Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two trials using the splenomegaly assay were conducted to assess the effects of adrenocorticotropin (ACTH) and dietary ascorbic acid (AA) on the ability of chickens to mount a graft-vs.-host reaction (GVHR). Broiler chicks served as blood donors. Birds received AA at levels of 0, 150, or 300 mg/kg of feed (ppm). At 6 wk of age, donor birds from each AA group received either three intramuscular injections of ACTH in gelatin at 12-h intervals, comparable injections of the gelatin, or no injections. Thirteen-day-old Single Comb White Leghorn embryos served as recipients. Two recipient embryos per donor were injected in a chorioallantoic vein with either whole blood (Trial 1) or saline-washed and reconstituted blood cells (Trial 1). Eggs were further incubated for 6 days, at which time the embryos were killed and each spleen excised. Relative spleen weights were expressed as milligrams of spleen/100 g embryonic body weight. Significant differences in relative spleen weight or donor plasma corticosterone (CS) levels did not occur in Trial 1. In Trial 2, regardless of AA treatment, relative spleen weights of embryos that received blood cells from donors treated with ACTH were significantly lower than controls. Donor CS was significantly lower in birds that received ACTH. These results indicate that, when washed and reconstituted blood cells are injected into recipients and donor plasma CS is decreased, GVHR capacity is suppressed in ACTH-treated donors.
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PMID:Effect of adrenocorticotropin and dietary ascorbic acid on the graft-versus-host reaction capacity of chickens. 283 55

Subcutaneous injection of nonspecific irritants such as magnesium silicate (talc) provokes granulomatous inflammation in the rat. Part of the acute phase response (APR) in these animals is the loss of trabecular bone at sites distant from the site of inflammation. To assess the possible involvement of vitamin D in the bone loss, we studied the development of the acute phase response in vitamin D-deprived rats. The serum APR provoked by subcutaneous inflammation in rachitic rats consisted of hypozincemia, hypercupremia, increased alkaline phosphatase activity and adrenocorticotropic hormone (ACTH) concentration, and was similar to that in control animals except for the absence of hypoferremia. Control rats with talc-induced subcutaneous inflammation also had splenomegaly and decreased total and mononuclear peripheral blood cell counts, while subcutaneous inflammation did not induce spleen changes in rachitic rats. Subcutaneous inflammation induced the loss of trabecular bone and decreased the osteoblastic cell count in tibial metaphyses in control animals. Rachitic rats had abundant osteoid on trabecular surfaces, and the number of osteoblasts and osteoclasts was comparable to that of the controls. Subcutaneous inflammation did not affect any of the bone parameters in rachitic rats. These results indicate that vitamin D plays an important role in the generation of the acute phase response during inflammation, particularly in the induction of spleen and bone cell changes. The discrepancy of the blood on one hand and bone and spleen indices of the APR on the other, indicate that they may be divergent pathways in the generation of the inflammatory response, some of which may be dependent on vitamin D.
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PMID:Role of 1,25-dihydroxyvitamin D3 in the generation of the acute-phase response in rats with talc-induced granulomatosis. 835 76