Nickel is associated with reproductive toxicity. However, the reproductive toxicity of nickel nanoparticles (Ni NPs) is unclear. Our goal was to determine the association between nickel nanoparticle exposure and reproductive toxicity. According to the one-generation reproductive toxicity standard, rats were exposed to nickel nanoparticles by gavage and we selected indicators including sex hormone levels, sperm motility, histopathology, and reproductive outcome etc. Experimental results showed nickel nanoparticles increased follicle stimulating hormone (FSH) and luteinizing hormone (LH), and lowered etradiol (E2) serum levels at a dose of 15 and 45 mg/kg in female rats. Ovarian lymphocytosis, vascular dilatation and congestion, inflammatory cell infiltration, and increase in apoptotic cells were found in ovary tissues in exposure groups. For male rats, the weights decreased gradually, the ratio of epididymis weight over body weight increased, the motility of rat sperm changed, and the levels of FSH and testosterone (T) diminished. Pathological results showed the shedding of epithelial cells of raw seminiferous tubule, disordered arrangement of cells in the tube, and the appearance of cell apoptosis and death in the exposure group. At the same time, Ni NPs resulted in a change of the reproductive index and the offspring development of rats. Further research is needed to elucidate exposure to human populations and mechanism of actions.
The overall percentage of missed fractures in the extremities was 3.7%. Only 33% of the initially missed fractures were attributed to radiographically imperceptible lesions. Adequate training for physicians and radiologists in the ED may reduce the rate of missed fractures.
Anxiety disorders are prevalent in youth. Despite demonstrated efficacy of cognitive behavioral therapy (CBT), approximately 40% of anxiety-disordered youth remain unresponsive to treatment. Because developmental and etiological models suggest that parental factors are relevant to the onset and maintenance of childhood anxiety, researchers have proposed and investigated family-based interventions with increased parent work in treatment, aiming to improve the efficacy of treatment for childhood anxiety. However, contrary to what theoretical models suggest, data to date did not indicate additive benefit of family-based CBT in comparison with child-centered modality. Is parent/family involvement unnecessary when treating childhood anxiety disorders? Or could there be the need for specificity (tailored family-based treatment) that is guided by a revised conceptualization that improves the implementation of a family-based intervention? The current review examines (1) relevant parental factors that have been found to be associated with the development and maintenance of childhood anxiety and (2) interventions that incorporate parental involvement. Relevant findings are integrated to formulate a "targeted" treatment approach for parental involvement in CBT for youth anxiety. Specifically, there is potential in the assessment of parent/family factors prior to treatment (for appropriateness) followed by a target-oriented implementation of parent training.
a b s t r a c tSilent mating type information regulation 1 (SIRT1) is implicated in tumorigenesis through its effect on autophagy. In gastric cancer (GC), SIRT1 is a marker for prognosis and is involved in cell invasion, proliferation, epithelial-mesenchymal transition (EMT) and drug resistance. Autophagy can function as a cell-survival mechanism or lead to cell death during the genesis and treatment of GC. This functionality is determined by factors including the stage of the tumor, cellular context and stress levels. Interestingly, SIRT1 can regulate autophagy through the deacetylation of autophagy-related genes (ATGs) and mediators of autophagy. Taken together, these findings support the need for continued research efforts to understand the mechanisms mediating the development of gastric cancer and unveil new strategies to eradicate this disease.
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