REVISITING THE PROFESSIONAL MOBILITY OF TECHNICAL COLLEGE SPECIALISTS

В статье излагается взгляд на проблему развития профессиональной мобильности студентов технических специальностей колледжа посредством использования ряда дидактически значимых инструментов, объединенных в систему контрольно-оценочных мероприятий, также позволяющих формировать личностные качества студентовThe article presents a look at the problem of technical students’ professional mobility development through the use of a number of didactically significant tools, combined into a system of check and assessment activities, also allowing the formation of students' personal qualitie

Hydrogen sulfide in regulation of frog myocardium contractility

Hydrogen sulfide (H2S) is an endogenously synthesized gaseous molecule which, along with nitric oxide and carbon monoxide, induces a number of effects in cardiovascular system under normal and pathological conditions. In the present work, the effects and underlying mechanisms of the H2S donor sodium hydrosulfide (NaHS) on the isometric force of frog myocardium contraction have been studied. NaHS at the concentration of 100 μM induced negative inotropic effect and reduced the maximum velocity of the contraction and relaxation of the isolated ventricle strips. The substrate of H2S synthesis, L-cysteine (200 μM and 1 mM), induced the same effect, while the inhibitors of cystathionin-γ-lyase, the H2S-producing enzyme in heart, β-cyanoalanine (500 μM) and propargylglycine (500 μM), increased the amplitude of contraction. Inhibition of cystathionin-γ-lyase by β-cyanoalanine prevented the negative inotropic effect of L-cysteine. After the inhibition of adenylate cyclase by MDL-12,330A (3 μM) or phosphodiesterases by IBMX (200 μM), the effect of NaHS was less than that in the control. In the presence of membrane-penetrating analogous of cAMP, 8Br-cAMP (100 μM) and pCPT-cAMP (100 μM), the negative inotropic effect of NaHS was completely retained. The effect of NaHS significantly decreased after preliminary application of the NO donor, SNAP (10 μM), and did not change after the inhibition of NO synthases by L-NAME (100 μM). The results suggest the possibility of endogenous synthesis of H2S in frog myocardium and regulation of its contractility by the activation of phosphodiesterases hydrolyzing cAMP, which leads to a decrease in the activation of cAMP-dependent protein kinases and phosphorylation of voltage-dependent L-type Ca channels. As a result, the reduction of calcium entry into cardiomyocytes decreases the contractility of frog myocardium. © 2013 Pleiades Publishing, Ltd

Hydrogen sulfide in regulation of frog myocardium contractility

Hydrogen sulfide (H2S) is an endogenously synthesized gaseous molecule which along with nitric oxide and carbon monoxide induces a number of effects in cardiovascular system in normal and pathological conditions. In the present study the effects and underlying mechanisms of H2S donor, sodium hydrosulfide (NaHS), on isometric force of frog myocardium contraction were studied. NaHS in the concentration of 100 μM induced a negative inotropic effect and decreased the maximal velocity of contraction and relaxation of isolated ventricle strips. The substrate Of H2S synthesis L-cystein (200 μM and 1 mM) induced the same effect and the inhibitors of cystationin y-lyase, H2S-producing enzyme in heart, ß-cyanoalanin (500 μM) and propargylglycine (500 μM) increased the amplitude of contraction. Inhibition of cystationin y-lyase by ß-cyanoalanin prevented the negative inotropic effect of L-cystein. After inhibition of adenylate cyclase by MDL12,330A (3 μM) or phosphodiesterases by IBMX (200 μM) effect of NaHS was lesser than in control. In the presence of membrane-penetrating analogous of cAMP, 8Br-cAMP (100 μM) and pCPT-cAMP (100 μM), negative inotropic effect of NaHS completely retained. The effect of NaHS significantly decreased after preliminary application of the NO donor, SNAP (10 μM), and did not change after inhibition of NO-synthases by LNAME ( 100 μM). The obtained data suggest the possibility of endogenous synthesis of H2S in frog myocardium and regulation of its contractility by activation of phosphodiesterases hydrolyzing cAMP, which leads to a decrease of activation of cAM P-dependent protein kinases and phosphorylation of voltage-dependent L-type Ca-channels. As the result, a reduction of calcium entry into cardiomyocytes decreases the contractility of frog myocardium

Hydrogen sulfide in regulation of frog myocardium contractility

Hydrogen sulfide (H2S) is an endogenously synthesized gaseous molecule which, along with nitric oxide and carbon monoxide, induces a number of effects in cardiovascular system under normal and pathological conditions. In the present work, the effects and underlying mechanisms of the H2S donor sodium hydrosulfide (NaHS) on the isometric force of frog myocardium contraction have been studied. NaHS at the concentration of 100 μM induced negative inotropic effect and reduced the maximum velocity of the contraction and relaxation of the isolated ventricle strips. The substrate of H2S synthesis, L-cysteine (200 μM and 1 mM), induced the same effect, while the inhibitors of cystathionin-γ-lyase, the H2S-producing enzyme in heart, β-cyanoalanine (500 μM) and propargylglycine (500 μM), increased the amplitude of contraction. Inhibition of cystathionin-γ-lyase by β-cyanoalanine prevented the negative inotropic effect of L-cysteine. After the inhibition of adenylate cyclase by MDL-12,330A (3 μM) or phosphodiesterases by IBMX (200 μM), the effect of NaHS was less than that in the control. In the presence of membrane-penetrating analogous of cAMP, 8Br-cAMP (100 μM) and pCPT-cAMP (100 μM), the negative inotropic effect of NaHS was completely retained. The effect of NaHS significantly decreased after preliminary application of the NO donor, SNAP (10 μM), and did not change after the inhibition of NO synthases by L-NAME (100 μM). The results suggest the possibility of endogenous synthesis of H2S in frog myocardium and regulation of its contractility by the activation of phosphodiesterases hydrolyzing cAMP, which leads to a decrease in the activation of cAMP-dependent protein kinases and phosphorylation of voltage-dependent L-type Ca channels. As a result, the reduction of calcium entry into cardiomyocytes decreases the contractility of frog myocardium. © 2013 Pleiades Publishing, Ltd

Alger [un cordonnier dans la rue] / Philippe Joudiou

Hydrogen sulfide (H2S) is an endogenously synthesized gaseous molecule which along with nitric oxide and carbon monoxide induces a number of effects in cardiovascular system in normal and pathological conditions. In the present study the effects and underlying mechanisms of H2S donor, sodium hydrosulfide (NaHS), on isometric force of frog myocardium contraction were studied. NaHS in the concentration of 100 μM induced a negative inotropic effect and decreased the maximal velocity of contraction and relaxation of isolated ventricle strips. The substrate Of H2S synthesis L-cystein (200 μM and 1 mM) induced the same effect and the inhibitors of cystationin y-lyase, H2S-producing enzyme in heart, ß-cyanoalanin (500 μM) and propargylglycine (500 μM) increased the amplitude of contraction. Inhibition of cystationin y-lyase by ß-cyanoalanin prevented the negative inotropic effect of L-cystein. After inhibition of adenylate cyclase by MDL12,330A (3 μM) or phosphodiesterases by IBMX (200 μM) effect of NaHS was lesser than in control. In the presence of membrane-penetrating analogous of cAMP, 8Br-cAMP (100 μM) and pCPT-cAMP (100 μM), negative inotropic effect of NaHS completely retained. The effect of NaHS significantly decreased after preliminary application of the NO donor, SNAP (10 μM), and did not change after inhibition of NO-synthases by LNAME ( 100 μM). The obtained data suggest the possibility of endogenous synthesis of H2S in frog myocardium and regulation of its contractility by activation of phosphodiesterases hydrolyzing cAMP, which leads to a decrease of activation of cAM P-dependent protein kinases and phosphorylation of voltage-dependent L-type Ca-channels. As the result, a reduction of calcium entry into cardiomyocytes decreases the contractility of frog myocardium

Hydrogen sulfide in regulation of frog myocardium contractility

Hydrogen sulfide (H2S) is an endogenously synthesized gaseous molecule which along with nitric oxide and carbon monoxide induces a number of effects in cardiovascular system in normal and pathological conditions. In the present study the effects and underlying mechanisms of H2S donor, sodium hydrosulfide (NaHS), on isometric force of frog myocardium contraction were studied. NaHS in the concentration of 100 μM induced a negative inotropic effect and decreased the maximal velocity of contraction and relaxation of isolated ventricle strips. The substrate Of H2S synthesis L-cystein (200 μM and 1 mM) induced the same effect and the inhibitors of cystationin y-lyase, H2S-producing enzyme in heart, ß-cyanoalanin (500 μM) and propargylglycine (500 μM) increased the amplitude of contraction. Inhibition of cystationin y-lyase by ß-cyanoalanin prevented the negative inotropic effect of L-cystein. After inhibition of adenylate cyclase by MDL12,330A (3 μM) or phosphodiesterases by IBMX (200 μM) effect of NaHS was lesser than in control. In the presence of membrane-penetrating analogous of cAMP, 8Br-cAMP (100 μM) and pCPT-cAMP (100 μM), negative inotropic effect of NaHS completely retained. The effect of NaHS significantly decreased after preliminary application of the NO donor, SNAP (10 μM), and did not change after inhibition of NO-synthases by LNAME ( 100 μM). The obtained data suggest the possibility of endogenous synthesis of H2S in frog myocardium and regulation of its contractility by activation of phosphodiesterases hydrolyzing cAMP, which leads to a decrease of activation of cAM P-dependent protein kinases and phosphorylation of voltage-dependent L-type Ca-channels. As the result, a reduction of calcium entry into cardiomyocytes decreases the contractility of frog myocardium

Hydrogen sulfide in regulation of frog myocardium contractility

Hydrogen sulfide (H2S) is an endogenously synthesized gaseous molecule which along with nitric oxide and carbon monoxide induces a number of effects in cardiovascular system in normal and pathological conditions. In the present study the effects and underlying mechanisms of H2S donor, sodium hydrosulfide (NaHS), on isometric force of frog myocardium contraction were studied. NaHS in the concentration of 100 μM induced a negative inotropic effect and decreased the maximal velocity of contraction and relaxation of isolated ventricle strips. The substrate Of H2S synthesis L-cystein (200 μM and 1 mM) induced the same effect and the inhibitors of cystationin y-lyase, H2S-producing enzyme in heart, ß-cyanoalanin (500 μM) and propargylglycine (500 μM) increased the amplitude of contraction. Inhibition of cystationin y-lyase by ß-cyanoalanin prevented the negative inotropic effect of L-cystein. After inhibition of adenylate cyclase by MDL12,330A (3 μM) or phosphodiesterases by IBMX (200 μM) effect of NaHS was lesser than in control. In the presence of membrane-penetrating analogous of cAMP, 8Br-cAMP (100 μM) and pCPT-cAMP (100 μM), negative inotropic effect of NaHS completely retained. The effect of NaHS significantly decreased after preliminary application of the NO donor, SNAP (10 μM), and did not change after inhibition of NO-synthases by LNAME ( 100 μM). The obtained data suggest the possibility of endogenous synthesis of H2S in frog myocardium and regulation of its contractility by activation of phosphodiesterases hydrolyzing cAMP, which leads to a decrease of activation of cAM P-dependent protein kinases and phosphorylation of voltage-dependent L-type Ca-channels. As the result, a reduction of calcium entry into cardiomyocytes decreases the contractility of frog myocardium