5 resultados para Doris Dörrie

em DigitalCommons@The Texas Medical Center


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Background: Children's active commuting to school, i.e. walking or cycling to school, was associated with greater moderate-to-vigorous physical activity, although studies among ethnic minorities are sparse. Objectives: Among a low-income, ethnic minority sample of fourth grade students from eight public schools, we examined (1) correlates of active commuting to school and (2) the relationship between active commuting to school and moderate-to-vigorous physical activity. Methods: We conducted a cross-sectional analysis of baseline measurements from a sample of participants (n=149) aged 9-12 years from a walk to school intervention study in Houston, Texas. The primary outcome was the weekly rate of active commuting to school. Daily moderate-to-vigorous physical activity, measured by accelerometers, was a secondary outcome. Child self-efficacy (alpha=0.75), parent self-efficacy (alpha=0.88), and parent outcome expectations (alpha=0.78) were independent variables. Participant characteristics (age, gender, race/ethnicity, distance from home to school, acculturation, and BMI percentile) were independent sociodemographic variables. We used mixed-model regression analyses to account for clustering by school and a stepwise procedure with backward elimination of non-significant interactions and covariates to identify significant moderators and predictors. School-level observations of student pedestrians were assessed and compared using chi-square tests of independence. Results: Among our sample, which was 61.7% Latino, the overall rate of active commuting to school was 43%. In the mixed model for active commuting to school, parent self-efficacy (std. beta = 0.18, p=0.018) and age (std. beta = 0.18, p=0.018) were positively related. Latino students had lower rates of active commuting to school than non-Latinos ( 16.5%, p=0.040). Distance from home to school was inversely related to active commuting to school (std. beta = 0.29, p<0.001). In the mixed model for moderate-to-vigorous physical activity, active commuting to school was positively associated (std. beta = 0.31, p <0.001). Among the Latino subsample, child acculturation was negatively associated with active commuting to school (std. beta = -0.23, p=0.01). With regard to school-level pedestrian safety observations, 37% of students stopped at the curb and 2.6% looked left-right-left before crossing the street. Conclusion: Although still below national goals, the rate of active commuting was relatively high, while the rate of some pedestrian safety behaviors was low among this low-income, ethnic minority population. Programs and policies to encourage safe active commuting to school are warranted and should consider the influence of parents, acculturation, and ethnicity.

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Case control and retrospective studies have identified parental substance abuse as a risk factor for physical child abuse and neglect (Dore, Doris, & Wright, 1995, May; S. R. Dube et al., 2001; Guterman & Lee, 2005, May; Walsh, MacMillan, & Jamieson, 2003). The purpose of this paper is to present the findings of a systematic review of prospective studies from 1975 through 2005 that include parental substance abuse as a risk factor for physical child abuse or neglect. Characteristics of each study such as the research question, sample information, data collection methods and results, including the parent assessed and definitions of substance abuse and physical child abuse and neglect, are discussed. Five studies were identified that met the search criteria. Four of five studies found that parental substance abuse was a significant variable in predicting physical child abuse and neglect.^

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c-Src, a protein tyrosine kinase (PTK) the specific activity of which is increased $>$20-fold in $\sim$80% of colon tumors and colon tumor cell lines, plays a role in both growth regulation and tumorigenicity of colon tumor cells. To examine the effect of increased c-Src specific activity on colon tumor cells, coumarin-derived tyrosine analog PTK inhibitors were assessed in a standard colon tumor cell line, HT-29. Of the nine compounds tested for inhibiting c-Src activity in a standard immune complex kinase assay from c-Src precipitated from HT-29 cells, the 7,8-dihydroxy-containing compounds daphnetin and fraxetin were most effective, with IC$\sb{50}$s of 0.6 $\pm$ 0.2 mM and 0.6 $\pm$ 0.3 mM, respectively. Treatment of HT-29 cells with daphnetin resulted in inhibition of cell growth in a dose-dependent manner. In contrast, scopoletin, a relatively poor Src inhibitor in vitro, did not inhibit HT-29 cell growth in the concentration range tested. In daphnetin treated cells, a dose-dependent decrease of c-Src activity paralleling cell growth inhibition was also observed; the IC$\sb{50}$ was 0.3 $\pm$ 0.1 mM for c-Src autophosphorylation. In contrast, the IC$\sb{50}$ for c-Src protein level was $>$ 0.6 mM, indicating that the effects of daphnetin were primarily an enzymatic activity of c-Src, rather than protein level in HT-29 cells. These results are the first to demonstrate that c-Src specific activity regulates colon tumor cell growth.^ To elucidate the signaling pathways activated by c-Src in colon tumor cells, the Src family substrate FAK, which has been shown to play a role in both extracellular matrix-dependent cell growth and survival, was examined. Coprecipitation assays showed Src-FAK association in detergent insoluble fractions of both attached and detached HT-29 cells, indicating that Src-FAK association in HT-29 cells is stable and, unlike untransformed cells, not dependent on cell-substratum contact. FAK also coprecipitated with Grb2, an adaptor protein also playing a role in cell proliferation and survival, in both attached and detached HT-29 cells, suggesting that a Src-FAK-Grb2-mediated signaling pathway(s) in HT-29 cells is/are constitutively activated.^ FAK was also analyzed in c-src antisense HT-29 clones AS15 and AS33 in which c-Src is specifically reduced by transfection of an antisense expression vector. FAK protein level is unexpectedly decreased in both AS15 and AS33 cells by 5-fold and 1.5-fold compared to HT-29, respectively, corresponding with the decreased expression of c-Src observed in these cells. FAK protein level was not decreased compared to parental in the c-src "sense" clone S8. Northern blot analyses showed decreased FAK mRNA levels compared to parental in AS15 and AS33, correlating with decreased FAK protein level, indicating that FAK activity in the antisense cells is regulated, at least in part, by altering FAK expression, and that this regulation is Src dependent. Because FAK has been implicated in anoikis, the ability of c-src antisense cells to survive in the absence of cell-substratum contact was examined. Decreased cell survival is seen in both AS15 and AS33, correlating with the decreases in c-Src and FAK levels and tumorigenicity in these cells. These results suggest that at least one mechanism by which activation of c-Src contributes to tumorigenic phenotype of colon tumor cells is by aberrantly promoting a survival signal through unregulated Src-FAK-Grb2 complexes. (Abstract shortened by UMI.) ^