Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because pyridoxal phosphate does not normally cross membranes, it was intriguing that the concentration of pyridoxal phosphate is much higher in goat milk than in human milk. We also noted that, although the total vitamin B-6 concentration of bovine milk was similar to that of caprine milk, the bovine milk had lower pyridoxal phosphate. Preliminary data from five Alpine goats, five Brown Swiss cows, five Holstein cows and three humans suggested that there was an inverse relationship between pyridoxal phosphate concentration and phosphatase activity in the goats and cows but not in the humans. This was confirmed with additional data from Nubian goats, Jersey and Guernsey cows, and crossbred sows. Combining the animal data yielded the following relationship between pyridoxal phosphate (PLP, mumol/L) and alkaline phosphatase (P'ase) activity (mmol/(min.L): PLP = 2.03e(-2.26 P'ase) + 0.03. The human milk samples were low in both pyridoxal phosphate and alkaline phosphatase. We conclude that in goats, cows and pigs a significant fraction of the vitamin B-6 appearing in the milk is secreted as pyridoxal phosphate, probably bound to protein, and varying amounts may then be hydrolyzed back to pyridoxal depending on the alkaline phosphatase activity. Human mammary tissue apparently secretes very little pyridoxal phosphate.
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PMID:Alkaline phosphatase activity and pyridoxal phosphate concentrations in the milk of various species. 145 18

Brown Hisex chicks were fed diets containing 2% and 5% Azadirachta indica leaf from their 7th to 35th day of age. Thereafter, the chicks were fed control diet for 2 weeks. A depression in body weight gain and efficiency of feed utilization was observed in chicks fed A. indica leaf when compared with the control. The main clinicopathological changes were increases in lactic dehydrogenase, glutamic oxaloacetic transaminase and alkaline phosphatase activities and uric acid and bilirubin concentrations and decreases in the total protein levels in serum. Changes in the values of erythrocyte count, haemoglobin concentration, packed cell volume, mean corpuscular volume and mean corpuscular haemoglobin were remarkable and associated with yellow discoloration on the legs and combs and hepatonephropathy. Tissue recovery was incomplete 2 weeks after removal from the experimental diets.
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PMID:On the toxicology of Azadirachta indica leaves. 804 48

The authors describe the technique employed for percutaneous transhepatic sphincterotomy as performed on 3 patients with common bile duct (CBD) stones. In all patients, previous endoscopic attempt had failed for anatomical reasons (Billroth II gastric resection or partial gastric resection with Brown anastomosis), and the ampulla could not be correctly incannulated with the sphincterotome. In all patients endoscopy was useful to check the position of the diathermic loop inserted percutaneously. Complete and immediate success was obtained in all 3 cases. No major complications occurred during transhepatic treatment. To date, 1 recurrence has been observed, and the patient has been retreated with bilioplasty. All patients were followed after 5-6 months with US, plain X-rays of the abdomen and blood tests (gamma Gt, alkaline phosphatase, and bilirubinemia). The authors suggest that percutaneous transhepatic sphincterotomy be employed electively in patients with biliary tree diseases in case the endoscopic approach failes.
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PMID:[Percutaneous transhepatic sphincterotomy]. 228 Nov 74

Cyclosporine metabolites (CM) were compared with cyclosporine for their in vitro and in vivo immunosuppressive, nephrotoxic, and hepatotoxic effects using (A) in vitro mixed lymphocyte induction of monocyte/macrophage procoagulant activity (PCA), an accurate marker of allograft rejection; (B) in vitro toxic effects on renal cells in culture; and (C) a unidirectional rejection model of rat small intestinal transplantation (SIT). CM were composed of OL1, OL17, OL18, and two additional peaks C and H, (peak C: mass = 1235, 15.3% of total CM, peak H: mass = 1205, 6.3% of total CM). In vitro, CM fully suppressed the one-way mixed lymphocyte culture-induced PCA from 52.5 +/- 8.2 mU/10(6) PBM to the basal level 22.3 +/- 6.6 mU/10(6) PBM (P less than 0.01), which was comparable to CsA (21.3 +/- 5.5 mU/10(6) PBM). Lewis rats that had received Lewis-Brown Norway F1 hybrid intestinal allografts when treated with CM, demonstrated near-normal histology with minimal signs of rejection as compared with the fulminant clinical and histological rejection observed in the control (untreated and Cremaphor/NaCl treated) animals. PCA was markedly elevated in the control animals, 278 +/- 172 (untreated) and 160 +/- 98 mU/10(6) PBM (Cremaphor/normal saline treated), whereas CsA-treated allogeneic transplants expressed only basal levels of PCA (14.0 +/- 4 mU/10(6) PBM) (P less than 0.01), associated with normal histology. CM-treated animals expressed PCA levels of 27.0 +/- 10 mU/10(6) PBM, which was significantly different from both control and CsA-treated animals (P less than 0.01). In contrast to CsA-treated animals, CM-treated allogeneic transplants demonstrated no apparent renal or hepatic toxicity, as measured by blood urea nitrogen (25.3 +/- 9.5 vs. 10.0 +/- 5.3 mg/dl), alkaline phosphatase (160.7 +/- 29.3 vs. 100.3 +/- 19.5 U/L), and aspartate transaminase (96.7 +/- 23.7 vs. 61.7 +/- 11.7 U/L) (P less than 0.01). Similarly, in contrast to CsA, CM had minimal or no toxicity in renal epithelial and mesangial cells in culture, as measured by minimal or no inhibition of DNA, RNA, and protein synthesis. These results suggest that CM have potent immunosuppressive properties with no apparent nephrotoxicity and hepatotoxicity in vitro and in vivo.
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PMID:The effects of cyclosporine and cyclosporine metabolites in experimental small intestinal transplantation. 236 Feb 47

Diamine oxidase (DAO; EC 1.4.3.6) is an enzyme found in high activity in the mature upper villus cells of rat intestinal mucosa and only in very low activity in all other tissues except for the placenta in the pregnant rat. The present study was designed to investigate whether plasma and mucosal DAO could be used to monitor the timing and severity of injury and recovery of the intestinal mucosa after administration of the chemotherapeutic agent 1-beta-D-arabinofuranosylcytosine (ara-C). A dose of 0.3 g/kg s.c. every 8 hr for 6 doses was given to adult Lewis x Brown Norway rats. This resulted in death of the proliferating crypt cells, followed by regeneration of the mucosa from the surviving crypt cells, with recovery by Day 8. This mucosal damage and recovery was reflected by histological changes and a decrease in activity of mucosal disaccharidases and alkaline phosphatase. Both mucosal and plasma DAO levels also fell markedly to less than 10% of basal levels (N = 30, p less than 0.005) by Day 4 and recovered with a time course similar to the histological and biochemical changes indicative of injury and recovery. With increasing dosage and/or increasing duration of ara-C treatment, mucosal injury was progressive, with increasing loss of both plasma and mucosal DAO levels as compared to controls (N = 38, p less than 0.005). Plasma DAO levels in three patients with leukemia following ara-C chemotherapy decreased markedly to less than 30% of basal pretreatment levels (p less than 0.05) by Days 9 to 12, with a time course that was compatible with clinical intestinal mucosal injury. Our data document that plasma DAO levels reflect the mucosal injury and subsequent recovery after ara-C treatment in the rat and humans. Thus, plasma DAO may serve as a marker of the integrity of the intestinal mucosa after chemotherapy.
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PMID:Diamine oxidase as a plasma marker of rat intestinal mucosal injury and regeneration after administration of 1-beta-D-arabinofuranosylcytosine. 678 36

Chondrocyte hypertrophy involves de novo acquisition and/or increased expression of certain gene products including, among others, type X collagen, alkaline phosphatase, and matrix metalloproteinases. To analyze further the genetic program associated with chondrocyte hypertrophy, we have employed a modification of the polymerase chain reaction-mediated subtractive hybridization method of Wang and Brown (Wang and Brown [1991] Proc. Natl. Acad. Sci 88:11505). Cultures of hypertrophic tibial chondrocytes and nonhypertrophic sternal cells were used for poly A+ RNA isolation. Among 50 individual cDNA fragments isolated for up-regulated hypertrophic genes, 18 were tentatively identified by their similarities to entries in the GenBank database, whereas the other 32 showed no significant similarity. The identified genes included translational and transcriptional regulatory factors, ribosomal proteins, the enzymes transglutaminase and glycogen phosphorylase, type X collagen (highly specific for hypertrophic cartilage matrix), gelsolin, and the carbohydrate-binding protein galectin. Two of these, transglutaminase and galectin, were cloned and were further characterized. The chondrocyte transglutaminase revealed previously in hypertrophic cartilage by immunochemical methods appears to be the chicken equivalent of mammalian factor XIIIa (showing 75% overall protein similarity). The chicken chondrocyte galectin is a variant of mammalian galectin-3. Galectins are known to bind to components found in hypertrophic cartilage, and factor XIIIa is known to crosslink some of the same components, possibly modifying them for calcification and/or removal.
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PMID:Identification and characterization of up-regulated genes during chondrocyte hypertrophy. 889 82

The effect of an orally administered glutamine-enriched elemental diet was examined following orthotopic small bowel allotransplantation using Brown Norway rats as donors and Lewis rats as recipients. The recipients was treated with FK 506 and randomized to receive glutamine-free elemental enteral diet solution (glutamine-free group), glutamine-enriched elemental diet solution containing 7500 mg of glutamine per 100 g diet (glutamine-enriched group) or standard chow (chow group) ad libitum for 7 d. There were no histological changes due to resection. Weight loss in the glutamine-enriched group was significantly less than that of the chow group. Both plasma glutamine levels and the ratio of glutamine to total amino acids in the homogenate of the graft mucosa of the glutamine-enriched group were significantly higher than those of the glutamine-fee group. Villous height and crypt depth were significantly decreased in the glutamine-free group. The BrdU labeling index in the graft epithelium and alkaline phosphatase activity in the homogenate of the graft mucosa of the glutamine-enriched group were significantly higher than those of the glutamine-free group. Therefore, orally administered glutamine-enriched elemental diet appears to promote the regeneration and differentiation of the graft mucosa following small bowel allotransplantation.
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PMID:Effect of a glutamine-enriched diet on small bowel allograft during immunosuppressive therapy. 929 90

1. Plasma alkaline phosphatase (ALP) activity was determined in 4 laying strains (White Leghorn, New Hampshire, Native Brown and Native Barred) at 48 and 54 weeks of age. Birds were fed 1 of 2 isoenergetic diets with calculated crude protein contents of 152 and 181 g/kg. 2. No significant differences in plasma ALP activity were noted between the strains, although significant differences in laying performance between strains were evident. 3. There was no response in plasma ALP activity to the high dietary protein level in any strain. Depressed plasma ALP activity was associated with increasing age of birds. 4. The results failed to confirm the suggestion that ALP activity is related to egg production of the laying hen.
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PMID:Plasma alkaline phosphatase and production traits in laying hens as influenced by dietary protein, strain and age. 980 45

Ozone is known to induce airway hyperresponsiveness (AHR) in humans and animals. Previous studies in animals used high exposure levels and reported inconsistent results. The aim of this study was to investigate the effect of a single low-level ozone exposure on different inbred rat strains. Nine rat strains were exposed to 0.05 parts per million (ppm) for 4 h and airway responsiveness to intravenous 5-hydroxytryptamine (HT) examined. Bronchoalveolar lavage fluid (BALF) was examined for the presence of inflammatory cells and markers. Lewis, BDII and Long-Evans rats developed AHR 90 min after ozone exposure, whereas Wistar, Sprague-Dawley, Fisher 344, Brown-Norway, BDE and DA rats did not. Baseline airway responsiveness to 5-HT differed significantly between rat strains, but did not correlate with the presence or absence of ozone-induced AHR. No inflammatory cell influx was found in BALF of any rat strain. In Long-Evans rats, AHR lasted up to 12 h after ozone exposure despite the absence of an inflammatory cell influx or increase in lactate dehydrogenase, alkaline phosphatase or total protein in BALF. In conclusion, exposure to an ambient concentration of ozone induced airway hyperresponsiveness without airway inflammation in some highly inbred rat strains. Genetic factors are likely to account for the observed variability in sensitivity of the airways to ozone.
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PMID:Ambient ozone concentrations induce airway hyperresponsiveness in some rat strains. 1048 39

In order to test the hypothesis (Munn, Zhou, Attwood, Bondarev, Conway, Marshall, Brown, Mellor, Science 281 (1998) 1191-1193) that localized placental tryptophan catabolism prevents immune rejection of the mammalian fetus, the cellular localization and characteristics of human placental indoleamine 2,3-dioxygenase (EC 1.13.11.42) were studied. The localization of indoleamine 2, 3-dioxygenase activity was determined quantitatively using cell fractionation by differential and discontinuous sucrose gradient centrifugation. Enzyme activity was looked for in isolated brush border microvillous plasma membranes of placental syncytiotrophoblast. We found that this membrane preparation (which showed a 32.4-fold purification from the starting homogenate with reference to the activity of a membrane marker enzyme, alkaline phosphatase (EC 3.1.3.1)) was strongly negatively enriched with indoleamine 2,3-dioxygenase (which showed a one twenty-fifth decrease in its specific activity). Placental indoleamine 2, 3-dioxygenase is thus not expressed in the maternal facing brush border membrane of syncytiotrophoblast. 1-Methyl-DL-tryptophan which was used by Munn et al. as a key experimental tool for inhibiting indoleamine 2,3-dioxygenase in the murine model showed a competitive inhibition of human placental indoleamine 2,3-dioxygenase with L-tryptophan. The hypothesis, based on experiments performed in mouse, may therefore be applicable to avoidance of immune rejection of the fetus in human pregnancy.
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PMID:Human placental indoleamine 2,3-dioxygenase: cellular localization and characterization of an enzyme preventing fetal rejection. 1056 24


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