Characterization of edge damage induced on REBCO superconducting tape by mechanical slitting

Rare-earth barium-copper-oxide (REBCO) superconductors are high-field superconductors fabricated in a tape geometry that can be utilized in magnet applications well in excess of 20 T. Due to the multilayer architecture of the tape, delamination is one cause of mechanical failure in REBCO tapes. During a mechanical slitting step in the manufacturing process, edge cracks can be introduced into the tape. These cracks are thought to be potential initiation sites for crack propagation in the tapes when subjected to stresses in the fabrication and operation of magnet systems. We sought to understand which layers were the mechanically weakest by locating the crack initiation layer and identifying the geometrical conditions of the slitter that promoted or suppressed crack formation. The described cracking was investigated by selectively etching and characterizing each layer with scanning electron microscopy, laser confocal microscopy, and digital image analysis. Our analysis showed that the average crack lengths in the REBCO, LaMnO3 (LMO) and Al2O3 layers were 34 μm, 28 μm, and 15 μm, respectively. The total number of cracks measured in 30mmof wire length was between 3000 and 5700 depending on the layer and their crack densities were 102 cracks mm-1 for REBCO, 108 cracks mm-1 for LMO, and 183 cracks mm-1 for Al2O3. These results indicated that there are separate crack initiation mechanisms for the REBCO and the LMO layers, as detailed in the paper. With a better understanding of the crack growth behavior exhibited by REBCO tapes, the fabrication process can be improved to provide a more mechanically stable and cost-effective superconductor

Financial incentives to promote retention in care and viral suppression in adults with HIV initiating antiretroviral therapy in Tanzania: a three-arm randomised controlled trial

Background: Financial incentives promote use of HIV services and might support adherence to the sustained antiretroviral therapy (ART) necessary for viral suppression, but few studies have assessed a biomarker of adherence or evaluated optimal implementation. We sought to determine whether varying sized financial incentives for clinic attendance effected viral suppression in patients starting ART in Tanzania. Methods: In a three-arm, parallel-group, randomised controlled trial at four health facilities in Shinyanga region, Tanzania, adults aged 18 years or older with HIV who had started ART within the past 30 days were randomly assigned (1:1:1) using a tablet-based application (stratified by site) to receive usual care (control group) or to receive a cash incentive for monthly clinic attendance in one of two amounts: 10 000 Tanzanian Shillings (TZS; about US$4·50) or 22 500 TZS (about$10·00). There were no formal exclusion criteria. Participants were masked to the existence of two incentive sizes. Incentives were provided for up to 6 months via mobile health technology (mHealth) that linked biometric attendance monitoring to automated mobile payments. We evaluated the primary outcome of retention in care with viral suppression (<1000 copies per mL) at 6 months using logistic regression. This trial is registered with ClinicalTrials.gov, NCT03351556. Findings: Between April 24 and Dec 14, 2018, 530 participants were randomly assigned to an incentive strategy (184 in the control group, 172 in the smaller incentive group, and 174 in the larger incentive group). All participants were included in the primary intention-to-treat analysis. At 6 months, approximately 134 (73%) participants in the control group remained in care and had viral suppression, compared with 143 (83%) in the smaller incentive group (risk difference [RD] 9·8, 95% CI 1·2 to 18·5) and 150 (86%) in the larger incentive group (RD 13·0, 4·5 to 21·5); we identified a positive trend between incentive size and viral suppression (p trend=0·0032), although the incentive groups did not significantly differ (RD 3·2, −4·6 to 11·0). Adverse events included seven (4%) deaths in the control group and 11 (3%) deaths in the intervention groups, none related to study participation. Interpretation: Small financial incentives delivered using mHealth can improve retention in care and viral suppression in adults starting HIV treatment. Although further research should investigate the durability of effects from short-term incentives, these findings strengthen the evidence for implementing financial incentives within standard HIV care

Pass a Law, Any Law, Fast! State Legislative Responses to the Kelo Backlash

The Supreme Court in Kelo v. City of New London left protection of property against takings for economic development to the states. Since Kelo, thirty-seven states have enacted legislation to update their eminent domain laws. This paper is the first to theoretically and empirically analyze the factors that influence whether, in what manner, and how quickly states change their laws through new legislation. Fourteen of the thirty-seven new laws offer only weak protections against development takings. The legislative response to Kelo was responsive to measures of the backlash but only in the binary decision whether to pass any new law. The decision to enact a meaningful restriction was more a function of relevant political economy measures. States with more economic freedom, greater value of new housing construction, and less racial and income inequality are more likely to have enacted stronger restrictions, and sooner. Of the thirteen states that have not updated, Arkansas, Oklahoma and Mississippi are highly likely to do so in the future. Hawaii, Massachusetts and New York are unlikely to update ever if at all

Development of Social Variation in Reproductive Schedules: A Study from an English Urban Area

Background: There is striking social variation in the timing of the onset of childbearing in contemporary England, with the mean age at first motherhood about 8 years earlier in the most deprived compared to the least deprived neighbourhoods. However, relatively little is known about how these social differences in reproductive schedule develop in childhood. Methodology/Principal Findings: We studied the development of differences in reproductive schedules, using a crosssectional survey over 1000 school students aged 9–15 in the metropolitan borough of North Tyneside. Students from more deprived neighbourhoods had earlier ideal ages for parenthood than those from more affluent ones, and these differences were fully apparent by age 11. We found evidence consistent with three mechanisms playing a role in maintaining the socioeconomic gradient. These were: vertical intergenerational transmission (students whose own parents were younger at their birth wanted children younger); oblique intergenerational transmission (students in neighbourhoods where parents were younger in general wanted children earlier); and low parental investment (students who did not feel emotionally supported by their own parents wanted children at a younger age). Conclusions/Significance: Our results shed some light on the proximate factors which may be involved in maintaining early childbearing in disadvantaged communities. They help understand why educational initiatives aimed at adolescents tend to have no effect, whereas improving the well-being of poor families with young children may do so. Our results also sugges

Genetic effects on gene expression across human tissues

Characterization of the molecular function of the human genome and its variation across individuals is essential for identifying the cellular mechanisms that underlie human genetic traits and diseases. The Genotype-Tissue Expression (GTEx) project aims to characterize variation in gene expression levels across individuals and diverse tissues of the human body, many of which are not easily accessible. Here we describe genetic effects on gene expression levels across 44 human tissues. We find that local genetic variation affects gene expression levels for the majority of genes, and we further identify inter-chromosomal genetic effects for 93 genes and 112 loci. On the basis of the identified genetic effects, we characterize patterns of tissue specificity, compare local and distal effects, and evaluate the functional properties of the genetic effects. We also demonstrate that multi-tissue, multi-individual data can be used to identify genes and pathways affected by human disease-associated variation, enabling a mechanistic interpretation of gene regulation and the genetic basis of diseas

Genome-wide association study identifies six new loci influencing pulse pressure and mean arterial pressure.

Numerous genetic loci have been associated with systolic blood pressure (SBP) and diastolic blood pressure (DBP) in Europeans. We now report genome-wide association studies of pulse pressure (PP) and mean arterial pressure (MAP). In discovery (N = 74,064) and follow-up studies (N = 48,607), we identified at genome-wide significance (P = 2.7 × 10(-8) to P = 2.3 × 10(-13)) four new PP loci (at 4q12 near CHIC2, 7q22.3 near PIK3CG, 8q24.12 in NOV and 11q24.3 near ADAMTS8), two new MAP loci (3p21.31 in MAP4 and 10q25.3 near ADRB1) and one locus associated with both of these traits (2q24.3 near FIGN) that has also recently been associated with SBP in east Asians. For three of the new PP loci, the estimated effect for SBP was opposite of that for DBP, in contrast to the majority of common SBP- and DBP-associated variants, which show concordant effects on both traits. These findings suggest new genetic pathways underlying blood pressure variation, some of which may differentially influence SBP and DBP

Genome-wide association identifies nine common variants associated with fasting proinsulin levels and provides new insights into the pathophysiology of type 2 diabetes.

OBJECTIVE: Proinsulin is a precursor of mature insulin and C-peptide. Higher circulating proinsulin levels are associated with impaired β-cell function, raised glucose levels, insulin resistance, and type 2 diabetes (T2D). Studies of the insulin processing pathway could provide new insights about T2D pathophysiology. RESEARCH DESIGN AND METHODS: We have conducted a meta-analysis of genome-wide association tests of ∼2.5 million genotyped or imputed single nucleotide polymorphisms (SNPs) and fasting proinsulin levels in 10,701 nondiabetic adults of European ancestry, with follow-up of 23 loci in up to 16,378 individuals, using additive genetic models adjusted for age, sex, fasting insulin, and study-specific covariates. RESULTS: Nine SNPs at eight loci were associated with proinsulin levels (P < 5 × 10(-8)). Two loci (LARP6 and SGSM2) have not been previously related to metabolic traits, one (MADD) has been associated with fasting glucose, one (PCSK1) has been implicated in obesity, and four (TCF7L2, SLC30A8, VPS13C/C2CD4A/B, and ARAP1, formerly CENTD2) increase T2D risk. The proinsulin-raising allele of ARAP1 was associated with a lower fasting glucose (P = 1.7 × 10(-4)), improved β-cell function (P = 1.1 × 10(-5)), and lower risk of T2D (odds ratio 0.88; P = 7.8 × 10(-6)). Notably, PCSK1 encodes the protein prohormone convertase 1/3, the first enzyme in the insulin processing pathway. A genotype score composed of the nine proinsulin-raising alleles was not associated with coronary disease in two large case-control datasets. CONCLUSIONS: We have identified nine genetic variants associated with fasting proinsulin. Our findings illuminate the biology underlying glucose homeostasis and T2D development in humans and argue against a direct role of proinsulin in coronary artery disease pathogenesis