Experimental Demonstration of Continuous Electronic Structure Tuning via Strain in Atomically Thin MoS₂

We demonstrate the continuous tuning of the electronic structure of atomically thin MoS₂ on flexible substrates by applying a uniaxial tensile strain. A redshift at a rate of ∼70 meV per percent applied strain for direct gap transitions, and at a rate 1.6 times larger for indirect gap transitions, has been determined by absorption and photoluminescence spectroscopy. Our result, in excellent agreement with first principles calculations, demonstrates the potential of two-dimensional crystals for applications in flexible electronics and optoelectronics

Forest plot of mortality relative risks reported by 22 studies.

<p>The relative risks correspond to the estimated effect of receiving vs. not receiving TB treatment at the time of cART initiation on subsequent mortality among HIV-infected adults. Estimates are ordered according to length of follow-up time. Estimates were abstracted according to the precision used by the original authors; estimates calculated using available data are reported to 2 decimal places. Abbreviations: cART, combination antiretroviral therapy; CI, confidence interval; HIV, human immunodeficiency virus; RR, relative risk; TB, tuberculosis. </p

Table1_The genetics of occupational asthma development among workers exposed to diisocyanates: A systematic literature review with meta-analysis.XLSX

Diisocyanates are widely used compounds that pose a safety concern for workers in occupations within the spray-paint, spray-foam insulation, and furniture varnish industries. Epidemiological studies show that only a subset of workers exposed to diisocyanates develop diisocyanate-induced occupational asthma (diisocyanate asthma, DA), indicating that genetic susceptibility may play a role. The purpose of this systematic literature review was to compile and meta-analyze the reported data on genetic susceptibility markers for DA. Three databases (Embase, Pubmed, and Scopus) were searched and 169 non-duplicate publications were identified, of which 22 relevant occupational studies were included in this review. Researchers reported prevalence odds ratios (PORs) for 943 comparisons in 82 different genes/serotypes. Protein network functions for the DA-associated genes from this review include: antigen processing, lymphocyte activation, cytokine production regulation, and response to oxidative stress. Meta-analysis of comparisons between workers with DA and controls was conducted for 23 genetic markers within: CTNNA3, GSTM1, GSTP1, GSTT1, HLA-C, HLA-DQB1, HLA-DR1, HLA-DR3, HLA-DR4, HLA-DR7, and HLA-DR8. These genes code for proteins that are involved in cell-cell adhesions (CTNNA3), glutathione conjugation for xenobiotic metabolism (GST gene family), and immune system response (HLA gene family). The most compelling pooled PORs were for two studies on CTNNA3 (increased DA risk: rs10762058 GG, rs7088181 GG, rs4378283 TT; PORs 4.38–4.97) and three studies on HLA-DR1 (decreased DA risk, POR 0.24). Bioinformatics of the predicted protein pathways for DA shows overlap with biomarker-associated pathways in workers before development of asthma, suggesting overlap in toxicokinetic and toxicodynamic pathways of diisocyanates. The control groups were also compared against each other and differences were negligible. Suggestions for improving future research are also presented. Of the highest importance, the literature was found to be profoundly publication-biased, in which researchers need to report the data for all studied markers regardless of the statistical significance level. We demonstrate the utility of evaluating the overlap in predicted protein pathway functions for identifying more consistency across the reported literature including for asthma research, biomarker research, and in vitro studies. This will serve as an important resource for researchers to use when generating new hypothesis-driven research about diisocyanate toxicology.</p

The Effect of Tuberculosis Treatment at Combination Antiretroviral Therapy Initiation on Subsequent Mortality: A Systematic Review and Meta-Analysis

<div><p>Objective</p><p>We aimed to perform a systematic review and meta-analysis examining the impact of TB treatment at the time of combination antiretroviral therapy (cART) initiation on subsequent mortality.</p> <p>Methods</p><p>We searched PubMed, EMBASE, and selected conference proceedings for studies that report adult mortality on cART, stratified by TB treatment status at cART initiation. Stratified random-effects and meta-regression analyses were used to examine the influence of study and population characteristics.</p> <p>Results</p><p>22 eligible cohort studies reported data on 98,350 (range 74-15,225) adults, of whom 14,779 (15%) were receiving TB treatment at cART initiation. Studies of those receiving vs. not receiving TB treatment had an average mortality relative risk of 1.10 (95% confidence interval 0.87-1.40) at 1-3 months (based upon 8 estimates), 1.15 (0.94-1.41) at 6-12 months (11 estimates), and 1.33 (1.02-1.75) at 18-98 months (10 estimates) following cART initiation. However, there was a wide range of estimates and those at later time points were markedly heterogeneous. Meta-regression identified factors associated with elevated average risk estimates: lower median baseline CD4 counts and adjustment for baseline hemoglobin at 1-3 months; longer length of follow-up and women-only studies at 6-12 months; and not adjusting for BMI/weight at 18-98 months.</p> <p>Conclusions</p><p>Patients receiving TB treatment at cART initiation did not have a statistically significant estimated increase in short-term risk of all-cause mortality as compared to those not receiving TB treatment. TB treatment was significantly associated with increased mortality after about a year of cART, suggesting that patients with concurrent TB treatment at cART initiation may benefit from continued support after TB treatment completion.</p> </div

Identification and selection of eligible studies.

<p>Identification and selection of eligible studies.</p

Adolescent Expectations of Early Death Predict Adult Risk Behaviors

<div><p>Only a handful of public health studies have investigated expectations of early death among adolescents. Associations have been found between these expectations and risk behaviors in adolescence. However, these beliefs may not only predict worse adolescent outcomes, but worse trajectories in health with ties to negative outcomes that endure into young adulthood. The objectives of this study were to investigate perceived chances of living to age 35 (Perceived Survival Expectations, PSE) as a predictor of suicidal ideation, suicide attempt and substance use in young adulthood. We examined the predictive capacity of PSE on future suicidal ideation/attempt after accounting for sociodemographics, depressive symptoms, and history of suicide among family and friends to more fully assess its unique contribution to suicide risk. We investigated the influence of PSE on legal and illegal substance use and varying levels of substance use. We utilized the National Longitudinal Study of Adolescent Health (Add Health) initiated in 1994–95 among 20,745 adolescents in grades 7–12 with follow-up interviews in 1996 (Wave II), 2001–02 (Wave III) and 2008 (Wave IV; ages 24–32). Compared to those who were almost certain of living to age 35, perceiving a 50–50 or less chance of living to age 35 at Waves I or III predicted suicide attempt and ideation as well as regular substance use (i.e., exceeding daily limits for moderate drinking; smoking ≥ a pack/day; and using illicit substances other than marijuana at least weekly) at Wave IV. Associations between PSE and detrimental adult outcomes were particularly strong for those reporting persistently low PSE at both Waves I and III. Low PSE at Wave I or Wave III was also related to a doubling and tripling, respectively, of death rates in young adulthood. Long-term and wide-ranging ties between PSE and detrimental outcomes suggest these expectations may contribute to identifying at-risk youth.</p> </div

Heavy metals, organic solvents, and multiple sclerosis: An exploratory look at gene-environment interactions

<div><p>ABSTRACT</p><p>Exposure to heavy metals and organic solvents are potential etiologic factors for multiple sclerosis (MS), but their interaction with MS-associated genes is under-studied. The authors explored the relationship between environmental exposure to lead, mercury, and solvents and 58 single-nucleotide polymorphisms (SNPs) in MS-associated genes. Data from a population-based case-control study of 217 prevalent MS cases and 496 age-, race-, gender-, and geographically matched controls were used to fit conditional logistic regression models of the association between the chemical, gene, and MS, adjusting for education and ancestry. MS cases were more likely than controls to report lead (odds ratio [OR] = 2.03; 95% confidence interval [CI]: 1.07, 3.86) and mercury exposure (OR = 2.06; 95% CI: 1.08, 3.91). Findings of potential gene-environment interactions between SNPs in <i>TNF-</i>α, <i>TNF-</i>β, TCA-β, <i>VDR, MBP,</i> and <i>APOE</i>, and lead, mercury, or solvents should be considered cautiously due to limited sample size.</p></div

Perceived Survival Expectations (PSE) as a predictor of Wave IV suicidal behavior, Add Health.

<p>PSE = Perceived Survival Expectations. Assessed via: “What are your chances of living to age 35?”.</p><p>Unweighted sample size; Percentages, Relative Risks (95% Confidence Intervals) are weighted.</p>a<p>Log-binomial regression model controlled for age, sex, race/ethnicity, foreign-birth, parental education, family structure, childhood physical maltreatment, childhood sexual abuse and Wave I values for block group poverty, family history of suicide, history of suicide among friends, depressive symptoms, religiosity, parental attachment/support, cigarette smoking, binge drinking, illicit drug use and self-rated health.</p>b<p>Log-binomial regression model controlled for the above-listed Wave III equivalent covariates.</p>c<p>Log-binomial regression model controlled for the above-listed Wave I equivalent covariates.</p

Percent deceased (n = 131) by Wave I and Wave III PSE.

<p>Percent deceased (n = 131) by Wave I and Wave III PSE.</p

Perceived Survival Expectations (PSE) as a predictor of Wave IV heavy drinking, smoking and illicit substance use, Add Health.

<p>PSE = Perceived Survival Expectations. Assessed via: “What are your chances of living to age 35?”.</p><p>Unweighted sample size, All other estimates are weighted.</p>a<p>Model controlled for age, sex, race/ethnicity, foreign-birth, parental education, family structure, childhood physical abuse, childhood sexual abuse and Wave I values for block group poverty, depressive symptoms, religiosity, parental attachment/support and self-rated health.</p>b<p>Model controlled for the above-listed Wave III covariates.</p>c<p>Model controlled for the above-listed Wave I covariates.</p