Phelpshutchison1634
ATP-binding cassette transporter (ABC transporter) subfamilies ABCA-C and ABCG-H have been implicated in insecticide detoxification, mostly based on findings of elevated gene expression in response to insecticide treatment. We previously characterized TcABCA-C genes from the model beetle and pest Tribolium castaneum and demonstrated that TcABCA and TcABCC genes are involved in the elimination of diflubenzuron, because RNA interference (RNAi)-mediated gene silencing increased susceptibility. In this study, we focused on the potential functions of TcABCG and TcABCH genes in insecticide detoxification.
When we silenced the expression of TcABCG-H genes using RNAi, we noticed a previously unreported developmental RNAi phenotype for TcABCG-4F, which is characterized by 50% mortality and ecdysial arrest during adult moult. When we knocked down the Drosophila brown orthologue TcABCG-XC, we did not obtain apparent eye colour phenotypes but did observe a loss of riboflavin uptake by Malpighian tubules. Next, we det response, and hence underlines the significance of functional studies on insecticide detoxification. © 2021 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.
To determine what proportion of the inter-country variation in death rates can be explained in terms of obesity rates and other known risk factors for coronavirus disease 2019 (COVID-19).
COVID-19 death rates from 30 industrialized countries were analysed using linear regression models. Covariates modelled population density, the age structure of the population, obesity, population health, per capita gross domestic product (GDP), ethnic diversity, national temperature and the delay in the government imposing virus control measures.
The multivariable regression model explained 63% of the inter-country variation in COVID-19 death rates. The initial model was optimized using stepwise selection. In descending order of absolute size of model coefficient, the covariates in the optimized model were the obesity rate, the hypertension rate, population density, life expectancy, the percentage of the population aged older than 65 years, the percentage of the population aged younger than 15 years, the diabetes ratefinition of a COVID-19 death and in the completeness of the recording of COVID-19 deaths.
Although genome-wide association studies have identified many loci that influence smoking behaviors, much of the genetic variance remains unexplained. We characterized the genetic architecture of four smoking behaviors using single nucleotide polymorphism (SNP) heritability (h
). BIBR 1532 supplier This is an estimate of narrow-sense heritability specifically estimating the proportion of phenotypic variation due to causal variants (CVs) tagged by SNPs.
Partitioned h
analysis of smoking behavior traits.
UK Biobank.
UK Biobank participants of European ancestry. The number of participants varied depending on the trait, from 54 792 to 323 068.
Smoking initiation, age of initiation, cigarettes per day (CPD; count, log-transformed, binned and dichotomized into heavy versus light) and smoking cessation with imputed genome-wide SNPs.
We estimated that, in aggregate, approximately 18% of the phenotypic variance in smoking initiation was captured by imputed SNPs [h
=0.18, standard error (SE)=0.01] and 12% [SE=0.02] for smoking cessation, both of which were more than twice the previously reported estimates. Estimated age of initiation (h
=0.05, SE=0.01) and binned CPD (h
=0.1, SE=0.01) were substantially below published twin-based h
of 50%. CPD encoding influenced estimates, with dichotomized CPD h
=0.28. There was no evidence of dominance genetic variance for any trait.
A biobank study of smoking behavior traits suggested that the phenotypic variance explained by SNPs of smoking initiation, age of initiation, cigarettes per day and smoking cessation is modest overall.
A biobank study of smoking behavior traits suggested that the phenotypic variance explained by SNPs of smoking initiation, age of initiation, cigarettes per day and smoking cessation is modest overall.
Research linking orbitofrontal cortex (OFC) structure and substance use disorders (SUDs) is largely correlational and often implies a causal effect of addiction/substance exposure on the brain, but familial risk factors (e.g. genetic liability) may confound these associations. We tested whether associations between alcohol, cannabis and tobacco use disorders and OFC thickness reflected the potential causal effects of familial risk or SUDs-related consequences (e.g. substance exposure).
A co-twin control/discordant twin design separated familial risk confounding from SUD-related consequences.
A population-based sample of 436 24-year-old twins (62% monozygotic) from the Minnesota Twin Family Study, USA.
Alcohol, cannabis and tobacco use disorders were assessed using the Composite International Diagnostic Interview-Substance Abuse Module. Cortical thickness of the medial and lateral OFC (mOFC and lOFC, respectively) was assessed using magnetic resonance imaging (MRI).
Lower mOFC (P-values ≤0.006) but nlial risk effect, the experience of an alcohol or cannabis use disorder in emerging adulthood reduces the thickness of the medial orbitofrontal cortex, a region associated with value-guided decision-making.
To examine the long-term efficacy and safety of dapagliflozin, a sodium-glucose co-transporter-2 (SGLT2) inhibitor used to treat type 1 diabetes, in the Japanese subpopulation of the DEPICT-2 study.
Patients with type 1 diabetes were randomized to dapagliflozin 5 mg (n = 55), dapagliflozin 10 mg (n = 41) or placebo (n = 58) plus insulin for a 24-week, double-blind period followed by a 28-week, single-blind extension phase.
From baseline to 24 weeks, dapagliflozin reduced HbA1c compared with placebo (mean change of -0.58% and -0.80% for 5 and 10 mg, respectively), and an HbA1c reduction was observed up to 52 weeks. Compared with placebo, dapagliflozin 5 and 10 mg increased the proportion of patients achieving HbA1c reductions of 0.5% or more without severe hypoglycaemia events and reduced glycaemic variability assessed via continuous glucose monitoring. Both dapagliflozin doses decreased body weight and total daily insulin dose at 24 weeks compared with placebo; these reductions were maintained up to 52 weeks.
