RESUMO
Chinese Americans demonstrate greater prevalence of diabetes than non-Hispanic whites and find standard diabetes care disregards their cultural health beliefs. Academic researchers and Chinatown agencies collaborated to culturally adapt and test an efficacious cognitive-behavioral intervention using community-based participatory research. Using a delayed-treatment repeated-measures design, 145 adult Chinese immigrants with Type 2 diabetes completed treatment. Immediate benefits of treatment were evident in the improvement (p < .05) in diabetes self-efficacy, diabetes knowledge, bicultural efficacy, family emotional and instrumental support, diabetes quality of life, and diabetes distress. Prolonged benefits were evident in all changed variables 2 months post-intervention. The CBPR approach enabled the development of a culturally acceptable, efficacious behavioral intervention, and provides a model for working with communities that demonstrate health disparities.
Assuntos
Asiático/psicologia , Pesquisa Participativa Baseada na Comunidade , Diabetes Mellitus Tipo 2/etnologia , Diabetes Mellitus Tipo 2/psicologia , Conhecimentos, Atitudes e Prática em Saúde , Aceitação pelo Paciente de Cuidados de Saúde/psicologia , Cooperação do Paciente/etnologia , Adaptação Psicológica , Adulto , Idoso , Idoso de 80 Anos ou mais , Atitude Frente a Saúde , Características Culturais , Diabetes Mellitus Tipo 2/terapia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Cooperação do Paciente/psicologia , Avaliação de Programas e Projetos de SaúdeRESUMO
Human T cell leukemia virus 1 (HTLV-1) gene expression is regulated by both the viral Tax protein and by cellular transcriptional factors. We have previously shown that immune activation stimuli such as phorbol esters (PMA) and phytohemagglutinin (PHA) cooperate with HTLV-1 Tax expression to enhance HTLV-1 gene expression in infected T cells through increased activity of the HTLV-1 LTR. We now extend these studies to demonstrate roles for the T cell receptor complex, Lck, and Ras molecules in the coactivation of the HTLV-1 LTR by Tax and T cell activation stimuli. We also observe coactivation of Tax-responsive cellular promoter elements containing NF-kappaB and serum response factor (SRF) binding sites by Tax and T cell activation stimuli. These results suggest a model whereby T cell receptor stimulation and Tax expression coactivate HTLV-1 gene expression and cellular gene expression, enhancing activation of latent HTLV-1 and expression of cellular genes involved in disease pathogenesis.