2,2′-(1,10-Phenanthrolin-2-ylimino)di­ethanol

In the title compound, C16H17N3O2, symmetry-related mol­ecules are linked into one-dimensional chains along the a axis by a combination of inter­molecular O—H⋯N and O—H⋯O hydrogen bonds and weak π–π stacking inter­actions with a centroid–centroid distance of 3.5494 (12) Å

护理分层管理的现状与发展趋势

Through implementing hierarchical management and monitor, improving and perfecting the hospital nurse training mechanism, implementing wages and labor outcomes in association with mechanism, further cultivating high-quality and high-level nursing management personnel, constantly improving quality, which maximize all the nursing staff 's enthusiasm and creativity, enhance the cohesion of nursing team, and improve the quality of hospital care.通过实施分层管理，逐层监控，完善和健全医院护士培训机制，实现工资待遇与劳动成果挂钩机制，进一步培养高素质、高层次的护理管理人才，持续质量改进，从而最大限度地发挥了全体护理人员的积极性和创造性，提升了护理队伍的凝聚力，提高了医院的护理质量

Associations of Muscle Mass and Strength with All-Cause Mortality among US Older Adults

INTRODUCTION: Recent studies suggested that muscle mass and muscle strength may independently or synergistically affect aging-related health outcomes in older adults; however, prospective data on mortality in the general population are sparse. METHODS: We aimed to prospectively examine individual and joint associations of low muscle mass and low muscle strength with all-cause mortality in a nationally representative sample. This study included 4449 participants age 50 yr and older from the National Health and Nutrition Examination Survey 1999 to 2002 with public use 2011 linked mortality files. Weighted multivariable logistic regression models were adjusted for age, sex, race, body mass index (BMI), smoking, alcohol use, education, leisure time physical activity, sedentary time, and comorbid diseases. RESULTS: Overall, the prevalence of low muscle mass was 23.1% defined by appendicular lean mass (ALM) and 17.0% defined by ALM/BMI, and the prevalence of low muscle strength was 19.4%. In the joint analyses, all-cause mortality was significantly higher among individuals with low muscle strength, whether they had low muscle mass (odds ratio [OR], 2.03; 95% confidence interval [CI], 1.27-3.24 for ALM; OR, 2.53; 95% CI, 1.64-3.88 for ALM/BMI) or not (OR, 2.66; 95% CI, 1.53-4.62 for ALM; OR, 2.17; 95% CI, 1.29-3.64 for ALM/BMI). In addition, the significant associations between low muscle strength and all-cause mortality persisted across different levels of metabolic syndrome, sedentary time, and LTPA. CONCLUSIONS: Low muscle strength was independently associated with elevated risk of all-cause mortality, regardless of muscle mass, metabolic syndrome, sedentary time, or LTPA among US older adults, indicating the importance of muscle strength in predicting aging-related health outcomes in older adults

An Implementation of List Successive Cancellation Decoder with Large List Size for Polar Codes

Polar codes are the first class of forward error correction (FEC) codes with a provably capacity-achieving capability. Using list successive cancellation decoding (LSCD) with a large list size, the error correction performance of polar codes exceeds other well-known FEC codes. However, the hardware complexity of LSCD rapidly increases with the list size, which incurs high usage of the resources on the field programmable gate array (FPGA) and significantly impedes the practical deployment of polar codes. To alleviate the high complexity, in this paper, two low-complexity decoding schemes and the corresponding architectures for LSCD targeting FPGA implementation are proposed. The architecture is implemented in an Altera Stratix V FPGA. Measurement results show that, even with a list size of 32, the architecture is able to decode a codeword of 4096-bit polar code within 150 us, achieving a throughput of 27MbpsComment: 4 pages, 4 figures, 4 tables, Published in 27th International Conference on Field Programmable Logic and Applications (FPL), 201

Ginsenoside Rb1 Preconditioning Enhances eNOS Expression and Attenuates Myocardial Ischemia/Reperfusion Injury in Diabetic Rats

Diabetes mellitus is associated with decreased NO bioavailability in the myocardium. Ginsenoside Rb1 has been shown to confer cardioprotection against ischemia reperfusion injury. The aim of this study was to investigate whether Ginsenoside Rb1 exerts cardioprotective effects during myocardial ischemia-reperfusion in diabetic rats and whether this effect is related to increase the production of NO via enhancing eNOS expression in the myocardium. The myocardial I/R injury were induced by occluding the left anterior descending artery for 30 min followed by 120 min reperfusion. An eNOS inhibitor L-NAME or Rb1 were respectively administered 25 min or 10 min before inducing ischemia. Ginsenoside Rb1 preconditioning reduced myocardial infarct size when compared with I/R group. Ginsenoside Rb1 induced myocardial protection was accompanied with increased eNOS expression and NO concentration and reduced plasma CK and LDH (P < 0.05). Moreover, the myocardial oxidative stress and tissue histological damage was attenuated by Ginsenoside Rb1 (P < 0.05). L-NAME abolished the protective effects of Ginsenoside Rb1. It is concluded that Ginsenoside Rb1 protects against myocardium ischemia/reperfusion injury in diabetic rat by enhancing the expression of eNOS and increasing the content of NO as well as inhibiting oxidative stress