Two surgical treatment methods for open angle glaucoma and cataract

AIM: To compare the curative effects of two surgical treatment methods for open angle glaucoma and cataract patients.<p>METHODS: Totally 69 patients with primary open angle glaucoma and cataract were divided into two groups: group A and group B. Thirty-four patients(34 eyes)in group A underwent small incision non-phacoemulsification cataract surgery combined with trabeculectomy, just combined operations, 35 patients(35 eyes)in group B underwent small incision non-phacoemulsification cataract surgery beyond 6mo after trabeculectomy, just two stage operations. Postoperative intraocular pressure at 1wk and 3mo, postoperative corrected visual acuity and filtering bleb at 3mo were observed, and intraoperative and postoperative complications were compared. All the patients were followed up for 3-6mo.<p>RESULTS: All the visual acuity were increased compared with that before surgery in two groups, the difference was not statistically significant. All the intraocular pressure was controlled in two groups, the difference was not statistically significant, and the difference about the filtering bleb was neither statistically significant(<i>P</i>>0.05). There were no serious intraoperative and postoperative complications in two groups.<p>CONCLUSION: The two stage operations and the combined operations both can control theintraocular pressure and improved visual acuity of open angle glaucoma and cataract. The two stage operations may prevent a second operation for post trabeculectomy cataract, allowing earlier visual rehabilitation

Late cardioprotection of exercise preconditioning against exhaustive exercise-induced myocardial injury by up-regulatation of connexin 43 expression in rat hearts

AbstractObjectiveTo investigate the expression of myocardium connexin 43 (Cx43) in late exercise preconditioning (LEP) cardioprotection.MethodsEight-week-old adult male Sprague Dawley rats were randomly assigned into four groups (n = 8). Myocardial injury was judged in accordance with serum levels of cTnⅠ and NT-proBNP as well as hematoxylin basicfuchsin picric acid staining of myocardium. Cx43 mRNA was detected by in situ hybridization and qualified by real-time fluorescence quantitative PCR. Cx43 protein was localized by immunohistochemistry and its expression level was determined by western blotting.ResultsThe LEP obviously attenuated the myocardial ischemia/hypoxia injury caused by exhaustive exercise. There was no significant difference of Cx43 mRNA level between the four groups. Cx43 protein level was decreased significantly in group EE (P < 0.05). However, LEP produced a significant increase in Cx43 protein level (P < 0.05), and the decreased Cx43 protein level in exhaustive exercise was significantly up-regulated by LEP (P < 0.05).ConclusionsLEP protects rat heart against exhaustive exercise-induced myocardial injury by up-regulating the expression of myocardial Cx43

Transcriptional activation of microRNA-34a by NF-kappa B in human esophageal cancer cells

<p>Abstract</p> <p>Background</p> <p>miR-34a functions as an important tumor suppressor during the process of carcinogenesis. However, the mechanism of miR-34a dysregulation in human malignancies has not been well elucidated. Our study aimed to further investigate the regulation mechanism of miR-34a.</p> <p>Results</p> <p>We found that overexpression of NF-kappa B p65 subunit could increase miR-34a levels in EC109, an esophageal squamous cancer cell line, while ectopic expression of DN IkappaB leaded to a significant reduction of miR-34a expression. Bioinformatics analysis suggested three putative KB sites in promoter region of miR-34a gene. Mutation two of these KB sites impaired p65 induced miR-34a transcriptional activity. Chromatin immunoprecipitation and electrophoretic mobility shift assays both showed that NF-kappaB could specifically bind to the third KB site located in miR-34a promoter. In addition, we found that overexpression of NF-kappaB p65 could not successfully induce miR-34a expression in esophageal cancer cell lines with mutant p53 or decreased p53. Reporter assay further showed that NF-kappaB-induced miR-34a transcriptional activity was reduced by p53 impairment. Nevertheless, CHIP analysis suggested binding of NF-kappaB to miR-34a promoter was not affected in cells with mutant p53.</p> <p>Conclusions</p> <p>Our work indicates a novel mechanism of miR-34a regulation that NF-kappaB could elevate miR-34a expression levels through directly binding to its promoter. And wildtype p53 is responsible for NF-kappaB-mediated miR-34a transcriptional activity but not for NF-kappaB binding. These findings might be helpful in understanding miR-34a abnormality in human malignancies and open new perspectives for the roles of miR-34a and NF-kappaB in tumor progression.</p