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Michael L. Goodman Miriam S. Mutambudzi Stanley Gitari Philip H. Keiser Sarah E. Seidel 《Vulnerable children and youth studies》2016,11(4):366-378
There are an estimated 56 million orphans and vulnerable children across sub-Saharan Africa. Communities typically care for orphan children through informal caring arrangements – either within or outside of kinship networks. Within Kenya, an estimated 250,000 children live on the streets. There is less research related to fostering attitudes of this special population than orphans and vulnerable children generally. Important research over the past decade has illuminated multiple ways in which children are made more vulnerable because of HIV, including parental death and street-migration from HIV-affected households. As HIV transitions from a terminal illness to a chronic, manageable one, research is also required to establish how parents living with HIV can be an asset to children. In this study, we assess whether mothers living with HIV were very willing to foster biologically-related children, and street-involved children, how these fostering attitudes differed from mothers not living with HIV, and whether differences in fostering attitudes by reported HIV status were mediated by social support, family functioning and general self-rated health. Approximately 40% of mothers living with HIV were very willing to provide long-term foster care to biologically-related or street-involved children. This was less than the percentage of mothers not living with HIV, who were very willing to foster biologically-related children (61%) or street-involved children (58%). Significant portions of these differences were explained by social support, family functioning and general self-rated health. Multi-sectoral approaches are suggested by these findings in order to improve the child-fostering capacity of mothers living with HIV. Improving social support, family functioning and general self-rated health among HIV-infected mothers may not only provide protective benefits for the mothers and their children, but also expand the community’s capacity to care for orphan and vulnerable children. 相似文献
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目的:探讨miR-26b参与原发性肝细胞肝癌(HCC)侵袭的机制。方法:在细胞培养液中培养人肝细胞系HL-7702和HCC细胞各系Hepb-3、HuH-7、MHCC97-L、MHCC97-H。实时荧光定量PCR法(qRT-PCR)检测miR-26b的表达水平;用miR-26b mimics、miR-26b inhibitors和Notch1-siRNA分别转染HCC细胞;MTT实验检测转染后HCC细胞的活力;采用Western blot检测Notch1受体蛋白表达水平的变化;Transwell小室测定不同处理后的HCC细胞的侵袭能力。结果:人正常肝细胞系HL-7702和HCC细胞系Hepb-3、HuH-7、MHCC97-L、MHCC97-H中的miR-26b相对表达含量随其侵袭和迁移能力的升高而依次下降;抑制miR-26b的表达,Notch1受体蛋白表达明显增高,而此时HCC细胞的侵袭性显著增强;相反,上调miR-26b的表达,Notch1受体蛋白表达明显降低,而HCC细胞侵袭性显著下降;miR-26b可能通过调控Notch1信号通路调节HCC细胞侵袭性。结论:miR-26b通过负调控Notch1信号通路抑制HCC细胞侵袭能力,为HCC侵袭的机制奠定了理论基础,miR-26b可能成为HCC治疗的新靶点。 相似文献
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