RESUMEN
A 75-year-old woman presented with consciousness disturbance accompanied by hematemesis. Brain imaging revealed ischemia in the bilateral caudate nuclei and right cerebral watershed area due to stenosis of the right anterior cerebral artery (ACA) and bilateral internal carotid arteries (ICA), and hypoperfusion in the right caudate nucleus. The patient's only symptom was abulia, which gradually resolved. Further brain scans showed that the ICA stenosis had improved, although the right ACA stenosis persisted. This was a rare case of bilateral caudate nucleus infarctions with a hemodynamic etiology.
Asunto(s)
Estenosis Carotídea/complicaciones , Núcleo Caudado/irrigación sanguínea , Hemorragia Gastrointestinal/complicaciones , Infarto de la Arteria Cerebral Anterior/etiología , Anciano , Estenosis Carotídea/diagnóstico por imagen , Estenosis Carotídea/fisiopatología , Núcleo Caudado/diagnóstico por imagen , Angiografía Cerebral/métodos , Circulación Cerebrovascular , Imagen de Difusión por Resonancia Magnética , Femenino , Hematemesis/etiología , Hemodinámica , Humanos , Infarto de la Arteria Cerebral Anterior/diagnóstico por imagen , Infarto de la Arteria Cerebral Anterior/fisiopatología , Angiografía por Resonancia Magnética , Tomografía Computarizada de Emisión de Fotón ÚnicoRESUMEN
The transcription factor OASIS gene, which encodes for a CREB/ATF family member, is specifically expressed in the salivary gland, the cartilage and the tooth germs of the mouse embryo. In the present study, the expression patterns were compared between OASIS mRNA and major vertebrate proteoglycans, which might be the downstream genes of OASIS in the tooth germs of mouse first mandibular molars, through in situ hybridization histochemistry. OASIS mRNA expression was observed in the inner enamel epithelium during the cap and bell stages (E14.5-E18.5) in the preodontoblasts during differentiation stage (E18.5-P0) and in the differentiating odontoblasts during the early secretory stage (P2.5-P4.5). Proteoglycans (versican, decorin, biglycan, glypican, syndecan-1, and syndecan-3) were expressed in the tooth germs in various patterns. Decorin, biglycan, syndecan-1 and syndecan-3 showed gene expressions overlapping with OASIS. Especially the expression pattern of decorin and syndecan-3 coincided temporally and spatially exactly with that of OASIS. These results suggest that the OASIS gene might be related to proteoglycan expression and may play an important role in the differentiation of the odontoblast and cells in inner enamel epithelium.
Asunto(s)
Proteína de Unión a Elemento de Respuesta al AMP Cíclico/metabolismo , Proteínas de la Matriz Extracelular , Glicoproteínas/metabolismo , Proteínas del Tejido Nervioso/metabolismo , Odontogénesis , Proteoglicanos , Germen Dentario/embriología , Germen Dentario/metabolismo , Factores de Transcripción/metabolismo , Agrecanos , Animales , Proteína de Unión a Elemento de Respuesta al AMP Cíclico/genética , Regulación del Desarrollo de la Expresión Génica , Glicoproteínas/genética , Hibridación in Situ , Lectinas Tipo C , Ratones , Ratones Endogámicos ICR , Proteínas del Tejido Nervioso/genética , Odontogénesis/genética , ARN Mensajero/metabolismo , Especificidad de la Especie , Factores de Transcripción/genéticaRESUMEN
Bacterial lipopolysaccharide (LPS) triggers innate immune responses through the Toll-like receptor (TLR) 4. Regulation of TLR signaling is a key step for inflammation, septic shock and innate/adaptive immunity. TLR signaling is shown to be regulated by cytokines, such as interferon-gamma (positive) and interleukin-10 and IL-4 (negative). However, molecular mechanisms of the regulation of LPS signaling by cytokines have not been clarified. Cytokine signaling is regulated by CIS/SOCS family proteins. Both SOCS1 and SOCS3 can inhibit JAK tyrosine kinase activity. We demonstrate that SOCS1 and SOCS3 play an important regulatory role in macrophages and dendritic cells (DCs) by modulating TLR signaling. SOCS1 negatively regulates not only the JAK/STAT pathway, but also the TLR-NF-kappaB pathway. SOCS3 protein was strongly induced by both IL-6 and IL-10 in the presence of LPS, but selectively inhibited IL-6 signaling. Therefore lack of SOCS3 gene in macrophages resulted in suppression of TLR signaling by hyperactivation of STAT3.