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51	Účinnost technologie ČOV České Budějovice pro eliminaci farmak / Efficiency of the technology of WWTP České Budějovice for the elimination of pharmaceuticals BARTOŇ, Jiří January 2013 (has links) The main aim of this study was to investigate the efficiency of wastewater treatment plant (WWTP) in České Budějovice for the elimination of selected pharmaceuticals (carbamazepine, diclofenac, atenolol, metoprolol, sotalol, bisoprolol, valsartan, verapamil and tramadol) over a long time period (March 2011 - February 2012). Time-proportional 24 hours pooled samples of wastewater from influent and effluent of the WWTP were used to assess the efficiency of WWTP. The concentrations of target compounds were determined by using in line SPE/LC-MS/MS analysis. The average annual concentrations in the effluent of WTP were in the range of 0,019 microgram/l (verapamil) to 1,00 microgram/l (atenolol). Average annual efficiencies of pharmaceutical elimination in WWTP based on pooled samples were found in the case of carbamazepine (-22 %), tramadol (-15 %), sotalol (-1 %), diclofenac (15 %), metoprolol (16 %), verapamil (43 %), bisoprolol (48 %) and valsartan (85 %). The statistical analysis of daily results in the winter and in the summer period showed significantly higher efficiency of the WWTP in the summer for 5 target compounds (diclofenac, atenolol, valsartan, sotalol and bisoprolol). Removal efficiency for the rest of pharmaceuticals did not show significant differences. Elevated temperature and longer irradiation period in summer can positively affect biodegradation or increased photolysis respectively.
52	Études in vitro et in vivo évaluant le rôle du métabolisme des médicaments par les CYP450s comme facteurs de variabilité interindividuelle dans la réponse aux médicaments Michaud, Véronique January 2008 (has links) Thèse numérisée par la Division de la gestion de documents et des archives de l'Université de Montréal. Cytochromes P450 Cytochromes P450 Cytochrome b5 Cytochrome b5 Complexe métabolique intermédiaire Metabolic intermediate complex Pharmacogénétique Pharmacogenetic Pharmacocinétique Pharmacokinetic Variabilité interindividuelle Intersubject variability Clarithromycine Clarithromycin Dompéridone Domperidone Vérapamil Verapamil Warfarine Warfarin
53	Études in vitro et in vivo évaluant le rôle du métabolisme des médicaments par les CYP450s comme facteurs de variabilité interindividuelle dans la réponse aux médicaments Michaud, Véronique January 2008 (has links) Thèse numérisée par la Division de la gestion de documents et des archives de l'Université de Montréal Cytochromes P450 Cytochromes P450 Cytochrome b5 Cytochrome b5 Complexe métabolique intermédiaire Metabolic intermediate complex Pharmacogénétique Pharmacogenetic Pharmacocinétique Pharmacokinetic Variabilité interindividuelle Intersubject variability Clarithromycine Clarithromycin Dompéridone Domperidone Vérapamil Verapamil Warfarine Warfarin
54	Regulation of Myoplasmic Ca2+ During Fatigue in KATP Channel Deficient FDB Muscle Fibres Selvin, David 23 September 2013 (has links) It is known that muscles that lack KATP channel activity generate much greater unstimulated [Ca2+]i and force than normal muscles during fatigue. The increase in unstimulated force in KATP channel deficient muscles is abolished by a partial inhibition of L-type Ca2+ channels, suggesting that it is due to a Ca2+ influx through L-type Ca2+ channels and a subsequent increased myoplasmic Ca2+. However, there is also evidence that the increase in resting force is abolished by NAC, a ROS scavenger. The objective of this study was to reconcile these observations by studying the hypothesis that “the increase in resting [Ca2+]i during fatigue in KATP channel deficient muscles starts with an excess Ca2+ influx through L-type Ca2+ channels, followed by an excess ROS production that causes a further increase in resting [Ca2+]i”. To test the hypothesis, single FDB fibres were fatigued with one tetanic contraction/sec for 180 sec. KATP channel deficient fibres were obtained i) by exposing wild type muscle fibers to glibenclamide, a KATP channel blocker and ii) by using fibres from Kir6.2-/- mice, which are null mice for the Kir6.2 gene that encodes for the protein forming the channel pore. Verapamil, a L-type Ca2+ channel blocker, applied at 1 μM, significantly reduced resting [Ca2+]i during fatigue in glibenclamide-exposed wild type fibres. NAC (1 mM) also reduced resting [Ca2+]i in glibenclamide-exposed muscles. The results suggest that the increase in resting [Ca2+]i during fatigue in KATP channel deficient FDB fibres is due to an influx through L-type Ca2+ channels, and an excess ROS production. muscle katp katp channel calcium verapamil nac ros reactive oxygen species n-acetyl cysteine glibenclamide atp sarcomere physiology fatigue FDB single fibre fibre fiber tension collagenase digestion mem dmem fbs fetal bovine serum
55	Regulation of Myoplasmic Ca2+ During Fatigue in KATP Channel Deficient FDB Muscle Fibres Selvin, David January 2013 (has links) It is known that muscles that lack KATP channel activity generate much greater unstimulated [Ca2+]i and force than normal muscles during fatigue. The increase in unstimulated force in KATP channel deficient muscles is abolished by a partial inhibition of L-type Ca2+ channels, suggesting that it is due to a Ca2+ influx through L-type Ca2+ channels and a subsequent increased myoplasmic Ca2+. However, there is also evidence that the increase in resting force is abolished by NAC, a ROS scavenger. The objective of this study was to reconcile these observations by studying the hypothesis that “the increase in resting [Ca2+]i during fatigue in KATP channel deficient muscles starts with an excess Ca2+ influx through L-type Ca2+ channels, followed by an excess ROS production that causes a further increase in resting [Ca2+]i”. To test the hypothesis, single FDB fibres were fatigued with one tetanic contraction/sec for 180 sec. KATP channel deficient fibres were obtained i) by exposing wild type muscle fibers to glibenclamide, a KATP channel blocker and ii) by using fibres from Kir6.2-/- mice, which are null mice for the Kir6.2 gene that encodes for the protein forming the channel pore. Verapamil, a L-type Ca2+ channel blocker, applied at 1 μM, significantly reduced resting [Ca2+]i during fatigue in glibenclamide-exposed wild type fibres. NAC (1 mM) also reduced resting [Ca2+]i in glibenclamide-exposed muscles. The results suggest that the increase in resting [Ca2+]i during fatigue in KATP channel deficient FDB fibres is due to an influx through L-type Ca2+ channels, and an excess ROS production. muscle katp katp channel calcium verapamil nac ros reactive oxygen species n-acetyl cysteine glibenclamide atp sarcomere physiology fatigue FDB single fibre fibre fiber tension collagenase digestion mem dmem fbs fetal bovine serum

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