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Interleukin-1 and tumour necrosis factor are involved in cutaneous hyperalgesia.
The mechanism is thought to be mediated by tumour necrosis factor inhibition.
Little information is currently available on the role of interleukin 1 and tumour necrosis factor in inflammatory bowel disease.
Infliximab works by binding tumour necrosis factor alpha.
Additional products (tumour necrosis factor, therapeutic enzymes)
Epithelial cells showed no expression of tumour necrosis factor or interleukin 1 mRNA.
It is a monoclonal antibody that inhibits the pro-inflammatory cytokine tumour necrosis factor alpha.
Adalimumab, marketed as Humira, like infliximab is an antibody that targets tumour necrosis factor.
The mechanism is unknown, although it has been suggested that activation of tumour necrosis factor (TNF) may be responsible.
Tumour necrosis factor mRNA was detected in four of nine controls compared with 11/15 inflammatory bowel disease patients.
Structurally, it is unlike any other superantigen, but is remarkably similar the Tumour necrosis factor and viral capsid proteins.
Tumour necrosis factor, interferon alfa, and interleukin 2 have already been expressed and secreted in high concentrations within certain tumours.
For example, experimental staphylococcal enterotoxin shock depends on superantigen-induced release of tumour necrosis factor mediated via T cells.
Mutations in RHBDF2 inhibit tumour necrosis factor alpha.
Serum zinc and copper in active rheumatoid arthritis: correlation with interleukin 1 beta and tumour necrosis factor alpha.
It causes toxic shock syndrome (TSS) by stimulating the release of large amounts of interleukin-1, interleukin-2 and tumour necrosis factor.
Infliximab, marketed as Remicade, is a mouse-human chimeric antibody that targets tumour necrosis factor, a cytokine in the inflammatory response.
Endo et al have shown that tumour necrosis factor, transforming growth factor, and interleukin-8 increase ET-1 synthesis in guineapig tracheal epithelial cell cultures.
The induction of KCC3 is up-regulated by vascular endothelial growth factor and down-regulated by tumour necrosis factor.
This reduces expression of tumour necrosis factor (TNF), interleukin 1α and β, and interleukin 6.
The tumour necrosis factor signal was located mainly in the deeper lamina propria whereas the interleukin 1β was seen in subepithelial macrophages.
This study cannot conclude with certainty the nature of the cells expressing mRNA for interleukin 1 or tumour necrosis factor, although the majority are probably macrophages.
Double labelling studies will be required to show definitely that tumour necrosis factor mRNA and RFD9 antigen are expressed by the same cells.
Increased values of tumour necrosis factor (TNF-α) were also found during intestinal perfusionof the patients and correlated with those of IL-8.
Helson L, Green S, Carswell E, et al.: Effect of tumour necrosis factor on cultured human melanoma cells.