The wide detection band comes from the transitions from the quantum ring (QR) ground states to different excited states. The shallow confinement states generate higher dark current and enhance the carrier flow between the QRs PERK inhibitor within the same QR layer. This carrier flow averages out the repulsive potential and makes QRIPs behave similarly to the quantum well infrared photodetectors instead of QDIPs.

With an Al0.27Ga0.73As current blocking layer, the performance of QRIPs was greatly enhanced.”
“Background-Mutations in KCNJ2, the gene encoding the human inward rectifier potassium channel Kir2.1 (I(K1) or I(Kir2.1)), have been identified in Andersen-Tawil syndrome. Andersen-Tawil syndrome is a multisystem inherited disease exhibiting periodic paralysis, cardiac arrhythmias, and dysmorphic features at times mimicking catecholaminergic polymorphic ventricular tachycardia.

Methods and Results-Our

proband displayed dysmorphic features including micrognathia, clinodactyly, and syndactyly and exhibited multiform extrasystoles and bidirectional ventricular tachycardia both at rest and during exercise testing. The patient’s symptoms continued after administration of nadolol but subsided after treatment with flecainide. Molecular genetic screening revealed a novel heterozygous mutation (c. 779G>C/p.R260P) GSK J4 in KCNJ2. Whole-cell patch-clamp studies conducted in TSA201 cells transfected with wild-type human KCNJ2 cDNA (WT-KCNJ2) yielded robust I(Kir2.1) but AZD6738 clinical trial no measurable current in cells expressing the R260P mutant. Coexpression of WT and R260P-KCNJ2 (heterozygous expression) yielded a markedly reduced inward I(Kir2.1) compared with WT alone (-36.5 +/- 9.8 pA/pF versus -143.5 +/- 11.4 pA/pF, n=8 for both, P<0.001, respectively, at -90 mV), indicating a strong dominant negative effect of the mutant. The outward component of I(Kir2.1) measured at -50 mV was also markedly reduced with the heterozygous expression versus WT (0.52 +/- 5.5 pA/pF versus 23.4 +/- 6.7 pA/pF, n=8 for both, P< 0.001, respectively). Immunocytochemical analysis indicates that impaired trafficking of R260P-KCNJ2 channels.

Conclusions-We

report a novel de novo KCNJ2 mutation associated with classic phenotypic features of Andersen-Tawil syndrome and catecholaminergic polymorphic ventricular tachycardia mimicry. The R260P mutation produces a strong dominant negative effect leading to marked suppression of I(K1) secondary to a trafficking defect. (Circ Cardiovasc Genet. 2011; 4: 51-57.)”
“By using a multipulse femtosecond pump-probe technique, we achieved an in situ characterization of terahertz wave shaping in the periodically poled Mg:LiNbO3 crystal. The analysis method, which includes fast-Fourier transform (frequency spectrum) and Morlet wavelet transform (time-frequency spectrum) that detailed information on the shaping of the terahertz waves, is demonstrated.