Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A rapid, inexpensive method for the separation of 5-1-isoleucyl[14C] angiotensin II (A-II) from its various metabolites has been devised. A-II was extracted from tissues with absolute methanol (recovery 96%) and paper chromatographed in a butanol-acetic acid-water (18:2:5) medium for two ascents at 60 degrees C. The resulting RF for A-II of 0.45 was then compared with the RF values of three A-II metabolites produced by enzymatic degradation of the 14C-A-II and [14C]isoleucine. Trypsin degradation produced the [14C]hexapeptide metabolite, chymotryptic degradation produced the [14C]tetrapeptide metabolite and carboxypeptidase A degradation produced the [14C]heptapeptide. Increases in temperature produced a continuous increase in RF values for all the substances examined but the resolution decreased above 60 degrees C. Similarly, increases in the temperature caused the appearance of secondary peaks with some but not all peptides. The tryptic digest (hexapeptide) and the chymotryptic digest (tetrapeptide) are apparently acid- and heat-stable under the experimental conditions. All of the peptides examined failed to produce secondary peaks when heated at neutral pH. The method was used to study the tissue distribution of 14C-A-II after intravenous injection.
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PMID:Rapid paper chromatographic separation of [14C] angiotensen II from some metabolites: application to organ distribution. 3 36

Polypeptide VII of cytochrome c oxidase was isolated and purified by gel filtration on Bio-Gel P-10 in 10% acetic acid. Automatic Edman degradation of this peptide chain was not successful, because it is blocked at the N-terminus. The amino acid analysis shows a relatively high content of hydrophilic residues (54%). On the basis of this analysis and the apparent molecular weight by sodium dodecyl sulfate gel electrophoresis and gel filtration, a chain length of about 80 residues was calculated. Among the tryptic peptides one blocked heptapeptide was found. Cleavage of this peptide with thermolysin gave two peptide fragments, one of which was not retained on a cation exchange resin. Mass spectrometric sequence determination of this peptide revealed the structure Ac-Ala-Glu-Asp for the N-terminus of polypeptide VII. Treatment with carboxypeptidase A at two different pH values showed that the C-terminal amino acid is isoleucine and the penultimate amino acid is lysine.
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PMID:Studies on cytochrome c oxidase, VII. Isolation and chemical characterization of polypeptide VII. 22 66

Lyophilized bovine, porcine, and human choroid plexuses contain .02-.09 U of antidiuretic activity per milligram. The antidiuretic factor in bovine choroid plexus was concentrated 100 times by extraction with acetic acid, fractional precipitation with acetone and ethyl ether, gel filtration, and paper chromatography. Resulting choroid plexus fraction IIgammaB2 was eluted from Sephadex G-25 in position corresponding to molecular weight between 750 and 3,500; its antidiuretic activity was destroyed by trypsin, performic acid, and thioglycollic acid, but was not affected by leucine aminopeptidase, carboxypeptidase A or B, or cyanogen bromide. HgammaB2 possesses antidiuretic, pressor, and oxytocic potencies (measured in anesthetized-hydrated rat, anesthetized rat, and isolated rat uterus, respectively) of 1.9, 0.5, and 0.1 U/mg, respectively.
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PMID:Antidiuretic peptide in mammalian choroid plexus. 81 22

Studies on the identification of the terminal residues in protease-free hog pancreatic alpha-amylase, prepared by glycogen precipitation, demonstrated the absence of free amino terminals when four different chemical procedures were used. These methods were based on reaction with fluorodinitrobenzene, trinitrobenzenesulfonic acid, dansyl chloride, and cyanate. In the search for the presence of a possible alpha-N-blocking group, an acetyl group was detected as acetic acid dinitrophenyl hydrazide after hydrazinolysis and dinitrophenylation. Quantitation of acetyl groups by a gas chromatographic or a specific enzymatic method yielded 0.7 mol of acetyl group per 51,000 g of protein. Other acyl groups, such as formyl or propionyl, were not found. Leucine was shown to be the carboxyl terminal residue by hydrazinolysis or by carboxypeptidase A digestion of acid denatured amylase. With either procedure, 0.8 mol of carboxyl terminal leucine was found per 51,000 g of protein. These findings are consistent with the proposal that hog pancreatic alpha-amylase is composed of a single, alpha-N-acetylated chain of molecular weight 50,000. Claims of other investigators for subunit and multichain structures for this enzyme are discussed in view of these end group data.
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PMID:Terminal residues of hog pancreatic amylase. 98 1

Magnolol, isolated from Magnolia officinalis, inhibited mouse hind-paw edema induced by carrageenan, compound 48/80, polymyxin B and reversed passive Arthus reaction. Acetic acid-induced writhing response was depressed by magnolol, indomethacin and ibuprofen. The lethality of endotoxin challenge was reduced by pretreatment with magnolol, indomethacin and BW755C, a dual cyclo-oxygenase/lipoxygenase inhibitor. The recovered myeloperoxidase activity in edematous paw was significantly decreased in mice pretreated with magnolol and BW755C. Suppression of edema was demonstrated not only in normal mice but also in adrenalectomized animals. Magnolol was less potent on reducing PGD2 formation in rat mast cell than that of indomethacin. Unlike dexamethasone, magnolol did not increase liver glycogen level. The results suggest that the anti-inflammatory effect of magnolol was neither mediated by glucocorticoid activity nor through releasing steroid hormones from adrenal gland. The action of magnolol is proposed to be dependent on reducing the level of eicosanoid mediators.
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PMID:Anti-inflammatory and analgesic effects of magnolol. 133 74

The effects of ketotifen, a 'mast cell stabiliser,' on two models of experimental colitis were examined. The inflammatory response elicited by either trinitrobenzene sulphonic acid or acetic acid resulted in increased colonic synthesis of platelet activating factor, prostaglandin E2, thromboxane B2, leukotrienes B4 and C4, and myeloperoxidase activity. Intragastric administration of ketotifen 100 micrograms/100 grams twice daily significantly decreased mucosal damage when given prophylactically 48 hours before the induction of colitis and then throughout the experiment. This effect was consistent in both models and was accompanied by a significant reduction in mucosal generation of platelet activating factor, prostaglandin E2, thromboxane B2, and leukotrienes C4 and B4. Myeloperoxidase activity was reduced as well, reaching significance only in the acetic acid model. This study shows that both trinitrobenzene sulphonic acid and acetic acid colitis can be pharmacologically manipulated by ketotifen. The mechanism of action of ketotifen has not yet been determined. Ketotifen's potential in the treatment of active inflammatory bowel disease or in the prevention of exacertations, or both, remains to be elucidated.
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PMID:Ketotifen effectively prevents mucosal damage in experimental colitis. 145 75

Quazolast, a mast cell stabilizer, was evaluated for efficacy against acid independent (alcohol, HCl), or dependent (aspirin, indomethacin) gastric damage in rats. Its gastroprotective profile was compared to that of ranitidine. In addition, the antisecretory and gastric ulcer (acetic acid induced) healing capabilities of these agents were examined. Quazolast, in direct contrast to ranitidine, protected the rat gastric mucosa from acid-independent, but not acid-dependent gastric damage. Quazolast lacked antisecretory activity in rats; however, it did heal acetic acid induced gastric ulcers in this species. On day 15 after acetic acid injection, quazolast significantly healed such ulcers, while ranitidine did not. Although the exact mechanisms of gastroprotection and ulcer healing action for quazolast remain to be determined, it may be an effective agent for the treatment of gastric ulcers.
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PMID:Gastroprotective and ulcer healing profile of the mast cell stabilizer quazolast in rats. 168 5

Anti-inflammatory activity of a hot water extract (A-ext) of Aconiti Tuber (Aconitum calmicaeli DEBX.) has been studied by using various experimental models. The successive administration of A-ext from the day of injection of adjuvant agent or 5 d after the injection it significantly inhibited the adjuvant-induced arthritis developed in the primary and secondary lesions in rats. However, when A-ext was administered from 11 d after the injection of adjuvant, the arthritic paw edema was not reduced. A-ext did not inhibit an acetic acid-induced increase in vascular permeability in mice and carrageenin-induced paw edema in rats. A-ext inhibited cotton pellet-induced granuloma in rats, but did not suppress the weight of thymus and adrenal gland. In vitro experiment, A-ext contracted the isolated ileum of guinea pig, but the contractive activity was reduced by pretreatment of anti-histamine agent, diphenhydramine, but not by pretreatment of papaverine or atropine. A-ext did not release histamine from peritoneal mast cell. These results suggest that A-ext prevents the adjuvant-induced arthritis and has a histamine-like effect.
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PMID:[Pharmacological study on Aconiti Tuber. I. Effect of water extract from Aconiti Tuber on adjuvant-induced arthritis]. 169 57

Modern image analysers automatically perform densitometric measurements and elaborate digital images. Elaboration however is subject to operator interpretation and often eliminates precious information from the areas of interest. For this reason, it was appropriate to find a staining method which would overcome this drawback and, in the case of mast cell histochemistry, limit staining to granule content. The following current staining techniques were tested: Toluidine Blue in buffered solution (solut. a) and in 0.003% alcoholic solution (solut. b) and alcoholic Astra Blue, pH 0.2 Densitometric analysis was performed on both 5 microns and semithin sections of mouse tongue fixed in Isotonic formaldehyde-acetic acid (IFAA). Digital images were obtained using 630 nm and 546 nm wavelengths for Toluidine Blue and 610 nm for Astra Blue. Direct comparison between the two Toluidine Blue solutions revealed that more pixels were captured by the 5 microns sections stained with solut. a, whilst the opposite occurred in semithin sections. Both dyes introduced a certain amount of error due to the orthochromatic component of the nucleus and cytoplasmic basophily, which had to be eliminated through image elaboration. Because of its subjective nature, this operation may in turn lead to further errors. The choice of Astra Blue as an alternative to Toluidine Blue in densitometric analysis of mastocytes is based on its property to restrict staining to the granules of mast cells. A comparison between Astra Blue and the two Toluidine Blue solutions showed that, at all transmission levels, preparations stained with Astra Blue captured more pixels than those stained with Toluidine Blue. Consequently our results suggest that the most suitable technique for densitometric image analysis is fixation of mast cells in IFAA followed with Astra Blue.
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PMID:Mast cell fixation and staining in image analysis. 172 8

We compared the time course of histamine release with other markers of intestinal injury in a rabbit model of necrotizing enterocolitis. Injury was induced by luminal acetic acid (200 mM) and casein (10 mg/ml) and experiments terminated after 45 min or 3 hr. Compared to saline controls there was a significant elevation of epithelial permeability (51Cr-EDTA clearance) and luminal protein levels at both time points. Luminal fluid histamine levels were approximately 120-fold greater than saline controls at 45 min but were indistinguishable from control values at 3 hr. We conclude that although mast cell activation is a characteristic of this model, elevations in histamine levels are transient.
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PMID:Histamine is a transient marker of small intestinal injury induced by luminal acetic acid and casein. 179 25


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