ScienceAnalysisTheSCImago Journal & Country Rank is a portal that includes the journals andcountry scientific indicators developed from the information contained in theScopus database (Elsevier B.V.). These indicators can be used to assess andanalyze scientific domains.Thisplatform takes its name from the SCImago Journal Rank (SJR) indicator, developedby SCImago from the widely known algorithm Google PageRankTM. This indicatorshows the visibility of the journals contained in the Scopus database from1996. 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) PROTOCOLOS (Signalipedia)Signalipedia - os membros do grupo vao adicionando informacoes e dados sobre os protocolos em uso - portanto, esta pagina esta em construcao. Regras basicas no laboratorioProteinasRNA-DNACelulasGeraisLise CelularRegras Basicas Regras Basicas Solucoes e TampoesDosagem de ProteinasExtracao de RNA TransfeccaoBanco de DadosAnticorposTranscripcao Reversa Lentivirus e BiosegurancaBiologia de SistemasSDS-PAGEPCR CitometriaSequenciasWestern Blot (transferencia)Transformacao de BacteriasLDH, CaspaseReagentesWestern Blot (imunodeteccao)MiniprepMicroscopioLiteraturaImunoprecipitacaoRNAiImunocitoquimicaProtocolos GeraisEspectrometria de MassaGliomas in vivoProgramasSenescencia AutofagiaCelulas Tronco Tumorais 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) ATENCAO PROGRAMEM-SE, para mais detalhes consultem aqui: ver8 o Congresso Internacional sobreAuto-imunidade9-13 maio 2012Granada, Espanhahttp://www2.kenes.com/autoimmunity/Pages/Home.aspxOs neutrofilos na imunidade09-12 junho de 2012Quebec City,Canadawww.neutrophil2012.caCongresso Europeu de Imunologia5-8 setembro de 2012Glasgow, ReinoUnidohttp://www.eci-glasgow2012.com/12 o Simposio Internacional sobreCelulas Dendriticas7-11 07 de outubro de 2012Daegu, na Coreiahttp://www.people-x.com/homepage/DC2012/mail/m-e01.htm15 Congresso Internacional deImunologia22-27 agosto de 2013Roma, Italiahttp://www.ici2013.orgCongresso Internacional de Adjuvantes eVacinas Allergen6-11 maio