Gap junctions(GJ) form the chemical signal channels between cardiocytes.The core proteins of these channels are the connexins(Cx).The quantity or distribution of Cx will lead to the remodeling of GJ, which contributed to arrhythmia and remodeling following the acute myocardial infarction.GJ remodeling is the key reason and pathological basis of arrhythmia following acute myocardial infarction.How to increase the number of myocardial cells and lighten or reverse the heart reconstitution have become a focal point.In the acute myocardial infarction cell transplantation treatment, stem cells are characterized by self-renewal and multi-directional differentiation have been paid great attention.This study summarized the basis and clinical research of GJ structure, function, distribution, remodeling and stem cell transplantation treatment following myocardial infarction.

Biological performances of Ni-Cr porcelain alloy are highly correlated with released metallic ions. Released metal ions from Ni-Cr porcelain alloy, particularly Ni, Be can induce inflammation of the adjacent periodontal tissue and oral mucosa. In vitro evidence has indicated that the immune response can be altered by various metal ions. Allergic reactions due to metallic dental restorations have been documented. Ni has especially been identified as being highly allergenic. The cytotoxicity and corrosion level of Ni-Cr porcelain alloy is increased after recasting. The Ni-Cr porcelain alloy produced according to technology requirements has good biological safety. Ni-Cr porcelain alloy released a few of metal ions which might induce allergy and density of adjacent periodontal tissues, for the stimulation effect of these metal ions. There is no evidence to suggest that Ni-Cr porcelain alloy restorations has systemic toxicity or carcinogenic/genotoxic effect to human.

Smooth muscle cell (SMC) proliferation, platelet free calcium level and aggregation of experimental atherosclerotic rabbits were investigated in this study. Aortic SMC ofhyperlipidemic rabbits in vitro showed higher growth activity than did normal rabbit SMC. And also hyperlipidemic serum stimulated SMC to proliferate at a significantly greater rate than control serum. Moreover, the level of platelet free calcium and the platelet aggregation was also higher in hyperlipidemic rabbits, indicating that activitated platelets possibly release more PDGF to act as a stimulator to SMC proliferation and calcium is an important factor to activate platelets. Furthermore, SMC from 8501-treated rabbits appeared lower proliferative rate than thecells from hyperlipidemic rabbits. And serum from those rabbits inhibited SMC proliferation compared with hyperlipidemic serum, the inhibitory effect was even stronger than that of normal serum. It may be relevant to the favorable effects of 8501 to TXA2/PGI2 balance.

Objective To evaluate the value of cranial MRI on diagnosing nonalcoholic Wernickes encephalopathy (WE). Methods The clinical characters, cranial MRI features, and outcomes materials in six cases of nonalcoholic Wernickes encephalopathy were analyzed.Results Cranial MR and Flair imaging of the patients exhibited areas of increased T 2W and flair signals symmetrically surrounding the aqueduct and third ventricle and within the medial thalamus. One patient who became persistent vegetative state coexistenced increased T 2W and flair signal of the cortex. According to the follow-up results, the alterations of four patients in T 2W and Flair signals showed to resolve being consistent with the clinical recovery. One patient with persistent vegetative state had no change within two years of the follow-up.Conclusions Cranial MRI is of great value in diagnosing nonalcoholic Wernickes encephalopathy and reflects appropriately the pathological evolution of this disease.

Objective To study the effect of Tongxinluo on the plasma C-reactive protein(CRP)and endothelin-1(ET-1)in acute coronary syndrome(ACS) patients.Methods 100 patients with ACS were randomly divided into conventional therapy group and treatment group(conventional therapy+Tongxinluo gelatin capsule).The changes of CRP and ET-1 in the first day,7th and 14th day were observed.Results In the treatment group,CRP and ET-1 were significantly decreased in the 7th and 14th day(P＜0.05,P＜0.01),and there was significant decrease only in the 14th day(P＜0.05)in the conventional therapy group.CRP and ET-1 levels in the treatment group were significantly different as compared with conventional thereapy group(P＜0.01).Conclusion Tongxinluo capsule may protect blood vessel endothelium through inhibiting CRP and ET-1 to decrease the inflammatory response of endangium.

Objective:To explore the effect of endothelin-1 on atrial ifbrosis in patients with atrial ifbrillation (AF).
Methods: A total of 72 patients with thoracotomy were studied, the patients were divided into 2 groups:AF group, n=39 and Sinus rhythm (SR) group, n=33. The mRNA and protein expressions of endothelin-1 (ET-1), platelet derived growth factor-B (PDGF-B) and collagen I (COL1) in right atrial appendage (RAA) tissue were measured by RT-PCR and Western blot analysis;meanwhile, the impact of ET-1 stimulation and non-selective ET-1 receptor antagonist (sulfafurazole SIZ) on PDGF-B mRNA and protein expressions in H9c2 cells were measured.
Results: ①The RAA tissue mRNA and protein expressions in AF group were higher than those in SR group, as for ET-1 (2.830 ± 2.276) vs (1.220 ± 0.887) and (0.835 ± 0.241) vs (0.286 ± 0.083), both P<0.01;for PDGF-B (2.568 ± 2.348) vs (1.567 ± 0.831) and (0.807±0.241) vs (0.381 ± 0.105), both P<0.05;for COL1α1 (3.376 ± 1.598) vs (1.629 ± 0.833) and (0.652 ± 0.210) vs (0.312 ± 0.12), both P<0.05.②The protein expressions of ET-1 and COL1 had positive correlation (r=0.580, P<0.01).③ET-1 promoted PDGF-B secretion in H9c2 cells in a concentration and time-dependent manner;SIZ could reduce such promotion.
Conclusion: ET-1 plays an important role in AF occurrence which might be related to PDGF-B regulation.

Objective To investigate the effect of microRNA-101 (miRNA-101) on atrial fibrosis in human chronic atrial fibrillation (AF). Methods Right atrial appendages were obtained from 59 patients (30 with AF) undergoing cardiac surgery, including 47 patients with valve heart disease and 12 patients with congenital heart disease. The expression of miRNA-101 was determined by quantitative real-time PCR in the right atrial appendages of patients with and without AF. The cell-specific localization of miRNA-101 was detected by in situ hybridization assay. The mRNA and protein expression levels of transforming growth factor β typeⅠreceptor (TGFβRⅠ) and collagen type I (COL1) were determined by quantitative real-time PCR and Western-blot assay, respectively. Collagen in the right atrial appendages was observed by Masson staining assay. Results The expression of miRNA-101 was found to be significantly down-regulated in AF patients compared with patients with sinus rhythm (SR) (P < 0.05). The result of miRNA-ISH showed that miRNA-101, which was highly distributed within the connective tissues of heart, was down-regulated at about 24.9% in patients with AF compared with patients with SR. No significant differences at the mRNA expression level of TGFβRI was found between patients with AF and patients with SR (P > 0.05). But the protein expression of TGFβRI in patients with AF was significantly higher than that of patients with SR (P < 0.05). The mRNA and protein expressionsl of COL1 were significantly higher in patients with AF than thoset of patients with SR (P < 0.05). The collagen was significantly increased in patients with AF than that of patients with SR (P < 0.05). Conclusions Downregulation of miRNA-101 may contribute to atrial fibrosis in human atrial fibrillation by targeting TGFβRⅠ.

AIM: To investigate the effects of heptanol preconditioning on the changes of structure, function and connexin 43 (Cx43) content in mitochondria in a rabbit model of myocardial isehemia-reperfusion (IR) injury. METHODS: In anesthetized open-chest rabbits, the left anterior descending artery (LAD) was occluded for 30 min and reperfused for 4 h. Sixty-four rabbits were randomly divided into 4 groups (n=16 in each group): sham operation group (sham group), ischemia-reperfusion group (IR group), ischemic preconditioning group (IP group) and heptanol preconditioning group (HT group). All rabbits in the 4 groups were killed 4 h after reperfusion. Myocardial infarct size was determined at the end of the experiment. Mitochondria was isolated by centrifugations. The ultrastructural changes of the mitochondria were observed under electronic microscope. The mitochondrial membrane potential, Ca~(2+) concentration, MDA content and SOD activity of myocardial mitochondria were also examined. The content of mitochondria Cx43 was detected by Western blotting. RESULTS: Compared to IR group, the myocardial infarct size was significantly reduced in IP (18.97%±2.80%) and HT (19.97%±3.80%) groups, the damage of mitoehondrial ultrastructure was milder (P<0.05), mitochondrial membrane potential was significantly higher and Ca~(2+) concentration was much lower (P<0.01) in IP group and HT group. No significant difference of MDA content and SOD activity in myocardial mitochondria between IR group and HT group was found. However, MDA content were much lower and SOD activity was significantly higher in IP group as compared to IR group (P<0.01). Compared to sham group, the mitochondria Cx43 expression was distinctly decreased compared to IR group (P<0.05) and no significant difference was found between IP group and HT group (P>0.05). CONCLUSION: Heptanol preconditioning protects myocardium from ischemia-reperfusion injury. The mechanism may be related to increasing in mitochondrial membrane potential, alleviating Ca~(2+) overload in myocardial mitochondria and attenuating the decrease in mitochondria Cx43 expression induced by isehemia-reperfusion.

Objective To investigate the diagnostic value of endoscopic ultrasonography (EUS) for duodenal cysts.Methods Clinical manifestations, results of conventional gastroscopy and EUS, as well as follow-up, of patients with duodenal cysts were retrospectively analyzed.Results A total of 105 patients with duodenal cysts presented with no lesion-related symptoms, but displayed characteristic imaging changes under EUS, which could reveal the origin, size and nature of duodenal cysts, and differentiate it from other submucosal lesions.A maximum follow-up of 5 years showed no changes in duodenal cysts.Conclusion Duodenal cyst is a benign disease, and EUS plays a very important role in diagnosis of the disease.

Objective To observe the injury of some chief organ induced by paraquat (PQ) poisoning in rats, and to explore the mechanism. Method A total of 60 inbred line SD rats were randomly divided into experimental group (n = 30) and control group (n = 30), and each group was further divided into 6 subgroups (n =5) as per the sacrifice of rats at different intervals. The rats of experimental group received the intra-abdominal injection of paraquat (1 mg/mL, 18 mg/kg), and the rats of control group were treated with the same amount of saline solution instead. The rats of each subgroup were sacrificed separately 2 h,6 h, 12 h,24 h,72 h and 120 h after administration of PQ or saline. Lungs, livers and kidneys were taken for histopathological study. Results There was noticeable exudate in lung tissue of rats in experimental group in the early stage. And then the cystic changes in the liver of rats in experimental group were found. A noticeable hemoglobin was found in the renal tubules 24 h after modeling. But the exudation in lung decreased 24 h later, and in the mean time, the disorganization of pulmonary alveoli was obvious and some remarkable collagen appeared in the interstitial tissue of lung, and it was significantly obvious 72 h after modeling. In the liver of rats in experimental group, the injured tissue had some extent of repair in 72 h after modeling, and recovered gradually. But the injury of kidney was exacerbated 72 h after modeling. In the control group, the lung, liver and kidney were not changed in all stages after modeling.Conclusions The paraquat could induce failure of some chief organs in SD rats. The injury was most remarkable in the lung in a progressive way. The kidney injury was not more severe than that of lung tissue, but the pathological changes of the kidney became worse and worse as time taken. The injury of liver induced by paraquat was slight, and the injury could heal up gradually.