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)

Chicken erythrocyte histone H5 has been suggested repeatedly to be a general suppressor of transcription and replication. Therefore, the biological functions of H5 were investigated and compared with those of H1 (H1a + H1b) by microinjection of the purified proteins into proliferating L6 rat myoblasts. By pulse-labelling of the injected cells with [3H]uridine and [3H]thymidine it was shown that H5 blocked both transcription and replication substantially, and that the chromatin of the injected cells became densely compacted. H1 also suppressed these functions, but to a much lesser degree. The effects were specific and not caused by change in intracellular pH caused by introduction of the very basic H5, or its non-specific interaction with nucleic acid, since injection of protamine or lysozyme did not affect the cells. The migration and localization of injected H5 was monitored at different times after injection by immunofluorescence, which revealed that H5 was efficiently and stably concentrated in the nucleus. The results indicate that H5 indeed might function as an inactivator of the erythroid genome in its natural environment, probably by keeping the chromatin in a very condensed state.
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PMID:Chicken histone H5 inhibits transcription and replication when introduced into proliferating cells by microinjection. 307 39

To determine changes in the cell lineages of metaphases karyotyped following different culture times, marrow from 11 healthy individuals was studied using a technique that allows simultaneous analysis of karyotype and cell lineage. Cell lineage was identified as erythroid by surface glycophorin A, granulocytic by Sudan black B and PM-81, and monocytic by lysozyme. Marrow examined sequentially showed granulocytic mitoses to initially decrease from a mean of 40% at 1.75 hr to 6% at 3.5 hr and then increase, being 46% by 6 hr and 82% after 1 day, and remain high for the 10 days studied. Erythroid mitoses were most frequent (mean, 72%) at 3.5 hr and then decreased rapidly, being 16% by 6 hr, 7% at 1 day, and absent thereafter. When granulocytic mitoses were least frequent, 20-36% of mitoses were also unreactive with glycophorin A. Double staining experiments to identify these cells found some to be monocytic, but most remained unidentified. The authors conclude that mitoses of different hematopoietic lineages predominate when normal marrow is studied cytogenetically at different times following aspiration, and that the major changes occur during the first 8 hours. These findings have importance for how cytogenetic studies are performed in leukemia.
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PMID:Bone marrow cytogenetics: the lineage of dividing cells changes during the first few hours in culture. 366 33

A retrospective analysis of 30 patients with chronic myelomonocytic leukemia (CrMML) was performed to define the natural history of the disease and the risk of acute transformation. Our patients fulfilled the following criteria of diagnosis: blood monocytosis over 1 X 10(9)/l, blast cell percentage in bone marrow up to 30, and in peripheral blood less than 5. The most common presenting feature was anemia; seven patients had fever; three patients complained of purpura and bleeding. Anysopoikilocytosis and macrocytosis were frequent. Abnormal granulocyte morphology, defective granulation and abnormal leukocyte alkaline phosphatase were often observed. Blast cells in peripheral blood smears were found in 14 patients. Serum and urine lysozyme levels were increased in 82 per cent and 93 per cent, respectively. Dysplastic changes involving erythroid, granulocytic and megakaryocytic lineages were constant features in all cases. Agranulated blasts above 5 per cent of marrow nucleated cells were seen in 13 patients (43 per cent). Seven of the 20 patients showed non-specific chromosomal abnormalities at diagnosis. Median survival from diagnosis was 18 months (range, 3-112). Evolution into acute myeloid leukemia occurred in 11 patients. No difference in survival was found between patients who developed acute leukemia and patients who did not. A shorter survival has correlated to the following parameters: leukocytes greater than 10 X 10(9)/l, the presence of blasts in peripheral blood and agranulated blasts in the marrow above 5 per cent.
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PMID:Chronic myelomonocytic leukemia: clinical features, cytogenetics, and prognosis in 30 consecutive cases. 386 Apr 66

Human bone marrow was cultured and cells from individual monocyte colonies stained with a variety of polyclonal and monoclonal antibodies. Erythroid colonies and peripheral blood monocytes were used as controls. Both bone marrow cultured and peripheral blood monocytes stained with antibodies to lysozyme, non-specific cross reacting antigen (NCA) and alpha-1-antitrypsin and the cells stained variably for HLA-DR. A small number of cells in each cultured bone marrow colony stained with antibody to human thymic antigen (HTA T6) and most of the cells stained with variable intensity using anti-S-100 protein. No cells reactive with these two antibodies were detected in peripheral blood monocyte preparations and erythroid colony cells were negative for all antigens studied. The presence of cells within individual bone marrow colonies with phenotypic properties of both phagocytic macrophages (lysozyme positive, NCA positive, alpha-1-antitrypsin positive) and Langerhans cells/interdigitating reticulum cells (HTA(T6) positive, S-100 protein positive) suggests that these cells share a common stem cell and are both components of the mononuclear phagocyte system.
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PMID:Immunocytochemical characterization of monocyte colonies of human bone marrow: a clue to the origin of Langerhans cells and interdigitating reticulum cells. 389 94

The extension of myeloproliferative malignant tumors to lymph nodes was studied in seven excision biopsies and 27 autopsies in which lymph nodes were obtained from all nodal regions. We observed the proliferation of poorly, partially, and well differentiated neoplastic cells with a predominance of immature cells of the granulocytic series and fewer cells of the erythroid and megakaryocytic cells lines. Disturbances of the lymph node architecture consisted of invasion by abnormal cells of the trabecular stroma, disrupting the reticulin mesh and extending toward the pericapsular area. In the lymph node a loose network of thin and thick fibers replaced the original framework. Generalized lymph node involvement at autopsy showed preservation of the architecture, both in cases with total replacement of the lymphoid population by abnormal cells and in cases with involvement by single cells or small groups of cells. Partial involvement occurred chiefly in the medullary zone, probably the result of hematogenous dissemination from the vascular plexus in medullary cords. Further abnormal cell development was linked to trabecular infiltration. The extensive involvement seen at autopsy took place by lymphatic dissemination. In lymph nodes studied at autopsy an abnormal immunoblastic reaction was observed. At first these abnormal cells were suspected of representing the myeloproliferative malignant disease, but the application of special staining techniques revealed their polyclonal cytoplasmic immunoglobulins. The chloroacetate esterase stain and the immunohistochemical stains for muramidase and hemoglobulin were especially useful in demonstrating that myeloproliferative diseases develop in the environment found in lymph nodes.
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PMID:Nonlymphoid hematopoietic malignant disease of the lymph nodes. 617 May 64

The bone marrow biopsy specimens of 35 patients with benign and malignant erythroid hyperplasias were examined for the presence of hemoglobin A, hemoglobin F, muramidase (lysozyme), and transferrin, using an indirect immunoperoxidase method (PAP) on Zenker's-fixed paraffin-embedded bone marrow biopsy specimens and particles. Five cases of each of the following entities were studied: erythroleukemia and erythremic myelosis, acute granulocytic leukemia with maturation (FAB M2), polycythemia rubra vera, myeloproliferative syndrome in childhood, megaloblastic anemia (B12 and folate deficiency), erythroid hyperplasia (regenerating bone marrow and hemolytic anemia), and Ph' chromosome positive chronic granulocytic leukemia. Hemoglobin A was present in both the early and late erythroid precursors in all conditions. Hemoglobin F was the predominant hemoglobin in early erythroblasts of pernicious anemia and in both early and late erythroid elements in erythroleukemia and erythremic myelosis. Small quantities of hemoglobin F were present in a few isolated clusters in other conditions. Staining for hemoglobin F may be useful in identifying immature erythroid precursors and in distinguishing some cases of dysplastic erythroid hyperplasia from neoplasia. Additionally, these findings suggest that the maturational switch in hemoglobin synthesis operates with distinct pathways under different conditions.
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PMID:An immunohistochemical study of hemoglobin A, hemoglobin F, muramidase, and transferrin in erythroid hyperplasia and neoplasia. 619 99

Mice were immunized with purified eosinophils obtained from patients with the idiopathic hypereosinophilic syndrome. A hybridoma initially producing an IgM antibody which switched to an IgG1 antibody was selected for cloning and further testing. This IgG1 antibody reacted with human eosinophils, granulocytes, monocytes and large granular lymphocytes, but did not react with T lymphocytes, B lymphocytes, platelets, erythrocytes, or a panel of human leukemia cells and cell lines. Bone marrow analysis revealed staining of myeloid precursor cells but not erythroid precursors or plasma cells. This IgG1 antibody had no effect on aggregation of granulocytes, lysozyme release, superoxide production, chemotaxis, or killing activity; however, there was some stimulation of beta-glucuronidase secretion. While the antibody did not augment the killing of Staphylococcus aureus by granulocytes, the antibody itself was bactericidal. By immunoprecipitation of granulocytes, eosinophils and monocytes, a molecule with a molecular weight of 95 kD was identified.
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PMID:Monoclonal antibody to human eosinophils recognizing 95 kD surface membrane antigen. 667 4

Myelomonocytic myeloproliferative disease in a horse was diagnosed on the basis of hematologic, enzymatic, and histopathologic findings. It was characterized clinically by depression, weight loss splenomegaly, lymphadenopathy, coagulopathy, and bacteremia. Hematologic findings included severe refractory anemia, thrombocytopenia, monocytosis, and pleomorphic leukocytes, with a left shift of the myeloid series. The serum lysozyme concentration was 14.5 microgram/ml (normal, less than 5 microgram/ml). The bone marrow contained many immature cells of the myeloid series and had a myeloid-to-erythroid ratio of 30.5 to 1. The horse died after brief hospitalization. Necropsy revealed generalized lymphadenopathy and hemorrhages throughout the body. Histopathologically, primitive cells were seen in several tissues. Cells that proliferated in the bone marrow were primarily myeloblastic, with some additional erythropoietic cells. Myeloblastic cells with evidence of normal erythropoiesis were seen in numerous lymph nodes and in the spleen, whereas primarily normal erythropoietic cells proliferated in the adrenal glands. Myeloid blast-type cells predominated in the lungs, myocardium, liver, and kidneys.
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PMID:Myelomonocytic myeloproliferative diseases in a horse. 705 85

Six children with severe congenital neutropenia and repeated life-threatening infections were investigated by examining clinical features and myeloid cell ultrastructure, cytochemistry, and in vitro proliferation. Despite the presence of neutropenia, normal numbers of colony-forming cells (CFC) were present in blood and marrow specimens, and colony-stimulating activities (CSA) from blood cells and serum were normal or slightly increased in all patients. In vitro maturation of the progenitors to neutrophils was also uniformly present in the colonies. No patients had demonstrable antineutrophil antibodies or serum inhibitors of myelopoiesis. Serum lysozyme levels were normal. Ultrastructural and cytochemical studies of directly sampled marrow cells revealed several abnormalities in most neutrophilic myeloid cells from each of the patients consistent with an intrinsic myeloid precursor cell defect. These included (1) the defective synthesis or degeneration of primary granules, (2) an absence or marked decrease of secondary granules in the few late neutrophils observed in the bone marrow, and (3) the presence of autophagy. Phagocytosis of intact myeloid cells with subsequent degeneration was not observed; however, neutrophil debris was evident in phagocytic vacuoles of marrow macrophages. Our demonstration of ultrastructurally dysmorphic neutrophilic granulocytes, intramedullary cell lysis, normal stem cell numbers, and negative serology is comparable to similar observations of erythroid cells from patients with congenital dyserythropoietic anemia. We therefore hypothesize that the dysgranulopoiesis in these children results in neutropenia and propose the descriptive name congenital dysgranulopoietic neutropenia.
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PMID:Congenital dysgranulopoietic neutropenia: clinical, serologic, ultrastructural, and in vitro proliferative characteristics. 740 13

Using an in vitro expansion and differentiation system for human CD34+ cord blood (CB) progenitor cells, we analyzed the induction and expression kinetics of the granulomonocyte associated lysosomal proteins myeloperoxidase (MPO), lysozyme (LZ), lactoferrin (LF), and macrosialin (CD68). Freshly isolated CD34+ CB cells were negative for LZ and LF, and only small proportions expressed MPO (4% +/- 2%) or CD68 (3% +/- 1%). Culturing of CD34+ cells for 14 days with interleukin (IL)-1, IL-3, IL-6, stem cell factor, granulocyte-macrophage colony-stimulating factor (GM-CSF), and G-CSF resulted in on average a 1,750-fold amplification of cell number, of which 83% +/- 7% were MPO+. Without addition of GM-CSF and G-CSF, lower increases in total cell numbers (mean, 211-fold) and lower proportions of MPO+ cells (54% +/- 11%) were observed. The proportion of MPO+ cells slightly exceeded but clearly correlated with the proportion of cells positive for the granulomonocyte associated surface molecules CD11b (Mac-1), CD15 (LeX), CD64 (Fc gamma RI) CD66, or CD89 (Fc alpha R). At day 14 MPO+ and LZ+ cells were virtually identical. However, at earlier time points during culture (days 4 and 7), single MPO+ or LZ+ cell populations were also observed, which only later acquired LZ and MPO, respectively. Maturation of cells into the neutrophilic pathway was indicated by the acquisition of MPO, followed by LZ. In contrast, maturation of cells into the monocytic pathway was indicated by the acquisition of LZ followed by MPO and CD14. CD68 was found to be expressed at day 4 by the majority of cells and was not restricted to the granulomonocytic cells, as cells with megakariocytic (CD41+) or erythroid (CD71hi) features were CD68+. LF expression was observed only in GM- plus G-CSF-supplemented cultures, in which only 26% +/- 5% of cells expressed LF by day 14.
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PMID:Granulomonocyte-associated lysosomal protein expression during in vitro expansion and differentiation of CD34+ hematopoietic progenitor cells. 749 68


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