428 research outputs found

    PAR9 CO-PRESCRIPTION OF GASTROPROTECTIVE AGENTS FOR PATIENTS AT RISK OF NSNSAID-INDUCED GASTROINTESTINAL HARM

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    PMH37 BURDEN OF ILLNESS OF PATIENTS WITH ANXIETY IN THE UK

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    An attempt to partition stomatal and non-stomatal ozone deposition parts on a short grassland

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    To evaluate the damaging effect of tropospheric ozone on vegetation, it is important to evaluate the stomatal uptake of ozone. Although the stomatal flux is a dominant pathway of ozone deposition onto vegetated surfaces, non-stomatal uptake mechanisms such as soil and cuticular deposition also play a vital role, especially when the leaf area index LAI<4. In this study, we partitioned the canopy conductance into stomatal and non-stomatal components. To calculate the stomatal conductance of water vapour for sparse vegetation, we firstly partitioned the latent heat flux into effects of transpiration and evaporation using the Shuttleworth–Wallace (SW) model. We then derived the stomatal conductance of ozone using the Penman–Monteith (PM) theory based on the similarity to water vapour conductance. The non-stomatal conductance was calculated by subtracting the stomatal conductance from the canopy conductance derived from directly-measured fluxes. Our results show that for short vegetation (LAI=0.25) dry deposition of ozone was dominated by the non-stomatal flux, which exceeded the stomatal flux even during the daytime. At night the stomatal uptake of ozone was found to be negligibly small. In the case of vegetation with LAI≈1, the daytime stomatal and non-stomatal fluxes were of the same order of magnitude. These results emphasize that non-stomatal processes must be considered even in the case of well-developed vegetation where cuticular uptake is comparable in magnitude with stomatal uptake, and especially in the case of vegetated surfaces with LAI<4 where soil uptake also has a role in ozone deposition

    Excitation of Giant Spin-Isospin Multipole Vibrations in 54,56-Fe and 58,60-Ni

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    This work was supported by the National Science Foundation Grant NSF PHY 81-14339 and by Indiana Universit

    Recent Upgrades of the Gas Handling System for the Cryogenic Stopping Cell of the FRS Ion Catcher

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    In this paper, the major upgrades and technical improvements of the buffer gas handling system for the cryogenic stopping cell of the FRS Ion Catcher at GSI/FAIR (in Darmstadt, Germany) are described. The upgrades include implementation of new gas lines and gas purifiers to achieve a higher buffer gas cleanliness for a more efficient extraction of reactive ions as well as suppression of the molecular background ionized in the stopping cell. Furthermore, additional techniques have been implemented for improved monitoring and quantification of the purity of the helium buffer gas

    Diclofenac Prolongs Repolarization in Ventricular Muscle with Impaired Repolarization Reserve

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    Background: The aim of the present work was to characterize the electrophysiological effects of the non-steroidal anti- inflammatory drug diclofenac and to study the possible proarrhythmic potency of the drug in ventricular muscle. Methods: Ion currents were recorded using voltage clamp technique in canine single ventricular cells and action potentials were obtained from canine ventricular preparations using microelectrodes. The proarrhythmic potency of the drug was investigated in an anaesthetized rabbit proarrhythmia model. Results: Action potentials were slightly lengthened in ventricular muscle but were shortened in Purkinje fibers by diclofenac (20 mM). The maximum upstroke velocity was decreased in both preparations. Larger repolarization prolongation was observed when repolarization reserve was impaired by previous BaCl 2 application. Diclofenac (3 mg/kg) did not prolong while dofetilide (25 mg/kg) significantly lengthened the QT c interval in anaesthetized rabbits. The addition of diclofenac following reduction of repolarization reserve by dofetilide further prolonged QT c . Diclofenac alone did not induce Torsades de Pointes ventricular tachycardia (TdP) while TdP incidence following dofetilide was 20%. However, the combination of diclofenac and dofetilide significantly increased TdP incidence (62%). In single ventricular cells diclofenac (30 mM) decreased the amplitude of rapid (I Kr ) and slow (I Ks ) delayed rectifier currents thereby attenuating repolarization reserve. L-type calcium current (I Ca ) was slightly diminished, but the transient outward (I to ) and inward rectifier (I K1 ) potassium currents were not influenced. Conclusions: Diclofenac at therapeutic concentrations and even at high dose does not prolong repolarization markedly and does not increase the risk of arrhythmia in normal heart. However, high dose diclofenac treatment may lengthen repolarization and enhance proarrhythmic risk in hearts with reduced repolarization reserve
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