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Recently, researchers from the University of Cambridge published a research paper titled "Arachidonic acid inhibition of the NLRP3 inflammasome is a mechanism to explain the anti-inflammatory effects of fasting" in Cell Reports. The study uncovers how fasting helps prevent inflammation. Fasting can increase the level of arachidonic acid in the blood, and arachidonic acid can reduce the activity of the NLRP3 inflammasome, thereby inhibiting inflammation. The findings also help explain some of the beneficial health effects of drugs like aspirin.
Bacterial infections can lead to the formation of abscesses, pockets of dead cells and debris surrounded by inflammatory immune cells. Bacteria can multiply in an abscess and cause more infections, further damaging surrounding tissue. In severe cases, these immune responses can spread throughout the body and eventually cause life-threatening organ failure or sepsis. But how these abscesses form and how to prevent them have not been better understood.
Decades of research into chronic pain in humans have deepened scientists' understanding of the cellular mechanisms underlying this process. However, the inability to account for the biological variables underlying gender may limit the clinical application of these groundbreaking findings. Recently, in a research report titled "Sex differences in peripheral immune cell activation: Implications for pain and pain resolution" published in the international journal Brain, Behavior, and Immunity, scientists from the University of Alberta and other institutions have revealed differences in the way male and female mice develop and relieve chronic pain in their bodies. The findings point to potential ways for scientists to develop targeted therapies for use in humans in the future.
Cancer cells use various tricks to achieve immune evasion. For example, a recent research result published by a Columbia University team in Cell found that cancer cells use the same regulatory factor to suppress anti-tumor immune responses through two different mechanisms.
Professor Dan Yang, an academician of the National Academy of Sciences and University of California, Berkeley, published a research paper titled "Microglia regulate sleep through calcium-dependent modulation of norepinephrine transmission" in the journal Nature Neuroscience. The study found that activation of inhibitory G protein (Gi protein) signaling in microglia, immune cells in the brain, promotes sleep, and that this effect is mediated, at least in part, through its intracellular Ca2+ signaling, resulting in a decrease in extracellular norepinephrine (NE) concentration.
Malignant tumors are one of the major causes of human death, and the complexity of the tumor immune microenvironment (TIME) limits the effectiveness of various conventional therapies. Although various PD-1/PD-L1 immunosuppressants have achieved significant efficacy in some patients with advanced cancer, their therapeutic effects on most solid tumors are still limited. It may be related to the fact that solid tumor TIME has less T cell infiltration and is rich in immunosuppressive myeloid cells.
Understanding how the virus spreads in the human body is critical to developing effective drugs and treatments to stop its spread. In a new study, researchers from the Texas Biomedical Research Institute have found that the Ebola virus (EBOV) can build and use intercellular tunnels to move from one cell to another, thereby evading treatment. Relevant research results were recently published in the Journal of Infectious Diseases, with the title of "Ebola Virus Uses Tunneling Nanotubes as an Alternate Route of Dissemination."
α-synuclein is an important drug target for Parkinson's disease therapy, but it is also an intrinsically disordered protein that lacks a typical small molecule binding pocket. In contrast, the SNCA-encoding mRNA has an ordered structural region in its 5′ untranslated region (UTR). Recently, a research report titled "Decreasing the intrinsically disordered protein α-synuclein levels by targeting its structured mRNA with a ribonuclease-targeting chimera" was published in the international journal Proceedings of the National Academy of Sciences. Scientists from The Scripps Research Institute and other institutions have developed a new method to combat α-synuclein by targeting the mRNA that forms α-synuclein. This platform can be used to expand druggability of many challenging disease targets.
Mice enter their twilight years at around two years of age, which is roughly equivalent to 80 years in humans. When scientists introduce specific mutated genes into mice and age them over time, the mice become forgetful and irritable, eventually displaying the same symptoms of Alzheimer's disease that many older adults experience.
Recently, Cancer Discovery journal published the latest research results led by the research team of Fox Chase Cancer Center in the United States, which proposed a new strategy for transforming the immune microenvironment of "cold" tumors such as small cell lung cancers (SCLCs). With the help of screening based on CRISPR technology, the study found that inhibiting RNA helicase DHX9 can increase endogenous nucleic acids such as double-stranded RNA in cancer cells. Then a state similar to viral infection is created to activate "endogenous immune" mechanisms such as interferon response and successfully transform "cold" tumors.
