cell

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cell

an independent team of operatives who work together in a CELLULAR MANUFACTURING production environment.
References in periodicals archive ?
Key words: Alcohol consumption; alcoholic liver disease; alcoholic liver injury; alcoholic hepatitis; alcohol-related liver inflammation; liver; immunity; innate immune response; adaptive immune response; macrophage; macrophage phenotypic switch; Kupffer cell
Hepatic injury by TNF-alpha is modulated by the prevalent pro-inflammatory or anti-inflammatory mediator profile elaborated by Kupffer cells (Kara et al.
Specific super-paramagnetic iron oxide-based (eg, ferucarbotran [Resovist; Schering, Berlin, Germany]) and manganese-based (ie, mangafodipirtrisodium [Tesla-scan; Nycomed Amersham, Oslo, Norway]) contrast media are targeted at the Kupffer cells and hepatocytes, respectively.
Numerical density of Kupffer cells on the area (Nak): It expresses the number of Kupffer cells per unit area (per [cm.
Some of the highlights include the concept of Kupffer cell activation and the role of these cells in liver inflammation, oxidative stress--related injury, stellate cell activation, and liver fibrosis.
Lead stimulates intercellular signalling between hepatocytes and Kupffer cells.
1991]: 'Ultrastructural and Immunohistologic Study of Kupffer Cells in Orthotopic Transplanted Rat Liver', Transplantation Proceedings, 23, pp.
Small Kupffer cell clusters and, rarely, discrete noncaseating granulomas or fibrin-ring granulomas, may be seen in Epstein-Barr virus infection of the liver.
MP, a naturally occurring fatty acid methyl ester, can be considered a universal macrophage inhibitor as it was shown to suppress isolated Kupffer cells, rat peritoneal macrophages and RAW cells.
Activation of toll-like receptor 3 attenuates alcoholic liver injury by stimulating Kupffer cells and stellate cells to produce interleukin-10 in mice.
Kupffer cell expressed membrane- bound TNF mediates melphalan hepatotoxicity via acti- vation of both TNF receptors.
Additional hepatic lesions analyzed as binary variables included steatosis, inflammation, Kupffer cell hyperplasia, oval cell hyperplasia, multinucleated hepatocytes, hepatocyte hypertrophy, and lipofuscin deposition.