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Biomedical subjects

G DiPasquale

Publications and source records attributed to G DiPasquale.

At least 37 records · Page 2Linked to original sources
PubMed1986

Lack of response of rat chondrosarcoma chondrocytes to interleukin-1 to produce proteoglycan- and collagen-degrading enzymes.

Chondrocytes obtained from rat articular cartilage and Swarm rat chondrosarcoma were maintained in culture. Human interleukin-1 (IL-1) was added at confluency, and three days later the spent media was evaluated for proteoglycan- and collagen-degrading enzymes. Unlike chondrocytes from articular cartilage from several species, chondrocytes from Swarm rat chondrosarcoma did not respond to IL-1 stimulation. This lack of sensitivity to IL-1 may be a useful biochemical marker to classify various types of chondrosarcomas. However, it appears that the use of chondrosarcoma chondrocyte cultures are not useful as a source for metalloproteinases.

Animals↗
PubMed1985

Effect of antirheumatic agents on the mitogen response of arthritic rat spleen cells.

Splenic lymphoid cells from rats with adjuvant induced polyarthritis show a diminished response to the T-cell mitogens Con A and PHA. This report describes the in vitro effects of various antirheumatic agents on the mitogen induced proliferative response of normal (NSC) and arthritic (ASC) rat spleen cells. Indomethacin enhanced only the arthritic responses. Other PG synthesis inhibitors such as ibuprofen and naproxen enhanced the arthritic as well as the normal spleen cell proliferative responses. Gold sodium thiomalate augmented arthritic but not normal blastogenesis. Penicillamine significantly enhanced only the Con A response of arthritic cells at 10(7)M. Levamisole produced a significant increase in the PHA response of arthritic cells and the Con A NSC response. Chloroquine diphosphate enhanced the Con A response of normal cells at 10(-5)M and 10(-6)M; both chloroquine and tilorone suppressed blastogenesis of arthritic spleen cells at 10(-4)M and 10(-5)M. When classifying antirheumatic agents as stimulator or suppressors of immune function, one must account for their effects on arthritic as well as normal lymphoid cells at the predicted pharmacologic plasma levels.

Animals↗
PubMed1985

Comparison of spontaneous and retinoic acid stimulated rabbit articular cartilage degradation in vitro.

The in vitro degradation of rabbit articular cartilage explants was evaluated with and without the addition of retinoic acid under various experimental conditions. Retinoic acid at nontoxic concentrations ranging from 1 X 10(-7) to 1 X 10(-5) M significantly increased cartilage degradation. The addition of phenanthroline or cycloheximide, but not pepstatin, significantly inhibited spontaneous and retinoic-acid-stimulated cartilage degradation at pH 7. When the pH was reduced to 5, only pepstatin inhibited spontaneous and retinoic-acid-stimulated cartilage degradation. No chondroitin sulphate release was observed when the temperature was reduced to 4 degrees C. The different inhibitory profiles observed at pH 7 and pH 5 suggest that cartilage degradation at pH 7 is associated with the presence and synthesis of a neutral metalloproteinase.

Animals↗
PubMed1982

Isoxicam and related 4-hydroxy-N-isoxazolyl-2H-1,2-benzothiazine-3-carboxamide 1,1-dioxides. Potent nonsteroidal antiinflammatory agents.

A novel series of antiinflammatory agents, N-isoxazolyl-3-carboxamides of 4-hydroxy-2H-1,2-benzothiazine 1,1-dioxide, was synthesized and evaluated as antiinflammatory agents in the carrageenin-induced rat paw edema (CIRPE) assay and adjuvant-induced polyarthritis (AIP) assay. Several analogues were found to be equipotent or more potent than aspirin and phenylbutazone. Structure-activity relationships are discussed. One of the compounds, 4-hydroxy-2-methyl-N-(5-methyl-3-isoxazolyl)-2H-1,2-benzothiazine 3-carboxamide 1,1-dioxide (3a; isoxicam), was found to be 3 times as potent as phenylbutazone in the CIRPE and in the therapeutic AIP assays. Isoxicam (3a) is presently undergoing phase III clinical trial as an antiarthritic drug.

Animals↗
PubMed1977

Inhibition of arachidonic acid induced mortality in rabbits with several non-steroidal anti-inflammatory agents.

The intravenous administration of arachidonic acid to rabbits is an effective in vivo model for evaluating potential anti-thrombotic drugs. Most of the non-steroidal anti-inflammatory agents (NSAIFA) inhibit this arachidonic acid induced mortality (except sodium salicylate and acetaminophen). However, there is a lack of correlation between the relative potencies from various assays (rabbit anti-thrombotic, anti-inflammatory, alalgesic, ulcerogenic and inhibition of prostaglandin synthetase evaluations). These studies imply other actions with NSAIFA than an effect solely on the prostaglandin biosynthetic pathway.

Animals↗