The synthesis of 3D organic-inorganic hybrid heterojunctions of g-CN nanoneedles@TiC MXene with superior photocatalytic H evolution.

3D organic-inorganic hybrid heterojunctions of 1D carbon nitride (g-CN) nanoneedles anchoring on 2D TiC MXene nanosheets have been constructed a green molten salt treatment. The TiC MXene nanosheets and molten salt treatment guide the formation of ordered nanoneedle-like g-CN. Both the formed heterojunctions and the nanoneedle-like structures contribute charge separation and transfer for superior photocatalytic H evolution.

Verapamil reverses cardiac iron overload in streptozocin-induced diabetic rats.

Accumulating evidence shows that iron overload is a new risk factor for diabetes mellitus. L-type Ca(2+) channel (LTCC) has been identified as an important mediator for ferrous iron uptake into cardiomyocytes. In this study, we aimed to examine the effects of verapamil, the LTCC blocker, on myocardial iron metabolism in diabetic rats.

Myocardial iron metabolism in the regulation of cardiovascular diseases in rats.

The iron homeostasis plays an important role in cardiac function. To understand how it acts in diabetic and ischemic myocardial injury, we studied the myocardial iron metabolism in diabetic and myocardial ischemic rats. Diabetic rats were induced by intraperitoneal injection of streptozocin (STZ) after intragastric administration of a high-fat diet while the ischemic rat hearts were subjected to coronary artery ligation for 0.

Reciprocal regulation between M3 muscarinic acetylcholine receptor and protein kinase C-epsilon in ventricular myocytes during myocardial ischemia in rats.

We have studied the association between M(3) muscarinic acetylcholine receptors (M(3)-mAChR) and protein kinase C-epsilon (PKC-epsilon) during ischemic myocardial injury using Western blot analysis and immunoprecipitation technique. Myocardial ischemia (MI) induced PKC-epsilon translocation from cytosolic to membrane fractions. This translocation participated in the phosphorylation of M(3)-mAChR in membrane fractions, which could be abolished by the inhibitor of PKC, chelerythrine chloride.