AI Networking Cookbook: Practical recipes for AI-assisted network automation and development
TL;DR
Under HG conditions, silencing of SNHG12 promoted cell proliferation, inhibited apoptosis, and mitigated inflammatory responses, as well as attenuated fibrosis, reflected by decreased expression of transforming growth factor-beta 1 and alpha-smooth muscle actin.
FBXL19-AS1 appears to interact with and modulate miR-650, thereby affecting ITGB3 expression and potentially participating in the pathological progression of AD.
Overexpression of Gm10451 suppressed G6PD, aggravated oxidative/ER stress and inflammation, inhibited insulin secretion and promoted β-cell apoptosis, representing a poteniall therapeutic target for diabetes-related β-cell dysfunction.
NR2F1-AS1 serves as a potential non-invasive biomarker and promising therapeutic target for DPN by driving Schwann cell dysfunction via the NR2F1-AS1/miR-150-5p/TP53 axis.
It is suggested that lnc-DNAJC3-AS1 promotes GC progression, at least in part, through the miR-576-5p/LYPLA1 pathway, providing a potential target for GC treatment.
A progressive dysregulation of miR-182-5p/NRF2 axis is closely linked to the deterioration of glycemic control, inflammation and iron metabolism in type 2 diabetes mellitus and could be useful for disease stratification and as potential targets for future therapies and risk assessment.
Overexpression of GAS6-AS1 could mitigate the reduction in cell viability and the elevation in apoptosis induced by DOX in H9c2 cells, and inhibit the expression of pro-inflammatory factors.
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