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Biomedical subjects

O Meyer

Publications and source records attributed to O Meyer.

At least 289 records · Page 16Linked to original sources
PubMed1986

[Autoimmunity to collagen, experimental arthritis and rheumatic disease].

Auto-immunity to type II collagen is now recognised as a good experimental model of arthritis. The possibility of a post-immunization treatment with collagen to suppress or abrogate the arthritic response is particularly interesting in the therapeutical trends suggested by such a possibility. In human pathology, if the pathogenic role of anti-native collagen type II auto-antibodies is well demonstrated in relapsing polychondritis, in the contrary, this hypothesis does not seem relevant to rheumatoid arthritis. In this disease, the role of the auto-immunity to native collagen appears secondary.

Animals↗
PubMed1985

[Fetal death caused by myocarditis and isolated congenital auriculoventricular block].

A 26-year old woman gave birth, at term, to a child with isolated complete heart block. A second pregnancy was interrupted by foetal death. Among other immunological abnormalities, this young woman had an antibody resembling the anti-SS-B antibody. At pathological examination the foetus' heart was found to be free of malformation but presented with subacute myocarditis associated with microcalcifications of the conductive tissue. Such findings suggest that an incipient myocarditis may either result in foetal death or lead to fibrosis of conduction pathways with isolated complete heart block.

Adult↗
PubMed1985

[Antiphospholipid antibodies, thrombosis and lupus disease. Value of the assay of anticardiolipin antibodies by the ELISA technic].

The authors have developed a sensitive immunoenzymatic method for assaying anti-cardiolipin antibodies in the serum of patients with lupus (SLE). These antibodies were present in the serum of 43/108 SLE patients, particularly in those patients with either false syphilis serology (p less than 0.02) or circulating anticoagulant (p less than 0.05). The mean titre of anti-cardiolipin antibodies was higher in the group with positive VDRL (less than 0.03). The anti-cardiolipin antibody titre was independent of the anti-native DNA antibody titre, but there was a correlation with the anti-denatured DNA antibody titre (p less than 0.02). This correlation can be partially explained by the antigenic similarity (phosphodiester bridge) between the two molecules. The preliminary clinical studies have not shown any correlation between the presence of anti-cardiolipin antibodies and the presence of signs such as thrombocytopenia, haemolysis, cerebral vascular accident, venous thrombosis, recurrent abortion. A longitudinal study of certain patients suggests that the anti-cardiolipin antibodies may disappear at the time of thrombotic accidents, which induces fixation of these antibodies to a platelet or vascular target and as a result of corticosteroid therapy.

Antibodies, Antinuclear↗
PubMed1985

Genetic deficiency of C4, C2 or C1q and lupus syndromes. Association with anti-Ro (SS-A) antibodies.

Sera from 15 patients with genetically determined complement component deficiencies were studied for the presence of antibodies to various nuclear antigens. One of three patients with C2 deficiency presented with systemic lupus erythematosus (SLE); all eight patients with C4 deficiency had either SLE or a lupus-like syndrome, and two of four patients with functional C1q deficiency had SLE. Five of nine complement deficiency patients with SLE studied had measurable antinuclear antibody titres, but only two had antibodies against native DNA. Precipitating antibodies against extractable nuclear antigens were found in sera from seven of the 11 complement deficient patients with SLE; one had only antibodies against antigens extracted from calf thymus (ECT), six patients (one with C2 deficiency, four with C4 deficiency and one with C1q deficiency) had anti-Ro (SS-A) antibodies with or without anti-ECT antibodies. The frequency of anti-Ro antibodies in the complement deficient population with SLE (55%) was significantly higher (P less than 0.02) than that of a control population of SLE patients without genetically determined complement deficiencies (27%).

Adolescent↗
PubMed1984

[Determination of anti-native DNA antibodies by immunofluorescence on Crithidia luciliae. Correlation between renal involvement and the presence of high-avidity anti-native DNA antibodies in lupic disease].

Low avidity native DNA - anti-native DNA complexes dissociate at alkaline pH and in high molarity solutions. This property was used to modify the indirect immunofluorescence reaction on Crithidia luciliae in order to assay high avidity anti-native DNA antibodies resistant to alkaline and strongly saline solutions. Assays were performed in the sera of 36 patients (31 women and 5 men) with systemic lupus erythematosus (SLE). Seventeen of these patients had histologically significant lupus nephritis (WHO types III, IV and V) and 19 had no renal, urinary or biochemical abnormalities. The mean titer of total anti-native DNA antibodies was similar in both groups, but the titer of high avidity anti-native DNA antibodies was significantly higher in patients with lupus nephritis. The percentage of patients with high avidity antibodies was 87% in the group with renal involvement and 28% in the group with no kidneys involvement. Thus, lupus nephritis should be feared when anti-native DNA antibodies with high dissociation constant are found in the sera of SLE patients.

Animals↗
PubMed1984

Immunocytochemical localization of carbon monoxide oxidase in Pseudomonas carboxydovorans. The enzyme is attached to the inner aspect of the cytoplasmic membrane.

The localization of carbon monoxide oxidase (CO oxidase), the key enzyme in CO metabolism of Pseudomonas carboxydovorans, was examined using modified immunoferritin and protein A-gold techniques. Cell extracts were incubated with specific immunoglobulin G antibodies raised against CO oxidase, followed by treatment with ferritin-conjugated goat-anti-rabbit immunoglobulin G antibodies (pre-embedding labeling). Electron microscopic examination of ultrathin sections showed cytoplasmic membranes and inside-out vesicles labeled at the inner aspect, whereas the outer sides of protoplasts and membrane vesicles remained completely unlabeled. The highly sensitive protein A-gold method has been modified to allow labeling of CO oxidase with good ultrastructural preservation of the bacterial cell. Glutaraldehyde-fixed cells of P. carboxydovorans were osmificated and embedded in glycol methacrylate. Etched ultrathin sections were treated with sodium metaperiodate and incubated with the specific antibodies against CO oxidase. These antibodies were then allowed to react with protein A-gold complexes (postembedding labeling). Exponentially grown cells showed 87% of CO oxidase associated with the cytoplasmic membrane and 13% of the enzyme in the cytoplasm. The results indicate that CO oxidase is attached in vivo to the inner aspect of the cytoplasmic membrane and suggest interaction of the enzyme with a membrane-bound electron acceptor. The ratio of enzyme associated with the cytoplasmic membrane decreased to 50% in the stationary growth phase.

Aldehyde Oxidoreductases↗
PubMed1984

Selenite binding to carbon monoxide oxidase from Pseudomonas carboxydovorans. Selenium binds covalently to the protein and activates specifically the CO----methylene blue reaction.

The CO----methylene blue and CO----dichlorophenol indophenol activities of carbon monoxide oxidase were specifically activated upon aerobic incubation with selenite, whereas the NADH----methylene blue activity was not altered. Fully active enzyme contained selenium, molybdenum, and flavin adenine dinucleotide in a 1:1:1 ratio. Selenium was covalently bound to the protein, probably between the sulfurs of half-cystine residues, and not a constituent of the molybdenum cofactor. The action of selenite was directed to the cytoplasmic species of carbon monoxide oxidase exclusively, whereas the CO----methylene blue activity of the membrane-bound enzyme remained unaffected.

Aldehyde Oxidoreductases↗
PubMed1984

Toxicological studies on malachite green: a triphenylmethane dye.

The oral LD50 for malachite green oxalate was found to be 275 mg/kg in rats while the approximate lethal dose for NMRI mice was 50 mg/kg. No systemic effects were seen after dermal application of 2,000 mg/kg. Repeated administration in the diet for 28 days to rats produced only minor changes in serum urea and aspartate aminotransferase levels. The rats at the highest dose level showed decreased weight gain and appeared clinically to have elevated motor activity. No sex differences were observed in either acute or prolonged experiments. In accord with human experience malachite green was irritating to mucous membranes, but no effects were seen on intact skin nor was it shown to be sensitizing. It was found to be a mutagen in the Salmonella/microsome test after metabolic activation but without clastogenic activity when tested at maximally tolerated levels in mice in the micronucleus test.

Animals↗
PubMed1984

[Complement activation during extracorporeal circulation. A model for understanding lesional pulmonary edema].

The complement system (CH50, C3, C4, C3 PA) was monitored during extra-corporeal circulation in 10 patients with ischemic-heart disease. Mean concentrations of CH50, C3, C4, and C3 PA significantly decreased as early as 5 minutes after initiation of the extra-corporeal circulation and decrement remain steady all over the surgical procedure. Transient neutropenia occurred early during the procedure. A significant hypoxemia was present only 24 hours after surgery. We suggest that a complement mediated leukostasis might occur with sequestration in the lungs and contribute to endothelial cell damage with pulmonary edema known as the "post-pump syndrome".

Adult↗
PubMed1984

Molybdopterin in carbon monoxide oxidase from carboxydotrophic bacteria.

The carbon monoxide oxidases (COXs) purified from the carboxydotrophic bacteria Pseudomonas carboxydohydrogena and Pseudomonas carboxydoflava were found to be molybdenum hydroxylases, identical in cofactor composition and spectral properties to the recently characterized enzyme from Pseudomonas carboxydovorans (O. Meyer, J. Biol. Chem. 257:1333-1341, 1982). All three enzymes exhibited a cofactor composition of two flavin adenine dinucleotides, two molybdenums, eight irons and eight labile sulfides per dimeric molecule, typical for molybdenum-containing iron-sulfur flavoproteins. The millimolar extinction coefficient of the COXs at 450 nm was 72 (per two flavin adenine dinucleotides), a value similar to that of milk xanthine oxidase and chicken liver xanthine dehydrogenase at 450 nm. That molybdopterin, the novel prosthetic group of the molybdenum cofactor of a variety of molybdoenzymes (J. Johnson and K. V. Rajagopalan, Proc. Natl. Acad. Sci. U.S.A. 79:6856-6860, 1982) is also a constituent of COXs from carboxydotrophic bacteria is indicated by the formation of identical fluorescent cofactor derivatives, by complementation of the nitrate reductase activity in extracts of Neurospora crassa nit-l, and by the presence of organic phosphate additional to flavin adenine dinucleotides. Molybdopterin is tightly but noncovalently bound to the protein. COX, sulfite oxidase, xanthine oxidase, and xanthine dehydrogenase each contains 2 mol of molybdopterin per mol of enzyme. The presence of a trichloroacetic acid-releasable, so-far-unidentified, phosphorous-containing moiety in COX is suggested by the results of phosphate analysis.

Aldehyde Oxidoreductases↗
PubMed1984

[What can be expected of biological tests in scleroderma?].

Biological investigations are useful from three main view points in systemic scleroderma: diagnosis: the demonstration of antinuclear antibodies which are quite specific for these conditions: antinuclear anti-ECT (nRNP, Scl 70, KU, PM 1) and anticentromere antibodies; prognosis: the presence of some antibodies is associated with a more favourable outcome: anti-nRNP and Sharp's syndrome, anti-centromere and the CREST syndrome, anti-KU and syndromes overlapping with polymyositis; pathogenic: the study of abnormalities of T-lymphocyte function, immunogenetic (HLA grouping) studies, cytotoxic factors for vascular endothelium, mitogenic factors of fibroblasts and the "chromosome breaking" factor.

Antibodies, Antinuclear↗