Atomic and electronic structure of crystalline and amorphous alloys. I. Calcium-magnesium compounds.
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Verapamil and nifedipine, known as calcium channel blockers, inhibited the phytochrome-mediated movements induced on Cassia fasciculata leaflets by a light-off signal, whereas they had no effect on the ;blue' pigment-mediated movements induced by a light-on signal. LaCl(3) inhibited both types of reactions, but the inhibition of light-induced opening needed a 10 times higher concentration than that of dark-induced closure. Bay K 8644, an activator of calcium channels, increased the rate of dark-induced closure, whereas it had no effect on the light-induced opening. These data suggest that calcium ions are not mobilized in the same way in the two types of movements: possibly from external stores in the phytochrome-mediated reaction and from internal stores in the ;blue' pigment-mediated reaction.
The effects of opioid agonists on veratrine-stimulated Ca2+ influx and amino acid neurotransmitter release in rat cerebrocortical brain slices were studied. Inhibitory effects were seen on both of these parameters with all of the opioid agonists used. None of the drugs used affected basal 45Ca2+ uptake, basal K+ content or basal amino acid release from the slices. At high concentrations (100 microM) fentanyl, tifluadom, U50,488H, butorphanol and bremazocine greatly inhibited the depolarization of the slices by veratrine as determined by the reduced release of K+. The opioid receptor subtypes at which the drugs were acting were characterized by the antagonistic effects of naloxone and WIN44441-3. The opioid-induced inhibition of stimulated Ca2+ uptake and amino acid release were not antagonized by WIN44441-2, the inactive enantiomer of WIN44441-3. It is concluded that opioid agonists acting through mu- and kappa-receptors and probably through delta- and sigma-receptors, have an inhibitory effect on Ca2+ uptake into cerebrocortical brain slices and the subsequent release of aspartate, glutamate and gamma-aminobutyric acid (GABA).
1. The effects of 1,1'-diheptyl-4,4'-bipyridinium dibromide (DHBP), a viologen for electrochromic memory display agent, on calcium release and ryanodine binding were studied with triad-rich sarcoplasmic reticulum (SR) vesicles isolated from rabbit skeletal muscle. 2. DHBP inhibited the calcium release induced by 2 mM caffeine and 2 micrograms ml-1 polylysine with an IC50 value of 5 micrograms ml-1 and 4 micrograms ml-1 respectively. 3. DHBP inhibited [3H]-ryanodine binding in a dose-dependent manner with an IC50 of 2.5 micrograms ml-1 and 90-100% inhibition at 20-30 micrograms ml-1. 4. Calcium uptake by SR was inhibited in the presence of caffeine and this inhibition was antagonized by concomitant addition of DHBP. 5. The effect of DHBP on muscle twitches was studied on the mouse diaphragm. Muscle twitches elicited by direct electrical muscle stimulation and contractions induced by either 10 mM caffeine or 1 microM ryanodine were blocked by pretreatment with DHBP. 6. Data from this study provided evidence that DHBP blocked the calcium release from SR by direct interaction with the calcium release channel, also known as the ryanodine receptor. A possible use of this agent as a specific inhibitor for calcium release and as a muscle relaxant was suggested.
Rats were injected with Calcein and killed 1 h, and 1, 2 and 3 days after injection. Incisors were stained with glyoxal-bis-(2-hydroxyanil) (GBHA) and the enamel surface examined in a fluorescence microscope with incident-light excitation. In maturing enamel Calcein produced five fluorescent double bands across the long axis of the tooth. GBHA produced a series of single red stripes, each of which was imposed on a double Calcein band 1 h after injection. At longer intervals after injection GBHA stripes were seen to be gradually displaced in the apical direction from the Calcein double bands. Since GBHA is known to stain enamel adjacent to smooth-ended ameloblasts this supports the view of a cyclic modulation of ameloblast morphology and function.
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Calcium-deprived rats have elevated intakes of CaCl2, other calcium salts, and some non-calcium compounds. We used taste reactivity to examine the effects of calcium deprivation on the palatability of CaCl2 and other solutions. Nine male Sprague-Dawley rats were calcium-deprived by maintenance on a low-calcium diet, and eight replete rats were used as controls. All rats were videotaped during intraoral infusion of the following solutions: 30 and 300 mM CaCl2, 30 mM calcium lactate, 100 and 600 mM NaCl, 30 mM MgCl2, 1 mM quinine.HCl, 2.5 mM sodium saccharin, and deionized water. We counted individual orofacial and somatic movements elicited by the infusions and used them to calculate total ingestive and aversive scores. Relative to controls, calcium-deprived rats gave a significantly larger number of tongue protrusions and had higher total ingestive scores for CaCl2, calcium lactate, NaCl, and MgCl2. Our results suggest that CaCl2, calcium lactate, NaCl, and MgCl2 taste more palatable to rats when they are calcium-deprived than replete, and this may be responsible for the increased intake of these solutions following calcium deprivation.
The preparation of a series of 24 N-benzhydrylpiperazine derivatives is described. Their efficacy as calcium antagonists was examined with reference to changes in the permeability of the cell membrane to extracellular and intracellular calcium. Compounds 14, 15, 17 and 19 were the most powerful when compared with known calcium antagonists such as cinnarizine, flunarizine, and aligeron ([1-diphenylmethyl)-4-(2-propenyl)]-piperazine), and were selected for further study.
The loss of calcium from plasma-sprayed calcium phosphate ceramics (CPCs) on bioinert metal substrate (Ti-6Al-4V) immersed in cell culture medium with or without human osteoblast culture was measured. The ceramics were a CPC and a duplex system composed of a CPC layer on an alumina coating. The dissolution of calcium compounds was monitored by measuring the calcium leaked from the coatings into the culture medium in 15 days. Calcium was measured by flame photometry. The surfaces of the ceramics exposed to the culture medium and in contact with osteoblasts were analysed by X-ray diffraction (XRD). The dissolution process occurred in the first 6 days of contact, but the calcium released into the culture medium was only a small fraction of the calcium content of the coatings. The presence or absence of osteoblasts on the surface of the ceramics did not make significant difference for the calcium release. The XRD spectra of the ceramics before and after immersion and in contact with cells did not show a significant change in the compounds of the coatings.
To examine the biostability and calcification-resistance of polyurethanes (PUs), the surface of PU was grafted with hydrophobic perfluorodecanoic acid (PFDA) (PU-PFDA), hydrophilic polyethyleneoxide (PEO) (PU-PEO1000), and further negatively charged sulfonate groups (PU-PEO1000-SO3). An in vivo animal test was conducted by subcutaneous implantation in rats during 2, 4 and 6 months. A scanning electron microscope study demonstrated that the degree of surface cracking on explanted PUs was increased in the following order: PU-PFDA > PU > PU-PEO1000 > PU-PEO1000-SO3. In the results of energy dispersive x-ray analysis and inductively coupled plasma atomic emission spectrometry, the deposition of calcium was found abundantly, but that of phosphorus was hardly in existence in all implanted PUs, suggesting that this calcium compound is not a hydroxyapatite. The calcium contents, regardless of implantation time, were also increased in the same order (PU-PFDA > PU > PU-PEO1000 > PU-PEO1000-SO3). After 6 months implantation, no severe tissue reactions were observed and calcification almost occurred on polymer surfaces in all implants. Such superior biostability and anticalcification of PU-PEO1000-SO3 might be attributed to synergistic effects of its excellent surface smoothness, sulfonate acid (SO3-) groups, nonadhesive and mobile PEO, and the high hydrophilicity and enhanced blood compatibility. Therefore, PU-PEO1000-SO3 is promising as biostable and calcification-resistant biomaterial.