A security proof of continuous-variable QKD using three coherent states

We introduce a ternary quantum key distribution (QKD) protocol and asymptotic security proof based on three coherent states and homodyne detection. Previous work had considered the binary case of two coherent states and here we nontrivially extend this to three. Our motivation is to leverage the practical benefits of both discrete and continuous (Gaussian) encoding schemes creating a best-of-both-worlds approach; namely, the postprocessing of discrete encodings and the hardware benefits of continuous ones. We present a thorough and detailed security proof in the limit of infinite signal states which allows us to lower bound the secret key rate. We calculate this is in the context of collective eavesdropping attacks and reverse reconciliation postprocessing. Finally, we compare the ternary coherent state protocol to other well-known QKD schemes (and fundamental repeaterless limits) in terms of secret key rates and loss.Comment: Close to the published versio

Oxidized low-density lipoprotein inhibits hepatitis C virus cell entry in human hepatoma cells.

Cell entry of hepatitis C virus, pseudoparticles (HCVpp) and cell culture grown virus (HCVcc), requires the interaction of viral glycoproteins with CD81 and other as yet unknown cellular factors. One of these is likely to be the scavenger receptor class B type I (SR-BI). To further understand the role of SR-BI, we examined the effect of SR-BI ligands on HCVpp and HCVcc infectivity. Oxidized low-density lipoprotein (oxLDL), but not native LDL, potently inhibited HCVpp and HCVcc cell entry. Pseudoparticles bearing unrelated viral glycoproteins or bovine viral diarrhea virus were not affected. A dose-dependent inhibition was observed for HCVpp bearing diverse viral glycoproteins with an approximate IC50 of 1.5 microg/mL apolipoprotein content, which is within the range of oxLDL reported to be present in human plasma. The ability of lipoprotein components to bind to target cells associated with their antiviral activity, suggesting a mechanism of action which targets a cell surface receptor critical for HCV infection of the host cell. However, binding of soluble E2 to SR-BI or CD81 was not affected by oxLDL, suggesting that oxLDL does not act as a simple receptor blocker. At the same time, oxLDL incubation altered the biophysical properties of HCVpp, suggesting a ternary interaction of oxLDL with both virus and target cells. In conclusion, the SR-BI ligand oxLDL is a potent cell entry inhibitor for a broad range of HCV strains in vitro. These findings suggest that SR-BI is an essential component of the cellular HCV receptor complex

Chromosomal instability and copy number alterations in Barrett’s esophagus and esophageal adenocarcinoma

Purpose: Chromosomal instability, as assessed by many techniques, including DNA content aneuploidy, LOH, and comparative genomic hybridization, has consistently been reported to be common in cancer and rare in normal tissues. Recently, a panel of chromosome instability biomarkers, including LOH and DNA content, has been reported to identify patients at high and low risk of progression from Barrett’s esophagus (BE) to esophageal adenocarcinoma (EA), but required multiple platforms for implementation. Although chromosomal instability involving amplifications and deletions of chromosome regions have been observed in nearly all cancers, copy number alterations (CNAs) in premalignant tissues have not been well characterized or evaluated in cohort studies as biomarkers of cancer risk. Experimental Design: We examined CNAs in 98 patients having either BE or EA using BAC array CGH to characterize CNAs at different stages of progression ranging from early BE to advanced EA. Results: CNAs were rare in early stages (<HGD) but were progressively more frequent and larger in later stages (HGD and EA), including high level amplifications. The number of CNAs correlated highly with DNA content aneuploidy. Patients whose biopsies contained CNAs involving more than 70 Mbp were at increased risk of progression to DNA content abnormalities or EA (HR=4.9, 95% CI 1.6-14.8, p=0.0047), and the risk increased as more of the genome was affected. Conclusions: Genome wide analysis of CNAs provides a common platform for evaluation of chromosome instability for cancer risk assessment as well as identification of common regions of alteration that can be further studied for biomarker discovery

Reliability and validity of subjective measures of aerobic intensity in adults with spinal cord injury: a systematic review

Objective: To systematically synthesize and appraise research regarding test-retest reliability or criterion validity of subjective measures for assessing aerobic exercise intensity in adults with spinal cord injury (SCI). Data Sources: Electronic databases (Pubmed, PsychINFO, SPORTDiscus, EMBASE and CINAHL) were searched from inception to 1-1-2016. Study Selection: Studies involving at least 50% of participants with SCI who performed an aerobic exercise test that included measurement of subjective and objective intensity based on test-retest reliability or criterion validity protocols. Data Extraction: Characteristics were extracted on study design, measures, participants, protocols, and results. Each study was evaluated for risk of bias based on strength of the study design and a quality checklist score (COnsensus-based Standards for the selection of health Measurement Instruments [COSMIN]). Data Synthesis: The seven eligible studies (one for reliability, six for validity) evaluated overall, peripheral and/or central ratings of perceived exertion on a 6-20 scale (RPE 6-20). No eligible studies were identified for other subjective intensity measures. The evidence for reliability and validity were synthesized separately for each measure, and assessed using Grading of Recommendations Assessment, Development, and Evaluation (GRADE). Overall, very low GRADE confidence ratings were established for reliability and validity evidence generalizable to the entire population with SCI and various upper-body and lower-body modalities. There was low confidence for the evidence showing that overall RPE 6-20 has acceptable validity for adults with SCI and high fitness levels performing moderate to vigorous-intensity upper-body aerobic exercise. Conclusions: Health care professionals and scientists need to be aware of the very low to low confidence in the evidence, which currently prohibits a strong clinical recommendation for the use of subjective measures for assessing aerobic exercise intensity in adults with SCI. However, a tentative, conditional recommendation regarding overall RPE 6-20 seems applicable depending on participants’ fitness level as well as the exercise intensity and modality used

Effects of Hybrid Cycle and Handcycle Exercise on Cardiovascular Disease Risk Factors in People with Spinal Cord Injury:A Randomized Controlled Trial

Objective: To examine the effects of a 16-week exercise programme, using either a hybrid cycle or a handcycle, on cardiovascular disease risk factors in people with spinal cord injury.Participants: Nineteen individuals with spinal cord injury &gt;= 8 years.Design: Multicentre randomized controlled trial. Both the hybrid cycle group (n = 9) and the handcycle group (n = 10) trained twice a week for 16 weeks on the specific cycle. Outcome measures obtained pre and post the programme were: metabolic syndrome components (waist circumference, systolic and diastolic blood pressure, high-density lipoprotein cholesterol, triglycerides and insulin resistance), inflammatory status (C-reactive protein (CRP), interleukin (1)-6 and -10), and visceral adiposity (trunk and android fat).Results: For all outcome measures, there were no significant differences over time between the 2 training groups. Overall significant reductions were found for waist circumference (p = 0.001), diastolic blood pressure (p = 0.03), insulin resistance (p = 0.006), CRP (p = 0.05), IL-6 (p = 0.04), IL-6/IL-10 ratio (p = 0.03), and trunk (p = 0.04) and android (p = 0.02) fat percentage. No significant main effects for time were observed for systolic blood pressure, triglycerides, high-density lipoprotein cholesterol, IL-10, and trunk and android fat mass.Conclusion: The 16-week exercise programme, using either a hybrid cycle or a handcycle, found similar beneficial effects on metabolic syndrome components, inflammatory status and visceral adiposity, indicating that there were no additional benefits of functional electrical stimulation-induced leg exercise over handcycle exercise alone.</p

Cell proliferation, cell cycle abnormalities, and cancer outcome in patients with Barrett’s esophagus: A long-term prospective study

Purpose: Elevated cellular proliferation and cell cycle abnormalities, which have been associated with premalignant lesions, may be caused by inactivation of tumor suppressor genes. We measured proliferative and cell cycle fractions of biopsies from a cohort of patients with Barrett's esophagus to better understand the role of proliferation in early neoplastic progression and the association between cell cycle dysregulation and tumor suppressor gene inactivation. Experimental Design: Cell proliferative fractions (determined by Ki67/DNA multiparameter flow cytometry) and cell cycle fractions (DNA content flow cytometry) were measured in 853 diploid biopsies from 362 patients with Barrett's esophagus. The inactivation status of CDKN2A and TP53 was assessed in a subset of these biopsies in a cross-sectional study. A prospective study followed 276 of the patients without detectable aneuploidy for an average of 6.3 years with esophageal adenocarcinoma as an endpoint. Results: Diploid S and 4N (G2/tetraploid) fractions were significantly higher in biopsies with TP53 mutation and LOH. CDKN2A inactivation was not associated with higher Ki67-positive, diploid S, G1, or 4N fractions. High Ki67-positive and G1 phase fractions were not associated with the future development of esophageal adenocarcinoma (p=0.13 and p=0.15, respectively), while high diploid S phase and 4N fractions were (p=0.03 and p<0.0001, respectively). Conclusions: High Ki67-positive proliferative fractions were not associated with inactivation of CDKN2A and TP53 or future development of cancer in our cohort of patients with Barrett's esophagus. Bi-allelic inactivation of TP53 was associated with elevated 4N fractions, which have been associated with the future development of esophageal adenocarcinoma

NSAIDs Modulate Clonal Evolution in Barrett's Esophagus

Cancer is considered an outcome of decades-long clonal evolution fueled by acquisition of somatic genomic abnormalities (SGAs). Non-steroidal anti-inflammatory drugs (NSAIDs) have been shown to reduce cancer risk, including risk of progression from Barrett's esophagus (BE) to esophageal adenocarcinoma (EA). However, the cancer chemopreventive mechanisms of NSAIDs are not fully understood. We hypothesized that NSAIDs modulate clonal evolution by reducing SGA acquisition rate. We evaluated thirteen individuals with BE. Eleven had not used NSAIDs for 6.2±3.5 (mean±standard deviation) years and then began using NSAIDs for 5.6±2.7 years, whereas two had used NSAIDs for 3.3±1.4 years and then discontinued use for 7.9±0.7 years. 161 BE biopsies, collected at 5–8 time points over 6.4–19 years, were analyzed using 1Million-SNP arrays to detect SGAs. Even in the earliest biopsies there were many SGAs (284±246 in 10/13 and 1442±560 in 3/13 individuals) and in most individuals the number of SGAs changed little over time, with both increases and decreases in SGAs detected. The estimated SGA rate was 7.8 per genome per year (95% support interval [SI], 7.1–8.6) off-NSAIDs and 0.6 (95% SI 0.3–1.5) on-NSAIDs. Twelve individuals did not progress to EA. In ten we detected 279±86 SGAs affecting 53±30 Mb of the genome per biopsy per time point and in two we detected 1,463±375 SGAs affecting 180±100 Mb. In one individual who progressed to EA we detected a clone having 2,291±78 SGAs affecting 588±18 Mb of the genome at three time points in the last three of 11.4 years of follow-up. NSAIDs were associated with reduced rate of acquisition of SGAs in eleven of thirteen individuals. Barrett's cells maintained relative equilibrium level of SGAs over time with occasional punctuations by expansion of clones having massive amount of SGAs

Retired A Stars and Their Companions VI. A Pair of Interacting Exoplanet Pairs Around the Subgiants 24 Sextanis and HD200964

We report radial velocity measurements of the G-type subgiants 24 Sextanis (=HD90043) and HD200964. Both are massive, evolved stars that exhibit periodic variations due to the presence of a pair of Jovian planets. Photometric monitoring with the T12 0.80m APT at Fairborn Observatory demonstrates both stars to be constant in brightness to <= 0.002 mag, thus strengthening the planetary interpretation of the radial velocity variations. 24 Sex b,c have orbital periods of 453.8 days and 883~days, corresponding to semimajor axes 1.333 AU and 2.08 AU, and minimum masses (Msini) 1.99 Mjup and 0.86 Mjup, assuming a stellar mass 1.54 Msun. HD200964 b,c have orbital periods of 613.8 days and 825 days, corresponding to semimajor axes 1.601 AU and 1.95 AU, and minimum masses 1.85 Mjup and 0.90 Mjup, assuming M* = 1.44 Msun. We also carry out dynamical simulations to properly account for gravitational interactions between the planets. Most, if not all, of the dynamically stable solutions include crossing orbits, suggesting that each system is locked in a mean motion resonance that prevents close encounters and provides long-term stability. The planets in the 24 Sex system likely have a period ratio near 2:1, while the HD200964 system is even more tightly packed with a period ratio close to 4:3. However, we caution that further radial velocity observations and more detailed dynamical modelling will be required to provide definitive and unique orbital solutions for both cases, and to determine whether the two systems are truly resonant.Comment: AJ accepte

Transkingdom Networks: A Systems Biology Approach to Identify Causal Members of Host-Microbiota Interactions

Improvements in sequencing technologies and reduced experimental costs have resulted in a vast number of studies generating high-throughput data. Although the number of methods to analyze these "omics" data has also increased, computational complexity and lack of documentation hinder researchers from analyzing their high-throughput data to its true potential. In this chapter we detail our data-driven, transkingdom network (TransNet) analysis protocol to integrate and interrogate multi-omics data. This systems biology approach has allowed us to successfully identify important causal relationships between different taxonomic kingdoms (e.g. mammals and microbes) using diverse types of data

Axonal inclusions in spinocerebellar ataxia type 3

Protein aggregation is a major pathological hallmark of many neurodegenerative disorders including polyglutamine diseases. Aggregation of the mutated form of the disease protein ataxin-3 into neuronal nuclear inclusions is well described in the polyglutamine disorder spinocerebellar ataxia type 3 (SCA3 or Machado–Joseph disease), although these inclusions are not thought to be directly pathogenic. Neuropil aggregates have not yet been described in SCA3. We performed a systematic immunohistochemical study of serial thick sections through brains of seven clinically diagnosed and genetically confirmed SCA3 patients. Using antibodies against ataxin-3, p62, ubiquitin, the polyglutamine marker 1C2 as well as TDP-43, we analyzed neuronal localization, composition and distribution of aggregates within SCA3 brains. The analysis revealed widespread axonal aggregates in fiber tracts known to undergo neurodegeneration in SCA3. Similar to neuronal nuclear inclusions, the axonal aggregates were ubiquitinated and immunopositive for the proteasome and autophagy associated shuttle protein p62, indicating involvement of neuronal protein quality control mechanisms. Rare TDP-43 positive axonal inclusions were also observed. Based on the correlation between affected fiber tracts and degenerating neuronal nuclei, we hypothesize that these novel axonal inclusions may be detrimental to axonal transport mechanisms and thereby contribute to degeneration of nerve cells in SCA3