Congressos, simpósios e Encontros de Imunologia 2012

ATENÇÃO PROGRAMEM-SE, para mais detalhes consultem aqui: ver

8 º Congresso Internacional sobre Auto-imunidade

9-13 maio 2012

Granada, Espanha

http://www2.kenes.com/autoimmunity/Pages/Home.aspx

Os neutrófilos na imunidade

09-12 junho de 2012

Quebec City, Canadá

www.neutrophil2012.ca

Congresso Europeu de Imunologia

5-8 setembro de 2012

Glasgow, Reino Unido

http://www.eci-glasgow2012.com/

12 º Simpósio Internacional sobre Células Dendríticas

7-11 07 de outubro de 2012

Daegu, na Coréia

http://www.people-x.com/homepage/DC2012/mail/m-e01.htm

15 Congresso Internacional de Imunologia

22-27 agosto de 2013

Roma, Itália

http://www.ici2013.org

Congresso Internacional de Adjuvantes e Vacinas Allergen

6-11 maio 2012

Varadero, Cuba

Reunião Anual da Associação Americana de imunologistas

4 - 08 de maio de 2012

Boston, Massachusetts, Estados Unidos

Identificação de Estresse Oxidativo e Toll-like receptor 4 de sinalização como um caminho chave de lesão pulmonar aguda

Multiple lung pathogens such as chemical agents, H5N1 avian flu, or SARS cause high lethality due to acute respiratory distress syndrome. Here we report that Toll-like receptor 4 (TLR4) mutant mice display natural resistance to acid-induced acute lung injury (ALI). We show that TLR4-TRIF-TRAF6 signaling is a key disease pathway that controls the severity of ALI. The oxidized phospholipid (OxPL) OxPAPC was identified to induce lung injury and cytokine production by lung macrophages via TLR4-TRIF. We observed OxPL production in the lungs of humans and animals infected with SARS, Anthrax, or H5N1. Pulmonary challenge with an inactivated H5N1 avian influenza virus rapidly induces ALI and OxPL formation in mice. Loss of TLR4 or TRIF expression protects mice from H5N1-induced ALI. Moreover, deletion of ncf1, which controls ROS production, improves the severity of H5N1-mediated ALI. Our data identify  oxidative stress and innate immunity as key lung injury pathways that control the severity of ALI. ver (aqui)

Mechanisms for suppressing NADPH oxidase in the vascular wall

Oxidative stress underlies many forms of vascular disease as well as tissue injury following ischemia and reperfusion. The major source of oxidative stress in the artery wall is an NADPH oxidase. This enzyme complex as expressed in vascular cells differs from that in phagocytic leucocytes both in biochemical structure and functions. The crucial flavin-containing catalytic subunits, Nox1 and Nox4, are not found in leucocytes, but are highly expressed in vascular cells and upregulated with vascular remodeling, such as that found in hypertension and atherosclerosis. The difference in catalytic subunits offers the opportunity to develop “vascular specific” NADPH oxidase inhibitors that do not compromise the essential physiological signaling and phagocytic functions carried out by reactive oxygen and nitrogen species.  Nitric oxide and targeted inhibitors of NADPH oxidase that block the source of oxidative stress in the vasculature are more likely to prevent the deterioration of vascular function that leads to stroke and heart attack, than are conventional antioxidants. The roles of Nox isoforms in other inflammatory conditions are yet to be explored.ver (aqui)

Role of Nicotinamide Adenine Dinucleotide Phosphate Oxidase 1 in Oxidative Burst Response to Toll-Like Receptor 5 Signaling in Large Intestinal Epithelial Cells

The NADPH oxidase 1 (Nox1) is a gp91^phox homologue preferentially expressed in the colon. We have established primary cultures of guinea pig large intestinal epithelial cells giving 90% purity of surface mucous cells. These cells spontaneously released superoxide anion (O₂^-) of 160 nmol/mg protein/h and expressed the Nox1, p22^phox,p67^phox, and Rac1 mRNAs, but not the gp91^phox, Nox4, p47^phox, p40^phox, and Rac2mRNAs. They also expressed novel homologues of p47^phox and p67^phox (p41^nox and p51^nox, respectively). Human colon cancer cell lines (T84 and Caco2 cells) expressed theNox1, p22^phox, p51^nox, and Rac1 mRNAs, but not the other NADPH component mRNAs, and secreted only small amounts of O₂^- (<2 nmol/mg protein/h). Cotransfection of p41^noxand p51^nox cDNAs in T84 cells enhanced PMA-stimulated O₂^- release 5-fold. Treatment of the transfected T84 cells with recombinant flagellin (rFliC) from Salmonella enteritidisfurther augmented the O₂^- release in association with the induction of Nox1 protein. The enhanced O₂^- production by cotransfection of p41^nox and p51^nox vectors further augmented the rFliC-stimulated IL-8 release from T84 cells. T84 cells expressed the Toll-like receptor 5, and rFliC rapidly phosphorylated TGF--activated kinase 1 and TGF--activated kinase 1-binding protein 1. A potent inhibitor for NF-κB (pyrrolidine dithiocarbamate) significantly blocked the rFliC-primed increase in O₂^- production and induction of Nox1 protein. These results suggest that p41^nox and p51^nox are involved in the Nox1 activation in surface mucous cells of the colon, and besides that, epithelial cells discern pathogenicities among bacteria to appropriately operate Nox1 for the host defense. ver (aqui)

Cursos recomendados e reconhecidos pela CAPES

Constam da relação abaixo apresentada os programas e cursos de pós-graduação que obtiveram nota igual ou superior a "3" na avaliação da CAPES e que, portanto, atendem ao requisito básico estabelecido pela legislação vigente para serem reconhecidos pelo Ministério da Educação por meio do Conselho Nacional de Educação (CNE) e, em decorrência, expedirem diplomas de mestrado e/ou doutorado com validade nacional. Nela são incluídos os programas e cursos cujos atos de reconhecimento ou de renovação de reconhecimento já foram oficializados pelo Ministro da Educação (Cursos reconhecidos) como também aqueles cujas propostas foram recentemente aprovadas pela CAPES e encaminhadas ao CNE para a instrução de seus processos de reconhecimento (Cursos recomendados).

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