A note on q-Euler numbers and polynomials

The purpose of this paper is to construct q-Euler numbers and polynomials by using p-adic q-integral equations on Zp. Finally, we will give some interesting formulae related to these q-Euler numbers and polynomials.Comment: 6 page

Simple deterministic dynamical systems with fractal diffusion coefficients

We analyze a simple model of deterministic diffusion. The model consists of a one-dimensional periodic array of scatterers in which point particles move from cell to cell as defined by a piecewise linear map. The microscopic chaotic scattering process of the map can be changed by a control parameter. This induces a parameter dependence for the macroscopic diffusion coefficient. We calculate the diffusion coefficent and the largest eigenmodes of the system by using Markov partitions and by solving the eigenvalue problems of respective topological transition matrices. For different boundary conditions we find that the largest eigenmodes of the map match to the ones of the simple phenomenological diffusion equation. Our main result is that the difffusion coefficient exhibits a fractal structure by varying the system parameter. To understand the origin of this fractal structure, we give qualitative and quantitative arguments. These arguments relate the sequence of oscillations in the strength of the parameter-dependent diffusion coefficient to the microscopic coupling of the single scatterers which changes by varying the control parameter.Comment: 28 pages (revtex), 12 figures (postscript), submitted to Phys. Rev.

Restricted Expression of Epstein-Barr Virus Latent Genes in Murine B Cells Derived from Embryonic Stem Cells

Background: Several human malignancies are associated with Epstein-Barr virus (EBV) and more than 95 % of the adult human population carries this virus lifelong. EBV efficiently infects human B cells and persists in this cellular compartment latently. EBV-infected B cells become activated and growth transformed, express a characteristic set of viral latent genes, and acquire the status of proliferating lymphoblastoid cell lines in vitro. Because EBV infects only primate cells, it has not been possible to establish a model of infection in immunocompetent rodents. Such a model would be most desirable in order to study EBV’s pathogenesis and latency in a suitable and amenable host. Methodology/Principal Findings: We stably introduced recombinant EBV genomes into mouse embryonic stem cells and induced their differentiation to B cells in vitro to develop the desired model. In vitro differentiated murine B cells maintained the EBV genomes but expression of viral genes was restricted to the latent membrane proteins (LMPs). In contrast to human B cells, EBV’s nuclear antigens (EBNAs) were not expressed detectably and growth transformed murine B cells did not arise in vitro. Aberrant splicing and premature termination of EBNA mRNAs most likely prevented the expression of EBNA genes required for B-cell transformation. Conclusions/Significance: Our findings indicate that fundamental differences in gene regulation between mouse and ma

Cryptanalysis of The Lifted Unbalanced Oil Vinegar Signature Scheme

In 2017, Ward Beullens \textit{et al.} submitted Lifted Unbalanced Oil and Vinegar (LUOV)\cite{beullens2017field}, a signature scheme based on the famous multivariate public key cryptosystem (MPKC) called Unbalanced Oil and Vinegar (UOV), to NIST for the competition for post-quantum public key scheme standardization. The defining feature of LUOV is that, though the public key $\mathcal{P}$ works in the extension field of degree $r$ of $\mathbb{F}_2$, the coefficients of $\mathcal{P}$ come from $\mathbb{F}_2$. This is done to significantly reduce the size of $\mathcal{P}$. The LUOV scheme is now in the second round of the NIST PQC standardization process. In this paper we introduce a new attack on LUOV. It exploits the lifted structure of LUOV to reduce direct attacks on it to those over a subfield. We show that this reduces the complexity below the targeted security for the NIST post-quantum standardization competition

Ecosystem Services in Conservation Planning: Targeted Benefits vs. Co-Benefits or Costs?

There is growing support for characterizing ecosystem services in order to link conservation and human well-being. However, few studies have explicitly included ecosystem services within systematic conservation planning, and those that have follow two fundamentally different approaches: ecosystem services as intrinsically-important targeted benefits vs. substitutable co-benefits. We present a first comparison of these two approaches in a case study in the Central Interior of British Columbia. We calculated and mapped economic values for carbon storage, timber production, and recreational angling using a geographical information system (GIS). These ‘marginal’ values represent the difference in service-provision between conservation and managed forestry as land uses. We compared two approaches to including ecosystem services in the site-selection software Marxan: as Targeted Benefits, and as Co-Benefits/Costs (in Marxan's cost function); we also compared these approaches with a Hybrid approach (carbon and angling as targeted benefits, timber as an opportunity cost). For this analysis, the Co-Benefit/Cost approach yielded a less costly reserve network than the Hybrid approach (1.6% cheaper). Including timber harvest as an opportunity cost in the cost function resulted in a reserve network that achieved targets equivalently, but at 15% lower total cost. We found counter-intuitive results for conservation: conservation-compatible services (carbon, angling) were positively correlated with each other and biodiversity, whereas the conservation-incompatible service (timber) was negatively correlated with all other networks. Our findings suggest that including ecosystem services within a conservation plan may be most cost-effective when they are represented as substitutable co-benefits/costs, rather than as targeted benefits. By explicitly valuing the costs and benefits associated with services, we may be able to achieve meaningful biodiversity conservation at lower cost and with greater co-benefits

A Polynomial-Time Key-Recovery Attack on MQQ Cryptosystems

International audienceWe investigate the security of the family of MQQ public key cryptosystems using multivariate quadratic quasigroups (MQQ). These cryptosystems show especially good performance properties. In particular, the MQQ-SIG signature scheme is the fastest scheme in the ECRYPT benchmarking of cryptographic systems (eBACS). We show that both the signature scheme MQQ-SIG and the encryption scheme MQQ-ENC, although using different types of MQQs, share a common algebraic structure that introduces a weakness in both schemes. We use this weakness to mount a successful polynomial time key-recovery attack. Our key-recovery attack finds an equivalent key using the idea of so-called {\it good keys} that reveals the structure gradually. In the process we need to solve a MinRank problem that, because of the structure, can be solved in polynomial-time assuming some mild algebraic assumptions. We highlight that our theoretical results work in characteristic $2$ which is known to be the most difficult case to address in theory for MinRank attacks. Also, we emphasize that our attack works without any restriction on the number of polynomials removed from the public-key, that is, using the minus modifier. This was not the case for previous MinRank like-attacks against \MQ\ schemes. From a practical point of view, we are able to break an MQQ-SIG instance of $80$ bits security in less than $2$ days, and one of the more conservative MQQ-ENC instances of $128$ bits security in little bit over $9$ days. Altogether, our attack shows that it is very hard to design a secure public key scheme based on an easily invertible MQQ structure

Many Labs 5:Testing pre-data collection peer review as an intervention to increase replicability

Replication studies in psychological science sometimes fail to reproduce prior findings. If these studies use methods that are unfaithful to the original study or ineffective in eliciting the phenomenon of interest, then a failure to replicate may be a failure of the protocol rather than a challenge to the original finding. Formal pre-data-collection peer review by experts may address shortcomings and increase replicability rates. We selected 10 replication studies from the Reproducibility Project: Psychology (RP:P; Open Science Collaboration, 2015) for which the original authors had expressed concerns about the replication designs before data collection; only one of these studies had yielded a statistically significant effect (p < .05). Commenters suggested that lack of adherence to expert review and low-powered tests were the reasons that most of these RP:P studies failed to replicate the original effects. We revised the replication protocols and received formal peer review prior to conducting new replication studies. We administered the RP:P and revised protocols in multiple laboratories (median number of laboratories per original study = 6.5, range = 3?9; median total sample = 1,279.5, range = 276?3,512) for high-powered tests of each original finding with both protocols. Overall, following the preregistered analysis plan, we found that the revised protocols produced effect sizes similar to those of the RP:P protocols (?r = .002 or .014, depending on analytic approach). The median effect size for the revised protocols (r = .05) was similar to that of the RP:P protocols (r = .04) and the original RP:P replications (r = .11), and smaller than that of the original studies (r = .37). Analysis of the cumulative evidence across the original studies and the corresponding three replication attempts provided very precise estimates of the 10 tested effects and indicated that their effect sizes (median r = .07, range = .00?.15) were 78% smaller, on average, than the original effect sizes (median r = .37, range = .19?.50)

The Drosophila speciation factor HMR localizes to genomic insulator sites

Hybrid incompatibility between Drosophila melanogaster and D. simulans is caused by a lethal interaction of the proteins encoded by the Hmr and Lhr genes. In D. melanogaster the loss of HMR results in mitotic defects, an increase in transcription of transposable elements and a deregulation of heterochromatic genes. To better understand the molecular mechanisms that mediate HMR's function, we measured genome-wide localization of HMR in D. melanogaster tissue culture cells by chromatin immunoprecipitation. Interestingly, we find HMR localizing to genomic insulator sites that can be classified into two groups. One group belongs to gypsy insulators and another one borders HP1a bound regions at active genes. The transcription of the latter group genes is strongly affected in larvae and ovaries of Hmr mutant flies. Our data suggest a novel link between HMR and insulator proteins, a finding that implicates a potential role for genome organization in the formation of species