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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.

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.

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 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.

BACKGROUND: Stem cell transplantation in repairing infarct myocardium and in improving cardiac function has been widely accepted. However, whether transplanted cells and host cells formed an effective electricity and mechanical couple, whether a relevant independent electrical system with contractile function formed or whether severe malignant ventricular arrhythmia formed, are still unclear.OBJECTIVE: To investigate electrophysiological abnormaltiy and left ventricular remodeling in rats with myocardial infarction following allogenic bone marrow mesenchymal stem cell (BMSC) transplantation.DESIGN, TIME AND SETTING: The randomized controlled animal study was performed at the Experimental Center, Guangxi Medical University from December 2005 to October 2008.MATERIALS: A total of 120 healthy Wistar rats were equally randomized into normal control, sham operation, saline control and cell transplantation groups. Healthy Wister rats aged 1 month were selected to harvest bone marrow.METHODS: At the third passage, rat BMSCs were collected and treated with 5-aza, and differentiated into cerdiomyocytes.BMSCs were labeled with DAPI at 2 hours before transplantation. In the saline control and cell transplantation groups, rat models of myocardial infarction were established by ligating the left anterior descending coronary artery. In the sham operation group, the coronary artery was not ligated, but only braid. At 7 days following ligation, BMSCs in the cell transplantation group at 2×10-1/L were infused into the edge and center of myocardial infarct region by multipoint injection. Rats in the other three groups were subjected to an equal volume of saline.MAIN OUTCOME MEASURES: Electrocardiogram and cardiac electrophysiology were performed. Ultrasonic cardiography was used to detect left ventricular function. Infarct size was determined. DAPl-labeled donor cell migration and distribution was observed with a fluorescence microscope.RESULTS: BMSCs could differentiate into cardiacmuscle cell-like cells which were capable of pulsing spontaneously, expressing cardiactoponin T and forming myofilament in vitro. Compared with the saline control group, PR interval, QRS duration and ventdcular effective refractory period shortened, ventricular fibrillation threshold increased at 4, 8 and 12 weeks (P < 0.05); left ventricular internal diameter at end-systole reduced, and left ventricular ejection fraction and shortening traction was significantly increased (P< 0.05). At 8 and 12 weeks, infarct size was significantly smaller (P < 0.05). At 4 weeks, DAPl-labeled BMSCs could be seen under the fluorescence microscope, and still could he detected at 12 weeks. However, the fluorescence became weak with prolonged time.CONCLUSION: BMSCs have the plasticity of differentiating into cardiac muscle cell-like cells, which can modulate theelectrophysiological abnormality and left ventricular remodeling following myocardial infarction.

Objective The present study was designed to investigate whether pulsing DCs with tumor-derived extracts is an ef- fective way to induce CTL. and antitumor immunity, Methods DCs were propagated from bone marrow (BM)of C57BL/6J(H-2Kb. I- Ab)mice in vitro with GM-CSF + IL-4tumor associated antigen (TAA) extracted from actively growing Hepa 1-6 cells was used to activate DCs. The phenotypes of DCs were detected by FACS, the cytotoxicity of CTL was as- sayed by 3H-TdR labbel assay. Result and Conclusion The TAA extract pulsed DCs exhibited much more and longer cell processes and increased expression of MHC- Ⅰ, MHC-Ⅱ, CD80 (B7-1 ) 、 CD86 (B7-2 ). This experiment has shown that DCs pulsed with TAA extracts of C57B/6J cells could stimulate effectively the responsiveness of syngenic splenic T cells to induce specific CTL against C57BL/6J cells.