Topological phase-fluctuations, amplitude fluctuations, and criticality in extreme type-II superconductors

We study the effect of critical fluctuations on the $(B,T)$ phase diagram in extreme type-II superconductors in zero and finite magnetic field using large-scale Monte Carlo simulations on the Ginzburg-Landau model in a frozen gauge approximation. We show that a vortex-loop unbinding gives a correct picture of the zero field superconducting-normal transition even in the presence of amplitude fluctuations, which are far from being critical at $T_c$. We extract critical exponents of the dual model by studying the topological excitations of the original model. From the vortex-loop distribution function we extract the anomalous dimension of the dual field $\eta \simeq -0.18$, and conclude that the charged Ginzburg-Landau model and the neutral 3DXY model belong to different universality classes. We find are two distinct scaling regimes for the vortex-line lattice melting line: a high-field scaling regime and a distinct low-field 3DXY critical scaling regime. We also find indications of an abrupt change in the connectivity of the vortex-tangle in the vortex liquid along a line $T_L \geq T_M$. This is the finite field counter-part of the zero-field vortex-loop blowout. Which at low enough fields appears to coincide with $T_M$. Here, a description of the vortex system only in terms of field induced vortex lines is inadequate at and above the VLL melting temperature.Comment: 30 pages, 14 figure

Extreme Type-II Superconductors in a Magnetic Field: A Theory of Critical Fluctuations

A theory of critical fluctuations in extreme type-II superconductors subjected to a finite but weak external magnetic field is presented. It is shown that the standard Ginzburg-Landau representation of this problem can be recast, with help of a novel mapping, as a theory of a new "superconductor", in an effective magnetic field whose overall value is zero, consisting of the original uniform field and a set of neutralizing unit fluxes attached to $N_{\Phi}$ fluctuating vortex lines. The long distance behavior is related to the anisotropic gauge theory in which the original magnetic field plays the role of "charge". The consequences of this "gauge theory" scenario for the critical behavior in high temperature superconductors are explored in detail, with particular emphasis on questions of 3D XY vs. Landau level scaling, physical nature of the vortex "line liquid" and the true normal state, and fluctuation thermodynamics and transport. A "minimal" set of requirements for the theory of vortex-lattice melting in the critical region is also proposed and discussed.Comment: 28 RevTeX pages, 4 .ps figures; appendix A added, additional references, streamlined Secs. IV and V in response to referees' comment

MiRNA Profile Associated with Replicative Senescence, Extended Cell Culture, and Ectopic Telomerase Expression in Human Foreskin Fibroblasts

Senescence is a highly regulated process that limits cellular replication by enforcing a G1 arrest in response to various stimuli. Replicative senescence occurs in response to telomeric DNA erosion, and telomerase expression can offset replicative senescence leading to immortalization of many human cells. Limited data exists regarding changes of microRNA (miRNA) expression during senescence in human cells and no reports correlate telomerase expression with regulation of senescence-related miRNAs. We used miRNA microarrays to provide a detailed account of miRNA profiles for early passage and senescent human foreskin (BJ) fibroblasts as well as early and late passage immortalized fibroblasts (BJ-hTERT) that stably express the human telomerase reverse transcriptase subunit hTERT. Selected miRNAs that were differentially expressed in senescence were assayed for expression in quiescent cells to identify miRNAs that are specifically associated with senescence-associated growth arrest. From this group of senescence-associated miRNAs, we confirmed the ability of miR-143 to induce growth arrest after ectopic expression in young fibroblasts. Remarkably, miR-143 failed to induce growth arrest in BJ-hTERT cells. Importantly, the comparison of late passage immortalized fibroblasts to senescent wild type fibroblasts reveals that miR-146a, a miRNA with a validated role in regulating the senescence associated secretory pathway, is also regulated during extended cell culture independently of senescence. The discovery that miRNA expression is impacted by expression of ectopic hTERT as well as extended passaging in immortalized fibroblasts contributes to a comprehensive understanding of the connections between telomerase expression, senescence and processes of cellular aging

Nature of the Low Field Transition in the Mixed State of High Temperature Superconductors

We have numerically studied the statics and dynamics of a model three-dimensional vortex lattice at low magnetic fields. For the statics we use a frustrated 3D XY model on a stacked triangular lattice. We model the dynamics as a coupled network of overdamped resistively-shunted Josephson junctions with Langevin noise. At low fields, there is a weakly first-order phase transition, at which the vortex lattice melts into a line liquid. Phase coherence parallel to the field persists until a sharp crossover, conceivably a phase transition, near $T_{\ell} > T_m$ which develops at the same temperature as an infinite vortex tangle. The calculated flux flow resistivity in various geometries near $T=T_{\ell}$ closely resembles experiment. The local density of field induced vortices increases sharply near $T_\ell$, corresponding to the experimentally observed magnetization jump. We discuss the nature of a possible transition or crossover at $T_\ell$(B) which is distinct from flux lattice melting.Comment: Updated references. 46 pages including low quality 25 eps figures. Contact [email protected] or visit http://www.physics.ohio-state.edu:80/~ryu/ for better figures and additional movie files from simulations. To be published in Physical Review B1 01Jun9

Whole-Genome Sequencing of Sake Yeast Saccharomyces cerevisiae Kyokai no. 7

The term ‘sake yeast’ is generally used to indicate the Saccharomyces cerevisiae strains that possess characteristics distinct from others including the laboratory strain S288C and are well suited for sake brewery. Here, we report the draft whole-genome shotgun sequence of a commonly used diploid sake yeast strain, Kyokai no. 7 (K7). The assembled sequence of K7 was nearly identical to that of the S288C, except for several subtelomeric polymorphisms and two large inversions in K7. A survey of heterozygous bases between the homologous chromosomes revealed the presence of mosaic-like uneven distribution of heterozygosity in K7. The distribution patterns appeared to have resulted from repeated losses of heterozygosity in the ancestral lineage of K7. Analysis of genes revealed the presence of both K7-acquired and K7-lost genes, in addition to numerous others with segmentations and terminal discrepancies in comparison with those of S288C. The distribution of Ty element also largely differed in the two strains. Interestingly, two regions in chromosomes I and VII of S288C have apparently been replaced by Ty elements in K7. Sequence comparisons suggest that these gene conversions were caused by cDNA-mediated recombination of Ty elements. The present study advances our understanding of the functional and evolutionary genomics of the sake yeast

A Mutation in the Gene Encoding Mitochondrial Mg2+ Channel MRS2 Results in Demyelination in the Rat

The rat demyelination (dmy) mutation serves as a unique model system to investigate the maintenance of myelin, because it provokes severe myelin breakdown in the central nervous system (CNS) after normal postnatal completion of myelination. Here, we report the molecular characterization of this mutation and discuss the possible pathomechanisms underlying demyelination. By positional cloning, we found that a G-to-A transition, 177 bp downstream of exon 3 of the Mrs2 (MRS2 magnesium homeostasis factor (Saccharomyces cerevisiae)) gene, generated a novel splice acceptor site which resulted in functional inactivation of the mutant allele. Transgenic rescue with wild-type Mrs2-cDNA validated our findings. Mrs2 encodes an essential component of the major Mg2+ influx system in mitochondria of yeast as well as human cells. We showed that the dmy/dmy rats have major mitochondrial deficits with a markedly elevated lactic acid concentration in the cerebrospinal fluid, a 60% reduction in ATP, and increased numbers of mitochondria in the swollen cytoplasm of oligodendrocytes. MRS2-GFP recombinant BAC transgenic rats showed that MRS2 was dominantly expressed in neurons rather than oligodendrocytes and was ultrastructurally observed in the inner membrane of mitochondria. Our observations led to the conclusion that dmy/dmy rats suffer from a mitochondrial disease and that the maintenance of myelin has a different mechanism from its initial production. They also established that Mg2+ homeostasis in CNS mitochondria is essential for the maintenance of myelin

Automatic Detection of User Abilities through the SmartAbility Framework

This paper presents a proposed smartphone application for the unique SmartAbility Framework that supports interaction with technology for people with reduced physical ability, through focusing on the actions that they can perform independently. The Framework is a culmination of knowledge obtained through previously conducted technology feasibility trials and controlled usability evaluations involving the user community. The Framework is an example of ability-based design that focuses on the abilities of users instead of their disabilities. The paper includes a summary of Versions 1 and 2 of the Framework, including the results of a two-phased validation approach, conducted at the UK Mobility Roadshow and via a focus group of domain experts. A holistic model developed by adapting the House of Quality (HoQ) matrix of the Quality Function Deployment (QFD) approach is also described. A systematic literature review of sensor technologies built into smart devices establishes the capabilities of sensors in the Android and iOS operating systems. The review defines a set of inclusion and exclusion criteria, as well as search terms used to elicit literature from online repositories. The key contribution is the mapping of ability-based sensor technologies onto the Framework, to enable the future implementation of a smartphone application. Through the exploitation of the SmartAbility application, the Framework will increase technology amongst people with reduced physical ability and provide a promotional tool for assistive technology manufacturers

The SOX2 response program in glioblastoma multiforme: an integrated ChIP-seq, expression microarray, and microRNA analysis

<p>Abstract</p> <p>Background</p> <p><it>SOX2 </it>is a key gene implicated in maintaining the stemness of embryonic and adult stem cells. <it>SOX2 </it>appears to re-activate in several human cancers including glioblastoma multiforme (GBM), however, the detailed response program of <it>SOX2 </it>in GBM has not yet been defined.</p> <p>Results</p> <p>We show that knockdown of the <it>SOX2 </it>gene in LN229 GBM cells reduces cell proliferation and colony formation. We then comprehensively characterize the <it>SOX2 </it>response program by an integrated analysis using several advanced genomic technologies including ChIP-seq, microarray profiling, and microRNA sequencing. Using ChIP-seq technology, we identified 4883 <it>SOX2 </it>binding regions in the GBM cancer genome. <it>SOX2 </it>binding regions contain the consensus sequence wwTGnwTw that occurred 3931 instances in 2312 <it>SOX2 </it>binding regions. Microarray analysis identified 489 genes whose expression altered in response to <it>SOX2 </it>knockdown. Interesting findings include that <it>SOX2 </it>regulates the expression of SOX family proteins <it>SOX1 </it>and <it>SOX18</it>, and that <it>SOX2 </it>down regulates <it>BEX1 </it>(brain expressed X-linked 1) and <it>BEX2 </it>(brain expressed X-linked 2), two genes with tumor suppressor activity in GBM. Using next generation sequencing, we identified 105 precursor microRNAs (corresponding to 95 mature miRNAs) regulated by <it>SOX2</it>, including down regulation of miR-143, -145, -253-5p and miR-452. We also show that miR-145 and <it>SOX2 </it>form a double negative feedback loop in GBM cells, potentially creating a bistable system in GBM cells.</p> <p>Conclusions</p> <p>We present an integrated dataset of ChIP-seq, expression microarrays and microRNA sequencing representing the <it>SOX2 </it>response program in LN229 GBM cells. The insights gained from our integrated analysis further our understanding of the potential actions of <it>SOX2 </it>in carcinogenesis and serves as a useful resource for the research community.</p