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Biomedical subjects

C W Denko

Publications and source records attributed to C W Denko.

14 recordsLinked to original sources
PubMed1979

Protective role of ceruloplasmin in inflammation.

Experimental inflammation in copper (Cu)-deficient rats is greater than that induced in controls eating normal diet. Cu-supplementation of the Cu-deficient diet results in a reduced swelling, down to normal levels. Injection of the naturally occurring acute phase reactant, ceruloplasmin (Cp) a Cu-bearing serum protein, also results in reduction of experimental inflammation. Since a rise in serum Cp occurs in normal pregnancy this protective anti-inflammatory action of Cp is proposed as an explanation for the widely-observed phenomenon of spontaneous control of rheumatoid arthritis in pregnancy.

Adult↗
PubMed1978

Sympathetic or reflex footpad swelling due to crystal-induced inflammation in the opposite foot.

Sympathetic or reflex footpad swelling occurred in rats when several crystals known to be pathogenic in human joints or soft tissues were injected into the opposite footpad. Monosodium urate (MSU), calcium pyrophosphate dihydrate (CaPPD), hydroxyapatite, calcium oxalate (CaOx), and xanthine (X) suspension induced varying degrees of such reflex of sympathetic swelling. In the second cycle of crystal-induced swelling, the foot that had been the initial or primary site of inflammation reacted with greater reflex swelling, when compared to the first cycle. Similarly, reflex increases in temperature occurred when CaPPD was injected. These reflex increases in swelling and temperature may relate to signs and symptoms of patients with reflex neurovascular dystrophy or shoulder--hand syndrome.

Animals↗
PubMed1978

Restorative chemotherapy in degenerative hip disease.

Twenty patients with degenerative joint disease (DJD) of the hip were treated for prolonged periods with an extract of cartilage and bone marrow. Although clinical improvement, lessened joint pain and increased function, occurred in a majority of the patients, the most significant changes were in four who had concomitant x-ray improvement. These patients had roentgenographic evidence of recovery of joint space and regeneration of the femoral head. Discussion is presented of possible mechanisms by which this tissue extract induces changes in chondrocyte metabolism. A theory is proposed to explain DJD as a multifactorial disorder in which liver impairment in processing growth hormone is the key malfunction. Treatment of DJD of the hip by injections of the tissue extract of cartilage and bone marrow is a rational and effective therapy without significant toxicity.

Aged↗
PubMed1978

Temporal changes in histone acetylation.

The incorporation of tritiated acetate was studied in developing and aging rats. Thymus, liver and serum were collected 30 minutes after injection of acetate. The trichloroacetic acid precipitable histone fraction was then extracted from liver and thymus and its radioactivity determined. Serum and cytoplasmic fractions were also counted. Serum activity declined with age. Thymus histone and cytoplasmic fractions showed a cyclic pattern. Acetylation of liver histones showed a straight line decline to a relatively constant level. The decline in acetylation of liver histones is postulated to be due to repression of acetylation processes and is thought to parallel the change of hepatocytes from a diploid to a polyploid state.

Acetates↗
PubMed1978

A new mechanical method for measuring rat paw edema.

A new method is presented for measuring swelling or rat paw edema in inflammation induced by carrageenin injection. This technique is compared to other widely used ones. A spring-loaded dial indicator produces results that are accurate, precise and reproducible. It is recommended for investigators seeking the advantages of a noninvasive, low cost, rapid method quantifying the swelling of inflammation.

Animals↗
PubMed1978

Chernogubov's syndrome: a translation of the first modern case report of the Ehlers-Danlos syndrome.

The heritable disorder of connective tissue, now termed Ehlers--Danlos syndrome, was described by Chernogubov, a Russian dermatologist, in 1892. His graphic description of the first modern case with multisystemic features is presented in English translation. Chernogubov attributed the development of this disorder to a generalized defect in the embryological formation of connective tissue fibers. Chernogubov's observations were recognized by his colleagues as providing new insights in explaining an interesting and puzzling case. In the literature of the Soviet Union this syndrome is known as Chernogubov's syndrome. This work is justifiably recognized as a seminal publication in rheumatology.

Adolescent↗
PubMed1977

Prostaglandin A2 and 35S uptake in connective tissue.

Rats deficient in essential fatty acids (EFA) incorporated lesser amounts of radioactive sulfate into lung, kidney, spleen, heart, costal cartilage, long bone and skull bone than did normal control animals. Administration of prostaglandin A2 stimulated 35S uptake by lung, kidney and aorta while 35S levels in costal cartilage, tibial cap and long bone were strikingly reduced. Comments are presented suggesting that this metabolic mechanism may explain, in part, cartilage and bone resorption in areas of inflammation, such as arthritis, both rheumatoid arthritis and osteoarthritis.

Animals↗
PubMed1976

Modification of adjuvant inflammation in rats deficient in essential fatty acids.

Rats deficient in essential fatty acids (EFA) did not develop as much foot swelling on receiving injections of complete Freund's adjuvant as did normal controls. Both the acute inflammation and the chronic inflammation were affected. This reduction in the chronic phase of adjuvant inflammation was restored to normal levels by feeding a small supplement of corn oil as a dietary source of EFA. Since the EFA are biologic precursors of prostaglandins (PG), the lack of EFA is thought to influence adjuvant-induced inflammation by reducing available PG mediators of inflammation.

Acute Disease↗
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↗
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↗