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3.
Am J Surg ; 205(2): 163-8, 2013 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-23331981

RESUMO

BACKGROUND: On July 1, 2011, the Accreditation Council for Graduate Medical Education (ACGME) eliminated 30-hour call in an attempt to improve resident wakefulness. We surveyed interns on the Newton Wellesley Hospital (NWH) surgery service before and after the transition from Q4 overnight call to a night float schedule. METHODS: For 15 weeks, interns completed weekly surveys including the Epworth Sleepiness Scale (ESS). The service changed to a night float schedule after 3 weeks (ie, first to 3-4 and then to 6 nights in a row). RESULTS: The average ESS score rose from 9.8 ± 5.2 to 14.9 ± 3.1 and 14.4 ± 4.5 (P = .042) on the 3/4 and 6/1 schedules, respectively. Interns were more likely to be abnormally tired on either night float schedule (relative risk = 2.86; 95% confidence interval, 1.17-6.97, P = .029). CONCLUSIONS: The new ACGME work hours increased the ESS scores among interns at NWH and caused interns to be more tired than interns on the Q4 schedule. This is likely caused by the multiple nights of poor sleep without a post-call day to make up sleep.


Assuntos
Fadiga/prevenção & controle , Hospitais Comunitários , Hospitais de Ensino , Internato e Residência , Assistência Noturna , Admissão e Escalonamento de Pessoal/organização & administração , Privação do Sono/complicações , Fases do Sono , Especialidades Cirúrgicas/educação , Tolerância ao Trabalho Programado , Acreditação , Adulto , Análise de Variância , Educação de Pós-Graduação em Medicina , Fadiga/etiologia , Feminino , Humanos , Masculino , Massachusetts , Admissão e Escalonamento de Pessoal/normas , Admissão e Escalonamento de Pessoal/tendências , Estudos Prospectivos , Projetos de Pesquisa , Risco , Viés de Seleção , Privação do Sono/etiologia , Inquéritos e Questionários , Estados Unidos , Recursos Humanos , Carga de Trabalho/normas , Carga de Trabalho/estatística & dados numéricos
4.
Glia ; 56(16): 1780-90, 2008 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-18649404

RESUMO

S100B is a calcium-binding protein released by astroglial cells of the brain capable of producing numerous extracellular effects. Although the direct molecular mechanism remains unknown, these effects can be trophic including differentiation, growth, recovery, and survival of neurons when the S100B protein is mainly oxidized and neurotoxic including apoptosis and neuroinflammatory processes marked by microglial activation when in a reduced state. S100B and its receptor RAGE (receptor for advanced glycation end products) have been found to be increased in Alzheimer's disease, Down syndrome, with tissue trauma and ischemia. In the current study, we examined the binding of the S100B receptor (RAGE) on microglial cells and the developmental effects of the antioxidant vitamin E on microglial activation and the upregulation of RAGE in an S100B over-expressing mouse model of pathological aging. We report that RAGE is co-localized on activated microglial cells and vitamin E induced dramatic increases in microglial activation as well as total microglial relative optical density that was accompanied by upregulation of the RAGE receptor, particularly in the CA1 region of the hippocampus. Our findings suggest further investigation into the potential role of vitamin E in reducing the oxidation state of the S100B protein and its influence on neuroinflammatory processes marked by microglial activation in vivo.


Assuntos
Senilidade Prematura/metabolismo , Antioxidantes/farmacologia , Hipocampo/efeitos dos fármacos , Microglia/efeitos dos fármacos , Fatores de Crescimento Neural/metabolismo , Proteínas S100/metabolismo , Tocoferóis/farmacologia , Senilidade Prematura/patologia , Animais , Modelos Animais de Doenças , Encefalite/metabolismo , Hipocampo/metabolismo , Hipocampo/patologia , Camundongos , Camundongos Transgênicos , Microglia/metabolismo , Proteínas Quinases Ativadas por Mitógeno/efeitos dos fármacos , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Fármacos Neuroprotetores/metabolismo , Fármacos Neuroprotetores/farmacologia , Estresse Oxidativo/efeitos dos fármacos , Estresse Oxidativo/fisiologia , Subunidade beta da Proteína Ligante de Cálcio S100
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