37 resultados para Vidal, José, 1630-1702
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Fecha: 10-10-1936/31-1-1939 / Unidad de instalación: Carpeta 25 - Expediente 21 / Nº de pág.: 33 (28 mecanografiadas, 5 manuscritas)
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Fecha: 29-9-1947 / Unidad de instalación: Carpeta 25 - Expediente 23-4 / Nº de pág.: 1 (mecanografiada)
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Fecha: 29-12-1937 original (>1970 copia) / Unidad de instalación: Carpeta 48 - Expediente 8-9 / Nº de pág.: 3 (mecanografiadas)
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Fecha: 26-2-1985 / Unidad de instalación: Carpeta 48 - Expediente 7-8 / Nº de pág.: 4 (mecanografiadas)
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1 carta (mecanografiada) ; 210x290mm. Ubicación: Caja 1 - Carpeta 5
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1 carta (mecanografiada) ; 162x224mm. Ubicación: Caja 1 - Carpeta 9
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7 cartas (mecanografiadas) ; entre 215x286mm y 157x215mm. Ubicación: Caja 1 - Carpeta 10
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3 cartas (mecanografiadas) ; entre 220x340mm y 220x310mm. Ubicación: Caja 1 - Carpeta 11
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5 cartas (manuscritas y mecanografiadas) ; 215x160mm. Ubicación: Caja 1 - Carpeta 12
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Background: Patients with chronic obstructive pulmonary disease (COPD) often experience exacerbations of the disease that require hospitalization. Current guidelines offer little guidance for identifying patients whose clinical situation is appropriate for admission to the hospital, and properly developed and validated severity scores for COPD exacerbations are lacking. To address these important gaps in clinical care, we created the IRYSS-COPD Appropriateness Study. Methods/Design: The RAND/UCLA Appropriateness Methodology was used to identify appropriate and inappropriate scenarios for hospital admission for patients experiencing COPD exacerbations. These scenarios were then applied to a prospective cohort of patients attending the emergency departments (ED) of 16 participating hospitals. Information was recorded during the time the patient was evaluated in the ED, at the time a decision was made to admit the patient to the hospital or discharge home, and during follow-up after admission or discharge home. While complete data were generally available at the time of ED admission, data were often missing at the time of decision making. Predefined assumptions were used to impute much of the missing data. Discussion: The IRYSS-COPD Appropriateness Study will validate the appropriateness criteria developed by the RAND/UCLA Appropriateness Methodology and thus better delineate the requirements for admission or discharge of patients experiencing exacerbations of COPD. The study will also provide a better understanding of the determinants of outcomes of COPD exacerbations, and evaluate the equity and variability in access and outcomes in these patients.
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Background: Human melanoma frequently colonizes bone marrow (BM) since its earliest stage of systemic dissemination, prior to clinical metastasis occurrence. However, how melanoma cell adhesion and proliferation mechanisms are regulated within bone marrow stromal cell (BMSC) microenvironment remain unclear. Consistent with the prometastatic role of inflammatory and angiogenic factors, several studies have reported elevated levels of cyclooxygenase-2 (COX-2) in melanoma although its pathogenic role in bone marrow melanoma metastasis is unknown. Methods: Herein we analyzed the effect of cyclooxygenase-2 (COX-2) inhibitor celecoxib in a model of generalized BM dissemination of left cardiac ventricle-injected B16 melanoma (B16M) cells into healthy and bacterial endotoxin lipopolysaccharide (LPS)-pretreated mice to induce inflammation. In addition, B16M and human A375 melanoma (A375M) cells were exposed to conditioned media from basal and LPS-treated primary cultured murine and human BMSCs, and the contribution of COX-2 to the adhesion and proliferation of melanoma cells was also studied. Results: Mice given one single intravenous injection of LPS 6 hour prior to cancer cells significantly increased B16M metastasis in BM compared to untreated mice; however, administration of oral celecoxib reduced BM metastasis incidence and volume in healthy mice, and almost completely abrogated LPS-dependent melanoma metastases. In vitro, untreated and LPS-treated murine and human BMSC-conditioned medium (CM) increased VCAM-1-dependent BMSC adherence and proliferation of B16M and A375M cells, respectively, as compared to basal medium-treated melanoma cells. Addition of celecoxib to both B16M and A375M cells abolished adhesion and proliferation increments induced by BMSC-CM. TNF alpha and VEGF secretion increased in the supernatant of LPS-treated BMSCs; however, anti-VEGF neutralizing antibodies added to B16M and A375M cells prior to LPS-treated BMSC-CM resulted in a complete abrogation of both adhesion-and proliferation-stimulating effect of BMSC on melanoma cells. Conversely, recombinant VEGF increased adherence to BMSC and proliferation of both B16M and A375M cells, compared to basal medium-treated cells, while addition of celecoxib neutralized VEGF effects on melanoma. Recombinant TNFa induced B16M production of VEGF via COX-2-dependent mechanism. Moreover, exogenous PGE2 also increased B16M cell adhesion to immobilized recombinant VCAM-1. Conclusions: We demonstrate the contribution of VEGF-induced tumor COX-2 to the regulation of adhesion-and proliferation-stimulating effects of TNFa, from endotoxin-activated bone marrow stromal cells, on VLA-4-expressing
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9 cartas (mecanografiadas) ; 207x300mm. Ubicación: Caja 1 - Carpeta 36
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1 carta (manuscrita) ; 270x180mm. Ubicación: Caja 1 - Carpeta 37
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1 carta (mecanografiada) ; 215x135mm. Ubicación: Caja 1 - Carpeta 51
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1 carta (mecanografiada) ; 340x165mm. Ubicación: Caja 1 - Carpeta 61