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ToF-SIMS depth profiling analysis of the uptake of Ba2+ and Co2+ ions by natural kaolinite clay.

The sorption behavior of Ba(2+) and Co(2+) ions on a natural clay sample rich in kaolinite was studied using time-of-flight secondary ion mass spectrometry (ToF-SIMS). Depth profiling at 10-A steps was performed up to a 70-A matrix depth of the clay prior to and following sorption. The results showed that Co(2+) is sorbed in slightly larger quantities than Ba(2+), with significant numbers of ions fixed on the outermost surface of the clay. Depletion of the ions K(+), Mg(2+), and Ca(2+) from the clay lattice was observed to accompany enrichment with Co(2+) and Ba(2+) ions. The data obtained using X-ray powder diffraction (XRPD) and scanning electron microscopy (SEM) indicated insignificant structural and morphological changes in the lattice of the clay upon sorption of both Ba(2+) and Co(2+) ions. Analysis using energy dispersive X-ray spectroscopy (EDS) showed that the average atomic percentage (+/-S.D.) of Ba and Co on kaolinite surface were 0.49 +/- 0.11 and 0.61 +/- 0.19 , respectively, indicating a limited uptake capacity of natural kaolinite for both ions.

Aluminum Silicates↗

Thermal decomposition kinetics of the Pb0.25Ba0.75(TNR).H2O complex.

Studies of the non-isothermal decomposition of Pb(0.25)Ba(0.75)(TNR).H(2)O (TNR=2,4,6-trinitro-1,3-dihydroxy-benzene) were carried out by means of TG-DTA, DSC and IR techniques. The thermal decomposition mechanism and the associated kinetics have been investigated. The kinetic parameters were obtained from the analysis of the DSC curves by integral and differential methods. The most probable kinetic model function of the dehydration reaction of Pb(0.25)Ba(0.75)(TNR).H(2)O were suggested by comparison of the kinetic parameters.

Barium Compounds↗

Solubility and stability of barium arsenate and barium hydrogen arsenate at 25 degrees C.

The inconsistency among current thermodynamic data of Ba3(AsO4)2(c) and BaHAsO4.H2O(c) led the authors to obtain independent solubility data of barium arsenate by both precipitation and dissolution experiments. Low and neutral pH (3.63-7.43) favored the formation of BaHAsO4.H2O(c). Both BaHAsO4.H2Oc and Ba3(AsO4)2(c) formed at the neutral pH conditions (7.47, 7.66), whereas Ba3(AsO4)2(c) was the only solid phase precipitated at high pH (13.03, 13.10). The Ba3(AsO4)2(c) precipitate acquired at 50 degrees C appeared as small leafy crystal, while the Ba3(AsO4)2(c) solid precipitated at 25 degrees C comprised granular aggregate with some smaller crystal clusters. XRD and SEM analyses of Ba3(AsO4)2(c) and BaHAsO4.H2O(c) indicated that the solids were indistinguishable before and after the dissolution experiments. In the present work, the solubility products (Ksp) for Ba3(AsO4)2(c) and BaHAsO4.H2O(c) were determined to be 10(-23.53)(10(-23.01) to 10(-24.00)) and 10(-5.60)(10(-5.23) to 10(-5.89)), respectively. DeltaGf degrees for Ba3(AsO4)2(c) and BaHAsO4.H2O(c) were calculated to be -3113.40 and -1544.47 kJ/mol, respectively. There was no difference between the solubility products of the leafy and the granular Ba3(AsO4)2(c) solids.

Arsenates↗

A simple etching technique for improving the retention of fiber posts to resin composites.

Coupling of fiber posts to composites is hampered by absence of chemical union between epoxy resins and methacrylate-based resins. This study examined a clinically feasible protocol for creating micromechanical retention on the surface of fiber posts, using hydrogen peroxide etching to remove the surface layer of epoxy resin. This was followed by silanization of the exposed quartz fibers to enhance their chemical bonding to composites. Etching with 24% H2O2 for 10 min or 10% H2O2 for 20 min produced a 50 microm thick surface zone that is depleted of epoxy resin, leaving intact, undamaged quartz fibers for silanization. Low viscosity flowable composites were employed to infiltrate this zone, to simulate the creation of hybrid layers in acid-etched dentin by dentin adhesives. Interfacial strengths were enhanced with the adjunctive use of H2O2 etching and silanization, and were probably dependent on the ability of the flowable composites to completely infiltrate this interdiffusion zone.

Barium Compounds↗

Acetylcholine-related bowel dysmotility in homozygous mutant NCX/HOX11L.1-deficient (NCX-/-) mice-evidence that acetylcholine is implicated in causing intestinal neuronal dysplasia.

BACKGROUND/PURPOSE: Homozygous mutant Ncx/Hox11L.1-deficient (Ncx-/-) mice develop mega-ileo-ceco-colon (mega-ICC) with a caliber change in the proximal colon. The authors investigated the mechanism of intestinal dysmotility in these mice. METHODS: Five-week-old Ncx-/- mice with mega ICC were compared with age-matched BDF1 control mice. Jejunum, ileum, and colon were excised from all mice and 1.0-cm-long strips of each organ, each with a resting tension of 0.5g, were suspended in an organ bath filled with Tyrode's solution at 37 degrees C and bubbled with a mixture of 95% oxygen and 5% carbon dioxide. Contractile responses to acetylcholine chloride (ACh), histamine, serotonin, and barium chloride (BaCl2) were recorded isometrically. RESULTS: For ACh, Ncx-/- mice had decreased distal colon circular muscle contraction only at lower doses and decreased distal colon longitudinal muscle contraction for all doses compared with controls (P <.05 or P <.01). In the proximal colon, Ncx-/- mice had increased circular muscle contraction only at higher doses and decreased longitudinal muscle contraction only at lower doses compared with controls (P <.01 or P <.05). ACh did not affect jejunum, and there were no significant effects on ileum. There was no response to histamine and serotonin by any part of the bowel, and the response to BaCl2 was the same for both Ncx-/- mice and controls. CONCLUSIONS: Only ACh differentially affected muscle contraction in Ncx-/- mice in the proximal and distal colon. Thus, ACh is implicated in causing the bowel dysmotility seen in Ncx-/- mice and human IND.

Acetylcholine↗

Effects of androgen manipulation on alpha1-adrenoceptor subtypes in the rat seminal vesicle.

This study analyses possible changes during surgical and chemical castration in the expression and pharmacological characteristics of alpha1-adrenoceptor in adult rat seminal vesicle. Ribonuclease protection assays indicated that alpha1a--was the predominant mRNA, while alpha1b-and alpha1d-adrenoceptor transcripts were detected in lower abundance in this tissue. alpha1a-adrenoceptor mRNA expression presented a complex dependency on androgens, while alpha1b- and alpha1d-adrenoceptor transcripts were both upregulated with surgical and chemical castration, suggesting a negative modulation by androgens. Testosterone treatment reversed the effects caused by surgical castration. Functional studies confirmed the involvement of alpha1A- and alpha1B-adrenoceptor in the seminal vesicle contractile responses, and suggested that alpha1B-induced contractile response was upregulated after castration. Taken together, the results suggest that alpha1-adrenoceptor expression in seminal vesicle is differentially regulated by the androgen status of the rat.

Adrenergic alpha-1 Receptor Antagonists↗

Identification of the RAG-1 as a suitable mouse model for mitochondrial DNA disease.

Previous studies have shown that transfer of human myoblasts carrying a mitochondrial DNA mutation into muscles of the severe combined immunodeficient mouse may provide an important animal model for mitochondrial myopathy. However, a major drawback of this mouse is its extreme sensitivity to ionising radiation, a pre-treatment which enhances the efficiency of myoblast transfer success. We implanted human myoblasts into the tibialis anterior muscles of another immunodeficient mouse, mutated in the recombinase activating gene-1 (RAG-1), to determine if this mouse could be an alternative to the severe combined immunodeficient for our mitochondrial myoblast transfer model. We also examined several different methods of muscle degeneration prior to myoblast transfer to determine which method resulted in the greatest amount of human tissue in implanted muscles. Our results show that the RAG-1 mouse displayed no sensitivity to the irradiation process compared to the high sensitivity in the severe combined immunodeficient mouse which resulted in early termination of the study. We also show that degeneration of host muscles by the myotoxin barium chloride (BaCl(2)) resulted in the greatest amount of regenerating human muscle fibres in both the severe combined immunodeficient and RAG-1 mice. In addition, the maximum amount of human fibres observed in transplanted muscles was similar in each mouse strain. The average number of fibres throughout muscles was significantly greater in severe combined immunodeficient mice injured by BaCl(2), but was similar between all other muscle groups. This study suggests that the RAG-1 mouse is a suitable host for the mitochondrial myoblast transfer model and may also prove valuable for other myoblast transfer models such as muscular dystrophy.

Analysis of Variance↗

The relaxant effect of urocortin in rat pulmonary arteries.

Urocortin is a potent vasodilator, which plays physiological or pathophysiological roles in systemic circulation. However, little is known about its action on pulmonary circulation. The present study was aimed to characterize some cellular mechanisms underlying the relaxant effect of urocortin in isolated rat pulmonary arteries. Changes in isometric tension were measured on small vessel myographs. Urocortin inhibited U46619-induced contraction with reduction of the maximal response. Urocortin-induced relaxation was independent of the presence of endothelium. Inhibitors of nitric oxide (NO)-dependent dilator, NG-nitro-L-arginine methyl ester or 1H-[1,2,4]oxadizolo[4,3-a]quinoxalin-1-one, did not affect the relaxation. Astressin (100-500 nM), a corticotropin-releasing factor (CRF) receptor antagonist and KT5720, a protein kinase A (PKA) inhibitor reduced urocortin-induced relaxation. Urocortin produced less relaxant effect in 30 mM K+- than U46619-contracted arterial rings. Urocortin did not reduce CaCl2-induced contraction in 60 mM K+-containing solution. Ba2+ (100-500 microM) but not other K+ channel blockers reduced the relaxant responses to urocortin. Urocortin also relaxed the rings preconstricted by phorbol 12,13-diacetae in normal Krebs solution while this relaxation was less in a Ca2+-free solution. Our results show that urocortin relaxed rat pulmonary arteries via CRF receptor-mediated and PKA-dependent but endothelium/NO or voltage-gated Ca2+ channel-independent mechanisms. Stimulation of Ba2+-sensitive K+ channel may contribute to urocortin-induced relaxation. Finally, urocortin relaxed pulmonary arteries partly via inhibition of a PKC-dependent contractile mechanism.

Animals↗

Theoretical investigations of the EPR g factors and the local structure for Er3+ in BaWO4.

The electron paramagnetic resonance (EPR) parameters g factors g(parallel) and g(perpendicular) as well as the local structure for Er3+ in scheelite-type BaWO4 are theoretically investigated by using the perturbation formulas of the EPR parameters for a 4f11 ion under tetragonal symmetry. In these formulas, the contributions to the EPR parameters arising from the second-order perturbation terms and the admixture of different states are included. It is found that the impurity-ligand bonding angles (or the polar angles) related to the fourfold axis in the tetragonal Er3+ center are about 1.5 degrees smaller than those in pure crystal. The calculated EPR parameters are in agreement with the observed values. The validity of the results is discussed.

Barium Compounds↗

Growth and vibrational spectroscopic studies of pure and yttrium doped single crystals of trisodium barium pentachloride dihydrate.

Single crystals of pure and rare earth doped trisodium barium pentachloride dihydrate have been grown by slow evaporation solution growth. The solubility of both pure and doped forms of Na3BaCl5 x 2H2O has been estimated. Vibrational spectra were recorded to determine the symmetries of molecular vibrations. The observed Raman and infrared bands were assigned and discussed in detail. The optical transparencies of the grown crystals were tested by UV-vis spectrophotometer.

Barium Compounds↗

Application of principal component analysis and Raman spectroscopy in the analysis of polycrystalline BaTiO3 at high pressure.

The principal component analysis (PCA) was applied to Raman spectra of polycrystalline BaTiO(3) under pressure from atmospheric pressure to approximately 6.72 GPa. For the system utilized, PCA was able to distinguish spectral features and to determine the phase transition pressure: tetragonal to cubic at approximately 2.0 GPa. The present study demonstrates the potentialities of the application of PCA to the investigation on phase transitions at high pressure by Raman spectroscopy.

Barium Compounds↗

Upconversion in Er3+-doped Bi2O3-Li2O-BaO-PbO tertiary glass.

Radiative properties of Er3+-doped tertiary bismuth glass has been analyzed by the Judd-Ofelt theory. NIR to visible upconversion in the Er3+-doped glass has been reported. The mechanism for the upconversion is explained on the basis of quadratic dependence on excitation power and on the energy-matching scheme. Energy transfer is noted as the dominant process including the long-lived 4I11/2 level as the intermediate state for the green and red upconversion emissions. The effect of temperature on the fluorescence intensity of the two bands due to 2H11/2-->4I15/2 and 4S3/2-->4I15/2 transitions as well as on the transitions due to Stark components of the 4S3/2 level have been monitored and it is concluded that their intensity ratio may serve as better temperature sensing device.

Barium Compounds↗

Metamizol acts as an ATP sensitive potassium channel opener to inhibit the contracting response induced by angiotensin II but not to norepinephrine in rat thoracic aorta smooth muscle.

Clinically metamizol (MZ) has been related to alteration on haemodynamic parameters and modifications on blood pressure in humans when administered intravenously. These effects have been observed at MZ therapeutic doses. Experimentally, MZ is able to induce relaxation on several types of vascular smooth muscles and modulates the contraction induced by phenylephrine. However, the mechanism underlying the MZ effects on vascular reactivity is not clear. Potassium channels (K) present on vascular smooth muscle cells closely regulate the vascular reactivity and membrane potential. There are four described types of K in vascular tissue: K voltage sensitive (K(V)), K calcium sensitive (K(Ca)2+), K ATP sensitive (K(ATP) and K inward rectification (K(IR), voltage sensitive). The aim of this work was to investigate MZ effects on angiotensin II (AT II) and noradrenaline (NA) induced contraction and to evaluate the K participation on MZ modulating effect on vascular smooth muscle contraction, using isometric and patch clamp techniques. MZ induces relaxation in a concentration dependent manner. Furthermore, MZ strongly inhibits in a concentration dependent fashion the contraction induced by AT II. However, MZ inhibition on NA induced contraction was moderated compared with that observed on AT II. MZ effects on AT II induced contraction was blocked by glybenclamide (a specific K(ATP) blocker, 3 microM, *p < 0.01). In patch clamp experiments, MZ (3 mM) induces an increase on potassium current (K+) mediated by K(ATP) in similar way as diazoxide (a specific K(ATP) opener, 3 microM). Our results suggest that MZ induces relaxation and inhibits contraction induced by AT II acting as a K(ATP) opener.

Adenosine Triphosphate↗

Functional properties of a truncated recombinant GIRK5 potassium channel.

Xenopus laevis oocytes codify a G-protein-activated inward rectifier potassium channel (GIRK5 or Kir3.5). Coinjection of other GIRKs, the muscarinic m2 receptor, or Gbetagamma protein cRNAs is required to observe functional GIRKx-GIRK5 heteromultimers in oocytes. Studies with GIRK2 isoforms have shown that the size of the amino or carboxyl terminus plays a crucial role on giving functional K(+) channels. In this work we studied the properties of a GIRK5 with 25 amino acids deleted toward its amino-terminal domain. Injection of GIRK5-Delta25 cRNA alone displayed large basal and transient inward rectifying currents in oocytes. The instantaneous currents reached a stationary level after a long duration voltage pulse (10 s). For this relaxation, fast (tau(1)) and slow (tau(2)) time constants were estimated at different voltages. Recovery from inactivation followed a monoexponential function (tau=0.95+/-0.07 s). By contrast with other inward rectifier channels, blockade of GIRK5-Delta25 by extracellular Ba(2+) was voltage-independent (K(d)=102+/-2 microM), suggesting the presence of a Ba(2+) site at the external channel vestibule. To confirm this hypothesis, the Ba(2+) sensitivity of two charged mutants GIRK5-Delta25(N129E) and GIRK5-Delta25(K157E) at each of the external loops was determined. GIRK5-Delta25(N129E) and GIRK5-Delta25(K157E) showed a 100-fold and 2-fold higher affinity to Ba(2+), respectively, supporting the existence of this Ba(2+) binding site.

Animals↗

The sodium pump modulates the influence of I(Na) on [Ca2+]i transients in mouse ventricular myocytes.

To investigate whether activity of the sarcolemmal Na pump modulates the influence of sodium current on excitation-contraction (E-C) coupling, we measured [Ca(2+)](i) transients (fluo-3) in single voltage-clamped mouse ventricular myocytes ([Na+](pip) = 15 or 0 mM) when the Na pump was activated (4.4 mM K(+)(o)) and during abrupt inhibition of the pump by exposure to 0 K with a rapid solution-switcher device. After induction of steady state [Ca2+](i) transients by conditioning voltage pulses (0.25 Hz), inhibition of the Na pump for 1.5 s immediately before and continuing during a voltage pulse (200 ms, -80 to 0 mV) caused a significant increase (15 +/- 2%; n = 16; p < 0.01) in peak systolic [Ca2+](i) when [Na+](pip) was 15 mM. In the absence of sodium current (I(Na), which was blocked by 60 microM tetrodotoxin (TTX)), inhibition of the Na pump immediately before and during a voltage pulse did not result in an increase in peak systolic [Ca2+](i). Abrupt blockade of I(Na) during a single test pulse with TTX caused a slight decrease in peak [Ca2+](i), whether the pump was active (9%) or inhibited (10%). With the reverse-mode Na/Ca exchange inhibited by KB-R 7943, inhibition of the Na pump failed to increase the magnitude of the peak systolic [Ca2+](i) (4 +/- 1%; p = NS) when [Na+](pip) was 15 mM. When [Na+](pip) was 0 mM, the amplitude of the peak systolic [Ca2+](i) was not altered by abrupt inhibition of the Na pump immediately before and during a voltage pulse. These findings in adult mouse ventricular myocytes indicate the Na pump can modulate the influence of I(Na) on E-C coupling in a single beat and provide additional evidence for the existence of Na fuzzy space, where [Na+] can significantly modulate Ca2+ influx via reverse Na/Ca exchange.

Animals↗

Calcium channels activated by depletion of internal calcium stores in A431 cells.

Depletion of intracellular calcium stores induces transmembrane Ca2+ influx. We studied Ca(2+)- and Ba(2+)-permeable ion channels in A431 cells after store depletion by dialysis of the cytosol with 10 mM BAPTA solution. Cell-attached patches of cells held at low (0.5 microM) external Ca2+ exhibited transient channel activity, lasting for 1-2 min. The channel had a slope conductance of 2 pS with 200 mM CaCl2 and 16 pS with 160 mM BaCl2 in the pipette. Channel activity quickly ran down in excised inside-out patches and was not restored by InsP3 and/or InsP4. Thapsigargin induced activation in cells kept in 1 mM external Ca2+ after BAPTA dialysis. These channels represent one Ca2+ entry pathway activated by depletion of internal calcium stores and are clearly distinct from previously identified calcium repletion currents.

Barium Compounds↗

The role of intrinsic and agonist-activated conductances in determining the firing patterns of preoptic area neurons in the guinea pig.

Whole-cell and intracellular recordings were made in coronal hypothalamic slices prepared from ovariectomized female guinea pigs. 62% of preoptic area (POA) neurons fired action potentials in a bursting manner, and exhibited a significantly greater afterhyperpolarization (AHP) than did non-bursting POA neurons. The majority (70%) of POA neurons (n=76) displayed a time-dependent inward rectification (I(h)) that was blocked by CsCl (3 mM) or by ZD 7288 (30 microM). In addition, 51% of the cells expressed a low-threshold spike (LTS) associated with a transient inward current (I(T)) that was blocked by NiCl(2) (200 microM). A smaller percentage of POA neurons (29%) expressed a transient outward, A-type K(+) current that was antagonized by a high concentration of 4-aminopyridine (3 mM). Moreover, POA neurons responded to bath application of the mu-opioid receptor agonist DAMGO (93%) or the GABA(B) receptor agonist baclofen (83%) with a membrane hyperpolarization or an outward current. These responses were accompanied by a decrease in input resistance or an increase in conductance, respectively, and were attenuated by BaCl(2) (100 microM). In addition, the reversal potential for these responses closely approximated the Nernst equilibrium potential for K(+). These results suggest that POA neurons endogenously express to varying degrees an AHP, an I(h), an I(T) and an A-type K(+) current. The vast majority of these neurons also are inhibited upon mu-opioid or GABA(B) receptor stimulation via the activation of an inwardly-rectifying K(+) conductance. Such intrinsic and transmitter-activated conductances likely serve as important determinants of the firing patterns of POA neurons.

4-Aminopyridine↗

Nociceptin/orphanin FQ and [Phe(1)psi(CH2-NH)Gly2]nociceptin(1-13)NH2 modulates the activity of hypothalamic paraventricular nucleus neurons in vitro.

Nociceptin, also known as orphanin FQ (N/OFQ), an endogenous ligand for the orphan opioid receptor-like(1) (ORL(1)) receptor, is moderately expressed in the hypothalamic paraventricular nucleus (PVN) involved in the integrative control of the function of the endocrine and autonomic nervous systems. Our previous study demonstrated that intracerebroventricular administration of N/OFQ elicits an inhibitory action on the function of the cardiovascular and sympathetic nervous systems in conscious rats. However, the effects of N/OFQ on PVN neurons have not been examined. We investigated the effects of N/OFQ on PVN neurons using a whole-cell patch-clamp recording technique in rat brain slices. N/OFQ (30-1000 nM) hyperpolarized membrane potentials in type 1 and type 2 neurons of the PVN classified by the electrophysiological property. [Phe(1)psi(CH2-NH)Gly2]nociceptin(1-13)NH2 (Phepsi) (1-9 microM), a presumed competitive antagonist of the ORL(1) receptor, also hyperpolarized membrane potential in both types of neurons. In voltage clamp studies, N/OFQ (3-3000 nM) activated a K+ current concentration-dependently in 69.7% of PVN neurons with an EC(50) of 72.4+/-12 nM. Phepsi (100-9000 nM) also activated a K+ current with an EC(50) of 818+/-162 nM in PVN neurons, and significantly reduced the amplitude of the N/OFQ-stimulated current. The N/OFQ-induced current was not antagonized by the classical opioid receptor antagonist naloxone and putative antagonist nocistatin. These findings suggest that N/OFQ may have a functional role in the PVN.

Animals↗