Background: Mitral Regurgitation (MR) is a severe complication after percutaneous valvulopalsty for Mitral Stenosis (MS). Objective: To study some predictors, mechanisms and outcome of MR immediately and 3 months after percutaneous valvuloplasty (PMV) by the Inoue technique for mitral stenosis.Subjects and method: 43 patients with MS were followed up for 3 months after PMV by the Inoue technique in the Viet Nam National Heart Institute at Bach Mai Hospital between Jan 2007 to Oct 2007. Results: Uneven mitral leaflets and calcium commissures with Padial\u2019s criteria scoring over 10 was a significant predicator of influence of severe MR after PMV.According to Wilkins\u2019 score, only the calcium commissures affected the MR after PMV (p<0.05). Conclusion: Patients with aortic regurgitation and/or mild MR who\u2019s Wilkins\u2019 scores less than 8 and Padial's scores less than 10 had not be influenced by severe MR after PMV.
Mitral stenosis ; Percutaneous valvuloplasty (PMV)

Aims: This study aimed to isolate the fungal strains causing brown spot disease on dragon fruit and identify them using molecular biology techniques. The study also investigated the inhibitory effects of silver (Ag) and ZnO nanoparticles on the isolated fungal strains. Methodology and results : Six fungal strains (TL1, TL2, TL3, TL4, TL5, TL6) causing brown spot disease (stem-canker) were isolated. TL1 and TL2 isolates were used for testing the antifungal features of nanoparticles. Nanoparticles were directly added to the PDA medium to make a solution with concentrations of 50, 75 and 100 ppm. The antifungal feature of nanoparticles was screened by inoculating with the fungal samples for 72 h. The inhibitory capacity of ZnO and Ag nanoparticles against fungal strains was then investigated. TL1 and TL2 samples were identified as Neocytalidium dimidiatum using the internal transcribed spacer (ITS) region. The study also revealed that silver nanoparticles were more effective than zinc oxide nanoparticles in inhibiting the growth of fungal strains that cause brown spot disease on dragon fruit. Specifically, ZnO nanoparticles had the highest inhibitory effect on TL2, 61.27% at 100 ppm and Ag nanoparticles gave the highest inhibitory effect on TL2, 85.83% at 100 ppm. Conclusion, significance and impact of study The research findings suggest that the use of Ag and ZnO nanoparticles may be an effective way to control brown dragon fruit spot disease. It may help in improving dragon fruit yield and aesthetic quality. As a result, it may help in reducing economic loss for farmers. However, further research is required.

Objective: To examine the in vitro and in vivo anti-inflammatory effects of the alkaloid enriched extract (ELA) from the roots of Eurycoma longifolia. Methods: The in vitro antiinflammatory effects of ELA were evaluated by examining its inhibitory activities against nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) expressions in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. The level of NO produced in the culture media was determined by Griess method. The iNOS and COX-2 protein expressions were analyzed by Western blot. The in vivo effect of ELA was evaluated on LPS-induced septic shock in mice model. Mice mortality was monitored for 5 days after injection of LPS. The chemical contents of the ELA were determined by using various chromatographic and spectroscopic techniques. Results: The ELA was found to exhibit a significant anti-inflammatory effect in both in vitro and in vivo models. The results demonstrated that ELA dose-dependently inhibited LPS-induced NO production as well as the protein iNOS and COX-2 expressions. In the septic shock model, ELA dose-dependently protected mice from LPS-induced mortality. Further study on the isolated components of ELA indicated that 9,10-dimethoxycanthin-6-one may contribute significantly to the anti-inflammatory effects of the extract. Conclusions: These results suggest that ELA exhibits the anti-inflammatory activity via suppression of pro-inflammatory mediators such as NO, iNOS, and COX-2 and protects mice from LPS-induced mortality in septic shock model.