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Identified by Associate Professor Julie Rayes and Dr Martina Colicchia from the Birmingham Platelet Group, and described in a recent paper in Blood, this previously unknown axis comprises platelet receptor glycoprotein I alpha (GPIbα), and an anti-microbial protein S100A8/A9, which is released from activated immune cells. High levels of S100A8/A9 are seen in the blood in thrombo-inflammatory diseases including myocardial infarction (MI), deep vein thrombosis (DVT) and infections such as COVID-19 and sepsis, and their presence correlates with thrombotic complications, and worse outcomes for patients. [Source(s): University of Birmingham, EurekAlert] Researchers from the University of Birmingham, UK, who identified a novel mechanism for platelet activation in pathogenic blood clotting (thrombosis) are now turning their attention to sepsis. Identified by Associate Professor Julie Rayes and Dr Martina Colicchia from the Birmingham Platelet Group, and described in a recent paper in Blood, this previously unknown axis comprises platelet receptor glycoprotein I alpha (GPIbα), and an anti-microbial protein S100A8/A9, which is released from activated immune cells. High levels of S100A8/A9 are seen in the blood in thrombo-inflammatory diseases including myocardial infarction (MI), deep vein thrombosis (DVT) and infections such as COVID-19 and sepsis, and their presence correlates with thrombotic complications, and worse outcomes for patients.

[...]therapeutics are important because there are currently no disease-modifying treatments for osteoarthritis; the best we can do for now is minimize pain and disability,” said Fabrisia Ambrosio, PhD, MPT, inaugural director of the Atlantic Charter Discovery Center for Musculoskeletal Recovery of the Schoen Adams Research Institute at Spaulding Rehabilitation Network, and Member of the Faculty of Physical Medicine and Rehabilitation at Harvard Medical School. “Since matrix stiffening is a feature of aged tissues throughout the body, we anticipate that these findings may also have implications beyond cartilage repair for the field of aging research.” Using advanced mass spectrometry technology, the researchers mapped out the trajectory of structural and protein changes in mice with knee osteoarthritis over the course of their lifetimes and according to sex. Future Research Aims to Address Therapeutic Gaps in Age-Related Conditions With the latest findings, the researchers plan to study whether there are ways to intervene with the disease process that leads to osteoarthritis, such as by blocking the pathway that represses Klotho, even in the face of a stiff extracellular matrix environment.

[...]after a decade of research, a group of Brazilian scientists has succeeded in describing a mechanism associated with the production of neuropathic pain, opening up a new stage of their exploration in search of drugs that can act on the metabolic pathway in question and pointing to an avenue for the development of targeted therapies. According to Mattar Cunha, the discovery has opened up a hitherto unexplored field of research into the role of the meninges in the production of pain. Inflammation Previous research had already shown that the kynurenine pathway, whose formation depends on several enzymes but primarily on IDO1, is involved in pain. Because IDO1 is induced during pathological processes, especially inflammation, by pro-inflammatory cytokines, the researchers hypothesized that the neuroinflammation that causes neuropathic pain could increase IDO, raising the levels of these neurotoxic or neurostimulatory metabolites.