994 resultados para 4-31


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CTLA-4 is a critical negative regulator of T cell responses and CTLA-4-deficient (CTLA-4(-/-)) mice die of a lymphproliferative disease. Nevertheless, RAG-2-deficient mice reconstituted with a mixture of CTLA-4(-/-) and normal (CTLA-4(+/+)) bone marrow survive in the absence of any signs of disease, although 50% of their T cells do not express CTLA-4. Using such mixed chimeras, we analyzed the role of CTLA-4 in specific T cell responses to lymphocytic choriomeningitis virus, Leishmania major and mouse mammary tumor virus, which cause acute, chronic and persistent infections, respectively. The populations of antigen-specific CTLA-4(-/-)CD4(+) and CTLA-4(-/-)CD8(+) T cells became activated, expanded and contracted indistinguishably from CTLA-4(+/+)CD4(+) and CTLA-4(+/+)CD8(+) T cells after infection with all three pathogens. Thus, CTLA-4 is not involved in the down-regulation of specific T cell responses and peripheral deletion in a T cell-autonomous fashion.

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Newsletter produced by the Iowa Board of Nursing for nurses to keep them informed to CE classes, renewals, board meetings, etc. Produced 4 times a year. Also known as Nursing Newsletter.

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Newsletter produced by the Iowa Board of Nursing for nurses to keep them informed to CE classes, renewals, board meetings, etc. Produced 4 times a year. Also known as Nursing Newsletter.

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Newsletter produced by the Iowa Board of Nursing for nurses to keep them informed to CE classes, renewals, board meetings, etc. Produced 4 times a year. Also known as Nursing Newsletter.

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En aquest article revisem la Historia de l'actual Escola Universitaria de Ciencies de la Salut (EUCS), de la Universitat de Vic. És a dir, repassem els seus 3 1 anys de vida institucional al servei de la formació professional de la Infermeria, primer i posteriorment, de les altres professions sanitaries: Nutrició Humana i Dietktica, Fisioterapia i Terapia Ocupacional. Després de fer una breu referencia a alguns antecedents instructius del segle XIX i XX, ens endinsem a la Histbria de I'EUCS prbpiament dita. Aquesta s'ha dividit en 4 etapes. La primera etapa és la de 1'Escola Femenina d'Ajudants Tecnics Sanitaris (ATS); la segona, 1'Escola Universitaria d'lnfermeria Osona (EUIO); la tercera, la dels Estudis Universitaris de Vic (EUIO-EUV); i, la quarta, la de la Universitat de Vic (EUCS-Wic). Hem procurat alternar-hi il-lustracions i experiencies viscudes per alguns testimonis, a fi de fer-ho més ame. Aixb ha estat possible gdcies a la col.laboració de les persones que es ressenyen al final (vegeu fonts consultades). 1, molt especialment, gracies al cornitl: organitzador d'aquesta Jornada. No obstant, cal advertir que aquesta nota és més aviat una pinzellada. La veritable reconstrucció de la vida de la nostra institució requeriria un treball molt rnés aprofundit, fet amb més temps, més testimonis, rnés estudi documental, ... En definitiva, més profunditat (currículum, professorat, estudiants, assignatures, llocs de practiques, metodologia docent, avaluació, inserció laboral, abandonaments, recursos, etc.). Deixo, doncs, la porta oberta per a qui s'anirni a continuar.

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Angioedema is a rare side effect of angiotensin converting enzyme (ACE) inhibitors. Its cause is probably related to the accumulation of bradykinin and substance P, i.e. two proinflammatory peptides normally inactivated by ACE. Angioedema occurs most of the time at the early phase of treatment, but may also develop during long-term treatment. It might involve the gastro-intestinal tract, leading to abdominal pain, vomiting and/or diarrhea, as well as pancreatitis. Dipeptidyl-ptidase-4 (DPP-4) is another enzyme allowing the degradation of bradykinin and substance P. Co-administering an ACE inhibitor and a DPP-4 inhibitor (as an antidiabetic agent) increases significantly the risk of angioedema.

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Early production of IL-4 by LACK-reactive Vbeta4-Valpha8 CD4(+) T cells instructs aberrant Th2 cell development and susceptibility to Leishmania major in BALB / c mice. This was demonstrated using Vbeta4(+)-deficient BALB / c mice as a result of chronic infection with MMTV (SIM), a mouse mammary tumor virus expressing a Vbeta4-specific superantigen. The early IL-4 response was absent in these mice which develop a Th1 response to L. major. Here, we studied the functional plasticity of LACK-reactive Vbeta4-Valpha8 CD4(+) T cells using BALB/ c mice inoculated with L. major shortly after infection with MMTV (SIM), i. e. before deletion of Vbeta4(+) cells. These mice fail to produce the early IL-4 response to L. major and instead exhibit an IFN-gamma response that occurs within LACK-reactive Vbeta4-Valpha8 CD4(+) T cells. Neutralization of IFN-gamma restores the production of IL-4 by these cells. These data suggest that the functional properties of LACK-reactive Vbeta4-Valpha8 CD4(+) T cells are not irreversibly fixed.