58 research outputs found
Quantum error rejection code with spontaneous parametric conversion
We propose a linear optics scheme with SPDC process to test the fault
tolerance property of quantum error correction code. To transmit an unknown
qubit robustly through the noisy channel, one may first encode it into a
certain quantum error correction code and then transmit it. The remote party
decodes it and stores it. Sending a qubit in such a way can significantly
reduces the error rate compared with directly sending the qubit itself. Here we
show how to realize such a scheme by linear optics.Comment: To appear in Phys. Rev. A. 18 pages, 2 figure, minor erros corrected
and more explanations added to increase the readabilit
Spectroscopy by frequency entangled photon pairs
Quantum spectroscopy was performed using the frequency-entangled broadband
photon pairs generated by spontaneous parametric down-conversion. An absorptive
sample was placed in front of the idler photon detector, and the frequency of
signal photons was resolved by a diffraction grating. The absorption spectrum
of the sample was measured by counting the coincidences, and the result is in
agreement with the one measured by a conventional spectrophotometer with a
classical light source.Comment: 11 pages, 5 figures, to be published in Phys. Lett.
Quantum spiral bandwidth of entangled two-photon states
We put forward the concept of quantum spiral bandwidth of the spatial mode
function of the two-photon entangled state in spontaneous parametric
downconversion. We obtain the bandwidth using the eigenstates of the orbital
angular momentum of the biphoton states, and reveal its dependence with the
length of the down converting crystal and waist of the pump beam. The
connection between the quantum spiral bandwidth and the entropy of entanglement
of the quantum state is discussed.Comment: 10 pages, 3 figure
Double-slit interference pattern from single-slit screen and its gravitational analogues
The double slit experiment (DSE) is known as an important cornerstone in the
foundations of physical theories such as Quantum Mechanics and Special
Relativity. A large number of different variants of it were designed and
performed over the years. We perform and discuss here a new verion with the
somewhat unexpected results of obtaining interference pattern from single-slit
screen. This outcome, which shows that the routes of the photons through the
array were changed, leads one to discuss it, using the equivalence principle,
in terms of geodesics mechanics. We show using either the Brill's version of
the canonical formulation of general relativity or the linearized version of it
that one may find corresponding and analogous situations in the framework of
general relativity.Comment: 51 pages, 12 Figures five of them contain two subfigures and thus the
number of figures is 17, 1 Table. Some minor changes introduced, especially,
in the reference
Bi-allelic JAM2 Variants Lead to Early-Onset Recessive Primary Familial Brain Calcification.
Primary familial brain calcification (PFBC) is a rare neurodegenerative disorder characterized by a combination of neurological, psychiatric, and cognitive decline associated with calcium deposition on brain imaging. To date, mutations in five genes have been linked to PFBC. However, more than 50% of individuals affected by PFBC have no molecular diagnosis. We report four unrelated families presenting with initial learning difficulties and seizures and later psychiatric symptoms, cerebellar ataxia, extrapyramidal signs, and extensive calcifications on brain imaging. Through a combination of homozygosity mapping and exome sequencing, we mapped this phenotype to chromosome 21q21.3 and identified bi-allelic variants in JAM2. JAM2 encodes for the junctional-adhesion-molecule-2, a key tight-junction protein in blood-brain-barrier permeability. We show that JAM2 variants lead to reduction of JAM2 mRNA expression and absence of JAM2 protein in patient's fibroblasts, consistent with a loss-of-function mechanism. We show that the human phenotype is replicated in the jam2 complete knockout mouse (jam2 KO). Furthermore, neuropathology of jam2 KO mouse showed prominent vacuolation in the cerebral cortex, thalamus, and cerebellum and particularly widespread vacuolation in the midbrain with reactive astrogliosis and neuronal density reduction. The regions of the human brain affected on neuroimaging are similar to the affected brain areas in the myorg PFBC null mouse. Along with JAM3 and OCLN, JAM2 is the third tight-junction gene in which bi-allelic variants are associated with brain calcification, suggesting that defective cell-to-cell adhesion and dysfunction of the movement of solutes through the paracellular spaces in the neurovascular unit is a key mechanism in CNS calcification
AD51B in Familial Breast Cancer
Common variation on 14q24.1, close to RAD51B, has been associated with breast cancer: rs999737 and rs2588809 with the risk of female breast cancer and rs1314913 with the risk of male breast cancer. The aim of this study was to investigate the role of RAD51B variants in breast cancer predisposition, particularly in the context of familial breast cancer in Finland. We sequenced the coding region of RAD51B in 168 Finnish breast cancer patients from the Helsinki region for identification of possible recurrent founder mutations. In addition, we studied the known rs999737, rs2588809, and rs1314913 SNPs and RAD51B haplotypes in 44,791 breast cancer cases and 43,583 controls from 40 studies participating in the Breast Cancer Association Consortium (BCAC) that were genotyped on a custom chip (iCOGS). We identified one putatively pathogenic missense mutation c.541C>T among the Finnish cancer patients and subsequently genotyped the mutation in additional breast cancer cases (n = 5259) and population controls (n = 3586) from Finland and Belarus. No significant association with breast cancer risk was seen in the meta-analysis of the Finnish datasets or in the large BCAC dataset. The association with previously identified risk variants rs999737, rs2588809, and rs1314913 was replicated among all breast cancer cases and also among familial cases in the BCAC dataset. The most significant association was observed for the haplotype carrying the risk-alleles of all the three SNPs both among all cases (odds ratio (OR): 1.15, 95% confidence interval (CI): 1.11–1.19, P = 8.88 x 10−16) and among familial cases (OR: 1.24, 95% CI: 1.16–1.32, P = 6.19 x 10−11), compared to the haplotype with the respective protective alleles. Our results suggest that loss-of-function mutations in RAD51B are rare, but common variation at the RAD51B region is significantly associated with familial breast cancer risk
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