L: -carnitine adjunct therapy appears to be associated with a reduced level of cardiac markers in patients with NSTEMI. These results support a larger clinical trial to investigate the effect of L: -carnitine on cardiac events following PCI.
Objective: Recently, the effect of long non-coding RNAs (lncRNAs) in hypertension (HTN) has been identified. This study aims to explore the expression of lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in HTN and its role in vascular lesion and remodeling of HTN rats.
Results: LncRNA MALAT1 expression was up-regulated in HTN patients, and lncRNA MALAT1 could be an effective index of HTN diagnosis. Down-regulated MALAT1 and inhibited Notch-1 could reduce relative factor expression, including inflammation-related factors, endothelial function-related factors and oxidative stress-related factors, and inhibit apoptosis of aortic endothelial cells of HTN rats.
Methods: LncRNA MALAT1 expression in HTN patients and healthy controls was detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Angiotensin II (Ang II)-induced HTN rat models were injected with MALAT1-siRNA, empty lentivirus vector, Notch pathway inhibitor (DAPT) and dimethyl sulphoxide (DMSO) via caudal vein. After three-week treatment, changes of blood pressure, inflammatory factor levels, endothelial function-related factors, oxidative stress indices and apoptosis of vascular endothelial cells were determined by a series of assays.
Conclusion: This study revealed that down-regulated lncRNA MALAT1 could alleviate the vascular lesion and remodeling of HTN rats, the mechanism may be related to the inhibited activation of Notch signaling pathway.
Clin Invest Med 2008; 31 (3): E117-E122.
AbstractPurpose: To investigate the effect of adrenomedullin on the cell numbers and apoptosis of endothelial progenitor cells (EPCs). Methods: Mononuclear cells were isolated from peripheral blood by Ficoll density gradient centrifugation. The cells were stimulated with adrenomedullin, before and after the treatment of adrenomedullin-receptor antagonist, adrenomedullin 22-52, or a PI3K inhibitor LY294002. Results: Adrenomedullin dose-dependently increased the number of EPCs (P<0.05). Adrenomedullin also significantly decreased apoptosis rate of EPCs in a concentrationdependent manner (P<0.05). In the isolated human mononuclear cells pretreated with adrenomedullin 22-52 or LY294002, adrenomedullin failed to increase the number of EPCs or to reduce the level of apoptosis. Conclusions: Adrenomedullin increases the number of EPCs and decreases their apoptosis. These actions are likely mediated by PI3K signaling pathways. The clinical importance of these favourable effects on EPCs remains to be determined.There is growing evidence that endothelial progenitor cells (EPCs) isolated from peripheral blood are able to travel to the sites of ischemia and endothelial disruption, enhancing endothelial function and neovascularization. 1 A recent study suggests that the level of circulating EPCs predicts the occurrence of cardiovascular events and death from cardiovascular causes and may help to identify patients with increased cardiovascular risk. 2 Augmentation of EPCs with improved functional activity might represent a useful strategy for clinical therapy of coronary artery disease. 3 Adrenomedullin is a potent and long lasing vasodilating peptide, comprising 52 amino acids. It is secreted from endothelial cells, smooth muscle cells and adventitial fibroblasts in various organs, such as the heart, lung, kidney, adipose tissues, and the central nervous system. 4,5 Adrenomedullin signaling is of particular importance in endothelial cell biology, since this peptide protects cells from apoptosis, promotes angiogenesis, and affects vascular tone and permeability. 5 Adrenomedullin has also been shown to enhance the angiogenic potency of bone marrowderived mononuclear cell transplantation, and to improve the cardiac function in rats with myocardial infarction. 6 These beneficial effects are believed to be mediated partly by the angiogenic property of adrenomedullin itself and by its antiapoptotic effect on ORIGINAL RESEARCH
Aims: To evaluate the safety and efficacy of a new approach for transseptal catheterization in patients undergoing percutaneous balloon mitral valvuloplasty (PBMV). Methods: One hundred and two patients with rheumatic mitral stenosis were randomized into two groups. In the study group (RA approach), an imaginary horizontal line was drawn from the top end of the tricuspid valve under anteroposterior fluoroscopic view. The intersection of the horizontal line and the right edge of the corresponding thoracic vertebra was defined as the upper border of the Fossa ovalis. The atrial septum was punctured from a point 0.5 cm below the upper border of the Fossa ovalis. In the control group (LA approach), an imaginary horizontal line was drawn between the upper and middle third of the left atrium, and the intersection of this horizontal line and the right edge of the corresponding thoracic vertebra was used as an atrial septum puncture point. Results: Atrial septum puncture succeeded in all patients in the study group and in 72.6% of the patients in the control group (p < 0.01). The average fluoroscopy times for transseptal catheterization in the study and the control groups were 2.0 ± 0.5 and 3.0 ± 1.0 min, respectively (p < 0.01). Transseptal catheterization was subsequently achieved using the RA approach in the 14 patients from the control group in whom the LA approach failed. Conclusions: The RA approach is a safe and effective means for transseptal catheterization in patients undergoing PBMV.
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