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Biomedical subjects

O Haferkamp

Publications and source records attributed to O Haferkamp.

At least 55 records · Page 3Linked to original sources
PubMed1982

Alterations in chondrocyte morphology, proliferation and binding of 35SO4 due to Fe(III), Fe(II), ferritin and haemoglobin in vitro.

Lapine articular chondrocytes in vitro were used to study the effects of Fe3+, Fe2+, ferritin and haemoglobin on cell proliferation, synthesis of proteoglycans and morphological structure. Fe3+ (10, 100 and 500 micrograms/ml) reduced the DNA content of cultures by approximately 35% as well as inhibiting proteoglycan synthesis. Chondrocytes showed positive cytoplasmic staining for both ferric and ferrous ions at the 500 micrograms/ml concentration. Fe2+ (100 micrograms/ml) also decreased DNA content and proteoglycan synthesis, although no iron uptake by the chondrocytes could be detected. Ferritin (1.0, 0.5 and 0.1 micrograms/ml) elicited a significant inhibition of proteoglycan synthesis without affecting cellular DNA synthesis. 1 and 5 micrograms/ml of haemoglobin each reduced the DNA content of cultures by 60%, whilst markedly inhibiting proteoglycan synthesis (75 and 99% respectively). None of the substances tested caused chondrocyte toxicity. The ability of Fe3+, Fe2+, ferritin and, in particular, haemoglobin to inhibit chondrocyte proteoglycan synthesis may represent a pathway whereby cartilage is susceptible to destruction in the haemophilic joint.

Animals↗
PubMed1982

Selective inhibition of human neutrophilic chemotaxis by echo virus, type 9. Virus-induced changes in membrane fluidity.

By means of the excimer-forming lipid technique changes of membrane fluidity of human PMNs exposed to a chemoattractant (FMLP) and/or Echo virus, type 9, strain A. Barty has been investigated. It was shown that preincubation of PMNs with Echo 9 virus results in a viral dose-dependent decrease of membrane fluidity of granulocytes exposed to FMLP. The virus-induced rigidity of cell membrane causes obviously a disturbance in the aggregation of membrane particles to form receptors, and thus can lead to a failure of regular processing of chemotactic signals.

Chemotactic Factors↗
PubMed1982

Influence of zinc and copper on lapine articular chondrocytes in monolayer culture: morphology, proliferation and proteoglycan synthesis.

The effects of zinc and copper ions on the structure, proliferative capacity and proteoglycan metabolism of lapine articular chondrocytes were studied in a monolayer culture system. Zn++ was cytotoxic at a concentration of 100 mumol/l, whereas 50 mumol/l caused a stimulation of chondrocyte proliferation with simultaneous reduction (p less than 0.01) in macro-molecular binding of 35 SO4. 10 mumol/Zn++ failed to evoke any alteration in these parameters. Cu++ concentrations of 100 and 50 mumol/1 significantly reduced cell proliferation (p less than 0.01) with a concomitant stimulation of 35 SO4 uptake into proteoglycans 10 mumol/Cu++ did not significantly alter chondrocyte multiplication nor binding of 35SO4. It is proposed that Zn++ may play a role in chondrocyte damage in joint disease. Furthermore, the possible therapeutic efficacy of copper in maintaining cartilage integrity is supported.

Animals↗
PubMed1981

Selective inhibition of human neutrophil chemotaxis by ECHO-virus, type 9.

Preincubation (37 degrees C, 60 min) of human neutrophilic granulocytes with various concentrations of infectious ECHO virus, type 9, strain A. Barty resulted in virus-dose dependent inhibition of neutrophil chemotactic reactivity (Boyden-chamber assay) to chemoattractants (F-Met-Leu-Phen: zymosan-activated human serum). Other cellular functions-phagocytosis, increase of oxidative cell metabolism, intracellular killing of live staphylococci--remained intact. This selective inhibition of human neutrophilic chemotaxis was due to viral induced cytotoxicity or competitive inhibition of chemotactic cell surface receptors.

Animals↗
PubMed1981

Ultrastructure of platelets before and during atrial stimulation. Differences in the coronary sinus and aortic blood in patients with angina pectoris.

We studied 15 patients with strain-induced angina pectoris performing an ultrastructural analysis of platelets withdrawn simultaneously from the aorta and coronary sinus. In coronary sinus blood, all platelets exhibited shape changes with pseudopod formation but without degranulation. In the aortic blood we observed on average fewer shape changes of the platelets. During tachycardia stress, shape change formation did not increase in most patients. In three patients however, micro-aggregation of the platelets was observed only in the aortic blood. These patients had a paucity of risk factors. They also had fewer critical coronary artery stenoses compared with the other patients. We conclude that there may be minority among the patients with angina pectoris exhibiting hyper-aggregation of the platelets.

Angina Pectoris↗
PubMed1981

[Yersinioses. Clinical, patho-anatomical and pathogenetic problems (author's transl)].

On the basis of a selected patient group and bioptic material, the difficulties in diagnosing Y. pseudotuberculosis and Y. enterocolitica infections are presented from the clinical and morphological point of view, particularly when extraintestinal complications are present. Taking one patient with Y. enterocolitica infection and recurrent oligoarthritis as an example, the possible pathogenetic significance of circulating immune complexes for the development of extraintestinal symptoms is being discussed.

Adolescent↗
PubMed1981

The effect of soluble sodium urate on the proliferation and proteoglycan synthesis of lapine articular chondrocytes in monolayer culture.

The effects of soluble monosodium urate (350, 50, and 5 mumol/l) on the proliferation and proteoglycan synthesis of lapine articular chondrocytes were studied in a monolayer culture system. Cellular proliferation in vitro was unaffected by urate treatment. Chondrocytes treated with 50 mumol/l sodium urate showed a 26% reduction in binding of 35SO4 to matrix macromolecules. However, this reduction did not achieve statistical significance. The 350 and 5 mumol/l concentrations did not alter 35SO4 binding. It is proposed that monosodium urate has no marked direct effect on chondrocyte viability, proliferation and proteoglycan synthesis.

Animals↗
PubMed1981

Ultrastructural degenerative changes of age-dependent ECHO 9 virus-induced polymyositis in infant mice.

Experimental inoculation of newborn NMRI mice with Echo virus, type 9, strain A. Barty *ECHO 9 virus AB) resulted in diffuse polymyositis 4 days later. The disease, after a delay of 1 day, increased in intensity and was accompanied by a rapid, progressive paresis leading to death 7-11 days following infection. As early as 24-48 h after inoculation, we detected initial ultrastructural degenerative changes, characterized by segmental dilation fo the sarcoplasmic reticulum. Disruption and breakage of myofibrils followed, and lead to the formation of increasing numbers of contraction bands. Ultimately, virus-mediated nuclear and other organellar injury resulted in muscle fiber necrosis. In addition, we observed some substructural cellular events related to virus propagation. Beginning on the 4th day after infection, pronounced proliferation of the sarcoplasmic-reticulum membranes became evident in perinuclear and subsarcolemmal areas in the mature muscle fibers, myoblasts, and post-fused myotubes of mice inoculated within 18 h after birth. These cytological alterations were not noted in the myoblasts and myotubes of NMRI mice injected with virus 2 or 4 days after birth.

Age Factors↗
PubMed1981

Development of necrosis and its sequelae in the myocardium of polymyopathic hamsters (BIO 8262). An electron microscopic study.

Beginning about 30 days after birth, polymyopathic Syrian hamsters of the strain BIO 8262 develop calcifying myocardial necrosis. In the final stage the resorptive granulation tissue is followed by scars with multi-nucleated giant cells containing huge amorphous calcium plaques. The ultrastructural findings reveal the importance of myocardial mitochondria as starting points for calcification. The pattern of cell damage shows marked similarity to the changes observed in the myocardiocytes of magnesium-deficient rats. However, it is different from the alterations described in degenerating myocardiocytes of dehydrotachysterol-treated animals. Spicular electron-dense inclusions are the first and only kind of intramitochondrial calcification. Granular and annular-granular inclusions, as observed in ischaemic and infarcted canine myocardium, could not be detected, indicating that different pathogenetic mechanisms operate. The increased intracellular calcium level triggering myocardial necrosis is regarded as a secondary phenomenon, based on a genetic abnormality.

Animals↗
PubMed1981

[Sclerosing mesenteritis: case reports and review of literature (author's transl)].

Sclerosing mesenteritis is a rare, non-systemic disease confined to the mesenteric adipose tissue and typified by a variety of inflammatory pseudo-tumours. Histological investigation uncovers a wide spectrum of pathological changes, with collections of foam cells, fibrosis and for the most part sparse mononuclear inflammatory infiltrates in the mesenteric fat tissue. In the course of several weeks to months the pseudotumours generally resolve without therapeutic measures. The disease entity is discussed on the basis of three clinical cases.

Adipose Tissue↗
PubMed1980

[Influenza A virus infection, a precipitating factor for the major heart attack (author's transl)].

A report on 5 men aged from 53 to 75 years whose clinical symptoms were characterized by a major attack. There was a striking temporal relationship between the onset of this and an influenza infection which, in these 5 patients with chronic heart diseases led to a severe, and in the youngest patient, even to a fatal course. In an acute heart attack it seems rational to take into consideration an acute influenza virus infection as a precipitating factor in existing chronic heart disease and to institute virological studies.

Aged↗
PubMed1980

Interaction of circulating immune complexes with granulocyte function in patients with rheumatoid arthritis.

The sera and peripheral blood granulocytes of 10 patients with rheumatoid arthritis and of 10 healthy controls were investigated for the presence of soluble immune complexes and for cellular dysfunction. Using the Rajicell-radioimmunoassay, immune complexes were detected in 7 out of 10 rheumatoid sera. In one patient the presence of immune complexes was demonstrated by immunofluorescence. In all rheumatoid patients with circulating immune complexes decreased chemotactic reactivity and diminished bactericidal capacity of the neutrophils were observed. Incubation of rheumatoid granulocytes with pooled AB-serum or pretreatment of neutrophils of healthy controls with immune complexes containing rheumatoid sera resulted in a reduced number of comparable cellular dysfunctions including increased release of lysosomal enzymes, strongly correlated with the presence of intracellular phagocytosed immune complexes. Phagocytosis and increase of oxidative cell metabolism during phagocytosis were not influenced by circulating immune complexes. Based on our in vitro findings we suggest that the described immune complex-dependent granulocyte dysfunctions are possible responsible for the high risk of local or systemic bacterial diseases in patients with rheumatoid arthritis.

Adult↗