RESUMO
Autoimmune diseases are some of the most common yet least understood maladies in medicine today. Some estimates place the number of sufferers of such diseases as high as 20% of the U.S. population, most of them women. The disorders involved range from the familiar to the relatively uncommon to the obscure. What these disorders have in common is that they cause the immune system to attack the body's own tissues. Uncertainty in the field of autoimmune disease extends even to the fundamental questions of what an autoimmune disease is and how many people are affected; identifying specific environmental risk factors for autoimmune diseases is still highly speculative. To gain some sense of direction, scientists are looking at a few documented environmental exposures that have led to autoimmune syndromes, as well as some animal models that exhibit autoimmune syndromes similar to those seen in humans. At a September 1998 NIEHS workshop on environmental links to autoimmune diseases, participants prioritized research needs in five main categories, a step that should help scientists develop strategies for investigating this family of diseases.
Assuntos
Doenças Autoimunes/etiologia , Animais , Artrite Reumatoide/etiologia , Diabetes Mellitus Tipo 1/etiologia , Exposição Ambiental , Feminino , Humanos , Lúpus Eritematoso Sistêmico/etiologia , Masculino , Fatores de Risco , Fatores SexuaisAssuntos
Antineoplásicos/farmacologia , Neoplasias Encefálicas/fisiopatologia , Glioma/fisiopatologia , Animais , Neoplasias Encefálicas/tratamento farmacológico , Neoplasias Encefálicas/genética , Dano ao DNA/efeitos dos fármacos , DNA de Neoplasias/efeitos dos fármacos , Resistencia a Medicamentos Antineoplásicos , Glioma/tratamento farmacológico , Glioma/genética , Glutationa/efeitos dos fármacos , Humanos , Compostos de Nitrosoureia/farmacologiaAssuntos
Epilepsia Tipo Ausência/genética , Glutamatos/genética , Transmissão Sináptica/genética , Ácido gama-Aminobutírico/genética , Animais , Encéfalo/fisiopatologia , Mapeamento Encefálico , Epilepsia Tipo Ausência/fisiopatologia , Feminino , Glutamato Descarboxilase/genética , Glutamato Descarboxilase/fisiologia , Glutamatos/fisiologia , Ácido Glutâmico , Masculino , Camundongos , Camundongos Endogâmicos C57BL/genética , Camundongos Mutantes Neurológicos , Receptores de GABA-A/genética , Receptores de GABA-A/fisiologia , Receptores de Glutamato/genética , Receptores de Glutamato/fisiologia , Transdução de Sinais , Transmissão Sináptica/fisiologia , Ácido gama-Aminobutírico/fisiologiaRESUMO
The C57BL/10 sps/sps mouse mutant displays generalized absence seizure-like behavior. In these mice, glutamic acid decarboxylase activity is reduced in the cortex and hippocampus. Tritiated flunitrazepam binding (3H-flu) is reduced in these areas, as well as in midbrain, cerebellum, and pons-medulla. Quantitative [3H]-flunitrazepam binding autoradiography confirms these observations. GABA uptake by synaptosomes from sps/sps mice is also reduced in all the areas studied. Potassium-stimulated, Ca(2+)-dependent release of radioactivity from synaptosomes preloaded with [14C]-GABA is reduced in the hippocampus, increased in midbrain and pons-medulla, but remains unaltered in the cortex. These results suggest region-specific alterations in GABAergic neurotransmission that may be responsible for the absence-like seizures in C57BL/10 sps/sps mice.