Enhanced indistinguishability of in-plane single photons by resonance fluorescence on an integrated quantum dot

Integrated quantum light sources in photonic circuits are envisaged as the building blocks of future on-chip architectures for quantum logic operations. While semiconductor quantum dots have been proven to be the highly efficient emitters of quantum light, their interaction with the host material induces spectral decoherence, which decreases the indistinguishability of the emitted photons and limits their functionality. Here, we show that the indistinguishability of in-plane photons can be greatly enhanced by performing resonance fluorescence on a quantum dot coupled to a photonic crystal waveguide. We find that the resonant optical excitation of an exciton state induces an increase in the emitted single-photon coherence by a factor of 15. Two-photon interference experiments reveal a visibility of 0.80 ± 0.03, which is in good agreement with our theoretical model. Combined with the high in-plane light-injection efficiency of photonic crystal waveguides, our results pave the way for the use of this system for the on-chip generation and transmission of highly indistinguishable photons

Geometrothermodynamics of black holes

The thermodynamics of black holes is reformulated within the context of the recently developed formalism of geometrothermodynamics. This reformulation is shown to be invariant with respect to Legendre transformations, and to allow several equivalent representations. Legendre invariance allows us to explain a series of contradictory results known in the literature from the use of Weinhold's and Ruppeiner's thermodynamic metrics for black holes. For the Reissner-Nordstr\"om black hole the geometry of the space of equilibrium states is curved, showing a non trivial thermodynamic interaction, and the curvature contains information about critical points and phase transitions. On the contrary, for the Kerr black hole the geometry is flat and does not explain its phase transition structure.Comment: Revised version, to be published in Gen.Rel.Grav.(Mashhoon's Festschrift

Quantum Chaos Versus Classical Chaos: Why is Quantum Chaos Weaker?

We discuss the questions: How to compare quantitatively classical chaos with quantum chaos? Which one is stronger? What are the underlying physical reasons

Geometric Strategy for the Optimal Quantum Search

We explore quantum search from the geometric viewpoint of a complex projective space $CP$, a space of rays. First, we show that the optimal quantum search can be geometrically identified with the shortest path along the geodesic joining a target state, an element of the computational basis, and such an initial state as overlaps equally, up to phases, with all the elements of the computational basis. Second, we calculate the entanglement through the algorithm for any number of qubits $n$ as the minimum Fubini-Study distance to the submanifold formed by separable states in Segre embedding, and find that entanglement is used almost maximally for large $n$. The computational time seems to be optimized by the dynamics as the geodesic, running across entangled states away from the submanifold of separable states, rather than the amount of entanglement itself.Comment: revtex, 10 pages, 7 eps figures, uses psfrag packag

Localization of the human homolog of the yeast cell division control 27 gene (CDC27) proximal to ITGB3 on human chromosome 17q21.3

The human homolog of the Saccharomyces cerevisiae cell division control 27 gene (CDC27) was mapped to human chromosome 17q12-q21 using a panel of human/rodent somatic cell hybrids and localized distal to the breast cancer susceptibility gene, BRCA1 , using a panel of radiation hybrids. The radiation hybrid panel indicates that the most likely position of human CDC27 on human chromosome 17 is between the marker D17S409 and the beta 3 subunit of integrin (ITGB3). Further confirmation of this localization comes from the sequence tagged site (STS) mapping of human CDC27 to the same yeast artificial chromosomes (YACs) positive for ITGB3 . The estimated distance between ITGB3 and human CDC27 is less than 600 kb.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/45546/1/11188_2005_Article_BF02257470.pd

Exome sequencing of child–parent trios with bladder exstrophy: Findings in 26 children

Bladder exstrophy (BE) is a rare, lower ventral midline defect with the bladder and part of the urethra exposed. The etiology of BE is unknown but thought to be influenced by genetic variation with more recent studies suggesting a role for rare variants. As such, we conducted paired-end exome sequencing in 26 child/mother/father trios. Three children had rare (allele frequency ≤ 0.0001 in several public databases) inherited variants in TSPAN4, one with a loss-of-function variant and two with missense variants. Two children had loss-of-function variants in TUBE1. Four children had rare missense or nonsense variants (one per child) in WNT3, CRKL, MYH9, or LZTR1, genes previously associated with BE. We detected 17 de novo missense variants in 13 children and three de novo loss-of-function variants (AKR1C2, PRRX1, PPM1D) in three children (one per child). We also detected rare compound heterozygous loss-of-function variants in PLCH2 and CLEC4M and rare inherited missense or loss-of-function variants in additional genes applying autosomal recessive (three genes) and X-linked recessive inheritance models (13 genes). Variants in two genes identified may implicate disruption in cell migration (TUBE1) and adhesion (TSPAN4) processes, mechanisms proposed for BE, and provide additional evidence for rare variants in the development of this defect

Exome sequencing identifies variants in infants with sacral agenesis

Background: Sacral agenesis (SA) consists of partial or complete absence of the caudal end of the spine and often presents with additional birth defects. Several studies have examined gene variants for syndromic forms of SA, but only one has examined exomes of children with non-syndromic SA. Methods: Using buccal cell specimens from families of children with non-syndromic SA, exomes of 28 child–parent trios (eight with and 20 without a maternal diagnosis of pregestational diabetes) and two child–father duos (neither with diagnosis of maternal pregestational diabetes) were exome sequenced. Results: Three children had heterozygous missense variants in ID1 (Inhibitor of DNA Binding 1), with CADD scores >20 (top 1% of deleterious variants in the genome); two children inherited the variant from their fathers and one from the child's mother. Rare missense variants were also detected in PDZD2 (PDZ Domain Containing 2; N = 1) and SPTBN5 (Spectrin Beta, Non-erythrocytic 5; N = 2), two genes previously suggested to be associated with SA etiology. Examination of variants with autosomal recessive and X-linked recessive inheritance identified five and two missense variants, respectively. Compound heterozygous variants were identified in several genes. In addition, 12 de novo variants were identified, all in different genes in different children. Conclusions: To our knowledge, this is the first study reporting a possible association between ID1 and non-syndromic SA. Although maternal pregestational diabetes has been strongly associated with SA, the missense variants in ID1 identified in two of three children were paternally inherited. These findings add to the knowledge of gene variants associated with non-syndromic SA and provide data for future studies

Chromosomal localization of 15 ion channel genes

Several human Mendelian diseases, including the long-QT syndrome, malignant hyperthermia, and episodic ataxia/myokymia syndrome, have recently been demonstrated to be due to mutations in ion channel genes. Systematic mapping of ion channel genes may therefore reveal candidates for other heritable disorders. In this study, the GenBank and dbEST databases were used to identify members of several ion channel families (voltage-gated calcium and sodium cardiac chloride, and all classes of potassium channels). Genes and ESTs without prior map localization were identified based on GDB and OWL database information and 15 genes and ESTs were selected for mapping. Of these 15, only the serotonin receptor 5HT3R had been previously mapped to a chromosome. A somatic cell hybrid panel (SCH) was screened with an STS from each gene and, if necessary, the results verified by a second SCH panel. For three ESTs, rodent derived PCR products of the same size as the human STS precluded SCH mapping. For these three, human Pl clones were isolated and the genomic location was determined by metaphase FISH. These genes and ESTs can now be further evaluated as candidate genes for inherited cardiac, neuromuscular, and psychiatric disorders mapped to these chromosomes. Furthermore, the ESTs developed in this study can be used to isolate genomic clones, enabling the determination of each transcript's genomic structure and physical map location. This approach may also be applicable to other gene families and may aid in the identification of candidate genes for groups of related heritable disorders.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/45548/1/11188_2006_Article_BF02369898.pd