PREVALÊNCIA DOS DISTÚRBIOS DO SONO EM ADULTOS CADASTRADOS A ESTRATÉGIA DE SAÚDE DA FAMÍLIA DE MUCUGÊ, BAHIA

O sono é um estado biológico vital e complexo que possui um papel essencial no crescimento, no processo de aprendizado, na memória e no funcionamento do organismo (Zanuto, 2015)

Comorbid mood and anxiety disorders in victims of violence with posttraumatic stress disorder

OBJETIVO: Buscar estudos que avaliem a comorbidade entre transtorno de estresse pós-traumático e transtornos do humor, bem como entre transtorno de estresse pós-traumático e outros transtornos de ansiedade. MÉTODO: Revisamos a base de dados do Medline em busca de estudos publicados em inglês até abril de 2009, com as seguintes palavras-chave: "transtorno de estresse pós-traumático", "TEPT", "transtorno de humor", "transtorno depressivo maior", "depressão maior", "transtorno bipolar", "distimia", "transtorno de ansiedade", "transtorno de ansiedade generalizada", agorafobia", "transtorno obsessivo-compulsivo", "transtorno de pânico", "fobia social" e "comorbidade". RESULTADOS: Depressão maior é uma das condições comórbidas mais frequentes em indivíduos com transtorno de estresse pós-traumático, mas eles também apresentam transtorno bipolar e outros transtornos ansiosos. Essas comorbidades impõem um prejuízo clínico adicional e comprometem a qualidade de vida desses indivíduos. Comportamento suicida em pacientes com transtorno de estresse pós-traumático, com ou sem depressão maior comórbida, é também uma questão relevante, e sintomas depressivos mediam a gravidade da dor em sujeitos com transtorno de estresse pós-traumático e dor crônica. CONCLUSÃO: Os estudos disponíveis sugerem que pacientes com transtorno de estresse pós-traumático têm um risco maior de desenvolver transtornos afetivos e, por outro lado, transtornos afetivos pré-existentes aumentam a propensão ao transtorno de estresse pós-traumático após eventos traumáticos. Além disso, vulnerabilidades genéticas em comum podem ajudar a explicar esse padrão de comorbidades. No entanto, diante dos poucos estudos encontrados, mais trabalhos são necessários para avaliar adequadamente essas comorbidades e suas implicações clínicas e terapêuticas.OBJECTIVE: To review studies that have evaluated the comorbidity between posttraumatic stress disorder and mood disorders, as well as between posttraumatic stress disorder and other anxiety disorders. METHOD: We searched Medline for studies, published in English through April, 2009, using the following keywords: "posttraumatic stress disorder", "PTSD", "mood disorder", "major depressive disorder", "major depression", "bipolar disorder", "dysthymia", "anxiety disorder", "generalized anxiety disorder", "agoraphobia", "obsessive-compulsive disorder", "panic disorder", "social phobia", and "comorbidity". RESULTS: Major depression is one of the most frequent comorbid conditions in posttraumatic stress disorder individuals, but individuals with posttraumatic stress disorder are also more likely to present with bipolar disorder, other anxiety disorders and suicidal behaviors. These comorbid conditions are associated with greater clinical severity, functional impairment, and impaired quality of life in already compromised individuals with posttraumatic stress disorder. Depression symptoms also mediate the association between posttraumatic stress disorder and severity of pain among patients with chronic pain. CONCLUSION: Available studies suggest that individuals with posttraumatic stress disorder are at increased risk of developing affective disorders compared with trauma-exposed individuals who do not develop posttraumatic stress disorder. Conversely, pre-existing affective disorders increase a person's vulnerability to the posttraumatic stress disorder--inducing effects of traumatic events. Also, common genetic vulnerabilities can help to explain these comorbidity patterns. However, because the studies addressing this issue are few in number, heterogeneous and based on a limited sample, more studies are needed in order to adequately evaluate these comorbidities, as well as their clinical and therapeutic implications

Na busca das origens da dramaturgia do movimento

Este artigo procura, através de um breve estudo sobre as origens da dança moderna alemã, extrair o conceito dramaturgia do movimento como um modelo de composição dramática presente na atualidade cênica

Effect of fish oil intake on glucose levels in rat prefrontal cortex, as measured by microdialysis

Background: Brain glucose sensing may contribute to energy homeostasis control. the prefrontal cortex (PFC) participates in the hedonic component of feeding control. As high-fat diets may disrupt energy homeostasis, we evaluated in male Wistar rats whether intake of high-fat fish-oil diet modified cortical glucose extracellular levels and the feeding induced by intracerebroventricular glucose or PFC glucoprivation.Methods: Glucose levels in PFC microdialysates were measured before and after a 30-min meal. Food intake was measured in animals receiving intracerebroventricular glucose followed, 30-min. later, by 2-deoxy-D-glucose injected into the PFC.Results: the fish-oil group showed normal body weight and serum insulin while fat pads weight and glucose levels were increased. Baseline PFC glucose and 30-min. carbohydrates intake were similar between the groups. Feeding-induced PFC glucose levels increased earlier and more pronouncedly in fish-oil than in control rats. Intracerebroventricular glucose inhibited feeding consistently in the control but not in the fish-oil group. Local PFC glucoprivation with 2-DG attenuated glucose-induced hypophagia.Conclusions: the present experiments have shown that, following food intake, more glucose reached the prefrontal cortex of the rats fed the high-fat fish-oil diet than of the rats fed the control diet. However, when administered directly into the lateral cerebral ventricle, glucose was able to consistently inhibit feeding only in the control rats. the findings indicate that, an impairment of glucose transport into the brain does not contribute to the disturbances induced by the high-fat fish-oil feeding.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Universidade Federal de São Paulo Unifesp, Dept Fisiol, BR-04023062 São Paulo, BrazilUniversidade Federal de São Paulo Unifesp, Dept Fisiol, BR-04023062 São Paulo, BrazilWeb of Scienc

Lateral hypothalamic serotonin is not stimulated during central leptin hypophagia

Whether leptin targets the hypothalamic serotonergic system to inhibit food intake is not established. We examined the effect of a short-term i.c.v. leptin treatment on serotonin microdialysate levels in rat lateral hypothalamus. Adipose tissue gene expression was also evaluated.Male rats received four daily injections of leptin (5 mu g) or vehicle (with pair-feeding to leptin-induced intake) and a fifth injection during collection of LH microdialysates. We found that serotonin and 5-HIAA levels were not affected by the leptin pre-treatment, as basal levels were similar between the leptin and the pair-fed group. These levels remained unaltered after the acute leptin injection.For gene expression studies, rats were pre-treated with five daily injections of either leptin (5 mu g) or vehicle (with either pair-feeding or ad libitum intake). mRNA levels of resistin, adiponectin, lipoprotein lipase, and PPAR-gamma were unaltered by either leptin or pair-feeding. Leptin gene expression was significantly reduced by leptin but not by pair-feeding, in both the retroperitoneal (- 74%) and the epididymal (- 99%) depots while no differences were observed in the subcutaneous depot.The observations confirmed the absence of an acute stimulatory effect of central leptin on serotonin release in the lateral hypothalamus and showed that the pre-treatment with leptin failed to modify this pattern. This indicates that components of the serotonergic system are probably not directly affected by leptin. Additionally, the central effect of leptin was able to downregulate its own adipose tissue gene expression in a depot-specific manner while other adipokine genes were not affected. (C) 2013 Elsevier B.V. All rights reserved.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Universidade Federal de São Paulo, UNIFESP, Dept Fisiol, Disciplina Fisiol Nutr, BR-04023062 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Ciencias Biol, Diadema, SP, BrazilUniversidade Federal de São Paulo, UNIFESP, Dept Fisiol, Disciplina Fisiol Nutr, BR-04023062 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Ciencias Biol, Diadema, SP, BrazilWeb of Scienc

L-arginine abolishes the hypothalamic serotonergic activation induced by central interleukin-1 beta administration to normal rats

IL-1 beta-induced anorexia may depend on interactions of the cytokine with neuropeptides and neurotransmitters of the central nervous system control of energy balance and serotonin is likely to be one catabolic mediator targeted by IL-1 beta. in the complex interplay involved in feeding modulation, nitric oxide has been ascribed a stimulatory action, which could be of significance in counteracting IL-1 beta effects.The present study aims to explore the participation of the nitric oxide and the serotonin systems on the central mechanisms induced by IL-1 beta and the relevance of their putative interactions to IL-1 beta hypophagia in normal rats. Serotonin levels were determined in microdialysates of the ventromedial hypothalamus after a single intracerebroventricular injection of 10 ng of IL-1 beta, with or without the pre-injection of 20 mu g of the nitric oxide precursor L-arginine. IL-1 beta significantly stimulated hypothalamic serotonin extracellular levels, with a peak variation of 130 +/-37% above baseline. IL-1 beta also reduced the 4-h and the 24-h food intakes (by 23% and 58%, respectively). the IL-1 beta-induced serotonergic activation was abolished by the pre-injection of L-arginine while the hypophagic effect was unaffected.The data showed that one central effect of IL-1 beta is serotonergic stimulation in the ventromedial hypothalamus, an action inhibited by nitric oxide activity. It is suggested that, although serotonin participates in IL-1 beta anorexia, other mechanisms recruited by IL-1 beta in normal rats are able to override the absence of the serotonergic hypophagic influence.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Universidade Federal de São Paulo, Dept Physiol, BR-04023060 São Paulo, BrazilUniversidade Federal de São Paulo, Div Appl Stat, BR-04023060 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Physiol, BR-04023060 São Paulo, BrazilUniversidade Federal de São Paulo, Div Appl Stat, BR-04023060 São Paulo, BrazilWeb of Scienc

SARS-COV-2 e a atuação do enfermeiro frente a pandemia / SARS-COV-2 and the performance of nurses against the pandemic

O vírus do COVID-19 pertence à ordem Nidovirales e família Coronaviridae. A subfamília Coronavirinae é formada pelos gêneros Alphacoronavirus e Betacoronavirus, indivíduos quem infectam os mamíferos e Gammacoronavirus e Deltacoronavirus, esses que infectam de tal maneiras as aves como os mamíferos. O SARS-CoV-2 é um β-coronavírus ou seja, um subgênero Sarbecovírus e Subfamília Orthocoronavirinae, dispondo como elemento genético o RNA de curso positivo sem segmentação. Este estudo rata-se de uma revisão integrativa. Portanto, elaborou-se a seguinte questão norteadora: Qual assistência da enfermagem sanitária ao paciente portador do SARS-CoV-2.?. O enfermeiro ao realizar atendimento ao cliente com o diagnóstico de COVID-19 de usar as Precauções Padrões respiratória e de contato, lembrando da importância de higienizar as mãos de forma correta e ao desparamentar seguir todo passo a passo para evitar contaminação

Mental Disorders in Megacities: Findings from the São Paulo Megacity Mental Health Survey, Brazil

Background: World population growth is projected to be concentrated in megacities, with increases in social inequality and urbanization-associated stress. São Paulo Metropolitan Area (SPMA) provides a forewarning of the burden of mental disorders in urban settings in developing world. The aim of this study is to estimate prevalence, severity, and treatment of recently active DSM-IV mental disorders. We examined socio-demographic correlates, aspects of urban living such as internal migration, exposure to violence, and neighborhood-level social deprivation with 12-month mental disorders. Methods and Results: A representative cross-sectional household sample of 5,037 adults was interviewed face-to-face using the WHO Composite International Diagnostic Interview (CIDI), to generate diagnoses of DSM-IV mental disorders within 12 months of interview, disorder severity, and treatment. Administrative data on neighborhood social deprivation were gathered. Multiple logistic regression was used to evaluate individual and contextual correlates of disorders, severity, and treatment. Around thirty percent of respondents reported a 12-month disorder, with an even distribution across severity levels. Anxiety disorders were the most common disorders (affecting 19.9%), followed by mood (11%), impulse-control (4.3%), and substance use (3.6%) disorders. Exposure to crime was associated with all four types of disorder. Migrants had low prevalence of all four types compared to stable residents. High urbanicity was associated with impulse-control disorders and high social deprivation with substance use disorders. Vulnerable subgroups were observed: women and migrant men living in most deprived areas. Only one-third of serious cases had received treatment in the previous year. Discussion: Adults living in São Paulo megacity had prevalence of mental disorders at greater levels than similar surveys conducted in other areas of the world. Integration of mental health promotion and care into the rapidly expanding Brazilian primary health system should be strengthened. This strategy might become a model for poorly resourced and highly populated developing countries