A IMPORTÂNCIA DOS PROCESSOS INFLAMATÓRIOS NA FISIOPATOLOGIA DAS DOENÇAS OCUPACIONAIS: UM FOCO NA REABILITAÇÃO FISIOTERAPÊUTICA

INTRODUÇÃO As doenças ocupacionais formam hoje um grupo de patologias que mais atingem a população, isso porque as atividades realizadas pelos trabalhadores tornaram-se repetitivas, além da má alimentação, sedentarismo e estresse, enfrentado pelos profissionais. Esses fatores modificam o sistema imunológico e desencadeiam processos inflamatórios. Através deste trabalho buscamos verificar e compreender como ocorrem as modificações e os processos inflamatórios causados pelo estresse ocupacional e o que desencadeiam nas doenças ocupacionais, além de analisar como a Fisioterapia pode ajudar na reabilitação desses processos.   METODOLOGIA Este estudo foi elaborado por meio de uma revisão sistemática da literatura onde foram efetuadas consultas a artigos científicos através de buscas em bancos de dados como Pubmed; Science Direct, LILACS; BIREME; Scielo para positivá-lo, tendo como palavras chaves descritores como: “Doenças ocupacionais”, “Lesão por esforço repetitivo”, “Inflamação”, “Sistema Imunológico” e “Fisioterapia”.   RESULTADOS E DISCUSSÃO Os processos inflamatórios liberados através das atividades repetitivas geram doenças e lesões ocupacionais e que possuem como característica comum a dor.  O tratamento fisioterapêutico visa, então, o controle do processo inflamatório, diminuição do nível da dor e manutenção/reabilitação da função do membro ou tecido acometido pela doença/lesão ocupacional.   Tabela 01 – Principais Doenças Ocupacionais Asma Ocupacional Dermatose Ocupacional LER/DORT Perda Auditiva Induzida pelo Ruído (PAIR) Pneumoconioses Distúrbios Mentais Fonte: Ministério da Saúde   CONCLUSÃO Não existem muitos estudos que relacionem doença ocupacional, inflamação e fisioterapia, entretanto foi possível compreender como as doenças ocupacionais se desencadeiam dentro dos processos inflamatórios e concluir a importância da fisioterapia no controle dessas doenças e na diminuição dos processos inflamatórios causados pela atividade ocupacional do trabalhador.   REFERÊNCIAS   FERNANDES, R. C. P. et al. Repetitive tasks under time pressure: the musculoskeletal disorders and the industrial work. Revista Ciência e Saúde Coletiva, Rio de Janeiro, v.15, n. 3, p. 931-42, mai. 2010.   MARQUES, N.R. et al.Características biomecânicas, ergonômicas e clínicas da postura sentada: uma revisão. Fisioterapia & Pesquisa. São Paulo, v.17, nº3, julho/setembro de 2010.   Norma Regulamentadora nº 17 - Ergonomia. Ministério do Trabalho e do Emprego. Portaria MTPS nº 3.751, 23 de novembro de 1990.   SOARES, R. et al. Searching for elements at work that could explain the low attendance to a labor gymnastics program. Revista Brasileira de Saúde Ocupacional, São Paulo, v. 31, n.114, p.149-60, jul./ago. 2006.   PASTRE, E. et al. Work-related musculoskeletal complaints by women in a social rehabilitation center. Revista Cadernos de Saúde Pública, Rio de Janeiro, v 23, n.11, p. 2605-12, nov. 2007.

A Rodent Model of Schizophrenia Reveals Increase in Creatine Kinase Activity with Associated Behavior Changes

Schizophrenia is a debilitating mental disorder characterized by positive (delusions, hallucinations, disorganized speech) and negative (affective flattering, avolition and social withdrawal) symptoms as well as cognitive deficits. The frequency, severity and topography characterize the disorder as heterogeneous, the pathophysiology of schizophrenia is poorly understood. Sub-anesthetic doses of ketamine produce hyperactivity, stereotypy and abnormal social interaction and it is used as a model of schizophrenia. In this study, we induced an animal model by acute sub-anesthetic doses of ketamine and tested different behavioral parameters. We also evaluated the activity of creatine kinase (CK) in brain of rats treated with ketamine. Our results demonstrated that administration of 10, 25 and 50 mg/kg of ketamine induced an increase of covered distance in habituated and non-habituated rats to the behavioral apparatus. Ketamine administration induced significant social deficits and stereotypic behavioral in all doses tested. Finally we evaluated the effect of different doses of ketamine on creatinine kinase (CK) activity and we observed that CK activity is increased inspecific regions of the brain. Our study suggests that our animal model may be used as a model of schizophrenia and that cerebral energy metabolism might be altered in the brain of schizophrenic patients, probably leading to alterations that might be involved in the pathogenesis of schizophrenia

Reduction of acethylcolinesterase activity in the brain of mdx mice

Lack of dystrophin in brain structures have been involved with impaired cognitive functions. Acethylcolinesterase (AChE) is implicated in many cognitive functions and probably plays important roles in neurodegenerative disorders. In the present study, we investigated AChE activity in the prefrontal cortex, hippocampus, striatum and cortex of mdx mice. To this aim, brain tissues from male dystrophic mdx and normal control mice were used. We observed that mdx mice display a reduction in AChE activity of 40-60% in all brain structures evaluated. In conclusion, dystrophin deficiency may be affecting AChE activity and contributing negatively, in part, to memory storage and restoring. (C) 2011 Elsevier B.V. All rights reserved.Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)CNPqFAPESCFundação de Amparo à Pesquisa e Inovação do Estado de Santa Catarina (FAPESC)United Nations Educational, Scientific and Cultural Organization (UNESCO)UNES

Ketamine alters behavior and decreases BDNF levels in the rat brain as a function of time after drug administration

Objective: To evaluate behavioral changes and brain-derived neurotrophic factor (BDNF) levels in rats subjected to ketamine administration (25 mg/kg) for 7 days. Method: Behavioral evaluation was undertaken at 1 and 6 hours after the last injection. Results: We observed hyperlocomotion 1 hour after the last injection and a decrease in locomotion after 6 hours. Immobility time was decreased and climbing time was increased 6 hours after the last injection. BDNF levels were decreased in the prefrontal cortex and amygdala when rats were killed 6 hours after the last injection, compared to the saline group and to rats killed 1 hour after the last injection. BDNF levels in the striatum were decreased in rats killed 6 hours after the last ketamine injection, and BDNF levels in the hippocampus were decreased in the groups that were killed 1 and 6 hours after the last injection. Conclusion: These results suggest that the effects of ketamine on behavior and BDNF levels are related to the time at which they were evaluated after administration of the drug

A Rodent Model of Schizophrenia Reveals Increase in Creatine Kinase Activity with Associated Behavior Changes

Schizophrenia is a debilitating mental disorder characterized by positive (delusions, hallucinations, disorganized speech) and negative (affective flattering, avolition and social withdrawal) symptoms as well as cognitive deficits. The frequency, severity and topography characterize the disorder as heterogeneous, the pathophysiology of schizophrenia is poorly understood. Sub-anesthetic doses of ketamine produce hyperactivity, stereotypy and abnormal social interaction and it is used as a model of schizophrenia. In this study, we induced an animal model by acute sub-anesthetic doses of ketamine and tested different behavioral parameters. We also evaluated the activity of creatine kinase (CK) in brain of rats treated with ketamine. Our results demonstrated that administration of 10, 25 and 50 mg/kg of ketamine induced an increase of covered distance in habituated and non-habituated rats to the behavioral apparatus. Ketamine administration induced significant social deficits and stereotypic behavioral in all doses tested. Finally we evaluated the effect of different doses of ketamine on creatinine kinase (CK) activity and we observed that CK activity is increased inspecific regions of the brain. Our study suggests that our animal model may be used as a model of schizophrenia and that cerebral energy metabolism might be altered in the brain of schizophrenic patients, probably leading to alterations that might be involved in the pathogenesis of schizophrenia