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

With a view to finding more effective antiulcer agents, a series of 2-benzylthio-5,6,7,8-tetrahydro-4(3H)-quinazolinones and related compounds were synthesized and evaluated in a histamine-stimulated gastric secretion model. The sodium salt of the 2-(dimethylamino)benzylthio derivative (8) showed gastric mucosal protection and gastric antisecretion activities, and was also effective against experimental gastric and duodenal ulcers induced by some ulcerogenic agents. Based on a comparison of the antiulcer properties of 8 with those of the lead compounds (1 and 2) and cimetidine, it appears that, for improvement of antiulcer activity, the reduction of gastric acidity is a more important factor than the reduction of gastric volume output or gastric total acid output.
 ...
PMID:Studies on antiulcer agents. IV. Antiulcer effects of 2-benzylthio5,6,7,8-tetrahydro-4(3H)-quinazolinones and related compounds. 857 39

It has been observed previously that xanthan gum (XG) and hydroxypropylmethyl cellulose (HPMC) show different drug release behavior. In order to clarify these findings, the rheological properties of both polymers have been determined by oscillatory as well as by steady shear measurements. Aqueous solutions of 4 and 7% (w/w) polymer have been used to simulate the outer surface of a hydrated tablet. The dynamic moduli, i.e., storage modulus (G') and loss modulus (G") of the two polymers have been determined in pure water and USP phosphate buffer pH 7.4 at different dilutions. In this concentration range XG solution exhibits "gel-like" behavior, while HPMC behaves as a typical polymer solution. These findings are quite consistent with the reported higher ability of XG matrices to retard drug release than HPMC matrices for controlled-release formulation. The effects of differences in drug solubility and acidity, as well as the addition of lactose, and of the ionic strength of the medium on the rheological properties of XG and HPMC solutions have been studied in detail. Among these parameters, only the salt concentration exerts an enhancing effect on both moduli of XG, while no detectable influence on HPMC solution could be observed.
 ...
PMID:Rheological characterization of xanthan gum and hydroxypropylmethyl cellulose with respect to controlled-release drug delivery. 874 47

Occlusion of feeding tubes is a common and costly complication of enteral feeding. Although the composition of feeding formulas, the size, design, and material of the feeding tube, and the rate of delivery have been considered as factors that determine the rate of tube occlusion, little information is available on the effect of the luminal content of the gut on tube occlusion. Enteral feeding tubes are placed either in the stomach or postpylorically, in the small intestine. The chemical composition of these regions including acidity and bile salt concentration may vary. Since acidity has been shown to promote tube occlusion and bile salts have detergent-like properties, these chemical differences in the luminal environment may be important to tube occlusion. To test the idea that bile salt inhibits acid-promoted occlusion of feeding tubes, in an in vitro study, we compared the time-to-complete occlusion of four groups of formula-filled feeding tubes (six tubes in each group) immersed in an acidic solution (pH 3.0) containing 0 (control), 10, 20, or 40 mM of taurocholate. We found that although 33% of the feeding tubes were occluded within 12 hours in the absence of exposure to bile salt, none were occluded when 20 or 40 mM of taurocholate was added to the acidic solution. After 24 hours, 40 mM of taurocholate inhibited acid-promoted occlusion of 67% of the feeding tubes. Thus 0 to 40 mM of taurocholate still inhibited acid-promoted tube occlusion in a dose-dependent fashion (p < .05). Acidity and the concentration of bile salt may work together, but in opposite directions, as luminal factors that determine the rate of occlusion of feeding tubes.
 ...
PMID:Bile salt inhibits acid-promoting feeding tube occlusion. 880 28

An attempt was carried out for prolongation of the shelf-life of Mozzarella cheese by incorporation of potassium sorbate into the cheese. Three manufacturing techniques were used: a) addition of potassium sorbate to kneading water (at level of 6%), b) addition during brine salting (at level of 0.5%) and c) dipping the cheese into potassium sorbate solution (6%) directly prior to packaging. Control cheese was made without potassium sorbate treatment. The resulting cheeses were divided into two portions, one of which was contaminated with Penicillium roqueforti and then packaged, while the second one was packaged without contamination. Both were stored at refrigerator (5 +/- 1 degree C) temperature and analysed periodically until spoilage. The results showed that treatment with potassium sorbate did not affect the organoleptic properties of the cheeses, except that a slight objectionable bitter flavour was observed in fresh cheeses treated with sorbate using the techniques of dipping or in brine salting then it was disappeared during storage. However, the overall acceptabilities of the sorbate-treated cheese were increased up to 10 weeks of storage compared with 4 weeks for untreated cheeses. Treatment with potassium sorbate in kneading water or brine appeared to be more effective than dipping. Addition of potassium sorbate inhibited microbial growth, especially that of moulds and yeasts. The sorbate-treated cheeses had higher moisture, pH values and lower acidity than the control. Fat, salt and total nitrogen were unaffected during storage. Levels of soluble N, non-protein N and total volatile fatty acids in sorbate-treated cheeses were slightly higher than in the control. Furthermore, addition of potassium sorbate increased the meltability and improved the fat leakage of Mozzarella cheese.
 ...
PMID:Prolongation of the keeping quality of Mozzarella cheese by treatment with sorbate. 881 83

Guanylin and uroguanylin are intestinal peptides that stimulate chloride secretion by activating a common set of receptor-guanylate cyclase signaling molecules located on the mucosal surface of enterocytes. High mucosal acidity, similar to the pH occurring within the fluid microclimate domain at the mucosal surface of the intestine, markedly enhances the cGMP accumulation responses of T84 human intestinal cells to uroguanylin. In contrast, a mucosal acidity of pH 5.0 renders guanylin essentially inactive. T84 cells were used as a model epithelium to further explore the concept that mucosal acidity imposes agonist selectivity for activation of the intestinal receptors for uroguanylin and guanylin, thus providing a rationale for the evolution of these related peptides. At an acidic mucosal pH of 5.0, uroguanylin is 100-fold more potent than guanylin, but at an alkaline pH of 8.0 guanylin is more potent than uroguanylin in stimulating intracellular cGMP accumulation and transepithelial chloride secretion. The relative affinities of uroguanylin and guanylin for binding to receptors on the mucosal surface of T84 cells is influenced dramatically by mucosal acidity, which explains the strong pH dependency of the cGMP and chloride secretion responses to these peptides. The guanylin-binding affinities for peptide-receptor interaction were reduced by 100-fold at pH 5 versus pH 8, whereas the affinities of uroguanylin for these receptors were increased 10-fold by acidic pH conditions. Deletion of the N-terminal acidic amino acids in uroguanylin demonstrated that these residues are responsible for the increase in binding affinities that are observed for uroguanylin at acidic pH. We conclude that guanylin and uroguanylin evolved distinctly different structures, which enables both peptides to regulate, in a pH-dependent fashion, the activity of receptors that control intestinal salt and water transport via cGMP.
 ...
PMID:Regulation of intestinal uroguanylin/guanylin receptor-mediated responses by mucosal acidity. 912 60

2D-NMR experiments were used to determine the pKa values ranging from 8.0 to >/=11.1 of seven basic residues in turkey ovomucoid third domain (OMTKY3) and were compared to values predicted as described by Antosiewicz et al. [(1996) Biochemistry 35, 7819-7833]. Lys 13, 29, and 34 were previously attributed with increasing the acidity of numerous acidic residues [Schaller, W., and Robertson, A. D. (1995) Biochemistry 34, 4714-4723]. These interactions were expected to raise the pKa values of those basic groups; however, the pKa values of Lys 13 and 34 are less than the model compound values. The pKa values of the other basic residues are greater than the model compound values and, unlike the acidic residues, all are surprisingly insensitive to salt. While the calculations properly predict the direction of most of the pKa shifts and provide valuable insight into the possible molecular origins of the interactions that perturb pKa values, there is a tendency to overestimate the magnitude of the shifts and their salt dependence. Interestingly, the shapes of both the calculated and observed transitions are often more complex than expected for a simple titration, suggesting that pKa values at many sites are changing during the transition. Differences between predicted and experimental pKa values and titration profiles for some residues may be due to as yet uncharacterized structural changes at the extremes of pH.
 ...
PMID:Theoretical and experimental analysis of ionization equilibria in ovomucoid third domain. 962 26

Helicobacter pylori acquisition is the main cause of chronic gastritis in humans. In up to half of the infected subjects, chronic gastritis progresses to atrophic gastritis and intestinal metaplasia. During this course, various mechanisms are triggered that may contribute to the pathogenesis of gastric cancer. Such mechanisms include the inflammation-related cascades of cytokine and free radical reactions, up- and downregulation of growth factors and their receptors, and the atrophy-related impairment of acid output and intraluminal acidity. An array of other factors may also have become significant including overgrowth of bacteria other than H. pylori in the hypochlorhydric or achlorhydric stomach, a high dietary consumption of salt, nitrate, or nitrite, smoking, deficiency of vitamins or micronutrients, influence of sex hormones, or an inherited liability of the dividing epithelial cells to gene errors. These factors may vary in effect between populations and individuals but, if active, may affect the cell genome which may further influence the course and progression of chronic gastritis, and can finally result in overt gastric neoplasia. The molecular biology of gastric cancer has revealed a spectrum of gene errors which vary in type and extent between different histological types of cancer, and between individual cases. There now is evidence that the intestinal metaplasia or the gastric epithelium in atrophic gastritis reveal signs of abnormal expression of various regulatory genes well before the appearance of gastric neoplasia. It is possible that the mechanisms leading to mutation of the genes in epithelial cells are triggered very early in the H. pylori gastritis cascade, and that atrophic gastritis and intestinal metaplasia result from these processes.
 ...
PMID:Review article: Pathogenesis of the transformation from gastritis to malignancy. 970 Oct 4

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.
 ...
PMID:Survival of Escherichia coli O157:H7 during the manufacture of pepperoni. 970 71

A current model for carotenoid transport and absorption in the gut proposes an initial solubilization in the oil phase of dietary emulsions followed by incorporation of the carotenoids in mixed bile salt micelles. To assess the relevance of the first stage of this model to what is observed in vivo we have examined the transfer of carotene from carrot juice to olive oil. Increased acidity enhanced the transfer from both whole juice and carotene crystals isolated from carrot chromoplasts. The transfer was significantly slower from whole juice. By using exogenous beta-carotene and measuring its transfer to oil in the presence and absence of carrot juice we have demonstrated that the inhibition of the transfer in juice arises, at least in part, from soluble juice factors. The inhibition is relieved by a fall in pH, which leads to lowering of the electric potential at the oil/aqueous phase interface and aggregation of carrot tissue including crystalline carotene. Under conditions of low pH, oil droplets adhere to the tissue aggregates, allowing carotene to pass into the oil. Our results provide an explanation for why carotene absorption in vivo is depressed by conditions of low gastric acidity.
 ...
PMID:Low pH enhances the transfer of carotene from carrot juice to olive oil. 983 78

Hypophosphatemia caused by renal phosphate loss occurs frequently after kidney transplantation. In assumption of systemic phosphorus depletion, the presumed deficit commonly is replaced by oral phosphate supplements. However, such treatment is debatable, because intracellular phosphorus stores have not been assessed in this setting and may not be accurately reflected by serum phosphate concentrations. Moreover, disturbances in mineral metabolism from chronic renal failure, such as hypocalcemia and hyperparathyroidism, may be prolonged with oral phosphate supplements. Conversely, a neutral phosphate salt might improve renal acid excretion and systemic acid/base homeostasis for its properties as a urinary buffer and a poorly reabsorbable anion. Twenty-eight patients with mild early posttransplantation hypophosphatemia (0.3-0.75 mmol/L) were randomly assigned to receive either neutral sodium phosphate (Na(2)HPO(4)) or sodium chloride (NaCl) for 12 weeks and examined with regard to (1) correction of serum phosphate concentration and urinary phosphate handling; (2) muscular phosphate content; (3) serum calcium and parathyroid hormone (PTH); and, (4) renal acid handling and systemic acid/base homeostasis. Mean serum phosphate concentrations were similar and normal in both groups after 12 weeks of treatment; however, more patients in the NaCl group remained hypophosphatemic (93% versus 67%). Total muscular phosphorus content did not correlate with serum phosphate concentrations and was 25% below normophosphatemic controls but was completely restored after 12 weeks with and without phosphate supplementation. However, the percentage of the energy-rich phosphorus compound adenosine triphosphate (ATP) was significantly higher in the Na(2)HPO(4) group, as was the relative content of phosphodiesters. Also, compensated metabolic acidosis (hypobicarbonatemia with respiratory stimulation) was detected in most patients, which was significantly improved by neutral phosphate supplements through increased urinary titratable acidity. These benefits of added phosphate intake were not associated with any adverse effects on serum calcium and PTH concentrations. In conclusion, oral supplementation with a neutral phosphate salt effectively corrects posttransplantation hypophosphatemia, increases muscular ATP and phosphodiester content without affecting mineral metabolism, and improves renal acid excretion and systemic acid/base status.
 ...
PMID:Metabolic aspects of phosphate replacement therapy for hypophosphatemia after renal transplantation: impact on muscular phosphate content, mineral metabolism, and acid/base homeostasis. 1056 Nov 44


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>