348 research outputs found

    The Changing Role of Pharmacists as Evidenced by the Strong Vocational Interest Blank

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    The Strong Vocational Interest Blank/Strong Campbell Interest Inventory-Merged Form, or simply Strong Vocational Interest Blank (SVIB), is widely used to determine the suitability of a student\u27s interests to a particular field. In the process of norming the instrument, data concerning the satisfaction of practitioners of a field and their responses on the instrument are gathered. Such data lend themselves to analysis of trends in the characteristics of those practitioners both over time and over the satisfaction spectrum. Hence changes in the field and characteristics lending themselves to satisfaction can be ascertained

    Developing a framework for the analysis of power through depotentia

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    Stakeholder participation in tourism policy-making is usually perceived as providing a means of empowerment. However participatory processes drawing upon stakeholders from traditionally empowered backgrounds may provide the means of removing empowerment from stakeholders. Such an outcome would be in contradiction to the claims that participatory processes improve both inclusivity and sustainability. In order to form an understanding of the sources through which empowerment may be removed, an analytical perspective has been developed deriving from Lukes�s views of power dating from 1974. This perspective considers the concept of depotentia as the removal of �power to� without speculating upon the underlying intent and also provides for the multidimensionality of power to be examined within a single study. The application of this analytical perspective has been tested upon findings of the government-commissioned report of the Countryside and Community Research Unit in 2005. The survey and report investigated the progress of Local Access Forums in England created in response to the Countryside and Rights of Way Act 2000. Consideration of the data from this perspective permits the classification of individual sources of depotentia which can each be addressed and potentially enable stakeholder groups to reverse loss of empowerment where it has occurred

    Role of lifestyle and aging on the longitudinal change in cardiorespiratory fitness

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    Background - Cardiorespiratory fitness (CRF) in adults decreases with age and is influenced by lifestyle. Low CRF is associated with risk of diseases and the ability of older persons to function independently. We defined the longitudinal rate of CRF decline with aging and the association of aging and lifestyle with CRF. Methods - We studied a cohort of 3429 women and 16,889 men, aged 20 to 96 years, from the Aerobics Center Longitudinal Study who completed 2 to 33 health examinations from 1974 to 2006. The lifestyle variables were body mass index, self-reported aerobic exercise, and smoking behavior. Cardiorespiratory fitness was measured by a maximal Balke treadmill exercise test. Results - Linear mixed models regression analysis stratified by sex showed that the decline in CRF with age was not linear. After 45 years of age, CRF declined at an accelerated rate. For each unit of increase in body mass index, the CRF of women declined 0.20 metabolic equivalents (METs) (95% confidence interval, -0.21 to -0.19); that of men, 0.32 METs (-0.33 to -0.20). Current smokers of both sexes also had lower CRF (-0.29 METs [95% confidence interval, -0.40 to -0.19] for women and -0.41 METS [-0.44 to -0.38] for men). Cardiorespiratory fitness was positively associated with self-reported physical activity. Conclusions - Cardiorespiratory fitness in men and women declines at a nonlinear rate that accelerates after 45 years of age. Maintaining a low BMI, being physically active, and not smoking are associated with higher CRF across the adult life span

    Outdoor, Indoor, and Personal Exposure to VOCs in Children

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    We measured volatile organic compound (VOC) exposures in multiple locations for a diverse population of children who attended two inner-city schools in Minneapolis, Minnesota. Fifteen common VOCs were measured at four locations: outdoors (O), indoors at school (S), indoors at home (H), and in personal samples (P). Concentrations of most VOCs followed the general pattern O ≈ S < P ≤ H across the measured microenvironments. The S and O environments had the smallest and H the largest influence on personal exposure to most compounds. A time-weighted model of P exposure using all measured microenvironments and time–activity data provided little additional explanatory power beyond that provided by using the H measurement alone. Although H and P concentrations of most VOCs measured in this study were similar to or lower than levels measured in recent personal monitoring studies of adults and children in the United States, p-dichlorobenzene was the notable exception to this pattern, with upper-bound exposures more than 100 times greater than those found in other studies of children. Median and upper-bound H and P exposures were well above health benchmarks for several compounds, so outdoor measurements likely underestimate long-term health risks from children’s exposure to these compounds

    Multiple functional risk variants in a SMAD7 enhancer implicate a colorectal cancer risk haplotype

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    Genome-wide association studies (GWAS) of colorectal cancer (CRC) have led to the identification of a number of common variants associated with modest risk. Several risk variants map within the vicinity of TGFβ/BMP signaling pathway genes, including rs4939827 within an intron of SMAD7 at 18q21.1. A previous study implicated a novel SNP (novel 1 or rs58920878) as a functional variant within an enhancer element in SMAD7 intron 4. In this study, we show that four SNPs including novel 1 (rs6507874, rs6507875, rs8085824, and rs58920878) in linkage disequilibrium (LD) with the index SNP rs4939827 demonstrate allele-specific enhancer effects in a large, multi-component enhancer of SMAD7. All four SNPs demonstrate allele-specific protein binding to nuclear extracts of CRC cell lines. Furthermore, some of the risk-associated alleles correlate with increased expression of SMAD7 in normal colon tissues. Finally, we show that the enhancer is responsive to BMP4 stimulation. Taken together, we propose that the associated CRC risk at 18q21.1 is due to four functional variants that regulate SMAD7 expression and potentially perturb a BMP negative feedback loop in TGFβ/BMP signaling pathways

    Molecular Mapping of the Thrombin-Heparin Cofactor II Complex

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    We used 55 Ala-scanned recombinant thrombin molecules to define residues important for inhibition by the serine protease inhibitor (serpin) heparin cofactor II (HCII) in the absence and presence of glycosaminoglycans. We verified the importance of numerous basic residues in anion-binding exosite-1 (exosite-1) and found 4 additional residues, Gln24, Lys65, His66, and Tyr71 (using the thrombin numbering system), that were resistant to HCII inhibition with and without glycosaminoglycans. Inhibition rate constants for these exosite-1 (Q24A, K65A, H66A, Y71A) thrombin mutants (0.02-0.38 x 10(8) m(-1) min(-1) for HCII-heparin when compared with 2.36 x 10(8) m(-1) min(-1) with wild-type thrombin and 0.03-0.53 x 10(8) m(-1) min(-1) for HCII-dermatan sulfate when compared with 5.23 x 10(8) m(-1) min(-1) with wild-type thrombin) confirmed that the structural integrity of thrombin exosite-1 is critical for optimal HCII-thrombin interactions in the presence of glycosaminoglycans. However, our results are also consistent for HCII-glycosaminoglycan-thrombin ternary complex formation. Ten residues surrounding the active site of thrombin were implicated in HCII interactions. Four mutants (Asp51, Lys52, Lys145/Thr147/Trp148, Asp234) showed normal increased rates of inhibition by HCII-glycosaminoglycans, whereas four mutants (Trp50, Glu202, Glu229, Arg233) remained resistant to inhibition by HCII with glycosaminoglycans. Using 11 exosite-2 thrombin mutants with 20 different mutated residues, we saw no major perturbations of HCII-glycosaminoglycan inhibition reactions. Collectively, our results support a "double bridge" mechanism for HCII inhibition of thrombin in the presence of glycosaminoglycans, which relies in part on ternary complex formation but is primarily dominated by an allosteric process involving contact of the "hirudin-like" domain of HCII with thrombin exosite-1
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