Work Hours and Self rated Health of Hospital Doctors in Norway and Germany. A comparative study on national samples

<p>Abstract</p> <p>Background</p> <p>The relationship between extended work hours and health is well documented among hospital doctors, but the effect of national differences in work hours on health is unexplored. The study examines the relationship between work hours and self rated health in two national samples of hospital doctors.</p> <p>Methods</p> <p>The study population consisted of representative samples of 1,260 German and 562 Norwegian hospital doctors aged 25-65 years (N = 1,822) who received postal questionnaires in 2006 (Germany) and 2008 (Norway). The questionnaires contained items on demography, work hours (number of hours per workday and on-call per month) and self rated subjective health on a five point scale - dichotomized into "good" (above average) and "average or below".</p> <p>Results</p> <p>Compared to Norway, a significantly higher proportion of German doctors exceeded a 9 hour work day (58.8% vs. 26.7%) and 60 hours on-call per month (63.4% vs. 18.3%). Every third (32.2%) hospital doctor in Germany worked more than this, while this pattern was rare in Norway (2.9%). In a logistic regression model, working in Norway (OR 4.17; 95% CI 3.02-5.73), age 25-44 years (OR 1.66; 95% CI 1.29-2.14) and not exceeding 9 hour work day and 60 hours on-call per month (OR 1.35; 95% CI 1.03-1.77) were all independent significant predictors of good self reported health.</p> <p>Conclusion</p> <p>A lower percentage of German hospital doctors reported self rated health as "good", which is partly explained by the differences in work time pattern. Initiatives to increase doctors' control over their work time are recommended.</p

Translational Regulation of Utrophin by miRNAs

Background Utrophin is the autosomal homolog of dystrophin, the product of the Duchenne Muscular Dystrophy (DMD) locus. Its regulation is of therapeutic interest as its overexpression can compensate for dystrophin's absence in animal models of DMD. The tissue distribution and transcriptional regulation of utrophin have been characterized extensively, and more recently translational control mechanisms that may underlie its complex expression patterns have begun to be identified. Methodology/Principal Findings Using a variety of bioinformatic, molecular and cell biology techniques, we show that the muscle isoform utrophin-A is predominantly suppressed at the translational level in C2C12 myoblasts. The extent of translational inhibition is estimated to be ~99% in C2C12 cells and is mediated by both the 5′- and 3′-UTRs of the utrophin-A mRNA. In this study we identify five miRNAs (let-7c, miR-150, miR-196b, miR-296-5p, miR-133b) that mediate the repression, and confirm repression by the previously identified miR-206. We demonstrate that this translational repression can be overcome by blocking the actions of miRNAs, resulting in an increased level of utrophin protein in C2C12 cells. Conclusions/Significance The present study has identified key inhibitory mechanisms featuring miRNAs that regulate utrophin expression, and demonstrated that these mechanisms can be targeted to increase endogenous utrophin expression in cultured muscle cells. We suggest that miRNA-mediated inhibitory mechanisms could be targeted by methods similar to those described here as a novel strategy to increase utrophin expression as a therapy for DMD

Dietary phytochemicals, HDAC inhibition, and DNA damage/repair defects in cancer cells

Genomic instability is a common feature of cancer etiology. This provides an avenue for therapeutic intervention, since cancer cells are more susceptible than normal cells to DNA damaging agents. However, there is growing evidence that the epigenetic mechanisms that impact DNA methylation and histone status also contribute to genomic instability. The DNA damage response, for example, is modulated by the acetylation status of histone and non-histone proteins, and by the opposing activities of histone acetyltransferase and histone deacetylase (HDAC) enzymes. Many HDACs overexpressed in cancer cells have been implicated in protecting such cells from genotoxic insults. Thus, HDAC inhibitors, in addition to unsilencing tumor suppressor genes, also can silence DNA repair pathways, inactivate non-histone proteins that are required for DNA stability, and induce reactive oxygen species and DNA double-strand breaks. This review summarizes how dietary phytochemicals that affect the epigenome also can trigger DNA damage and repair mechanisms. Where such data is available, examples are cited from studies in vitro and in vivo of polyphenols, organosulfur/organoselenium compounds, indoles, sesquiterpene lactones, and miscellaneous agents such as anacardic acid. Finally, by virtue of their genetic and epigenetic mechanisms, cancer chemopreventive agents are being redefined as chemo- or radio-sensitizers. A sustained DNA damage response coupled with insufficient repair may be a pivotal mechanism for apoptosis induction in cancer cells exposed to dietary phytochemicals. Future research, including appropriate clinical investigation, should clarify these emerging concepts in the context of both genetic and epigenetic mechanisms dysregulated in cancer, and the pros and cons of specific dietary intervention strategies

Dark Current and Noise Measurements of an InAs/GaSb Superlattice Photodiode Operating in the Midwave Infrared Domain

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