Research Triangle Park

About: Research Triangle Park is a nonprofit organization based out in Durham, North Carolina, United States. It is known for research contribution in the topics: Population & Receptor. The organization has 24961 authors who have published 35800 publications receiving 1684504 citations. The organization is also known as: RTP.

A TOMM40 variable-length polymorphism predicts the age of late-onset Alzheimer's disease.

Abstract: The ɛ4 allele of the apolipoprotein E (APOE) gene is currently the strongest and most highly replicated genetic factor for risk and age of onset of late-onset Alzheimer's disease (LOAD). Using phylogenetic analysis, we have identified a polymorphic poly-T variant, rs10524523, in the translocase of outer mitochondrial membrane 40 homolog (TOMM40) gene that provides greatly increased precision in the estimation of age of LOAD onset for APOE ɛ3 carriers. In two independent clinical cohorts, longer lengths of rs10524523 are associated with a higher risk for LOAD. For APOE ɛ3/4 patients who developed LOAD after 60 years of age, individuals with long poly-T repeats linked to APOE ɛ3 develop LOAD on an average of 7 years earlier than individuals with shorter poly-T repeats linked to APOE ɛ3 (70.5±1.2 years versus 77.6±2.1 years, P=0.02, n=34). Independent mutation events at rs10524523 that occurred during Caucasian evolution have given rise to multiple categories of poly-T length variants at this locus. On replication, these results will have clinical utility for predictive risk estimates for LOAD and for enabling clinical disease prevention studies. In addition, these results show the effective use of a phylogenetic approach for analysis of haplotypes of polymorphisms, including structural polymorphisms, which contribute to complex diseases.

Interventions for Individuals with Low Health Literacy: A Systematic Review

Abstract: The US Department of Health and Human Services recently called for action on health literacy An important first step is defining the current state of the literature about interventions designed to mitigate the effects of low health literacy We performed an updated systematic review examining the effects of interventions that authors reported were specifically designed to mitigate the effects of low health literacy We searched MEDLINE®, The Cumulative Index to Nursing and Allied Health Literature (CINAHL), PsycINFO, Educational Resources Information Center (ERIC), and the Cochrane Library databases (2003 forward for health literacy; 1966 forward for numeracy) Two reviewers independently reviewed titles, abstracts, and full-text articles for inclusion and included studies that examined outcomes by health literacy level and met other pre-specified criteria One reviewer abstracted article information into evidence tables; a second checked accuracy Two reviewers independently rated study quality using predefined criteria Among 38 included studies, we found multiple discrete design features that improved comprehension in one or a few studies (eg, presenting essential information by itself or first, presenting information so that the higher number is better, adding icon arrays to numerical information, adding video to verbal narratives) In a few studies, we also found consistent, direct, fair or good-quality evidence that intensive self-management interventions reduced emergency department visits and hospitalizations; and intensive self- and disease-management interventions reduced disease severity Evidence for the effects of interventions on other outcomes was either limited or mixed Multiple interventions show promise for mitigating the effects of low health literacy and could be considered for use in clinical practice

Functional analysis of regulatory sequences controlling PR-1 gene expression in Arabidopsis.

Abstract: The Arabidopsis PR-1 gene is one of a suite of genes induced co-ordinately during the onset of systemic acquired resistance (SAR), a plant defense pathway triggered by pathogen infection or exogenous application of chemicals such as salicylic acid (SA) and 2,6-dichloroisonicotinic acid (INA). We have characterized cis-acting regulatory elements in the PR-1 promoter involved in INA induction using deletion analysis, linker-scanning mutagenesis, and in vivo footprinting. Compared to promoter fragments of 815 bp or longer (which show greater than 10-fold inducibility after INA treatment), induction of a 698 bp long promoter fragment is reduced by half and promoter fragments of 621 bp or shorter have lost all inducibility. Additionally, two 10-bp linker-scanning mutations centered at 640 bp and 610 bp upstream from the transcription initiation site are each sufficient to abolish chemical inducibility of a GUS reporter fusion. The -640 linker-scanning mutation encompasses a region highly homologous to recognition sites for transcription factors of the basic leucine zipper class, while the -610 linker-scanning mutation contains a sequence similar to a consensus recognition site for the transcription factor NF-kappa B. Furthermore, several inducible in vivo footprints located at or nearby these motifs demonstrate significant and highly reproducible changes in DNA accessibility following SAR induction. This in vivo signature of protein-DNA interactions after INA induction is tightly correlated with the functionally important regions of the promoter identified by mutation analysis.