Oxygen impurities in NiAl: Relaxation effects

We have used a full-potential linear muffin-tin orbital method to calculate the effects of oxygen impurities on the electronic structure of NiAl. Using the supercell method with a 16-atom supercell we have investigated the cases where an oxygen atom is substitutionally placed at either a nickel or an aluminum site. Full relaxation of the atoms within the supercell was allowed. We found that oxygen prefers to occupy a nickel site over an aluminum site with a site selection energy of 138 mRy (21,370 K). An oxygen atom placed at an aluminum site is found to cause a substantial relaxation of its nickel neighbors away from it. In contrast, this steric repulsion is hardly present when the oxygen atom occupies the nickel site and is surrounded by aluminum neighbors. We comment on the possible relation of this effect to the pesting degradation phenomenon (essentially spontaneous disintegration in air) in nickel aluminides.Comment: To appear in Phys. Rev. B (Aug. 15, 2001

Quantum inference of states and processes

The maximum-likelihood principle unifies inference of quantum states and processes from experimental noisy data. Particularly, a generic quantum process may be estimated simultaneously with unknown quantum probe states provided that measurements on probe and transformed probe states are available. Drawbacks of various approximate treatments are considered.Comment: 7 pages, 4 figure

Systematic Review of Medicine-Related Problems in Adult Patients with Atrial Fibrillation on Direct Oral Anticoagulants

New oral anticoagulant agents continue to emerge on the market and their safety requires assessment to provide evidence of their suitability for clinical use. There-fore, we searched standard databases to summarize the English language literature on medicine-related problems (MRPs) of direct oral anticoagulants DOACs (dabigtran, rivaroxban, apixban, and edoxban) in the treatment of adults with atri-al fibrillation. Electronic databases including Medline, Embase, International Pharmaceutical Abstract (IPA), Scopus, CINAHL, the Web of Science and Cochrane were searched from 2008 through 2016 for original articles. Studies pub-lished in English reporting MRPs of DOACs in adult patients with AF were in-cluded. Seventeen studies were identified using standardized protocols, and two reviewers serially abstracted data from each article. Most articles were inconclusive on major safety end points including major bleeding. Data on major safety end points were combined with efficacy. Most studies inconsistently reported adverse drug reactions and not adverse events or medication error, and no definitions were consistent across studies. Some harmful drug effects were not assessed in studies and may have been overlooked. Little evidence is provided on MRPs of DOACs in patients with AF and, therefore, further studies are needed to establish the safety of DOACs in real-life clinical practice

Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990-2015: A systematic analysis for the Global Burden of Disease Study 2015

Background: The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. Methods: We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors—the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. We characterised risk exposure in relation to a Socio-demographic Index (SDI). Findings: Between 1990 and 2015, global exposure to unsafe sanitation, household air pollution, childhood underweight, childhood stunting, and smoking each decreased by more than 25%. Global exposure for several occupational risks, high body-mass index (BMI), and drug use increased by more than 25% over the same period. All risks jointly evaluated in 2015 accounted for 57·8% (95% CI 56·6–58·8) of global deaths and 41·2% (39·8–42·8) of DALYs. In 2015, the ten largest contributors to global DALYs among Level 3 risks were high systolic blood pressure (211·8 million [192·7 million to 231·1 million] global DALYs), smoking (148·6 million [134·2 million to 163·1 million]), high fasting plasma glucose (143·1 million [125·1 million to 163·5 million]), high BMI (120·1 million [83·8 million to 158·4 million]), childhood undernutrition (113·3 million [103·9 million to 123·4 million]), ambient particulate matter (103·1 million [90·8 million to 115·1 million]), high total cholesterol (88·7 million [74·6 million to 105·7 million]), household air pollution (85·6 million [66·7 million to 106·1 million]), alcohol use (85·0 million [77·2 million to 93·0 million]), and diets high in sodium (83·0 million [49·3 million to 127·5 million]). From 1990 to 2015, attributable DALYs declined for micronutrient deficiencies, childhood undernutrition, unsafe sanitation and water, and household air pollution; reductions in risk-deleted DALY rates rather than reductions in exposure drove these declines. Rising exposure contributed to notable increases in attributable DALYs from high BMI, high fasting plasma glucose, occupational carcinogens, and drug use. Environmental risks and childhood undernutrition declined steadily with SDI; low physical activity, high BMI, and high fasting plasma glucose increased with SDI. In 119 countries, metabolic risks, such as high BMI and fasting plasma glucose, contributed the most attributable DALYs in 2015. Regionally, smoking still ranked among the leading five risk factors for attributable DALYs in 109 countries; childhood underweight and unsafe sex remained primary drivers of early death and disability in much of sub-Saharan Africa. Interpretation: Declines in some key environmental risks have contributed to declines in critical infectious diseases. Some risks appear to be invariant to SDI. Increasing risks, including high BMI, high fasting plasma glucose, drug use, and some occupational exposures, contribute to rising burden from some conditions, but also provide opportunities for intervention. Some highly preventable risks, such as smoking, remain major causes of attributable DALYs, even as exposure is declining. Public policy makers need to pay attention to the risks that are increasingly major contributors to global burden. Funding: Bill & Melinda Gates Foundation

Advanced Glycation End Products Down-regulate Gap Junctions in Human Hepatoma SKHep 1 Cells via the Activation of Src-Dependent ERK1/2 and JNK/SAPK/AP1 Signaling Pathways

Hyperglycemia and advanced glycation end products (AGEs) are associated with an elevated risk of developing several cancers in diabetic patients. However, the detailed mechanisms remain to be elucidated. The mechanism of AGE-bovine serum albumin (BSA) on gap junction intercellular communication in human hepatoma cell line, SKHep 1, was investigated. Both Cx32 and Cx43 are major gap junction forming proteins in the liver, the loss of which has been shown to facilitate tumorigenesis. Although the MTT assay results showed that AGE-BSA significantly increased cell growth by 31%, AGE-BSA down-regulated Cx32 and Cx43 expression in a dose- and time-dependent manner. The present study also demonstrated that ERK1/2 and JNK/SAPK were significantly activated by AGE BSA and that Src, ERK1/2, and JNK/SAPK inhibitors significantly reversed the reduction of Cx32 and Cx43 proteins by AGE-BSA. Taken together, these results strongly support the hypothesis that Src-dependent ERK1/2 and JNK/SAPK/AP1 signaling pathways play a key role in AGE BSA-mediated down-regulation of Cx32 and Cx43 protein expression in SKHep 1 cells