472 research outputs found
Anion vacancies as a source of persistent photoconductivity in II-VI and chalcopyrite semiconductors
Using first-principles electronic structure calculations we identify the
anion vacancies in II-VI and chalcopyrite Cu-III-VI2 semiconductors as a class
of intrinsic defects that can exhibit metastable behavior. Specifically, we
predict persistent electron photoconductivity (n-type PPC) caused by the oxygen
vacancy VO in n-ZnO, and persistent hole photoconductivity (p-type PPC) caused
by the Se vacancy VSe in p-CuInSe2 and p-CuGaSe2. We find that VSe in the
chalcopyrite materials is amphoteric having two "negative-U" like transitions,
i.e. a double-donor transition e(2+/0) close to the valence band and a
double-acceptor transition e(0/2-) closer to the conduction band. We introduce
a classification scheme that distinguishes two types of defects (e.g., donors):
type-alpha, which have a defect-localized-state (DLS) in the gap, and
type-beta, which have a resonant DLS within the host bands (e.g., conduction
band). In the latter case, the introduced carriers (e.g., electrons) relax to
the band edge where they can occupy a perturbed-host-state (PHS). Type alpha is
non-conducting, whereas type beta is conducting. We identify the neutral anion
vacancy as type-alpha and the doubly positively charged vacancy as type-beta.
We suggest that illumination changes the charge state of the anion vacancy and
leads to a crossover between alpha- and beta-type behavior, resulting in
metastability and PPC. In CuInSe2, the metastable behavior of VSe is carried
over to the (VSe-VCu) complex, which we identify as the physical origin of PPC
observed experimentally. We explain previous puzzling experimental results in
ZnO and CuInSe2 in the light of this model.Comment: submitted to Phys. Rev.
Inflammation, insulin resistance, and diabetes-mendelian randomization using CRP haplotypes points upstream
Background
Raised C-reactive protein (CRP) is a risk factor for type 2 diabetes. According to the Mendelian randomization method, the association is likely to be causal if genetic variants that affect CRP level are associated with markers of diabetes development and diabetes. Our objective was to examine the nature of the association between CRP phenotype and diabetes development using CRP haplotypes as instrumental variables.
Methods and Findings
We genotyped three tagging SNPs (CRP + 2302G > A; CRP + 1444T > C; CRP + 4899T > G) in the CRP gene and measured serum CRP in 5,274 men and women at mean ages 49 and 61 y (Whitehall II Study). Homeostasis model assessment-insulin resistance (HOMA-IR) and hemoglobin A1c (HbA1c) were measured at age 61 y. Diabetes was ascertained by glucose tolerance test and self-report. Common major haplotypes were strongly associated with serum CRP levels, but unrelated to obesity, blood pressure, and socioeconomic position, which may confound the association between CRP and diabetes risk. Serum CRP was associated with these potential confounding factors. After adjustment for age and sex, baseline serum CRP was associated with incident diabetes (hazard ratio = 1.39 [95% confidence interval 1.29-1.51], HOMA-IR, and HbA1c, but the associations were considerably attenuated on adjustment for potential confounding factors. In contrast, CRP haplotypes were not associated with HOMA-IR or HbA1c (p=0.52-0.92). The associations of CRP with HOMA-IR and HbA1c were all null when examined using instrumental variables analysis, with genetic variants as the instrument for serum CRP. Instrumental variables estimates differed from the directly observed associations (p=0.007-0.11). Pooled analysis of CRP haplotypes and diabetes in Whitehall II and Northwick Park Heart Study II produced null findings (p=0.25-0.88). Analyses based on the Wellcome Trust Case Control Consortium (1,923 diabetes cases, 2,932 controls) using three SNPs in tight linkage disequilibrium with our tagging SNPs also demonstrated null associations.
Conclusions
Observed associations between serum CRP and insulin resistance, glycemia, and diabetes are likely to be noncausal. Inflammation may play a causal role via upstream effectors rather than the downstream marker CRP
Perpetrating Cyber Dating Abuse: A Brief Report on the Role of Aggression, Romantic Jealousy and Gender
There is increasing evidence that the use of elec-tronic communication technology (ECT) is being integrated into romantic relationships, which can be used as a medium to control a romantic partner. Most research focuses on the vic-tims of cyber dating abuse, however, we focused on the factors that predict perpetration of cyber dating abuse. We explored whether aggression (verbal aggression, physical aggression, anger and hostility), romantic jealousy (emotional, cognitive and behavioral jealousy), and gender predicted perpetration of cyber dating abuse (n = 189). We found that hostility, behav-ioral jealousy and gender significantly predicted perpetration of cyber dating abuse. The findings of this study contribute to our understanding of the psychological factors that drive cyber dating abuse in romantic relationships
Genetic regulatory signatures underlying islet gene expression and type 2 diabetes
The majority of genetic variants associated with type 2 diabetes (T2D) are located outside of genes in noncoding regions that may regulate gene expression in disease-relevant tissues, like pancreatic islets. Here, we present the largest integrated analysis to date of high-resolution, high-throughput human islet molecular profiling data to characterize the genome (DNA), epigenome (DNA packaging), and transcriptome (gene expression). We find that T2D genetic variants are enriched in regions of the genome where transcription Regulatory Factor X (RFX) is predicted to bind in an islet-specific manner. Genetic variants that increase T2D risk are predicted to disrupt RFX binding, providing a molecular mechanism to explain how the genome can influence the epigenome, modulating gene expression and ultimately T2D risk
Interactions between genetic variation and cellular environment in skeletal muscle gene expression
From whole organisms to individual cells, responses to environmental conditions are influenced by genetic makeup, where the effect of genetic variation on a trait depends on the environmental context. RNA-sequencing quantifies gene expression as a molecular trait, and is capable of capturing both genetic and environmental effects. In this study, we explore opportunities of using allele-specific expression (ASE) to discover cis-acting genotype-environment interactions (GxE)-genetic effects on gene expression that depend on an environmental condition. Treating 17 common, clinical traits as approximations of the cellular environment of 267 skeletal muscle biopsies, we identify 10 candidate environmental response expression quantitative trait loci (reQTLs) across 6 traits (12 unique gene-environment trait pairs; 10% FDR per trait) including sex, systolic blood pressure, and low-density lipoprotein cholesterol. Although using ASE is in principle a promising approach to detect GxE effects, replication of such signals can be challenging as validation requires harmonization of environmental traits across cohorts and a sufficient sampling of heterozygotes for a transcribed SNP. Comprehensive discovery and replication will require large human transcriptome datasets, or the integration of multiple transcribed SNPs, coupled with standardized clinical phenotyping.Peer reviewe
Implementation of an all-electron GW approximation based on the PAW method without plasmon pole approximation: application to Si, SiC, AlAs, InAs, NaH and KH
A new implementation of the GW approximation (GWA) based on the all-electron
Projector-Augmented-Wave method (PAW) is presented, where the screened Coulomb
interaction is computed within the Random Phase Approximation (RPA) instead of
the plasmon-pole model. Two different ways of computing the self-energy are
reported. The method is used successfully to determine the quasiparticle
energies of six semiconducting or insulating materials: Si, SiC, AlAs, InAs,
NaH and KH. To illustrate the novelty of the method the real and imaginary part
of the frequency-dependent self-energy together with the spectral function of
silicon are computed. Finally, the GWA results are compared with other
calculations, highlighting that all-electron GWA results can differ markedly
from those based on pseudopotential approaches.Comment: 11pages,3figures, submitted to PR
Allelic spectrum of the natural variation in CRP
With the recent completion of the International HapMap Project, many tools are in hand for genetic association studies seeking to test the common variant/common disease hypothesis. In contrast, very few tools and resources are in place for genotype–phenotype studies hypothesizing that rare variation has a large impact on the phenotype of interest. To create these tools for rare variant/common disease studies, much interest is being generated towards investing in re-sequencing either large sample sizes of random chromosomes or smaller sample sizes of patients with extreme phenotypes. As a case study for rare variant discovery in random chromosomes, we have re-sequenced ~1,000 chromosomes representing diverse populations for the gene C-reactive protein (CRP). CRP is an important gene in the fields of cardiovascular and inflammation genetics, and its size (~2 kb) makes it particularly amenable medical or deep re-sequencing. With these data, we explore several issues related to the present-day candidate gene association study including the benefits of complete SNP discovery, the effects of tagSNP selection across diverse populations, and completeness of dbSNP for CRP. Also, we show that while deep re-sequencing uncovers potentially medically relevant coding SNPs, these SNPs are fleetingly rare when genotyped in a population-based survey of 7,000 Americans (NHANES III). Collectively, these data suggest that several different types re-sequencing and genotyping approaches may be required to fully understand the complete spectrum of alleles that impact human phenotypes. ELECTRONIC SUPPLEMENTARY MATERIAL: Supplementary material is available for this article at http://dx.doi.org/10.1007/s00439-006-0160-y and is accessible for authorized users
The new enclosures: critical perspectives on corporate land deals
The contributions to this collection use the tools of agrarian political economy to
explore the rapid growth and complex dynamics of large-scale land deals in recent
years, with a special focus on the implications of big land deals for property and
labour regimes, labour processes and structures of accumulation. The first part of
this introductory essay examines the implications of this agrarian political
economy perspective. First we explore the continuities and contrasts between
historical and contemporary land grabs, before examining the core underlying
debate around large- versus small-scale farming futures. Next, we unpack the
diverse contexts and causes of land grabbing today, highlighting six overlapping
mechanisms. The following section turns to assessing the crisis narratives that
frame the justifications for land deals, and the flaws in the argument around there
being excess, empty or idle land available. Next the paper turns to an examination
of the impacts of land deals, and the processes of inclusion and exclusion at play,
before looking at patterns of resistance and constructions of alternatives. The
final section introduces the papers in the collection.ESR
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