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Biomedical subjects

Y Sultan

Publications and source records attributed to Y Sultan.

At least 127 records · Page 7Linked to original sources
PubMed1984

An immunoradiometric assay for factor VIII related antigen (VIIIRAg) using two monoclonal antibodies-comparison with polyclonal rabbit antibodies for use in von Willebrand's disease diagnosis.

Two monoclonal antibodies raised against FVIII/von Willebrand protein were used in an immunoradiometric assay (IRMA) to measure this antigen in normal plasma and plasma of patients with different forms of von Willebrand's disease. The first antibody, an IgG1, was used to coat polystyrene tubes, the second one, an IgG2a, iodinated and used in the second step. Both antibodies inhibit ristocetin induced platelet agglutination and react strongly with platelets, megakaryocytes and endothelial cells. The IRMA test using these antibodies showed greater sensitivity than that using rabbit polyclonal anti VIIIRAg antibodies. A good correlation between the two tests was nevertheless found when VIIIRAg was measured in the majority of patient's plasma. However 5 patients from 3 different families showed more antigenic material in the rabbit antibody IRMA than in the monoclonal antibody IRMA. It is suggested therefore that the monoclonal antibodies identify part of the VIIIR:Ag molecule showing structural abnormalities in these vWd patients, these structural changes remaining undetected by the polyclonal antibodies.

Animals↗
PubMed1984

Anti-idiotypic suppression of autoantibodies to factor VIII (antihaemophilic factor) by high-dose intravenous gammaglobulin.

In two patients with high-titre autoantibodies to antihaemophilic factor (VIIIc), treatment with high-dose intravenous immunoglobulin (IVIg) resulted in rapid and prolonged, although not total, suppression of antibody. IVIg also inhibited anti-VIIIc activity in patients' plasma in vitro; IVIg and F(ab')2 fragments from IVIg inhibited anti-VIIIc activity of the IgG fraction and of the Fab'2 fragments of the IgG fraction from patients' plasma, indicating that the in-vivo effect of IVIg was due to the presence in the therapeutic immunoglobulins of anti-idiotypic antibodies against idiotypes expressed by anti-VIIIc autoantibodies. In contrast, IVIg had little or no effect on antibody titre in two haemophilic patients with anti-VIIIc alloantibodies. These observations suggest that IVIg contains anti-idiotypes against autoantibodies and may be effective in the treatment of some autoimmune diseases through idiotypic/anti-idiotypic interactions.

Adolescent↗
PubMed1984

A solid-phase fibrin immunoassay for the specific detection of monoclonal antibodies against different epitopic determinants of tissue-plasminogen activators.

The selective detection of hybridomas producing monoclonal antibodies against tissue-plasminogen activators (t-PA) by means of a solid-phase fibrin immunoassay (SOFIA) is described. The screening method is based on the specific and high affinity binding of t-PA for fibrin solid phase. This, as in the physiological fibrin-t-PA interaction, provides a molecular structure conserving its antigenic and functional properties. The solid-fibrin-state support is prepared by thrombin proteolysis of fibrinogen coupled to a poly-glutaraldehyde activated polyvinylchloride plate. This procedure avoids fibrinogen desorption and provides a uniform fibrin network onto which t-PA from crude extracts or purified preparations, can be specifically absorbed. The fibrin-t-PA solid-phase support is able to fix anti-t-PA antibodies which can be subsequently revealed by a second enzyme- or radiolabelled anti-mouse Ig antibody. The results demonstrate the effectiveness of the SOFIA method for the selection of hybridomas producing anti-t-PA antibodies against different epitopic determinants of t-PAs.

Animals↗
PubMed1984

[Lymphocyte subpopulations in hemophilic patients].

Monoclonal antibody analysis of peripheral blood T-cell subsets was performed in 23 multitransfused haemophiliacs, 5 children and 10 adults. Although none of the patients exhibited symptoms of acquired immune deficiency, 5 of them showed an abnormally low proportion of T-cells with reversal of the OKT4 (helper/inducer) to OKT8 (cytotoxic/suppressor) ratio. No evidence of cytomegalovirus infection was found. A search for antibodies to human leukaemia virus antigen P24 gave negative results. The relationship between this abnormality and transfusions is discussed.

Adolescent↗
PubMed1984

Use of monoclonal antibody and colloidal gold in E.M. localization of von Willebrand factor in megakaryocytes and platelets.

The subcellular localization of Factor VIII/von Willebrand protein (VIII R:Ag) is studied with monoclonal antibody and gold immunocytochemical technique. Monoclonal antibody against purified VIII R:Ag is brightly fluorescent on megakaryocytes and platelets. In E.M., gold immunolabeling is performed on thin cell sections of human megakaryocytes and platelets. Different embedding materials are used to preserve the antigenicity : Epon embedded megakaryocytes show a high concentration of VIII R:Ag in alpha-granules using 4F9 monoclonal antibody. In comparison, lowicryl K4M embedded material does not improve the same specificity, only a few platelets granules were stained. This subcellular localization, in full agreement with biochemical results appears visualized for the first time in E.M.

Antibodies, Monoclonal↗
PubMed1984

Monoclonal antibodies against the human factor VIII von Willebrand molecule: characterization and potential for screening of von Willebrand patients.

Two new monoclonal antibodies (M.Abs) 4F91C5 and 202D3 which are capable of inhibiting ristocetin cofactor activity have been raised against high molecular weight detergent denatured Factor VIII/von Willebrand preparations. Characterized in a simple solid phase radioimmune binding assay (RIA) the binding activity of the two M.Abs can be shown to be absorbed by normal plasma, and plasma from type A hemophilia patients but not by plasma from patients suffering from severe von Willebrand disease. Both monoclonal antibodies are capable of inhibiting strongly the FVIII.vWF associated ristocetin cofactor activity. Competition radioimmune assays have shown that the two monoclonal antibodies recognize different epitopes on the Factor VIII/vWF molecule. This has been confirmed by the differential binding of the two M.Abs observed to monkey plasma. Whilst inhibition curves for the two M.Abs with normal plasma and FVIII/vWF preparations in solid phase RIA are similar, quite different reactivities with commercially available F VIII preparations have been found. The high sensitivity of these reagents for the FVIII/vWF molecule and their ability to inhibit strongly the associated biological activity suggest the potential usefulness of these monoclonal antibodies as diagnostic reagents.

Animals↗
PubMed1983

Immunocytochemical localization of factor VIII/von Willebrand factor antigen in human platelets.

Specific antibodies against anti-human FVIII/vW protein were isolated by affinity chromatography on glutaraldehyde-activated gel (Ultrogel AcA22). They were coupled directly with peroxidase or visualized with anti-rabbit IgG (sheep)-peroxidase (Institut Pasteur). Fab fragments of the same specific antibodies were prepared to enhance the intracellular penetration and coupled to peroxidase. In washed human platelets, staining was observed on the plasma membrane and in the canalicular system, whereas in previous studies whole specific antibodies incubated with fixed platelets showed the labeling only on the plasma membrane. After thrombin activation, the release of granules containing FVIII/vW protein was better visualized in the surface canalicular system. This localization was discussed in regard to the exocytosis process: membrane fusion, granule labeling.

Antigens↗
PubMed1982

Monoclonal antibodies against human factor VIII molecular neutralize antihemophilic factor and ristocetin cofactor activities.

A series of monoclonal antibodies have been raised against a preparation of the factor VIII/von Willebrand factor molecule. Of the seven hybridomas showing specific activity against the factor VIII molecule in a solid-phase radioimmunoassay, three (F4.55, F4.77, and F4.264) have been shown to partially inhibit ristocetin-induced platelet aggregation and two (F4.115 and F4.415) inhibit the antihemophilic activity of the factor VIII molecule. An additional monoclonal antibody was directed against a contaminant of the factor VIII preparation and is an antifibrinogen antibody.

Animals↗
PubMed1982

Localization of factor VIII/von Willebrand factor antigen by immunoelectron microscopy in human endothelial cells using Fab fragments coupled to peroxidase.

Factor VIII/von Willebrand factor antigen (VIII R:Ag) has been localized in human endothelial cells by an immunoperoxidase method and electron microscopy. Specific antibodies against VIII R:Ag were isolated from monospecific rabbit antisera by an immunoadsorbant. Fab fragments were prepared and coupled to peroxidase. Native human endothelial cells from umbilical cord veins were incubated with the Fab conjugates. Peroxidase labeling was seen on the plasma membrane, in vesicles, and in the Golgi apparatus. In order to eliminate nonspecific antibody internalization, the same procedure was reproduced on fixed endothelial cells and similar localization was observed. Staining was only found when specific VIII R:Ag Fab conjugates were used. All the controls were devoid of labeling, thus the peroxidase reaction product localized in the Golgi cisternae is specific for VIII R:Ag and suggests VIII R:Ag synthesis in endothelial cells.

Antigens↗
PubMed1981

[Intra-osseus hemorrhagic lesions in congenital afibrinogenemia. A new case (author's transl)].

Congenital afibrinemia is a rare disease, transmitted by an autosomal recessive mode, and due to deficient fibrinogen. Osseous involvement is exceptional, since only 2 cases have been reported. We describe a third case. The roentgenographic features are well limited radiolucent lesions, arising in the medullary space, and slightly expanding. These lesions are related to fibrous cysts, resulting from intraosseous hemorrhages. Spontaneous resolution may occur: the absence of fibrin deposits and blood clot probably favours resorption.

Afibrinogenemia↗
PubMed1980

Circulating immune complexes containing anti-VIII antibodies in multi-transfused patients with haemophilia A.

Evidence for the presence of circulating immune complexes was found in thirty-four out of fifty-five samples from forty-seven patients with haemophilia A. In eleven patients the complexes, precipitated from the blood with polyethylene glycol, were digested with pepsin. The F(ab')2 antibody was tested, and found to have neutralizing activity against coagulant Factor VIII in two patients. In one of these no free antibody had ever been found in the plasma, while in the other the antibody was concentrated tenfold in the complex. In two other samples free without complexed antibody was found. In comparison, IgG-containing complexes were found in nine out of nineteen patients with von Willebrand's disease and no complexes were found in the sera from twelve multi-transfused thalassaemics. PEG precipitation is a useful technique for the preparation of concentrated immune complexes for further study such as antigen identification.

Adolescent↗
PubMed1979

[Purification of the vascular plasminogen activator].

We have isolated a purified preparation of the vascular plasminogen activator. Plasma obtained from post occlusion venous blood has been chromatographed with low and high ionic strength buffers. The purified protein has a relative molecular weight of 71,000.

Fibrinolysis↗
PubMed1979

[Disseminated intravascular coagulation (D.I.C.) and fibrinolysis in patients with acute leukemia (author's transl)].

Biological symptoms of D.I.C. were investigated in 43 patients with acute leukemia. Ten of them were found to be positive either at the onset or at the relapse of the disease and in some cases D.I.C. was triggered by chemotherapy. Among the ten positive cases 3 patients had an acute promyelocytic leukemia, 4 had an acute lymphoblastic leukemia, 2 a myeloblastic and 1 a monoblastic leukemia. D.I.C. was found either in patients with an hypercellular form of the disease or in patients with a normal or low white cell count. Symptoms of D.I.C. in acute leukemia must be systematicaly sought at the onset and during treatment by chemotherapy and treated with heparin and platelet transfusions as it is now admitted for acute promyelocytic leukemia.

Acute Disease↗