Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.2.1.17 (lysozyme)
21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

For the isolation of human lysozyme from the urine of leukemia patients, a simple method has been established which involves precipitation of urinary proteins by 60% saturation with ammonium sulfate, fractionation of crude lysozyme on Sephadex G-50 and purification by CM-Sepharose chromatography. By this method approximately 60% of the lysozyme in the urine was isolated in a pure state in ten days.
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PMID:Isolation of human urinary lysozyme. 71 8

134 cases of acute leukemia in adults were classified according a "double blind" cytological diagnosis, a cytochemical study, and lysozyme assay. Each type has distinct characters, allowing a good nosological definition. The histochemical methods, as well as lysozyme assay are usually unnecessary, particularly in well differenciated myeloblastic, promyelocytic or myelo-monocytic acute leukemia. They are, on the contrary, frequently useful in poorly differenciated myeloblastic or monoblastic leukemia. But, they cannot help to solve every problem in cytological diagnosis: there are still 10% of undifferenciated acute leukemia, the lymphoblastic acute leukemia are not clearly defined and 4% of cases of acute leukemia have atypical characters leading to difficulties in cytological classification. The need for new methods and markers is emphasized.
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PMID:[Cytological classification of adult acute leukemia (author's transl)]. 79 Feb 73

Cytochemical and electron-microcopic studies have been carried out on leukemic monocytes and 'hairy cells' (HC), 'reticulosarcoma' (RS) cells and cells of cases of 'reticulosis' and 'reticulosarcoma cell leukemia'. Additional investigations included equantitative determinations of the urinary lysozyme excretion, skin window studies, testing of the phagocytosis of ferritin by HC, and labelling of the Fc receptors on CH at the ultrastructural level. Clear evidences against any cytological relationship among leukemic HC and monocytes have been provided. Further results argued also against the frequently stressed relationship among leukemic monocytes and RS cells. Cases of 'RS cell leukemia' and 'reticulosis' had to be reclassified as lymphosarcoma cell leukemia, acute lymphatic, and myeloblastic leukemias. Besides distinct ultrastructural differences among HC, RS cells, and lymphocytes, mainly gradual differences have been noted using cytochemical methods and by evaluating the phagocytosis of ferritin particles. A further common trait of HC, RS cells, and B lymphocytes seems to be the presence of surface Fc receptors. A more precise classification instead of the diagnosis 'reticulosarcoma' and 'reticulosarcoma cell leukemia' is required, and the use of the term 'hairy cell' leukemia is suggested stead of the misleading term 'leukemic reticuloendotheliosis'.
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PMID:Hairy cell leukemia ('leukemic reticuleondotheliosis'), reticulosarcoma, and monocytic leukemia. Cytochemical and ultrastructural investigations. 80 67

The unsaturated vitamin B12-binding capacities of the 'large molecular size vitamin B12-binding protein' (LBP) and the 'small molecular size vitamin B12-binding protein' (SBP) were determined by a Sephadex G 150 gel filtration method in 9 patients with chronic myelocytic leukaemia (CML), 5 patients with blast cell leukaemia and 12 patients with non-neoplastic leucocytosis. EDTA plasma and serum separated after 20 min and after 120 min were examined. In the 20 min EDTA plasma samples, the mean LBP value was 8,009 pg/ml in CML, 2,468 in blast leukaemia, 175 in non-neoplastic leucocytosis, and 57 in normal controls. The in vitro release of LBP into serum was much smaller in the leukaemias than in non-neoplastic leucocytosis. No correlation was found between the LBP values and the white blood cell counts or lysozyme values, but lysozyme was correlated to white cell count in CML. It is suggested that the plasma LBP levels reflect the fraction of LBP decay taking place at sites, e.g. the spleen, from which the released LBP can enter the circulation.
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PMID:Granulocyte release of vitamin B12-binders in vivo and in vitro in leukaemia and non-neoplastic leucocytosis. 81 75

A gradient was developed for isoelectric focusing in the pH range 2-5. Cobalophilin (earlier called R proteins or vitamin B12-binding proteins of R-type) was isolated from saliva and amniotic fluid in homogeneous form. It was found to be a glycoprotein with a molecular weight of 59,300-69,100. The preparation from amniotic fluid contained 33% carbohydrate. Cobalophilin variants in plasma, serum, granulocytes, platelets, amniotic fluid, milk, saliva and gastric juice were characterized by isoelectric focusing. Most fluids and cells contained the same isoproteins, with pI values between 2.3 and 5.0. Isoproteins of presumably myelogenic origin (e.g. those in granulocytes and plasma) had pI values below 4.2, whereas those of glandular origin (in milk and saliva) had a pI range of 4.0-5.0. Serum contained more cobalophilin than plasma, owing to release of this protein from granulocytes during clotting. This phenomenon also changed the isoprotein pattern. Plasma and serum from newborn infants and from patients with leucocytosis, polycythaemia vera and chronic myelogenous leukaemia contained the same isoproteins as were found in plasma from healthy subjects. In addition to these, isoproteins with lower than 'normal' pI values were often found in chronic myelogenous leukaemia and occasionally in leucocytosis. It is concluded that cobalophilin from different fluids and cells is a single microheterogeneous protein with a variable carbohydrate composition. The distribution of cobalophilin in different body fluids and cells supports the suggestion that cobalophilin is an antimicrobial protein (Gullberg 1972) like lactoferrin and lysozyme.
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PMID:Vitamin B12-binding proteins of r-type, cobalophilin. 105 22

Two cases of the development of acute myeloid leukemia (AML) after treatment with alkylating agents are reported. In Case 1, melphalan and then cyclophosphamide had been given for multiple myeloma. 46 months after onset of cytostatic treatment AML occurred, as confirmed cytochemically and by qualitative determination of urinary lysozyme. In Case 2, cyclophosphamide had been given for rheumatoid arthritis. After a latency of 34 months 'smouldering leukaemia' developed with an atypical monocytic leukaemic cell population. In a third case, multiple myeloma and monocytic leukaemia developed synchronously. The causative role of melphalan and cyclophosphamide in the development of AML seems securely established. Despite the risk of alkylating agents in the treatment of multiple myeloma or Hodgkin's disease causing AML, they should not be replaced, as other drugs have been shown to be less beneficial. On the other hand, alkylating agents should be used with great caution in the treatment of non-malignant diseases.
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PMID:[Plasmocytoma, alkylating agents, and acute myeloid leukemia (author's transl)]. 105 6

Purified human lysozyme (muramidase) stimulated potassium excretion by the isolated perfused rat kidney. Lysozyme is filtered and reabsorbed, without a tubular maximum. Over 90% of lysozyme filtered is retained within the kidney; 50% was recovered by enzymic assay and histologically localized to the proximal tubular cells. Hypokalaemia seen in some patients with myelomonocytic leukaemia may be directly attributed to an elevated circulating lysozyme level.
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PMID:Effect of human lysozyme (muramidase) on potassium handling by the perfused rat kidney. A mechanism for renal damage in human monocytic leukaemia. 105 11

Pretreatment serum lysozyme activity was high in 2 children with myelomonocytic leukemia, 800 and 1 000 mug/ml, normal in all 10 cases of acute lyelocytic leukemia and subnormal in 21 of 34 cases of acute lymphocytic leukemia. Normal values were found in all but one case of acute lymphocytic leukemia during complete remission including 8 cases after all therapy had been discontinued. All 8 are still in complete remission. Low serum lysozyme activity was found in 5 patients with acute lymphocytic leukemia in complete relapse, this could possibly be helpful in the diagnosis of early relapse. Activity was subnormal in 5 of 17 children with malignant tumours, and in 3 of 65 cases of various benign hematological disorders.
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PMID:Serum lysozyme activity in children with hematological and malignant disorders. 105 25

The natural history and haematological features of 18 patients with a chronic form of myelomonocytic leukaemia are described. The majority were elderly and, in this series, females predominated. Haematological prodomata, such as unexplained monocytosis, leucopenia, or thrombocytopenia were common, and the clinical onset was insidious. Splenomegaly was variable but tended to increase as the disease progressed. Anaemia was usually less than in the acute disease, unless compounded by iron deficiency. The blood film typically showed a mixed monocytosis and granulocytosis, cells in both lines showing abnormalities. 'Paramyeloid' cells, appearing in Romanowsky stained films intermediate between myelocytes and monocytes, were characteristic, although cytochemical and electron microscopical analysis suggests that these cells may be allotted to one or other cell line. The marrow aspirate was characteristically hypercellular, showed granulocytic hyperplasia, and, in contrast to the well-differentiated blood picture, the proportion of poorly differentiated cells, including blasts, was high. Serum lysozyme levels were usually raised. Five of the 18 cases survived more than 5 years, while 10 lived 2 years or longer. The morphological and clinical features form part of a spectrum including acute myelomonocytic leukaemia, into which several of the patients transformed. Recognition of the syndrome is important because the patients are probably best managed without intensive chemotherapy.
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PMID:Chronic myelomonocytic leukaemia. 105 74

Lysozyme [EC 3.2.1.17] was purified from human tears, serum, and urine of acute monocytic leukemia patients, renal disease patients, and residents in cadmium-polluted areas of Tsushima Island using an affinity adsorbent containing lysozyme-lysate of Micrococcus lysodeikticus cell walls as the ligand. By means of this procedure, leukemia lysozyme was purified 100- to 200-fold with an activity recovery of 80%. It was crystallized at pH 10. This purified preparation appeared homogeneous in disc electrophoresis and showed a specific activity 2.5-fold higher than that of crystalline lysozyme from hen egg-white. Tear lysozyme was also purified to a nearly homogeneous state while the enzymes from normal serum and urine of a nephrosis patient and of residents in cadmium-polluted area were still disc electrophoretically heterogeneous and showed low specific activity as compared with purified leukemia lysozyme.
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PMID:Affinity chromatographic purification of human lysozyme, with special reference to human leukemia lysozyme. 107 Apr 87


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