122 research outputs found
Precision Measurements Using Squeezed Spin States via Two-axis Counter-twisting Interactions
We show that the two-axis counter twisting interaction squeezes a coherent
spin state into three states of interest in quantum information, namely, the
twin-Fock state, the equally-weighted superposition state, and the state that
achieves the Heisenberg limit of optimal sensitivity defined by the Cramer-Rao
inequality in addition to the well-known Heisenberg-limited state of spin
fluctuations.Comment: 5 pages, 3 figure
Charge-Order Pattern of the Low-Temperature Phase of NaV2O5 Uniquely Determined by Resonant X-Ray Scattering from Monoclinic Single Domain
The present resonant x-ray scattering from each of monoclinically-split
single domains of NaV2O5 has critically enhanced contrast between V4+ and V5+
ions strong enough to lead to unambiguous conclusion of the charge-order
pattern of its low-temperature phase below Tc = 35 K. The zig-zag type
charge-order patterns in the -plane previously confirmed have four kinds of
configurations (A, A', B and B') and the stacking sequence along the c-axis is
determined as the AAA'A' type by comparison with model calculations. By
assigning the A and A' configurations to Ising spins, one can reasonably
understand the previously discovered "devil's staircase"-type behavior with
respect to the modulation of the layer-stacking sequences at high pressures and
low temperatures, which very well resembles the global phase diagram
theoretically predicted by the ANNNI model.Comment: 4 pages, 3 figure
Survival predictors of heart rate variability after myocardial infarction with and without low left ventricular ejection fraction
Background: Heart rate variability (HRV) and heart rate (HR) dynamics are used to predict the survival probability of patients after acute myocardial infarction (AMI), but the association has been established in patients with mixed levels of left ventricular ejection fraction (LVEF).
Objective: We investigated whether the survival predictors of HRV and HR dynamics depend on LVEF after AMI.
Methods: We studied 687 post-AMI patients including 147 with LVEF ≤35% and 540 with LVEF \u3e35%, of which 23 (16%) and 22 (4%) died during the 25 month follow-up period, respectively. None had an implanted cardioverter-defibrillator. From baseline 24 h ECG, the standard deviation (SDNN), root mean square of successive difference (rMSSD), percentage of successive difference \u3e50 ms (pNN50) of normal-to-normal R-R interval, ultra-low (ULF), very-low (VLF), low (LF), and high (HF) frequency power, deceleration capacity (DC), short-term scaling exponent (α
Results: The predictors were categorized into three clusters; DC, SDNN, α
Conclusion: The mortality risk in post-AMI patients with low LVEF is predicted by indices reflecting decreased HRV or HR responsiveness and cardiac parasympathetic dysfunction, whereas in patients without low LVEF, the risk is predicted by a combination of indices that reflect decreased HRV or HR responsiveness and indicator that reflects abrupt large HR changes suggesting sympathetic involvement
Scaling the stimulated emission of polarization-entangled photons using passive optical components
Bright sources of polarization-entangled photon pairs are essential
components for quantum information technologies. In general, it is necessary to
introduce a resonator that combines active optical components such as an
electric optical modulator to enhance the stimulated emission of
polarization-entangled photons. It is technically difficult to perform the time
series operation to output the stimulated entangled photons in the resonator by
synchronizing laser pulses. In this paper, we propose a scheme to scale up the
stimulated emission of polarization-entangled photon pairs using a resonator
with only passive optical components. We show the theoretical aspects of the
scheme and also perform a proof-of-principle experimental demonstration of the
scheme in a double-pass configuration.Comment: 8 pages, 6 figures, Physical Review A to be publishe
A stem cell-derived gene (Sddr) negatively regulates differentiation of embryonic stem cells
金沢大学医薬保健研究域医学系Embryonic stem (ES) cells, derived from the inner cell mass of blastocysts, are pluripotent and continue to self-renew. To better understand the molecular mechanisms under-lying self-renewal, we have been searching for a gene(s) which is specifically expressed in self-renewing ES cells. Here we report the isolation and characterization of a novel gene, Sddr (stem cell-derived differentiation regulator). Sddr was highly expressed in undifferentiated ES cells, and its expression was downregulated upon differentiation. In addition to ES cells, Sddr expression was observed strongly in ovary, and weakly in lung. Immunostaining and cellular fractionation analyses suggested that Sddr is a cytoplasmic protein associated with the cytoskeleton. Sddr-null ES cells showed no remarkable abnormalities in their undifferentiated state. In contrast, in differentiating Sddr-null cells, induction of several differentiation-associated markers was enhanced, and downregulation of self-renewal marker genes was accelerated, as compared with wild-type cells. These results suggest that although it is dispensable for ES cell self-renewal, Sddr is a negative regulator of ES cell differentiation. © 2009 UBC Press
Sustained activation of the unfolded protein response induces cell death in Fuchs' endothelial corneal dystrophy
Purpose: The unfolded protein response (UPR) is believed to play a role in the pathogenesis of Fuchs' endothelial corneal dystrophy (FECD). The purpose of this study was to investigate whether unfolded proteins accumulate in the corneal endothelium in FECD and if they are involved in triggering cell death. Methods: Descemet's membranes with corneal endothelial cells (CECs) were obtained during keratoplasty, and expression of aggresomes, type 1 collagen, fibronectin, and agrin was evaluated. Endoplasmic reticulum (ER) stress of immortalized human CECs from non-FECD subjects and from FECD patients (iHCEC and iFECD, respectively) were evaluated. The effect of MG132-mediated aggresome formation on the UPR and intrinsic pathway and the effect of mitochondrial damage on UPR were also examined. The effect of CHOP knockdown on the ER stress–mediated intrinsic pathway was also evaluated. Results: Aggresome formation was higher in iFECD than in iHCEC and was colocalized with type 1 collagen, fibronectin, and agrin. GRP78, phosphorylated IRE1, PERK, and CHOP showed higher activation in iFECD than in iHCEC. MG132-mediated aggresome formation upregulated ER stress sensors, the mitochondrial membrane potential drop, cytochrome c release to the cytoplasm, and activation of caspase-9 and -3. By contrast, staurosporine-mediated mitochondrial damage did not induce ER stress. Knockdown of CHOP attenuated the ER stress-induced cleavage of caspase-9, which is caused by intrinsic pathway activation. Conclusions: Excessive synthesis of extracellular matrix proteins induced unfolded protein accumulation in FECD. Prolonged ER stress–mediated cell death, occurring via the intrinsic apoptotic signaling pathway, therefore might be associated with the pathogenesis of FECD
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