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Query: CAS:7440-70-2 (calcium)
333,191 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The digestive and metabolic effects of inulin (from chicory) were studied in rats adapted to semipurified diets containing 0, 5, 10 or 20% inulin (wt/wt). Moderate levels of inulin (5-10%) did not significantly affect food intake or body weight gain. Dietary inulin resulted in considerably greater cecal fermentation and a significantly greater intraluminal concentration of propionate (peaking at 58.4 mmol/L). A lower concentration of acetate (42.6 mmol/L) was observed in rats fed 20% inulin. Lactic fermentations were observed in rats fed the 10 or 20% inulin diets. The cecal pool of volatile fatty acids tended to reach a plateau in rats fed diets containing more than 10% inulin (up to 600-700 mumol), but volatile fatty acid absorption was a slightly hyperbolic function of the dietary inulin level. Butyrate absorption was proportionally lower than that of propionate. Inulin-containing diets induced an enlargement of the cecal pool of calcium, phosphate and (to a lesser extent) magnesium. There was also an enhanced absorption of these divalent cations. The cecal pool of bile acids was greater in rats fed inulin, and this oligosaccharide displayed a slight hypocholesterolemic effect, even in rats fed the 5% inulin diet. However, plasma triglycerides were depressed only in rats fed the 20% inulin diet. In conclusion, inulin seems very effective in promoting propionic fermentation and in enhancing the calcium content of the large intestine. However, high levels of inulin (greater than 10%) may affect growth in rats and lead to acidic (pH 5.65) cecal fermentation.
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PMID:High propionic acid fermentations and mineral accumulation in the cecum of rats adapted to different levels of inulin. 194 Nov 80

To study the mechanisms underlying plasmalemmal expansion in the nerve growth cone, a cell-free assay was developed to quantify membrane addition, using ligand binding and sealed growth cone particles isolated by subcellular fractionation from fetal rat brain. Exposed versus total binding sites of 125I-wheat germ agglutinin were measured in the absence or presence of saponin, respectively, after incubation with various agents. Ca2(+)-ionophore A23187 in the presence of Ca2+ increases the number of binding sites (Bmax) but does not change their affinity (KD), indicating that new receptors appear on the plasma membrane. Similarly, membrane depolarization by high K+ or veratridine significantly induces, in a Ca2(+)-dependent manner, the externalization of lectin binding sites from an internal pool. Morphometric analysis of isolated growth cones indicates that A23187 and high K+ treatment cause a significant reduction in a specific cytoplasmic membrane compartment, thus confirming the lectin labeling results and identifying the plasmalemmal precursor. The isolated growth cones take up gamma-amino-butyric acid and serotonin, but show no evidence for Ca2(+)-dependent transmitter release so that transmitter exocytosis is dissociated from plasmalemmal expansion. The data demonstrate that plasmalemmal expansion in the growth cone is a regulated process and identify an internal pool of precursor membrane.
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PMID:Regulated plasmalemmal expansion in nerve growth cones. 199 70

Acamprosate is an homotaurine derivative, structural analogue of Gamma amino butyric acid and upper homologue of taurine. Its crossing through the blood brain barrier is facilitated by acetylation and calcium salification. Acamprosate has a very weak toxicity attributable to the ingested dose of calcium. Acamprosate is a GABAagonist showing pharmacological activity on direct and indirect tests of GABA activity and a high binding capacity with GABA receptors. Acamprosate also shows beta-adrenergic and serotoninergic activity, probably due to its GABAergic activity. Acamprosate is neither and antidepressant, nor a neuroleptic or a tranquillizer. In experimental alcohology, on different animal models (alcohol preferring or alcohol dependent) acamprosate induces a very clear and highly significant reduction of alcohol consumption. This effect is progressive and dose dependent, antagonized by bicuculine which is a GABA agonist. Besides, acamprosate reduces the intensity of the alcohol withdrawal syndrome. Clinical alcohology is a very difficult field for strict methodology in therapeutic trials: determination of inclusion characters, choice of judgment criteria, reduction of the number of drop out and lost subjects, length of evaluation... Different clinical controlled studies, most in double blind against placebo, on patients suffering from signs of physical or psychical alcohol addiction as well as biological modifications due to their ethylic consumption showed beneficial effects of acamprosate (in weaned alcoholics after withdrawal) according to clinical criteria (the number of abstinents after 3 months was doubled: 60% with active drug--30% with placebo) and for biological criteria (Normalization of Gamma Glutamyl Transpeptidase level in blood). The tolerance is good.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acamprosate. From pharmacology to therapeutics]. 216

The action of the polyether antibiotic monensin on the release of gamma-[3H]amino-n-butyric acid [( 3H]GABA) from mouse brain synaptosomes is characterized. Monensin enhances the release of this amino acid transmitter in a dose-dependent manner and does not modify the efflux of the nontransmitter amino acid alpha-[3H]aminoisobutyrate. The absence of external Ca2+ fails to prevent the stimulatory effect of monensin on [3H]GABA release. Furthermore, monensin is less effective in stimulating [3H]GABA release in the presence of Ca2+. The releasing response to monensin is absolutely dependent on external Na+. The blockade of voltage-sensitive Na+ or Ca2+ channels does not modify monensin-induced release of the transmitter. Also, the blockade of the GABA uptake pathway fails to prevent the stimulatory effect of monensin on [3H]GABA release. Although monensin markedly increases Na+ permeability in synaptosomes, these data indicate that the Ca2+-independent monensin-stimulated transmitter release is not mediated by the Na+-dependent uptake pathway. It is concluded that the entrance of Na+ through monensin molecules inserted in the presynaptic membrane might be sufficient to initiate the intraterminal molecular events underlying transmitter release.
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PMID:Characterization of the effect of monensin on gamma-amino-n-butyric acid release from isolated nerve terminals. 274 31

A capillary gas chromatographic method with selected-ion monitoring (GC-SIM) was applied to eight common herbicides: 2-(4-chloro-o-tolyl-oxy)propionic acid, 3,6-dichloro-2-methoxybenzoic acid, 2-methyl-4-chlorophenoxyacetic acid, 2,3,6-trichlorobenzoic acid, 2,4-dichlorophenoxyacetic acid, 3,5,6-trichloro-2-pyridyloxy-acetic acid, 2,4,5-trichlorophenoxyacetic acid and alpha-(2-methyl-4-chlorophenoxy) butyric acid. The method involves extraction with saturated calcium hydroxide solution, esterification with pentafluorobenzyl bromide, clean-up with a silica gel column and determination by capillary GC-SIM. Recoveries from soil and sediment are over 89% (with the exception of 77% for TBA) with coefficients of variation below 5% (n = 7). The method is suitable for the simultaneous determination of the eight herbicides in environmental samples with high sensitivity and accuracy.
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PMID:Capillary gas chromatographic-mass spectrometric determination of acid herbicides in soils and sediments. 276 77

With eukaryotic cells, butyrate is known to induce a series of morphological and biochemical changes that mimic cellular differentiation. With platelets, we have found that butyrate (10 mmol/L) caused an approximately threefold increase in sensitivity to calcium ionophore A23187 and arachidonate. Maximum aggregation was observed at agonist concentrations of 3 mumol/L and 170 mumol/L, respectively, as compared with required concentrations of 10 mumol/L and 400 mumol/L in the absence of butyrate. Similar effects were seen with isobutyric acid, and about one-half the effect was shown with valerate and caproate, but lower homologues showed no synergistic effect. No ultrastructural changes were observed in platelets incubated with butyrate, and the aggregation effects were reversible and returned to normal on removal of butyrate. Membrane fluidity was unchanged by butyrate as measured by changes in the fluorescence depolarization of diphenylhexatriene. Butyrate caused a 60% to 70% increase in the uptake of 3H-arachidonate. Butyrate also potentiated the inhibition of platelet function by prostaglandin E1 and forskolin and uptake of 3H-forskolin was increased approximately 20%. In contrast, platelet response to other agonists (ADP, epinephrine, collagen, thrombin, and platelet-activating factor) was essentially unaffected by butyrate. These results suggest that butyrate may increase the uptake of certain hydophobic agonists and antagonists by platelets. Similar mechanisms for uptake of endogenous effectors may explain the response of eukaryotic cells to butyrate in culture.
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PMID:Synergistic effects of butyrate on platelet responses to arachidonate, A23187, PGE1, and forskolin. 308 38

The effects of 3,4-dihydro-2,2-dimethyl-2H-1-benzopyran-6-butyric acid (DBA), an antisickling agent, on the rates of Ca2+-dependent ATP hydrolysis by the human red cell (Ca2+ + Mg2+)-ATPase, have been studied in membranes (normal and sickle-cell) stripped of endogenous calmodulin. The activity of the enzyme is increased by DBA in a manner which is dependent on both the concentrations of DBA and Ca2+. At 37 degrees C, the normal red cell (Ca2+ + Mg2+)-ATPase activity is stimulated maximally by 133% in the presence of 1 mM DBA and 0.2 mM CaCl2, while the sickle-cell enzyme is stimulated maximally by 81% in the presence of 0.5 mM DBA and 0.2 mM CaCl2. The stimulation of the enzyme in both systems is antagonized by increasing the CaCl2 concentration in the medium to 0.5 mM, in contrast to the well established mode of activation by the modulator protein, calmodulin. This suggests that the two effectors, DBA and calmodulin, probably act by different mechanisms. From our present observations, we suggest that the antisickling effect of DBA may be connected with the mobilization of calcium within red cells.
Cell Calcium 1985 Jun
PMID:Sickle-cell membrane-bound (Ca2+ + Mg2+)-ATPase: activation by 3,4-dihydro-2,2-dimethyl-2H-1-benzopyran-6-butyric acid, a novel antisickling agent. 316 Apr 69

The composition of pooled resting plaque fluid from 10 population samples, grouped according to age (8-11, 14-17, 18-25 years) and caries status (caries-free, CF, DMFS = 0; caries-susceptible, CS, DMFS greater than 10), was determined by means of ion chromatography. Subjects received a dental prophylaxis one week prior to plaque collection, abstained from oral hygiene for 48 hours, and did not eat or drink for at least one hour prior to plaque collection. Plaque samples from each group were pooled under mineral oil and centrifuged (15,000 g) for 45 minutes at ambient temperature. Supernatants were analyzed for organic acids, inorganic anions, mono- and divalent cations, and pH value. The ions Na+, NH4+, K+, Ca2+, Mg2+, Cl-, and phosphate were present in all samples. Acetic and propionic acids were predominant, comprising over 75% of the acid (anions) present under resting conditions. Succinic, lactic, formic, and butyric acids were present in lower concentrations. Within each age group, the mean values for pH and NH4+ concentration were higher in the caries-free group; the differences between mean values (CF: pH, 6.35; NH4+, 52 mmol/L; CS: pH, 5.85; NH4+, 37 mmol/L) were found to be statistically significant (p less than 0.05) when all data for the CF and CS groups were combined. Significantly higher concentrations of Mg2+ and butyric acid were also found for the combined CF data. Concentrations of all other constituents were similar. Calculations indicate that plaque fluid is supersaturated with respect to enamel mineral and dicalcium phosphate dihydrate, with a significantly higher degree of saturation with respect to enamel mineral in the CF group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Composition of pooled resting plaque fluid from caries-free and caries-susceptible individuals. 319 44

The baseline efflux of gamma-amino[2,3-3H]butyric acid ([3H]GABA) and [3H]dopamine ([3H]DA) from caudate synaptosomes was greatly enhanced by the sodium-ionophore monensin; this stimulatory effect of monensin on transmitter release was markedly inhibited by trifluoperazine (TFP), a potent calmodulin antagonist. TFP also decreased the depolarization-induced, calcium-dependent release of [3H]GABA and this effect was unrelated to the calcium-flux across the plasma membrane since TFP also inhibited the release of GABA elicited by the calcium-ionophore A23187. Our data indicate that transmitter release induced by both increased intraterminal sodium levels and by the calcium entry into the nerve endings during depolarization might be mediated by calmodulin-dependent processes.
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PMID:Sodium-dependent, calmodulin-dependent transmitter release from synaptosomes. 392 1

A growth cone-enriched fraction isolated from neonatal rat forebrain was shown to accumulate gamma-amino [3H]butyric acid ([3H]-GABA) and [3H]noradrenaline ([3H]NA). Uptake of both neurotransmitters was sodium- and temperature-dependent and exhibited saturation kinetics with Km values of 17.7 microM and 4.5 microM respectively and Vmax values of 114 pmol/min/mg protein and 59 pmol/min/mg protein respectively. Electron microscopic autoradiography showed that about 50% of isolated growth cones can accumulate [3H]GABA. Inhibitor studies showed that beta-alanine was a relatively weak inhibitor of [3H]GABA uptake compared to nipecotic acid and diamino-butyric acid. Growth cone fractions preloaded with [3H]GABA and [3H]NA demonstrated a K+ (25 mM) -induced release of both neurotransmitters. Of the K+-stimulated release of [3H]GABA 50% was Ca2+-dependent, whereas the release of [3H]NA was entirely Ca2+-independent.
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PMID:Growth cones isolated from developing rat forebrain: uptake and release of GABA and noradrenaline. 404 8


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