Enhancing quantum entropy in vacuum-based quantum random number generator

Information-theoretically provable unique true random numbers, which cannot be correlated or controlled by an attacker, can be generated based on quantum measurement of vacuum state and universal-hashing randomness extraction. Quantum entropy in the measurements decides the quality and security of the random number generator. At the same time, it directly determine the extraction ratio of true randomness from the raw data, in other words, it affects quantum random numbers generating rate obviously. In this work, considering the effects of classical noise, the best way to enhance quantum entropy in the vacuum-based quantum random number generator is explored in the optimum dynamical analog-digital converter (ADC) range scenario. The influence of classical noise excursion, which may be intrinsic to a system or deliberately induced by an eavesdropper, on the quantum entropy is derived. We propose enhancing local oscillator intensity rather than electrical gain for noise-independent amplification of quadrature fluctuation of vacuum state. Abundant quantum entropy is extractable from the raw data even when classical noise excursion is large. Experimentally, an extraction ratio of true randomness of 85.3% is achieved by finite enhancement of the local oscillator power when classical noise excursions of the raw data is obvious.Comment: 12 pages,8 figure

A 0.1–5.0 GHz flexible SDR receiver with digitally assisted calibration in 65 nm CMOS

© 2017 Elsevier Ltd. All rights reserved.A 0.1–5.0 GHz flexible software-defined radio (SDR) receiver with digitally assisted calibration is presented, employing a zero-IF/low-IF reconfigurable architecture for both wideband and narrowband applications. The receiver composes of a main-path based on a current-mode mixer for low noise, a high linearity sub-path based on a voltage-mode passive mixer for out-of-band rejection, and a harmonic rejection (HR) path with vector gain calibration. A dual feedback LNA with “8” shape nested inductor structure, a cascode inverter-based TCA with miller feedback compensation, and a class-AB full differential Op-Amp with Miller feed-forward compensation and QFG technique are proposed. Digitally assisted calibration methods for HR, IIP2 and image rejection (IR) are presented to maintain high performance over PVT variations. The presented receiver is implemented in 65 nm CMOS with 5.4 mm2 core area, consuming 9.6–47.4 mA current under 1.2 V supply. The receiver main path is measured with +5 dB m/+5dBm IB-IIP3/OB-IIP3 and +61dBm IIP2. The sub-path achieves +10 dB m/+18dBm IB-IIP3/OB-IIP3 and +62dBm IIP2, as well as 10 dB RF filtering rejection at 10 MHz offset. The HR-path reaches +13 dB m/+14dBm IB-IIP3/OB-IIP3 and 62/66 dB 3rd/5th-order harmonic rejection with 30–40 dB improvement by the calibration. The measured sensitivity satisfies the requirements of DVB-H, LTE, 802.11 g, and ZigBee.Peer reviewedFinal Accepted Versio

Somatostatin receptors differentially affect spontaneous epileptiform activity in mouse hippocampal slices

Somatostatin-14 (SRIF) reduces hippocampal epileptiform activity but the contribution of its specific receptors (sst1-5) is poorly understood. We have focused on sst1 and sst2 role in mediating SRIF modulation of epilepsy using hippocampal slices of wild type (WT) and sst1 or sst2 knock out (KO) mice. Recordings of epileptiform discharge induced by Mg2+-free medium with 4-aminopyridine were performed from the CA3 region before and after the application of SRIF compounds. In WT mice, SRIF and the sst1 agonist CH-275 reduce epilepsy whereas sst1 blockade with its antagonist SRA-880 increases bursting discharge. Activation of sst2 does not affect bursting frequency unless its agonist octreotide is applied with SRA-880, indicating that sst1 masks sst2-mediated modulation of epilepsy. In sst1 KO mice: i. bursting frequency is lower than in WT; ii. SRIF, CH-275 and SRA-880 are ineffective on epilepsy; iii. octreotide is also devoid of effects, whereas blockade of sst2 with the antagonist D-Tyr8 Cyn 154806 increases bursting frequency. In sst2 KO mice, SRIF ligand effects are similar to those in WT. In the whole hippocampus of sst1 KO mice, sst2 mRNA, protein and binding are higher than in WT and RT-PCR of the CA3 subarea confirms an increase of the sst2 messenger. We conclude that sst1 mediates inhibitory actions of SRIF and that interactions between sst1 and sst2 may prevent sst2 modulation of epilepsy. We suggest that, in sst1 KO mice, activation of over-expressed sst2 reduces bursting frequency, indicating that sst2 density represents the rate-limiting factor for sst2-mediated modulation of epilepsy.L'articolo è disponibile sul sito dell'editore http://onlinelibrary.wiley.com

1, 25-D3 Protects From Cerebral Ischemia by Maintaining BBB Permeability via PPAR-γ Activation

The blood-brain barrier (BBB) is a physical and biochemical barrier that maintains cerebral homeostasis. BBB dysfunction in an ischemic stroke, results in brain injury and subsequent neurological impairment. The aim of this study was to determine the possible protective effects of 1, 25-dihydroxyvitamin D3 [1, 25(OH)2D3, 1, 25-D3, vit D] on BBB dysfunction, at the early stages of an acute ischemic brain injury. We analyzed the effects of 1, 25-D3 on BBB integrity in terms of histopathological changes, the neurological deficit, infarct size and the expression of brain derived neurotrophic factor (BDNF), in a middle cerebral artery occlusion/reperfusion (MCAO/R) rat model. BBB permeability and the expression of permeability-related proteins in the brain were also evaluated by Evans blue (EB) staining and Western blotting respectively. To determine the possible mechanism underlying the role of 1, 25-D3 in BBB maintenance, after MCAO/R, the rats were treated with the specific peroxisome proliferator-activated receptor gamma (PPARγ) inhibitor GW9662. Supplementation with 1, 25-D3 markedly improved the neurological scores of the rats, decreased the infarct volume, prevented neuronal deformation and upregulated the expression of the tight junction (TJ) and BDNF proteins in their brains. Furthermore, it activated PPARγ but downregulated neuro-inflammatory cytokines such as nuclear factor kappa-B (NF-κB) and tumor necrosis factor-α (TNF-α), after MCAO/R. Taken together, 1, 25-D3 protects against cerebral ischemia by maintaining BBB permeability, upregulating the level of BDNF and inhibiting PPARγ-mediated neuro-inflammation

New insight into the phylogeographic pattern of Liriodendron chinense (Magnoliaceae) revealed by chloroplast DNA: east–west lineage split and genetic mixture within western subtropical China

Background Subtropical China is a global center of biodiversity and one of the most important refugia worldwide. Mountains play an important role in conserving the genetic resources of species. Liriodendron chinense is a Tertiary relict tree largely endemic to subtropical China. In this study, we aimed to achieve a better understanding of the phylogeographical pattern of L. chinense and to explore the role of mountains in the conservation of L. chinense genetic resources. Methods Three chloroplast regions (psbJ-petA, rpl32-ndhF, and trnK5’-matK) were sequenced in 40 populations of L. chinense for phylogeographical analyses. Relationships among chloroplast DNA (cpDNA) haplotypes were determined using median-joining networks, and genetic structure was examined by spatial analysis of molecular variance (SAMOVA). The ancestral area of the species was reconstructed using the Bayesian binary Markov Chain Monte Carlo (BBM) method according to its geographic distribution and a maximum parsimony (MP) tree based on Bayesian methods. Results Obvious phylogeographic structure was found in L. chinense. SAMOVA revealed seven groups matching the major landscape features of the L. chinense distribution area. The haplotype network showed three clades distributed in the eastern, southwestern, and northwestern regions. Separate northern and southern refugia were found in the Wu Mountains and Yungui Plateau, with genetic admixture in the Dalou Mountains and Wuling Mountains. BBM revealed a more ancient origin of L. chinense in the eastern region, with a west–east split most likely having occurred during the Mindel glacial stage. Discussion The clear geographical distributions of haplotypes suggested multiple mountainous refugia of L. chinense. The east–west lineage split was most likely a process of gradual genetic isolation and allopatric lineage divergence when the Nanling corridor was frequently occupied by evergreen or coniferous forest during Late Quaternary oscillations. Hotspots of haplotype diversity in the Dalou Mountains and Wuling Mountains likely benefited from gene flow from the Wu Mountains and Yungui Plateau. Collectively, these results indicate that mountain regions should be the main units for conserving and collecting genetic resources of L. chinense and other similar species in subtropical China

The Airlines’ Recent Experience Under the Railway Labor Act

Silky-feather has been selected and fixed in some breeds due to its unique appearance. This phenotype is caused by a single recessive gene (hookless, h). Here we map the silky-feather locus to chromosome 3 by linkage analysis and subsequently fine-map it to an 18.9 kb interval using the identical by descent (IBD) method. Further analysis reveals that a C to G transversion located upstream of the prenyl (decaprenyl) diphosphate synthase, subunit 2 (PDSS2) gene is causing silky-feather. All silky-feather birds are homozygous for the G allele. The silky-feather mutation significantly decreases the expression of PDSS2 during feather development in vivo. Consistent with the regulatory effect, the C to G transversion is shown to remarkably reduce PDSS2 promoter activity in vitro. We report a new example of feather structure variation associated with a spontaneous mutation and provide new insight into the PDSS2 function