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Biomedical subjects

C W Denko

Publications and source records attributed to C W Denko.

At least 55 records · Page 3Linked to original sources
PubMed1976

Experimental inflammation induced by naturally occurring microcrystalline calcium salts.

Inflammation caused by insoluble microcrystalline calcium salts was compared with inflammation elicited by soluble carrageenan and monosodium urate crystals, in rats' paws. Local and systemic responses to four calcium crystals, viz. pyrophosphate, triphosphate, oxalate, and tartrate were studied. Changes in liver function, reflected in reduced serum albumin and increased sleep times in response to barbiturates, indicative of systemic inflammation, occurred despite the localized nature of the crystal induced inflammation. Serum thiol levels were also reduced. These altered functions were similar to, but less pronounced than, those accompanying the severe systemic inflammation produced by Freund's adjuvant. A copper glycine complex was effective in reducing foot swelling due to triphosphate, and edema due to oxalate. Colchicine had very little effect on the inflammation caused by the insoluble calcium salts but inhibited inflammation due to sodium urats crystals and soluble carrageenan. Crystal-induced inflammation that is outwardly localized may induce biochemical changes that are similar to changes found in systemic inflammation.

Animals↗
PubMed1976

35S and 3H-proline incorporation in rats deficient in essential fatty acids.

The effects of essential fatty acid (EFA) deficiency on connective tissue metabolism were studied in rats deficient in EFA and prostaglandins (PG). In chronic EFA deficiency, 3H-proline fixation, a measure of protein synthesis, was markedly reduced in the stomach, liver, adrenal, kidney, spleen, heart, and small intestine. Collagen rich tissues, such as lung, aorta, and cartilage also demonstrated reduced 3H-proline incorporation. 35S uptake, a measure of glycosaminoglycan synthesis, was inhibited in the lung, kidney, spleen, aorta, small intestine, and cartilage. Shorter periods of EFA deficiency resulted in similar diminished 35S incorporation. However, corn oil supplements largely corrected these metabolic defects. PGE1 injections stimulated 35S uptake in the mucus secreting tissues of the stomach and intestine. Comments are presented suggesting that the anti-PG actions of steroids and non-steroidal anti-inflammatory drugs contribute to ulcer formation during drug therapy.

Animals↗
PubMed1975

Anti-prostaglandin action of colchicine.

Colchicine, given locally, inhibits urate-crystal- and CaPPD-crystal-induced inflammation. Since this inflammation is known to be mediated in part by PGE1 these observations indicate colchicine acts as an anti-PG agent. Colchicine counteracts the phlogistic action of exogenous PGE1 in both urate- and CaPPD-crystal-induced inflammation. With use of large excesses of colchicine, its anti-inflammatory action appears limited to its anti-PGE1 activity. In turn, PGE1 counteracts the antiphlogistic action of colchicine. Colchicine is less effective in reducing swelling due to CaPPD-crystals than that due to urate-crystals, a finding similar to the clinical observations that colchicine is more effective therapy for gout than for pseudogout. Some relationships are reviewed to suggest that CaPPD-crystal inflammation is a more severe membrane disorder than is urate-crystal inflammation.

Animals↗
PubMed1975

A phlogistic function of PGE1 in calcium pyrophosphate dihydrate crystal-induced inflammation.

Promotion of calcium pyrophosphate dihydrate (CaPPD) crystal-induced inflammation by prostaglandin (PG) E1 has been demonstrated by two new techniques: (1) Rats deficient in essential fatty acids, biological precursors of PG, developed less footpad swelling than did normal rats following injections of unheated CaPPD. Addition of one ng of PGE1 to these crystals resulted in normal swelling. (2) This phlogistic effect of PGE1 was also demonstrated in normal rats fed a normal dietwho received injections of CaPPD crystals heated to 200 degrees C for three hours. The heated crystals induced less footpad swelling than did unheated crystals. When one ng of PGE1 was added to the suspensions of heated crystals the resultant swelling approximated that obtained by unheated crystals. The possible role of PGE1 in mediating CaPPD crystal-induced inflammation is suggested. An analysis of urate and CaPPD crytal-induced inflammation is presented with comments setting forth the concept that these metabolic crystal disorders are membrane diseases.

Animals↗
PubMed1974

Effect of prostaglandins in urate crystal inflammation.

By use of two novel techniques for detecting extremely small amounts of PGs, studies were conducted elucidating the mechanism of urate crystal-induced inflammation. Rats deficient in EFA and thus deficient in PGs received injections of monosodium urate crystals into the footpad. The EFA-deficient animals developed less swelling than did normal animals. However, when a 1-ng dose of PGE-1, PGE-2, PGA-2, or PGF-2-alpha was added along with the urate injection the swelling was enhanced to approximately normal levels. In the second technique the swelling induced by injection of two different urate crystals was compared. Urate crystals heated to 200 degrees C produced less swelling in normal rats than did similar urate crystals heated only to 50 degrees C. However when a 1-ng dose of PGE-1, PGE-2 or PGF-2-alpha was added to the heated urate crystals injection the swelling increased to approximately the swelling in normal controls receiving urate heated to 50 degrees C. Comments are presented suggesting that urate crystal inflammation may be a membrane disease.

Animals↗
PubMedDate not supplied

Serum proteins--transferrin, ceruloplasmin, albumin, alpha 1-acid glycoprotein, alpha 1-antitrypsin--in rheumatic disorders.

Serum levels of carrier proteins, transferrin, ceruloplasmin and albumin were determined in patients with rheumatic disorders, along with serum levels of acute phase proteins, ceruloplasmin, alpha 1-acid glycoprotein and alpha 1-antitrypsin. Depressed levels of transferrin occurred in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Albumin was reduced in SLE and RA men. Acute phase reactants which are protective in inflammation were elevated in RA, osteoarthritis (OA), gout, pseudogout (PsG), and SLE. All of these rheumatic disorders show biochemical changes compatible with systemic inflammatory disease including gout and PsG which are considered local disorders and OA which is considered noninflammatory arthritis.

Arthritis, Rheumatoid↗
PubMedDate not supplied

Hydroxyapatite crystal-induced inflammation and prostaglandin E1.

Hyroxyapatite (HOAp), tribasic calcium phosphate, crystals induced typical signs of inflammation when injected into the footpad of the rat. Rats deficient in essential fatty acids (EFA) and thereby deficient in prostaglandins (PG) demonstrated less swelling than did normal controls. Similar reduced inflammatory swelling resulted from the use of HOAp crystals heated to 200 degrees C. The reduced inflammogenic effect of the heated crystal and the reduced response of the EFA-deficient rat were comparable and were corrected by adding PGE1. This PGE1 influence was of short duration in both test systems. A new theory of crystal induced inflammation is presented based on experiments using PGE1 with monosodium urate, calcium pyrophosphate and HOAp crystals. It is suggested that this inflammation is a membrane phenomenon related to synthesis or release of PG from cellular membranes stimulated by an electrostatic force from the crystals.

Animals↗