Fidelity susceptibility and long-range correlation in the Kitaev honeycomb model

We study exactly both the ground-state fidelity susceptibility and bond-bond correlation function in the Kitaev honeycomb model. Our results show that the fidelity susceptibility can be used to identify the topological phase transition from a gapped A phase with Abelian anyon excitations to a gapless B phase with non-Abelian anyon excitations. We also find that the bond-bond correlation function decays exponentially in the gapped phase, but algebraically in the gapless phase. For the former case, the correlation length is found to be $1/\xi=2\sinh^{-1}[\sqrt{2J_z -1}/(1-J_z)]$, which diverges around the critical point $J_z=(1/2)^+$.Comment: 7 pages, 6 figure

Universal role of correlation entropy in critical phenomena

In statistical physics, if we successively divide an equilibrium system into two parts, we will face a situation that, within a certain length $\xi$, the physics of a subsystem is no longer the same as the original system. Then the extensive properties of the thermal entropy $S($AB$)= S($A$)+S($B$)$ is violated. This observation motivates us to introduce the concept of correlation entropy between two points, as measured by mutual information in the information theory, to study the critical phenomena. A rigorous relation is established to display some drastic features of the non-vanishing correlation entropy of the subsystem formed by any two distant particles with long-range correlation. This relation actually indicates the universal role of the correlation entropy in understanding critical phenomena. We also verify these analytical studies in terms of two well-studied models for both the thermal and quantum phase transitions: two-dimensional Ising model and one-dimensional transverse field Ising model. Therefore, the correlation entropy provides us with a new physical intuition in critical phenomena from the point of view of the information theory.Comment: 10 pages, 9 figure

Efficient Concentration Protocols for the Single-Photon Entanglement State with Polarization Feature

We propose two efficient entanglement concentration protocols (ECPs) for arbitrary less-entangled single-photon entanglement state, in which the photon qubit has the polarization feature. The first ECP is in linear optics, and the second ECP is in nonlinear optics. The two ECPs have some attractive advantages. First, they can preserve the polarization feature of the photon qubit, while all the other existing ECPs for single photon state cannot achieve this goal. Second, they only require one pair of less-entangled single-photon entanglement state and some auxiliary single photons. Third, they only require local operations. Especially, the second ECP can be used repeatedly, which can increase its success probability largely. Based on above properties, our two ECPs, especially the second one may be useful in current and future quantum communication

Protein disulfide isomerase modulation of TRPV1 controls heat hyperalgesia in chronic pain

Protein disulfide isomerase (PDI) plays a key role in maintaining cellular homeostasis by mediating protein folding via catalyzing disulfide bond formation, breakage, and rearrangement in the endoplasmic reticulum. Increasing evidence suggests that PDI can be a potential treatment target for several diseases. However, the function of PDI in the peripheral sensory nervous system is unclear. Here we report the expression and secretion of PDI from primary sensory neurons is upregulated in inflammatory and neuropathic pain models. Deletion of PDI in nociceptive DRG neurons results in a reduction in inflammatory and neuropathic heat hyperalgesia. We demonstrate that secreted PDI activates TRPV1 channels through oxidative modification of extracellular cysteines of the channel, indicating that PDI acts as an unconventional positive modulator of TRPV1. These findings suggest that PDI in primary sensory neurons plays an important role in development of heat hyperalgesia and can be a potential therapeutic target for chronic pain

Transient elastography with controlled attenuation parameter (CAP) for diagnosis of moderate or severe steatosis in people with suspected non-alcoholic fatty liver disease

© 2020 The Cochrane Collaboration. This article [Turankova T, Blyuss O, Brazhnikov A, Svistunov A, Gurusamy KS, Pavlov CS. Transient elastography with controlled attenuation parameter (CAP) for diagnosis of moderate or severe steatosis in people with suspected non-alcoholic fatty liver disease (Protocol). Cochrane Database of Systematic Reviews 2020, Issue 7. Art. No.: CD013670. DOI: 10.1002/14651858.CD013670.], has been published in final form at https://doi.org/10.1002/14651858.CD013670.Objectives: This is a protocol for a Cochrane Review (diagnostic). The objectives are as follows:. To determine the diagnostic accuracy of transient elastography with CAP for diagnosis of moderate and severe hepatic steatosis in people with suspected NAFLD when compared with liver biopsy as reference standard. To achieve this, we will compare none/mild hepatic steatosis (S0 to S1) versus moderate/severe hepatic steatosis (S2 to S3); and none/mild/moderate hepatic steatosis (S0 to S2) versus severe hepatic steatosis (S3). Secondary objectives We aim to also identify the pooled sensitivity and specificity for the most common cut-off values of CAP for diagnosis of none/mild hepatic steatosis (S0 to S1) and moderate/severe hepatic steatosis (S2 to S3); or none/mild/moderate hepatic steatosis (S0 to S2) and severe hepatic steatosis (S3) in people with suspected NAFLD, and to explore potential sources of heterogeneity influencing the diagnostic test accuracy of CAP (see: Investigations of heterogeneity).Peer reviewe

A comprehensive overview of radioguided surgery using gamma detection probe technology

The concept of radioguided surgery, which was first developed some 60 years ago, involves the use of a radiation detection probe system for the intraoperative detection of radionuclides. The use of gamma detection probe technology in radioguided surgery has tremendously expanded and has evolved into what is now considered an established discipline within the practice of surgery, revolutionizing the surgical management of many malignancies, including breast cancer, melanoma, and colorectal cancer, as well as the surgical management of parathyroid disease. The impact of radioguided surgery on the surgical management of cancer patients includes providing vital and real-time information to the surgeon regarding the location and extent of disease, as well as regarding the assessment of surgical resection margins. Additionally, it has allowed the surgeon to minimize the surgical invasiveness of many diagnostic and therapeutic procedures, while still maintaining maximum benefit to the cancer patient. In the current review, we have attempted to comprehensively evaluate the history, technical aspects, and clinical applications of radioguided surgery using gamma detection probe technology

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

Pan-cancer analysis of whole genomes

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale(1-3). Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter(4); identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation(5,6); analyses timings and patterns of tumour evolution(7); describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity(8,9); and evaluates a range of more-specialized features of cancer genomes(8,10-18).Peer reviewe