Sequential Proteomic and N-Glycoproteomic Analyses of Bronchoalveolar Lavage Fluids for Potential Biomarker Discovery of Lung Adenocarcinoma.

Lung adenocarcinoma (LUAD) is the most common histological subtype of nonsmall-cell lung cancer. Herein, a multiomics method, which combined proteomic and N-glycoproteomic analyses, was developed to analyze the normal and cancerous bronchoalveolar lavage fluids (BALFs) from six LUAD patients to identify potential biomarkers of LUAD. The data-independent acquisition proteomic analysis was first used to analyze BALFs, which identified 59 differentially expressed proteins (DEPs).

Somatostatin-expressing neurons in the medial prefrontal cortex promote sevoflurane anesthesia in mice.

Background: The medial prefrontal cortex plays a crucial role in regulating consciousness. However, the specific functions of its excitatory and inhibitory networks during anesthesia remain uncertain. Here we explored the hypothesis that somatostatin interneurons in the medial prefrontal cortex enhance the effects of sevoflurane anesthesia by increasing GABA transmission to pyramidal neurons.

Characterization of a novel D-sorbitol dehydrogenase from Faunimonas pinastri A52C2.

The enzyme D-sorbitol dehydrogenase (SLDH) facilitates the conversion of D-sorbitol to L-sorbose. While current knowledge of this enzyme class predominantly centers on Gluconobacter oxydans, the catalytic properties of enzymes from alternative sources, particularly their substrate specificity and coenzyme dependency, remain ambiguous. In this investigation, we conducted BLASTp analysis and screened out a novel SLDH (Fpsldh) from Faunimonas pinastri A52C2.

Liposomes-Loaded miR-9-5p Alleviated Hypoxia-Ischemia-Induced Mitochondrial Oxidative Stress by Targeting ZBTB20 to Inhibiting Nrf2/Keap1 Interaction in Neonatal Mice.

Hypoxia ischemia (HI) is a leading cause of cerebral palsy and long-term neurological sequelae in infants. Given that mitochondrial dysfunction in neurons contributes to HI brain damage, this study aimed to investigate the regulatory role of miR-9-5p in mitochondrial function following HI injury. Overexpression of miR-9-5p in HI mice or HO-exposed PC12 cells suppressed neuronal injury, associated with increased mitochondrial copy number, normalizing mitochondrial membrane potential, improved nuclear factor-erythroid factor 2-related factor 2 (Nrf2) activation, and downregulation of Keap1.