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PubMed2001

Response of the pulp of dogs to capping with mineral trioxide aggregate or a calcium hydroxide cement.

This study was conducted to observe the response of dogs' dental pulp to mineral trioxide aggregate (MTA) and a calcium hydroxide cement when used as pulp capping materials. After the pulps of 30 teeth were exposed, they were capped with either MTA or a calcium hydroxide cement. Histological analysis was performed 2 months after treatment. Results showed a healing process with complete tubular dentin bridge formation and no inflammation in any of the pulps capped with MTA. On the other hand, only five specimens from the calcium hydroxide cement group formed a complete dentin bridge. In this experimental group, pulp inflammation was observed in all but three cases. In conclusion, MTA exhibited better results than the calcium hydroxide cement for the capping of the pulp in dogs.

Aluminum Compounds↗
PubMed1994

Vascular smooth-muscle cells contain AT1 angiotensin receptors coupled to phospholipase D activation.

We previously showed that angiotensin II (Ang II) and angiotensin-(2-8)-peptide [Ang-(2-8)] activate a phosphoinositide-specific phospholipase C (PLC) and cause calcium mobilization in rat aortic vascular smooth-muscle cells (VSMC), while Ang II and Ang-(1-7) produce prostaglandins. To define further the signal-transduction mechanisms activated by angiotensin peptides in smooth-muscle cells, we measured diacylglycerol (DAG) accumulation in response to different angiotensin peptides and its inhibition by subtype-selective receptor antagonists. Both an initial (10 s) and secondary (10 min) phase of DAG production in response to 100 nM Ang II were inhibited by 1 microM losartan (DuP 753), an AT1 antagonist, while 1 microM PD 123177, an AT2 antagonist, was ineffective. In contrast, the heptapeptide Ang-(1-7) did not produce DAG in VSMC. Ang II also caused the hydrolysis of phosphatidylinositol and phosphatidylcholine, the formation of phosphatidic acid and the formation of phosphatidylethanol (PEt) in the presence of ethanol, through activation of a PLD and a PLD-induced transphosphatidylation reaction. A similar concentration of Ang-(2-8) also activated PLD; in contrast, Ang-(1-7) was ineffective. PEt production by 100 nM Ang II was significantly attenuated by the AT1 antagonists losartan, its metabolite EXP 3174 or L-158,809 (all at 1 microM), whereas a similar concentration of the AT2 antagonists CGP 42112A or PD 123177 was ineffective. The production of PEt by Ang II was also partially attenuated by the removal of extracellular calcium and potentiated by increasing calcium concentrations, indicating that PLD activity is partially dependent on extracellular calcium. Thus VSMC PLD is coupled to an AT1 receptor and occurs in response to Ang II or Ang-(2-8), but not Ang-(1-7). Since AT1 receptors in VSMC are also coupled to activation of PLC, both PLC and PLD may be coupled to the same or a different AT1 receptor. Alternatively, PLD may be sequentially activated in response to Ang II activation of PLC and a subsequent increase in calcium concentration.

Angiotensin II↗
PubMed2006

Human pulpal response to mineral trioxide aggregate (MTA): a histologic study.

The purpose of this study was to study the histologic changes in the dental pulp following pulpotomy with Mineral Trioxide Aggregate (MTA) and Calcium hydroxide. Pulpotomies were performed on premolar teeth that were to be extracted for orthodontic reasons. The radicular pulp was capped with either MTA or Calcium hydroxide and restored with IRM. The teeth were extracted at 4 and 8 week intervals, fixed in 10% formalin and then kept in 5% nitric acid for 28 days for demineralization. Longitudinal sections were then prepared and viewed under light microscope. The pulps capped with MTA (at the end of 4 weeks and 8 weeks) showed dentin bridge formation which was more homogenous and continuous with the original dentin when compared to the pulps capped with calcium hydroxide. The pulpal inflammation was also less in the MTA group as compared to the calcium hydroxide group at the end of 4 and 8 weeks.

Adolescent↗
PubMed1987

Effects of sodium and calcium concentration on the barium chloride-induced electrical and contractile responses of the guinea pig vas deferens.

1. The mechanism of 10 mM barium chloride-induced electrical and contractile responses of the guinea pig vas deferens was investigated using calcium channel blockers and by modifying the Na+ and Ca2+ concentrations of the nutritional solution. Isometric contraction and membrane depolarization were measured simultaneously by the sucrose-gap technique. 2. In the absence of added Ca2+ there was a decay of the contractile but not of the depolarizing effect, which was independent of the frequency of 10 mM barium chloride administration. However, both barium-induced contraction and depolarization were reduced and the former more rapidly in a Ca2+-free solution (0.5 mM EGTA). 3. In low-Na+ solution (16 mM) there was a 3-fold increase in depolarization and no change in contraction, but in a low-Na+ Ca2+-free solution (0.5 mM EGTA), only contraction was reduced. 4. Nifedipine blocked both barium-induced contraction and depolarization in a dose-dependent manner when the organs were bathed in regular nutrient solution. In contrast, in low-Na+ solution only 50% of the depolarization was blocked by 10(-6) M nifedipine, which completely inhibited contraction. Both barium-induced contraction and depolarization in low-Na+ Ca2+-free solution were blocked by 10(-3) M LaCl3. 5. These data indicate that in the presence of calcium, barium mobilizes extracellular calcium through voltage-dependent channels and the contraction is due to the entry of calcium. In contrast, in the absence of added Ca2+ or in Ca2+-free solutions (0.5 mM EGTA), barium enters through the voltage-dependent channel and the contraction is reduced because the intracellular stores of calcium are limited.

Animals↗
PubMed1979

Protective effect of creatinol O-phosphate (COP) on ventricular fibrillation and death induced by intravenous CaCl2 in mice.

The activity of N-methyl-N-(beta-hydroxyethyl)guanidine O-phosphate (creatinol O-phosphate, COP) on the acute toxicity of CaCl2 in mice was studied. The results obtained in the present investigation show that COP administered i.v. is able to antagonize, in a dose-dependent way, the lethal ventricular fibrillation provoked by CaCl2 in unanesthetized mice. Prenalamine and cinnarizine, two calcium antagonistic compounds, proved to be active in a way qualitatively similar to COP.

Animals↗
PubMed1996

Adsorption of bacteriocins by ingestible silica compounds.

Bacteriocins including nisin, pediocin PO2, brevicin 286 and piscicolin 126 were adsorbed from culture supernates by various food-grade porous silica anti-caking agents and the food colourant, titanium dioxide. All the porous silica (calcium silicate or silicon dioxide) materials showed substantial capacity in adsorbing bacteriocin activities from the culture supernate and biological activity was recovered in the adsorbents. In contrast, the food colourant titanium dioxide adsorbed most of the bacteriocin activity from the supernate, with minimal biological activity retained in the adsorbent. Experiments with piscicolin 126 showed that optimum adsorption could be achieved with Micro-Cel E within 30 min, independent of the supernate pH (2.0-10.0). Piscicolin activity of up to 5 x 10(7) AU g(-1) of Micro-Cel E was obtained after adsorption from culture supernates and the adsorbed piscicolin demonstrated substantial biological activity against Listeria monocytogenes in both broth and a milk growth medium.

Adsorption↗
PubMed1995

Antibacterial effects of some root end filling materials.

In addition to having good sealing ability, root end filling materials should "ideally" have some antibacterial activity to prevent bacterial growth. This investigation compared the antibacterial effects of amalgam, zinc oxide-eugenol, Super EBA and a mineral trioxide aggregate on nine facultative bacteria Streptococcus fecalis, Streptococcus mitis, Streptococcus mutans, Streptococcus salivarius, Lactobacillus species, Staphylococcus aureus, Staphylococcus epidermidis, Bacillus subtilis, and Escherichia coli B and seven strict anaerobic bacteria, Prevotella (Bacteroides) buccae, Bacteroides fragilis, Prevotella (Bacteroides) intermedia, Prevotella (Bacteroides) melaninogenica, Fusobacterium necrophorum, Fusobacterium nucleatum, and Peptostreptococcus anaerobius. After growing these bacteria on solid media, freshly mixed and 24-h set test materials were placed on the surface of these inoculated media and incubated in the appropriate atmosphere for 24 to 48 h at 37 degrees C. Impregnated discs with the Super EBA liquid were used as positive controls. The antibacterial effects of each material were measured in millimeters and the data were analyzed using one-way and two-way analysis of variance and Scheffé tests to determine the statistical differences between the antibacterial effects of the test materials. Impregnated discs with Super EBA liquid caused varying degrees of growth inhibition for both facultative and strict anaerobic bacteria. Both types of amalgam had no antibacterial effect against any of the bacteria tested in this study. Mineral trioxide aggregate had an antibacterial effect on some of the facultative bacteria and no effect on any of the strict anaerobic bacteria. Zinc oxide-eugenol and Super EBA pastes had some antibacterial effects on both types of bacteria tested.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum Compounds↗
PubMed1987

Biochemical and functional interactions of a selective kappa opioid agonist with calcium.

The discovery of the selective kappa opioid receptor agonist, U-50488H, has provided a tool for the study of the mechanisms and function of the kappa receptor-effector. We have investigated the interactions of this compound with calcium in several biochemical and functional studies to assess the involvement of calcium mechanisms in the kappa receptor-linked effector. In rat brain synaptosomes, U-50488H attenuated the uptake of 45Ca++ induced by K+ (40 mM) depolarization. This effect was concentration-related (U-50488H 10(-5) to 10(-7) M), was apparent in short (8-second) but not longer (1-minute) term incubations, and did not occur in the presence of a non-polarizing concentration (5.6 mM) of K+. Naloxone (10(-7) M) did not block this effect of U-50488H (10(-6) M), and higher concentrations (10(-5) M) alone blocked calcium uptake. We have found that the binding of the depolarizing amino acid analog, kainic acid, is enhanced by CaCl2. U-50488H (10(-4) to 10(-6) M) blocks this enhancement of 3H-kainic acid binding in vitro and also blocks the in vivo effects of kainic acid. In mice, intravenous injection of kainic acid causes scratching, convulsions, and death, depending on the dose administered. U-50488H blocks all of these effects (ED50 = 4.5 mg/kg for antagonism of convulsions induced by 27.5 mg/kg kainic acid). The convulsions induced by intracerebroventricularly administered kainic acid are also blocked by U-50488H as are those induced by similarly administered Bay K 8644, a calcium channel activator. All of these anticonvulsant effects of U-50488H were antagonized by naltrexone. Together these data indicate that the kappa agonist U-50488H has functionally relevant interactions with depolarization-related Ca++ mechanisms in the central nervous system.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1992

Cardiac glycosides in the treatment of experimental overdose with calcium-blocking agents.

The ability of digitalis compounds to counteract calcium antagonist overdose was studied in anesthetized dogs (n = 6, 13.5 +/- 0.7 kg) and isolated trabeculae from human hearts (n = 7). Digitalis caused by increasing intracellular cytosolic Ca2+ concentration through Na+/Ca(2+)-exchange across the cell membrane, was postulated to overcome the detrimental effects of excessive slow calcium-channel blockade. In anesthetized dogs, an infusion of verapamil (40 mg/30 min, i.v.) decreased mean arterial pressure from 88 +/- 6 to 66 +/- 6 mm Hg (P < 0.05), reduced systemic vascular resistance (SVR) from 3838 +/- 916 to 2200 +/- 669 dyne.s/cm5 (P < 0.05), and induced total atrio-ventricular (A-V) block in three animals. Stroke volume (SV) remained unchanged. Administration (i.v.) of NaCl (0.9%, 200 ml) and calcium gluconate (100 mg)--to increase the availability of Na+ and Ca(2+)--together with atropine (0.2 mg)--to block the parasympathetic effects of digoxin on A-V conduction--increased left ventricular contractility (15%) but had no significant effects on blood pressure, SV, or A-V block. Digoxin (0.125 mg) returned sinus rhythm in all dogs and, by increasing SVR (P < 0.05) and left ventricular contractility (P < 0.05), returned arterial pressures to baseline. Because of increased afterload, SV decreased slightly (15%) despite increased cardiac contractility. In experiments with isolated trabeculae from diseased human hearts, TA 3090 (Clentiazem) depressed contractile force and ouabain, another glycoside, restored contractile force within 30 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Effects of cation interactions on sugar anion conformation in complexes of lactobionate and gluconate with calcium, sodium or potassium.

In the investigated compounds, the tetrahydrated calcium chloride salt of lactobionic acid (Ca2+.-Cl(-).C12H21O12(-).4H2O), potassium lactobionate (K+.-C12H21O12-), sodium lactobionate monohydrate (Na+.-C12H21O12-.H2O) and calcium galactonate hydrate (Ca2+.2C6H11O7(-).5H2O), the cations and hydrogen-bonding systems have a strong influence on the geometries and conformations of the carbohydrate anions.

Anions↗
PubMed1977

Improved adhesion of acrylic restorative materials to dental enamel by precoating with monomers containing phosphonate groups.

The adhesion of acrylic composite restorative materials to etched dental enamel is increased by a factor of two or more when the enamel is coated with a thin layer of vinyl-benzyl phosponic acid (VBPA) prior to forming the enamel-restorative bond. The present results support the suggestion that the enhanced adhesion is attributable to bonding between calcium ions in the enamel surface and phosphonate groups in the VBPA.

Acrylic Resins↗
PubMed1998

Possible Ca2+-dependent mechanism of apical outer hair cell modulation within the cochlea of the guinea pig.

Calcium ions were precipitated with potassium antimonate after injection of the inorganic calcium channel blocker MnCl2 or the inorganic potassium channel blockers BaCl2 or CsCl into the perilymph of the scala vestibuli of the guinea pig. The spatial distribution of the formed histochemical reaction products within the organ of Corti was studied by energy-filtering transmission-electron microscopy. Compared with untreated control ears, the number of the formed precipitates drastically increased at the extracellular side of the lamina reticularis after application of the various inorganic channel blockers. The apical side of the outer hair cells and the intervening Deiter cells were covered by a thick layer of calcium precipitates, whereas the number of histochemical reaction products was clearly reduced in the nearby acellular tectorial membrane. The high calcium content within the formed reaction products at the lamina reticularis could be demonstrated by elemental mapping and by electron energy-loss spectroscopy. To ascertain the alterations in the amounts of the calcium precipitates within the tectorial membrane after application of the various inorganic channel blockers, the precipitate densities were determined semiquantitatively by an image processing system and the values obtained compared with those of untreated control specimens. The observed histochemical results are in good agreement with published electrophysiological findings concerning the spatial distribution of ion channels located at the apical outer hair cell membrane. The detected alterations in the spatial distribution of calcium precipitates might correspond to calcium-dependent processes involved in outer hair cell modulation.

Animals↗
PubMed1997

Simulatory effect of porcine insulin on noradrenaline secretion in guinea-pig ileum myenteric nerve terminals.

1. The effect of insulin on the release of noradrenaline (NA) from nerve terminals was investigated in isolated ileal synaptosomes of guinea-pig. Release was determined as the amount of NA, quantified by h.p.l.c.-electrochemical detection, from samples incubated with insulin minus that in parallel blanks treated with some volume of vehicle. 2. Porcine insulin stimulated the secretion of NA in a concentration-dependent manner from 0.01 i.u. ml-1, while the value of lactate dehydrogenase in the incubated medium was not influenced by insulin. 3. The presence of insulin receptors in this preparation was illustrated by immunoblotting with insulin receptor monoclonal antibodies. 4. The release of NA by insulin was reduced by guanethidine and bretylium and it was markedly lowered in the samples obtained from guinea-pigs that had received an intraperitoneal injection of DSP-4, the noradrenergic neurotoxin. 5. Tetrodotoxin attenuated the action of insulin at concentrations sufficient to block sodium channels. The depolarizing effect of insulin on the membrane potential was also illustrated by a concentration-dependent increase in the fluorescence of bisoxonol, a potential-sensitive dye. 6. The action of insulin was attenuated by removal of calcium chloride from the bathing medium. The induction of calcium ion influx by insulin into the synaptosomes is supported by the inhibitory effects of the calcium channel blockers omega-conotoxin GVIA (for the N-type channels) and nifedipine (for the L-type channels). 7. These findings suggest that insulin can stimulate NA release from noradrenergic terminals via activation of calcium influx.

Adrenergic Agents↗
PubMed2003

Inositol 1,4,5-trisphosphate-induced calcium release is necessary for generating the entire light response of limulus ventral photoreceptors.

The experiments reported here were designed to answer the question of whether inositol 1,4,5-trisphosphate (IP3)-induced calcium release is necessary for generating the entire light response of Limulus ventral photoreceptors. For this purpose the membrane-permeable IP3 receptor antagonist 2-aminoethoxydiphenyl borate (2APB) (Maruyama, T., T. Kanaji, S. Nakade, T. Kanno, and K. Mikoshiba. 1997. J. Biochem. (Tokyo). 122:498-505) was used. Previously, 2APB was found to inhibit the light activated current of Limulus ventral photoreceptors and reversibly inhibit both light and IP3 induced calcium release as well as the current activated by pressure injection of calcium into the light sensitive lobe of the photoreceptor (Wang, Y., M. Deshpande, and R. Payne. 2002. Cell Calcium. 32:209). In this study 2APB was found to inhibit the response to a flash of light at all light intensities and to inhibit the entire light response to a step of light, that is, both the initial transient and the steady-state components of the response to a step of light were inhibited. The light response in cells injected with the calcium buffer 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) was reversibly inhibited by 2APB, indicating that these light responses result from IP3-mediated calcium release giving rise to an increase in Cai. The light response obtained from cells after treatment with 100 microM cyclopiazonic acid (CPA), which acts to empty intracellular calcium stores, was reversibly inhibited by 2APB, indicating that the light response after CPA treatment results from IP3-mediated calcium release and a consequent rise in Cai. Together these findings imply that IP3-induced calcium release is necessary for generating the entire light response of Limulus ventral photoreceptors.

Animals↗
PubMed1998

Intracellular calcium dynamics during photolysis.

The objective of this investigation was to gain a deeper understanding of the intracellular events that precede photolysis of cells. A model system, consisting of malignant melanoma cells pretreated with the calcium sensitive fluorescent dye, Fluo-3, was used to examine the intracellular calcium dynamics in single-cell photolysis experiments. Exposure of the cells to 632 nm laser light in the presence of photosensitizer, tin chlorin e6, resulted in a rise in intracellular calcium. The increase in intracellular calcium was blocked using a variety of calcium channel blocking agents, including verapamil, nifedipine, and nickel. Treatment with the channel blockers was also effective in either decreasing or eliminating cell death despite the presence of lethal doses of photosensitizer and irradiation. These results show that intracellular calcium rises prior to plasma membrane lysis, and that this early rise in intracellular calcium is necessary for membrane rupture.

Aniline Compounds↗