Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastrin-releasing peptide is a 27-amino acid peptide recently isolated from porcine gut. It shares a common C-terminal decapeptide homology with bombesin (except for a His/Gln interchange at residue 8 from C-terminus). Synthetic porcine gastrin-releasing peptide was shown to release gastrin 5 min after intravenous injection in rats. Given intracisternally (0.3--3 microgram), but not intravenously (1--10 micrograms), gastrin-releasing peptide caused a dose-dependent reduction in gastric secretion (volume and acidity) and elevation in plasma gastrin levels measured 2 h after peptide injection and pylorus ligation in rats. Gastrin-releasing peptide given intracisternally had long acting, reversible, and specific inhibitory effects. Gastrin-releasing peptide blocked the secretion of acid evoked by 2-deoxy-D-glucose or TRH given intracisternally or by histamine given subcutaneously. The acetylated C-terminal octapeptide fragment of gastrin-releasing peptide inhibited gastric acid secretion as effectively as gastrin-releasing peptide. Acetylated C-terminal heptapeptide did not. These results demonstrated that gastrin-releasing peptide has the capability to act in the brain to inhibit basal and stimulated gastric secretion and its antisecretory effect does not depend on a decrease in gastrin release. The presence of bombesin immunoactivity in rat brain and its ability to act through the brain to inhibit gastric acid secretion suggest that bombesinlike peptides may be chemical messengers involved in central nervous regulation of gastric secretion.
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PMID:Central nervous system inhibition of gastric secretion in the rat by gastrin-releasing peptide, a mammalian bombesin. 723 37

Three of five isolates of Sporidesmium sclerotivorum, a mycoparasite of Sclerotinia spp., grew well on an agar medium containing mineral salts, glucose, thiamine, and glutamine or Casamino acids as the nitrogen source. The nitrogen requirement for two of the isolates was satisfied by NH4Cl, Casamino acids, or glutamine. Glutamine was the best single nitrogen source. Only one isolate, CS-1, was used in further nutritional studies. The optimum concentration of glutamine for growth was 5 g/L. Glucose, mannose, mannitol, and cellobiose were excellent carbon sources. A glucose concentration of 20 g/L was optimum. Mannitol supported greater growth than glucose with Casamino acids as the nitrogen source but glucose was the superior carbon source with glutamine as the nitrogen source. Greatest growth was achieved with a combination of these carbon and nitrogen sources. Sporidesmium sclerotivorum, isolate CS-1, required thiamine for growth and sporulation. Biotin stimulated growth. The fungus developed maximally within the range of pH 5.0-5.5 and growth was greatly reduced at a pH below 4.0 or above 6.0. Control of acidity by the periodic addition of NaOH solution permitted substantially increased growth. The optimum temperature for growth was 22.5-25.0 degrees C but production of macroconidia was greatest at 15-20 degrees C.
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PMID:Nutritional and environmental factors affecting growth and sporulation of Sporidesmium sclerotivorum. 729 4

Gastric emptying rates of hypertonic (10%) dextrose liquid meals were studied in five dogs before, and 3, 6, and 12 months after proximal gastric vagotomy (PGV) without drainage. The purpose of this study was to determine if operation-related changes in emptying rates normalized or became more disparate during the year after PGV. An increased rate of emptying during the first 5 min after ingestion was seen at 3 months after PGV, which significantly increased (P less than 0.025) after 6 and 12 months. The remainder of the meal after PGV emptied at a regulated expotential rate unchanged throughout the postoperative year from its preoperative rate. Total volumes of gastric aspirate at four intervals after meal ingestion did not significantly change across the four test periods in respect to endogenous secretion or pH acidity.
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PMID:Progression of changes in gastric emptying of hypertonic liquids after proximal gastric vagotomy. An experimental study. 746 Jul 14

D-glucose solution injected into the portal vein influences efferent tonic activities of the vagal nerve innervating the stomach. This suggested the existence of a neural connection between hepatic vagal branch afferents and gastric vagal efferents in the brain. Considering this observation together with findings indicating that electrical stimulation of the proximal cut end of the hepatic vagal branch changes acidity in the gastric perfusing fluid or pressure within the stomach, it has been presumed that hepatic afferent signals related to glucose may regulate the motor or secretory function of the stomach through a change in central nervous activity. Recently active interaction between the portal and medullary glucose signals in gastric function was discovered, and analysis of the characteristic features of the system is in progress.
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PMID:Control of motor and secretory functions of the stomach by a portal glucose signal. 756 48

The ulcerogenic activity of NS-398 was compared with that of indomethacin and the effects of NS-398 on stress-induced ulceration, gastric acid secretion and gastric mucosal prostaglandin (PG) contents were investigated in rats. NS-398 in a single dose of up to 1,000 mg/kg, p.o. did not significantly cause gastric ulceration while other nonsteroidal anti-inflammatory drugs such as, loxoprofen, indomethacin, diclofenac and ibuprofen, produced distinct gastric lesions. In cases of stress-induced ulcerations, NS-398 at 30 mg/kg, p.o. had no significant influence while indomethacin markedly potentiated the ulceration in a dose dependent manner. In basal gastric secretion studies, both NS-398 and indomethacin decreased secretion volume and acidity. However, in the 2-deoxy-D-glucose-stimulated gastric acid secretion study, NS-398 had no significant influence on gastric secretions while indomethacin significantly potentiated the secretion. Both NS-398 and indomethacin to much the same extent significantly decreased prostaglandin E2 (PGE2) contents in inflammatory tissue. However, with respect to gastric mucosal PGE2 contents, NS-398 did not decrease PGE2 contents while indomethacin significantly decreased the contents. It would thus appear that the absence of ulcerogenic properties of NS-398 is due to a relative lack of activity in inhibiting gastric PG synthesis.
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PMID:Effect of NS-398, a new nonsteroidal anti-inflammatory agent, on gastric ulceration and acid secretion in rats. 823 61

We have determined the relative importance of the transmembrane proton electrochemical gradient to the transport of D-[14C]glucose and [14C]glycylsarcosine (gly-sar) in rat kidney brush-border membrane vesicles (BBMV) from superficial renal cortex. Electrogenic [14C]gly-sar transport was first optimised by imposing a pH gradient (pHo = 5.7, pHi = 8.4) and an interior negative p.d. (using outwardly directed K+ gradient plus valinomycin). Under identical conditions (pHo = 5.7, pHi = 8.4), an acceleration of initial D-[14C]glucose (at 100 microM) transport by 2.0 +/- 0.7-fold was observed compared to no proton gradient (pHo = 8.4, pHi = 8.4). This increase was due primarily to an effect of external protons, since acidic conditions (pHo = pHi = 5.7) also resulted in acceleration of D-glucose influx (2-fold). The increase in D-glucose transport in the presence of external acidity was reduced by the uncoupler FCCP, even in the absence of a proton gradient. Furthermore, the increased D-glucose transport with external acidity in the presence of a proton gradient was insensitive to a K+ gradient-driven diffusion potential in the presence of valinomycin. In no instance was an overshoot accumulation of D-[14C]glucose observed in H+ gradient conditions. H(+)-stimulated D-[14C]glucose transport showed a linear dependence on D-glucose concentration up to 20 mM D-glucose, unlike electrogenic Na(+)-dependent D-glucose transport, whose Km was 1.77 +/- 0.35 mM. In contrast, the initial rate of [14C]gly-sar (100 microM) transport by the renal H+/di-tripeptide transporter was accelerated 15.7 +/- 3.3-fold and stimulated a marked overshoot of 5.1 +/- 0.4-fold over equilibrium values. Conversely, the electrogenic, Na+/glucose transporter could be readily demonstrated, whilst [14C]gly-sar transport could not be energised by an inward Na+ gradient. The absence of electrogenic D-glucose transport in H+ gradient conditions is clear evidence against H+/glucose cotransport in Na(+)-free conditions mediated by SGLT2 (sodium-glucose transporter, renal cortex). Furthermore, since a proton gradient does not increase brush-border membrane D-glucose uptake in Na(+)-rich media, it is unlikely that in vivo renal D-glucose transport mediated via SGLT2 may be energised by the transmembrane proton gradient.
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PMID:Proton/solute cotransport in rat kidney brush-border membrane vesicles: relative importance to both D-glucose and peptide transport. 862 55

Most intravenous infusion fluids and non-sterile liquid products contain dextrose which serves as a sweetener or an energy source for critically ill or traumatized patients. Hence dextrose was critically examined for stability in the presence of some micro-organism which are commonly known to contaminated i.v. infusion fluids. In the presence of these test organisms, the dextrose component of these solutions was found to be remarkably degraded with average rates of 0.065-3.153% per hour depending on the type of organism. Micro-organisms such as Ps. aeruginosa and E. coli gave low rates of degradation of 0.065-0.88% per hour while the values of 0.770-3.153% per hour were obtained for K. pneumonia; B-lac+ Staph. aureus and B. subtilis. The degradation of dextrose by C. albicans however, increased with dextrose concentration with average rate of 1.147-1.21% per hour. The degradations were gradually accompanied by increases in total acidity and decreases in pH of the dextrose solutions. The variation in the rates of degradation of dextrose by the test organisms is attributable to their survival rates in dextrose solutions and it is of great significance especially at the low inoculum size of 100 cells/ml. The results thus obtained necessitate the maintenance of a high level of aseptic procedures to prevent inadvertent contamination of i.v. fluids and other glucose containing solutions during clinical and other use conditions.
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PMID:Consequences of inadvertent microbial contamination of dextrose solutions. 902 May 94

Parallel increments of gastric acid and pepsinogen secretion generally occur after the application of cholinergic stimuli. However, it still remains to be established whether the changes in acid output associated with cholinergic stimulation play a role in regulation of the concomitant peptic secretory activity. In the present study, an anesthetized rat model was used for the evaluation of pepsinogen secretion in order to pursue a dual purpose: 1) to assess the relative functional relevance of direct and acid-dependent control exerted by cholinergic pathways on pepsinogen output; 2) to characterize the mechanisms through which changes in acidity within the stomach lumen may affect the peptic secretory activity of gastric mucosa. Bethanechol, 2-deoxy-D-glucose or electrical vagal stimulation caused parallel and atropine-sensitive increments of peptic and acid secretions. Omeprazole, a selective inhibitor of gastric H+:K+-adenosintriphosphatase, blocked the increase in acid but not pepsinogen secretion induced by bethanechol. However, 2-deoxy-D-glucose or electrical vagal stimulation failed to increase either pepsinogen or acid secretion in omeprazole-pretreated rats. When tested in animals pretreated with both omeprazole and physostigmine (a drug able to prevent the enzymatic breakdown of vagally released ACh through the blockade of acetylcholinesterase), 2-deoxy-D-glucose or electrical vagal stimulation significantly increased pepsinogen secretion without affecting acid secretion. In omeprazole-pretreated rats, perfusion of the gastric lumen with acid solutions caused a pH-dependent and atropine-sensitive increase in peptic output only when applied in combination with electrical vagal stimulation. Functional ablation of capsaicin-sensitive sensory neurons did not modify the gastric secretory responses induced by bethanechol or electrical vagal stimulation. However, after topical application of lidocaine to the gastric mucosal surface, bethanechol stimulated both peptic and acid outputs, whereas electrical vagal stimulation only evoked acid secretion without affecting basal peptic output. The present results indicate that the activation of muscarinic receptors by vagally released ACh is not sufficient by itself to stimulate pepsinogen secretion and that a facilitatory action mediated by acid secretion is necessary to allow an increment of peptic output in response to vagal cholinergic stimuli. It is suggested that such facilitatory input is driven to chief cells by local intramural reflexes that involve capsaicin-insensitive intrinsic nerves.
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PMID:Positive modulation of pepsinogen secretion by gastric acidity after vagal cholinergic stimulation. 939 75

This study investigated the growth and survival of Escherichia coli O157:H7 during the manufacture of pepperoni to determine whether a 5-log10-unit decline in numbers, as recommended by the U.S. Food Safety and Inspection Service (FSIS), could be achieved. A range of pepperoni formulations with variations in salt (2.5 to 4.8%) and sodium nitrite (100 to 400 ppm) levels, and with pH (4.4 to 5.6) adjusted by manipulation of dextrose concentrations were prepared. The batters produced were inoculated with E. coli O157:H7 380-94 at a level of approximately 6.70 log10 CFU/g; changes in pathogen numbers, pH, titratable acidity, and sodium nitrite concentrations were monitored during fermentation and drying. With the standard commercial formulation (i.e., 2.5% salt, 100 ppm sodium nitrite, pH 4.8) E. coli O157:H7 numbers declined by approximately 0.41 log10 CFU/g during fermentation and a further 0.43 log10 CFU/g during subsequent drying (7 days). A regression equation was fitted to the data which showed significantly (P < 0.001) greater reductions in pathogen numbers in samples with increased salt and sodium nitrite contents and lowered pH. However declines were in all cases less than the target reduction of 5 log10 CFU/g.
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PMID:Survival of Escherichia coli O157:H7 during the manufacture of pepperoni. 970 71

Titratable acidity of the extracellular medium was compared with that calculated from pH changes in a suspension of Saccharomyces cerevisiae. After addition of cells to normal water the ratio of titratable acidity to the computed one was about 25, after addition of 50 mmol/L D-glucose it was about 13, after subsequent addition of K+ ions it was only 2. In heavy water the respective values were 30, 9, and 1. Apparently, the principal buffer-generating processes have to do with glucose metabolism but little with the K+/H+ exchange observed after addition of K+. D2O appears to block processes producing the buffering capacity of the medium, among them possibly extrusion of organic acids.
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PMID:Extracellular acidification by Saccharomyces cerevisiae in normal and in heavy water. 1006 11


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