Please use this identifier to cite or link to this item: https://doi.org/10.2741/3561
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dc.titleSepsis as a model of SIRS
dc.contributor.authorBhatia, M.
dc.contributor.authorHe, M.
dc.contributor.authorZhang, H.
dc.contributor.authorMoochhala, S.
dc.date.accessioned2016-11-11T08:00:40Z
dc.date.available2016-11-11T08:00:40Z
dc.date.issued2009-01-01
dc.identifier.citationBhatia, M., He, M., Zhang, H., Moochhala, S. (2009-01-01). Sepsis as a model of SIRS. Frontiers in Bioscience 14 (12) : 4703-4711. ScholarBank@NUS Repository. https://doi.org/10.2741/3561
dc.identifier.issn10939946
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/130076
dc.description.abstractSepsis describes a complex clinical syndrome that results from the host inability to regulate the inflammatory response against infection. Despite more than 20 years of extensive study, sepsis and excessive systemic inflammatory response syndrome (SIRS) are still the leading cause of death in intensive care units. The clinical study of sepsis and new therapeutics remains challenging due to the complexity of this disease. Therefore, many animal models have been employed to investigate the pathogenesis of sepsis and to preliminarily test potential therapeutics. However, so far, most therapeutics that have shown promising results in animal models failed in human clinical trials. In this chapter we will present an overview of different experimental animal models of sepsis and compare their advantages and disadvantage. The studies in animal models have greatly improved our understanding about the inflammatory mediators in sepsis. In this chapter we will also highlight the roles of several critical mediators including TNF-α, IL-1β, IL-6, chemokines, substance P, hydrogen sulfide and activated protein C in animal models of sepsis as well as in clinical studies.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.2741/3561
dc.sourceScopus
dc.subjectChemokines
dc.subjectHydrogen sulfide
dc.subjectRat
dc.subjectReview
dc.subjectSepsis; Mouse
dc.subjectSubstance P
dc.typeArticle
dc.contributor.departmentPHARMACOLOGY
dc.description.doi10.2741/3561
dc.description.sourcetitleFrontiers in Bioscience
dc.description.volume14
dc.description.issue12
dc.description.page4703-4711
dc.identifier.isiut000270060800077
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