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PubMed2001

The effect of pH on the dimensionality of coordination polymers.

Hydrothermal reactions of simple alkaline salts or their hydroxides with 3,5-pyrazoledicarboxylic acid (H(3)pdc) yielded seven new compounds. At a lower pH level three one-dimensional structures [Ca(Hpdc)(H(2)O)(4)].2H(2)O (1), [Ca(Hpdc)(H(2)O)(4)].H(2)O (2), and [Ba(H(2)pdc)(2)(H(2)O)(4)].2H(2)O (6) were obtained by evaporation of the solutions resulting from hydro(solvo)thermal reactions of MCl(2) (M = Ca, Ba) with H(3)pdc in water (1, 6) or in water/Et(3)N (2) at 150 degrees C for 3 days. Crystal structures of 1 and 2 contain zigzag chains of metal centers bridged by a single Hpdc(2-) ligand, whereas structure 6 consists of linear chains of metal centers bridged by two H(2)pdc(-) ligands. A dimer molecule [Sr(H(3)pdc)(H(2)pdc)(2)(H(2)O)(3)](2).2(H(3)pdc).4H(2)O (4) was obtained from a similar hydrothermal reaction using Sr(ClO(4))(2).6H(2)O instead of MCl(2). This compound contains [2+2] metallomacrocycles. At higher pH levels (pH = 4-6), the three-dimensional polymers [M(Hpdc)(H(2)O)] (Ca 3, Sr 5, Ba 7 ) were isolated by reactions of MCl(2) (M = Ca, Sr, Ba) with H(3)pdc in water/Et(3)N or in M(OH)(2) (M = Ca, Sr, Ba) with H(3)pdc in water under hydro(solvo)thermal conditions (150 degrees C, 3 days). Calcium and strontium are seven- and nine-coordinated in 3 and 5, respectively; barium is nine- and ten-coordinated in 7. It was observed that the increase in pH resulted in a higher connectivity level of ligands, which in turn leads to a higher dimensionality of the crystal structures. The correlation between the structures and pH values will be discussed. Crystal data: for 1, monoclinic, space group P2(1)/n (No. 14), with a = 8.382(2), b = 12.621(3), c = 11.767(2) A, beta = 98.91(3) degrees, Z = 4; for 2, 3, and 5, monoclinic, space group P2(1)/c (No. 14), Z = 4, a = 7.711(2), b = 15.574(3), c = 9.341(2) A, beta = 96.73(3) degrees, Z = 4 (2), a = 6.616(1), b = 12.654(3), c = 8.782(2) A, beta = 103.65(3) degrees, Z = 4 (3), a = 9.213(2), b = 12.088(3), c = 6.196(2) A, beta = 98.96(3) degrees (5); for 4 and 7, triclinic, space group P1 (No. 2), with a = 11.263(2), b = 11.460(3), c = 12.904(2) A, alpha = 71.54(3), beta = 98.96(3), gamma = 89.03(3) degrees, Z = 1 (4), a = 7.107(1), b = 9.780(2), c = 11.431(2) A, alpha = 74.69(3), beta = 73.39(3), gamma = 85.29(3) degrees, Z = 2 (7); for 6, monoclinic, space group C2/c (No. 15), with a = 20.493(4), b = 6.708(1), c = 15.939(3) A, beta = 123.56(3) degrees, Z = 4.

Journal Article↗
PubMed2002

Boar semen controlled delivery system: storage and in vitro spermatozoa release.

Swine spermatozoa were encapsulated in barium alginate and protamine-barium alginate membranes to lengthen their preservation time and to provide a means of controlling their release. Precocious acrosome reactions and secondary anomalies were measured as indices of semen quality. These characteristics were observed for two forms of encapsulated spermatozoa when stored at 18 and 38 degrees C for 24 h and for semen diluted in a classical extender at both temperatures. The results indicate that encapsulation enhances semen preservation, providing protection against membrane damage upon dilution. The effect is even more evident at the higher temperature (38 degrees C), where cell metabolism is higher. An in vitro release test of spermatozoa showed a massive cell delivery from barium alginate capsules within 6 h, and a slow release from protamine-barium alginate capsules. The properties of spermatozoa 24 h after release did not differ from the semen stored at the same temperature in capsules, indicating that the release process does not impair semen quality.

Alginates↗
PubMed2003

Barium-deficient celsian, Ba1-xAl2-2xSi2+2xO8 (x = 0.20 or 0.06).

Barium-deficient forms of celsian (barium aluminium silicate) with the formula Ba(1-x)Al(2-2x)Si(2+2x)O(8) (x = 0.20 and 0.06) have been identified. In contrast with the celsian-orthoclase solid solutions which have been reported previously, these forms, refined in the space group C2/m, with Ba and one O atom in the 4i sites with m site symmetry, and a further O atom in a 4g site with twofold axial symmetry, suggest a slight solid solution with silica. The serendipitous preparation of the compounds represents a possible hazard associated with solid-state synthesis.

Journal Article↗
PubMed1997

A comparison of EDHF-mediated and anandamide-induced relaxations in the rat isolated mesenteric artery.

1. Relaxation of the methoxamine-precontracted rat small mesenteric artery by endothelium-derived hyperpolarizing factor (EDHF) was compared with relaxation to the cannabinoid, anandamide (arachidonylethanolamide). EDHF was produced in a concentration- and endothelium-dependent fashion in the presence of NG-nitro-L-arginine methyl ester (L-NAME, 100 microM) by either carbachol (pEC50 [negative logarithm of the EC50] = 6.19 +/- 0.01, Rmax [maximum response] = 93.2 +/- 0.4%; n = 14) or calcium ionophore A23187 (pEC50 = 6.46 +/- 0.02, Rmax = 83.6 +/- 3.6%; n = 8). Anandamide responses were independent of the presence of endothelium or L-NAME (control with endothelium: pEC50 = 6.31 +/- 0.06, Rmax = 94.7 +/- 4.6%; n = 10; with L-NAME: pEC50 = 6.33 +/- 0.04, Rmax = 93.4 +/- 6.0%; n = 4). 2. The selective cannabinoid receptor antagonist, SR 141716A (1 microM) caused rightward shifts of the concentration-response curves to both carbachol (2.5 fold) and A23187 (3.3 fold). It also antagonized anandamide relaxations in the presence or absence of endothelium giving a 2 fold shift in each case. SR 141716A (10 microM) greatly reduced the Rmax values for EDHF-mediated relaxations to carbachol (control, 93.2 +/- 0.4%; SR 141716A, 10.7 +/- 2.5%; n = 5; P < 0.001) and A23187 (control, 84.8 +/- 2.1%; SR 141716A, 3.5 +/- 2.3%; n = 6; P < 0.001) but caused a 10 fold parallel shift in the concentration-relaxation curve for anandamide without affecting Rmax. 3. Precontraction with 60 mM KCl significantly reduced (P < 0.01; n = 4 for all) relaxations to 1 microM carbachol (control 68.8 +/- 5.6% versus 17.8 +/- 7.1%), A23187 (control 71.4 +/- 6.1% versus 3.9 +/- 0.45%) and anandamide (control 71.1 +/- 7.0% versus 5.2 +/- 3.6%). Similar effects were seen in the presence of 25 mM K+. Incubation of vessels with pertussis toxin (PTX; 400 ng ml-1, 2 h) also reduced (P < 0.01; n = 4 for all) relaxations to 1 microM carbachol (control 63.5 +/- 7.5% versus 9.0 +/- 3.2%), A23187 (control 77.0 +/- 5.8% versus 16.2 +/- 7.1%) and anandamide (control 89.8 +/- 2.2% versus 17.6 +/- 8.7%). 4. Incubation of vessels with the protease inhibitor phenylmethylsulphonyl fluoride (PMSF; 200 microM) significantly potentiated (P < 0.01), to a similar extent (approximately 2 fold), relaxation to A23187 (pEC50: control, 6.45 +/- 0.04; PMSF, 6.74 +/- 0.10; n = 4) and anandamide (pEC50: control, 6.31 +/- 0.02; PMSF, 6.61 +/- 0.08; n = 8). PMSF also potentiated carbachol responses both in the presence (pEC50: control, 6.25 +/- 0.01; PMSF, 7.00 +/- 0.01; n = 4; P < 0.01) and absence (pEC50: control, 6.41 +/- 0.04; PMSF, 6.88 +/- 0.04; n = 4; P < 0.001) of L-NAME. Responses to the nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP) were also potentiated by PMSF (pEC50: control, 7.51 +/- 0.06; PMSF, 8.00 +/- 0.05, n = 4, P < 0.001). 5. EDHF-mediated relaxation to carbachol was significantly attenuated by the K+ channel blocker tetraethylammonium (TEA; 1 mM) (pEC50: control, 6.19 +/- 0.01; TEA, 5.61 +/- 0.01; n = 6; P < 0.01). In contrast, TEA (1 mM) had no effect on EDHF-mediated relaxation to A23187 (pEC50: control, 6.47 +/- 0.04; TEA, 6.41 +/- 0.02, n = 4) or on anandamide (pEC50: control, 6.28 +/- 0.06; TEA, 6.09 +/- 0.02; n = 5). TEA (10 mM) significantly (P < 0.01) reduced the Rmax for anandamide (control, 94.3 +/- 4.0%; 10 mM TEA, 60.7 +/- 4.4%; n = 5) but had no effect on the Rmax to carbachol or A23187. 6. BaCl2 (100 microM), considered to be selective for blockade of inward rectifier K+ channels, had no significant effect on relaxations to carbachol or A23187, but caused a small shift in the anandamide concentration-response curve (pEC50: control, 6.39 +/- 0.01; Ba2+, 6.20 +/- 0.01; n = 4; P < 0.01). BaCl2 (1 mM; which causes non-selective block of K+ channels) significantly (P < 0.01) attenuated relaxations to all three agents (pEC50 values: carbachol, 5.65 +/- 0.02; A23187, 5.84 +/- 0.04; anandamide, 5.95 +/- 0.02; n = 4 for each). 7. Apamin (1mu M), a selective blocker of small conductance, Ca2+-activated, K+ channels (SKCa), 4-aminopyridine (1mM), a blocker of delayed rectifier, voltage-dependent, K+ channels (Kv), and ciclazindol (10mu M), an inhibitor of Kv and adenosine 5'-triphosphate (ATP)-sensitive K+ channels (KATP), significantly reduced EDHF-mediated relaxations to carbachol, but had no significant effects on A23187 or anandamide responses. 8. Glibenclamide (10mu M), a KATP inhibitor and charybdotoxin (100 or 300nM), a blocker of several K+ channel subtypes, had no significant effect on relaxations to any of the agents. Iberiotoxin (50nM), an inhibitor of large conductance, Ca2+-activated, K+ channels (BKCa), had no significant effect on the relaxation responses, either alone or in combination with apamin (1muM). Also, a combination of apamin (1muM) with either glibenclamide (10muM) or 4-aminopyridine (1mM) did not inhibit relaxation to carbachol significantly more than apamin alone. Neither combination had any significant effect on relaxation to A23187 or anandamide. 9. A combination of apamin (1muM) with charybdotoxin (100nM) abolished EDHF-mediated relaxation to carbachol, but had no significant effect on that to A23187. Apamin (1muM) and charybdotoxin (300nM) together consistently inhibited the response to A23187, while apamin (1muM) and ciclazindol (10muM) together inhibited relaxations to both carbachol and A23187. None of these toxin combinations had any significant effect on relaxation to anandamide. 10. It was concluded that the differential sensitivity to K+ channel blockers of EDHF-mediated responses to carbachol and A23187 might be due to actions on endothelial generation of EDHF, as well as its actions on the vascular smooth muscle, and suggests care must be taken in choosing the means of generating EDHF when making comparative studies. Also, the relaxations to EDHF and anandamide may involve activation of cannabinoid receptors, coupled via PTX-sensitive G-proteins to activation of K+ conductances. The results support the hypothesis that EDHF is an endocannabinoid but relaxations to EDHF and anandamide show differential sensitivity to K+ channel blockers, therefore it is likely that anandamide is not identical to EDHF in the small rat mesenteric artery.

4-Aminopyridine↗
PubMed2003

(3 + 1)-dimensional structure refinement of the fresnoite framework-structure type compound Ba(2)TiGe(2)O(8).

The incommensurately modulated structure of the fresnoite framework-structure type compound Ba(2)TiGe(2)O(8) has been solved using a (3 + 1)-dimensional superspace approach. The structure is orthorhombic and adopts the superspace group Cmm2(0,beta,1/2)s00 with beta approximately 0.635 at room temperature. The refinement was based on neutron powder diffraction data obtained from a powdered single crystal grown by Czochralski pulling. The modulation parameters that were obtained support the idea that frozen-in rigid-unit modes cause the modulation. The modulation is mainly manifested by positional displacements of O atoms. Barium ions are either eightfold, ninefold or tenfold coordinated in the one-dimensional modulated structure. A significant improvement of the bond-valence sum for both barium positions is achieved by the introduction of the positional modulation. This finding strongly suggests that underbonded barium positions are critically involved in provoking the incommensurate modulation in Ba(2)TiGe(2)O(8).

Journal Article↗
PubMed1997

Spasmolytic activity of aurapten analogs.

Seven coumaric compounds analogous to aurapten were synthesized. Their spasmolytic activity against Ba2+, acetylcholine and histamine was evaluated to investigate their structure-activity relationship. The results of the bioassay demonstrated the important roles of the cis type of double bond at C-2' and the epoxide between c-6' and 7'.

Acetylcholine↗
PubMed1998

A case of zinc chloride ingestion.

Zinc chloride is a powerful corrosive agent. Reports of zinc chloride ingestion are uncommon, and there is little information about its toxicity and management. The authors report the clinical course of a 10-year-old girl who accidentally ingested an acid soldering flux solution (pH, 3.0; zinc chloride, 30% to < 60%). Systemic effects after the ingestion were unremarkable except for lethargy. Thus, chelation therapy was not considered. Severe gastric corrosion was caused by local caustic action. An antral stricture of the stomach approximately 3 weeks after the ingestion developed, and she underwent a modified Heineke-Mikulicz antropyloroplasty. Postoperatively, she made an uneventful recovery. On follow-up, although she was tolerating a normal diet, results of a barium meal showed her stomach to be totally aperistaltic. Results of a nuclear medicine study showed moderately delayed gastric emptying. Careful long-term follow-up is necessary, because there is potential risk for malignancy in the damaged stomach.

Burns, Chemical↗
PubMed1985

Splenotoxicity associated with splenic sarcomas in rats fed high doses of D & C Red No. 9 or aniline hydrochloride.

A histopathologic review of F344 rat spleens from the National Toxicology Program-National Cancer Institute bioassays of barium salt of 5-chloro-2-(2-hydroxy-1-naphthalenyl)-azo-4-methylbenzenesulfonic acid [(D & C Red No. 9) CAS: 516-00-21] and aniline HCI (CAS: 142-04-1) was conducted to assess splenotoxic changes associated with splenic sarcomas induced by these aromatic amines. Four splenic changes--fatty metamorphosis (FM), splenic fibrosis (FIB), capsule hyperplasia (CH), and hemorrhage--were markedly increased in incidence and severity in males treated with high doses of either D & C Red No. 9 or aniline HCI. Females treated with high doses of either of these compounds showed similar but less severe changes. FIB and FM showed strong group correlations with tumor incidence (r greater than or equal to 0.87). All groups that demonstrated FM also demonstrated splenic sarcomas; groups without the FM lesions did not exhibit splenic tumors. The morphologic similarity of the FIB and CH lesions to the induced splenic sarcomas suggests that these lesions are preneoplastic. Moreover, the treatment-related splenic lesions appear to be precursors of the induced splenic sarcomas. Carcinogenicity studies with serial sacrifices at varying intervals will be required for experimental verification of these conclusions. A schema, based on the findings of the study, suggests a hypothetical pathway for the progression of the treatment-related splenic lesions from onset to tumor formation.

Aniline Compounds↗
PubMed2006

Volume regulation following hyposmotic shock in isolated turbot (Scophthalmus maximus) hepatocytes.

Regulatory volume decrease (RVD) following hyposmotic stimulation was studied in isolated turbot, Scophthalmus maximus, hepatocytes. Exposed to a reduced osmolality (from 320 to 240 mosm kg(-1)), cells first swelled and then exhibited a RVD. Volume regulation was significantly inhibited in presence of NPPB, 9-AC, acetazolamide, DIDS and barium. Taken together, these results could suggest that RVD operated via separate K+ and Cl- channels and probably Cl-/HCO3(-) exchanger in turbot hepatocytes. The K+/Cl- cotransporter could also be involved as furosemide and DIOA strongly inhibited the process whereas NEM, a K+/Cl- cotransporter activator, added under isosmotic conditions, led to cell shrinkage. RVD in turbot hepatocytes appeared also to depend on proteins p38 MAP kinase and tyrosine kinase but not on proteins ERK 1/2. Arachidonic acid and leukotrienes could also be involved since inhibition of synthesis of both these compounds by quinacrine and NDGA, respectively, inhibited the volume regulation. Likewise, Ca2+ has been proved to be an essential messenger as RVD was prevented in absence of Ca2+. Finally, this work provides bases for novel studies on cell volume regulation in marine teleosteans.

Animals↗
PubMed1985

[General pharmacologic studies on the analgesic flupirtine].

In the present study the general pharmacological properties of ethyl-N-[2-amino-6-(4-fluor-phenylmethylamino)pyridin-3-yl]carbama te (flupirtine, D 9998), a structural new analgesic, are described. In several tests with mice flupirtine shows a centrally depressant component of action. However, regarding undesirable side effects as ataxia, inhibition of motor activity etc. this action is, with respect to the analgesic effective doses less pronounced than those of comparable analgesics, for instance phenacetin. In relatively low doses flupirtine antagonizes tremor induced by oxotremorine in mice. This activity is probably not caused by a central anticholinergic action, because other anticholinergic effects have not been observed. It should be pointed out that flupirtine antagonizes the morphine-induced tail phenomenon in mice in relatively low doses. This action obviously differentiates flupirtine from opiates. Up to high doses flupirtine does not cause catalepsia in mice, consequently its centrally depressant activity does not resemble that of reserpine and also is not comparable with those of neuroleptic agents. The corneal and pinnal reflexes are not influenced by flupirtine and the righting reflex is slightly delayed in high doses. The anticonvulsive activity of flupirtine observed in the pentetrazol shock test (mouse) after high doses probably cannot be considered to occur within the analgesic dose range. Inhibition of amphetamine toxicity in mice observed in doses near the hypnotic doses may be caused by non-specific effects. In vitro tests with isolated trachea or ileum of guinea pigs show that flupirtine possesses no or very weak antagonism against histamine-induced spasms. In spasms caused by barium chloride flupirtine shows a weak musculotropic-spasmolytic activity. Investigations on the circulatory system of dogs do not indicate any incompatibilities with flupirtine. No evidence of antiarrhythmic activity was found in rats. Flupirtine has no local anesthetic activity in mice but some weak effects on the cornea of rabbits. Like several other analgesics flupirtine shows in rats a reversible antidiuretic action including sodium and chloride retention which is of relatively short duration and is not observed in long-term studies in rats and dogs. In contrast to many stronger antiinflammatory compounds, flupirtine does not possess ulcerogenic activity in rats up to high doses. A minimal inhibition of intestinal motility (mouse) is observed only in doses higher than the analgesic effective doses.

Aminopyridines↗
PubMed2002

Interaction of the cytosolic domains of the Kir6.2 subunit of the K(ATP) channel is modulated by sulfonylureas.

The NH(2)- and COOH-termini of the ATP-sensitive potassium (K(ATP)) channel pore-forming subunit, Kir6.2, both lie intracellularly and interact with one another. To study this interaction, cyan fluorescent protein (CFP) and yellow fluorescent protein (YFP) were fused to the NH(2)- and COOH-termini of Kir6.2, respectively (CFP-Kir6.2-YFP). These fluorescent proteins have sufficient spectral overlap to allow distance-dependent fluorescence resonance energy transfer (FRET). When CFP-Kir6.2-YFP was expressed in human embryonic kidney cells and illuminated at 440 nm to excite CFP, significant fluorescence was recorded at 535 nm, the peak of the YFP emission spectrum. This indicated that FRET was occurring and thus that the NH(2)- and COOH-termini of Kir6.2 lie in close proximity to one another. The emission ratio, F(535)/F(480), was increased by co-expression of SUR2A, but not SUR1, suggesting that SUR2A but not SUR1 influences the Kir6.2 NH(2)- and COOH-terminal interaction. This interaction was reduced by the sulfonylureas tolbutamide and gliclazide, but not by the pore blocker barium. The properties of the tolbutamide response indicate that the drug disrupts the interaction between the NH(2)- and COOH-termini of Kir6.2 by binding to a low-affinity site on Kir6.2.

Animals↗
PubMed2004

Elevated levels of ferrimagnetic metals in foodchains supporting the Guam cluster of neurodegeneration: do metal nucleated crystal contaminants [corrected] evoke magnetic fields that initiate the progressive pathogenesis of neurodegeneration?

Elevated levels of aluminium (Al), strontium (Sr), barium (Ba), iron (Fe), manganese (Mn) cations - combined with deficiencies of magnesium (Mg)/calcium (Ca) - have been observed in the foodchains that traditionally support the Chamorro populations affected by high incidence clusters of Alzheimer (AD), Parkinson-like (PD), motor neurone diseases and multiple sclerosis on the island of Guam. Soils drawn from the cluster region demonstrated an excessive fivefold increase in 'magnetic susceptibility' readings in relation to soils from disease free adjoining regions. A multifactorial aetiological hypothesis is proposed that pivots upon the combined exposure to high levels of natural/industrial sources of ferrimagnetic/ferroelectric compounds incorporating Al, Fe, Mn, Sr, Ba (e.g., via yam/seafood consumption or exposure to world war 2 (WW2) munitions) and to low levels of Mg/Ca in all S. Pacific locations where these clusters of neurodegenerative disease have simultaneously erupted. Once gut/blood brain barrier permeability is impaired, the increased uptake of Al, Fe, Sr, Ba, or Mn into the Mg/Ca depleted brain leads to rogue metal substitutions at the Mg/Ca vacated binding domains on various enzyme/proteoglycan groups, causing a broad ranging disruption in Mg/Ca dependent systems - such as the glutamine synthetase which prevents the accumulation of neurotoxic glutamate. The rogue metals chelate sulphate, disrupting sulphated-proteoglycan mediated inhibition of crystal proliferation, as well as its regulation of the Fibroblast growth factor receptor complex which disturbs the molecular conformation of those receptors and their regulation of transphosphorylation between intracellular kinase domains; ultimately collapsing proteoglycan mediated cell-cell signalling pathways which maintain the growth and structural integrity of the neuronal networks. The depression of Mg/Ca dependent systems in conjunction with the progressive ferrimagnetisation of the CNS due to an overload of rogue ferroelectric/ferrimagnetic metal contaminants, enables 'seeding' of metal-protein crystalline arrays that can proliferate in the proteoglycan depleted brain. The resulting magnetic field emissions initiate a free radical mediated progressive pathogenesis of neurodegeneration. The co-clustering of these various types of disease in select geographical pockets around the world suggests that all of these conditions share a common early life exposure to ferromagnetic metal nucleating agents in their multifactorial aetiology. Factors such as individual genetics, the species of metal involved, etc., dictate which specific class of disease will emerge as a delayed neurotoxic response to these environmental insults.

Amyotrophic Lateral Sclerosis↗
PubMed1996

Value of technetium-99m HMPAO-labelled leucocyte scintigraphy as an initial screening test in patients suspected of having inflammatory bowel disease.

OBJECTIVE: This study was designed to evaluate the role of technetium-99m (99mTc) hexamethyl propylene amine oxime (HMPAO)-labelled leucocyte imaging as an initial screening test in patients suspected of having inflammatory bowel disease (IBD). PATIENTS AND METHODS: Thirty-one patients in whom a final diagnosis of irritable bowel syndrome (IBS) was made (group 1) and another 33 patients with established Crohn's disease (group 2) were studied. All patients had 99mTc HMPAO-labelled leucocyte scan with imaging at 40 and 120 min. Scans with abnormal bowel uptake were considered positive and this uptake was quantified by visual grading and computer-based methods (scan score). Group 1 patients with positive 99mTc HMPAO scan underwent an indium-111 (111In)-labelled leucocyte scan (imaging at 180 min) followed by endoscopy and barium radiology as deemed necessary in order to verify the 99m Tc HMPAO result. RESULTS: Three scan patterns were seen: well localized and unequivocally positive scans at both 40 min and 2 h were obtained from 28 patients. All but one had established Crohn's disease. Diffuse bowel uptake was seen in 14 scans. Ten of these (false positive) were obtained from symptomatic patients with IBS and four (false negative) from patients with asymptomatic Crohn's disease. No bowel uptake at 40 min and 2 h was seen in 22 scans. All but two of these (who had quiescent Crohn's disease) were obtained from patients with IBS. Active Crohn's disease is associated with significantly higher scan score (mean +/- SEM, 82.1 +/- 13.6) than the false positive scans (12.5 +/- 3.1, P > or = 0.001). Patients with false positive 99mTc HMPAO scans had negative 111In scans, endoscopy and barium radiology. CONCLUSION: Bowel scanning using either 111In or 99mTc HMPAO is useful in excluding active IBD. Because of radiation dose, image quality and availability 99mTc may be preferred to 111In.

Adult↗
PubMedDate not supplied

Scanning electron microscopy and energy dispersive analysis of machined denture base surfaces.

To relate the characteristics of rotary instruments to the surfaces they produce, acrylic resin, Molloplast B, and Novus were investigated with energy dispersive analysis and scanning electron microscopy (secondary and backscatter images) before and after machining. The chemical composition of cutting instruments, material surfaces, and residues was identified. Machined debris embedded in Molloplast B after machining with the Molloplast stone was found to contain a mean lead content of 45%. High concentrations of barium sulphate were discovered on the arbor band-machined surface of Novus. These differences were related to clinically appropriate instrumentation, and, therefore, biocompatibility studies that intimately relate to the in vivo situation should be considered for new materials.

Dental Polishing↗
PubMed1989

Calcium-activated chloride current in rat vascular smooth muscle cells in short-term primary culture.

Isolated cells from rat portal vein smooth muscle in short-term primary culture were studied using patch-clamp technique (whole-cell configuration). In order to study a calcium-activated chloride current, the potassium currents were blocked by intracellular cesium diffusion. Without EGTA in the pipette solution, depolarizing voltage pulses from a holding potential of -70 mV to positive potentials activated an early inward and a late outward current. The latter persisted as a long-lasting inward tail current when the membrane was repolarized to -70 mV. The outward current measured at the end of the pulse and the tail current were blocked by extracellular cobalt, after replacement of external calcium with barium, after removal of external calcium, and when the calcium concentration of the pipette solution was less than 0.5 microM, suggesting that they were calcium-dependent. The tail current decay was voltage sensitive, becoming faster with hyperpolarization. The reversal potential of the calcium-activated current was near the equilibrium potential for chloride ions, and was shifted as predicted by the Nernst equation when the extracellular or intracellular chloride concentration was changed. The calcium-activated current was blocked by adding micromolar concentrations of niflumic acid or millimolar concentrations of DIDS. This effect of compounds known to interfere with chloride channels together with the data on the equilibrium potential for chloride ions indicated above suggested the existence of a calcium-activated chloride current in vascular smooth muscle cells.

Animals↗
PubMed2006

Organic and inorganic di-cations for capillary silica coating and EOF modulation in CE: Example of application in PEG analysis.

EOF measurements, by using 1,4-di-(4-aza-1-azonia-bicyclo[2.2.2]octane)butane diiodide, barium and strontium tetraborate as silica wall modifiers, are reported and, as an example of application, analysis of PEG (PEG 400-2000) polydisperse preparations in free solution CZE is shown. PEGs have been derivatized with phthalic anhydride so as to form singly or doubly charged derivatives with strong UV absorbance at 214 nm. Whereas separations in plain tetraborate buffer, pH 9.0, without any EOF control, did not lead to good resolution of all-size oligomers and suffered from long analysis times, excellent resolution of all oligomers up to 40 ethylene oxide (EO) units could be obtained under EOF control. Such EOF modulation was engendered by addition of 1 mM M7C4M7, a doubly charged organic cation able to stick tenaciously to the silica wall. Further modulation of EOF and silica surface modification could be achieved also by addition of inorganic cations, notably those of group II, whereas monovalent cations did not seem to affect much the EOF flux. Among the doubly charged cations investigated, Ca++, Mg++, Sr++ and Ba++, the latter did seem to offer best EOF control and reproducible runs. A judicious blend of M7C4M7 (0.33-1 mM range) with barium (10-20 mM range) allowed baseline resolution of all PEG oligomers investigated up to PEG 2000 and >40 EO units in length. In this last case, best results in terms of reproducibility and separation efficiency of the more heavy homologues were obtained using Li+ salt in small amounts.

Aza Compounds↗
PubMedDate not supplied

Successful allotransplantation of microencapsulated parathyroids in rats.

Allotransplantation of parathyroid tissue in humans is desirable for treating long-term hypoparathyroidism (e.g., after inadvertent removal of parathyroid glands during thyroid surgery). Until now, parathyroid allotransplantation was not used clinically because its advantages were outweighted by the need of immunosuppression. To overcome the immunogenicity of the tissue to be transplanted, we employed the method of microencapsulation; first tried in islet cell transplantation for experimental allotransplantation of parathyroid tissue. We have been able to achieve long-term success in a rat model. After isolation and tissue culture, tissue pieces from parathyroid glands of 280 Lewis rats were encapsulated in barium alginate and grafted into hypocalcemic DA rats. From the 7th to the 90th day after transplantation the recipient rats (DA rats) showed a normal serum calcium concentration. This is the first report of successful long-term survival and function of microencapsulated allotransplanted parathyroid tissue.

Animals↗
PubMed2005

A Thr357 to Ser polymorphism in homozygous and compound heterozygous subjects causes absent or reduced P2X7 function and impairs ATP-induced mycobacterial killing by macrophages.

The P2X(7) receptor is a ligand-gated cation channel that is highly expressed on mononuclear leukocytes and that mediates ATP-induced apoptosis and killing of intracellular pathogens. There is a wide variation in P2X(7) receptor function between subjects, explained in part by four loss-of-function polymorphisms (R307Q, E496A, I568N, and a 5'-intronic splice site polymorphism), as well as rare mutations. In this study, we report the allele frequencies of 11 non-synonymous P2X(7) polymorphisms and describe a fifth loss-of-function polymorphism in the gene (1096C --> G), which changes Thr(357) to Ser (T357S) with an allele frequency of 0.08 in the Caucasian population. P2X(7) function was measured by ATP-induced ethidium(+) influx into peripheral blood lymphocytes and monocytes and, when compared with wild-type subjects, was reduced to 10-65% in heterozygotes, 1-18% in homozygotes, and 0-10% in compound heterozygotes carrying T357S and a second loss-of-function polymorphism. Overexpression of the T357S mutant P2X(7) in either HEK-293 cells or Xenopus oocytes gave P2X(7) function of approximately 50% that of wild-type constructs. Differentiation of monocytes to macrophages, which also up-regulates P2X(7), restored P2X(7) function to near normal in cells heterozygous for T357S and to a value 50-65% of wild-type in cells homozygous for T357S or compound heterozygous for T357S/E496A. However, macrophages from subjects that are compound heterozygous for either T357S/R307Q or T357S/stop codon had near-to-absent P2X(7) function. These functional deficits induced by T357S were paralleled by impaired ATP-induced apoptosis and mycobacteria killing in macrophages from these subjects. Lymphocytes, monocytes, and macrophages from subjects homozygous for T357S or compound heterozygous for T357S and a second loss-of-function allele have reduced or absent P2X(7) receptor function.

Adenosine Triphosphate↗