Introduction: Accurate genotyping of Killer cell Immunoglobulin-like Receptor (KIR) genes plays a pivotal role in enhancing our understanding of innate immune responses, disease correlations, and the advancement of personalized medicine. However, due to the high variability of the KIR region and high level of sequence similarity among different KIR genes, the generic genotyping workflows are unable to accurately infer copy numbers and complete genotypes of individual KIR genes from next-generation sequencing data. Thus, specialized genotyping tools are needed to genotype this complex region.
View Article and Find Full Text PDFBackground: Inflammatory bowel disease (IBD) is a chronic, immune-mediated inflammatory condition of the digestive tract associated with substantial psychosocial difficulties. Treatment often focuses on medications but may also include surgical approaches (e.g.
View Article and Find Full Text PDFBackground: Inflammatory bowel disease (IBD) is a chronic autoimmune disease often diagnosed during adolescence. IBD negatively impacts all aspects of health-related quality of life, resulting in physical, emotional, social, school, and work functioning challenges. Adolescents have identified the need for peer support in managing their disease and promoting positive health outcomes.
View Article and Find Full Text PDFDespite landmark breakthroughs in cancer research, African American adults (AA) bear the highest cancer burden compared to other racial groups in the United States (US). AA adults have twice the likelihood of dying from prostate and uterine cancers compared to White adults, suggesting that there are fundamental issues yet to be addressed when developing and implementing cancer-preventative programs for AA communities. Community-based participatory research (CBPR) empowers community members to identify and prioritize their health problems and preferred strategies to tackle these issues.
View Article and Find Full Text PDFThe β-amyloid precursor protein-cleaving enzyme 1 (BACE1) inhibitor JNJ-54861911, a candidate for the treatment of Alzheimer's disease, was withdrawn from clinical trials due to drug-induced liver injury (DILI). This paper describes our investigation of the metabolism of JNJ-54861911 to understand the potential contribution to the observed DILI. In human hepatocytes, JNJ-54861911 is metabolized by CYP450 3A4 to a reactive intermediate (RI), which undergoes glutathione (GSH) addition at C6 of the 2-amino-4-methyl-1,3-thiazin-4-yl moiety via glutathione S-transferase α1 (GSTA1) catalysis.
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