Activated PTHLH

Studies were done on analysis of biological processes in the same high expression (fold change ≥2) activated PTHLH feedback-mediated cell adhesion gene ontology (GO) network of human hepatocellular carcinoma (HCC) compared with the corresponding low expression activated GO network of no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection). Activated PTHLH feedback-mediated cell adhesion network consisted of anaphase-promoting complex-dependent proteasomal ubiquitin-dependent protein catabolism, cell adhesion, cell differentiation, cell-cell signaling, G-protein-coupled receptor protein signaling pathway, intracellular transport, metabolism, phosphoinositide-mediated signaling, positive regulation of transcription, regulation of cyclin-dependent protein kinase activity, regulation of transcription, signal transduction, transcription, and transport in HCC. We proposed activated PTHLH coupling feedback phosphoinositide to G-protein receptor signal-induced cell adhesion network. Our hypothesis was verified by the different activated PTHLH feedback-mediated cell adhesion GO network of HCC compared with the corresponding inhibited GO network of no-tumor hepatitis/cirrhotic tissues, or the same compared with the corresponding inhibited GO network of HCC. Activated PTHLH coupling feedback phosphoinositide to G-protein receptor signal-induced cell adhesion network included BUB1B, GNG10, PTHR2, GNAZ, RFC4, UBE2C, NRXN3, BAP1, PVRL2, TROAP, and VCAN in HCC from GEO dataset using gene regulatory network inference method and our programming

HIV and Stigma in Liuzhou, China

To describe emergent stigma-related themes from individual descriptions of living with HIV in Liuzhou, China

Interferon a-inducible protein 27 computational network construction and comparison between the frontal cortex of HIV Encephalitis (HIVE) and HIVE-control patients

Interferon α-inducible protein 27 (IFI27) computational network construction and analysis of frontal cortex of HIV encephalitis (HIVE) is very useful to identify novel markers and potential targets for prognosis and therapy. Based on integrated gene regulatory network infer (GRNInfer) method by linear programming and a decomposition procedure with analysis of the significant function cluster using Kappa statistics and fuzzy heuristic clustering from DAVID, we identified and constructed significant molecular IFI27 networks from 12 frontal cortex of HIVE-control patients and 16 HIVE in the same GEO Dataset GDS1726. Our integrative results reflected an IFI27 membrane module only in the upstream of the frontal cortex of HIVE-control patients (BTN3A2, RASGRP3, ROR1 inhibition), and the frontal cortex of HIVE (DGKG, LY96 activation; RASGRP3 inhibition); IFI27 organelle only in the upstream of HIVE-control patients (CREB5, OAS1, PDCD4 activation), and HIVE (PDCD4 activation; ZC3HAV1, ZNF652 inhibition); IFI27 sequence variant only in the upstream of HIVE-control patients (ISG15_2, OAS1, TNFRSF11B activation; BTN3A2, LCAT, ROR1 inhibition), and HIVE (CFB, DGKG, LCAT, LY96 activation; ISG15_2, TNFRSF11B, ZC3HAV1 inhibition)

Cartilage Oligomeric Matrix Protein (COMP)-Mediated Cell Differentiation to Proteolysis Mechanism Networks from Human Normal Adjacent Tissues to Lung Adenocarcinoma

Background: To understand cartilage oligomeric matrix protein (COMP) mechanism network from human normal adjacent tissues to lung adenocarcinoma

Ferrostatin-1 post-treatment attenuates acute kidney injury in mice by inhibiting ferritin production and regulating iron uptake-related proteins

Background Acute kidney injury (AKI) is a common and serious medical condition with high morbidity and mortality. Recent research has highlighted ferroptosis, a novel form of programmed cell death, as a potential therapeutic target in mitigating renal tubular injury in AKI. Ferrostatin-1, a specific ferroptosis inhibitor, has been demonstrated to prevent renal injury through ferroptosis inhibition. Methods Utilizing a murine AKI model, we investigated the effects of Ferrostatin-1 by administering it post-injury. Through high-throughput sequencing and pathological analysis, we focused on the critical role of ferroptosis-related pathways in the treatment. Results Ferrostatin-1 post-conditioning effectively mitigated oxidative damage and reduced iron content associated with AKI. Additionally, critical ferroptosis-related proteins, such as GPX4, SLC7A11, NRF2, and FTH1, exhibited increased expression levels. In vitro, Ferrostatin-1 treatment of HK-2 cells significantly diminished lipid peroxidation and iron accumulation. Furthermore, Ferrostatin-1 was found to downregulate the PI3K signalling pathway. Conclusion Ferrostatin-1 acted as a potential ferroptosis inhibitor with the capacity to enhance antioxidant defences. This study suggests that Ferrostatin-1 could serve as a promising novel strategy for improving the treatment of AKI and promoting recovery from the condition