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1-year primary patency, freedom from TLR, and assisted primary patency were 40% (median patent time 256 days), 67% (median patent time 524 days), and 77%, respectively. Conclusion Stenting for central venous occlusions and stenoses in the hemodialysis patients is safe and durable treatment option. However, considering its off-label use and potential hazard including vessel rupture, stent migration, and stent fracture, the indication for BMS deployment should be conservative, and interventionist should be well acquainted with prevention and measures to these complications. (This is a translation of Jpn J Vasc Surg 2019; 28 193-198.).Critical biological processes are under control of the circadian clock. Disruption of this clock, e.g. during aging, results in increased risk for development of chronic disease. Exercise is a protective intervention that elicits changes in both age and circadian pathologies, yet its role in regulating circadian gene expression in peripheral tissues is unknown. We hypothesized that voluntary wheel running would restore disrupted circadian rhythm in aged mice. We analyzed wheel running patterns and expression of circadian regulators in male and female C57Bl/6J mice in adult (~4 months) and old (~18 months) ages. As expected, young female mice ran further than male mice, and old mice ran significantly less than young mice. Older mice of both sexes had a delayed start time in activity which likely points to a disrupted diurnal running pattern and circadian disruption. Voluntary wheel running rescued some circadian dysfunction in older females. This effect was not present in older males, and whether this was due to low wheel running distance or circadian output is not clear and warrants a future study. Overall, we show that voluntary wheel running can rescue some circadian dysfunction in older female but not male mice; and these changes are tissue dependent. While voluntary running was not sufficient to fully rescue age-related changes in circadian rhythm, ongoing studies will determine if forced exercise (e.g. treadmill) and/or chrono-timed exercise can improve age-related cardiovascular, skeletal muscle, and circadian dysfunction.The snub-nosed monkey genus (Rhinopithecus) comprises five closely related species (R. avunculus, R. bieti, R. brelichi, R. roxellana, and R. strykeri). All are among the world's rarest and most endangered primates. However, the genomic impact associated with their population decline remains unknown. We analyzed population genomic data of all five snub-nosed monkey species to assess their genetic diversity, inbreeding level, and genetic load. For R. roxellana, R. bieti, and R. strykeri, population size is positively correlated with genetic diversity and negatively correlated with levels of inbreeding. Selleck ALK inhibitor Other species, however, which possess small population sizes, such as R. brelichi and R. avunculus, show high levels of genetic diversity and low levels of genomic inbreeding. Similarly, in the three populations of R. roxellana, the Shennongjia population, which possesses the lowest population size, displays a higher level of genetic diversity and lower level of genomic inbreeding. These findings suggest that alluable information concerning the genomic impact of population decline of the snub-nosed monkeys. We revealed multiple counterintuitive and unexpected patterns of genetic diversity in small and large population, which will be essential for conservation management of these endangered species.Accurate RNA secondary structure information is the cornerstone of gene function research and RNA tertiary structure prediction. However, most traditional RNA secondary structure prediction algorithms are based on the dynamic programming (DP) algorithm, according to the minimum free energy theory, with both hard and soft constraints. The accuracy is particularly dependent on the accuracy of soft constraints (from experimental data like chemical and enzyme detection). With the elongation of the RNA sequence, the time complexity of DP-based algorithms will increase geometrically, as a result, they are not good at coping with relatively long sequences. Furthermore, due to the complexity of the pseudoknots structure, the secondary structure prediction method, based on traditional algorithms, has great defects which cannot predict the secondary structure with pseudoknots well. Therefore, few algorithms have been available for pseudoknots prediction in the past. The ATTfold algorithm proposed in this article is a drease, our deep learning-based algorithm will have superior performance. In the future, this kind of algorithm will be more indispensable.

Extensive literature put forward the link between sleep and type 2 diabetes mellitus (T2DM), however, little is known about the underlying causality of the associations. Here we aim to assess the causal relationships between five major sleep-related traits and T2DM.

Two-sample Mendelian randomization (MR) was utilized to investigate the potential causal relations. Independent genetic variants associated with five sleep-related phenotypes-insomnia, sleep duration, short sleep duration, long sleep duration, and morningness-were chosen as instrumental variables to estimate the causal associations with T2DM. Summary statistics were acquired from the genome-wide association studies of UK Biobank and 23andMe (for sleep-related measures), the DIAbetes Genetics Replication And Meta-analysis and the FinnGen (for T2DM).

Individual Cochran's Q statistic was applied to remove the pleiotropic instruments, global Q statistics and MR-Egger regression were adopted to test for the global heterogeneity and horizontal ple and were robust among various sensitivity analyses.

Findings provide significant evidence for an adverse effect of insomnia on T2DM risk. The study extends fundamental knowledge to further understanding of the pathophysiological mechanisms of T2DM, and points out the non-negligible role of insomnia on epidemiologic intervention and clinical therapeutics of T2DM.

Findings provide significant evidence for an adverse effect of insomnia on T2DM risk. The study extends fundamental knowledge to further understanding of the pathophysiological mechanisms of T2DM, and points out the non-negligible role of insomnia on epidemiologic intervention and clinical therapeutics of T2DM.