Calf Bovine

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Klaus Steinmeyer - One of the best experts on this subject based on the ideXlab platform.

  • dcpib is a novel selective blocker of icl swell and prevents swelling induced shortening of guinea pig atrial action potential duration
    British Journal of Pharmacology, 2001
    Co-Authors: Niels Decher, Andreas E Busch, Hans Jochen Dr Lang, Bernd Nilius, Andrea Bruggemann, Klaus Steinmeyer
    Abstract:

    We identified the ethacrynic-acid derivative DCPIB as a potent inhibitor of ICl,swell, which blocks native ICl,swell of Calf Bovine pulmonary artery endothelial (CPAE) cells with an IC50 of 4.1 μM. Similarly, 10 μM DCPIB almost completely inhibited the swelling-induced chloride conductance in Xenopus oocytes and in guinea-pig atrial cardiomyocytes. Block of ICl,swell by DCPIB was fully reversible and voltage independent. DCPIB (10 μM) showed selectivity for ICl,swell and had no significant inhibitory effects on ICl,Ca in CPAE cells, on chloride currents elicited by several members of the CLC-chloride channel family or on the human cystic fibrosis transmembrane conductance regulator (hCFTR) after heterologous expression in Xenopus oocytes. DCPIB (10 μM) also showed no significant inhibition of several native anion and cation currents of guinea pig heart like ICl,PKA, IKr, IKs, IK1, INa and ICa. In all atrial cardiomyocytes (n=7), osmotic swelling produced an increase in chloride current and a strong shortening of the action potential duration (APD). Both swelling-induced chloride conductance and AP shortening were inhibited by treatment of swollen cells with DCPIB (10 μM). In agreement with the selectivity for ICl,swell, DCPIB did not affect atrial APD under isoosmotic conditions. Preincubation of atrial cardiomyocytes with DCPIB (10 μM) completely prevented both the swelling-induced chloride currents and the AP shortening but not the hypotonic cell swelling. We conclude that swelling-induced AP shortening in isolated atrial cells is mainly caused by activation of ICl,swell. DCPIB therefore is a valuable pharmacological tool to study the role of ICl,swell in cardiac excitability under pathophysiological conditions leading to cell swelling. British Journal of Pharmacology (2001) 134, 1467–1479; doi:10.1038/sj.bjp.0704413

Niels Decher - One of the best experts on this subject based on the ideXlab platform.

  • dcpib is a novel selective blocker of icl swell and prevents swelling induced shortening of guinea pig atrial action potential duration
    British Journal of Pharmacology, 2001
    Co-Authors: Niels Decher, Andreas E Busch, Hans Jochen Dr Lang, Bernd Nilius, Andrea Bruggemann, Klaus Steinmeyer
    Abstract:

    We identified the ethacrynic-acid derivative DCPIB as a potent inhibitor of ICl,swell, which blocks native ICl,swell of Calf Bovine pulmonary artery endothelial (CPAE) cells with an IC50 of 4.1 μM. Similarly, 10 μM DCPIB almost completely inhibited the swelling-induced chloride conductance in Xenopus oocytes and in guinea-pig atrial cardiomyocytes. Block of ICl,swell by DCPIB was fully reversible and voltage independent. DCPIB (10 μM) showed selectivity for ICl,swell and had no significant inhibitory effects on ICl,Ca in CPAE cells, on chloride currents elicited by several members of the CLC-chloride channel family or on the human cystic fibrosis transmembrane conductance regulator (hCFTR) after heterologous expression in Xenopus oocytes. DCPIB (10 μM) also showed no significant inhibition of several native anion and cation currents of guinea pig heart like ICl,PKA, IKr, IKs, IK1, INa and ICa. In all atrial cardiomyocytes (n=7), osmotic swelling produced an increase in chloride current and a strong shortening of the action potential duration (APD). Both swelling-induced chloride conductance and AP shortening were inhibited by treatment of swollen cells with DCPIB (10 μM). In agreement with the selectivity for ICl,swell, DCPIB did not affect atrial APD under isoosmotic conditions. Preincubation of atrial cardiomyocytes with DCPIB (10 μM) completely prevented both the swelling-induced chloride currents and the AP shortening but not the hypotonic cell swelling. We conclude that swelling-induced AP shortening in isolated atrial cells is mainly caused by activation of ICl,swell. DCPIB therefore is a valuable pharmacological tool to study the role of ICl,swell in cardiac excitability under pathophysiological conditions leading to cell swelling. British Journal of Pharmacology (2001) 134, 1467–1479; doi:10.1038/sj.bjp.0704413

H Bohni - One of the best experts on this subject based on the ideXlab platform.

  • a study of the potentials achieved during mechanical abrasion and the repassivation rate of titanium and ti6al4v in inorganic buffer solutions and Bovine serum
    Electrochimica Acta, 2004
    Co-Authors: F Contu, Bernhard Elsener, H Bohni
    Abstract:

    Abstract Titanium alloys in orthopaedic implants are susceptible to mechanical disruption of the passive film (fretting corrosion). To study this effect, open-circuit potential (ocp) measurements before, during and after mechanical disruption of the passive film in a tribo-electrochemical cell on commercial pure titanium and Ti6Al4V alloy in inorganic buffer solutions in the pH range from 2.0 to 12.0 and Calf Bovine serum at pH 4.0 and 7.0 are reported. Additionally, the effect of pH, electrolyte and sample composition on the repassivation rate has been investigated. The potentials achieved during the abrasion of Ti6Al4V are the same as those characterizing pure titanium, which indicates that the corrosion current of both materials in the active state is due to the oxidation of titanium. However, commercial pure titanium displays a tendency to repassivate faster than Ti6Al4V in inorganic buffer solutions thanks to the lower critical current density and the higher catalytic activity towards the hydrogen evolution reaction observed on the pure metal in comparison with the alloy. Proteinaceous solutions like Bovine serum, significantly slow down the anodic dissolution and the cathodic reactions both on titanium and the alloy. However, the repassivation rate of the Ti6Al4V is not affected by serum, while that of cp titanium significantly decreases both at pH 4.0 and 7.0.

Bernhard Elsener - One of the best experts on this subject based on the ideXlab platform.

  • a study of the potentials achieved during mechanical abrasion and the repassivation rate of titanium and ti6al4v in inorganic buffer solutions and Bovine serum
    Electrochimica Acta, 2004
    Co-Authors: F Contu, Bernhard Elsener, H Bohni
    Abstract:

    Abstract Titanium alloys in orthopaedic implants are susceptible to mechanical disruption of the passive film (fretting corrosion). To study this effect, open-circuit potential (ocp) measurements before, during and after mechanical disruption of the passive film in a tribo-electrochemical cell on commercial pure titanium and Ti6Al4V alloy in inorganic buffer solutions in the pH range from 2.0 to 12.0 and Calf Bovine serum at pH 4.0 and 7.0 are reported. Additionally, the effect of pH, electrolyte and sample composition on the repassivation rate has been investigated. The potentials achieved during the abrasion of Ti6Al4V are the same as those characterizing pure titanium, which indicates that the corrosion current of both materials in the active state is due to the oxidation of titanium. However, commercial pure titanium displays a tendency to repassivate faster than Ti6Al4V in inorganic buffer solutions thanks to the lower critical current density and the higher catalytic activity towards the hydrogen evolution reaction observed on the pure metal in comparison with the alloy. Proteinaceous solutions like Bovine serum, significantly slow down the anodic dissolution and the cathodic reactions both on titanium and the alloy. However, the repassivation rate of the Ti6Al4V is not affected by serum, while that of cp titanium significantly decreases both at pH 4.0 and 7.0.

Andreas E Busch - One of the best experts on this subject based on the ideXlab platform.

  • dcpib is a novel selective blocker of icl swell and prevents swelling induced shortening of guinea pig atrial action potential duration
    British Journal of Pharmacology, 2001
    Co-Authors: Niels Decher, Andreas E Busch, Hans Jochen Dr Lang, Bernd Nilius, Andrea Bruggemann, Klaus Steinmeyer
    Abstract:

    We identified the ethacrynic-acid derivative DCPIB as a potent inhibitor of ICl,swell, which blocks native ICl,swell of Calf Bovine pulmonary artery endothelial (CPAE) cells with an IC50 of 4.1 μM. Similarly, 10 μM DCPIB almost completely inhibited the swelling-induced chloride conductance in Xenopus oocytes and in guinea-pig atrial cardiomyocytes. Block of ICl,swell by DCPIB was fully reversible and voltage independent. DCPIB (10 μM) showed selectivity for ICl,swell and had no significant inhibitory effects on ICl,Ca in CPAE cells, on chloride currents elicited by several members of the CLC-chloride channel family or on the human cystic fibrosis transmembrane conductance regulator (hCFTR) after heterologous expression in Xenopus oocytes. DCPIB (10 μM) also showed no significant inhibition of several native anion and cation currents of guinea pig heart like ICl,PKA, IKr, IKs, IK1, INa and ICa. In all atrial cardiomyocytes (n=7), osmotic swelling produced an increase in chloride current and a strong shortening of the action potential duration (APD). Both swelling-induced chloride conductance and AP shortening were inhibited by treatment of swollen cells with DCPIB (10 μM). In agreement with the selectivity for ICl,swell, DCPIB did not affect atrial APD under isoosmotic conditions. Preincubation of atrial cardiomyocytes with DCPIB (10 μM) completely prevented both the swelling-induced chloride currents and the AP shortening but not the hypotonic cell swelling. We conclude that swelling-induced AP shortening in isolated atrial cells is mainly caused by activation of ICl,swell. DCPIB therefore is a valuable pharmacological tool to study the role of ICl,swell in cardiac excitability under pathophysiological conditions leading to cell swelling. British Journal of Pharmacology (2001) 134, 1467–1479; doi:10.1038/sj.bjp.0704413