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http://dx.doi.org/10.1042/bj0760102 | DOI Listing |
Immunol Res
January 2025
, Auckland, New Zealand.
Cytotoxic DNAs, methylation, histones and histones binding proteins are speculated to induce DNA sensors. Under stressed condition, the antigenic patterns, PAMPs and DAMPs, trigger the hyperactive innate response through DNA, DNA-RNA hybrids, oligonucleotides, histones and mtDNA to initiate cGAMP-STING-IFN I cascade. HSV -1&2, HIV, Varicella- Zoster virus, Polyomavirus, Cytomegalovirus, and KSHV negatively regulate the STING-MAVS-TBK-1/1KKE pathway.
View Article and Find Full Text PDFSwiss Med Wkly
December 2024
Center for Primary Care and Public Health (Unisanté), Department of Epidemiology and Health Systems, University of Lausanne, Lausanne, Switzerland.
Aim: To assess the perceptions of adults with diabetes regarding their care and health during the COVID-19 pandemic in the canton of Vaud, Switzerland.
Methods: Cross-sectional data was analysed from the 2021 follow-up questionnaire of the CoDiab-VD survey, a cohort of adults living with diabetes in the canton of Vaud. Various aspects of diabetes care and issues relating to the COVID-19 pandemic were assessed.
J Exp Biol
January 2025
Marine Science Program, Biological and Environmental Science and Engineering Division, King Abdullah University of Science and Technology (KAUST); Thuwal, Saudi Arabia.
Coastal deoxygenation poses a critical threat to tropical coral reefs. Dissolved oxygen (DO) depletion can cause hypoxia-induced stress and mortality for scleractinian corals. Coral hypoxic responses are species-specific and likely modulated by the duration and severity of low-DO conditions, although the physiological mechanisms driving hypoxia tolerance are not fully understood.
View Article and Find Full Text PDFElife
January 2025
The University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge, United Kingdom.
encodes three regulatory subunits of class IA phosphoinositide 3-kinase (PI3K), each associating with any of three catalytic subunits, namely p110α, p110β, or p110δ. Constitutional mutations cause diseases with a genotype-phenotype relationship not yet fully explained: heterozygous loss-of-function mutations cause SHORT syndrome, featuring insulin resistance and short stature attributed to reduced p110α function, while heterozygous activating mutations cause immunodeficiency, attributed to p110δ activation and known as APDS2. Surprisingly, APDS2 patients do not show features of p110α hyperactivation, but do commonly have SHORT syndrome-like features, suggesting p110α hypofunction.
View Article and Find Full Text PDFExpert Opin Drug Metab Toxicol
January 2025
EuroEspes Biomedical Research Center, International Center of Neuroscience and Genomic Medicine, Bergondo, Corunna, Spain.
Introduction: Genetic load influences the therapeutic response to conventional drugs in Alzheimer's disease (AD). Pharmacogenetics (PGx) is the best option to reduce drug-drug interactions and adverse drug reactions in patients undergoing polypharmacy regimens. However, there are important limitations that make it difficult to incorporate pharmacogenetics into routine clinical practice.
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