For annealing temperatures above T(g), however, the current density in the devices rapidly increases while their lifetime slightly decreases. Insight into the underlying processes is provided by atomic force microscopy
phase imaging and by UV/visible and fluorescence spectroscopy. We also investigated the influence of the operating temperature of the device: besides the commonly known fact that elevated operating temperatures reduce the lifetime, we discovered that the acceleration coefficient, which determines the scaling of the device lifetime with applied current density, was reduced. At the glass transition, Stattic purchase the device lifetime no longer depended on the current density. The device lifetime was improved even further by introducing an additional cross-linkable hole-transport Selleck LY2606368 layer. Optimized devices achieve a half-luminance lifetime of 1860 h when operated at room temperature and at an initial luminance of 500 cd m(-2). As a result of the relatively balanced stability of the three chromophores, the emission spectrum remains virtually unchanged over the entire device lifetime. Finally, to reduce the time required for the lifetime measurements, we propose to analyze the voltage increase over the
first 10-50 h of the lifetime test and find that this allows precisely estimating the lifetime of our devices. (C) 2009 American Institute of Physics. [DOI: 10.1063/1.3176502]“
“The present study was designed to see the effects of Angiotensin-II (Ang-II) on buffalo sperm capacitation, acrosome reaction (AR), and its relation to nitric oxide (NO center dot) production. The extent of capacitation or AR was determined by dual staining while the NO center dot production was determined by spectrophotometry. The results thus obtained revealed that Ang-II induced capacitation in a concentration and time dependent manner and 200 nM Ang-II was found to
find more be optimal for capacitation as it was comparable to heparin treatment (50.7 +/- 2.45% vs. 51.66 +/- 2.33%). In capacitated cells the extent of AR induced by Ang-II was significantly higher than the untreated control (48.13 +/- 2.31% vs. 22.16 +/- 2.11%) and comparable to lysophosphatidyl Choline (LPC) treatment (51.56 +/- 1.94%). The NO center dot production during Ang-II induced capacitation and AR was gradual and time dependent. These levels were significantly higher when compared to control (3.65 +/- 0.53 nmoles/10(8) cells vs. 9.12 +/- 0.30 nmoles/10(8) cells). All the actions of Ang-II were inhibited in the presence of Losartan but not PD123319, indicating the role of AT1 receptors in these actions. Further the NO center dot production was also significantly inhibited in the presence of neomycin and trifluoperazine pointing towards the role of phosphoinositide pathway in this process. In conclusion, Ang-II has a concentration and time dependent effect on buffalo sperm capacitation and AR, mediated via the AT1 receptors.