Identifying Pyroptosis-Hub Genes and Inflammation Cell Type-Related Genes in Ischemic Stroke.

Stroke is the second-leading global cause of death. The damage attributed to the immune storm triggered by ischemia-reperfusion injury (IRI) post-stroke is substantial. However, data on the transcriptomic dynamics of pyroptosis in IRI are limited.

Therapeutic Hypothermia Combined with Hydrogen Sulfide Treatment Attenuated Early Blood-Brain Barrier Disruption and Brain Edema Induced by Cardiac Arrest and Resuscitation in Rat Model.

Brain injury remains a major problem in patients suffering cardiac arrest (CA). Disruption of the blood-brain barrier (BBB) is an important factor leading to brain injury. Therapeutic hypothermia is widely accepted to limit neurological impairment.

ncRNA-Regulated LAYN Serves as a Prognostic Biomarker and Correlates with Immune Cell Infiltration in Hepatocellular Carcinoma: A Bioinformatics Analysis.

Liver hepatocellular carcinoma (LIHC) remains a lethal disease for humans. Immune checkpoint inhibitors (ICIs) targeting PD1/PD-L1 and CTLA4 offered new hopes for advanced-stage patients. Novel immune biomarkers and therapeutic targets are urgently needed.

Therapeutic hypothermia attenuates global cerebral reperfusion-induced mitochondrial damage by suppressing dynamin-related protein 1 activation and mitochondria-mediated apoptosis in a cardiac arrest rat model.

Therapeutic hypothermia is effective to attenuate brain ischemia/reperfusion (I/R) injury after cardiac arrest, and multiple mechanisms have been proposed. Dynamin-related protein 1 (Drp1), a large GTPases of dynamin superfamily, predominantly controls mitochondrial fission and is related to IR-induced Cyt C release and apoptosis. However, the effect of therapeutic hypothermia on Drp1 and mitochondrial fission after cardiac arrest remains still unclear.

Hydrogen-rich saline attenuates hippocampus endoplasmic reticulum stress after cardiac arrest in rats.

Background: Hydrogen-rich saline can selectively scavenge reactive oxygen species (ROS) and protect brain against ischemia reperfusion (I/R) injury. Endoplasmic reticulum stress (ERS) has been implicated in the pathological process of cerebral ischemia. However, very little is known about the role of hydrogen-rich saline in mediating pathophysiological reactions to ERS after I/R injury caused by cardiac arrest.