TRIOL Inhibits Rapid Intracellular Acidification and Cerebral Ischemic Injury: The Role of Glutamate in Neuronal Metabolic Reprogramming.

As one of the key injury incidents, tissue acidosis in the brain occurs very quickly within several minutes upon the onset of ischemic stroke. Glutamate, an excitatory amino acid inducing neuronal excitotoxicity, has been reported to trigger the decrease in neuronal intracellular pH (pHi) via modulating proton-related membrane transporters. However, there remains a lack of clarity on the possible role of glutamate in neuronal acidosis via regulating metabolism.

Coexistence of and (X) on a Novel Plasmid in sp. From Pig in Shanghai, China.

The purpose of this study was to characterize the complete sequence of a novel plasmid carrying tigecycline resistance gene (X) and carbapenemase gene from a swine sp. strain SH19PTT10. Minimal inhibitory concentration (MIC) was performed using microbroth dilution method.

The linear stability of Hunt-Rayleigh-Bénard flow.

The stability of a pressure driven flow in a duct heated from below and subjected to a vertical magnetic field (Hunt-Rayleigh-Bénard flow) is studied. We use the Chebyshev collocation approach to solve the eigenvalue problem for the small-amplitude perturbations. It is demonstrated that the magnetic field can stabilize the flow, while the temperature field can disturb the flow.

Protective effect of low dose gadolinium chloride against isoproterenol-induced myocardial injury in rat.

Acute myocardial injury remains a leading cause of morbidity and mortality worldwide, and large amount of released arachidonic acid (AA) is found to be related to cardiomyocyte apoptosis and necrosis. Previous study suggested that GdCl3 completely abolished AA-induced Ca(2+) response. Thus, this study aims to investigate possible cardioprotection effect of GdCl3 on isoproterenol (ISO)-induced myocardial injury and its underlying mechanism(s).