S. aureus showed higher susceptibility to PVA/GO-AgNPs films than E. coli. Inhibitory activity was higher when bacterial cells were in contact with nanocomposite films than when in contact with leachates coming out of the films. GO-AgNPs based PVA nanocomposites could find application as wound dressings for wound healing and infection prevention.AIMS In this study we analyzed the degree of genetic homozygosity among spina bifida patients with different degrees of neurogenic lesion (N = 82), as well as their clinical and neurological characteristics, compared to healthy control individuals (N = 100). METHODS According to clinical and electromyographic findings, we separately assessed the type of neurogenic lesion (paresis or paralysis). Regarding the degree of neurogenic lesion, patients were classified into three groups mild, moderate and severe. We analyzed six muscles. https://www.selleckchem.com/products/ficz.html For assessing the degree of individual genetic homozygosity, we tested the presence and distribution of 15 homozygous recessive characteristics (HRC). RESULTS The predominant type of neurogenic lesion was paresis. Every third evaluated muscle was affected in the group with mild neurogenic lesion, while more than half were affected in the group with severe neurogenic lesion. The average values of HRCs among different groups of patients and the control showed the population-genetic differences that exist among them (control HRC/15=3.0±0.2; mild HRC/15=3.6±0.2; moderate HRC/15=4.8±0.3; severe neurogenic lesion HRC/15=5.0±0.3). CONCLUSIONS Spina bifida patients have a significant increase of recessive homozygosity and a decreased variability compared to the control group. As neurogenic lesions are more severe, more affected muscles are present, as well as the increase of individual recessive homozygosity.Cycle-dependent damage evolution in self-healing, 2.5D woven Hi-NicalonTM SiC/[Si-B-C] and 2D woven Hi-NicalonTM SiC/[SiC-B4C] ceramic-matrix composites (CMCs) at 600 and 1200 °C was investigated. The cycle-dependent damage parameters of internal friction, dissipated energy, Kachanov's damage parameter, and broken fiber fraction were obtained to describe damage development in self-healing CMCs. The relationships between cycle-dependent damage parameters and multiple fatigue damage mechanisms were established. The experimental fatigue damage development of self-healing Hi-NicalonTM SiC/[Si-B-C] and Hi-NicalonTM SiC/[SiC-B4C] composites was predicted for different temperatures, peak stresses, and loading frequencies. The cycle-dependent damage evolution of self-healing Hi-NicalonTM SiC/[Si-B-C] and Hi-NicalonTM SiC/[SiC-B4C] composites depends on temperature, testing environment, peak stress, and loading frequency. For the Hi-NicalonTM SiC/[Si-B-C] composite, temperature is a governing parameter for the fatigue process. At an elevated temperature of 600 °C in an air atmosphere, the internal frictional parameter of Hi-NicalonTM SiC/[Si-B-C] composite decreases first and then increases with applied cycle number; however, at an elevated temperature of 1200 °C in an air atmosphere, the internal frictional parameter of Hi-NicalonTM SiC/[Si-B-C] composite decreases with applied cycle number, and the interface shear stress at 1200 °C is much lower than that at 600 °C. For Hi-NicalonTM SiC/[SiC-B4C] composite at 1200 °C, loading frequency is a governing parameter for the fatigue process. The degradation rate of interface shear stress is much higher at the loading frequency of 0.1 Hz than that at the loading frequency of 1 Hz.The aim of this study was to assess the influence of lead (Pb) at low concentrations (imitating Pb levels in human blood in chronic environmental exposure to this metal) on interleukin 1β (IL-1β) and interleukin 6 (IL-6) concentrations and the activity and expression of COX-1 and COX-2 in THP-1 macrophages. Macrophages were cultured in vitro in the presence of Pb at concentrations of 1.25 μg/dL; 2.5 μg/dL; 5 μg/dL; 10 μg/dL. The first two concentrations of Pb were selected on the basis of our earlier study, which showed that Pb concentration in whole blood (PbB) of young women living in the northern regions of Poland and in the cord blood of their newborn children was within this range (a dose imitating environmental exposure). Concentrations of 5 μg/dL and 10 μg/dL correspond to the previously permissible PbB concentrations in children or pregnant women, and adults. Our results indicate that even low concentrations of Pb cause an increase in production of inflammatory interleukins (IL-1β and IL-6), increases expression of COX-1 and COX-2, and increases thromboxane B2 and prostaglandin E2 concentration in macrophages. This clearly suggests that the development of inflammation is associated not only with COX-2 but also with COX-1, which, until recently, had only been attributed constitutive expression. It can be concluded that environmental Pb concentrations are able to activate the monocytes/macrophages similarly to the manner observed during inflammation.Retinal pigment epithelial cells are crucial for retina maintenance, making their cytoprotection an excellent way to prevent or slow down retinal degeneration. In addition, oxidative stress, inflammation, apoptosis, neovascularization, and/or autophagy are key pathways involved in degenerative mechanisms. Therefore, here we studied the effects of curcumin, lutein, and/or resveratrol on human retinal pigment epithelial cells (ARPE-19). Cells were incubated with individual or combined agent(s) before induction of (a) H2O2-induced oxidative stress, (b) staurosporin-induced apoptosis, (c) CoCl2-induced hypoxia, or (d) a LED-autophagy perturbator. Metabolic activity, cellular survival, caspase 3/7 activity (casp3/7), cell morphology, VEGF levels, and autophagy process were assessed. H2O2 provoked a reduction in cell survival, whereas curcumin reduced metabolic activity which was not associated with cell death. Cell death induced by H2O2 was significantly reduced after pre-treatment with curcumin and lutein, but not resveratrol. Staurosporin increased caspase-3/7 activity (689%) and decreased cell survival by 32%. Curcumin or lutein protected cells from death induced by staurosporin. Curcumin, lutein, and resveratrol were ineffective on the increase of caspase 3/7 induced by staurosporin. Pre-treatment with curcumin or lutein prevented LED-induced blockage of autophagy flux. Basal-VEGF release was significantly reduced by lutein. Therefore, lutein and curcumin showed beneficial protective effects on human-derived retinal cells against several insults.