800 meV localization energy in GaSb/GaAs/Al0.3Ga0.7As quantum dots

This article may be downloaded for personal use only. Any other use requires prior permission of the author and AIP Publishing. This article appeared in Appl. Phys. Lett. 102, 052115 (2013) and may be found at https://doi.org/10.1063/1.4791678.DFG, 120319092, ERA NanoSci - Coupling of Single Quantum Dots to Two-Dimensional System

Temporal solitons in free-space femtosecond enhancement cavities

Temporal dissipative solitons in nonlinear optical resonators are self-compressed, self-stabilizing and indefinitely circulating wave packets. Owing to these properties, they have been harnessed for the generation of ultrashort pulses and frequency combs in active and passive laser architectures, including mode-locked lasers1,2,3,4, passive fibre resonators5 and microresonators6,7,8,9,10,11. Here, we demonstrate the formation of temporal dissipative solitons in a free-space enhancement cavity with a Kerr nonlinearity and a spectrally tailored finesse. By locking a 100-MHz-repetition-rate train of 350-fs, 1,035-nm pulses to this cavity-soliton state, we generate a 37-fs sech²-shaped pulse with a peak-power enhancement of 3,200, which exhibits low-frequency intensity-noise suppression. The power scalability unique to free-space cavities, the unprecedented combination of peak-power enhancement and temporal compression, and the cavity-soliton-specific noise filtering attest to the vast potential of this platform of optical solitons for applications including spatiotemporal filtering and compression of ultrashort pulses and cavity-enhanced nonlinear frequency conversion.publishe

Myoglobin facilitates angiotensin II-induced constriction of renal afferent arterioles

Vasoconstriction plays an important role in the development of acute kidney injury in rhabdomyolysis. We hypothesized that myoglobin enhances the angiotensin II (ANG II) response in afferent arterioles by increasing superoxide and reducing nitric oxide (NO) bioavailability. Afferent arterioles of C57Bl6 mice were isolated perfused, and vasoreactivity was analyzed using video microscopy. NO bioavailability, superoxide concentration in the vessel wall, and changes in cytosolic calcium were measured using fluorescence techniques. Myoglobin treatment (10−5M) did not change the basal arteriolar diameter during a 20-min period compared with control conditions. NG-nitro-l-arginine methyl ester (l-NAME, 10−4M) and l-NAME + myoglobin reduced diameters to 94.7 and 97.9% of the initial diameter, respectively. Myoglobin or l-NAME enhanced the ANG II-induced constriction of arterioles compared with control (36.6 and 34.2%, respectively, vs. 65.9%). Norepinephrine responses were not influenced by myoglobin. Combined application of myoglobin and l-NAME further facilitated the ANG II response (7.0%). Myoglobin or l-NAME decreased the NO-related fluorescence in arterioles similarly. Myoglobin enhanced the superoxide-related fluorescence, and tempol prevented this enhancement. Tempol also partly prevented the myoglobin effect on the ANG II response. Myoglobin increased the fura 2 fluorescence ratio (cytosolic calcium) during ANG II application (10−12to 10−6M). The results suggest that the enhanced afferent arteriolar reactivity to ANG II is mainly due to a myoglobin-induced increase in superoxide and associated reduction in the NO bioavailability. Signaling pathways for the augmented ANG II response include enhanced cytosolic calcium transients. In conclusion, myoglobin may contribute to the afferent arteriolar vasoconstriction in this rhabdomyolysis model.</jats:p