Assuntos
Vértebras Cervicais/cirurgia , Debilidade Muscular/etiologia , Debilidade Muscular/fisiopatologia , Miopatias da Nemalina/fisiopatologia , Miopatias da Nemalina/cirurgia , Músculos do Pescoço/patologia , Músculos do Pescoço/fisiopatologia , Fusão Vertebral/métodos , Idoso , Movimentos da Cabeça/fisiologia , Humanos , Corpos de Inclusão/patologia , Corpos de Inclusão/ultraestrutura , Fixadores Internos , Masculino , Fibras Musculares Esqueléticas/metabolismo , Fibras Musculares Esqueléticas/patologia , Fibras Musculares Esqueléticas/ultraestrutura , Debilidade Muscular/cirurgia , Miopatias da Nemalina/diagnóstico , Músculos do Pescoço/ultraestrutura , Resultado do TratamentoAssuntos
Tronco Encefálico/fisiopatologia , Carcinoma de Células Pequenas/diagnóstico , Neoplasias Pulmonares/diagnóstico , Síndromes Paraneoplásicas do Sistema Nervoso/diagnóstico , Paralisia Respiratória/diagnóstico , Síndrome de Shy-Drager/diagnóstico , Idoso , Sistema Nervoso Autônomo/fisiopatologia , Carcinoma de Células Pequenas/fisiopatologia , Diagnóstico Diferencial , Coração/inervação , Humanos , Neoplasias Pulmonares/fisiopatologia , Masculino , Exame Neurológico , Síndromes Paraneoplásicas do Sistema Nervoso/fisiopatologia , Paralisia Respiratória/fisiopatologia , Síndrome de Shy-Drager/fisiopatologiaRESUMO
Graft versus host disease (GVHD) is a frequent complication of bone marrow transplantation (BMT). Peripheral neuropathies in association with chronic GVHD are uncommon. We report a patient with BHT for chronic myeloid leukemia, and chronic GVHD with severe sclerodermatitis resulting in bilateral medial antebrachial and saphenous sensory mononeuropathies.
Assuntos
Indóis/uso terapêutico , Transtornos de Enxaqueca/tratamento farmacológico , Pirrolidinas/uso terapêutico , Agonistas do Receptor de Serotonina/uso terapêutico , Sumatriptana/uso terapêutico , Vasoconstritores/uso terapêutico , Doença Aguda , Método Duplo-Cego , Humanos , Ensaios Clínicos Controlados Aleatórios como Assunto , TriptaminasRESUMO
The mechanism by which IL-1 beta exerts its actions in the brain during systemic inflammation is not fully understood, as neither IL-1 receptor gene expression nor IL-1 binding have been identified in significant levels in key areas that respond to IL-1 beta. Having hypothesized that perivascular nitric oxide (NO) might modulate the effects of systemic IL-1 beta in the brain, we studied the expression of the genes encoding for IL-1 beta, the signal-transducing IL-1 receptor type I (IL-1RI) and inducible NO synthase (iNOS) constitutively and during systemic inflammation in vascular and perivascular regions of the rat brain. Our results show that IL-1RI is constitutively expressed at the interface of the vascular wall and perivascular glia. During systemic inflammation there is induction of IL-1 beta gene expression in the vascular wall, accompanied by perivascular induction of iNOS mRNA. We conclude that during systemic inflammation vascular IL-1 beta, binding to vascular and perivascular IL-1RI receptors, may induce perivascular iNOS gene expression, leading to the production of NO and modulation of the effects of IL-1 beta in the brain. We propose that the vascular and peri-vascular induction of iNOS mRNA by IL-1 beta might represent a mechanism for the modulation of the central nervous system effects of peripheral inflammatory mediators.
Assuntos
Circulação Cerebrovascular/fisiologia , Expressão Gênica/genética , Interleucina-1/metabolismo , Óxido Nítrico Sintase/metabolismo , Receptores de Interleucina-1/metabolismo , Animais , Hibridização In Situ , Masculino , Ratos , Ratos Sprague-DawleyRESUMO
Pituitary function is regulated by hypothalamic releasing hormones secreted into hypophyseal-portal blood. A new hypothesis is that pituitary function might also be regulated at the local level by releasing hormones synthesized within the pituitary. Here we show that the pituitary expresses high levels of the gene encoding for urocortin. We suggest that urocortin synthesized by the pituitary may modulate pituitary function, and that adrenocorticotropic hormone (ACTH) secretion is dependent on input not only from the hypothalamus as previously described, but it may also be regulated by urocortin synthesized locally. Urocortin binds to the corticotropin-releasing hormone (CRH) receptor type 1 (CRH-R1) with high affinity and potently stimulates pituitary-adrenal function. Our group and others have previously localized high levels of CRH-R1 mRNA in the pituitary. Using a 35S-labeled rat urocortin riboprobe we have now localized urocortin mRNA in rat brain and pituitary. The finding of urocortin gene expression in the pituitary may help explain why proopiomelanocortin (POMC) mRNA levels are not decreased during hypothalamo-pituitary disconnection, and also describes a new level of complexity in the regulation of hypothalamo-pituitary function. Future studies should consider the possibility that pituitary function might be regulated at the local level by urocortin.
Assuntos
Química Encefálica/fisiologia , Hormônio Liberador da Corticotropina/genética , Hipófise/química , Animais , Autorradiografia , Tronco Encefálico/química , Tronco Encefálico/fisiologia , Cerebelo/química , Cerebelo/fisiologia , Expressão Gênica/fisiologia , Sistema Hipotálamo-Hipofisário/química , Sistema Hipotálamo-Hipofisário/fisiologia , Processamento de Imagem Assistida por Computador , Hibridização In Situ , Masculino , Hipófise/fisiologia , Prosencéfalo/química , Prosencéfalo/fisiologia , RNA Mensageiro/análise , Ratos , Ratos Sprague-Dawley , UrocortinasRESUMO
Inducible nitric oxide synthase (iNOS) is a transcriptionally regulated enzyme that synthesizes nitric oxide from L-arginine that has a key role in the pathophysiology of systemic inflammation and sepsis. Transgenic animals with a null mutation for the iNOS gene are resistant to hypotension and death caused by Escherichia coli lipopolysaccharide (LPS). The regulation of peripheral iNOS has been well studied in sepsis, but little is known about iNOS regulation in the brain during systemic inflammation or sepsis. We know that at baseline there is no detectable iNOS gene expression in the brain, but a detailed neuroanatomical study reveals that early in the course of systemic inflammation there is a profound induction of iNOS messenger RNA in vascular, glial and neuronal structures of the rat brain, accompanied by the production of nitric oxide (NO) metabolites in brain parenchyma and cerebrospinal fluid (CSF). We propose that the spillover of nitrite into the CSF has the potential to be a diagnostic marker for systemic inflammation and sepsis. Pharmacological interventions aimed at regulating iNOS function in the brain might represent a new treatment strategy in sepsis. Brain iNOS may be relevant to the pathophysiology, diagnosis and treatment of systemic inflammation and sepsis.