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Y Matzner

Publications and source records attributed to Y Matzner.

At least 37 records · Page 2Linked to original sources
PubMed1988

Generation of lipid neutrophil chemoattractant by irradiated bovine aortic endothelial cells.

Radiation injury to blood vessels is associated with an acute inflammatory process. We investigated the capacity of cultured bovine aortic endothelial cells (BAEC) to produce chemotactic factors after radiation injury. BAEC in serum-free media were irradiated with a cobalt-60 Gammacell 220 and the cell supernatants were assayed for chemotactic activity for human neutrophils in a Boyden chamber. There was a rapid release of chemotactic activity into the BAEC supernatants which was dependent both on the dose of radiation (5 to 40 Gy) and the time between irradiation and sample collection. In contrast, isolation of BAEC lysates by freeze-thawing was not associated with the presence of similar chemotactic activity. The chemotactic activity released from the irradiated BAEC was not destroyed by boiling nor by treatment with trypsin. The release of the chemotactic activity was, however, inhibited by the addition of a lipoxygenase inhibitor but not by the addition of a cyclooxygenase inhibitor before the irradiation. The chemotactic activity was recovered from the cell supernatants in the lipid phase after extraction with chloroform/methanol. Furthermore, the chloroform/methanol extracts co-eluted with authentic leukotriene B4 when the BAEC were prelabeled with [14C] arachidonic acid. However, we were unable to detect endogenous leukotriene B4 with RIA. Instead, the only detectable endogenous lipid present in the supernatants was 13-hydroxyoctadecadienoic acid which is derived from linoleic acid via the lipoxygenase pathway. 13-Hydroxyoctadecadienoic acid, however, had no chemotactic activity. These findings suggest that endothelial cells rapidly release a chemotactic agent after irradiation, the release of which is associated with a lipoxygenase pathway. The release of this chemotactic activity may account in part for the acute inflammatory response that is observed after ionizing irradiation.

Animals↗
PubMed1988

Glibenclamide causing thrombocytopenia and bleeding tendency: case reports and a review of the literature.

We described two patients with severe thrombocytopenia and bleeding tendency related to treatment with glibenclamide (short-acting sulfonylurea). To the best of our knowledge, thrombocytopenic purpura associated with this medication has been reported only twice previously. We suggest that platelet count should be carried out early after initiating glibenclamide treatment and every 3 months thereafter.

Diabetes Mellitus, Type 2↗
PubMed1988

Decreased neutrophil thromboxane A2 and endothelial PGI2 production in the postoperative period. An in vitro assay for detection of neutrophil and plasma dysfunction.

Severe trauma results in reversible abnormalities in neutrophil function, but the specific role in the pathogenesis of postoperative sepsis is undetermined. Twenty adult patients undergoing elective surgical procedures were studied. Blood samples were obtained prior to and 24 hours after operation. Blood neutrophils were isolated and incubated (10(7) cells/mL) on bovine vascular endothelial cell monolayers. Untreated plasma or zymosan-activated plasma (ZAP) or 65 C inactivated plasma was added, and TxB2 and 6-keto PGF1 alpha production measured after 2 hours. Endothelial damage was detected by light and scanning electron microscopy beginning 2 and 4 hours after treatment. Preoperatively, neutrophil TxB2 release was less than 200 pg/mL; following ZAP it was 2153 pg/mL (p less than 0.001), with untreated plasma 1055 pg/mL (p less than 0.005) and inactivated plasma 764 pg/mL (p less than 0.01). Neutrophil TxB2 release on a plastic dish was not different from incubation on endothelium. Endothelial 6-keto PGF1 alpha release following addition of untreated plasma preoperatively was 1308 pg/mL (p less than 0.01), and with ZAP 1305 pg/mL (p less than 0.01). Activated neutrophils did not alter 6-keto PGF1 alpha production. Postoperatively, neutrophil TxB2 production in response to ZAP was 1092 pg/mL, which was significantly reduced compared to the preoperative response (p less than 0.01). Endothelial damage by activated neutrophils in the postoperative period demonstrated on scanning electron microscopy was also reduced; 6-keto PGF1 alpha release in the postoperative period inducted by ZAP was 569 pg/mL and by untreated plasma 549 pg/mL, which was significantly lower than in the preoperative period (p less than 0.05 and p less than 0.05, respectively). No difference in chemotaxis was demonstrated. It is concluded that operative trauma is followed by lowered neutrophil TxB2 release, appearance of a plasmatic factor that depresses endothelial 6-keto PGF1 alpha production, as well as decreased neutrophil-induced endothelial damage. The neutrophil-endothelial monolayer system is a sensitive method for detection of neutrophil and plasmatic dysfunction.

Adult↗
PubMed1988

Differential induction of monocytic functions by dibutyryl cyclic AMP and retinoic acid in a human monoblast cell line U937.

Differentiation-inducing agents have recently been applied clinically in various myeloproliferative diseases, based on their in vitro ability to induce differentiation in myeloid and monocytic cell lines. In this study we compared the abilities of two agents, dibutyryl cyclic AMP (DBcAMP) and retinoic acid (RA) to induce monocytic functions in the human histiocytic lymphoma cell line U937. Both agents produced similar induction of phagocytosis and reduction of nitroblue tetrazolium (NBT). Other monocytic functions, including accumulation of lysozyme, spontaneous and directed migration toward zymosan-activated serum (ZAS), the chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) and leukotriene B4 (LTB4) were induced by DBcAMP, while RA induced migration toward LTB4 only. Simultaneous treatment with both inducers proved synergistic only with respect to phagocytosis. NBT reduction and migration toward FMLP and LTB4 were unchanged, while migration toward ZAS and lysozyme accumulation were suppressed by the addition of RA. The results suggest that the inducer affects the expression of cellular functions and characteristics specific to a particular lineage. In addition, the data presented indicate that the U937 cell line may serve as an excellent model system for the study of the regulation and mechanisms of chemotactic receptor expression in monocytes.

Bucladesine↗
PubMed1987

Serum ferritin in patients undergoing bone marrow transplantation.

Serum ferritin levels were monitored in nine patients with acute lymphoblastic leukemia (ALL), nine patients with acute nonlymphoblastic leukemia (ANLL), four patients with chronic myelogenous leukemia (CML), three patients with non-Hodgkin's lymphoma (NHL), and three patients with severe aplastic anemia (SAA) undergoing bone marrow transplantation (BMT) for hematologic malignancies or aplastic anemia. Serum ferritin analysis was performed before and after BMT at monthly intervals and/or according to the clinical condition of the patient. Serum ferritin increased considerably during the first 3 months following BMT and then decreased in patients with an uncomplicated course. Ferritin levels in the serum of patients who had undergone BMT decreased gradually when complete remission was achieved, but increased with any clinical complication. Thus, elevation of serum ferritin concentration was predictable for clinical complications and for relapse. Patients with acute leukemia with serum ferritin levels above 400 micrograms/l at time of BMT had a risk of relapse within 1 year, triple that patients with lower ferritin levels. All patients who underwent BMT to treat severe aplastic anemia have completely recovered. Accordingly, following an initial increase after BMT, serum ferritin levels returned to normal and remained so in line with the patients' good clinical condition. The findings indicate that serum ferritin yields useful information in the clinical evaluation of patients undergoing BMT.

Adolescent↗
PubMed1987

Cord compression as the presenting symptom of extradural malignant lymphoma.

Six patients with spinal cord compression as the presenting symptom of malignant lymphoma are described. These patients suffered from back pain for several months and were diagnosed after sudden paraparesis appeared. Five patients were treated by operative decompression followed by local irradiation, and all regained their motor function. A sixth patient presented with a more insidious paraparesis. A bone marrow aspiration established the diagnosis of malignant lymphoma, and this patient recovered with radiation and steroids alone. Thus, we recommend considering malignant lymphoma as a possible cause of acute cord compression, attempting to establish the diagnosis on an emergency basis within several hours, and attempting to achieve decompression with local radiotherapy and intravenous dexamethasone.

Adult↗
PubMed1987

HLA-B51 may serve as an immunogenetic marker for a subgroup of patients with Behçet's syndrome.

Epidemiologic data, family history, clinical data, HLA typing, neutrophilic chemotaxis, and immunofluorescence of clinically normal non-sun-exposed skin were studied in 46 Israeli non-Ashkenazi Jewish and Arab patients with Behçet's syndrome. HLA-B51 was present in 71 percent of the patient group as compared with 13 percent of the control group (relative risk = 17.1). In four of 30 families in the B51-positive group, there was a close relative of the proband with Behçet's syndrome who was carrying the HLA-B51 antigen. Neutrophilic chemotaxis in this group was enhanced in 80 percent of the patients, and in most patients no deposition of immunoglobulin in the dermo-epidermal junction was observed, whereas C3 was present in papillary vessels. In the B51-negative group, the family history was negative for Behçet's syndrome, neutrophilic chemotaxis was enhanced in only two of eight patients, and in four of six patients, IgM deposition was detected in the dermo-epidermal junction. It is concluded that in Israeli non-Ashkenazi Jews and Arabs, there is a significant association between HLA-B51 and the risk of developing Behçet's syndrome. The B51-positive patient group has a family history of the disease, enhanced neutrophilic chemotaxis, and a lack of immunoglobulin deposition in the dermo-epidermal junction.

Behcet Syndrome↗
PubMed1987

Expression of granulocytic functions by leukemic promyelocytic HL-60 cells: differential induction by dimethylsulfoxide and retinoic acid.

Recently, a novel approach has been used in the treatment of leukemia: induction of the leukemic cells to undergo terminal differentiation. Based on its in vitro ability to induce differentiation in several myeloid leukemic cell lines, retinoic acid (RA) has been applied clinically in cases of myelodysplastic syndromes and acute myeloid and promyelocytic leukemia. In the present study we have determined in detail the ability of RA to induce expression of granulocytic functions in a human promyelocytic leukemia cell line (HL-60) and compared it with that of dimethylsulfoxide (DMSO). Several granulocytic characteristics (phagocytosis, surface adherence and generation of free radicals in response to phorbol-ester) were induced to the same degree by both agents. Other normal neutrophil functions, including lysozyme accumulation, spontaneous migration, chemotactic activity toward zymosan-activated serum (containing C5a), the peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) and spontaneous motility in semi-solid medium were induced by DMSO, but they were absent or incompletely expressed in RA-induced cells. In contrast, only RA induced migration toward leukotriene B4 (LTB4). Simultaneous treatment with RA and DMSO proved synergistic with respect to morphological maturation and several functions (e.g. NBT reduction), but complementary stimulation of other activities (e.g. chemotaxis, lysozyme content) could not be demonstrated. Furthermore, characteristics induced by DMSO (i.e., expression of C5a and FMLP receptors and accumulation of lysozyme) were inhibited by the addition of RA.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Adhesion↗
PubMed1987

Neutrophil function studies in clinical medicine.

A complete evaluation of neutrophil function including: chemotaxis; adhesion; aggregation; phagocytosis; granule content and degranulation; respiratory burst activity; and bacterial killing; is expensive and requires the services of a specialized laboratory. However, preliminary screening of a patient with a predisposition toward infection, can be carried out using simple and inexpensive methods. These include examination of blood films, which may prove helpful in the diagnosis of Chediak-Higashi syndrome and specific granule deficiency; the Rebuck skin window test, which estimates chemotactic defects; the NBT test, which screens for chronic granulomatous disease patients; and peroxidase staining of the blood film in order to estimate the content of myeloperoxidase, when myeloperoxidase deficiency is suspected. For final diagnosis and determination of genetic transmission and radical treatment, ie, bone marrow transplantation, specific tests are indicated. Neutrophil function studies have also proved useful in detecting diseases in which defects in neutrophil function are secondary to the primary disorder. Indeed, increased neutrophil chemotaxis has been reported in the active phase of diseases such as: familial Mediterranean fever; psoriasis vulgaris, Behcet's syndrome and Sweet's syndrome. In these disorders the neutrophil chemotaxis assay has aided in the diagnosis and follow-up, particularly in evaluating the response to antiinflammatory agents, such as colchicine.

Cell Adhesion↗
PubMed1987

Sweet's syndrome.

Sweet's syndrome (acute neutrophilic dermatosis) is characterized by fever; polymorphonuclear neutrophilic leukocytosis; elevated ESR; and characteristic, raised, painful red plaques on the face and limbs. Since Sweet first described the syndrome in 1964, more than 150 cases have been reported, but it is assumed that the disorder is far more common than this number would indicate.

Acute Disease↗
PubMed1987

Idiopathic thrombocytopenic purpura presenting as iron-responsive thrombocytopenia.

We describe a patient with iron-deficiency anemia, thrombocytopenia and paucity of marrow megakaryocytes, in whom the anemia and the thrombocytopenia responded to the administration of iron. Thrombocytopenia recurred, despite maintenance of normal hemoglobin and iron levels and adequate marrow megakaryocytes. Corticosteroids and splenectomy were required for the control of the thrombocytopenia. In this patient, the initial manifestations of idiopathic thrombocytopenic purpura were modified by the presence of severe iron deficiency. This case strengthens the contention that iron is essential for megakaryopoiesis and thrombopoiesis.

Anemia↗
PubMed1987

Inhibition of heparanase-mediated degradation of extracellular matrix heparan sulfate by non-anticoagulant heparin species.

Incubation of human platelets, human neutrophils, or highly metastatic mouse lymphoma cells with sulfate-labeled extracellular matrix (ECM) results in heparanase-mediated release of labeled heparan sulfate cleavage fragments (0.5 less than Kav less than 0.85 on Sepharose 6B). This degradation was inhibited by native heparin both when brought about by intact cells or their released heparanase activity. Degradation of heparan sulfate in ECM may facilitate invasion of normal and malignant cells through basement membranes. The present study tested the heparanase inhibitory effect of nonanticoagulant species of heparin that might be of potential use in preventing heparanase mediated extravasation of bloodborne cells. For this purpose, we prepared various species of low-sulfated or low-mol-wt heparins, all of which exhibited less than 7% of the anticoagulant activity of native heparin. N-sulfate groups of heparin are necessary for its heparanase inhibitory activity but can be substituted by an acetyl group provided that the O-sulfate groups are retained. O-sulfate groups could be removed provided that the N positions were resulfated. Total desulfation of heparin abolished its heparanase inhibitory activity. Heparan sulfate was a 25-fold less potent heparanase inhibitor than native heparin. Efficiency of low-mol-wt heparins to inhibit degradation of heparan sulfate in ECM decreased with their main molecular size, and a synthetic pentasaccharide, representing the binding site to antithrombin III, was devoid of inhibitory activity. Similar results were obtained with heparanase activities released from platelets, neutrophils, and lymphoma cells. We propose that heparanase inhibiting nonanticoagulant heparins may interfere with dissemination of bloodborne tumor cells and development of experimental autoimmune diseases.

Animals↗
PubMed1986

Cerebrospinal fluid ferritin in malignant CNS involvement.

Cerebrospinal fluid (CSF) ferritin was measured in patients with benign inflammatory and noninflammatory neurologic disorders and in patients with malignant disease with and without documented central nervous system (CNS) involvement. CSF ferritin levels were increased in the majority of patients with inflammatory neurologic disease and in patients with malignant involvement of the CNS. In contrast, in patients with noninflammatory neurologic disorders and in malignant disease without CNS involvement, CSF ferritin levels were normal. These findings indicate that although the specificity of CSF ferritin measurement is limited, it is a highly sensitive test that may be useful in the initial evaluation of patients with malignant CNS involvement, and in assessing their response to therapy.

Adult↗
PubMed1986

Production of C5a antagonist by synovial and peritoneal tissue fibroblasts.

Fibroblasts grown from synovial and peritoneal tissues release into the medium an inhibitor of neutrophil chemotaxis. The inhibitor resembles the antagonist previously described in synovial and peritoneal fluids. It is a heat stable (56 degrees C) protein of MW approximately 40 kDa that counteracts the chemotactic activity of zymosan-activated serum or purified C5a but not the peptide chemoattractant F-met-leu-phe. No chemotactic inhibitor was detected in media from skin fibroblast cultures or in formal human sera. It is suggested that the inhibitor is produced locally by synovial and peritoneal fibroblasts and that it might play a role in the regulation of inflammation at sites lined with mesothelium.

Chemotactic Factors↗
PubMed1985

Isolation and fractionation of ferritin from human term placenta--a source for human isoferritins.

A method for isolating ferritin from human term placenta was described. The placenta was homogenized in water containing protease inhibitor and heated at 70 degrees C. The ferritin was precipitated with ammonium sulfate at pH 5.2 and purified by repeated cycles of ultracentrifugation and molecular sieve chromatography through Sepharose 4B columns. Isoelectric focusing revealed a broad spectrum of isoferritins. These isoferritins were separated by ion-exchange chromatography on Sephadex A-25 at pH 7.5 and stepwise elution with increasing concentrations of NaCl. By this method "basic," "intermediate," and "acid" isoferritins were separated. The most basic placental isoferritin was shown to be identical to splenic ferritin by isoelectric focusing, subunit analysis, and fluorescent ELISA. The acid placental isoferritin had similar characteristics to heart-type ferritin. It was suggested that the easily available placental tissue could serve as a source for human isoferritins in research and in clinical assays.

Carbonic Anhydrases↗