Cadmium Inhibits Proliferation of Human Bronchial Epithelial BEAS-2B Cells Through Inducing Ferroptosis via Targeted Regulation of the Nrf2/SLC7A11/GPX4 Pathway.

Cadmium (Cd)-induced pulmonary toxicity is closely associated with ferroptosis, a regulated form of cell death characterized by iron-dependent lipid peroxidation (LPO). Luteolin (Lut) is a natural flavonoid compound that exists in many plants. In this study, we used human bronchial epithelial BEAS-2B cells to explore the impact of ferroptosis in the inhibition of Cd-induced BEAS-2B cells proliferation.

[Luteolin inhibits proliferation of lung cancer A549 cells by increasing ROS production and inhibiting the AKT/mTOR signaling pathway and HO-1 expression].

Objectives: To investigate the mechanism of luteolin for inhibiting proliferation of lung cancer A549 cells.

Methods: A549 cells treated with different concentrations of luteolin for 48 h were evaluated for changes in cell viability, proliferation, reactive oxygen species (ROS) production and apoptosis using MTT assay, plate cloning assay, EdU staining, DCFH-DA assay and Hoechst33258 staining. The changes in cell autophagy were examined with MDC staining, and the expressions of apoptosis-related proteins (Bax, Bcl-2, and cleaved caspase-9), autophagy-related proteins (LC3B, Beclin 1, and P62), AKT/mTOR pathway proteins, and HO-1 protein were detected using Western blotting.

Solid-state molecular oxygen activation using ball milling and a piezoelectric material for aerobic oxidation of thiols.

The agitation of BaTiO ball milling converts mechanical energy into electrical energy, leading to the reduction of molecular oxygen a single electron transfer pathway analogous to the photocatalytic reaction. This mechanoredox strategy for the oxidative coupling of thiols could eliminate waste and develop a recyclable methodology to accomplish organic transformations in a greener fashion, exhibiting promising potential for large-scale chemical manufacturing.

The Analysis of Potential Diagnostic and Therapeutic Targets for the Occurrence and Development of Gastric Cancer Based on Bioinformatics.

Objective: Gastric cancer is among the most common malignant tumors of the digestive system. This study explored the molecular mechanisms and potential therapeutic targets for gastric cancer occurrence and progression using bioinformatics.

Methods: The gastric cancer microarray dataset was downloaded from the Gene Expression Omnibus (GEO) database.

Porous graphene oxide/chitosan beads with honeycomb-biomimetic microchannels as hydrophilic adsorbent for the selective capture of glycopeptides.

A porous hydrophilic affinity bead consisting of graphene oxide and chitosan (pGC) with the honeycomb-biomimetic microchannels has been synthesized and applied as hydrophilic adsorbent for selective capture of glycopeptides. The pGC beads have open-porous structure, honeycomb-like microchannels, large interior voids, and hydrophilic property. Based on the multivalent hydrophilic interactions between glycan moieties on glycopeptides and amino groups and hydroxyl groups on chitosan, the glycopeptides were enriched and separated by pGC beads.

miR‑146a improves hepatic lipid and glucose metabolism by targeting MED1.

Non‑alcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases worldwide. Increasing evidence has shown that microRNAs (miRNAs) play a vital role in the progression of NAFLD. The aim of the present study was to examine the expression level and roles of miR‑146a in fatty liver of high‑fat diet (HFD) and ob/ob mice and fatty acid‑treated hepatic cells using RT‑qPCR and western blot analysis.

Long non-coding RNA ANRIL enhances mitochondrial function of hepatocellular carcinoma by regulating the MiR-199a-5p/ARL2 axis.

Although the roles of long non-coding RNA (lncRNA) ANRIL (Antisense non-coding RNA in the INK4A locus) have been established in various tumors, its roles in mitochondrial metabolic reprogramming of hepatocellular carcinoma (HCC) cells are still unclear. This work aims to explore lncRNA ANRIL roles in regulating the mitochondrial metabolic reprogramming of liver cancer cells. First, we found that lncRAN ANRIL expression was significantly increased in HCC tissues or cells compared with the normal adjacent tissues and normal tissues or cells.