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Biomedical subjects

R Zubler

Publications and source records attributed to R Zubler.

10 recordsLinked to original sources
PubMed1988

[Reversal of positive serology for human immunodeficiency virus (HIV). Apropos of 2 case reports].

The medical history and laboratory data of two persons who have been in contact with HIV-I positive carrier individuals are reported. The serologic data of successive serum samples collected from these persons were first negative, then positive (including antibodies directed against Gag and Env gene products), and finally negative for presence of anti-HIV-I antibodies. Physical examination and other laboratory data, including absolute number of CD4 lymphocytes/mm3, were within the normal range in these two individuals, who presented a reversal of positive serology for HIV-I.

AIDS Serodiagnosis↗
PubMed1987

[Polyclonal B cell activation in infection caused by human immunodeficiency virus (HIV)].

87 patients with anti-HIV antibodies were divided into three groups based on the classification of the Centers for Disease Control and the following parameters reflecting polyclonal B cell activation were evaluated in these patients: immunoglobulin levels, circulating immune complexes and occurrence of autoantibodies. The results reported here indicate that intense polyclonal B cell activation occurs in both asymptomatic (CDC 2) and symptomatic patients (CDC 3 and CDC 4). Moreover, serological abnormalities were detected with similar frequency in the three groups studied.

Acquired Immunodeficiency Syndrome↗
PubMed1986

[Hemolytic anemia secondary to taking cyanidanol: demonstration of the mechanism of the erythrocyte damage].

A 36-year-old patient with chronic active hepatitis developed Coombs direct positive acute hemolytic anemia 2 weeks after a second course of cyanidanol (Cy). The patient's serum agglutinated control 0 Rh- erythrocytes only in the presence of Cy. Human anti-globulin test showed that the red cells were covered with IgG as well as C3 and C4. Control erythrocytes previously treated with Cy were also agglutinated by the patient's serum (dilution 1:64). Upon addition to the serum of Cy (concentration up to 10 micrograms/ml), the agglutination was enhanced up to a serum dilution of 1:256. Further increase of the Cy concentration (greater than 10 micrograms/ml) was followed by a decreased reaction. These results indicate that red cell damage in this patient was mediated by both mechanisms, i.e. with immune complexes acting on "normal" red cells and also with antibodies acting on cyanidanol-coated red cells.

Adult↗
PubMed1983

Prevention of cerebral malaria by adoptive transfer of malaria-specific cultured T cells into mice infected with Plasmodium berghei.

Murine T cell populations specific for Plasmodium berghei parasites were generated in vitro from BALB/c immune lymph node cells. The malaria-specific T lymphocytes were shown: a) to proliferate specifically in vitro in response to stimulation with P. berghei-infected red blood cells; b) to exhibit the Thy-1+, Lyt-1+2- cell surface phenotype; c) to provide specific helper activity for an in vitro anti-hapten (TNP) plaque-forming cell antibody response; and d) to protect P. berghei-infected mice from early mortality due to cerebral malaria.

Animals↗
PubMed1979

Complement activation in pneumonia.

Complement analyses performed on serially collected plasma samples from 10 patients during acute infectious pneumonia or bronchopneumonia showed normal or increased values for hemolytic activity and Clq, C4, C3, and factor B levels. However, the levels of C3 breakdown products (C3d) were significantly (greater than 2 SD) increased in six patients during the first three days of observation, suggesting that hypercatabolism of complement components may occur during the acute phase of infectious pneumonia concomitant with a hypersynthesis of some complement components. Evidence of circulating immune complexes was obtained only in two patients with the 125I-Clq Binding Test.

Acute Disease↗
PubMed1979

Decreased heat-labile opsonic activity and complement levels associated with evidence of C3 breakdown products in infected pleural effusions.

Heat-labile opsonic activity was measured simultaneously in serum and pleural fluid of patients with transudates, infectious exudates (with positive or negative bacterial culture) and neoplastic exudates, using two different complement-dependent phagocytic tests: the killing of Staphylococcus aureus Wood 46 variant strain (K50 opsonic titers) and the assessment of ingestion rate of endotoxin-coated paraffin particles (Oil Red 0 uptake test). K50 opsonic titers were lower in culture-positive pleural effusions as compared to culture-negative (P < 0.002) or neoplastic effusions (P < 0.002). These results were corroborated by the Oil Red 0 uptake test. The data obtained with the two assays showed a significant correlation (P < 0.001). The hemolytic activity of complement (CH50) as well as the levels of C3 breakdown product, C3d, were measured in the same sera and pleural fluid samples and in an additional group of patients with pleural effusions of the same etiology. Effusions with positive cultures showed lower CH50 values (P < 0.01) and higher C3d values (P < 0.05) when compared to culture-negative pleural fluids. Finally, evidence for immune complexes in pleural effusions and sera was looked for by determination of Clq binding activity. Levels were higher in culture-positive effusions when compared to culture-negative fluids (P = 0.005).K50 opsonic titers showed a positive correlation with CH50 values (P < 0.001) for all fluids tested. Similarly Clq binding activity correlated with C3d levels in effusions of infectious origin (P = 0.05). Recovery experiments using the various bacterial species isolated from culture-positive pleural effusions showed evidence of complement inactivation upon incubation with pooled sera at concentrations of 10(7)-10(8) microorganisms/ml. These results indicate that one important reason for bacterial persistence in empyema may be decreased opsonization secondary to local consumption of complement.

Adult↗
PubMed1977

[Evaluation of the role of circulating antigen-antibody complexes in the pathogenesis of glomerular nephropathies].

Immunofluorescence studies of the glomeruli in patients suffering from glomerulonephritis (GN) suggest the deposit of immune complexes from the circulating blood. Immune complexes were quantitated using a sensitive radioimmunoassay from sera of 41 patients with GN drawn at the time when renal biopsy was performed. Simultaneously, degradation products of C3 (C3d) were measured. Eleven of 12 patients with GN secondary to a systemic disease (usually LED) presented increased C1q-binding activity of their sera (C1q-BA). C3 was further demonstrated in 9 of these patients, suggesting the presence of circulating immune complexes. By contrast only 2 of 12 patients with idiopathic GN characterized by deposits of complement and IgG in the glomeruli exhibited increased C1q-BA. One of 17 patients with idiopathic GN without deposit of immunoglobulins and C3 in the glomeruli also had increased C1q-BA. The results observed in the group of patients with idiopathic GN with glomerular deposits could be accounted for either by a transitory or minimal presence of immune complexes or by local formation of complexes in the glomerular structures.

Antigen-Antibody Complex↗
PubMed1975

[Pathophysiological implications of antigen-antibody complexes (author's transl)].

Seventy years after the description of the Arthus phenomenon, the concept of immune complex mediated pathology is widely recognized in clinical pathophysiology. The availability of methods for the detection of soluble immune complexes opens new paths for clinical investigation in this field. This is demonstrated for systemic lupus erythematosus, viral hepatitis B and herpes zoster disease. New experimental approaches deal with the question of tissue localization of immune complex mediated diseases, e.g. through affinity of antigens for certain tissue structures.

Animals↗