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Biomedical subjects

W Mohr

Publications and source records attributed to W Mohr.

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

Cartilage choristoma of the eye.

A young girl had a rigid, white tumor that penetrated the sclera. It was partially resected, and histopathologic study demonstrated choristoma of elastic cartilage.

Cartilage↗
PubMed1983

A comparison of the effects of two gold-containing therapeutic agents on articular chondrocyte growth in vitro.

Chondrocyte structure and function under the influence of two gold-containing therapeutic agents, aurothioglucose and triethylphosphine gold, were studied in a monolayer culture system for cultivating lapine articular chondrocytes. The functional parameters investigated were chondrocyte proliferation and the incorporation of 35SO4 as indicator of glycosaminoglycan synthesis. Aurothioglucose (0.2, 1 and 10 micrograms/ml) failed to affect either parameter and caused no cytotoxic effect detectable with the light microscope. Triethylphosphine gold (1.5 and 3 micrograms/ml) prevented subcultured chondrocytes from forming monolayers and was cytotoxic to chondrocytes present in established monolayers, studied with the light and scanning electron microscope. A 0.3 microgram/ml concentration did not alter chondrocyte proliferation or sulphate incorporation and was not cytotoxic.

Animals↗
PubMed1983

The tissue architecture of synovial membranes in inflammatory and non-inflammatory joint diseases. I. The localization of the major synovial cell populations as detected by monoclonal reagents directed towards Ia and monocyte-macrophage antigens.

Utilizing monoclonal reagents directed towards antigens of the monocyte-macrophage lineage and Ia antigens, the tissue architecture of synovial membranes obtained from patients with non-inflammatory joint diseases and patients with rheumatoid arthritis was studied. Emphasis was placed on the localization of the type I, type II and type III synoviocytes that previously had been defined by their cell surface phenotype with regard to the expression of monocyte-macrophage lineage (M theta) and Ia antigens as well as by their phagocytic capacity or the ability to produce glycosaminoglycans. In patients with non-inflammatory joint diseases, cells with the M theta + Ia+ (type I) phenotype constituted the majority of synoviocytes immediately adjacent to the joint cavity; cells with this phenotype were also scattered in the subsynovial tissue and in the perivascular regions. The fibroblastoid type III cells defined by the absence of both M theta and Ia antigens formed the major cell population in the subsynovial tissue in this patient group. In patients with rheumatoid arthritis, the Ia+ M theta + cells were present in a characteristic double configuration forming an intensely positive layer adjacent to the intra-articular space followed by an Ia- M theta - layer that again was succeeded by an intensely Ia+ M theta + layer. Large numbers of synoviocytes bearing M theta + Ia+ antigens were also demonstrated in the diffusely inflamed subsynovial tissue, in the perivascular regions as well as around and within lymphoid infiltrates.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Monoclonal↗
PubMed1983

Effects of prostanoid precursors and indomethacin on chick embryonic cartilage growth in organ culture.

Using the Fell technique of organ culture of 8-day chick embryo femoral and tibial rudiments, the effects of indomethacin, dihomo-gamma-linolenic acid and arachidonic acid on limb rudiment linear growth and differentiation were investigated. Indomethacin (50 and 100 mumol/l) elicited a statistically significant decrease in rudiment linear growth without affecting differentiation or cell structure. Dihomo-gamma-linolenic acid and arachidonic acid, both at 100 mumol/l, exerted no effect on limb rudiment linear growth or differentiation. From previous work, it has been shown that PGA1 and PGB1 caused a marked inhibition of linear growth, PGA1 being cytotoxic. The failure of the prostaglandin (PG) precursors to reproduce these effects suggests that PGA or PGB biosynthesis in embryonic chondrocytes plays no significant role in cartilage growth regulatory mechanisms. Moreover, the growth inhibitory effect of the PG cyclooxygenase inhibitor, indomethacin, suggests that a product of arachidonic acid metabolism via the cyclooxygenase pathway may promote cartilage growth.

8,11,14-Eicosatrienoic Acid↗
PubMed1982

Lipid storage in cultured articular chondrocytes due to prostanoid precursors and a prostanoid synthesis inhibitor.

Lapine articular chondrocytes were subcultured in the presence or absence of the prostanoid precursors, arachidonic acid or dihomo-gamma-linolenic acid, and the cyclooxygenase inhibitor indomethacin. Lipid storage was studied microscopically using the Sudan black staining method. Control chondrocyte cultures showed a weakly positive staining reaction until confluence was reached, at which point the intra-cytoplasmic lipid content decreased. Both arachidonic acid and dihomo-gamma-linolenic acid at 100 mumol/l caused a marked increase in lipid storage which continued even after confluence was achieved. 1 mumol/l concentrations were indistinguishable from controls, whereas 10 mumol/l concentrations elicited a slight increase in lipid storage compared with controls. The prostaglandin cyclooxygenase inhibitor indomethacin did not affect chondrocyte lipid storage. However, administration of a prostanoid precursor in the presence of indomethacin caused a massive increase in intra-cytoplasmic storage of lipid, eventually leading to cell death. A possible explanation is that indomethacin may alter chondrocyte lipid metabolism in the presence of substrate molecules by rechanneling lipid synthesis away from the prostaglandin pathway to other lipid synthetic pathways.

8,11,14-Eicosatrienoic Acid↗
PubMed1982

Alterations in articular chondrocyte growth and proteoglycan synthesis due to prostanoid precursors.

The effects of the prostaglandin precursors, dihomo-gamma-linolenic acid and arachidonic acid, on chondrocyte proliferation, proteoglycan synthesis and morphological structure were studied using lapine articular chondrocytes in vitro. Neither substance exerted a cytotoxic effect on chondrocytes. Dihomo-gamma-linolenic acid caused a dose-dependent inhibition of chondrocyte proliferation (8% and 35% reduction at 10 and 100 mumol/l respectively) (P less than 0.01), whereas arachidonic acid failed to cause any significant alteration: 10 mumol/l of dihomo-gamma-linolenic acid stimulated proteoglycan synthesis by 14% (P less than 0.01), whilst 100 mumol/l elicited a reduction of 14% (P less than 0.01); 100 mumol/l of arachidonic acid also caused a statistically significant inhibition (31%) (P less than 0.001) of 35SO4 incorporation into proteoglycans. The inhibitory effects on proteoglycan synthesis may be mediated by intracellularly synthesized prostaglandins, which are known to exert this effect. This may also help explain the susceptibility of articular cartilage to damage with increasing age, as arachidonic acid is found in increasing concentrations in the superficial layers of articular cartilage.

8,11,14-Eicosatrienoic Acid↗
PubMed1982

The effects of nickel ions on articular chondrocyte growth in monolayer culture.

Monolayer cultures of lapine articular chondrocytes were used to study the effects of nickel ions (Ni++) on chondrocyte proliferative capacity, proteoglycan synthesis and cellular morphology. Nickel depressed chondrocyte proliferation at the highest concentration tested (100 mumol/l; P less than 0.01) and also exerted a dose-dependent inhibition of proteoglycan synthesis (50 and 100 mumol/l; P less than 0.01). Despite both these effects, no evidence of chondrocyte damage was detectable at the light-microscopical level. The possible significance of the nickel-induced reduction of articular chondrocyte proteoglycan synthesis for the functional integrity of the residual cartilage following hemiarthroplasty operations is discussed.

Animals↗
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

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↗