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Exogenous alpha-1-acid glycoprotein protects against renal ischemia-reperfusion injury by inhibition of inflammation and apoptosis
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Characterization of the interaction between murine tumour necrosis factor and monoclonal antibodies.
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Activated caspase-1 is not a central mediator of inflammation in the course of ischemia-reperfusion.
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How cells die counts - Reply.
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- Journal Article
- A1
- open access
Functional protection by acute phase proteins alpha(1)-acid glycoprotein and alpha(1)-antitrypsin against ischemia/reperfusion injury by preventing apoptosis and inflammation.
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- Journal Article
- A1
- open access
Inhibition of apoptosis induced by ischemia-reperfusion prevents inflammation.
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The role of endogenous IFN-gamma, TNF-alpha and IL-10 in LPS-induced nitric oxide release in a mouse model.
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Differential role of calcium in tumour necrosis factor-mediated apoptosis and secretion of granulocyte-macrophage colony-stimulating factor in a T cell hybridoma.
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Crucial role of tumor necrosis factor (TNF) receptor 2 and membrane-bound TNF in experimental cerebral malaria.
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Bactericidal permeability-increasing protein release in whole blood ex vivo: Strong induction by lipopolysaccharide and tumor necrosis factor-alpha.
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TNF receptor p55 plays a major role in centrally mediated increases of serum IL-6 and corticosterone after intracerebroventricular injection of TNF.
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Methylprednisolone differentially regulates IL-10 and tumour necrosis factor (TNF) production during murine endotoxaemia.
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Mechanism of induction of tolerance to tumour-necrosis-factor (TNF): No involvement of modulators of TNF bioavailability or receptor-binding.