Electro-optic properties of GaInAsSb/GaAs quantum well for high-speed integrated optoelectronic devices

The electro-optic properties of strained GaInAsSb/GaAs quantum wells (QWs) are investigated. A single QW p-i-n sample was grown by molecular beam epitaxy with antimony (Sb) pre-deposition technique. We numerically predict and experimentally verify a strong quantum confined Stark shift of 40 nm. We also predict a fast absorption recovery times crucial of high-speed optoelectronic devices mainly due to strong electron tunneling and thermionic emission. Predicted recovery times are corroborated by bias and temperature dependent time-resolved photoluminescence measurements indicating (<= 30 ps) recovery times. This makes GaInAsSb QW an attractive material particularly for electroabsorption modulators and saturable absorbers. (C) 2013 American Institute of Physics. (http://dx.doi.org/10.1063/1.4775371

A primate-specific, brain isoform of KCNH2 affects cortical physiology, cognition, neuronal repolarization and risk of schizophrenia

Organized neuronal firing is crucial for cortical processing and is disrupted in schizophrenia. Using rapid amplification of 5\u2032 complementary DNA ends in human brain, we identified a primate-specific isoform (3.1) of the ether-a-go-go-related K+ channel KCNH2 that modulates neuronal firing. KCNH2-3.1 messenger RNA levels are comparable to full-length KCNH2 (1A) levels in brain but three orders of magnitude lower in heart. In hippocampus from individuals with schizophrenia, KCNH2-3.1 expression is 2.5-fold greater than KCNH2-1A expression. A meta-analysis of five clinical data sets (367 families, 1,158 unrelated cases and 1,704 controls) shows association of single nucleotide polymorphisms in KCNH2 with schizophrenia. Risk-associated alleles predict lower intelligence quotient scores and speed of cognitive processing, altered memory-linked functional magnetic resonance imaging signals and increased KCNH2-3.1 mRNA levels in postmortem hippocampus. KCNH2-3.1 lacks a domain that is crucial for slow channel deactivation. Overexpression of KCNH2-3.1 in primary cortical neurons induces a rapidly deactivating K + current and a high-frequency, nonadapting firing pattern. These results identify a previously undescribed KCNH2 channel isoform involved in cortical physiology, cognition and psychosis, providing a potential new therapeutic drug targe