49 research outputs found
Reflective silicon binary diffraction grating for visible wavelengths
We introduce a new device based on sub-wavelength resonant gratings. We built a silicon-on-oxide reflective binary grating for visible light that mimics the functionality of a blazed diffraction grating in a flat geometry
GHZ extraction yield for multipartite stabilizer states
Let be an arbitrary stabilizer state distributed between three
remote parties, such that each party holds several qubits. Let be a
stabilizer group of . We show that can be converted by local
unitaries into a collection of singlets, GHZ states, and local one-qubit
states. The numbers of singlets and GHZs are determined by dimensions of
certain subgroups of . For an arbitrary number of parties we find a
formula for the maximal number of -partite GHZ states that can be extracted
from by local unitaries. A connection with earlier introduced measures
of multipartite correlations is made. An example of an undecomposable
four-party stabilizer state with more than one qubit per party is given. These
results are derived from a general theoretical framework that allows one to
study interconversion of multipartite stabilizer states by local Clifford group
operators. As a simple application, we study three-party entanglement in
two-dimensional lattice models that can be exactly solved by the stabilizer
formalism.Comment: 12 pages, 1 figur
Polarization-Correlated Photon Pairs from a Single Quantum Dot
Polarization correlation in a linear basis, but not entanglement, is observed
between the biexciton and single-exciton photons emitted by a single InAs
quantum dot in a two-photon cascade. The results are well described
quantitatively by a probabilistic model that includes two decay paths for a
biexciton through a non-degenerate pair of one-exciton states, with the
polarization of the emitted photons depending on the decay path. The results
show that spin non-degeneracy due to quantum-dot asymmetry is a significant
obstacle to the realization of an entangled-photon generation device.Comment: 4 pages, 4 figures, revised discussio
Sub-microsecond correlations in photoluminescence from InAs quantum dots
Photon correlation measurements reveal memory effects in the optical emission
of single InAs quantum dots with timescales from 10 to 800 ns. With above-band
optical excitation, a long-timescale negative correlation (antibunching) is
observed, while with quasi-resonant excitation, a positive correlation
(blinking) is observed. A simple model based on long-lived charged states is
presented that approximately explains the observed behavior, providing insight
into the excitation process. Such memory effects can limit the internal
efficiency of light emitters based on single quantum dots, and could also be
problematic for proposed quantum-computation schemes.Comment: 8 pages, 8 figure
Erythrocyte Transketolase Activity, Markers of Cardiac Dysfunction and the Diagnosis of Infantile Beriberi
Infantile beriberi, or clinical thiamin (vitamin B1) deficiency in infants, is a forgotten disease in Asia, where ∼100 years ago it was a major public health problem. Children aged ∼2–3 months present in cardiac failure but usually rapidly improve if given thiamin injections. It remains relatively common in Vientiane, Lao PDR (Laos) probably because of prolonged intra- and post-partum maternal food avoidance behaviours. There has been very little recent research on the best diagnostic techniques. We conducted a case control study of 47 infants with beriberi and age-matched afebrile and febrile controls in Vientiane. The conventional measures of thiamin deficiency, basal and activated erythrocyte transketolase activities (ETK) and activation (α) coefficients, were assayed along with three markers of cardiac dysfunction - plasma brain natriuretic peptide, N-terminal pro-brain natriuretic peptide, and troponin T. Basal ETK was a better biochemical marker of infantile beriberi than the activation coefficient. Raised plasma troponin T may be a useful indicator of infantile beriberi in babies at risk and in the absence of other evident causes
Clinically Unapparent Infantile Thiamin Deficiency in Vientiane, Laos
Infantile beriberi, or clinical thiamin (vitamin B1) deficiency in infants, is a forgotten disease in Asia, where 100 years ago it was a major public health problem. Infants with this deficiency, commonly aged ∼ 2–3 months, present in cardiac failure but usually rapidly improve if given thiamin injections. It remains relatively common in Vientiane, Lao PDR (Laos), probably because of prolonged intra- and post-partum food avoidance behaviours. Clinical disease may be the tip of an iceberg with subclinical thiamin deficiency contributing to sickness in infants without overt clinical beriberi. We therefore recruited 778 sick infants admitted during one year at Mahosot Hospital, Vientiane, without clinical evidence of beriberi, and performed erythrocyte transketolase (ETK) assays. 13.4 % of infants had basal ETK<0.59 micromoles/min/gHb suggesting biochemical thiamin deficiency. Mortality was 5.5% but, among infants ≥2 months old, mortality was higher in those with basal ETK<0.59 micromoles/min/gHb (3/47, 6.4%) than in those with basal ETK≥0.59 micromoles/min/gHb (1/146, 0.7%) (P = 0.045, relative risk = 9.32 (95%CI 0.99 to 87.5)). We conclude that clinically unapparent thiamin deficiency is common among sick infants (≥2 months old) admitted to hospital in Vientiane. This may contribute to mortality and a low clinical threshold for providing thiamin to sick infants may be needed
Inhibition of Neuroblastoma Tumor Growth by Targeted Delivery of MicroRNA-34a Using Anti-Disialoganglioside GD2 Coated Nanoparticles
Neuroblastoma is one of the most challenging malignancies of childhood, being associated with the highest death rate in paediatric oncology, underlining the need for novel therapeutic approaches. Typically, patients with high risk disease undergo an initial remission in response to treatment, followed by disease recurrence that has become refractory to further treatment. Here, we demonstrate the first silica nanoparticle-based targeted delivery of a tumor suppressive, pro-apoptotic microRNA, miR-34a, to neuroblastoma tumors in a murine orthotopic xenograft model. These tumors express high levels of the cell surface antigen disialoganglioside GD2 (GD(2)), providing a target for tumor-specific delivery.Nanoparticles encapsulating miR-34a and conjugated to a GD(2) antibody facilitated tumor-specific delivery following systemic administration into tumor bearing mice, resulted in significantly decreased tumor growth, increased apoptosis and a reduction in vascularisation. We further demonstrate a novel, multi-step molecular mechanism by which miR-34a leads to increased levels of the tissue inhibitor metallopeptidase 2 precursor (TIMP2) protein, accounting for the highly reduced vascularisation noted in miR-34a-treated tumors.These novel findings highlight the potential of anti-GD(2)-nanoparticle-mediated targeted delivery of miR-34a for both the treatment of GD(2)-expressing tumors, and as a basic discovery tool for elucidating biological effects of novel miRNAs on tumor growth
<i>GRIN2A</i>-related disorders:genotype and functional consequence predict phenotype
Alterations of the N-methyl-d-aspartate receptor (NMDAR) subunit GluN2A, encoded by GRIN2A, have been associated with a spectrum of neurodevelopmental disorders with prominent speech-related features, and epilepsy. We performed a comprehensive assessment of phenotypes with a standardized questionnaire in 92 previously unreported individuals with GRIN2A-related disorders. Applying the criteria of the American College of Medical Genetics and Genomics to all published variants yielded 156 additional cases with pathogenic or likely pathogenic variants in GRIN2A, resulting in a total of 248 individuals. The phenotypic spectrum ranged from normal or near-normal development with mild epilepsy and speech delay/apraxia to severe developmental and epileptic encephalopathy, often within the epilepsy-aphasia spectrum. We found that pathogenic missense variants in transmembrane and linker domains (misTMD+Linker) were associated with severe developmental phenotypes, whereas missense variants within amino terminal or ligand-binding domains (misATD+LBD) and null variants led to less severe developmental phenotypes, which we confirmed in a discovery (P = 10-6) as well as validation cohort (P = 0.0003). Other phenotypes such as MRI abnormalities and epilepsy types were also significantly different between the two groups. Notably, this was paralleled by electrophysiology data, where misTMD+Linker predominantly led to NMDAR gain-of-function, while misATD+LBD exclusively caused NMDAR loss-of-function. With respect to null variants, we show that Grin2a+/- cortical rat neurons also had reduced NMDAR function and there was no evidence of previously postulated compensatory overexpression of GluN2B. We demonstrate that null variants and misATD+LBD of GRIN2A do not only share the same clinical spectrum (i.e. milder phenotypes), but also result in similar electrophysiological consequences (loss-of-function) opposing those of misTMD+Linker (severe phenotypes; predominantly gain-of-function). This new pathomechanistic model may ultimately help in predicting phenotype severity as well as eligibility for potential precision medicine approaches in GRIN2A-related disorders