Single-Atom Nanocatalytic Therapy for Suppression of Neuroinflammation by Inducing Autophagy of Abnormal Mitochondria.

Catalysts have achieved efficacy in scavenging reactive oxygen species (ROS) to eliminate neuroinflammation, but it ignores the essential fact of blocking the source of ROS regeneration. Here, we report the single-atom catalysts (SACs) Pt/CeO, which can effectively catalyze the breakdown of existing ROS and induce mitochondrial membrane potential (Δψ) depolarization by interfering with the α-glycerophosphate shuttle pathway and malate-aspartate shuttle pathway, indirectly triggering the self-clearance of dysfunctional mitochondria and thus eradicating the source of ROS generation. In a therapeutic model of Parkinson's disease (PD), Pt/CeO wrapped by neutrophil-like (HL-60) cell membranes and modified by rabies virus glycoprotein (RVG29) effectively crosses the blood-brain barrier (BBB), enters dopaminergic neurons entering the neuroinflammatory region breaking down existing ROS and inducing mitophagy by electrostatic adsorption targeting mitochondria to prevent ROS regeneration after catalyst discharge.

Clinical characteristics and predictors of burn complicated with smoke inhalation injury: A retrospective analysis.

Fire smoke enters the human lungs through the respiratory tract. The damage to the respiratory tract and lung tissue is known as smoke inhalation injury (SII). Fire smoke can irritate airway epithelium cells, weaken endothelial cell adhesion and lyse alveolar type II epithelia cells, leading to emphysema, decreased lung function, pneumonia and risk of acute lung injury/acute respiratory distress syndrome (ARDS).