The Stroop revisited: a meta-analysis of interference control in AD/HD

Background: An inhibition deficit, including poor interference control, has been implicated as one of the core deficits in AD/HD. Interference control is clinically measured by the Stroop Colour-Word Task. The aim of this meta-analysis was to investigate the strength of an interference deficit in AD/HD as measured by the Stroop Colour-Word Task and to assess the role of moderating variables that could explain the results. These moderating variables included: methods of calculating the interference score, comorbid reading and psychiatric disorders, AD/HD-subtypes, gender, age, intellectual functioning, medication, and sample size. Methods: Seventeen independent studies were located including 1395 children, adolescents, and young adults, in the age range of 6-27 years. A meta-analysis was conducted to assess the effect sizes for the scores on the word and the colour card as well as the interference score. Results: Children with AD/HD performed more poorly on all three dependent variables. The effect sizes for word reading (d = .49) and colour naming (d = .58) were larger and more homogeneous than the effect size for the interference score (d = .35). The method used to calculate the interference score strongly influenced the findings for this measure. When interference control was calculated as the difference between the score on the colour card minus the score on the colour-word card, no differences were found between AD/HD groups and normal control groups. Discussion: The Stroop Colour-Word Task, in standard form, does not provide strong evidence for a deficit in interference control in AD/HD. However, the Stroop Colour-Word Task may not be a valid measure of interference control in AD/HD and alternative methodologies may be needed to test this aspect of the inhibitory deficit model in AD/HD. © Association for Child Psychology Psychiatry, 2004

Genetic Sharing with Cardiovascular Disease Risk Factors and Diabetes Reveals Novel Bone Mineral Density Loci.

Bone Mineral Density (BMD) is a highly heritable trait, but genome-wide association studies have identified few genetic risk factors. Epidemiological studies suggest associations between BMD and several traits and diseases, but the nature of the suggestive comorbidity is still unknown. We used a novel genetic pleiotropy-informed conditional False Discovery Rate (FDR) method to identify single nucleotide polymorphisms (SNPs) associated with BMD by leveraging cardiovascular disease (CVD) associated disorders and metabolic traits. By conditioning on SNPs associated with the CVD-related phenotypes, type 1 diabetes, type 2 diabetes, systolic blood pressure, diastolic blood pressure, high density lipoprotein, low density lipoprotein, triglycerides and waist hip ratio, we identified 65 novel independent BMD loci (26 with femoral neck BMD and 47 with lumbar spine BMD) at conditional FDR < 0.01. Many of the loci were confirmed in genetic expression studies. Genes validated at the mRNA levels were characteristic for the osteoblast/osteocyte lineage, Wnt signaling pathway and bone metabolism. The results provide new insight into genetic mechanisms of variability in BMD, and a better understanding of the genetic underpinnings of clinical comorbidity

The challenge of major reorganization Computers in Essex County Libraries

SIGLEAvailable from British Library Lending Division - LD:84/29748(Challenge) / BLDSC - British Library Document Supply CentreGBUnited Kingdo

Symbiotic Burkholderia species show diverse arrangements of nif/fix and nod genes and lack typical high-affinity cytochrome cbb3 oxidase genes

Genome analysis of fourteen mimosoid and four papilionoid beta-rhizobia together with fourteen reference alpha-rhizobia for both nodulation (nod) and nitrogen-fixing (nif/fix) genes has shown phylogenetic congruence between 16S rRNA/MLSA (combined 16S rRNA gene sequencing and multilocus sequence analysis) and nif/fix genes, indicating a free-living diazotrophic ancestry of the beta-rhizobia. However, deeper genomic analysis revealed a complex symbiosis acquisition history in the betarhizobia that clearly separates the mimosoid and papilionoid nodulating groups. Mimosoid-nodulating beta-rhizobia have nod genes tightly clustered in the nodBCIJHASU operon, whereas papilionoid-nodulating Burkholderia have nodUSDABC and nodlJ genes, although their arrangement is not canonical because the nod genes are subdivided by the insertion of nif and other genes. Furthermore, the papilionoid Burkholderia spp. contain duplications of several nod and nif genes. The Burkholderia nifHDKEN and fixABC genes are very closely related to those found in free-living diazotrophs. In contrast, nifA is highly divergent between both groups, but the papilionoid species nifA is more similar to alpha-rhizobia nifA than to other groups. Surprisingly, for all Burkholderia, the fixNOQP and fixGHIS genes required for cbb3 cytochrome oxidase production and assembly are missing. In contrast, symbiotic Cupriavidus strains have f1xN0QPGHIS genes, revealing a divergence in the evolution of two distinct electron transport chains required for nitrogen fixation within the beta-rhizobia