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Biomedical subjects

J Menzel

Publications and source records attributed to J Menzel.

At least 109 records · Page 6Linked to original sources
PubMed1983

Contribution of the antrum and duodenum to circulating forms of gastrin in the dog.

Gastrin release was stimulated in four anaesthetized dogs with meat extract and acetylcholine. The different forms of gastrin were analyzed in antral and duodenal mucosa and in blood from antral, duodenal and peripheral veins by use of radioimmunoassay with a region-specific antibody, Sephadex gel filtration, and SDS-gel electrophoresis. The duodenum contributed less than 4% of antral gastrin to circulating gastrin. The molecular forms of antral and duodenal gastrins were similar. On the basis of the electrophoretic results and the properties of the antibody, gastrin in the antral and duodenal veins consisted of a minor fraction of G 17 and a predominant fraction of C-terminal fragments of smaller molecular size. This fraction was even more marked in the peripheral venous circulation. In the peripheral blood, however, not only smaller forms of gastrin were present but also an increasing ratio of big gastrin immunoreactivity. Thus, there is active postsecretory processing of gastrin in the circulation of the anaesthetized dog.

Animals↗
PubMed1983

Influence of plasma fibronectin on collagen cleavage by collagenase.

The influence of plasma fibronectin on the cleavage of interstitial collagen types I, II, and III by mammalian collagenase was investigated. To this end, rheumatoid arthritis synovial tissue collagenase was isolated from tissue culture supernatants. A highly active enzyme preparation was obtained. Different dilutions of the collagenase were incubated in tubes coated with [3H]-labeled collagens. Liberation of labeled fragments in the presence (200 micrograms per ml) or absence of fibronectin was measured at different time intervals (1-30 min). A significant inhibition of collagen degradation was observed in case of type I and type III collagens. Analogous experiments were carried out using collagen-coated tubes preincubated with fibronectin at a concentration of 200 micrograms/ml. Here, a strong inhibition (76 percent) of type III collagen digestion by collagenase was observed, while the cleavage of type I or type II collagen was completely unchanged after preincubation with fibronectin. A direct attack of the collagenase preparation on plasma fibronectin could be excluded in control digestion experiments using radioiodinated fibronectin as substrate.

Arthritis, Rheumatoid↗
PubMed1982

[Immunological investigation in primary open angle glaucoma (author's transl)].

It is a matter of discussion in literature, if autoimmunological processes are involved in the pathogenesis of primary open angle glaucoma. Therefore we determined circulating Clq binding immune complexes, collagen antibodies, antinuclear antibodies and anit-nDNA-antibodies in the sera of patients with this disease. The result of our investigation and of recent papers lead to the conclusion that autoimmunological processes- are not involved in the pathogenesis of primary open angel glaucoma.

Adult↗
PubMed1981

Ocular manifestation of temporal arteritis. Immunological studies.

Since immunological mechanisms may be involved in the pathogenesis of temporal arteritis, serum samples of 15 patients with ocular manifestations of temporal arteritis were investigated for the presence of circulating immune compleses (CICs) and antinuclear antibodies (ANAs). In addition, the serum levels of IgG, IgA, IgM, and the complement components C3 and C4 were determined. In none of our patients could CICs be detected. Serum samples of two of the patients were positive for ANA. The values for IgG, IgM, C3, and C4 were within normal limits. Our data indicate that circulating C1q-binding immune complexes and ANAs are not the cause of ocular manifestation of temporal arteritis. This does not exclude the possibility that other forms of circulating immune complexes or the local formation of immune complexes might play a role in the pathogenesis of this disease.

Aged↗
PubMed1980

Angioma of the jugular foramen. Case report.

We describe a patient with a neoplasm closely mimicking a glumous jugulare tumour with regard to both clinical and radiological presentation. The tumour was removed by the transmastoid route. Only after histological examination of the excised neoplasm could the diagnosis of angioma be made. No other case of this nature has been found in the literature.

Diagnosis, Differential↗
PubMed1980

Demonstration of antibodies to denatured type I and type II collagen in juvenile rheumatoid arthritis, Still's syndrome and controls by [14C] collagen radioimmunoassay.

From 88 sera of patients with juvenile rheumatoid arthritis 30.6% showed antibodies to denatured type I collagen an 31.8% antibodies to type II collagen, a percentage which corresponds to radioimmunoassay results in adult RA. Rheumatoid factors were demonstrated with Waaler-Rose test in 14.7% and with latex test in 6.8% of investigated patients. Results of investigations with collagen types I and II correlated in 73.7%. Whilst type I collagen antibodies were found with equal frequency in active and non-active stages, type II antibodies were twice as frequent in active stages as in non-active stages. Sixteen sera of children with non-rheumatoid diseases had no collagen antibodies. JRA sera and controls differed with statistical significance in regard to collagen antibodies. 36 sera of children with Still's syndrome showed antibodies to type I collagen in 13.8% and antibodies to type II collagen in 33.3%. Both types of antibodies appeared more frequently in clinically active stages. The sera differed from controls with statistical significance in regard to collagen antibodies.

Adolescent↗
PubMed1980

Experimental arthritis induced by granulocyte collagenase.

Purified human granulocyte collagenase (1 mg %, 10 mg % or 50 mg %) was injected into rabbit knee joints (three groups of 6 animals each) three times within one week. Synovium and synovial fluid were investigated 18 hours, 1 week and 3 weeks after the last injection. After 18 hours, synovial fluids showed distinct cellular exudation, its size depending on the amount of collagenase applied. A smaller number of cells was seen after one week, while normal cell counts were observed 3 weeks after the last injection. Histologically, synovium showed an acute arthritis after 18 hours, whereas after 1 and 3 weeks a chronic proliferative form of arthritis with predominant activation of fibroblasts was diagnosed. As compared with an experimental arthritis induced with rheumatoid synovial collagenase, granulocyte collagenase was less arthritogenic. Neither trypsin nor saline injections induced distinct cellular exudation into synovial fluids nor histologic signs of arthritis.

Animals↗
PubMed1979

[Clinical experience with levamisole treatment of patients with systemic lupus erythematosus (author's transl)].

Levamisole treatment was started in 8 patients with inactive SLE. Four patients, who have now been followed up for over 12 months, have not shown clinical deterioration. Three of these patients received concomitant maintenance corticosteroid therapy, the dosage of which could be reduced in each case. A decrease in anti-DNA antibodies was observed in all 4 patients. Levamisole had to be withdrawn in the other 4 patients. One patient developed an exacerbation of her LE skin manifestations after two months, whilst in another patient fever and skin rash (probably drug-induced) were observed after one month. The cooperation of the 2 other patients was not satisfactory and the drug had, thus, to be withdrawn. In conclusion, 4 out of 8 patients with SLE showed a beneficial response to levamisole therapy.

Adolescent↗
PubMed1979

Failure to detect gliadin or gliadin binding sites in the skin of patients with dermatitis herpetiformis: immunofluorescence, organ culture and autoradiographic studies.

Recent investigations indicate an abnormal binding of gluten or gliadin to lymphocytes or intestinal mucosa cells in gluten sensitive enteropathy. Since dermatitis herpetiformis is closely associated to gluten sensitive enteropathy, similar receptors could also exist in the skin of patients with dermatitis herpetiformis. To prove this hypothesis, skin of normal volunteers and uninvolved skin of 3 patients with dermatitis herpetiformis was investigated for the presence of gliadin and gliadin binding sites. In vivo bound gliadin was not found by direct immunofluorescence using 3 different rabbit antigliadin antisera. In order to test skin for gliadin binding sites, normal sera and autologous dermatitis herpetiformis sera containing 25 mg% gliadin and tritium labeled gliadin, respectively, were used for incubation of normal and dermatitis herpetiformis skin cryocut sections and of normal and dermatitis herpetiformis skin specimens, grown under organ culture conditions. As checked by direct immunofluorescence and autoradiography, there was no specific in vitro binding of gliadin, indicating that gliadin does not fix to normal human or dermatitis herpetiformis skin. Thus, the role of gliadin in the fixation in vivo, of antibodies or immune complexes to skin in dermatitis herpetiformis, remains obscure.

Antibodies↗