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The demand for a facile approach for synthesizing multifunctional nanocomposites is increasingly vital across diverse applications. In this study, a polymerizable sol–gel synthesis has been reported to obtain nanocomposites of magnetic iron oxide deposited over alumina nanopowder. The synthesis is mediated by the deposition of a calculated amount of iron(III) methacrylate, along with ethylene glycol dimethacrylate crosslinker, over alumina nanopowder, followed by thermally-inducing free radical polymerization at 125 °C for 30 min. The powder thus obtained has been subjected to calcination at 400 °C for 150 min and the resultant nanocomposites were characterized using wide-angle x-ray scattering, attenuated total reflectance—Fourier transform infrared spectroscopy, x-ray photoelectron spectroscopy, field-emission scanning electron microscopy, ultraviolet-diffuse reflectance spectroscopy, vibrating sample magnetometer and Brunauer–Emmett–Teller surface area measurements. The nanocomposites containing 15 and 20 wt% of iron oxide have been found to exhibit a saturation magnetization (M s) value ranging from 12 to 14 emu g−1. To the nanocomposite containing 20 wt% of iron oxide, 5 wt% of AgBr was loaded through thoroughly mixing a surfactant-based precursor, silver-tetraoctyl ammonium bromide (Ag-TOAB), followed by thermolysis. All the nanocomposites have been studied for their antibacterial activity against a representative gram-negative bacterium, Escherichia coli, under dark and visible light conditions. While a 3 mg ml−1 loading of the AgBr-loaded nanocomposite has exhibited complete clearance of the bacterial growth by 90 min in the dark, a similar activity has been observed in 60 min under light. The study has revealed the multifunctionality and high potential of the AgBr-loaded iron oxide/alumina nanocomposite as a promising dual-mode antibacterial and magnetically recoverable photocatalyst material. [ABSTRACT FROM AUTHOR]

Purpose. The prevalence and severity of respiratory disorders are very high among coal miners as continuous exposure of workers in such an environment leads to accumulation of dust in the lungs. This study was designed to assess the prevalence of lung function impairment and to determine whether there is any correlation between dust exposure duration and lung function indices. Materials. Two hundred and thirty underground coal dust-exposed workers and 130 age-matched non-exposed workers were recruited from an underground mine in West Bengal, India. A spirometry test was performed for lung function and also basic information on personnel's dust exposure, smoking and respiratory morbidity was collected. Student's t test, Pearson's correlation coefficient (r), uncorrected Pearson's χ2 test and Fischer's exact test were performed for statistical analysis. Results. Lung function indices were significantly (p < 0.050) impaired between the exposed (43.91%) and non-exposed (23.85%) groups. In addition, highly significant decrements in the pulmonary volumes of exposed subjects were also noted. Furthermore, a high negative correlation was observed between spirometric results and exposure time in the exposed group compared with the non-exposed group. Conclusion. This study suggested a positive relationship between exposure time and lung function deterioration. [ABSTRACT FROM AUTHOR]

Ischaemia-reperfusion (I/R) injury is a serious problem subsequent to reperfusion treatment for ovarian torsion. The role of nitric oxide (NO) in ovarian I/R injury is debatable. The main focus of this study was to explore the protective role of L-arginine, a potent NO precursor, on ovarian I/R injury. Female Wistar rats were divided into three groups (n = 5). In the control group, only laparotomy was performed. In the I/R group, ischaemia and reperfusion were performed and no drug was given. In the I/R + arginine group, ischaemia was followed by reperfusion and 200 mg kg-1 L-arginine was injected 5 min before reperfusion. Concentration of malondialdehyde, NO and reduced glutathione, as well as activity of superoxide dismutase and catalase were analyzed. Hematoxylin and eosin-stained slides were microscopically examined for histological evaluation of the ovaries. Superoxide dismutase and catalase activity along with concentration of reduced glutathione and NO were significantly lower in the I/R group in comparison to the control group. Malondialdehyde concentration was significantly higher in the I/R group than in control group. These results were reversed with supplementation of L-arginine. Light microscopic examination revealed severe vascular congestion, edema, haemorrhage, and follicular degeneration in the ovary tissue. The extent of ovarian damage was much higher in the I/R group than in the I/R + L-arginine group. Treatment with L-arginine seems to have an ameliorating effect against oxidative stress in I/R injury in rat ovary. It considerably reduced the altered histological changes in the ovaries. Thus, it can be speculated that L-arginine might play a pivotal role as a potent therapeutic agent against ovarian torsion. [ABSTRACT FROM AUTHOR]

Abstract: Nicotine, one of the well‐known highly toxic components of cigarette smoke, causes a number of adverse health effects and diseases. Our previous study has shown that nicotine induces reactive oxygen species (ROS) in islet cell and disrupts islet cell mitochondrial membrane potential (ΔΨm). However, supplementation with folic acid and vitamin B12 were found effective against nicotine induced changes in pancreatic islet cells. But the toxicological effects and underlying mechanisms of nicotine‐induced mitochondrial dysfunction is still unknown. In this study, nicotine exposure decreases mitochondrial enzymes (pyruvate dehydrogenase, alpha‐ketoglutarate dehydrogenase, aconitase, malate dehydrogenase) activities by increasing cytosolic Ca2+ level which may contribute to increased mitochondrial ROS production by raising its flow to mitochondria. This in turn produces malondialdehyde and nitric oxide (NO) with a concomitant decrease in the activities of antioxidative enzymes and glutathione levels leading to loss of ΔΨm. Simultaneously, nicotine induces pancreatic islet cell apoptosis by modulating ΔΨm via increased cytosolic Ca2+ level, altered Bcl‐2, Bax, cytochrome c, caspase‐9, PARP expressions which were prevented by the supplementation of folic acid and vitamin B12. In conclusion, nicotine alters islet cell mitochondrial redox status, apoptotic machinery, and enzymes to cause disruption in the ΔΨm and supplementation of folic acid and vitamin B12 possibly blunted all these mitochondrial alterations. Therefore, this study may help to determine the pathophysiology of nicotine‐mediated islet cell mitochondrial dysfunction. [ABSTRACT FROM AUTHOR]

Nicotine, one of the well-known highly toxic components of cigarette smoke, causes a number of adverse health effects and diseases. Our previous study has shown that nicotine induces reactive oxygen species (ROS) in islet cell and disrupts islet cell mitochondrial membrane potential (ΔΨm). However, supplementation with folic acid and vitamin B 12 were found effective against nicotine induced changes in pancreatic islet cells. But the toxicological effects and underlying mechanisms of nicotine-induced mitochondrial dysfunction is still unknown. In this study, nicotine exposure decreases mitochondrial enzymes (pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, aconitase, malate dehydrogenase) activities by increasing cytosolic Ca 2+ level which may contribute to increased mitochondrial ROS production by raising its flow to mitochondria. This in turn produces malondialdehyde and nitric oxide (NO) with a concomitant decrease in the activities of antioxidative enzymes and glutathione levels leading to loss of ΔΨm. Simultaneously, nicotine induces pancreatic islet cell apoptosis by modulating ΔΨm via increased cytosolic Ca 2+ level, altered Bcl-2, Bax, cytochrome c, caspase-9, PARP expressions which were prevented by the supplementation of folic acid and vitamin B 12 . In conclusion, nicotine alters islet cell mitochondrial redox status, apoptotic machinery, and enzymes to cause disruption in the ΔΨm and supplementation of folic acid and vitamin B 12 possibly blunted all these mitochondrial alterations. Therefore, this study may help to determine the pathophysiology of nicotine-mediated islet cell mitochondrial dysfunction., (© 2018 Wiley Periodicals, Inc.)