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Combs McGrath posted an update 6 months, 1 week ago
To systematically review studies that examined the influence of the CYP1A2 -163C>A polymorphism on the ergogenic effects of caffeine and to discuss some of the reasons for the discrepancies in findings between the studies.
This review was performed in accordance with the PRISMA guidelines. The search for studies was performed through nine databases.
Seventeen studies were included in the review. Based on the included studies, it seems that individuals with the AA or AC/CC genotype may experience an increase in performance following caffeine ingestion. Significant differences between genotypes were found in four studies, and all four reported a more favorable response in the AA vs. AC/CC genotype. These results suggest that if there is an actual genotype-related effect of acute caffeine supplementation, it might be in that direction. In the studies that reported such data for aerobic endurance, the findings are specific to male participants performing cycling time trials (distances of ≥ 10km) and ingesting caffeine 60min before exercise. For high-intensity exercise, two studies reported that genotype variations determined the response to caffeine ingestion, even though the differences were either small (~ 1 additional repetition in high-load resistance exercise set performed to muscular failure) or inconsistent (i.e., observed only in one out of eight performance tests).
CYP1A2 genotype variations may modulate caffeine’s ergogenic effects, but the differences between genotypes were small, inconsistent, or limited to specific exercise scenarios. Future studies with larger sample sizes are needed to fully elucidate this research area.
CYP1A2 genotype variations may modulate caffeine’s ergogenic effects, but the differences between genotypes were small, inconsistent, or limited to specific exercise scenarios. Future studies with larger sample sizes are needed to fully elucidate this research area.
The Nod-like receptor protein-3 (NLRP3) inflammasome signalling pathway is involved in the inflammatory reaction of myocardial ischaemia-reperfusion (I/R) injury. Our previous study showed that miR-330-5p was differentially expressed in both cerebral and myocardial I/R injury, and thus might be a biomarker for I/R injury-related diseases. Another study also indicated that miR-330-5p could promote NLRP3 inflammasome activation in renal IRI. However, the role of miR-330-5p in myocardial I/R injury-induced inflammatory responses is unknown. This study aimed to investigate the role of miR-330-5p in NLRP3 inflammasome-mediated myocardial I/R injury.
Myocardial I/R injury was induced in mice by occlusion of the left anterior descending coronary artery for 45min followed by reperfusion. For NLRP3 inflammasome stimulation in vitro, cardiomyocytes were treated with 2h of oxygen and glucose deprivation (OGD) or LPS (100ng/ml). Myocardial miR-330-5p expression was examined by PCR at different treatment times. A miR-oth in-vivo and in-vitro models. Furthermore, TIM3 was confirmed as a potential target of miR-330-5p. As predicted, suppression of TIM3 by siRNA ameliorated the anti-miR-330-5p-mediated activation of the NLRP3 inflammasome induced by OGD and LPS, thus decreasing cardiomyocyte apoptosis.
Our study indicated that the miR-330-5p/TIM3 axis was involved in the regulatory mechanism of NLRP3 inflammasome-mediated myocardial inflammation.
Our study indicated that the miR-330-5p/TIM3 axis was involved in the regulatory mechanism of NLRP3 inflammasome-mediated myocardial inflammation.Mutations in kinases are abundant and critical to study signaling pathways and regulatory roles in human disease, especially in cancer. Somatic mutations in kinase genes can affect drug treatment, both sensitivity and resistance, to clinically used kinase inhibitors. Here, we present a newly constructed database, KinaseMD (kinase mutations and drug response), to structurally and functionally annotate kinase mutations. KinaseMD integrates 679 374 somatic mutations, 251 522 network-rewiring events, and 390 460 drug response records curated from various sources for 547 kinases. We uniquely annotate the mutations and kinase inhibitor response in four types of protein substructures (gatekeeper, A-loop, G-loop and αC-helix) that are linked to kinase inhibitor resistance in literature. In addition, we annotate functional mutations that may rewire kinase regulatory network and report four phosphorylation signals (gain, loss, up-regulation and down-regulation). Overall, KinaseMD provides the most updated information on mutations, unique annotations of drug response especially drug resistance and functional sites of kinases. KinaseMD is accessible at https//bioinfo.uth.edu/kmd/, having functions for searching, browsing and downloading data. YJ1206 To our knowledge, there has been no systematic annotation of these structural mutations linking to kinase inhibitor response. In summary, KinaseMD is a centralized database for kinase mutations and drug response.Innate lymphoid cells (ILCs) are a recently identified subset of leukocytes that play a central role in pathogen surveillance and resistance, modulation of immune response, and tissue repair. They are remarkably similar to CD4+ T-helper subsets in terms of function and transcription factors required for their development but are distinguished by their lack of antigen-specific receptors. Despite their similarities, the absence of a surface T-cell receptor (TCR) and presence of ILCs and precursors in adult bone marrow has led to speculation that ILCs and T cells develop separately from lineages that branch at the point of precursors within the bone marrow. Considering the common lineage markers and effector cytokine profiles shared between ILCs and T cells, it is surprising that the status of the TCR loci in ILCs was not fully explored at the time of their discovery. Here, we demonstrate that a high proportion of peripheral tissue ILC2s have TCRγ chain gene rearrangements and TCRδ locus deletions. Detailed analyses of these loci show abundant frameshifts and premature stop codons that would encode nonfunctional TCR proteins. Collectively, these data argue that ILC2 can develop from T cells that fail to appropriately rearrange TCR genes, potentially within the thymus.
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