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Biomedical subjects

C Steffen

Publications and source records attributed to C Steffen.

At least 181 records · Page 10Linked to original sources
PubMedDate not supplied

A kinetic evaluation of 14CO2 in expired air after 14C-methacetin administration in rats, used for the in vivo study of the metabolism of drugs.

The pharmacokinetics of the blood level and the patterns of 14CO2 exhalation were determined simultaneously following i.v. administration of 14C-methacetin to the conscious rat. The pattern of exhalation of 14CO2 did not parallel the biexponential decline of radioactivity in the blood and a delay of 30-40 min preceded the maximal rate of 14CO2 exhalation. The total radioactivity exhaled remained constant at 56 +/- 4.5% (SD) of the applied dose throughout a tenfold dose range of methacetin (0.6, 4.0 and 6.0 mg/kg i.p.), administered to groups of three rats each and measured over a period of 4 hours. The pattern of radiolabel exhalation was biexponential with the low dose, linear with the medium dose and convex with the high dose. Although the total fraction of the label expired after 4 hours remained constant, the rates of exhalation at the higher dosages exhibited saturation type kinetics. At the higher dosage, since the pattern of 14CO2 exhalation did not accurately reflect the decline of methacetin seen in blood, one of the steps occurring between the demethylation process and the production of expired CO2 appears to be rate limiting. Significant increases in the amount of 14CO2 exhaled within 1 hour were obtained by pretreatment with phenobarbital, rifampicin and 3-methylcholanthrene. Again the proportion of radiolabel expired in 4 hours remained constant. Acute hepatic injury produced by pretreatment with graded doses of carbon tetrachloride resulted in graded reductions in the amount of 14CO2 exhaled in the first hour, although the total amount exhaled during the 4 hour collection period did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetamides↗
PubMedDate not supplied

Collagen antibodies and collagen- anticollagen immune complexes in rheumatoid arthritis.

Serum, synovial fluid and synovial fluid cells of 14 patients with classic rheumatoid arthritis and of 5 controls were investigated serologically in regard to rheumatoid factors and collagen antibodies and by immunofluorescence double staining in regard to localization of collagen and gammaglobulin in fluid cells. Three patterns of staining were observed: a) gammaglobulin inclusions, b) gammaglobulin and collagen in identical localization, c) collagen inclusions. While distinct staining for gammaglobulin appeared only in seropositive cases, collagen inclusions were only observed in RA, however in seropositive and seronegative cases. In 5 RA cases collagen and gammaglobulin were demonstrated additionally in such identical localization that conclusion in regard to collagen-anticollagen immune complexes seems justified. 9 of 14 RA cases had collagen antibodies, all cases were collagen antibody positive which had collagen and gammaglobulin in identical localization in same inclusions.

Antigen-Antibody Complex↗
PubMedDate not supplied

Detection of collagenase-activity in RA synovial fluids using soluble 14C-labelled collagen.

14 RA synovial fluids and 7 non-RA synovial fluids were investigated as to their collagenase-activity using 14C-labelled type I human collagen in soluble form. Breakdown products were fractionated by gel filtration on Sephadex G 200 superfine. Cleavage of native and denatured labelled collagen was compared. 11 RA synovial fluids showed significant collagenase activity as manifested by degradation of native collagen, while only one synovial fluid of the control group displayed a significant collagenolytic activity. Results were compared with cleavage of reconstituted collagen fibrils. Influence of EDTA and KSCN on collagen degradation was also studied: EDTA completely blocked degradation of native or denatured collagen, while KSCN caused an increase of collagenolytic activity in two cases.

Arthritis, Rheumatoid↗
PubMedDate not supplied

[Basic studies on chronic polyarthritis as a collagen-autoimmune disease].

Clinical and experimental data establishing a hypothesis about rheumatoid arthritis (RA) as a collagen auto-immune disease are reviewed, beginning with the demonstration of rheumatoid synovial collagenase, the demonstration of collagen antibodies in the serum and the synovial fluid of patients with RA, the demonstration of collagen inclusion bodies and collagen-anticollagen immune complexes in synovial fluid cells and the synovial fluid of patients with RA, and leading to the in vitro demonstration of the inflammatory effect of such complexes, and the induction of experimental arthritis by these complexes. Each section contains tabular summaries of various investigations. Finally, a relation between these observations and the conclusions deduced from them and the appearance of rheumatoid factors in RA and the pathogenic effect of rheumatoid factor - gammaglobulin aggregates is considered.

Animals↗
PubMedDate not supplied

Collagenase-induced experimental arthritis.

Rabbits were injected intraarticularly three times with 0.5 ml of 10, 50 or 100 mg% purified rheumatoid synovial collagenase or with identical amounts of trypsin. 18 hours after the last injection the collagenase-injected animals showed distinct cellular exudation into the synovial fluid and acute arthritis; one week later there was a decrease of the cell count in the synovial fluid and appearance of proliferative synovitis, while 3 weeks later there was no exudation and less chronic inflammation but distinct fibrosis of the synovium. A direct action of collagenase on the connective tissue components would seem to be responsible for these changes. No pathologic alteration of the cartilage was observed. Trypsin-injected control animals showed negligible cellular exudation and no pathologic alteration of the synovium.

Animals↗
PubMedDate not supplied

[IgA rheumatoid factors in ankylosing spondylitis].

151 cases of ankylosing spondylitis, arranged in clinical stages I-IV, were investigated by immunological methods (determination of HLA-B27, immunocomplexes: conglutinin-, Clq-assay; IgG-, IgM-, IgA-rheumatoid factors) and with regard to acute phase proteins (CRP, C3/C4, alpha 1-acid glycoprotein). IgA-rheumatoid factors were demonstrated as dependent upon the stage of the disease in 23-41% of cases and appeared in 20-23% of cases simultaneously with immunocomplexes. Immunocomplexes appeared in 20-23% of cases. With regard to investigations of acute phase proteins, sedimentation rate and CRP correlated best. The frequent appearance of IgA-rheumatoid factors allows a definition of ankylosing spondylitis as seronegative only as far as the determination of IgG- and IgM- rheumatoid factors is concerned.

Acute-Phase Proteins↗
PubMedDate not supplied

Demonstration of collagen type conversion in culture supernatants from human chondrocytes by an inhibition ELISA.

Culture supernatants from monolayer cultures of human chondrocytes were tested for the presence of collagen type I and type II during subpassaging using an inhibition Elisa. The sensitivity of the Elisa was 404 +/- 50 ng/ml (mean +/- SEM) for the determination of type I collagen and 112 +/- 16 ng/ml for type II collagen. Whereas using immunofluorescence techniques, type II collagen was observed in human chondrocytes cultured under monolayer conditions only up to the first subpassage (1), in culture supernatants from human chondrocytes type II collagen could be found up to the fourth subpassage. Type I collagen was detectable in supernatants from the beginning of primary cultures and was present up to the tenth subpassage in increasing concentrations. Variations in the amount of collagen present in the culture supernatants seemed in part to be due to different growth characteristics of the chondrocytes. Cell shape was not associated with the release of a particular collagen type. In summary, the collagen inhibition Elisa appears to be equivalent to biochemical methods with regard to sensitivity and specificity. Investigations on influencing the switch in collagen production in human chondrocytes may benefit from the use of both techniques described.

Adult↗
PubMedDate not supplied

Absence of microsomal lipid peroxidation in acatalasemic mice.

Catalase (E.C. 1.11.1.6) activity and NADPH-dependent lipid peroxidation have been measured in liver microsomes from normal and acatalasemic mice. The absence of lipid peroxidation in acatalatic microsomes is not restituted by exogenous catalase as is microsomal methanol oxidation nor is it inhibited by sodium azide, thus suggesting an additional abnormality in these mice.

Acatalasia↗
PubMedDate not supplied

[Enzyme therapy in comparison with immune complex determinations in chronic polyarthritis].

42 patients with definite or classic rheumatoid arthritis were treated with an enzyme mixture (Wobenzym) for 6 weeks. Circulating immune complexes were investigated with a Clq-solid phase RIA in weekly intervals and also rheumatoid factors were determined together with other routine laboratory tests. The condition of patients after therapy was recorded together with amount of circulating immune complexes during treatment. 26 (61.9%) patients improved, 13 (30.9%) patients remained unchanged, and 3 (17.1%) showed impairment. No side effects were observed. Patients who primarily showed no immune complexes or patients who had immune complexes which became negative during enzyme therapy, showed improvement more often than patients which had immune complexes and remained positive during the entire course of therapy.

Adult↗
PubMedDate not supplied

Demonstration of C1q - binding to collagen - anticollagen immune complexes in synovial fluids of RA-patients.

Collagen-anticollagen immune complexes were demonstrated indirectly in RA synovial fluids by digestion with collagenase and subsequent antibody determination. Elimination of C1q was performed by affinity chromatography using an anti-C1q column. Binding of C1q to collagen-anticollagen complexes was proven by demonstrating that collagenase-caused liberation of collagen antibodies was abolished or distinctly reduced after passage through the anti-C1q column. Binding of C1q to collagen-anticollagen immune complexes was proven via the fixation of these aggregates onto the anti-C1q column. This was achieved in those 7 RA synovial fluids which contained distinctly demonstrable collagen-anticollagen complexes.

Antibodies↗
PubMedDate not supplied

Leucocyte migration inhibition with collagen type I and collagen type III in rheumatoid arthritis and degenerative joint diseases.

The leucocytes of 22 patients with classic rheumatoid arthritis were investigated with the direct leucocyte migration inhibition technique in agarose as described by Clausen. The leucocytes of 9 patients with degenerative joint diseases and of 9 healthy persons served as controls. Collagen type I and collagen type III were used as antigens. The leucocytes of 22 patients with rheumatoid arthritis showed in 15 cases a migration inhibition with collagen type III and in 10 cases with collagen type I. The inhibition with collagen type III was stronger and more frequent than with collagen type I. The frequent leucocyte migration inhibition with collagen type III in classic rheumatoid arthritis seems to be an expression of possible cell mediated reactivity against that type of collagen which appears especially in rheumatoid synovial tissue.

Adult↗
PubMedDate not supplied

[Enzyme breakdown of immune complexes].

4 types of immune complexes according to the Heidelberger curve were prepared as an in vitro model for immune complexes in rheumatoid arthritis and collagen diseases. Immune complexes of high and moderate antigen excess and immune complexes of high and moderate antibody excess were incubated with increasing concentrations of a mixture of enzymes or papain or pancreatin. The concentration of immune complexes was determined by a solid phase C1q radioimmunoassay before and after incubation. Up to 90% of the complexes of antigen excess were disintegrated even by low doses of enzymes (5-10 mg%); total cleavage appeared at 80 mg% enzyme concentration. Complexes of the antibody excess zone were gradually disintegrated by enzyme concentrations gradually increasing from 5 to 80 mg%, where total cleavage appeared. Single enzymes showed less cleavage activity than enzyme mixtures. Although enzymes were administered to supernatants of the Heidelberger precipitation containing soluble immune complexes as well as enzyme inhibitors, enzymatic activity was not impaired and immune complexes were disintegrated. The results of these investigations are discussed in regard to treatment with enzymes.

Animals↗
PubMedDate not supplied

Leukocyte locomotion and regulative serum effects in rheumatoid arthritis.

Leukocyte locomotion (LL) of 40 patients with rheumatoid arthritis (RA) was found to be unimpaired as compared to LL of 23 control individuals (p Greater Than 0.2). Casein and zymosan activated human sera were used as cytotaxins, and the sera of RA patients proved to be activatable in the same way as control sera in that they produced a similar chemotactic activity (p Greater Than 0.2). However, RA sera inhibited LL significantly (p Less Than 0.01) in comparison to control sera. This phenomenon was unchanged after elimination of immune complexes be ultracentrifugation, but could be reversed, after incubation of cells with RA sera, by reincubation with control sera.

Adult↗