsylvania in Philadelphia, University of Oxford, and The Francis Crick Institute in England.
Building on a series of studies over the past decade showing that microbiota broadly promote immune protection, the NIAID scientists and collaborators sought to discover how this occurs. They used Staphylococcus epidermidis, a common skin bacterium with known helpful and harmful features, as a study model in laboratory and mouse experiments.
The models helped them identify the important roles of skin cells called keratinocytes and of endogenous retroviruses in communication between microbiota and the skin immune system. Keratinocytes are the primary interface between the host and its microbiota. Their study showed that S. epidermidis triggered an antiviral response in keratinocytes, and that finding led them to discover that endogenous retroviruses coordinate responses to the microbiota that stimulate the immune system.
The mouse model also showed that a high-fat diet triggers an inflammatory immune response to S. epidermidis that can be controlled by providing antiretroviral treatment, suggesting a role for endogenous retroviruses in driving inflammatory responses caused by microbes under high-fat conditions. The researchers will continue exploring how these ancient viruses control the beneficial role of the microbiota and how nutrition can change this dialogue toward pro-inflammatory responses.
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Researchers from Charité — Universitätsmedizin Berlin and the University of California in San Francisco were able to show for the first time that a very low calorie diet significantly alters the composition of the microbiota present in the human gut. In a current Nature publication, the researchers report that dieting results in an increase of specific bacteria — notably Clostridioides difficile, which is associated with antibiotic-induced diarrhea and colitis. These bacteria apparently affect the body’s energy balance by exerting an influence on the absorption of nutrients from the gut.
The human gut microbiome consists of trillions of microorganisms and differs from one person to the next. In persons who are overweight or obese, for instance, its composition is known to be different to that found in individuals with a normal body weight. Many of us will, at some point in our lives, try dieting in order to lose weight. But what effect does such a drastic change in diet have on our bodies? An international team of researchers co-led by Charité has addressed this question. “For the first time, we were able to show that a very low calorie diet produces major changes in the composition of the gut microbiome and that these changes have an impact on the host’s energy balance,” says Prof. Dr. Joachim Spranger, Head of Charité’s Department of Endocrinology and Metabolic Diseases and one of the study’s lead authors.
To explore the effects of dieting, the team studied 80 older (post-menopausal) women whose weight ranged from slightly overweight to severely obese for a duration of 16 weeks. The women either followed a medically supervised meal replacement regime, consuming shakes totaling less than 800 calories a day, or maintained their weight for the duration of the study. The participants were examined at the Experimental and Clinical Research Center (ECRC), a facility jointly operated by Charité and the Max Delbrück Center for Molecular Medicine (MDC). Regular stool sample analysis showed that dieting reduced the number of microorganisms present in the gut and changed the composition of the gut microbiome. “We were able to observe how the bacteria adapted their metabolism in order to absorb more sugar molecules and, by doing so, make them unavailable to their human host. One might say we observed the development of a ‘hungry microbiome’,” says the study’s first author, Dr. Reiner Jumpertz von Schwartzenberg, a researcher and clinician at the Department of Endocrinology and Metabolic Diseases whose work on the study was funded by the Clinician Scientist program operated by Charité and the Berlin Institute of Health (BIH).
Stool samples, which had been collected before and after dieting, were then transferred into mice which had been kept under germ-free conditions and, as a result, lacked all gut microbiota. The results were staggering: Animals which received post-dieting stools lost more than 10 percent of their body mass. Pre-diet stools had no effect whatsoever. “Our results show that this phenomenon is primarily explained by changes in the absorption of nutrients from the animals’ guts,” says Prof. Spranger. He adds: “This highlights the fact that gut bacteria have a major impact on the absorption of food.”
When the researchers studied stool composition in greater detail, they were particularly struck by signs of increased colonization by a specific bacterium — Clostridioides difficile. While this microorganism is commonly found in the natural environment and in the guts of healthy human beings and animals, its numbers in the gut can increase in response to antibiotic use, potentially resulting in severe inflammation of the gut wall. It is also known as one of the most common hospital-associated pathogens. Increased quantities of the bacterium were found both in participants who had completed the weight loss regimen and in mice which had received post-dieting gut bacteria. “We were able to show that C. difficile produced the toxins typically associated with this bacterium and that this was what the animals’ weight loss was contingent upon,” explains Prof. Spranger. He adds: “Despite that, neither the participants nor the animals showed relevant signs of gut inflammation.”
Summing up the results of the research, Prof. Spranger says: “A very low calorie diet severely modifies our gut microbiome and appears to reduce the colonization-resistance for the hospital-associated bacterium Clostridioides difficile. These changes render the absorption of nutrients across the gut wall less efficient, notably without producing relevant clinical symptoms. What remains unclear is whether or to which extent this type of asymptomatic colonization by C. difficile might impair or potentially improve a person’s health. This has to be explored in larger studies.” Results from the current study, which also received funding from the German Center for Cardiovascular Disease (DZHK), might even give rise to treatment options for metabolic disorders such as obesity and diabetes. For this reason, the researchers will now explore how gut bacteria might be influenced in order to produce beneficial effects on the weight and metabolism of their human hosts.
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A typical Western high-fat diet can increase the risk of painful disorders common in people with conditions such as diabetes or obesity, according to a groundbreaking paper authored by a team led by The University of Texas Health Science Center at San Antonio, also referred to as UT Health San Antonio.
Moreover, changes in diet may significantly reduce or even reverse pain from conditions causing either inflammatory pain — such as arthritis, trauma or surgery — or neuropathic pain, such as diabetes. The novel finding could help treat chronic-pain patients by simply altering diet or developing drugs that block release of certain fatty acids in the body.
The paper, more than five years in the making, was published in the June edition of the journal Nature Metabolism by a collaborative team of 15 local researchers, headed by first co-authors Jacob T. Boyd, MD, PhD, and Peter M. LoCoco, PhD, of the Department of Endodontics at UT Health San Antonio.
In all, 11 of the co-authors are from UT Health San Antonio, including seven current or former students of its Graduate School of Biomedical Sciences; three represent the Department of Chemistry at the University of Texas at San Antonio; and one is from the Department of Neurology with the South Texas Veterans Health Care System.
“This study exemplifies team science at its best — multiple scientists and clinicians with complementary expertise working together to make lives better,” said Kenneth M. Hargreaves, DDS, PhD, professor and chair of the Department of Endodontics at UT Health San Antonio, and senior author of the paper.
Fatty acids and pain
Chronic pain is a major cause of disability around the world. But although fat-reduction often is advised to manage diabetes, auto-immune disorders and cardiovascular diseases, the role of dietary lipids, or fatty acids, in pain conditions has been relatively unknown.

The Queen has held her first in person meeting with the UK Prime Minister Boris Johnson in more than a year. Mr Johnson said it had been 15 months since the pair last met. HRH Queen Elizabeth II said she’d been talking to the Secretary of State for Health, Matt Hancock, calling him a “poor man”.

During the COVID-19 pandemic, cloth face masks became a way to help protect yourself and others from the virus. And for some people, they became a fashion statement, with many fabric choices available. But just how effective are they, especially in containing a sneeze? Now, researchers reporting in ACS Biomaterials Science & Engineering used high-speed videos of a person sneezing to identify the optimal cloth mask design.
Early in the pandemic, worldwide shortages of surgical masks and N95 respirators led many people to make or purchase cloth face masks. Now, with safe and effective COVID-19 vaccines available, mask restrictions are easing in many states. However, face masks will likely still be required in certain settings for a while, especially with possible vaccine-resistant variants emerging. They might also be useful in future pandemics. Face masks help reduce disease spread by blocking tiny, virus-laden droplets expelled through the nose and mouth when a person speaks, coughs or sneezes. A few studies have examined the effectiveness of various fabrics for blocking droplets and aerosols made by a machine, but until now, none have been conducted under the explosive conditions of a real human sneeze. Shovon Bhattacharjee, Raina MacIntyre and colleagues at the University of New South Wales wanted to see how well masks made of various fabrics and layers blocked respiratory droplets from the sneezes of a healthy adult.
The researchers made simple face masks with 17 commonly available fabrics. Each mask had one, two or three layers of the same or different fabrics. A healthy 30-year-old volunteer donned each mask, tickled the inside of his nose with tissue paper on a cotton swab, and then readjusted the mask just before the onset of a sneeze. The researchers captured high-speed videos of the sneezes and computed the intensity of droplets in the images in a region 2 cm from his mouth. With each fabric layer, the droplet-blocking capability improved by more than 20-fold. Interestingly, all of the three-layer cloth combinations the researchers tested were more effective than a three-layer surgical mask. The best masks for blocking droplets contained a hydrophilic inner layer of cotton or linen, an absorbent middle layer of a cotton/polyester blend and a hydrophobic outer layer of polyester or nylon. Machine washing the masks didn’t decrease their performance; in fact, masks containing cotton or polyester worked slightly better after washing because of pore shrinkage. Future studies are planned with more people and different age groups, the researchers say.
The authors acknowledge funding from the National Health and Medical Research Council of the Australian Government and the University of New South Wales (UNSW) Scientia Ph.D. Scholarship.
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Pairing blueberry pie with a scoop of ice cream is a nice summer treat. Aside from being tasty, this combination might also help people take up more of the “superfruit’s” nutrients, such as anthocyanins. Researchers reporting in ACS’ Journal of Agricultural and Food Chemistry show that α-casein, a protein found in cow’s milk, helped rats absorb more blueberry anthocyanins and their byproducts, boosting accessibility to these good-for-you nutrients.
In studies, anthocyanins have been shown to have antioxidant properties, lower blood pressure and reduce the risk of developing some cancers. However, only small amounts of these nutrients are absorbed from blueberries during digestion, despite their abundance in the fruit. Previous researchers have reported that consuming foods with ingredients such as citrus pectin, capcasin, capsicate and some proteins improve the uptake of anthocyanins. For instance, Bin Li and colleagues found that α-casein and β-casein proteins from cow’s milk protected blueberry anthocyanins in simulated digestion experiments. Now, this team wanted to see whether α-casein could help increase the absorption of blueberry anthocyanins in vivo.
The researchers fed rats purified blueberry anthocyanin extracts, adding α-casein to the solution given to one group of rats. During the next 24 hours, anthocyanin and metabolite concentrations were 1.5 to 10.1 times higher in the α-casein group than in the control rats. When examining α-casein’s molecular structure, the researchers observed that its amino acids allowed it to interact with and encapsulate the anthocyanin molecules, improving their stability in the intestines and allowing for better transport into the bloodstream. While the α-casein protein used in these experiments was derived and purified from milk, the results may not be the same for whole milk because its fats and sugars could impact absorption, the researchers explain. They say their next step is to conduct similar tests with human subjects.
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For patients who have inflammatory bowel syndrome (IBS), the condition is literally a pain in the gut. Chronic — or long-term — abdominal pain is common, and there are currently no effective treatment options for this debilitating symptom. In a new study in ACS Pharmacology & Translational Science, researchers identify a new potential source of relief: a molecule derived from spider venom. In experiments with mice, they found that one dose could stop symptoms associated with IBS pain.
The sensation of pain originates in electrical signals carried from the body to the brain by cells called neurons. Tiny channels in the surfaces of neurons help them transmit these signals by allowing positively charged sodium ions to pass into the cell. There are numerous types of sodium channels, and some pain-killing drugs work by blocking them. However, existing treatments interfere with channels indiscriminately and can only be used briefly — not for chronic pain. Stuart Brierley, Glenn King and colleagues wanted to find a way to selectively target the channels activated during chronic IBS pain.
The researchers focused on a particular sodium channel they suspected was responsible for chronic IBS pain. Then, to block it, they turned to the richest known source of molecules that alter the activity of sodium channels: spider venom. In the venom of a Peruvian tarantula, they discovered a molecule that they named Tsp1a, which had promising blocking activity. To test its potential as a treatment, the researchers used mice that had an IBS-related condition, and they monitored the mice during the experiment to detect a reflex associated with pain. A single Tsp1a treatment delivered into the mice’s colons significantly reduced the occurrence of this reflex, indicating pain relief. What’s more, Tsp1a appeared highly selective and did not interfere with other body functions, suggesting it could be used safely in humans. While Tsp1a shows promise as a potential treatment for chronic IBS pain, thorough studies of its activity in the body and the immune system’s reaction to it will be critical, the researchers write.
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