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Tag: Research

  • Liver cells effectively serve as immune checkpoint regulating anti-cancer immunity

    Liver cells effectively serve as immune checkpoint regulating anti-cancer immunity

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    Liver inflammation, a common side-effect of cancers elsewhere in the body, has long been associated with worse cancer outcomes and more recently associated with poor response to immunotherapy. Now, a team led by researchers from the Abramson Cancer Center and Perelman School of Medicine at the University of Pennsylvania has found a big reason why.

    In their study, published today in Nature Immunology, the researchers discovered that cancer-induced liver inflammation causes liver cells to secrete proteins called serum amyloid A (SAA) proteins, which circulate through the body and hinder the ability of T cells-;major anticancer weapons of the immune system-;to infiltrate and attack tumors elsewhere.

    We want to better understand what causes cancer to resist or respond to immunotherapy to help design more effective strategies for patients. Our findings show that liver cells-;with their release of SAA proteins-;effectively serve as an immune checkpoint regulating anti-cancer immunity, making them a promising therapeutic target.”


    Gregory Beatty, MD, PhD, senior author, associate professor of Hematology-Oncology and the director of Clinical and Translational Research for the Penn Pancreatic Cancer Research Center

    The study builds on previous research from the team, including co-lead authors Meredith Stone, PhD, a research associate, and Jesse Lee, a graduate student, into liver inflammation in cancer: In a 2019 study, they showed how it promotes pancreatic tumor metastasis to that organ. In 2021, researchers from the Beatty Laboratory observed that systemic inflammation, involving many of the same molecules implicated in liver metastasis, is associated with worse responses to immunotherapies in pancreatic cancer patients. The latest study was designed to investigate in more detail how liver inflammation may block the effects of these immune-boosting therapies.

    First, they looked at mouse models of pancreatic cancer, measuring the amount of T-cell infiltration in pancreatic tumors-;a basic indicator of anti-tumor immune activity. They found that mice with less T cell infiltration in their tumors tended to have more liver inflammation. These mice also showed stronger signs of an inflammatory signaling pathway called the IL-6/JAK/STAT3 pathway-;the same one the team had implicated in liver metastasis in their 2019 study.

    The researchers next showed that STAT3 activation in liver cells is associated with the reduced production of immune cells called dendritic cells, which are critical for normal T cell responses. When the scientists deleted STAT3 from liver cells, dendritic cell production and T cell activity picked up, and tumors that previously had only low T cell-infiltration developed high T cell-infiltration.

    Ultimately the team found that STAT3 activation in liver cells has its dendritic cell- and T cell-suppressing effect by inducing the production of SAA proteins, which target receptors on immune cells. Deleting the SAA proteins had the same immune-restoring effect as deleting STAT3, and increased survival times and the likelihood of cures in mice that had pancreatic tumors surgically removed.

    To get a sense whether the mouse model findings would translate to humans, the researchers measured SAA levels in tissue samples from patients whose pancreatic tumors had been surgically removed and found that those with low SAA levels at surgery went on to have significantly longer survival times afterward.

    “The translational findings in human patients highlight the likely clinical relevance of our discoveries in the mice,” Beatty said. “Now that we’ve shown how liver inflammation puts up a roadblock to immunotherapy, our next step is to see if the same pathway can be targeted to reverse inflammation in patients who already have liver metastasis.”

    The research team is now working to set up further preclinical and eventually clinical studies of STAT3- and/or SAA-inhibiting agents as potential add-on therapies in combination with immunotherapy-;for example, prior to surgery-;that could improve cancer patient outcomes.

    Support for the research was provided by the National Institutes of Health (T32 CA009140, T32-HL007439-41, K12-CA076931-21, R01-CA197916, R01CA245323, U01 CA224193 and U01 CA224175), the Damon Runyon Cancer Research Foundation, the PacMen Consortium, the US Department of Defense (W81XWH2110622, W81XWH2110621), Stand Up to Cancer, the Robert L. Fine Cancer Research Foundation, the Penn-Wistar SPORE in Skin Cancer, AACR-The Mark Foundation for Cancer Research, and the Pancreatic Cancer Action Network.

    Source:

    University of Pennsylvania School of Medicine

    Journal reference:

    Stone, M. L., et al. (2024). Hepatocytes coordinate immune evasion in cancer via release of serum amyloid A proteins. Nature Immunology. doi.org/10.1038/s41590-024-01820-1.

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  • WHO publishes report introducing updated terminology for airborne pathogens

    WHO publishes report introducing updated terminology for airborne pathogens

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    Following consultation with public health agencies and experts, the World Health Organization (WHO) publishes a global technical consultation report introducing updated terminology for pathogens that transmit through the air. The pathogens covered include those that cause respiratory infections, e.g. COVID-19, influenza, measles, Middle East respiratory syndrome (MERS), severe acute respiratory syndrome (SARS), and tuberculosis, among others.

    The publication, entitled “Global technical consultation report on proposed terminology for pathogens that transmit through the air”, is the result of an extensive, multi-year, collaborative effort and reflects shared agreement on terminology between WHO, experts and four major public health agencies: Africa Centres for Disease Control and Prevention; Chinese Center for Disease Control and Prevention; European Centre for Disease Prevention and Control; and United States Centers for Disease Control and Prevention. This agreement underlines the collective commitment of public health agencies to move forward together on this matter. 

    The wide-ranging consultation was conducted in multiple steps in 2021-2023 and addressed a lack of common terminology to describe the transmission of pathogens through the air across scientific disciplines. The challenge became particularly evident during the COVID-19 pandemic as experts from various sectors were required to provide scientific and policy guidance. Varying terminologies highlighted gaps in common understanding and contributed to challenges in public communication and efforts to curb the transmission of the pathogen.

    Together with a very diverse range of leading public health agencies and experts across multiple disciplines, we are pleased to have been able to address this complex and timely issue and reach a consensus. The agreed terminology for pathogens that transmit through the air will help set a new path for research agendas and implementation of public health interventions to identify, communicate and respond to existing and new pathogens.”


    Dr Jeremy Farrar, WHO Chief Scientist

    The extensive consultation resulted in the introduction of the following common descriptors to characterize the transmission of pathogens through the air (under typical circumstances):

    • Individuals infected with a respiratory pathogen can generate and expel infectious particles containing the pathogen, through their mouth or nose by breathing, talking, singing, spitting, coughing or sneezing. These particles should be described with the term ‘infectious respiratory particles’ or IRPs.

    • IRPs exist on a continuous spectrum of sizes, and no single cut off points should be applied to distinguish smaller from larger particles. This facilitates moving away from the dichotomy of previously used terms: ‘aerosols’ (generally smaller particles) and ‘droplets’ (generally larger particles).

    The descriptor ‘through the air’ can be used in a general way to characterize an infectious disease where the main mode of transmission involves the pathogen travelling through the air or being suspended in the air. Under the umbrella of ‘through the air transmission’, two descriptors can be used:

    1. Airborne transmission or inhalation, for cases when IRPs are expelled into the air and inhaled by another person. Airborne transmission or inhalation can occur at a short or long distance from the infectious person and distance depends on various factors (airflow, humidity, temperature, ventilation etc). IRPs can theoretically enter the body at any point along the human respiratory tract, but preferred sites of entry may be pathogen-specific.

    2. Direct deposition, for cases when IRPs are expelled into the air from an infectious person, and are then directly deposited on the exposed mouth, nose or eyes of another person nearby, then entering the human respiratory system and potentially causing infection.

    “This global technical consultation process was a concerted effort of many influential and experienced experts,” said Dr Gagandeep Kang, Christian Medical College, Vellore, India who is a Co-Chair of the WHO Technical Working Group. “Reaching consensus on these terminologies bringing stakeholders in an unprecedented way was no small feat. Completing this consultation gives us a new opportunity and starting point to move forward with a better understanding and agreed principles for diseases that transmit through the air,” added Dr Yuguo Li from the University of Hong Kong, Hong Kong SAR (China), who also co-chaired the Technical Working Group.

    This consultation was the first phase of global scientific discussions led by WHO. Next steps include further technical and multidisciplinary research and exploration of the wider implementation implications of the updated descriptors. 

    Source:

    The World Health Organization

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  • Delving into burning issues about heart disease and much more

    Delving into burning issues about heart disease and much more

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    The hottest science in the prevention of heart disease awaits at ESC Preventive Cardiology 2024, a scientific congress of the European Society of Cardiology (ESC). The annual congress of the European Association of Preventive Cardiology (EAPC), a branch of the ESC, takes place 25 to 27 April at the Megaron – Athens International Conference Centre, Greece. Explore the scientific programme.

    Don’t miss the late breaking science sessions for cutting-edge research in preventive cardiology, including unhealthy food and beverage trends in adolescents and the links between physical activity and smoking in children. Novel research will be presented in hundreds of scientific abstracts including data on stair climbing, insomnia, dairy products, and the potential connections between air pollution, mental health, and cardiovascular disease. Plus scientific sessions delving into burning issues about heart disease, sex, and much more…

    Patients often have insecurities after a heart event and we will discuss important questions such as when sexual activity can be resumed after a heart attack. We know that exercise helps prevent cardiovascular disease, so is sexual activity enough ‘exercise’?”

    Dr. Nicolle Kränkel, Congress Programme Committee Chair

    Hear experts examine the links between the heart and brain in a session exploring common pathways between depression and heart disease, and how patients with cardiac conditions can stop worrying.

    Dr. Kränkel said: “After a heart attack, patients are often scared and depressed. Depression and anxiety can also impact heart health. Additionally, awareness and cognition of one’s heart health play a large role in adhering to a healthy lifestyle. There is also crosstalk between the heart and other organs. That’s why this year’s congress theme is ‘Cardiovascular risk: The heart and beyond’ – exploring how we can harness these interactions to improve heart health and overall wellbeing.”

    Other important questions that you should attend to hear the answers to:

    Heart health and the young:

    • How do energy drinks affect the hearts of adolescents?
    • Is doping dangerous for the heart? Find out in a session dedicated to stimulants and their effects on the heart.
    • What is the impact of e-cigarettes on young hearts?

    Lifestyle issues:

    • Weight loss update: different approaches to weight loss are needed from childhood to old age – hear how one size does not fit all. And it’s not only about losing fat: learn about personalising exercise in obese patients.
    • What’s new in smoking cessation, including digital tools?
    • Can heart healthy diets be affordable? And the latest evidence on demographic and socio-economic disparities in nutrition. Check out nutrition for a better heart.

    And finally, could a vaccine prevent heart disease? Get up-to-the-minute scientific evidence on immunity and cardiovascular risk and what’s on the horizon.

    Source:

    European Society of Cardiology (ESC)

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  • Do neighborhood-level disparities in breast cancer–specific survival remain after accounting for individual, tumor, and treatment characteristics?

    Do neighborhood-level disparities in breast cancer–specific survival remain after accounting for individual, tumor, and treatment characteristics?

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    The screening, treatment, and survival in breast cancer cases have improved considerably, but differences in survival outcomes persist, especially in disadvantaged neighborhoods.

    A recent JAMA Network Open study assessed the role of neighborhood-level disparities in determining shorter breast cancer-specific survival after accounting for several confounding factors related to the tumor, individual, and treatment characteristics.

    Study: Neighborhood Disadvantage and Breast Cancer–Specific Survival in the US. Image Credit: Gorodenkoff/Shutterstock.comStudy: Neighborhood Disadvantage and Breast Cancer–Specific Survival in the US. Image Credit: Gorodenkoff/Shutterstock.com

    Background

    Neighborhoods are complex environments with distinct physical, cultural, and economic attributes. Communities facing economic challenges may have limited access to essential health services, including facilities for screening, mammography, and treatment. This lack of resources can affect breast cancer survival rates in these areas.

    Research has shown the association between neighborhood disadvantage and breast cancer survival, even after controlling for many of the neighborhood-level, individual-level, and structural factors.

    This suggests the presence of some unaccounted underlying mechanisms which have not been explored yet. Most prior research has focussed on specific geographic areas or subsets of the population, which has limited its generalizability.

    About this study

    This study used a robust index of neighborhood disadvantage (Yost index) to assess the association between neighborhood disadvantage and breast cancer-specific and overall survival post-controlling for tumor, individual, and treatment factors in a national cohort. The null hypothesis was the presence of survival disparities post-adjustment for confounders.

    The cohort comprised patients who were diagnosed with breast cancer from 2013 to 2018 and were sourced from the data held by the National Cancer Institute. The main exposure measure was the neighborhood disadvantage, captured by Yost index quintiles. The main outcome variable was breast cancer-specific survival.

    This was measured using a cause-specific hazard model controlling. Several factors were controlled for, including race, stage, rurality, age, ethnicity, insurance, subtype, and receipt of treatment.

    Study findings

    It was noted that patients in the most disadvantaged neighborhoods reported shorter breast cancer-specific and overall survival rates. This association prevailed even after adjusting for treatment characteristics that are commonly used to explain survival differences.

    This suggests the presence of unaccounted-for non-biological or biological mechanisms through which breast cancer-specific survival is influenced by neighborhood disadvantage.

    The findings raise an important question regarding whether neighborhood disadvantage could give rise to more malignant tumor biology and low survival rates.

    In social genomics studies, psychological and biological stress has been associated with neighborhood disadvantage. These stresses lead to upregulating stress-related neuroendocrine signaling pathways by placing demands on the sympathetic nervous system.

    The signaling pathways lead to a gene expression called conserved transcriptional response to adversity (CTRA). Research has associated the CTRA gene expression with upregulation of proinflammatory gene expression.

    This, in turn, facilitates a prometastatic environment, suggesting aggressive tumor biology. Therefore, this is how breast cancer survival could be affected by neighborhood disadvantage. It must be noted that more research is needed to closely examine the association between the CTRA gene, tumor expression, and neighborhood disadvantage in humans.

    Non-Hispanic Black patients were seen to have the highest mortality risk relative to non-Hispanic White and Hispanic patients. This is indicative of the fact that social determinants of health were not fully controlled for.

    For the relative risk of triple-negative breast cancer (TNBC), similar results were noted when contrasted with human epidermal growth factor receptor two negative (ERBB2−) disease.

    It was also mentioned that unaccounted-for non-biologic pathways could also be driving the persistent disparities in breast cancer-specific survival.

    The immeasurable effects of structural racism, financial burden, and trust on healthcare practitioners could all drive inequities in survival. Future research should appropriately account for these factors.

    Conclusions

    In sum, neighborhood disadvantage was noted to be independently associated with shorter survival in breast cancer patients despite accounting for tumor characteristics, individual-level factors, and treatment.

    In order to understand these residual disparities better, future research should consider the components of the built environment, which could influence outcomes.

    In this regard, a translational epidemiologic approach could be the way forward. This could consider neighborhood disadvantages when devising cancer control interventions and risk-stratifying vulnerable populations.

    In this way, the translational epidemiologic approach could advance precision medicine in oncology.

    Similar to previous retrospective observational studies, this study also has certain limitations. Information on comorbidities, medicine doses, treatment rationale, and completion of radiotherapy and chemotherapy could not be obtained.

    Another limitation concerns the important issue of access to care. Individual insurance coverage was used as a proxy for access to care; however, this is an incomplete representation of all access to care measures.

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  • Mitochondrial depletion in axons linked to protein accumulation in neurodegenerative diseases

    Mitochondrial depletion in axons linked to protein accumulation in neurodegenerative diseases

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    Researchers from Tokyo Metropolitan University have identified how proteins collect abnormally in neurons, a feature of neurodegenerative diseases like Alzheimer’s. They used fruit flies to show that depletion of mitochondria in axons can directly lead to protein accumulation. At the same time, significantly high amounts of a protein called eIF2β were found. Restoring the levels to normal led to a recovery in protein recycling. Such findings promise new treatments for neurodegenerative diseases.

    Every cell in our bodies is a busy factory, where proteins are constantly being produced and disassembled. Any changes or lapses in either the production or recycling phases can lead to serious illnesses. Neurodegenerative diseases such as Alzheimer’s and Amyotrophic Lateral Sclerosis (ALS), for example, are known to be accompanied by an abnormal build-up of proteins in neurons. However, the trigger behind this accumulation remains unknown.

    A team led by Associate Professor Kanae Ando of Tokyo Metropolitan University have been trying to determine the causes of abnormal protein build-up by studying Drosophila fruit flies, a commonly studied model organism that has many key similarities with human physiology. They focused on the presence of mitochondria in axons, the long tendril-like appendages that stretch out of neurons and form the necessary connections that allow signals to be transmitted inside our brains. It is known that the levels of mitochondria in axons can drop with age, and during the progress of neurodegenerative diseases.

    Now, the team have discovered that the depletion of mitochondria in axons has a direct bearing on protein build-up. They used genetic modification to suppress the production of milton, a key protein in the transport of mitochondria along axons. It was found that this led to abnormal levels of protein building up in fruit fly neurons, a result of the breakdown of autophagy, the recycling of proteins in cells. Through proteomic analysis, they were able to identify a significant upregulation in eIF2β, a key subunit of the eIF2 protein complex responsible for the initiation of protein production (or translation). The eIF2α subunit was also found to be chemically modified. Both of these issues hamper the healthy action of eIF2.

    Importantly, by artificially suppressing levels of eIF2β, the team discovered that they could restore the autophagy that was lost and regain some of the neuron function that was impaired due to axonal mitochondria loss. This not only shows that depletion of mitochondria in axons can cause abnormal protein accumulation, but that this happens via upregulation of eIF2β.

    As populations age and the prevalence of neurodegenerative conditions continues to increase, the team’s findings present a vital step in developing therapies to combat these serious illnesses.

    This work was supported by a Sasakawa Scientific Research Grant (2021-4087), the Takeda Science Foundation, a Hoansha Foundation Grant, a research award from the Japan Foundation for Aging and Health and the Novartis Foundation (Japan) for the Promotion of Science, a Grant-in-Aid for Scientific Research on Challenging Research (Exploratory) [JSPS KAKENHI Grant Number 19K21593], NIG-JOINT (National Institute of Genetics, 71A2018, 25A2019), and the TMU Strategic Research Fund for Social Engagement.

    Source:

    Tokyo Metropolitan University

    Journal reference:

    Shinno, K., et al. (2024). Axonal distribution of mitochondria maintains neuronal autophagy during aging via eIF2β. eLife. doi.org/10.7554/elife.95576.1.

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  • Innovative shoe insole technology mitigates the risk of diabetic foot ulcers

    Innovative shoe insole technology mitigates the risk of diabetic foot ulcers

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    Researchers have developed a new shoe insole technology that helps reduce the risk of diabetic foot ulcers, a dangerous open sore that can lead to hospitalization and leg, foot or toe amputations.

    The goal of this innovative insole technology is to mitigate the risk of diabetic foot ulcers by addressing one of their most significant causes: skin and soft tissue breakdown due to repetitive stress on the foot during walking.”


    Muthu B.J. Wijesundara, principal research scientist at The University of Texas at Arlington Research Institute (UTARI)

    Affecting about 39 million people in the U.S., diabetes can damage the small blood vessels that supply blood to the nerves, leading to poor circulation and foot sores, also called ulcers. About one-third of people with diabetes develop foot ulcers during their lifetime. In the U.S., more than 160,000 lower extremity amputations are performed annually due to complications from diabetic foot ulcers, costing the American health system about $30 billion a year. Those who have foot ulcers often die at younger ages than those without ulcers.

    “Although many shoe insoles have been created over the years to try to alleviate the problem of foot ulcers, studies have shown that their success in preventing them is marginal,” Wijesundara said. “We took the research a step further by creating a pressure-alternating shoe insole that works by cyclically relieving pressure from different areas of the foot, thereby providing periods of rest to the soft tissues and improving blood flow. This approach aims to maintain the health of the skin and tissues, thereby reducing the risk of diabetic foot ulcers.”

    In an article in the peer-reviewed International Journal of Lower Extremity Wounds, Wijesundara and UTA colleagues Veysel Erel, Aida Nasirian and Yixin Gu, along with Larry Lavery of UT Southwestern Medical Center, described their innovative insole technology. After this successful pilot project, the next step for the research team will be refining the technology to make it more accessible for users with varying weights and shoe sizes.

    “Considering the impact of foot ulcers, it’s exciting that we may be able to make a real difference in the lives of so many people,” Wijesundara said.

    Source:

    University of Texas at Arlington

    Journal reference:

    Erel, V., et al. (2024). Development of Cyclic Pressure Offloading Insole for Diabetic Foot Ulcer Prevention. The International Journal of Lower Extremity Wounds/International Journal of Lower Extremity Wounds. doi.org/10.1177/15347346241234825.

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  • Blessed thistle compound Cnicin speeds nerve growth, study finds

    Blessed thistle compound Cnicin speeds nerve growth, study finds

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    Blessed thistle (Cnicus benedictus) is a plant in the family Asteraceae and also grows in our climate. For centuries, it has been used as a medicinal herb as an extract or tea, e.g. to aid the digestive system. Researchers at the Center for Pharmacology of University Hospital Cologne and at the Faculty of Medicine of the University of Cologne have now found a completely novel use for Cnicin under the direction of Dr Philipp Gobrecht and Professor Dr. Dietmar Fischer. Animal models as well as human cells have shown that Cnicin significantly accelerates axon (nerve fibres) growth. The study ‘Cnicin promotes functional nerve regeneration’ was published in Phytomedicine.

    Rapid help for nerves

    Regeneration pathways of injured nerves in humans and animals with long axons are accordingly long. This often makes the healing process lengthy and even frequently irreversible because the axons cannot reach their destination on time. An accelerated regeneration growth rate can, therefore, make a big difference here, ensuring that the fibers reach their original destination on time before irreparable functional deficits can occur. The researchers demonstrated axon regeneration in animal models and human cells taken from retinae donated by patients. Administering a daily dose of Cnicin to mice or rats helped improve paralysis and neuropathy much more quickly.

    Compared to other compounds, Cnicin has one crucial advantage: it can be introduced into the bloodstream orally (by mouth). It does not have to be given by injection.

    The correct dose is very important here, as Cnicin only works within a specific therapeutic window. Doses that are too low or too high are ineffective. This is why further clinical studies on humans are crucial.”


    Professor Dr. Dietmar Fischer

    The University of Cologne researchers are currently planning relevant studies. The Center for Pharmacology is researching and developing drugs to repair the damaged nervous system.

    The current study received funding of around 1,200,000 euros from the Federal Ministry of Education and Research within the framework of the project PARREGERON.

    Source:

    Journal reference:

    Gobrecht, P., et al. (2024). Cnicin promotes functional nerve regeneration. Phytomedicine. doi.org/10.1016/j.phymed.2024.155641.

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  • Study identifies potential strategy to diminish the devastating impacts of traumatic brain injuries

    Study identifies potential strategy to diminish the devastating impacts of traumatic brain injuries

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    For the roughly 1.5 million Americans per year who survive a traumatic brain injury, health outcomes vary widely. Not only can these injuries lead to a loss of coordination, depression, impulsivity, and difficulty concentrating, but they come with an amplified risk for developing dementia in the future.

    The glaring absence of treatments for such a widespread condition drove a team of scientists at Gladstone Institutes to uncover, on a molecular level, how traumatic brain injuries trigger neurodegeneration-;and just as importantly, how to target that process to prevent long-term damage.

    “We set out to address the fundamental question of exactly what happens in the brain after injury to ignite the damaging process that destroys neurons,” says Jae Kyu Ryu, PhD, a scientific program leader in the lab of Katerina Akassoglou, PhD at Gladstone Institutes.

    Most traumatic brain injuries come as a result of falls, car crashes, or violent assaults, according to the Centers for Disease Control, but many also stem from sports accidents or certain military operations such as explosions. In each case, the external force is strong enough to move the brain within the skull, causing a significant breakdown in the blood-brain barrier and allowing blood to move in.

    “We knew that a specific blood protein, fibrin, was present in the brain after traumatic brain injury, but we didn’t know until now that it plays a causative role in brain damage after injury,” says Ryu, who led the study that appears in the Journal of Neuroinflammation.

    Ryu and others in Akassoglou’s lab have long investigated how blood that leaks into the brain triggers neurologic diseases, essentially by hijacking the brain’s immune system and setting off a cascade of harmful, often-irreversible effects. Fibrin, a protein that normally helps blood coagulate, is the culprit. 

    Across many neurological diseases, toxic immune responses in the brain are triggered by blood leaks and drive neurodegeneration. Neutralizing the toxic immune responses in the brain paves the way to new therapies for neurological diseases.”


    Katerina Akassoglou, senior investigator at Gladstone and director of the Center for Neurovascular Brain Immunology at Gladstone and UCSF

    In diseases such as Alzheimer’s and multiple sclerosis, abnormal leaks in the protective blood-brain barrier allow fibrin to seep into areas responsible for cognitive and motor functions causing neurodegeneration. But in this case, the traumatic brain injury itself causes the blood to leak into the brain. The new study showed, for the first time, that fibrin is responsible for turning good immune cells bad, causing dangerous inflammation and unleashing toxins that kill neurons.

    The Gladstone team used state-of-the-art imaging technology to study mouse brains, as well as brains from people who experienced a traumatic brain injury. They also produced three-dimensional imaging of a whole intact mouse brain, showing blood-brain barrier leaks and abundant fibrin in traumatic brain injury. In both mouse and human brains, fibrin was present together with activated immune cells.

    “It became clear that fibrin is activating these immune cells,” Ryu says. “We realized that we can prevent the toxic effects if we could block fibrin, but we had to do it in a precise way.”

    The team leveraged genetic tools with a specific mutation in fibrin that can block it from activating immune cells without affecting the protein’s beneficial blood-clotting abilities. This is especially critical for traumatic brain injuries, as excessive bleeding into the brain has been known to occur among patients who were taking anticoagulant medications before their injury.

    Akassoglou’s lab previously developed a drug, a therapeutic monoclonal antibody, that acts only on fibrin’s inflammatory properties, without adverse effects on blood coagulation. This fibrin-targeting immunotherapy protects from multiple sclerosis and Alzheimer’s disease in mice. A humanized version of this first-in-class fibrin immunotherapy is already in Phase 1 safety clinical trials by Therini Bio.

    “It’s exciting to have a therapeutic option to neutralize blood toxicity in neurologic diseases,” Ryu says. “Future studies are needed to test the effects of the fibrin immunotherapy in traumatic brain injury.”

    “This study identifies a potential new strategy to diminish the devastating impacts of brain injuries,” says Lennart Mucke, MD, director of the Gladstone Institute of Neurological Disease. “Brain injuries can have profound effects on a person’s cognitive abilities, emotional health, and motor skills, touching every part of their life. It will be interesting to explore whether blocking the disease-promoting effects of fibrin can improve the outcome of brain surgeries and reduce disability when implemented after traumatic brain injuries have occurred.”

    Source:

    Journal reference:

    Dean, T., et al. (2024). Fibrin promotes oxidative stress and neuronal loss in traumatic brain injury via innate immune activation. Journal of Neuroinflammation. doi.org/10.1186/s12974-024-03092-w.

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  • Public health efforts urged to reduce sodium in packaged foods

    Public health efforts urged to reduce sodium in packaged foods

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    In a recent review article published in Nutrients, researchers explored the dual role of sodium in water balance regulation and food formulation, noting its significant association with mortality due to excessive intake.

    Their conclusions underscore the importance of reducing sodium intake, promoting a global healthy lifestyle that includes both dietary adjustments and physical activity, and implementing educational interventions to optimize sodium balance and overall health.

    ​​​​​​​Study: Effect of active-duty military service on neonatal birth outcomes: a systematic review. Image Credit: beats1/Shutterstock.com​​​​​​​Study: Effect of active-duty military service on neonatal birth outcomes: a systematic review. Image Credit: beats1/Shutterstock.com

    Need to control sodium intake

    Sodium, crucial for extracellular fluid regulation and food science, poses risks when overconsumed. Global studies reveal high intake levels with associated cardiovascular risks.

    This has made reducing sodium in processed foods a global priority for public health agencies, and efforts are underway to reduce sodium in processed foods. While theoretical solutions exist, practical implementation requires addressing multiple factors such as taste, texture, and cost, highlighting ongoing efforts in food processing.

    The reduction or replacement of sodium in processed foods presents complex technological challenges. Strategies include reducing added salt, replacing sodium chloride with alternative salts or ingredients, and optimizing salt distribution for enhanced perception.

    However, global progress in reducing sodium intake has been low, and multidisciplinary approaches involving health professionals are needed to address this health challenge effectively.

    The Canadian government took initiatives to manage the excess sodium intake, including voluntary reduction targets and front-of-pack labeling regulations. Still, these efforts showed mixed success, suggesting that more than voluntary measures alone may be necessary and necessitate broader interventions.

    Possible solutions involve reducing sodium content in processed foods through policy interventions and enhancing individuals’ capacity to manage sodium intake, primarily through the guidance of health professionals such as dietitians.

    Dietary interventions

    Processed foods, notably prepackaged or prepared items, significantly contribute to sodium intake in the diet, with staples like processed meats, cheese, and bread being major sources.

    Studies indicate that reducing salt content in bread does not necessarily impact sales, suggesting potential for sodium reduction without compromising consumer acceptance, aligning with efforts to address excessive sodium intake.

    The Dietary Approaches to Stop Hypertension (DASH) diet, recommended for hypertensive patients, emphasizes potassium-rich foods while limiting the intake of sodium and saturated fats. Clinical studies consistently show its effectiveness in reducing blood pressure, even in individuals with type 2 diabetes.

    Despite challenges like high sodium preference in certain populations, DASH diet implementation through counseling and support strategies can aid in sodium reduction and hypertension management.

    Generating awareness of using salt-free seasonings, herbs, and spices can allow individuals to enhance food flavor without adding salt, potentially reducing sodium intake while maintaining taste satisfaction.

    Clinical studies suggest that replacing salt with low-sodium-salt substitutes (LSSS) may decrease sodium intake and slightly reduce blood pressure and cardiovascular risk. Still, concerns exist about potential adverse effects, particularly in high-risk populations, including people with chronic kidney disease.

    Research highlights the role of gut microbiota in cardiometabolic health, with studies showing the benefits of Lactobacillus rhamnosus probiotic supplementation on body composition and cardiometabolic markers.

    Recent findings suggest a link between gut microbiota depletion, high sodium intake, and blood pressure regulation, offering promise for microbiota-targeted interventions to improve sodium homeostasis.

    Digital platforms, like social media and electronic brochures, effectively supported a salt reduction initiative in the United Arab Emirates, with social media groups showing the most significant decrease in salt intake.

    Smartphone apps offer potential for DASH diet adherence, although their clinical effectiveness remains uncertain, emphasizing the need for further research and app improvement to maximize their public health impact.

    Mindful eating practices, such as those in the Mindfulness-Based Blood Pressure Reduction program, may improve compliance with low-sodium diets by promoting awareness of food choices.

    Improvement in emotional regulation can also mitigate the consumption of comfort foods that are high in sodium.

    Integrating these dietary strategies into interventions may effectively reduce sodium intake, complementing population-based approaches like policies to reduce salt and enhancing food labeling practices.

    Physical fitness and activity

    Recent findings suggest a complex interplay between body composition, aerobic fitness, and sodium intake, particularly in females. Interaction effects revealed a less favorable body composition profile in females with high sodium intake and low fitness levels.

    Mediation analysis indicated that both aerobic fitness and sodium intake mediate the association between body fitness and the genetic risk of obesity.

    Additionally, maintaining regular physical activity levels may mitigate the harmful impacts of high sodium intake, possibly through mechanisms like sweat sodium loss and reduced salt sensitivity.

    These insights advocate promoting physical activity alongside dietary sodium reduction strategies to achieve optimal sodium balance and metabolic health. Further research is warranted to elucidate the underlying mechanisms.

    Conclusions

    In summary, the crucial role of sodium in body homeostasis necessitates careful management to avoid cardiometabolic issues. While progress has been made in reducing sodium in processed foods, achieving optimal balance requires multifaceted interventions.

    These include nutritional counseling, lifestyle changes like increased physical activity, and potential microbiota modifications to promote sodium balance and overall health.

    Journal reference:

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  • Study shows yoga’s positive impact on emotional health in forensic psychiatry

    Study shows yoga’s positive impact on emotional health in forensic psychiatry

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    Previous studies in correctional facilities have shown positive effects of yoga on inmates. They experience increased impulse control and improved mental health. Are the same positive results seen in detained individuals with severe psychiatric disorders? Now, the first results from a large national and globally unique research study in forensic psychiatry from the University West are presented.

    It is the first scientific study of its kind to describe the effect and feasibility of trauma-adapted yoga in forensic psychiatry.

    It is a breakthrough that we can now demonstrate the possibility of using yoga as a complementary care intervention in psychiatry and the positive effects it brings.”


    Nóra Kerekes, Professor in Medical Sciences (Psychiatry) at the University West, and research leader of the study

    The results of the study are now published in the prestigious scientific journal, Psychiatry Research.

    “We wanted to explore whether previous positive results with the use of yoga in correctional facilities could be transferred to detained individuals suffering from severe psychiatric disorders. Therefore, we evaluated trauma-adapted yoga as a support within forensic psychiatry,” says Nóra Kerekes.

    Forensic psychiatry deals with the complex challenges that arise at the intersection of psychiatric illness, legal issues, and security concerns.

    “There are few high-quality clinical studies on individuals who have committed crimes and who have a serious mental disorder. What exists are either studies on inmates separately or studies of individuals suffering from various psychiatric disorders. For both of these groups, yoga has shown positive effects,” says Nóra Kerekes.

    Yoga class for 10 weeks

    Self-choice was a central component in the study design, where 56 patients at various forensic psychiatric clinics chose to participate. Over 10 weeks, they either participated in specially developed yoga classes or chose to engage in other forms of physical activity. Throughout the study, changes in their mental health, emotional states, antisocial and aggressive behaviors, pain perception, substance cravings, and ability to control their behavior and emotional reactions were observed.

    Positive effects measured

    In the current study, the yoga group showed remarkable reductions in negative emotional states, anxiety, paranoid ideation, hostility, and overall psychological distress. These reductions were not observed in the group performing other forms of physical activities. Additionally, the yoga group exhibited a significant reduction in pain frequency, and showed strengthened self-control and accountability.

    “We can conclude that trauma-iadapted yoga implemented in a forensic psychiatric setting demonstrates feasibility and results in several positive changes in patients’ mental health, emotional states, pain, and self-control,” says Nóra Kerekes.

    She continues:

    “A structured program of trauma-adapted yoga for patients and training for healthcare personnel has been developed and has now been confirmed to be feasible and beneficial within forensic psychiatry.”

     

    Source:

    Journal reference:

    Kerekes, N. (2024). Exploring the Impact of Trauma-Adapted Yoga in Forensic Psychiatry: Midterm Findings and Insights. Psychiatry Research. doi.org/10.1016/j.psychres.2024.115879.

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