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1.
J Korean Med Sci ; 26(7): 962-5, 2011 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-21738354

RESUMEN

Skull base osteomyelitis (SBO) is difficult to diagnose when a patient presents with multiple cranial nerve palsies but no obvious infectious focus. There is no report about SBO with septic pulmonary embolism. A 51-yr-old man presented to our hospital with headache, hoarseness, dysphagia, frequent choking, fever, cough, and sputum production. He was diagnosed of having masked mastoiditis complicated by SBO with multiple cranial nerve palsies, sigmoid sinus thrombosis, and septic pulmonary embolism. We successfully treated him with antibiotics and anticoagulants alone, with no surgical intervention. His neurologic deficits were completely recovered. Decrease of pulmonary nodules and thrombus in the sinus was evident on the follow-up imaging one month later. In selected cases of intracranial complications of SBO and septic pulmonary embolism, secondary to mastoiditis with early response to antibiotic therapy, conservative treatment may be considered and surgical intervention may be withheld.


Asunto(s)
Osteomielitis/diagnóstico , Embolia Pulmonar/diagnóstico , Antibacterianos/uso terapéutico , Anticoagulantes/uso terapéutico , Proteína C-Reactiva/análisis , Enfermedades de los Nervios Craneales/complicaciones , Enfermedades de los Nervios Craneales/diagnóstico , Diagnóstico Diferencial , Enterobacter aerogenes/aislamiento & purificación , Infecciones por Enterobacteriaceae/diagnóstico , Infecciones por Enterobacteriaceae/tratamiento farmacológico , Humanos , Pulmón/diagnóstico por imagen , Pulmón/patología , Imagen por Resonancia Magnética , Masculino , Mastoiditis/complicaciones , Mastoiditis/diagnóstico , Persona de Mediana Edad , Osteomielitis/complicaciones , Osteomielitis/tratamiento farmacológico , Embolia Pulmonar/complicaciones , Embolia Pulmonar/microbiología , Trombosis de los Senos Intracraneales/complicaciones , Trombosis de los Senos Intracraneales/diagnóstico , Base del Cráneo , Esputo/microbiología , Tomografía Computarizada por Rayos X
2.
Cancer Res Treat ; 42(2): 121-4, 2010 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-20622968

RESUMEN

Follicular dendritic cells (FDC) are non-lymphoid, non-phagocytic accessory cells of the immune system and these cells are essential for antigen presentation and regulation of the reactions in germinal centers. Follicular dendritic cell sarcoma (FDCS) is a rare neoplasm that shows a low-to-intermediate malignant potential. The most commonly involved sites are the lymph nodes, but FDCS may also occur at a variety of extranodal sites, including the oral cavity, tonsils, gastrointestinal tract and liver. We describe here a 79-year-old woman who had FDCS with extensive lymph node involvement, dry cough, and an itching sensation. The patient improved after systemic chemotherapy.

3.
Mol Cells ; 24(3): 372-7, 2007 Dec 31.
Artículo en Inglés | MEDLINE | ID: mdl-18182853

RESUMEN

The orphan nuclear receptor, SF-1, plays a pivotal role in the development and differentiation of the endocrine and reproductive systems, and also regulates the transcription of a host of genes, including those encoding several steroidogenic enzymes and gonadotropins. We found that a previously unidentified repressor, EID-1, is an SF-1-interacting protein that inhibits the transactivation of SF-1. A transient transfection assay revealed that EID-1 inhibits SF-1, but not LRH-1, ERRgamma, or mCAR. Using the yeast two hybrid and GST pull-down assays, we determined that EID-1 interacted strongly with SF-1. In addition, it colocalized with SF-1 in mammalian cells and interacted specifically with the AF-2 domain of SF-1, competing with SRC-1 to inhibit SF-1 transactivation. EID-1 is expressed in the mouse testis, and its expression decreases during testis development. The results of the present study suggest that EID-1 can act as a repressor, regulating the function of SF-1.


Asunto(s)
Proteínas Nucleares/metabolismo , Proteínas Represoras/metabolismo , Factor Esteroidogénico 1/metabolismo , Activación Transcripcional/efectos de los fármacos , Animales , Células COS , Proteínas de Ciclo Celular , Núcleo Celular/química , Chlorocebus aethiops , Humanos , Masculino , Ratones , Proteínas Nucleares/farmacología , Proteínas Represoras/farmacología , Factor Esteroidogénico 1/antagonistas & inhibidores , Testículo/crecimiento & desarrollo , Testículo/metabolismo , Células Tumorales Cultivadas
4.
Cancer Res ; 63(15): 4648-55, 2003 Aug 01.
Artículo en Inglés | MEDLINE | ID: mdl-12907645

RESUMEN

In our search for genes associated with gastric cancer progression, we identified macrophage inhibitory cytokine-1 (MIC-1), a member of the transforming growth factor beta superfamily, as an overexpressed gene in gastric tumor tissues. Expression analysis of MIC-1 in gastric tumor tissues revealed a specific expression in gastric cancer cells, and this expression level was well correlated with invasive potential in various human gastric cancer cell lines. Stable transfection of MIC-1 into SNU-216, a human gastric cancer cell line, significantly increased its invasiveness. The overexpression of MIC-1 into SNU-216 cells significantly increased the activity of urokinase-type plasminogen activator (uPA), and the expressions of uPA and urokinase-type plasminogen activator receptor (uPAR). Similarly, the stimulation of gastric cancer cell lines with purified recombinant MIC-1 dose-dependently increased cell invasiveness, uPA activity, and uPA and uPAR expression. However, MIC-1 did not significantly suppress the proliferation of gastric cancer cell lines. We also found that the stimulation of human gastric cell lines with recombinant MIC-1 strongly induced activation of mitogen-activated protein kinase kinase-1/2 and extracellular signal-regulated kinase-1/2. Additional analysis revealed that PD98059, a selective inhibitor of mitogen-activated protein kinase kinase-1/2, suppressed not only gastric cancer cell invasiveness and uPA activity, but also the mRNA expressions of uPA and uPAR, as induced by recombinant MIC-1. Our results indicate that MIC-1 may contribute to the malignant progression of gastric cancer cells by inducing tumor cell invasion through the up-regulation of the uPA activation system via extracellular signal-regulated kinase-1/2-dependent pathway.


Asunto(s)
Citocinas/fisiología , Neoplasias Gástricas/metabolismo , Activador de Plasminógeno de Tipo Uroquinasa/metabolismo , División Celular/efectos de los fármacos , División Celular/fisiología , Citocinas/biosíntesis , Citocinas/genética , Citocinas/farmacología , Relación Dosis-Respuesta a Droga , Activación Enzimática/efectos de los fármacos , Regulación Enzimológica de la Expresión Génica , Regulación Neoplásica de la Expresión Génica , Factor 15 de Diferenciación de Crecimiento , Humanos , Proteína Quinasa 1 Activada por Mitógenos/metabolismo , Proteína Quinasa 3 Activada por Mitógenos , Proteínas Quinasas Activadas por Mitógenos/metabolismo , Receptores de Superficie Celular/metabolismo , Receptores del Activador de Plasminógeno Tipo Uroquinasa , Proteínas Recombinantes/farmacología , Neoplasias Gástricas/enzimología , Neoplasias Gástricas/genética , Neoplasias Gástricas/patología , Transfección , Factor de Crecimiento Transformador beta/farmacología , Células Tumorales Cultivadas , Regulación hacia Arriba
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