Publications by authors named "M K Shimamura"
Prion diseases, including Creutzfeldt-Jakob disease (CJD), are deadly neurodegenerative disorders characterized by the buildup of abnormal prion proteins in the brain. This accumulation disrupts neuronal functions, leading to the rapid onset of psychiatric symptoms, ataxia, and cognitive decline. The urgency of timely diagnosis for effective treatment necessitates the identification of strongly correlated biomarkers in bodily fluids, which makes our research crucial.
View Article and Find Full Text PDFUnlabelled: Over 170 types of chemical modifications have been identified in cellular RNAs across the three domains of life. Modified RNA is eventually degraded to constituent nucleosides, and in mammals, modified nucleosides are released into the extracellular space. By contrast, the fate of modified nucleosides in bacteria remains unknown.
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- - The study focused on myofibroblasts and how a vaccine targeting fibroblast activation protein (FAP) might help reduce cardiac fibrosis in mice with chronic cardiac stress.
- - Mice were vaccinated with a FAP peptide while undergoing continuous treatment with angiotensin II and phenylephrine, resulting in a significant decrease in both cardiac fibrosis and the number of myofibroblasts.
- - The findings suggest that the FAP vaccine is a promising therapeutic option for cardiac fibrosis without causing harmful side effects in other injury models, indicating its potential for future treatments.
Immune checkpoint inhibitor (ICI) therapy is becoming the standard of care for the treatment of advanced non-small-cell lung cancer. However, T-cell activation by ICIs frequently induces a flare-up of preexisting autoimmune diseases such as rheumatoid arthritis (RA). Janus kinase (JAK) inhibitors are increasingly used in the treatment of RA, but they could interfere with the efficacy of ICIs by inhibiting interferon signaling.
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- - The study investigates the connection between CMV infection and Th17 cells in kidney transplant recipients, finding that both factors independently raise the risk of late allograft loss.
- - Researchers observed that CMV-specific Th17 cells were present in blood samples and expanded during CMV reactivation, showing distinct characteristics compared to general Th17 cells.
- - The findings suggest that CMV-induced Th17 cells might play a role in causing inflammation that can lead to damage in transplanted kidneys, highlighting a possible pathway for allograft injury.