Objective: The current study is a report of isolation and identification of Mycobacterium setense from a tap running water in a general surgery ward in a hospital in Isfahan, Iran. Materials and Methods: This bacterium was obtained from a hospital water sample according to the cetylpyridinium chloride 0.005% method on Lowenstein–Jensen slant and characterized to the species level as M. setense using results of phenotypic test and 16S rRNA sequencing. Results: This isolate identified to the species level using the conventional and molecular method as M. setense, this bacterium has highest similarity (100%) with those of M. setense CIP109395 16S rRNA gene sequences. Conclusion: This study can be useful and provide important information for learning about the natural habitats of pathogenic species of nontuberculosis mycobacteria. Furthermore, the molecular tests such as 16S rRNA gene sequencing can be applied for reliable and appropriate identification of mycobacterial species.

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Background and Objective: Dyslipidemia is a mechanistic factor between cigarette smoking and cardiovascular diseases (CVD). Normolipidemic smokers may still be at risk of CVD, hence the need to better characterize serum lipids with atherogenic indices. This study aimed at determining atherogenic indices in relation to smoking habits in cigarette smokers. Materials and Methods: The case–control study compared lipid indices of sixty male smokers with six anthropometrically matched non-smokers. Three comparable subgroups of smoking habits were statistically tested. Associations of serum lipids, atherogenic indices, and smoking habits were also determined. Results: Significant high (P < 0.001) atherogenic indices, proatherogenic lipids (total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL-c), very LDL-c, non-high-density lipoprotein cholesterol [HDL-c]), and significant low (P < 0.001) HDL-c were observed in smokers compared to controls. Significant differences (P < 0.002) in serum lipids and atherogenic indices were observed within the subgroups of cigarette sticks smoked per day. Significant positive (P < 0.002) correlation of cigarette sticks smoked per day with proatherogenic lipids and atherogenic indices was observed in smokers, whereas significant inverse (P < 0.001) correlation was observed with HDL-c. Conclusion: Atherogenic indices proved to be a better predictor of cardiovascular risk, especially in settings of seeming normal lipid profile.

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The prevalence of nonalcoholic fatty liver disease (NAFLD) has increased over the past few decades due to a rise in the incidence of Type 2 diabetes and obesity. Sedentary lifestyle coupled with exorbitant consumption of high-caloric diet has been associated with root cause of the epidemic increase in chronic liver diseases. NAFLD is a chronic liver disease which encompasses a spectrum of conditions ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), further leading to irreversible liver cirrhosis. A “multiple hit working model” is a recognized theory that explains the development and progression of NASH, the advanced stage of NAFLD. According to this model, initial hit leads to the development of steatosis, which makes the liver vulnerable to following hits induced by inflammatory cytokines, endotoxins, lipid peroxidation, oxidative stress, endoplasmic reticulum (ER) stress, saturated fatty acid deposition, and/or hepatic organelle dysfunction. These hits eventually result in hepatic fibrosis, inflammation, and apoptosis, which are considered the key features of NASH. Accumulation of hepatic fats leads to the activation of various pathways, including unfolded protein response, which is associated with intracellular stress and inflammation. ER plays a crucial role in restoring cellular homeostasis by directing either through the refolding of misfolded proteins or employing several alternative mechanisms such as ER-associated degradation. ER stress response also causes insulin resistance and inflammation and in the worst cases, culminates in severe liver damage and hepatic cell death, all of which are central to the pathogenesis of NASH. This review sheds some light on recent findings of ER stress response and oxidative stress in the progression of NAFLD.

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Background: Tobacco smoke, an endocrine and metabolic disruptor, is associated with increased abdominal adiposity in active smokers (ASs). However, the role of secondhand smoke (SHS) exposure in central adiposity is unclear. Abdominal adiposity, measured as sagittal abdominal diameter (SAD), is associated with increased risk of cardiometabolic disease and mortality. We assessed the role of SHS exposure in explaining patterns of SAD and evaluated this relationship for differences by age. Methods: Cross-sectional data from the National Health and Nutrition Examination Survey 2011–2012 were utilized for 6188 individuals aged 12–80 years. Using serum cotinine and self-reported smoking information, smoking status was categorized as nonsmoker (NS, <1 ng/ml), SHS (1–<10 ng/ml), and AS (≥10 ng/ml). SAD was compared across smoking categories including a Bonferroni correction. Age was grouped as 12–19, 20–49, and ≥50 years. Linear regression models assessing the association of SAD with smoking status were adjusted for sex, race/ethnicity (White, Black, Hispanic, and Asian/other), income, body mass index (BMI), and survey weights. The model (pooled over age) was adjusted for age, and the age-specific model included a smoking status by age group interaction. Results: AS, NS, and SHS constituted an estimated 41%, 53%, and 6% of the population, respectively. The estimated mean population SAD was 21.6 cm (standard error: 0.1). Before adjusting for risk factors, SAD was marginally greater among SHS (21.0 cm) than NS (20.8 cm). Adjusting for covariates, AS had greater mean SAD (20.5 cm) than both SHS (20.2 cm, p-Bon [p-Bonferroni] = 0.009) and NS (20.0, p-Bon ≤0.001). However, SHS did not have significantly greater mean SAD than NS (p-Bon = 1.000). Association of SAD and smoking status differed by age (smoking status × age interaction, P = 0.013), with inconsistent patterning in the oldest age group. Among individuals aged 20–49 years, SHS exposed (20.7 cm) had greater mean SAD than NS (20.1 cm), although not significantly so (p-Bon = 0.347). Among those aged ≥50 years, SHS (20.5 cm) had significantly lower mean SAD than NS (21.2 cm) (p-Bon = 0.033). Conclusion: Our results suggest a dose-response relationship between smoking and SAD. We discovered an unexpected U-shaped relationship between smoking and SAD among older adults that warrant further research.

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