CACNA1C rs1006737 SNP increases the risk of essential hypertension in both Chinese Han and ethnic Russian people of Northeast Asia.

Voltage-gated Ca2+ channels play a key role in the regulation of arterial tone and blood pressure. The aim of this study was to determine whether the association of calcium voltage-gated channel subunit alpha1 C (CACNA1C) rs1006737 with essential hypertension (EH) exists in both Chinese Han and ethnic Russian populations of Northeast Asia. We used a case-control study of 2 ethnic groups in the same latitude geographical area to investigate the association between the susceptibility of EH and rs1006737 polymorphism.

Electrochemical behavior of titanium and platinum in dicarboxilic amino acids solution.

Titanium and platinum samples as components of bimetallic implants for the osteoregeneration process have been modified in solutions modeling biological systems and studied by means of cyclic voltammetry, electrochemical impedance spectroscopy and scanning probe microscopy. While aspartic and glutamic acids did not adsorb significantly on platinum in the potential region investigated, the presence of the amino acids affects oxide layer growth on the titanium surface under anodic polarization. The two studied amino acids behave differently on the titanium electrode surface due to differences in adsorption modes of these substances.

Level of Blood Cell-Free Circulating Mitochondrial DNA as a Novel Biomarker of Acute Myocardial Ischemia.

Changes in the level of blood cell-free circulating mitochondrial DNA were examined during experimental adrenaline-induced myocardial injury in rats. The amount of mitochondrial DNA in the blood was significantly elevated at 48 and 72 h after subcutaneous injection of adrenaline solution, and it was accompanied by development of multiple small-focal myocardial ischemia. This suggests that the measured level of blood cell-free circulating mitochondrial DNA might be used as a biomarker of acute myocardial ischemia.

[Mechanisms of mitochondrial dysfunction development in vessels upon peroxidizes LDL influence].

The mechanisms of mitochondrial dysfunction development in vessels upon peroxodized LDL (pLDL) influence are discussed. Is is shown that the components of pLDL induce the formation of covalent complexes with cell proteins and destabilize cellular membrane microdomain structure that leads to membrane proteins dysfunction, Ca2+ liberation into cytosol from its stores, endoplasmic reticulum stress, increase in reactive oxygen species production by NADPH-oxidases. These effects cause disturbances in mitochondria of target cells, increases in reactive oxygen species production, mitochondrial pathway of cell death.