Almost quantum correlations

Quantum theory is not only successfully tested in laboratories every day but also constitutes a robust theoretical framework: small variations usually lead to implausible consequences, such as faster-than-light communication. It has even been argued that quantum theory may be special among possible theories. Here we report that, at the level of correlations among different systems, quantum theory is not so special. We define a set of correlations, dubbed 'almost quantum', and prove that it strictly contains the set of quantum correlations but satisfies all-but-one of the proposed principles to capture quantum correlations. We present numerical evidence that the remaining principle is satisfied too. © 2015 Macmillan Publishers Limited

Methods of histogram transformations and control processes of printing image reproduction

В статье предлагаются новые методы, позволяющие провести объективную оценку растровых структур по статистическим параметрам гистограммы, и метод коррекции изображения с использованием преобразования гистограммы по нормальному закону распределения, позволяющий автоматизировать процесс коррекции.There are new methods helping to do objective valuation of screen structures on statistical parameters of the histogram and method of image correction using histogram conversion with Gaussian distribution, allowing to automate correction process in our article

Measuring the thermodynamic cost of timekeeping

All clocks, in some form or another, use the evolution of nature toward higher entropy states to quantify the passage of time. Because of the statistical nature of the second law and corresponding entropy flows, fluctuations fundamentally limit the performance of any clock. This suggests a deep relation between the increase in entropy and the quality of clock ticks. Indeed, minimal models for autonomous clocks in the quantum realm revealed that a linear relation can be derived, where for a limited regime every bit of entropy linearly increases the accuracy of quantum clocks. But can such a linear relation persist as we move toward a more classical system? We answer this in the affirmative by presenting the first experimental investigation of this thermodynamic relation in a nanoscale clock. We stochastically drive a nanometer-thick membrane and read out its displacement with a radio-frequency cavity, allowing us to identify the ticks of a clock. We show theoretically that the maximum possible accuracy for this classical clock is proportional to the entropy created per tick, similar to the known limit for a weakly coupled quantum clock but with a different proportionality constant. We measure both the accuracy and the entropy. Once nonthermal noise is accounted for, we find that there is a linear relation between accuracy and entropy and that the clock operates within an order of magnitude of the theoretical bound

The second law and beyond in microscopic quantum setups

The Clausius inequality (CI) is one of the most versatile forms of the second law. Although it was originally conceived for macroscopic steam engines, it is also applicable to quantum single particle machines. Moreover, the CI is the main connecting thread between classical microscopic thermodynamics and nanoscopic quantum thermodynamics. In this chapter, we study three different approaches for obtaining the CI. Each approach shows different aspects of the CI. The goals of this chapter are: (i) To show the exact assumptions made in various derivations of the CI. (ii) To elucidate the structure of the second law and its origin. (iii) To discuss the possibilities each approach offers for finding additional second-law like inequalities. (iv) To pose challenges related to the second law in nanoscopic setups. In particular, we introduce and briefly discuss the notions of exotic heat machines (X machines), and "lazy demons".Comment: As a chapter of: F. Binder, L. A. Correa, C. Gogolin, J. Anders, and G. Adesso (eds.), "Thermodynamics in the quantum regime - Recent Progress and Outlook", (Springer International Publishing). v1 does not include references to other book chapter

Dnmt3a regulates myeloproliferation and liver-specific expansion of hematopoietic stem and progenitor cells

DNMT3A mutations are observed in myeloid malignancies, including myeloproliferative neoplasms (MPN), myelodysplastic syndromes (MDS), and acute myeloid leukemia (AML). Transplantation studies have elucidated an important role for Dnmt3a in stem cell self-renewal and in myeloid differentiation. Here we investigated the impact of conditional hematopoietic Dnmt3a loss on disease phenotype in primary mice. Mx1-Cre-mediated Dnmt3a ablation led to the development of a lethal, fully penetrant myeloproliferative neoplasm with myelodysplasia (MDS/MPN) characterized by peripheral cytopenias and by marked, progressive hepatomegaly. We detected expanded stem/progenitor populations in the liver of Dnmt3a-ablated mice. The MDS/MPN induced by Dnmt3a ablation was transplantable, including the marked hepatomegaly. Homing studies showed that Dnmt3a-deleted bone marrow cells preferentially migrated to the liver. Gene expression and DNA methylation analyses of progenitor cell populations identified differential regulation of hematopoietic regulatory pathways, including fetal liver hematopoiesis transcriptional programs. These data demonstrate that Dnmt3a ablation in the hematopoietic system leads to myeloid transformation in vivo, with cell autonomous aberrant tissue tropism and marked extramedullary hematopoiesis (EMH) with liver involvement. Hence, in addition to the established role of Dnmt3a in regulating self-renewal, Dnmt3a regulates tissue tropism and limits myeloid progenitor expansion in vivo

Direct In Vivo Evidence for Tumor Propagation by Glioblastoma Cancer Stem Cells

High-grade gliomas (World Health Organization grade III anaplastic astrocytoma and grade IV glioblastoma multiforme), the most prevalent primary malignant brain tumors, display a cellular hierarchy with self-renewing, tumorigenic cancer stem cells (CSCs) at the apex. While the CSC hypothesis has been an attractive model to describe many aspects of tumor behavior, it remains controversial due to unresolved issues including the use of ex vivo analyses with differential growth conditions. A CSC population has been confirmed in malignant gliomas by preferential tumor formation from cells directly isolated from patient biopsy specimens. However, direct comparison of multiple tumor cell populations with analysis of the resulting phenotypes of each population within a representative tumor environment has not been clearly described. To directly test the relative tumorigenic potential of CSCs and non-stem tumor cells in the same microenvironment, we interrogated matched tumor populations purified from a primary human tumor transplanted into a xenograft mouse model and monitored competitive in vivo tumor growth studies using serial in vivo intravital microscopy. While CSCs were a small minority of the initial transplanted cancer cell population, the CSCs, not the non-stem tumor cells, drove tumor formation and yielded tumors displaying a cellular hierarchy. In the resulting tumors, a fraction of the initial transplanted CSCs maintained expression of stem cell and proliferation markers, which were significantly higher compared to the non-stem tumor cell population and demonstrated that CSCs generated cellular heterogeneity within the tumor. These head-to-head comparisons between matched CSCs and non-stem tumor cells provide the first functional evidence using live imaging that in the same microenvironment, CSCs more than non-stem tumor cells are responsible for tumor propagation, confirming the functional definition of a CSC

Deregulated expression of TANK in glioblastomas triggers pro-tumorigenic ERK1/2 and AKT signaling pathways

Signal transmission by the noncanonical IkappaB kinases (IKKs), TANK-binding kinase 1 (TBK1) and IKKɛ, requires interaction with adapter proteins such as TRAF associated NF-κB activator (TANK). Although increased expression or dysregulation of both kinases has been described for a variety of human cancers, this study shows that deregulated expression of the TANK protein is frequently occurring in glioblastomas (GBMs). The functional relevance of TANK was analyzed in a panel of GBM-derived cell lines and revealed that knockdown of TANK arrests cells in the S-phase and prohibits tumor cell migration. Deregulated TANK expression affects several signaling pathways controlling cell proliferation and the inflammatory response. Interference with stoichiometrically assembled signaling complexes by overexpression or silencing of TANK prevented constitutive interferon-regulatory factor 3 (IRF3) phosphorylation. Knockdown of TANK frequently prevents constitutive activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2). TANK-mediated ERK1/2 activation is independent from the canonical MAP kinase or ERK kinase (MEK) 1/2-mediated pathway and utilizes an alternative pathway that uses a TBK1/IKKɛ/Akt signaling axis, thus identifying a novel pathway suitable to block constitutive ERK1/2 activity.Peer reviewe

Enhancement of COPD biological networks using a web-based collaboration interface

The construction and application of biological network models is an approach that offers a holistic way to understand biological processes involved in disease. Chronic obstructive pulmonary disease (COPD) is a progressive inflammatory disease of the airways for which therapeutic options currently are limited after diagnosis, even in its earliest stage. COPD network models are important tools to better understand the biological components and processes underlying initial disease development. With the increasing amounts of literature that are now available, crowdsourcing approaches offer new forms of collaboration for researchers to review biological findings, which can be applied to the construction and verification of complex biological networks. We report the construction of 50 biological network models relevant to lung biology and early COPD using an integrative systems biology and collaborative crowd-verification approach. By combining traditional literature curation with a data-driven approach that predicts molecular activities from transcriptomics data, we constructed an initial COPD network model set based on a previously published non-diseased lung-relevant model set. The crowd was given the opportunity to enhance and refine the networks on a website ( https://bionet.sbvimprover.com/) and to add mechanistic detail, as well as critically review existing evidence and evidence added by other users, so as to enhance the accuracy of the biological representation of the processes captured in the networks. Finally, scientists and experts in the field discussed and refined the networks during an in-person jamboree meeting. Here, we describe examples of the changes made to three of these networks: Neutrophil Signaling, Macrophage Signaling, and Th1-Th2 Signaling. We describe an innovative approach to biological network construction that combines literature and data mining and a crowdsourcing approach to generate a comprehensive set of COPD-relevant models that can be used to help understand the mechanisms related to lung pathobiology. Registered users of the website can freely browse and download the networks

Deletion of Asxl1 results in myelodysplasia and severe developmental defects in vivo

Somatic Addition of Sex Combs Like 1 (ASXL1) mutations occur in 10-30% of patients with myeloid malignancies, most commonly in myelodysplastic syndromes (MDSs), and are associated with adverse outcome. Germline ASXL1 mutations occur in patients with Bohring-Opitz syndrome. Here, we show that constitutive loss of Asxl1 results in developmental abnormalities, including anophthalmia, microcephaly, cleft palates, and mandibular malformations. In contrast, hematopoietic-specific deletion of Asxl1 results in progressive, multilineage cytopenias and dysplasia in the context of increased numbers of hematopoietic stem/progenitor cells, characteristic features of human MDS. Serial transplantation of Asxl1-null hematopoietic cells results in a lethal myeloid disorder at a shorter latency than primary Asxl1 knockout (KO) mice. Asxl1 deletion reduces hematopoietic stem cell self-renewal, which is restored by concomitant deletion of Tet2, a gene commonly co-mutated with ASXL1 in MDS patients. Moreover, compound Asxl1/Tet2 deletion results in an MDS phenotype with hastened death compared with single-gene KO mice. Asxl1 loss results in a global reduction of H3K27 trimethylation and dysregulated expression of known regulators of hematopoiesis. RNA-Seq/ChIP-Seq analyses of Asxl1 in hematopoietic cells identify a subset of differentially expressed genes as direct targets of Asxl1. These findings underscore the importance of Asxl1 in Polycomb group function, development, and hematopoiesisclos

Quantum majorization and a complete set of entropic conditions for quantum thermodynamics

What does it mean for one quantum process to be more disordered than another? Interestingly, this apparently abstract question arises naturally in a wide range of areas such as information theory, thermodynamics, quantum reference frames, and the resource theory of asymmetry. Here we use a quantum-mechanical generalization of majorization to develop a framework for answering this question, in terms of single-shot entropies, or equivalently, in terms of semi-definite programs. We also investigate some of the applications of this framework, and remarkably find that, in the context of quantum thermodynamics it provides the first complete set of necessary and sufficient conditions for arbitrary quantum state transformations under thermodynamic processes, which rigorously accounts for quantum-mechanical properties, such as coherence. Our framework of generalized thermal processes extends thermal operations, and is based on natural physical principles, namely, energy conservation, the existence of equilibrium states, and the requirement that quantum coherence be accounted for thermodynamically