Polymer/TiO2Nanorod Nanocomposite Optical Memristor Device

Modulation of resistive switching memory by light opens the route to new optoelectronic devices that can be controlled both optically and electronically. Applications include integrated circuits with memory elements switchable by light and neuromorphic computing with optically reconfigurable and tunable synaptic circuits. We report on a unique nanocomposite resistive switching material and device made from a low concentration (∼0.1% by mass) of titanium dioxide nanorods (TiO2-NRs) embedded within the azobenzene polymer, poly(disperse red 1 acrylate, PDR1A). The device exhibits both reversible electronic memristor switching and reversible polarization-dependent optical switching. Optical irradiation by circularly polarized light causes a trans-cis photochemical isomerization that modifies the conformation and orientation of the photoactive azo-unit within the polymer. The resulting expansion of the composite (PDR1A/TiO2-NR) polymer film modifies the conduction pathway, facilitated by the presence of the TiO2-NRs, as a semiconductor material, through the (PDR1A/TiO2-NR) polymer film, which provides a sensitive means to control resistive switching in the device. The effect is reversible by changing the polarization state of the incident light. A charge-flux memristor model successfully reproduces the current-voltage hysteresis loops and threshold switching properties of the device, as well as the effect of the illumination on the electrical characteristics

Nonsyndromic Cleft Lip with or without Cleft Palate: Increased Burden of Rare Variants within Gremlin-1, a Component of the Bone Morphogenetic Protein 4 Pathway

Background: The genes Gremlin-1 (GREM1) and Noggin (NOG) are components of the bone morphogenetic protein 4 pathway, which has been implicated in craniofacial development. Both genes map to recently identified susceptibility loci (chromosomal region 15q13, 17q22) for nonsyndromic cleft lip with or without cleft palate (nsCL/P). The aim of the present study was to determine whether rare variants in either gene are implicated in nsCL/P etiology. Methods: The complete coding regions, untranslated regions, and splice sites of GREM1 and NOG were sequenced in 96 nsCL/P patients and 96 controls of Central European ethnicity. Three burden and four nonburden tests were performed. Statistically significant results were followed up in a second case-control sample (n=96, respectively). For rare variants observed in cases, segregation analyses were performed. Results: In NOG, four rare sequence variants (minor allele frequency <1%) were identified. Here, burden and nonburden analyses generated nonsignificant results. In GREM1, 33 variants were identified, 15 of which were rare. Of these, five were novel. Significant p-values were generated in three nonburden analyses. Segregation analyses revealed incomplete penetrance for all variants investigated. Conclusion: Our study did not provide support for NOG being the causal gene at 17q22. However, the observation of a significant excess of rare variants in GREM1 supports the hypothesis that this is the causal gene at chr. 15q13. Because no single causal variant was identified, future sequencing analyses of GREM1 should involve larger samples and the investigation of regulatory elements. (C) 2014 Wiley Periodicals, Inc

Genome-wide association study identifies two susceptibility loci for nonsyndromic cleft lip with or without cleft palate

We conducted a genome-wide association study for nonsyndromic cleft lip with or without cleft palate (NSCL/P) in 401 affected individuals and 1,323 controls, with replication in an independent sample of 793 NSCL/P triads. We report two new loci associated with NSCL/P at 17q22 (rs227731, combined P = 1.07 x 10(-8), relative risk in homozygotes = 1.84, 95% CI 1.34-2.53) and 10q25.3 (rs7078160, combined P = 1.92 x 10(-8), relative risk in homozygotes = 2.17, 95% CI 1.32-3.56)