MiR-140-5p exerts a protective function in pregnancy-induced hypertension via mediating TGF-β/Smad signaling pathway.

Animal experiments showed that PIH rats had increased mean arterial pressure (MAP), systolic blood pressure (SBP), and diastolic blood pressure (DBP), but decreased litter size, number of viable fetuses, fetal weight, and placental weight. The higher Flt-1 and lower VEGF was observed in PIH rats with elevated TNF-α and IL-6 levels and decreased IL-10 levels. Treatment with agomiR-140-5p improved regarding the above indicators.

Oligomeric Aβ25-35 induces the tyrosine phosphorylation of PSD-95 by SrcPTKs in rat hippocampal CA1 subfield.

Purpose: Although amyloid-β (Aβ) is one of the neuropathological hallmarks of Alzheimer's Disease (AD), the mechanisms of Aβ neurotoxicity remain to be clarified. This study was aimed to evaluate the effect of Aβ on postsynaptic density-95 (PSD-95) tyrosine phosphorylation. Elucidating the regulatory mechanisms underlying it may be a promising therapy in AD.

The diagnostic value and regulatory mechanism of miR-200a targeting in pregnancy-induced hypertension.

Objective: To investigate the diagnostic value and regulatory mechanism of miR-200a targeting ZEB1 in pregnancy-induced hypertension (PIH).

Methods: The expression of miR-200a and ZEB1 was detected in the placenta of PIH patients, and then the human trophoblastic cell line JEG-3 was transfected and divided into different groups: control group, NC group, ZEB1 siRNA group, miR-200a inhibitor group and miR-200a inhibitor group + ZEB1 siRNA group. After transfection, cell proliferation and migration/invasion were evaluated byMTT and Transwell assays, respectively, whereas apoptosis was assessed byflow cytometry.

Current Trends for ST-segment Elevation Myocardial Infarction during the Past 5 Years in Rural Areas of China's Liaoning Province: A Multicenter Study.

Background: Since 2010, two versions of National Guidelines aimed at promoting the management of ST-segment elevation myocardial infarction (STEMI) have been formulated by the Chinese Society of Cardiology. However, little is known about the changes in clinical characteristics, management, and in-hospital outcomes in rural areas.

Methods: In the present multicenter, cross-sectional study, participants were enrolled from rural hospitals located in Liaoning province in Northeast China, during two different periods (from June 2009 to June 2010 and from January 2015 to December 2015).

Involvement of P38MAPK activation by NMDA receptors and non-NMDA receptors in amyloid-β peptide-induced neuronal loss in rat hippocampal CA1 and CA3 subfields.

Oligomeric amyloid-β peptide (Aβ) has been found to be associated with the pathogenesis of Alzheimer's disease (AD). Numerous studies have reported Aβ neurotoxicity, but the underlying molecular mechanisms remain to be fully illuminated. In the present study, we investigated the Aβ-induced activation and regulation of P38MAPKs in rat hippocampus in vivo.

Oligomerized Abeta25-35 induces increased tyrosine phosphorylation of NMDA receptor subunit 2A in rat hippocampal CA1 subfield.

Amyloid-beta peptide (Abeta) plays a causal role in the pathogenesis of Alzheimer's disease (AD). To elucidate the mechanisms underlying the over-activation of NMDA receptors in AD, we investigated the alteration of NR2A tyrosine phosphorylation after intracerebroventricular infusion of Abeta25-35 oligomers. Abeta25-35 treatment resulted in the elevated tyrosine phosphorylation of NR2A in rat hippocampal CA1 subfield and facilitated the interactions of NR2A or PSD-95 with Src kinases.

Mitochondrial Ca2+ flux and respiratory enzyme activity decline are early events in cardiomyocyte response to H2O2.

Oxidative stress is involved in mitochondrial apoptosis, and plays a critical role in ischemic heart disease and cardiac failure. Exposure of cardiomyocytes to H(2)O(2) leads to oxidative stress and mitochondrial dysfunction. In this study, we investigated the temporal order of mitochondrial-related events in the neonatal rat cardiomyocyte response to H(2)O(2) treatment.