Dextran Sulfate

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  Subject Areas on Research

  • A whole animal chemical screen approach to identify modifiers of intestinal neutrophilic inflammation. 
  • Colonic Epithelial-Derived Selenoprotein P Is the Source for Antioxidant-Mediated Protection in Colitis-Associated Cancer. 
  • Control of Intestinal Inflammation, Colitis-Associated Tumorigenesis, and Macrophage Polarization by Fibrinogen-Like Protein 2. 
  • Dextran sulfate sodium-induced colitis in immunodeficient rats. 
  • Dietary Salt Exacerbates Experimental Colitis. 
  • Differential inhibition of HIV-1 cell binding and HIV-1-induced syncytium formation by low molecular weight sulphated polysaccharides. 
  • Distinct Kinase-Independent Role of RIPK3 in CD11c+ Mononuclear Phagocytes in Cytokine-Induced Tissue Repair. 
  • Distinct cellular roles for PDCD10 define a gut-brain axis in cerebral cavernous malformation. 
  • Electroactive controlled release thin films. 
  • Environmental Factors Modify the Severity of Acute DSS Colitis in Caspase-11-Deficient Mice. 
  • Environmental factors regulate Paneth cell phenotype and host susceptibility to intestinal inflammation in Irgm1-deficient mice. 
  • Epithelial Smad4 Deletion Up-Regulates Inflammation and Promotes Inflammation-Associated Cancer. 
  • Fasting prevents experimental murine colitis produced by dextran sulfate sodium and decreases interleukin-1 beta and insulin-like growth factor I messenger ribonucleic acid. 
  • Glutamine therapy improves outcome of in vitro and in vivo experimental colitis models. 
  • IL-10-producing regulatory B10 cells inhibit intestinal injury in a mouse model. 
  • Inhibition of the beta-adrenergic receptor kinase by polyanions. 
  • Irgm1-deficient mice exhibit Paneth cell abnormalities and increased susceptibility to acute intestinal inflammation. 
  • NK-1 antagonist reduces colonic inflammation and oxidative stress in dextran sulfate-induced colitis in rats. 
  • Ornithine Decarboxylase in Macrophages Exacerbates Colitis and Promotes Colitis-Associated Colon Carcinogenesis by Impairing M1 Immune Responses. 
  • Targeting EZH2 histone methyltransferase activity alleviates experimental intestinal inflammation. 
  • The Crohn's Disease Risk Factor IRGM Limits NLRP3 Inflammasome Activation by Impeding Its Assembly and by Mediating Its Selective Autophagy. 
  • The NLRP3 inflammasome protects against loss of epithelial integrity and mortality during experimental colitis. 
  • The apolipoprotein E-mimetic peptide COG112 inhibits NF-kappaB signaling, proinflammatory cytokine expression, and disease activity in murine models of colitis. 
  • The importance of the retinoid X receptor alpha in modulating inflammatory signaling in acute murine colitis. 
  • The necroptosis adaptor RIPK3 promotes injury-induced cytokine expression and tissue repair. 
  • The scaffold-dependent function of RIPK1 in dendritic cells promotes injury-induced colitis. 
  • Tumor necrosis factor alpha and colitis-associated colon cancer. 
  • Vanilloid receptor-1 containing primary sensory neurones mediate dextran sulphate sodium induced colitis in rats. 
  • Vitamin D receptor and retinoid X receptor α status and vitamin D insufficiency in models of murine colitis. 
  • rHuKGF ameliorates symptoms in DSS and CD4(+)CD45RB(Hi) T cell transfer mouse models of inflammatory bowel disease.