Experimental study of temperature sensitivity of carrier lifetime and recombination coefficients in GaInNAs SQW lasers
This paper deals with the characterization of the differential carrier lifetime and the calculation of the monomolecular, radiative and non-radiative recombination coefficients and their temperature dependence as an evidence of the excellent temperature performance of this material system. The device characterized is a 1.25 /spl mu/m GaInNAs laser structure grown on a GaAs substrate. The active region consists of a single 6 nm thick single quantum well. Light current (L-I) characteristics performed over a temperature range of 20/spl deg/C to 80/spl deg/C, show a characteristic temperature of 50 K. Similar than in the case of commercial InGaAs. Good temperature performance of optical gain using Hakki-Paoli method, lasing wavelength and efficiency will also be presented and compared with modelling work.
Gain in 1.3 μm materials: InGaNAs and InGaPAs semiconductor quantum-well lasers
The absorption and gain for an InGaNAs/GaAs quantum-well structure is calculated and compared to that of a more conventional InGaAs/InGaPAs structure, both lasing in the 1.3 μm range. Despite significant differences in the band structures, the gain value is comparable for high carrier densities in both structures and the transition energy at the gain maximum shows a similar blueshift with increasing carrier density. For low and intermediate carrier densities, the calculated gain in the InGaPAs system is significantly lower and the bandwidth smaller than in the InGaNAs system.
Influence of inducers and inhibitors on the metabolism in vitro and neurochemical effects in vivo of MDMA.
(S)-(+)- and (R)-(-)-3,4-methylenedioxymethamphetamine (MDMA) were metabolized in vitro by rat liver microsomes via N-demethylation to 3,4-methylenedioxyamphetamine (MDA). Whereas no difference was found in the biotransformation of the two enantiomers in the male rat or in the phenobarbital (PB) treated animals of either sex, more than twice as much MDA was formed from (S)-(+)- than from (R)-(-)-MDMA in the untreated female rat. Although 3-methylcholanthrene (3MC) pretreated rat liver microsomes were less active than those from the untreated rats of the same sex, they formed more MDA from (+)- than from (-)-MDMA. The enantioselective metabolism thus appears to be associated with the relative abundance of individual cytochrome P-450 isozymes. (S)-(+)- and (R)-(-)-MDMA.HCl (20 mg/kg) were about equipotent in depleting serotonin (5-HT) levels in the frontal cortex at 3 hrs and 1 wk following oral administration to female rats. Pretreatment of rats with SKF-525A attenuated and that with PB enhanced the 5-HT depleting potential of either isomer at 3 hrs. The 5-HT depleting potency of (+)-MDMA was significantly greater than that of its (-)-antipode at 3 hr in PB pretreated, but not in SKF-525A pretreated animals. The results suggest that the neurochemical effects of MDMA are caused by the formation of an active metabolite in vivo, and since both enantiomers were N-demethylated in vitro to approximately the same extent by PB pretreated rat liver microsomes, the active metabolite may be other than MDA.