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Biomedical subjects

H Northoff

Publications and source records attributed to H Northoff.

At least 73 records · Page 4Linked to original sources
PubMed1994

Reactivation of antibodies of donor and recipient origin to platelet antigens early after allogeneic bone marrow transplantation: a case report.

Reactivation of platelet-reactive antibodies of donor and recipient origin is described in a patient following allogeneic BMT (donor: anti-HPA-5b; recipient: anti-HLA, anti-HPA-1b). The antibodies were detected around day 15 after BMT, peaked around day 25, and then decreased. These antibodies are interpreted as an antigen-independent reactivation of secondary B-cell responses, activated in the context of recognition of host antigens by the graft.

Adult↗
PubMed1994

A simple technique for red blood cell removal in major ABO-incompatible bone marrow transplantation.

A simple technique for red blood cell (RBC) removal in major ABO-incompatible bone marrow transplantation is reported requiring two centrifugation steps, special blood bags and a mechanical device to separate the buffy coat from RBCs within the bag. In 42 transplantations an average of 84% of nucleated cells was recovered with an average contamination of 7.5 ml packed RBCs. The preparations were well tolerated in all patients whose isoagglutinin titers had not been reduced. Bone marrow engraftment was not significantly different from control groups.

Adult↗
PubMed1994

[Demonstration of platelet-specific alloantibodies in HLA-sensitized hematologic oncologic patients].

Alloimmunization to the platelet-specific antigen systems HPA-1, -3 and -5 was studied in 59 multitransfused patients (31 females, 16 males, 12 children) with haematologic-oncologic disorders. All patients tested had broad-reacting or multispecific HLA antibodies. Of these, 10 (17%) were found to have additional platelet-specific alloantibodies. With respect to HLA sensitization, 9 out of 10 platelet-specific alloantibodies were found in sera which showed HLA antibodies reacting with more than 95% of unselected panel cells. Determination of antibody specificity revealed 6 patients with anti-HPA-1b, one patient with anti-HPA-3a, and 2 patients with anti-HPA-1b combined with anti-HPA-3a. One patient had anti-HPA-5b; in retrospect, only the HPA-5b antibody was demonstrable before the beginning of transfusion therapy and before HLA sensitization.

Adult↗
PubMed1993

CDw60 glycolipid antigens of human leukocytes: structural characterization and cellular distribution.

Monoclonal CDw60 antibodies recognize glycolipid antigens with restricted surface expression on human leukocytes. They allow us to define new functional subpopulations of T lymphocytes and are able to induce costimulatory signals. In this report, we describe the molecular composition of CDw60 glycolipid antigens derived from different human leukocyte subpopulations. The glycolipids were isolated and their structures were identified by immunochemical methods. All molecules containing the CDw60 determinant were found in the disialoganglioside fraction. They were O-acetylated derivatives of the gangliosides II3 (Neu5Ac)2-LacCer (GD3), IV3 (Neu5Ac)2-nLc4Cer (DSPG), and VI3 (Neu5Ac)2-nLc6Cer (DSnHC), respectively. The most common CDw60 glycolipid antigen in human leukocytes was 9-O-acetyl GD3. In a comparison of various cell types, the highest concentration of 9-O-acetyl GD3 on a per cell basis was determined in granulocytes and in blood T lymphocytes, whereas B lymphocytes, thymus cells, and monocytes contained considerably smaller amounts of this molecule. Polar CDw60 antigens such as 9-O-acetyl DSPG and 9-O-acetyl DSnHC were only detected in granulocytes.

Amino Acid Sequence↗
PubMed1993

Serological screening, using three different test systems of platelet-transfused patients with hematologic-oncologic disorders.

Sera of hematologic-oncologic patients were tested regularly after platelet transfusions in three test systems: lymphocytotoxicity test, platelet adhesion immunofluorescence test, and--only selected sera--in the monoclonal antibody-specific immobilization of platelet antigen test. Of 388 patients 53 (14%) had HLA antibodies 5 of these in combination with platelet-specific alloantibodies. Lymphocyte-restricted (non-HLA) reactions were observed in 20 patients, the majority of which was attributed to lymphocyte-specific auto- or alloantibodies. Sera of 27 patients showed platelet-specific reactions, usually cold-reacting autoantibodies which have no effect in vivo.

Adult↗
PubMed1993

Prevention of endotoxin-induced monokine release by human low- and high-density lipoproteins and by apolipoprotein A-I.

Interaction of endotoxin (lipopolysaccharide [LPS]) with human lipoproteins is known to prevent the LPS-induced activation of human monocytes and release of cytokines (monokines). LPS was exposed to lipoprotein classes separated by ultracentrifugation and to apolipoprotein A-I. Then monocytes were added, and the LPS activation of monocytes was determined by measuring the induced monokines. Failure of LPS to induce monokine release was called LPS inactivation caused by lipoproteins or apolipoproteins. The LPS inactivation is shown to be a function of low-density lipoproteins. High-density lipoproteins inactivate LPS to a much lesser extent. The very-low-density lipoproteins cannot inactivate LPS. Lipid components seemed not absolutely required for LPS inactivation, because purified human apolipoprotein A-I without its physiological lipid complement also inhibits LPS-induced monokine release.

Adult↗
PubMed1992

CDw 60 antibodies bind to acetylated forms of ganglioside GD3.

Four monoclonal antibodies, M-T21, M-T32, M-T41 and UM4D4, which belong to the new CDw 60 cluster of antibodies specific for a subpopulation of human T-lymphocytes, were found to bind mainly to acetylated forms of ganglioside GD3. After O-deacetylation of the antigen, binding was reduced ("M-T"-antibodies) or abolished (UM4D4).

Acetylation↗
PubMed1992

Growth control of cultured microglia.

Microglia, the resident macrophages of the brain, typically react to injuries or chronic diseases with proliferation and expression of differentiated features, such as production of cytokines associated with inflammatory events. Regulation and control of microglial cytokine expression, therefore, is a major focus of scientific interest. It has been shown that GMCSF and Il-3 are potent mitogens for microglia. Moreover, Il-3 and other cytokines are products of microglia. It is shown here that interleukin-1 (Il-1) as well as tumor necrosis factor (TNF alpha) increased microglial proliferation in mixed astrocyte-microglial cultures but had no mitogenic effects on isolated microglia. Lipopolysaccharide (LPS), the bacterial endotoxin, irreversibly inhibited microglial cell division in both mixed astrocyte-microglial cultures and in isolated microglial cultures. By contrast, the corticosteroids hydrocortisone and aldosterone and the synthetic glucocorticoid dexamethasone reversibly inhibited microglial proliferation. They also antagonized the stimulatory effects of Il-3 and granulocyte macrophage colony-stimulating factor (GMCSF). Estradiol and progesterone had no significant effects on mixed cultures but inhibited microglial proliferation in isolated cultures. Conditioned media from mixed cultures, isolated cultures, from the WEHI-2B cell line, or from fresh (serum-supplemented) media stimulated microglial proliferation to various extents. In summary, cytokine-mediated microglial proliferation can be down-regulated by a variety of steroid hormones. Along with their unimpaired access to brain cells in general, corticosteroids likely maintain an inhibitory tonus on microglial proliferation. It is hypothesized that this inhibition is overcome locally and temporally in brain injury and repair.

Acid Anhydride Hydrolases↗
PubMed1992

Results of the DGTI workshop on the evaluation of the reactivity of monoclonal anti-D.

All D+ samples were detected by all monoclonal antibodies without problems. Very few of the 3000 D- samples showed a +/- to ++ reaction with some of the IgG type mabs using the Coombs technique. It is still open whether these are specific reactions with weak positive samples, which were negative with polyclonal sera. IgM type mabs detected up to 100% of the Du samples dependent on the Rh-phenotype and the technique used (CCDuee greater than CcDuee greater than ccDuEe). Most of the CCDuee samples reacted very strong and should no longer be regarded as Du.

Antibodies, Monoclonal↗
PubMed1992

Biocompatibility of synthetic oxygen carriers and fluorosurfactants.

A system for testing the biocompatibility of synthetic oxygen carriers is described including tests of hemolysis, complement activation and proliferation of cell lines or lymphocytes. Of 17 surfactants tested in this system, 6 were compatible in all tests while the other compounds showed individually differing patterns of incompatibility. We conclude that, in order to conduct a meaningful screening, a series of different assays has to be applied. In addition to our system, further assays, covering cytokine induction and phagocytosis should be attempted.

Blood Substitutes↗
PubMed1992

The role of lipoproteins in the inactivation of endotoxin by serum.

The lipopolysaccharide (LPS)-induced release of cytokines from human monocytes can be prevented by previous interaction of serum with LPS. This inactivation is a function of lipoproteins. Here we show that LPS can be inactivated by low-density lipoproteins (LDL) as well as by high-density lipoproteins (HDL). The effects of heparin and EDTA on LPS inactivation by serum are also described.

Bacterial Toxins↗
PubMed1992

Low density lipoproteins inhibit endotoxin activation of monocytes.

Human serum and low density lipoproteins (LDLs) were shown to inactivate endotoxin (lipopolysaccharide [LPS]) by testing the effect of LPS interactions with serum or LDL on the activation of human monocytes. Sera and LDL preparations from four patients with familial hypercholesterolemia were used to demonstrate the inhibition of LPS from inducing interleukin-1 release. Before LDL removal by immunoapheresis, the patients' sera were able to inactive approximately fivefold more LPS than after LDL removal. The LPS-inactivating capacity lost during apheresis could essentially be retrieved in the LDL-rich eluate from the immunoadsorption columns. Because patients were treated frequently with immunoapheresis, their LDL levels before LDL removal were not markedly elevated. These patients' sera before LDL removal were shown to inactivate amounts of LPS comparable to those inactivated by the sera from three healthy volunteers. LDL prepared by ultracentrifugation showed similar LPS inactivation as LDL prepared by immunoapheresis. We conclude that the inhibition of LPS-induced monocyte activation by human serum is dependent to a large extent on the LDL fraction. LDLs were demonstrated to inhibit LPS from inducing interleukin-1 release by human monocytes.

Adult↗
PubMed1992

Syntheses, interfacial active properties and toxicity of new perfluoroalkylated surfactants.

New surfactants have been synthesized with perfluorohexyl-groups as hydrophobic tail, a polyethyleneglycol-methylether as hydrophilic head and a prolongator between them. The prolongator units are -C4H8-, -C2H4OC5H10-, -C2H4OC3H6C(O)- and -CH2CH(OEt)CH2-. The surface tension, CMC and the interfacial tension water/perfluorocarbon were measured and the surface excess concentrations of the surfactant molecules were calculated. The influence of the surfactants on in vitro proliferation of human cell lines Hela and Molt 4 was investigated as a parameter for biocompatibility. The influence of the surfactants led to a reduction of cell proliferation depending on the concentration and chemical nature of the surfactant. Thus the prolongators changed the properties of the surfactants. They reduced the interfacial tension water/perfluorocarbon and improved the biocompatibility of surfactants.

Biocompatible Materials↗
PubMed1992

The role of lipoproteins in inactivation of endotoxin by serum.

Lipopolysaccharide (LPS)-induced release of cytokines from human monocytes can be prevented by previous interference of serum with LPS. This inactivation is a function of lipoproteins. Here we show that low-density lipoproteins as well as high-density lipoproteins can inactivate LPS. The effects of heparin and EDTA on LPS inactivation by serum are also described.

Cytokines↗
PubMed1992

ABO-incompatible bone marrow transplantation.

In the past 10 years 201 HLA-identical bone marrow transplantations (BMT) were performed with major ABO incompatibility in 41 (20%) and minor ABO incompatibility in 35 (18%) patients. ABO compatibility between donor and recipient showed no influence on granulocyte and platelet recovery after BMT. Erythrocyte reconstitution was significantly (p < 0.01) delayed for about 1 week in major ABO-incompatible BMT. In addition, a pure red cell aplasia lasting for 2-5 months occurred in 6 out of 21 blood group 0 patients who received transplants of group A. The rate of graft rejection, incidence of graft-versus-host disease as well as the leukemic relapse rate were similar in ABO-compatible and ABO-incompatible BMT. The probability of a 10-year survival after BMT is independent of ABO compatibility between donor and recipient.

ABO Blood-Group System↗
PubMed1992

Results of the DGTI workshop on the evaluation of the reactivity of monoclonal anti-D.

All D+ samples were detected by all monoclonal antibodies (mabs) without any problem. Very few of the 3,000 D- samples showed a +/- to ++ reaction with some of the IgG type mabs using the Coombs technique. It is still open whether these are specific reactions with weakly positive samples, which were negative with polyclonal sera. IgM type mabs detected up to 100% of the Du samples dependent on the Rh phenotype and the technique used (CCDuee > CcDuee > ccDuEe). Most of the CCDuee samples reacted very strongly and should no longer be regarded as Du.

Antibodies, Monoclonal↗
PubMed1992

Biocompatibility of synthetic oxygen carriers and fluorosurfactants.

A system for testing the biocompatibility of synthetic oxygen carriers is described including tests of hemolysis, complement activation and proliferation of cell lines or lymphocytes. Of 17 surfactants tested in this system, 6 were compatible in all tests while the other compounds showed individually differing patterns of incompatibility. We conclude that, in order to conduct a meaningful screening, a series of different assays has to be applied. Addition to our system of further assays covering cytokine induction and phagocytosis should be attempted.

Biocompatible Materials↗