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

Enzymaticaly homogeneous fractions of lymphocytes, monocytes, and neutrophils were isolated by zonal centrifugation from peripheral blood of a patient with hairy cell leukemia, or leukemic reticuloendotheliosis, LRE,(with leukopenia, neutropenia, lymphocytosis, and massive splenomegaly). To detect enzymatic deficiencies, the cells were analyzed quantitatively for six leukocytic enzymes on three occasions: 1) before splenectomy, 2) 5 days after splenectomy, and 3) 6 weeks after splenectomy. Before splenectomy, the patient's cells showed moderate deficiency of beta-glucuronidase in lymphocytes and monocytes; server to modorate deficiency of lysozyme and myeloperoxidase in monocytes and granulocytes; and complete absence of neutral protease and alkaline phosphates in neutrophils. Full restoration of neutral protease and a three-fold rise in alkaline phosphatase activities occurred in the patient's neutrophils 5 days after splenectomy. Lysozyme and myeloperoxidase returned to normal in both monocytes and neutrophils of the patient. Six weeks following splenectomy, the alkaline phosphatase activity again disappeared from patient's neutrophils, although neutral protease remained normal. The patient's lymphocytes were unresponsive to PHA and PW mitogen before splenectomy but became responsive 6 weeks postoperatively. Monocytic transfomation into macrophges was supressed before and after splenectomy. The findings indicate that developmenally, in lymphocytic leukemia, a biochemical defect involves the patient's monocytes and neutrophils much more severely than it affects the leukemic lymphocytes. Functionally, the results partly explain the susceptibility of LRE patients to microbial infections.
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PMID:Absence of neutral protease and alkaline phosphatase in neutrophils of a case of hairy cell leukemia. 43 13

Reticuloendotheliosis virus strain T (REV-T) is a highly oncogenic avian retrovirus which causes a rapid neoplastic disease of the lymphoreticular system. We derived six cell lines (1-3, 1-5, 2-10, 2-14, 2-16, and 2-20) from chicken spleen cells infected with REV-T. These cells can produce both the REV-T and its associated reticuloendotheliosis helper virus, REV-A. Histochemical analyses of these cells indicate that, while they are not stained by benzidine, peroxidase, beta-glucuronidase or acid alpha-naphthyl acetate esterase, they contain a high proportion (95%) of cells positive for acid phosphatase. Light and electron microscopic studies of these cells also revealed morphologies of lymphoblasts or activated lymphocytes with irregular nuclei and dispersed chromatin. Immunochemical analyses indicate that essentially all (90 to 100%) of the cells contain the surface marker Ia, but no cytoplasmic immunoglobulin M and immunoglobulin G could be detected by immunofluorescence staining. Results also show that some of these cell lines contain a low level of terminal transferase (0.02 to 0.17 unit/10(9) cells), and a proportion (3 to 35%) of these cells can be stained by an antiserum directed against chicken bursa cells. These results are consistent with the conclusion that the cells transformed by the highly oncogenic REV-T are lymphoid in nature. In addition, at least some of these cell clones may contain features characteristic of activated B-lymphocytes. Analysis of these cell clones indicates that some cell lines contain an adherent and nonadherent population with some differences in morphologies. In addition, electron microscopic examination revealed that, while the non-adherent cells are actively producing type C viruses, type C viruses are either absent or very rare in the adherent cell populations. These results support the conclusion that some of these cell lines are heterogeneous and contain subpopulations of cells with differences in their ability to produce viruses.
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PMID:Morphological, immunological, and biochemical analyses of chicken spleen cells transformed in vitro by reticuloendotheliosis virus strain T. 628 48