The Power of One Clean Qubit in Communication Complexity

We study quantum communication protocols, in which the players\u27 storage starts out in a state where one qubit is in a pure state, and all other qubits are totally mixed (i.e. in a random state), and no other storage is available (for messages or internal computations). This restriction on the available quantum memory has been studied extensively in the model of quantum circuits, and it is known that classically simulating quantum circuits operating on such memory is hard when the additive error of the simulation is exponentially small (in the input length), under the assumption that the polynomial hierarchy does not collapse. We study this setting in communication complexity. The goal is to consider larger additive error for simulation-hardness results, and to not use unproven assumptions. We define a complexity measure for this model that takes into account that standard error reduction techniques do not work here. We define a clocked and a semi-unclocked model, and describe efficient simulations between those. We characterize a one-way communication version of the model in terms of weakly unbounded error communication complexity. Our main result is that there is a quantum protocol using one clean qubit only and using O(log n) qubits of communication, such that any classical protocol simulating the acceptance behaviour of the quantum protocol within additive error 1/poly(n) needs communication ?(n). We also describe a candidate problem, for which an exponential gap between the one-clean-qubit communication complexity and the randomized communication complexity is likely to hold, and hence a classical simulation of the one-clean-qubit model within constant additive error might be hard in communication complexity. We describe a geometrical conjecture that implies the lower bound

Quantum algorithm for robust optimization via stochastic-gradient online learning

Optimization theory has been widely studied in academia and finds a large variety of applications in industry. The different optimization models in their discrete and/or continuous settings has catered to a rich source of research problems. Robust convex optimization is a branch of optimization theory in which the variables or parameters involved have a certain level of uncertainty. In this work, we consider the online robust optimization meta-algorithm by Ben-Tal et al. and show that for a large range of stochastic subgradients, this algorithm has the same guarantee as the original non-stochastic version. We develop a quantum version of this algorithm and show that an at most quadratic improvement in terms of the dimension can be achieved. The speedup is due to the use of quantum state preparation, quantum norm estimation, and quantum multi-sampling. We apply our quantum meta-algorithm to examples such as robust linear programs and robust semidefinite programs and give applications of these robust optimization problems in finance and engineering.Comment: 21 page

Transient high level mammalian reovirus replication in a bat epithelial cell line occurs without cytopathic effect

Mammalian reoviruses exhibit a large host range and infected cells are generally killed; however, most studies examined only a few cell types and host species, and are probably not representative of all possible interactions between virus and host cell. Many questions thus remain concerning the nature of cellular factors that affect viral replication and cell death. In the present work, it was observed that replication of the classical mammalian reovirus serotype 3 Dearing in a bat epithelial cell line, Tb1.Lu, does not result in cell lysis and is rapidly reduced to very low levels. Prior uncoating of virions by chymotrypsin treatment, to generate infectious subviral particles, increased the initial level of infection but without any significant effect on further viral replication or cell survival. Infected cells remain resistant to virus reinfection and secrete an antiviral factor, most likely interferon, that is protective against the unrelated encephalomyocarditis virus. Although, the transformed status of a cell is believed to promote reovirus replication and viral “oncolysis”, resistant Tb1.Lu cells exhibit a classical phenotype of transformed cells by forming colonies in semisolid soft agar medium. Further transduction of Tb.Lu cells with a constitutively-active Ras oncogene does not seem cell growth or reovirus effect on these cells. Infected Tb1.Lu cells can produce low-level of infectious virus for a long time without any apparent effect, although these cells are resistant to reinfection. The results suggest that Tb1.Lu cells can mount an unusual antiviral response. Specific properties of bat cells may thus be in part responsible for the ability of the animals to act as reservoirs for viruses in general and for novel reoviruses in particular. Their peculiar resistance to cell lysis also makes Tb1.Lu cells an attractive model to study the cellular and viral factors that determine the ability of reovirus to replicate and destroy infected cells.Les réovirus de mammifères possèdent un large spectre d'hôtes et les cellules infectées sont généralement tuées par l'infection ; cependant, la plupart des études utilisent seulement certains types de cellules provenant de quelques espèces animales. Ceci n'est sans doute pas représentatif de toutes les interactions possibles entre virus et cellule hôte. Plusieurs questions demeurent concernant la nature des facteurs cellulaires qui affectent la réplication virale et la mort cellulaire. Dans la présente étude, il a été observé que la réplication du classique réovirus de mammifères (sérotype 3 Dearing) dans une lignée de cellules épithéliales de chauve-souris, Tb1.Lu, n'entraîne pas la lyse cellulaire et est rapidement réduite à un très faible niveau. La décapsidation des virions par traitement à la chymotrypsine, afin de générer des particules dites « sous-virales infectieuses », augmente le niveau initial d'infection sans effet significatif sur la réplication virale ou la survie cellulaire. Les cellules infectées demeurent résistantes à la réinfection et sécrètent un facteur antiviral, probablement de l'interféron, qui peut protéger contre l'infection par le virus de l'encéphalomyocardite. Malgré le fait que le statut de transformation cellulaire est considéré comme pouvant promouvoir la réplication de réovirus et l'oncolyse virale, les cellules Tb1.Lu résistantes démontrent un phénotype classique de cellules transformées et forment des colonies en milieu semi-solide contenant de l'agar. La transduction de cellules Tb1.Lu avec un oncogène Ras constitutivement actif ne semble pas affecter la croissance cellulaire ni la réplication virale. Les cellules Tb1.Lu infectées peuvent produire une faible quantité de virus infectieux pour une longue période sans effet apparent, malgré le fait que ces cellules soient résistantes à la réinfection. Ces résultats suggèrent que les cellules Tb1.Lu peuvent développer une réponse antivirale inhabituelle. Les propriétés spécifiques des cellules de chauve-souris pourraient donc être en partie responsables de la capacité de ces animaux à agir comme réservoirs de virus en général et de nouveaux réovirus en particulier. Leur résistance particulière à la lyse cellulaire fait aussi de ces cellules un modèle attrayant pour étudier les facteurs cellulaires et viraux qui déterminent la capacité de réovirus à se répliquer et à détruire les cellules infectées.Conseil de recherches en sciences naturelles et en génie du Canad

On quantum capacity of erasure channel assisted by back classical communication

We present a communication protocol for the erasure channel assisted by backward classical communication, which achieves a significantly better rate than the best prior result. In addition, we prove an upper bound for the capacity of the channel. The upper bound is smaller than the capacity of the erasure channel when it is assisted by two-way classical communication. Thus, we prove the separation between quantum capacities assisted by backward classical communication and two-way classical communication.Comment: 4 pages, 1 figur

Liver fibrosis and accelerated immune dysfunction (immunosenescence) among HIV-infected Russians with heavy alcohol consumption - an observational cross-sectional study

The multifactorial mechanisms driving negative health outcomes among risky drinkers with HIV may include immunosenescence. Immunosenescence, aging of the immune system, may be accentuated in HIV and leads to poor outcomes. The liver regulates innate immunity and adaptive immune tolerance. HIV-infected people have high prevalence of liver-related comorbidities. We hypothesize that advanced liver fibrosis/cirrhosis is associated with alterations in T-cell subsets consistent with immunosenescence. ART-naïve people with HIV with a recent history of heavy drinking were recruited into a clinical trial of zinc supplementation. Flow cytometry was used to characterize T-cell subsets. The two primary dependent variables were CD8+ and CD4+ T-cells expressing CD28-CD57+ (senescent cell phenotype). Secondary dependent variables were CD8+ and CD4+ T-cells expressing CD45RO + CD45RA- (memory phenotype), CD45RO-CD45RA+ (naïve phenotype), and the naïve phenotype to memory phenotype T-cell ratio (lower ratios associated with immunosenescence). Advanced liver fibrosis/cirrhosis was defined as FIB-4 > 3.25, APRI≥1.5, or Fibroscan measurement ≥10.5 kPa. Analyses were conducted using multiple linear regression adjusted for potential confounders. Mean age was 34 years; 25% female; 88% hepatitis C. Those with advanced liver fibrosis/cirrhosis (N = 25) had higher HIV-1 RNA and more hepatitis C. Advanced liver fibrosis/cirrhosis was not significantly associated with primary or secondary outcomes in adjusted analyses. Advanced liver fibrosis/cirrhosis was not significantly associated with these senescent T-cell phenotypes in this exploratory study of recent drinkers with HIV. Future studies should assess whether liver fibrosis among those with HIV viral suppression and more advanced, longstanding liver disease is associated with changes in these and other potentially senescent T-cell subsets

Investigation of the Proteolytic Functions of an Expanded Cercarial Elastase Gene Family in Schistosoma mansoni

Schistosome parasites are a major cause of disease in the developing world. The larval stage of the parasite transitions between an intermediate snail host and a definitive human host in a dramatic fashion, burrowing out of the snail and subsequently penetrating human skin. This process is facilitated by secreted proteases. In Schistosoma mansoni, cercarial elastase is the predominant secreted protease and essential for host skin invasion. Genomic analysis reveals a greatly expanded cercarial elastase gene family in S. mansoni. Despite sequence divergence, SmCE isoforms show similar expression profiles throughout the S. mansoni life cycle and have largely similar substrate specificities, suggesting that the majority of protease isoforms are functionally redundant and therefore their expansion is an example of gene dosage. However, activity-based profiling also indicates that a subset of SmCE isoforms are activated prior to the parasite's exit from its intermediate snail host, suggesting that the protease may also have a role in this process

A Random shRNA-Encoding Library for Phenotypic Selection and Hit-Optimization

RNA interference (RNAi) is a mechanism for inhibiting gene expression through the action of small, non-coding RNAs. Most existing RNAi libraries target single genes through canonical pathways. Endogenous microRNAs (miRNAs), however, often target multiple genes and can act through non-canonical pathways, including pathways that activate gene expression. To interrogate all possible functions, we designed, synthesized, and validated the first shRNA-encoding library that is completely random at the nucleotide level. Screening in an IL3-dependent cell line, FL5.12, yielded shRNA-encoding sequences that double cell survival upon IL3 withdrawal. Using random mutagenesis and re-screening under more stringent IL3-starvation conditions, we hit-optimized one of the sequences; a specific nucleotide change and the creation of a mismatch between the two halves of the stem both contributed to the improved potency. Our library allows unbiased selection and optimization of shRNA-encoding sequences that confer phenotypes of interest, and could be used for the development of therapeutics and tools in many fields of biology