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NEW DISCOVERY ON CHOLESTEROL MAY ONE DAY BE USED TO PREVENT CVD

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  NEW DISCOVERY ON CHOLESTEROL MAY ONE DAY BE USED TO PREVENT CVD         Researchers at the University of Leicester have discovered how cholesterol in our diet is absorbed into our cells. This discovery, which has just been published in the journal  Science,  opens up new opportunities for therapeutic intervention to control cholesterol uptake that could complement other therapies and potentially save lives. The research conducted with colleagues from the USA, China, and Australia has shown that two proteins (Aster B and Aster C) play a key role in transporting cholesterol from the membrane of the cells lining our intestine to the internal compartment, which is modified before circulation. The Leducq Foundation awarded $6 million to eight laboratories across the USA and Europe for collaborative research into how cholesterol is transported in our bodies. University of Leicester researchers from the Institute of Structural and Chemical Biology used thei...
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NEW DISCOVERY MAY EXPLAIN AGING AND DEGENERATIVE DISEASES IN HUMANS

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  NEW DISCOVERY MAY EXPLAIN AGING AND DEGENERATIVE DISEASES   IN HUMANS Researchers identify a new Mitophagy pathway highlighting the gut/brain connection.         Healthy mitochondria, the organelles that produce energy in all our cells, usually portend a long, healthy life in humans or  C. elegans , a tiny, short-lived nematode worm often used to study the aging process. Researchers at the Buck Institute have identified a new drug-like molecule that keeps mitochondria healthy via Mitophagy, which removes and recycles damaged mitochondria in multicellular organisms. The compound, dubbed MIC, is a natural compound that extended the lifespan in  C. elegans,  ameliorated pathology in neurodegenerative disease models of  C. elegans,  and improved mitochondrial function in mouse muscle cells. Results are published in the November 13, 2023, edition of  Nature Aging . Defective Mitophagy is implicated in many age-related disease...
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WHY IS LUPUS MORE PREVALENT IN FEMALES?

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  WHY IS LUPUS MORE PREVALENT IN FEMALES? A molecule associated with X chromosomes may contribute to developing lupus in females.         For years, researchers and clinicians have known that lupus, an autoimmune condition, occurs in women at a rate nine times higher than in men. Some of the factors that cause the disease's high prevalence in women have eluded discovery. Still, in a new study investigating the immune system processes in lupus and the X chromosome, Johns Hopkins Medicine researchers have uncovered answers about the disease's frequency in females. Several dysregulated genetic and biological pathways contribute to the development of lupus and its varied symptoms of muscle and joint pain, skin rashes, kidney problems, and other complications throughout the body. One such pathway involves a protein in the immune system called toll-like receptor 7 (TLR7), which, in lupus, reacts to the body's own RNA. These molecules act as messengers of genetic infor...
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Some benefits of exercise stem from the immune system Immune cells mobilized in the muscles during exercise fend off inflammation and boost endurance Date: November 3, 2023 Source: Harvard Medical School Summary: Research in mice shows that the anti-inflammatory properties of exercise may arise from immune cells mobilized to counter exercise-induced inflammation. Immune cells prevent muscle damage by lowering levels of interferon, a key driver of chronic inflammation, inflammatory diseases, and aging. Share: FULL STORY The connection between exercise and inflammation has captivated the imagination of researchers ever since an early 20th-century study showed a spike of white cells in the blood of Boston marathon runners following the race. Now, a new Harvard Medical School study published Nov. 3 in Science Immunology may offer a molecular explanation behind this century-old observation. The study, done in mice, suggests that the beneficial effects of exercise may be driven, at least partly, by the immune system. It shows that muscle inflammation caused by exertion mobilizes inflammation-countering T cells, or Tregs, which enhance the muscles' ability to use energy as fuel and improve overall exercise endurance. Long known for their role in countering the aberrant inflammation linked to autoimmune diseases, Tregs now also emerge as key players in the body's immune responses during exercise, the research team said. "The immune system, and the T cell arm in particular, has a broad impact on tissue health that goes beyond protection against pathogens and controlling cancer. Our study demonstrates that the immune system exerts powerful effects inside the muscle during exercise," said study senior investigator Diane Mathis, Morton Grove-Rasmussen Professor of Immunology in the Blavatnik Institute at HMS. Mice are not people, and the findings remain to be replicated in further studies, the researchers cautioned. However, the study is an important step toward detailing the cellular and molecular changes that occur during exercise and confer health benefits. Understanding the molecular underpinnings of exercise Protecting from cardiovascular disease, reducing the risk of diabetes, shielding against dementia. The salutary effects of exercise are well established. But exactly how does exercise make us healthy? The question has intrigued researchers for a long time. The new findings come amid intensifying efforts to understand the molecular underpinnings of exercises. Untangling the immune system's involvement in this process is but one aspect of these research efforts. "We've known for a long time that physical exertion causes inflammation, but we don't fully understand the immune processes involved," said study first author Kent Langston, a postdoctoral researcher in the Mathis lab. "Our study shows, at very high resolution, what T cells do at the site where exercise occurs, in the muscle." Most previous research on exercise physiology has focused on the role of various hormones released during exercise and their effects on different organs such as the heart and the lungs. The new study unravels the immunological cascade that unfolds inside the actual site of exertion -- the muscle. T cell heroes and inflammation-fueling villains Exercise is known to cause temporary damage to the muscles, unleashing a cascade of inflammatory responses. It boosts the expression of genes that regulate muscle structure, metabolism, and the activity of mitochondria, the tiny powerhouses that fuel cell function. Mitochondria play a key role in exercise adaptation by helping cells meet the greater energy demand of exercise. In the new study, the team analyzed what happens in cells taken from the hind-leg muscles of mice that ran on a treadmill once and animals that ran regularly. Then, the researchers compared them with muscle cells obtained from sedentary mice. The muscle cells of the mice that ran on treadmills, whether once or regularly, showed classic signs of inflammation -- greater activity in genes that regulate various metabolic processes and higher levels of chemicals that promote inflammation, including interferon. Both groups had elevated levels of Treg cells in their muscles. Further analyses showed that in both groups, Tregs lowered exercise-induced inflammation. None of those changes were seen in the muscle cells of sedentary mice. However, the metabolic and performance benefits of exercise were apparent only in the regular exercisers -- the mice that had repeated bouts of running. In that group, Tregs not only subdued exertion-induced inflammation and muscle damage, but also altered muscle metabolism and muscle performance, the experiments showed. This finding aligns with well-established observations in humans that a single bout of exercise does not lead to significant improvements in performance and that regular activity over time is needed to yield benefits. Further analyses confirmed that Tregs were, indeed, responsible for the broader benefits seen in regular exercisers. Animals that lacked Tregs had unrestrained muscle inflammation, marked by the rapid accumulation of inflammation-promoting cells in their hindleg muscles. Their muscle cells also had strikingly swollen mitochondria, a sign of metabolic abnormality. More importantly, animals lacking Tregs did not adapt to increasing demands of exercise over time the way mice with intact Tregs did. They did not derive the same whole-body benefits from exercise and had diminished aerobic fitness. These animals' muscles also had excessive amounts of interferon, a known driver of inflammation. Further analyses revealed that interferon acts directly on muscle fibers to alter mitochondrial function and limit energy production. Blocking interferon prevented metabolic abnormalities and improved aerobic fitness in mice lacking Tregs. "The villain here is interferon," Langston said. "In the absence of guardian Tregs to counter it, interferon went on to cause uncontrolled damage." Interferon is known to promote chronic inflammation, a process that underlies many chronic diseases and age-related conditions and has become a tantalizing target for therapies aimed at reducing inflammation. Tregs have also captured the attention of scientists and industry as treatments for a range of immunologic conditions marked by abnormal inflammation. The study findings provide a glimpse into the cellular innerworkings behind exercise's anti-inflammatory effects and underscore its importance in harnessing the body's own immune defenses, the researchers said. There are efforts afoot to design interventions targeting Tregs in the context of specific immune-mediated diseases. And while immunologic conditions driven by aberrant inflammation require carefully calibrated therapies, exercise is yet another way to counter inflammation, the researchers said. "Our research suggests that with exercise, we have a natural way to boost the body's immune responses to reduce inflammation," Mathis said. "We've only looked in the muscle, but it's possible that exercise is boosting Treg activity elsewhere in the body as well." RELATED TOPICS Health & Medicine Fitness Immune System Joint Pain Lymphoma Plants & Animals Mice Biology Biotechnology and Bioengineering Molecular Biology RELATED TERMS Necrosis Rheumatoid arthritis Chemotherapy Inflammation Immune system T cell Aerobic exercise White blood cell Story Source:

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  AN EXPLANATION OF HOW EXERCISE  HELPS TO BOOST THE IMMUNES SYSTEM Immune cells mobilized in the muscles during exercise fend off inflammation and boost endurance.         The connection between exercise and inflammation has captivated the imagination of researchers ever since an early 20th-century study showed a spike of white cells in the blood of Boston marathon runners following the race . Now, a new Harvard Medical School study published Nov. 3 in  Science Immunology  may offer a molecular explanation behind this century-old observation. The study, done in mice, suggests that the beneficial effects of exercise may be driven, at least partly, by the immune system. It shows that muscle inflammation caused by exertion mobilizes inflammation-countering T cells, or Tregs, which enhance the muscles' ability to use energy as fuel and improve overall exercise endurance. Long known for their role in countering the aberrant inflammation linked to auto...
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HIGH INSULIN LEVELS LINKED TO PANCREATIC CANCER

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  HIGH INSULIN LEVELS LINKED TO PANCREATIC CANCER First detailed explanation of why people with obesity and Type 2 diabetes are at an increased risk of pancreatic cancer         A new study from researchers at the University of British Columbia's Faculty of Medicine reveals a direct link between high insulin levels, common among patients with obesity and Type 2 diabetes, and pancreatic cancer. The study, published in  Cell Metabolism , provides the first detailed explanation of why people with obesity and Type 2 diabetes are at an increased risk of pancreatic cancer. The research demonstrates that excessive insulin levels overstimulate pancreatic acinar cells, which produce digestive juices. This overstimulation leads to inflammation that converts these cells into precancerous cells. "Alongside the rapid increase in both obesity and Type 2 diabetes, we're seeing an alarming rise in pancreatic cancer rates," said co-senior author Dr. James Johnson, a profess...
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SELENIUM-RICH DIET MAY REDUCE THE HARMFUL EFFECTS OF ENVIRONMENTAL POLLUTANTS

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  A SELENIUM-RICH DIET MAY REDUCE THE HARMFUL EFFECTS OF ENVIRONMENTAL POLLUTANTS         A study in mice conducted by the University of Cordoba proves that exposure to contaminating mixtures of metals and drug residue increases damage to health and evaluates the positive effects of a diet enriched in selenium to reduce this harm. People are exposed daily, through the environment and their diets, to external substances that can harm their health. Metals and the residue of pharmaceuticals, for example, in high doses, contaminate water and food, creating mixtures where they can interact, increasing their toxicity. Analyzing the effects of environmental pollution on organisms is essential to develop regulations establishing maximum doses of these pollutants for people. But what about mixtures of pollutants? What happens when, even when faced with accepted doses, the different compounds interact? To understand the health effects of exposure to these "cocktails of co...
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HOW BREAST CANCER SPREADS IS DISCOVERED

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  HOW BREAST CANCER SPREADS IS DISCOVERED     The most lethal feature of any cancer is metastasis, the spread of cancer cells throughout the body. New research led by Penn State reveals for the first time the mechanics behind how breast cancer cells may invade healthy tissues. The discovery, showing that a motor protein called dynein powers the movement of cancer cells in soft tissue models, offers new clinical targets against metastasis and has the potential to fundamentally change how cancer is treated. "This discovery marks a paradigm shift in many ways," said Erdem Tabdanov, assistant professor of pharmacology at Penn State and a lead co-corresponding author on the study, recently published in  Advanced Science . "Until now, dynein has never been caught in the business of providing the mechanical force for cancer cell motility, which is their ability to move themselves. Now we can see that if you target dynein, you could effectively stop motility of those cells a...
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