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1.
J Clin Psychiatry ; 71(7): 949-54, 2010 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-20492839

RESUMO

OBJECTIVE: Pediatric obesity (body mass index [BMI] > or = 95th percentile for sex and age) and overweight (BMI > or = 85th percentile < 95% percentile) are priority public health targets for the prevention of diabetes and cardiovascular disease. We examined the prevalence and risk of overweight and obesity in adolescents with serious mental disorders. METHOD: Height, weight, demographic, diagnostic, and treatment data were reviewed for 114 adolescents attending a partial hospitalization program over 18 consecutive months between January 2003 and July 2004. Sample data were compared to normative National Health and Nutrition Examination Survey data and regional county data for BMI. Unadjusted odds ratios and their 95% CIs were calculated for each categorical risk factor using the chi-squared test. A logistic regression model was conducted to detect the effects of these risk factors on the occurrence of overweight and obesity. RESULTS: The combined prevalence of overweight and obesity was 55.4% (n = 63); the prevalence for obesity alone was 30% (n = 34), approximately double the rate in national and county norms. Lack of private insurance, smoking, and antidepressant and antipsychotic treatment were associated with overweight and obese status. CONCLUSIONS: Adolescents with severe mental illness are at increased risk for overweight and obesity. Identification of elevated BMI, associated risk factors, and efforts to prevent weight gain should begin at initiation of mental health treatment.


Assuntos
Transtornos Mentais/tratamento farmacológico , Transtornos Mentais/epidemiologia , Obesidade/induzido quimicamente , Obesidade/epidemiologia , Sobrepeso/induzido quimicamente , Sobrepeso/epidemiologia , Psicotrópicos/efeitos adversos , Adolescente , Anticonvulsivantes/efeitos adversos , Anticonvulsivantes/uso terapêutico , Antidepressivos/efeitos adversos , Antidepressivos/uso terapêutico , Antipsicóticos/efeitos adversos , Antipsicóticos/uso terapêutico , Índice de Massa Corporal , Estudos Transversais , Hospital Dia/estatística & dados numéricos , Feminino , Humanos , Cobertura do Seguro/estatística & dados numéricos , Masculino , Países Baixos , Psicotrópicos/uso terapêutico , Fatores de Risco , Fumar/epidemiologia
2.
J Invest Dermatol ; 122(5): 1214-24, 2004 May.
Artigo em Inglês | MEDLINE | ID: mdl-15140225

RESUMO

Prostaglandins (PG) are key mediators of diverse functions in the skin and several reports suggest that PG mediate post-inflammatory pigmentary changes through modulation of melanocyte dendricity and melanin synthesis. The proteinase-activated receptor 2 (PAR-2) is important for skin pigmentation because activation of keratinocyte PAR-2 stimulates uptake of melanosomes through phagocytosis in a Rho-dependent manner. In this report, we show that activation of keratinocyte PAR-2 stimulates release of PGE(2) and PGF(2alpha) and that PGE(2) and PGF(2alpha) act as paracrine factors that stimulate melanocyte dendricity. We characterized the expression of the EP and FP receptors in human melanocytes and show that human melanocytes express EP1 and EP3, and the FP receptor, but not EP2 and EP4. Treatment of melanocytes with EP1 and EP3 receptor agonists resulted in increased melanocyte dendricity, indicating that both EP1 and EP3 receptor signaling contribute to PGE(2)-mediated melanocyte dendricity. Certain EP3 receptor subtypes have been shown to increase adenosine 3',5'-cyclic monophosphate (cAMP) through coupling to Gs, whereas EP1 is known to couple to Gq to activate phospholipase C with elevation in Ca(2+). The cAMP/protein kinase A system is known to modulate melanocyte dendrite formation through modulation of Rac and Rho activity. Neither PGF(2alpha) or PGE(2) elevated cAMP in human melanocytes showing that dendricity observed in response to PGE(2) and PGF(2alpha) is cAMP-independent. Our data suggest that PAR-2 mediates cutaneous pigmentation both through increased uptake of melanosomes by keratinocytes, as well as by release of PGE(2) and PGF(2alpha) that stimulate melanocyte dendricity through EP1, EP3, and FP receptors.


Assuntos
Dinoprosta/metabolismo , Dinoprostona/análogos & derivados , Dinoprostona/metabolismo , Queratinócitos/metabolismo , Melanócitos/metabolismo , Receptor PAR-2/metabolismo , Receptores de Prostaglandina E/metabolismo , Tamanho Celular/efeitos dos fármacos , Tamanho Celular/fisiologia , Células Cultivadas , AMP Cíclico/metabolismo , Dinoprosta/farmacologia , Dinoprostona/farmacologia , Expressão Gênica , Humanos , Queratinócitos/citologia , Queratinócitos/efeitos dos fármacos , Melanócitos/citologia , Melanócitos/efeitos dos fármacos , Misoprostol/farmacologia , Ocitócicos/farmacologia , Comunicação Parácrina/fisiologia , Receptores de Prostaglandina/genética , Receptores de Prostaglandina/metabolismo , Receptores de Prostaglandina E/agonistas , Receptores de Prostaglandina E/genética , Receptores de Prostaglandina E Subtipo EP1 , Receptores de Prostaglandina E Subtipo EP2 , Receptores de Prostaglandina E Subtipo EP3 , Receptores de Prostaglandina E Subtipo EP4
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