Objective To investigate the role of Kv1. 5 in the pathogenesis of pulmonary hypertension simulated by hypobaria and hypoxia, and the effects of dichloroacetate ( DCA) on the Kv1. 5 expression in pulmonary arterial smooth muscle cells ( PASMCs ) and mean pulmonary arterial pressure ( mPAP) . Methods Twenty-four SD rats were randomly divided into a normal group ( N group) , a high altitude group ( HA group) , and a DCA treated group ( DCA group) . The N group were fed in normalconditions, the HA group and DCA group were fed in a hypobaria and hypoxia chamber simulated to an altitude of 5000 meters. In addition, the DCA group rats were gastric gavaged with DCA ( 70 mg · kg - 1 · d - 1 ) .Twenty-one days later, percentage of wall thickness ( WT% ) and percentage of wall area ( WA% ) of the pulmonary arteriole, mPAP, and the ratio of right ventricle / left ventricle and septum ( RV/ LV + S) were evaluated. Real-time PCR, immunohistochemistry and Western blot were carried out to detect the Kv1. 5 expression in PASMCs. Results In the HA group, WT% , and WA% of pulmonary arteriole, mPAP and RV/ ( LV + S) all increased significantly compared with the N group ( P lt;0. 01) . These changes in the DCA group were significantly lower than those in the HA group( P lt; 0. 01) . Furthermore, the protein and mRNA expression of Kv1. 5 in the PASMCs deceased significantly in the HA group compared with the N group( P lt;0. 01) , but recovered in the DCA group ( P lt;0. 01) . Conclusions The expression of Kv1. 5 in PASMCs is tremendously inhibited in rats fed in high altitude, which might be a important role of pulmonaryhypertension. DCA can inhibit the remodeling of pulmonary arterials probably by recovering Kv1. 5 expression.
Abstract:Objective To investigate the expression and significance of Voltage-gated Cl channel-3 （ClC-3） in acute cardiac allograft rejection in rats. Methods The model of heterotopic cardiac allograft of SD to Wistar rats was established. The rats were divided into two groups： control group and cyclosporin A（CsA） treated group （CsA group）. Living span of the transplants in eight rats of each group were observed. Allograft samples were harvested separately on the day 1, 3, 5, 7 after operation （n = 6）. The rejection was evaluated by routine pathological examinations. The myocardial apoptosis by terminal deoxylnucleotidyl transferase mediated-dUTP nick end labeling （TUNEL） method and the local expression of ClC-3 were detected by reverse transcriptase polymerase chain reaction （RT-PCR）. Results The allografts survival time was significantly longer in CsA group compared with that in control group （15.4±5.1dvs. 7.6±1.5d, P〈0.05）. There was lesser pathological changes in CsA group than that in control group. The apoptosis index were significantly higher in control group and the expression of ClC-3 was significantly lower（P〈0.05）. CsA could inhibit the rise of apoptosis index and the decrease of the ClC-3 expression. Conclusion The ClC-3 expression is closely related with the severity of myocardial necrosis and apoptosis index, which indicates that ClC-3 plays a very important role in the necrosis and apoptosis during acute cardiac allograft rejection of rat.
目的 观察电压依赖性钙通道是否作用于大鼠脊髓背角胶状质层（SG）神经元大振幅微小兴奋性突触后电流的形成。 方法 选用成年雄性Sprague-Dawley（SD）大鼠，2%～3%异氟烷麻醉后，分离其腰骶部的脊髓，然后切片。采用全细胞电压钳技术，玻璃微电极的电阻为4~6 MΩ，钳制电压为?70 mV，记录胶状质层神经元微小兴奋性突触后电流（mEPSC）电流。将电流信号用Axopatch 200来放大并储存于电脑。对照组和用药结束后，持续采样mEPSC电流30 s。mEPSC电流的频率和振幅用Clampfit 8.1进行分析。 结果 钳制电压为?70 mV时，所有SG神经元均有自发性的EPSC。辣椒素增加mEPSC发生的频率和波幅。钴离子抑制辣椒素诱导的大振幅mEPSC。钴离子抑制辣椒素诱导的mEPSC的平均振幅，而不抑制其发生频率。 结论 电压依赖性钙离子通道参与了辣椒素引起的痛觉形成。
ObjectiveTo assess the image quality and radiation dose of gemstone CT coronary angiography (CCTA) with low tube voltage and low concentration contrast medium. MethodsSixty-nine patients who underwent CCTA from January to March 2014 were randomly divided into group A and B. CCTA was performed in thirty-four patients in group A with tube voltage of 100 kV and concentration of contrast medium of 300 mgI/mL. And thirty-five patients in group B underwent CCTA with 120 kV and 370 mgI/mL. According to upgrading American Heart Association standard all segments and all vessels were evaluated. We measured the CT value of ascending aortic root, left main coronary artery, and the initial segment of left anterior descending branch, left circumflex, right coronary artery, and also adjacent tissues. Besides, we recorded CT dose volume index (CTDIvol) and the dose length product (DLP) and calculated effective radiation dose. ResultsThe image quality scores were not significantly different between two groups (P>0.05). The density in the contrast enhanced vessel lumens in group A were signifcantly higher than that in group B (P<0.05). There was no significant difference in signal to noise ratio and carrier to noise ratio between the two groups (P>0.05). Noise in group A was higher than that in group B (P<0.05). The CTDIvol and effective radiation dose in group A were significantly lower than those in group B (P<0.05). ConclusionThe combination of 100 kV with low concentration contrast medium (300 mgI/mL) still maintains the image quality, as well as significantly lowers the radiation dose and the dose of iodine.
ObjectiveTo review the recent progress in the role of thrombospondins (TSPs) in synapse formation in the central nervous system (CNS).MethodsA wide range of domestic and foreign literature on the role of TSPs in the synapse formation of the CNS was reviewed. The role of TSPs in structural features, molecules, and related diseases was reviewed.ResultsAs an oligosaccharide protein, TSPs play important roles in angiogenesis, inflammation, osteogenesis, cell proliferation, and apoptosis. In the nervous system, they bind to voltage-dependent calcium channels, neuronectin, and other extracellular matrix proteins and cell surface receptors, and participate in and regulate multiple processes such as synapse formation, maturation, and function in the CNS.ConclusionTSPs as an oligomeric extracellular matrix protein play an important role in the formation of synapses and the repair of synapses after CNS injury.
Chloride voltage-gated channel 7 (CLCN7) gene mutations can cause the disorder of acidification in lacunas and osteolysis, leading to osteopetrosis characterized by increased bone density throughout the body and lysosomal storage diseases. Deafness can be caused by nerve injury for bone compression, negative pressure in the middle ear and otosclerosis. This article will introduce structure and function of CLCN7 gene and CLCN7 protein, osteolysis process, including the introduction of osteoclasts and the mechanism of osteolysis, osteopetrosis, mechanism and treatment of osteopetrosis caused by CLCN7 gene mutations, as well as osteopetrosis and syndromic deafness, in order to provide a basis for clinical diagnosis and treatment.