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esterase/necrose

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BACKGROUND Myocardial injury from ischemia can be aggravated by reperfusion of the jeopardized area. The precise underlying mechanisms have not been clearly defined, but proinflammatory events, including complement activation, leukocyte adhesion, and infiltration and release of diverse mediators,

[The application of unspecific esterase reaction to the study of cell necrosis].

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Expression of eotaxin, interleukin 13 and tumour necrosis factor-alpha in dermatitis herpetiformis.

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BACKGROUND The dermal and perivascular infiltrate in dermatitis herpetiformis (DH), which is mainly composed of CD4+ lymphocytes, neutrophils and eosinophils, is believed to play an important part in the pathogenesis of the disease. Previous studies suggest that cytokines such as interleukin (IL)

Tumor necrosis factor alpha: a costimulator for cytotoxic cell differentiation.

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Large granular lymphocytes (LGL) can be activated by interleukin-2 (IL-2) into lymphokine-activated killers (LAK). Tumor Necrosis factor alpha was found to act synergistically with very low concentrations of IL-2 which were ineffective by themselves in inducing LAK activity. We demonstrate that the

Tumor necrosis factor-alpha and interleukin-1 beta production by human fetal Kupffer cells.

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This study describes the isolation and characterization of human fetal Kupffer cells. We demonstrated that these cells have the potential to respond to cytokines and lipopolysaccharide with an increased production of tumor necrosis factor-alpha and interleukin-1 beta. Kupffer cells were

Measurement of tumor necrosis factor activity by flow cytometry.

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Tumor necrosis factor-alpha (TNF-alpha) is a monokine of 17 kDa produced by activated macrophages and various cells involved in the immune system. We propose a new method for the measurement of TNF activity using flow cytometry. After an incubation with TNF, L929 cells were harvested and treated
OBJECTIVE To clarify the relationship between changes in haemodynamics, liberation of tumour necrosis factor and generation of plasma kallikrein, and to see if treatment with a combination of drugs was successful in preventing activation of tumour necrosis factor and plasma kallikrein in

Effects of C1-esterase inhibitor in three models of acute pancreatitis.

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The present studies were done to evaluate the therapeutic potential of C1-esterase inhibitor in three different models of acute pancreatitis: (1) Edematous pancreatitis with acinar cell necrosis was induced by 7-h ip injections of 50 micrograms/kg cerulein in mice; (2) Hemorrhagic pancreatitis was

Cocaine hepatotoxicity: influence of hepatic enzyme inducing and inhibiting agents on the site of necrosis.

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Cocaine-induced hepatotoxicity has been reported in human beings and is well documented in mice. One interesting feature of this toxicity that appears to be common to both species is an apparent shift in the intraacinar site of necrosis under circumstances known to alter cocaine metabolism. However,
We have previously noted that the glutamine antagonist acivicin (alpha S,5S-alpha-amino-3-chloro-4,5-dihydro-5-isoxazoleacetic acid) induces monocytoid differentiation of freshly isolated human myeloid leukemia cells and cells of the myeloid leukemia cell line HL-60, and that the differentiation is
We describe the effects of stem cell factor (SCF) on the dendritic cell (DC) pathway and provide evidence for the existence of a post granulocyte-macrophage colony-forming unit (GM-CFU) DC progenitor. When employed with cytokines regulating DC development (tumor necrosis factor [TNF] + GM
Natural or recombinant human tumor necrosis factor (TNF) induced NBT-reducing activity of ML-1 cells in a dose-dependent manner. Interferon-gamma (IFN-gamma) induced NBT-reducing activity only marginally. However, when IFN-gamma was combined with TNF, induction of NBT-reducing activity was

Effects of choline-esterase inhibitor in experimental acute pancreatitis in rats. Preliminary results.

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Choline-esterase inhibitor (C1-INH), a regulatory alpha-glycoprotein, was administered at different dosages and intervals to rats with induced acute pancreatitis. When compared to controls, treated rats showed no significant differences in the severity of histopathological lesions, such as edema and
OBJECTIVE Myocardial injury from ischemia can be augmented after reperfusion due to proinflammatory events including complement activation, leukocyte adhesion, and release of various chemical mediators. It has been shown that intracoronary administration of a C1 esterase inhibitor (C1 INH)

Study of esterase-positive cells in swine atherosclerosis.

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Non-specific esterase activity was studied by light and electron microscopic histochemistry after 6 mos of progression of injury and diet-induced atherosclerotic lesions in the swine aorta, and after 6 wks, 5 mos and 14 mos on regression regimen. At each time period three cellular patterns of
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