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Background Atrial fibrillation (AF), an inflammatory process involving arrhythmia, is associated with severe morbidity and mortality and commonly seen in patients with diabetes mellitus (DM). The effect of metformin, the most commonly used medication for patients with DM, on AF has not been investigated. The primary aim of this study was to examine whether metformin prevented the occurrence of AF in type 2 DM patients by analyzing a nationwide, population-based dynamic cohort. Additionally, we investigated the effect of metformin on tachycardia-induced myolysis and oxidative stress in atrial cells. Methods The study population included 645,710 patients with type 2 diabetes and not using other antidiabetic medication from a subset of the Taiwan National Health Insurance Research Database. Of these patients, those who used metformin were categorized as the user group, and the remaining were classified as the non-user group. The time-dependent Cox's proportional hazard model was used to examine the effect of metformin on AF and the status of metformin use was treated as a time-dependent covariate. HL-1 atrial cells were paced with or without metformin, and then troponin and heavy-chain-myosin were measured as markers of myolysis. Results After 13 years of follow-up, 9,983 patients developed AF with an incidence rate of 1.5% (287 per 100,000 person-years). After adjusting for co-morbidities and medications, metformin independently protected the diabetic patients from new-onset AF with a hazard ratio of .81 (95% confidence interval 0.76-0.86, p < 0.0001). Metformin significantly decreased the extent of pacing-induced myolysis and the production of reactive oxygen species Conclusion Metformin use was associated with a decreased risk of AF in patients with type 2 DM who were not using other anti-diabetic medication, probably via attenuation of atrial cell tachycardia-induced myolysis and oxidative stress. [ABSTRACT FROM AUTHOR]

Background: In 2003, nosocomial infections caused by vancomycin-resistant enterococci (VRE) occurred rarely in Taiwan. Between 2003 and 2010, however, the average prevalence of vancomycin resistance among enterococci spp. increased from 2% to 16% in community hospitals and from 3% to 21% in medical centers of Taiwan. We used molecular methods to investigate the epidemiology of VRE in a tertiary teaching hospital in Taiwan. Methods: Between February 2009 and February 2011, rectal samples and infection site specimens were collected from all inpatients in the nephrology ward after patient consent was obtained. VRE strain types were determined by pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST). Results: A total of 59 vanA gene-containing VRE isolates (1 per patient) were obtained; 24 originated from rectal sample surveillance of patients who exhibited no symptoms (22 Enterococcus faecium and 2 Enterococcus faecalis), and 35 had developed infections over 3 days after admission (32 E. faecium, 2 E. faecalis, and 1 Enterococcus durans). The 59 VRE isolates demonstrated vancomycin minimum inhibitory concentrations (MICs) of ⩾256 μg/m. The MIC range for linezolid, tigecycline, and daptomycin was 0.25-1.5 μg/mL, 0.032-0.25 and 1-4 μg/mL, respectively. For 56 isolates, the MIC for teicoplanin was >8 μg/mL. The predominant types in the nephrology ward were MLST types 414, 78, and18 as well as PFGE types A, C, and D. Conclusion: VREs are endemic in nephrology wards. MLST 414 is the most predominant strain. The increase VRE prevalence is due to cross-transmission of VRE clones ST 414,78,18 by undetected VRE carriers. Because similar VRE STs had been reported in a different hospital of Taiwan, this finding may indicate inter-hospital VRE spread in Taiwan. Active surveillance and effective infection control policies are important controlling the spread of VRE in high risk hospital zones. All endemic VRE strains are resistant to teicoplanin but are sensitive to daptomycin, linezolid, and tigecycline. [ABSTRACT FROM AUTHOR]