The schematic illustrates the interplay between differentially expressed genes (DEGs) and autophagy-related genes (ARGs) in ischemic stroke pathogenesis. PPP1R15A emerges as a central regulator, linking these gene networks by activating the TLR4/NF-κB signaling pathway. This activation drives downstream processes, including cytotoxicity, apoptosis, autophagy, and neuroinflammation, ultimately exacerbating ischemic stroke progression.

In the hippocampus of AD rats, MT1 expression was slightly increased while MT2 expression was reduced. Ketogenic diet enhanced the immunoreactivity and protein expression of both MT1 and MT2 receptors, as shown by immunofluorescence staining and Western blotting.

A 4 cm defect was created in the nonhuman primate ulnar nerve and repaired with a sural nerve graft assisted with a collagen nerve guidance tube. At 6 months post repair, functional regeneration across the nerve lesion was assessed through electrophysiology and histology. (A) Graphical representation of the injury and repair. (B) Gross image of autograft repair. (C–E) Electrophysiological waveforms measuring activity in the first dorsal interosseus (FDI) muscle and abductor digiti minimi (ADM) muscle after stimulation of ulnar nerve. The autograft repaired nerve was compared to a naïve ulnar nerve.

This study reanalyzed single-nucleus RNA sequencing data from naïve and injured DRGs at 1 and 3 days post-sciatic nerve crush in mice. It identified differentially expressed genes and the biological processes associated with Schwann cells and satellite glial cells within the DRGs, highlighting the upregulation of Atf3 following injury.