Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this paper we show that TNF-alpha enhances platelet activation. Experiments were performed on a human polymorphonuclear neutrophil (PMN)-platelet cooperation system in which PMN, stimulated by FMLP, release cathepsin G (Cat.G), a serine proteinase responsible for the activation of nearby platelets. Pretreatment of the mixed cell suspension with 5 ng/ml TNF-alpha resulted in a strong platelet activation (37.7 +/- 3.2% aggregation; 46.0 +/- 14.4% serotonin release) in response to a weak concentration of FMLP (1.25 x 10(-8) M) inducing by itself only 7.7 +/- 4.0% of aggregation and 3.8 +/- 4.1% of serotonin release (mean +/- SD; n = 10). This effect was concentration dependent (maximum between 5 and 10 ng/ml) and was optimal for a brief preincubation time (5 min). Under these experimental conditions the target of TNF-alpha was PMN, as shown by beta-glucuronidase release. The observed potentiation was modified neither by 0.1 mM acetyl salicylic acid (a cyclo-oxygenase inhibitor) nor by 0.1 mM BN 52021 (a platelet-activating factor antagonist), while such a phenomenon was fully inhibited by 20 micrograms/ml eglin C, a strong and specific inhibitor of the human granulocytic proteinases, elastase and Cat.G. In fact, full inhibition was also observed with 300 nM alpha-1-antichymotrypsin, a specific inhibitor of Cat.G. This clear-cut evidence of Cat.G involvement was substantiated by the enhancement of Cat.G release from FMLP-activated PMN primed with TNF-alpha. These results demonstrate that the priming of PMN by TNF-alpha may modulate the activation of other inflammatory cells, particularly of platelets. It is hypothesized that this phenomenon could contribute to pulmonary pathologies, and more specifically to the adult respiratory distress syndrome, a disease for which PMN, platelet and TNF-alpha involvement has been proposed.
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PMID:Tumor necrosis factor-alpha enhances platelet activation via cathepsin G released from neutrophils. 200 99

The present report describes the results of a combined morphological, enzyme- and immunohistochemical analysis of nine cases of malignant non Hodgkin's lymphomas (NHL) clinically presenting as lethal midline granuloma. In a previous report written before antibodies directed against B and T lymphocytes were available, a histiocytic origin of such neoplasms had been suggested. A panel of antibodies reactive with most B cells (L26, MB1, KiB3) and a majority of T cells (MT1, UCHL1) was applied on paraffin sections of formalin fixed tissues as well as antibodies directed against leukocyte common antigen (LCA), myeloid/histiocyte antigen (MAC 387), lysozyme, alpha-1-antitrypsin, alpha-1-antichymotrypsin, S-100 protein, prekeratin and immunoglobulin light chains. Enzyme histochemistry included tests for non-specific acid esterase, acid phosphatase, beta-glucuronidase and chloroacetate esterase. As a result, five T, two B and two unclassified (malignant histiocytosis probable) NHL were identified, indicating distinct heterogeneity of NHL as causative disorders in lethal midline granuloma.
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PMID:Heterogeneous malignant non Hodgkin's lymphomas as a causative disorder in lethal midline granuloma. 252 38

To study the derivation of tumor cells of malignant fibrous histiocytomas (MFH), their phenotypical marker profile was investigated and compared with those of malignant histiocytosis (MH) and of different types of soft tissue tumors (STT). The presence of the following markers was investigated: on paraffin sections, alpha-1-antichymotrypsin (ACT); on frozen sections antigens associated with lymphocytes, macrophages and fibroblasts, the enzymes acid phosphatase, nonspecific esterase, and beta-glucuronidase; and, on isolated and cultured cells, the receptors for EA-gamma and complement. Furthermore, the capacity to phagocytose sensitized erythrocytes and carbon particles was studied in vitro. MFH tumor cells and a part of other types of STT shared the expression of ACT and lysosomal enzymes with MH. They differed, however, from MH by the absence of monocyte/macrophage-associated antigens and by the expression of fibroblast-associated antigens, which property they had in common with other STT. MFH tumor cells were not able to form rosettes or to phagocytose Ig-sensitized erythrocytes, but they showed phagocytosis of carbon particles. The results strongly indicate that MFH tumor cells originate from (primitive) fixed mesenchymal cells and are not related to monocyte-derived histiocytes.
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PMID:A study to analyze the origin of tumor cells in malignant fibrous histiocytomas. A multiparametric characterization. 299 48

Five out of eight consecutive cases with initial symptoms of a 'midline granuloma' were identified as malignant histiocytosis (histiocytic sarcoma) which within 5 months to 4 years led to generalization and death. The three remaining cases also fulfilled the morphological criteria of this type of neoplasia, though these patients are still alive 1/2 to 8 years after diagnosis, possibly as a result of local radiotherapy. The age of the individuals ranged from 18 to 71 years and there was a male preponderance of 7:1. The histiocytic nature of the atypical cells was primarily documented by intense activity of NaF-inhibitable non-specific esterase, of acid phosphatase and of beta-glucuronidase as demonstrated in cryostat sections of formaldehyde-saccharose-fixed fresh biopsy specimens and by the detection of alpha-1-antichymotrypsin, alpha-1-antitrypsin, and lysozyme antigens, in that order of constancy (immunohistochemical examination of formaldehyde-fixed paraffin sections, using the avidin-biotin-peroxidase complex method). There was among the reported cases a considerable heterogeneity with regard to these 'markers'. We conclude that malignant histiocytosis is a (the?) major cause of the 'midline granuloma syndrome'.
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PMID:Malignant histiocytosis (histiocytic sarcoma). A (the?) major cause of the 'midline granuloma syndrome'. 351 40