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1.
BMC Public Health ; 21(1): 672, 2021 04 07.
Artigo em Inglês | MEDLINE | ID: mdl-33827501

RESUMO

BACKGROUND: The United States needs to increase access to effective obesity prevention and treatment programming for impoverished youth at risk for health disparities. Although recommended, schools have difficulty consistently implement evidence-based obesity programing. We report on the effectiveness of adding structured nutrition education and minimum physical activity (PA) requirements to standard middle school after-school programming. METHODS: Using a longitudinal pre-post study design, we evaluated program effectiveness at one year on target behaviors on students recruited during three consecutive school years (2016-2018). We used generalized linear (or logistic) mixed-effects modeling to determine: 1) impact on healthy weight and target healthy behavior attainment, and 2) whether target behavior improvement and weight change were associated with after-school program attendance. The seven target behaviors relate to eating healthy, physical activity, and sleep. RESULTS: Over the three years, a total of 76 students enrolled and completed one year of programming (62% Hispanic, 46% girls, 72% with BMI > 85th %ile, 49% with BMI > 95th %ile). Of students with BMI > 85th %ile, 44% maintained or decreased BMI Z-score. There were improvements (non-significant) in BMI Z-score and the adoption of four healthy eating behaviors: fruit, vegetables, sugar-free beverages, and unhealthy snack food. Students with higher after-school attendance (> 75%) had greater improvements (non-significant) in composite behavior scores, BMI Z-score, and in most target behaviors (5/7) than students with lower after-school attendance (< 75%). Sleep improvements were significantly associated with BMI Z-score decrease (Beta = - 0.05, 95% CI (- 0.1,-0.003), p = 0.038.) CONCLUSIONS: Enhancement of existing after-school programming with structured nutrition education and minimum physical activity requirements demonstrates positive improvements in several health behaviors and weight outcomes. Adopting enhanced after-school programming increases access to health activities and may bring us closer to solving obesity in at-risk youth in impoverished communities. TRIAL REGISTRATION: ClinicalTrials.gov identifier (NCT number): NCT03565744 . Registered 21 June 2018 - Retrospectively registered.


Assuntos
Obesidade Infantil , Serviços de Saúde Escolar , Adolescente , Peso Corporal , Comportamento Alimentar , Feminino , Comportamentos Relacionados com a Saúde , Promoção da Saúde , Humanos , Obesidade Infantil/prevenção & controle , Instituições Acadêmicas
2.
Neurotoxicology ; 80: 71-75, 2020 09.
Artigo em Inglês | MEDLINE | ID: mdl-32621835

RESUMO

Environmental and occupational metal exposure poses serious global concerns. Metal exposure have severally been associated with neurotoxicity and brain damage. Furthermore, receptor for advanced glycation end products (RAGE) is also implicated in neurological disorders, particularly those with altered glucose metabolism. Here, we examine potential compounding effect of metal exposure and RAGE expression on dopamine (DA) and serotonin (SER) neurons in C. elegans. In addition, we evaluate the effect of RAGE expression on DA and SER neurons in hyperglycemic conditions. Newly generated RAGE-expressing C. elegans tagged with green fluorescent proteins (GFP) in DAergic and SERergic neurons were treated with cadmium (Cd) or manganese (Mn). Additionally, the RAGE-expressing worms were also exposed to high glucose conditions. Results showed metals induced neurodegeneration both in the presence and absence of RAGE expression, but the manner of degeneration differed between Cd and Mn treated nematodes. Furthermore, RAGE-expressing worms showed significant neurodegeneration in both DAergic and SERergic neurons. Our results indicate co-occurrence of metal exposure and RAGE expression can induce neurodegeneration. Additionally, we show that RAGE expression can exacerbate hyperglycemic induced neurodegeneration.


Assuntos
Intoxicação por Cádmio/metabolismo , Caenorhabditis elegans/metabolismo , Neurônios Dopaminérgicos/metabolismo , Intoxicação por Manganês/metabolismo , Degeneração Neural , Receptor para Produtos Finais de Glicação Avançada/metabolismo , Neurônios Serotoninérgicos/metabolismo , Animais , Animais Geneticamente Modificados , Cloreto de Cádmio , Intoxicação por Cádmio/etiologia , Intoxicação por Cádmio/genética , Intoxicação por Cádmio/patologia , Caenorhabditis elegans/genética , Cloretos , Neurônios Dopaminérgicos/efeitos dos fármacos , Neurônios Dopaminérgicos/patologia , Glucose/toxicidade , Compostos de Manganês , Intoxicação por Manganês/etiologia , Intoxicação por Manganês/genética , Intoxicação por Manganês/patologia , Receptor para Produtos Finais de Glicação Avançada/genética , Neurônios Serotoninérgicos/efeitos dos fármacos , Neurônios Serotoninérgicos/patologia
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