Effects of executive functioning on false memory in children

Misremembering is a common phenomenon in normal human development that has great potential to become problematic, especially in legal situations. The Deese/Roediger--McDermott (DRM; Deese, 1959; Roediger & McDermott, 1995) model has been commonly used in the literature to uncover mechanisms for why these false memories may occur. Children have only recently begun to be investigated using this paradigm. Some related mechanisms in children for false recollection that have yet to be investigated are child executive functioning and socioeconomic status. In the current study, executive functioning was investigated as a potential mechanism for false recollections using a DRM paradigm. Children completed a brief assessment of intelligence followed by assessments of executive functioning. Participants then engaged in the DRM recall and recognition task. Finally, they completed a semantic knowledge task. Results indicated that specific aspects of executive functioning (inhibition and cognitive flexibility) predicted false memory production at both recall and recognition. Additionally, maternal education and gross family income had predictive value at recall and recognition. However, a mediational model was not supported. These results help explain mechanisms for false memory and can provide valuable information regarding susceptibility to false memory production

It starts with the parents and ends with the parents

Alcohol is the most popular recreational drug in Australia. Despite the fact that many people gain enjoyment from alcohol related industries, alcohol is also implicated in much personal trauma and social damage. Parents play a key role in influencing alcohol use and driver behaviour in young people. The aim of this study was to gain an understanding of the attitudes and concerns of parents in Melbourne in relation to their teenage children\u27s use of alcohol and how they educate and/or provide role models for their adolescents with respect to alcohol usage. A convenience sample of parents with adolescent children participated in focus groups. Parents described patterns of alcohol use and perceived influences on consumption. They reported that they wanted to create safe environments for adolescents to consume alcohol but that they needed more support and information on which to base these decisions. There i, an opportunity for public health policy makers to specifically address parents and enhance their role in alcohol related road safety.<br /

Exotic pediculosis and hair-loss syndrome in deer (Odocoileus hemionus) populations in California

Infestation with nonnative, “exotic” lice was first noted in Washington black-tailed deer (Odocoileus hemionus columbianus) in 1994 and has since then spread throughout the western United States. In California, infestation with the exotic louse Damalinia (Cervicola) sp. was first detected in black-tailed deer from northern California in 2004, and, in 2009, the exotic louse species Bovicola tibialis and Linognathus africanus were identified on mule deer (Odocoileus hemionus californicus) in central Sierra Nevada in association with a mortality event. Exotic lice have since been detected in various locations throughout the state. We describe the geographic distribution of these exotic lice within California, using data from 520 live-captured and 9 postmortem-sampled, free-ranging mule deer examined between 2009 and 2014. Data from live-captured deer were used to assess possible associations between louse infestation and host age, host sex, migratory behavior, season, and blood selenium and serum copper concentrations. Damalinia (Cervicola) sp. and B. tibialis lice were distinctively distributed geographically, with D. (Cervicola) sp. infesting herds in northern and central coastal California, B. tibialis occurring in the central coastal mountains and the Sierra Nevada, and L. africanus occurring only sporadically. Younger age classes and low selenium concentrations were significantly associated with exotic louse infestation, whereas no significant relationship was detected with serum copper levels. Our results show that exotic lice are widespread in California, and younger age classes with low blood selenium concentrations are more likely to be infested with lice than older deer.This is the publisher’s final pdf. The published article is copyrighted by the author(s) and published by SAGE Publications for American Association of Veterinary Laboratory Diagnosticians. The published article can be found at: http://vdi.sagepub.com/content/28/4/399Keywords: Bovicola tibialis, hair-loss syndrome, selenium, deer, Damalinia (Cervicola) sp

Anthropogenic selection enhances cancer evolution in Tasmanian devil tumours

The Tasmanian Devil Facial Tumour Disease (DFTD) provides a unique opportunity to elucidate the long-term effects of natural and anthropogenic selection on cancer evolution. Since first observed in 1996, this transmissible cancer has caused local population declines by &gt;90%. So far, four chromosomal DFTD variants (strains) have been described and karyotypic analyses of 253 tumours showed higher levels of tetraploidy in the oldest strain. We propose that increased ploidy in the oldest strain may have evolved in response to effects of genomic decay observed in asexually reproducing organisms. In this study, we focus on the evolutionary response of DFTD to a disease suppression trial. Tumours collected from devils subjected to the removal programme showed accelerated temporal evolution of tetraploidy compared with tumours from other populations where no increase in tetraploid tumours were observed. As ploidy significantly reduces tumour growth rate, we suggest that the disease suppression trial resulted in selection favouring slower growing tumours mediated by an increased level of tetraploidy. Our study reveals that DFTD has the capacity to rapidly respond to novel selective regimes and that disease eradication may result in novel tumour adaptations, which may further imperil the long-term survival of the world\u27s largest carnivorous marsupial

Genome-wide meta-analysis of 241,258 adults accounting for smoking behaviour identifies novel loci for obesity traits

Few genome-wide association studies (GWAS) account for environmental exposures, like smoking, potentially impacting the overall trait variance when investigating the genetic contribution to obesity-related traits. Here, we use GWAS data from 51,080 current smokers and 190,178 nonsmokers (87% European descent) to identify loci influencing BMI and central adiposity, measured as waist circumference and waist-to-hip ratio both adjusted for BMI. We identify 23 novel genetic loci, and 9 loci with convincing evidence of gene-smoking interaction (GxSMK) on obesity-related traits. We show consistent direction of effect for all identified loci and significance for 18 novel and for 5 interaction loci in an independent study sample. These loci highlight novel biological functions, including response to oxidative stress, addictive behaviour, and regulatory functions emphasizing the importance of accounting for environment in genetic analyses. Our results suggest that tobacco smoking may alter the genetic susceptibility to overall adiposity and body fat distribution.Peer reviewe

The genetic architecture of type 2 diabetes

The genetic architecture of common traits, including the number, frequency, and effect sizes of inherited variants that contribute to individual risk, has been long debated. Genome-wide association studies have identified scores of common variants associated with type 2 diabetes, but in aggregate, these explain only a fraction of heritability. To test the hypothesis that lower-frequency variants explain much of the remainder, the GoT2D and T2D-GENES consortia performed whole genome sequencing in 2,657 Europeans with and without diabetes, and exome sequencing in a total of 12,940 subjects from five ancestral groups. To increase statistical power, we expanded sample size via genotyping and imputation in a further 111,548 subjects. Variants associated with type 2 diabetes after sequencing were overwhelmingly common and most fell within regions previously identified by genome-wide association studies. Comprehensive enumeration of sequence variation is necessary to identify functional alleles that provide important clues to disease pathophysiology, but large-scale sequencing does not support a major role for lower-frequency variants in predisposition to type 2 diabetes

Search for dark matter produced in association with bottom or top quarks in √s = 13 TeV pp collisions with the ATLAS detector

A search for weakly interacting massive particle dark matter produced in association with bottom or top quarks is presented. Final states containing third-generation quarks and miss- ing transverse momentum are considered. The analysis uses 36.1 fb−1 of proton–proton collision data recorded by the ATLAS experiment at √s = 13 TeV in 2015 and 2016. No significant excess of events above the estimated backgrounds is observed. The results are in- terpreted in the framework of simplified models of spin-0 dark-matter mediators. For colour- neutral spin-0 mediators produced in association with top quarks and decaying into a pair of dark-matter particles, mediator masses below 50 GeV are excluded assuming a dark-matter candidate mass of 1 GeV and unitary couplings. For scalar and pseudoscalar mediators produced in association with bottom quarks, the search sets limits on the production cross- section of 300 times the predicted rate for mediators with masses between 10 and 50 GeV and assuming a dark-matter mass of 1 GeV and unitary coupling. Constraints on colour- charged scalar simplified models are also presented. Assuming a dark-matter particle mass of 35 GeV, mediator particles with mass below 1.1 TeV are excluded for couplings yielding a dark-matter relic density consistent with measurements

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

A genome-wide association search for type 2 diabetes genes in African Americans.

African Americans are disproportionately affected by type 2 diabetes (T2DM) yet few studies have examined T2DM using genome-wide association approaches in this ethnicity. The aim of this study was to identify genes associated with T2DM in the African American population. We performed a Genome Wide Association Study (GWAS) using the Affymetrix 6.0 array in 965 African-American cases with T2DM and end-stage renal disease (T2DM-ESRD) and 1029 population-based controls. The most significant SNPs (n = 550 independent loci) were genotyped in a replication cohort and 122 SNPs (n = 98 independent loci) were further tested through genotyping three additional validation cohorts followed by meta-analysis in all five cohorts totaling 3,132 cases and 3,317 controls. Twelve SNPs had evidence of association in the GWAS (P<0.0071), were directionally consistent in the Replication cohort and were associated with T2DM in subjects without nephropathy (P<0.05). Meta-analysis in all cases and controls revealed a single SNP reaching genome-wide significance (P<2.5×10(-8)). SNP rs7560163 (P = 7.0×10(-9), OR (95% CI) = 0.75 (0.67-0.84)) is located intergenically between RND3 and RBM43. Four additional loci (rs7542900, rs4659485, rs2722769 and rs7107217) were associated with T2DM (P<0.05) and reached more nominal levels of significance (P<2.5×10(-5)) in the overall analysis and may represent novel loci that contribute to T2DM. We have identified novel T2DM-susceptibility variants in the African-American population. Notably, T2DM risk was associated with the major allele and implies an interesting genetic architecture in this population. These results suggest that multiple loci underlie T2DM susceptibility in the African-American population and that these loci are distinct from those identified in other ethnic populations