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Protection of zinc against tumor necrosis factor-induced lethal inflammation depends on heat shock protein 70 and allows safe antitumor therapy
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How glucocorticoids control their own strength and the balance between pro- and anti-inflammatory mediators
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A fully dissociated compound of plant origin for inflammatory gene repression
(2005) PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 102(44). p.15827-15832 -
Bilirubin release induced by tumor necrosis factor in combination with galactosamine is toxic to mice
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HSP70 protects against TNF-induced lethal inflammatory shock.
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Relaxation by vasoactive intestinal polypeptide in the gastric fundus of nitric oxide synthase-deficient mice.
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Detection, characterisation and purification of a murine liver factor capable of desensitising towards the lethal activity of tumour necrosis factor.
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Antisense knockdown of inducible nitric oxide synthase inhibits the relaxant effect of VIP in isolated smooth muscle cells of the mouse gastric fundus.
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Involvement of the acute phase protein alpha(1)-acid glycoprotein in nonspecific resistance to a lethal Gram-negative infection.
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Tumor necrosis factor-induced lethal hepatitis: pharmacological intervention with verapamil, tannic acid, picotamide and K76COOH.
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Protection against TNF-induced lethal shock by soluble guanylate cyclase inhibition requires functional inducible nitric oxide synthase.
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- Journal Article
- A1
- open access
The major acute-phase protein, serum amyloid P component, in mice is not involved in endogenous resistance against tumor necrosis factor alpha-induced lethal hepatitis, shock, and skin necrosis.
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Onderzoek naar de mechanismen leidend tot Tumor Necrosis Factor-geïnduceerde leverschade en hypotensie
(1999) -
The role of complement activation in tumour necrosis factor-induced lethal hepatitis.
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Caspase-1 is not involved in experimental hepatitis in mouse.