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Biomedical subjects

W Mohr

Publications and source records attributed to W Mohr.

At least 127 records · Page 7Linked to original sources
PubMed1981

Lysosomal elastase: effect on mechanical and biochemical properties of normal cartilage, inhibition by polysulfonated glycosaminoglycan, and binding to chondrocytes.

Rheumatic joint destruction usually starts with the destabilisation of cartilage. Lysosomal elastase is a candidate effector of this process, since this enzyme is found at the site of cartilage erosion by rheumatoid synovial tissue. In order to prove this hypothesis we assessed the mechanical stability of cartilage during treatment by this enzyme in vitro. An indentation apparatus was used for this purpose and biochemical as well as microscopic techniques were used to supplement the results thus obtained. Our findings show that elastase irreversibly impairs the stability of cartilage by lysis of matrix proteoglycans without the help of additive enzymes. Collagen fragmentation played no significant role during elastase-induced destabilisation, while specific collagenase attacked the collagen network within the matrix only subsequent to the removal of proteoglycans. These findings suggest that elastase is a leading enzyme during proteolytic cartilage degradation. In addition polysulfonated glycosaminoglycan was found to reduce the mechanical effect of elastase on normal cartilage. It is therefore concluded that local inhibition of elastase promises therapeutic benefit during rheumatic cartilage degradation. Upon treatment of cartilage with elastase we observed this enzyme not only within the matrix under destruction but also bound to chondrocytes. These findings support the hypothesis that elastase plays a role on the matrix not only by direct degradation, but also by an indirect effect mediated through living chondrocytes.

Adolescent↗
PubMed1981

Polymorphonuclear granulocytes in rheumatic tissue destruction. II. Demonstration of PMNs in rheumatoid nodules by electron microscopy.

Necrotic areas of rheumatoid nodules were investigated electron microscopically. PMNs in different stages of disintegration were present in all cases. Granular material, sometimes in a fiberlike orientation, and small fibrils without periodicity were detected between the collagenous fibers. It is assumed that granular material and fibrillar remnants represent degraded collagen. Often these degradation products were present in the neighborhood of disintegrating PMNs. From this morphological relationship it is concluded that enzymes of PMNs may in part be responsible for the fibrinoid necrosis in rheumatoid nodules.

Collagen↗
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

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

The body reaction to carbon fibre particles implanted into the medullary space of rabbits.

It is thought that abrasion particles can produce a tissue reaction when alloplastic material is used for prosthetic devices. Therefore it is important to examine the reaction of the tissues and the body to microparticles before introducing a new material. Carbon reinforced carbon is a new material which is suitable for artificial joints because of its physical properties (strength and elasticity). Carbon fibre fragments with a diameter of 7 microns and a length between 20-100 microns were injected in the medullary canal of 16 rabbits, and evaluated after periods of 2 and 12 weeks. Phagocytosis of small carbon fibre fragments by macrophages occurs, but only a minimal foreign body reaction to the intramedullary carbon fibre fragments. There is a small amount of fibrosis around some carbon fibres and a small amount of new bone formation with inclusion of carbon. Only a few carbon fragments are transported to the parenchymal organs. There is no foreign body reaction.

Animals↗
PubMed1981

[Ultrastructure of detritus synovitis ("hydroxylapatite synovitis?") (author's transl)].

Detritus synovitis is a sequel of cartilage and osseous destruction in diarthrosis. Cartilage and bone fragments are enclosed by granulation tissue. Remnants of the destroyed bone and calcified cartilage appear as defined accumulations of hydroxylapatite crystals in the granulation tissue. These hydroxylapatite tissues resemble those considered by other authors as being responsible for a "third crystal synovitis, namely, hydroxylapatite synovitis". However, the findings communicated here allow us to conclude that these crystals are the sequel of a destruction of diarthrosis, so that it is not justified to consider hydroxylapatite synovitis as a separate disease entity.

Aged↗
PubMed1981

Role of polymorphs in inflammatory cartilage destruction in adjuvant arthritis of rats.

The inflammatory destruction of cartilage in rat adjuvant arthritis has been studied by histochemistry and autoradiography. Naphthol-AS-D-chloroacetate esterase has been used as a marker for polymorphs. The evidence presented here shows that polymorphs accumulate at the cartilage-pannus border and in areas of cartilage loss. These cells appear therefore to be of decisive importance for the destruction of cartilage. Proteoglycans were demonstrated by safranin-O staining: there is a loss of PG that is particularly prominent in zones where pannus had invaded cartilage. By means of 35S labelling of proteoglycans it was possible to show that pannus containing polymorphs can invade living cartilage.

Animals↗
PubMed1981

Polymorphonuclear granulocytes in rheumatic tissue destruction. III. an electron microscopic study of PMNs at the pannus-cartilage junction in rheumatoid arthritis.

Metatarsophalangeal and metacarpophalangeal joints from 3 patients with rheumatoid arthritis were investigated electron microscopically with regard to the occurrence of polymorphonuclear granulocytes (PMNs) at the pannus-cartilage junction. In all 3 cases PMNs could be detected at the junction and within the cartilaginous matrix. PMN cytoplasmic processes surrounded collagenous islands in the cartilage. From the morphological findings it is deduced that PMNs are cells capable of destroying cartilage in inflammatory joint diseases, in particular in rheumatoid arthritis.

Arthritis, Rheumatoid↗
PubMed1980

Cyclophosphamide cardiotoxicity.

A 12-year-old boy with aplastic anemia developed severe but reversible cardiac failure after treatment with 200 mg/kg cyclophosphamide (4 x 50 mg/kg on four consecutive days) given as preparation for bone marrow grafting. This and previously reported cases demonstrate the possibility of cardiotoxicity after high doses of the drug.

Anemia, Aplastic↗
PubMed1980

Fibroelastosis of the right ventricle in two brothers of triplets.

We present an autopsy report of endocardial fibroelastosis of the right heart in two brothers of triplets. Beside this anomaly no other macroscopical malformations in the hearts were found. Morphologically an unusual hypertrophy of the subendocardial myocardiocytes in the right heart was observed. A history of tocolysis (sympathomimetic drugs for treatment of premature labour) was the main reason for publishing this case report. We could not answer the question if the drug was causative or only coincident with the observed lesions.

Autopsy↗
PubMed1979

Fibrin deposition and removal in disseminated intravascular coagulation induced by endotoxin and saline loading: radioautographic findings in rats.

In rats a single injection of endotoxin followed by an infusion of normal saline induced the generalized Shwartzman reaction. The presence of disseminated intravascular coagulation (DIC) was demonstrated by measuring plasma fibrinogen, platelet counts, schistocytes, plasma haemoglobin, fibrin(ogen) degradation products, and fibrin thrombi in the glomerular capillaries, 125I-fibrinogen was given after triggering DIC in order to examine the fibrinogen turnover in plasma and the kinetics of fibrin deposition and removal in kidney, liver, and spleen. 125I-fibrinogen turnover was found to be highly accelerated. Early deposition and removal were observed in the kidneys, while a later peak with a more delayed fall of radioactivity was noted in liver and spleen. On histological examination fibrin could be seen only in the glomerular capillaries and only in the early phase of DIC. In radioautographs radioactive material was localized in the glomerular capillaries, the Kupffer' cells of the liver, and in the perifollicular macrophages of the spleen. Comparing the results obtained by scintillation counting to those obtained by light microscopy it can be assumed that radioactivity in kidneys is correlated to fibrin deposition in glomerular capillaries and to an accumulation on fibrin(ogen) degradation products in liver and spleen.

Animals↗