Simvastatin ameliorates oxygen glucose deprivation/reoxygenation-induced pulmonary endothelial barrier dysfunction by restoring cell-cell junctions and actin cytoskeleton dynamics via the PI3K/Akt signaling pathway.

Endothelial barrier dysfunction is a critical pathophysiological process of pulmonary ischemia/reperfusion (I/R) injury in patients scheduled for cardiopulmonary bypass. Impaired actin cytoskeleton dynamics and cell-cell junctions are the main causes of endothelial dysfunction. Statins have protective effects on I/R-induced lung injury; however, the mechanism is unclear.

Angiotensin II Type I Receptor Agonistic Autoantibody Induces Podocyte Injury via Activation of the TRPC6- Calcium/Calcineurin Pathway in Pre-Eclampsia.

Background/aims: Angiotensin II type I receptor agonistic autoantibody (AT1-AA) is closely related to pre-eclampsia, which is characterized by proteinuria and hypertension. AT1-AA has been shown to enhance the effect of AngII in pre-eclampsia, such as production of endothelin-1, activation of ROS, and vasoconstriction, which are considered to be associated with hypertension; however, whether or not AT1-AA participates in podocyte damage leading to the generation of proteinuria has not been reported. In this study we investigated the role of pre-eclamptic serum AT1-AA on podocytes and the mechanism underlying the generation of proteinuria.

Inhibition of MiR-92a May Protect Endothelial Cells After Acute Myocardial Infarction in Rats: Role of KLF2/4.

BACKGROUND This study was designed to investigate the effects of microRNA-92 (miR-92), Kruppel-like factor 2 (KLF2), and Kruppel-like factor 4 (KLF4) on endothelial injury after acute myocardial infarction (AMI). MATERIAL AND METHODS Blood samples were collected from 50 AMI patients for detection of cardiac troponin I (cTnI), heart-type fatty acid-binding protein (H-FABP), and von Willebrand factor (vWF). The Sprague-Dawley rat models of AMI (n=30) were established by ligating their left anterior descending coronary artery.

Gastrodin blocks neural stem cell differentiation into glial cells mediated by kainic acid.

Kainic acid can simulate excitatory amino acids in vitro. Neural stem cells, isolated from newborn Wistar rats, were cultured in vitro and exposed to 100-4 000 μM kainic acid for 7 days to induce neuronal cell differentiation, causing the number of astrocytes to be significantly increased. Treatment with a combination of 0.

[The clinical application of the neurovascular island flap of the calf supported by perforating branches of peroneal artery].

Objective: To study the clinical application of the neurovascular island flap of the calf supported by perforating branches of peroneal artery for the soft tissue defects of ankle and the foot.

Methods: The flaps were used in 27 cases to repair the soft tissue defects of ankle and the lower leg from February 2004 to December 2007. Among them, 21 cases were male and 6 cases were female, ranging in age from 7 months to 64 years, with an average of 31.