1,609 research outputs found
Pseudogap temperature as a Widom line in doped Mott insulators
The pseudogap refers to an enigmatic state of matter with unusual physical
properties found below a characteristic temperature in hole-doped
high-temperature superconductors. Determining is critical for
understanding this state. Here we study the simplest model of correlated
electron systems, the Hubbard model, with cluster dynamical mean-field theory
to find out whether the pseudogap can occur solely because of strong coupling
physics and short nonlocal correlations. We find that the pseudogap
characteristic temperature is a sharp crossover between different
dynamical regimes along a line of thermodynamic anomalies that appears above a
first-order phase transition, the Widom line. The Widom line emanating from the
critical endpoint of a first-order transition is thus the organizing principle
for the pseudogap phase diagram of the cuprates. No additional broken symmetry
is necessary to explain the phenomenon. Broken symmetry states appear in the
pseudogap and not the other way around.Comment: 6 pages, 4 figures and supplementary information; published versio
Room temperature plasmon laser by total internal reflection
Plasmon lasers create and sustain intense and coherent optical fields below
light's diffraction limit with the unique ability to drastically enhance
light-matter interactions bringing fundamentally new capabilities to
bio-sensing, data storage, photolithography and optical communications.
However, these important applications require room temperature operation, which
remains a major hurdle. Here, we report a room temperature semiconductor
plasmon laser with both strong cavity feedback and optical confinement to
1/20th of the wavelength. The strong feedback arises from total internal
reflection of surface plasmons, while the confinement enhances the spontaneous
emission rate by up to 20 times.Comment: 8 Page, 2 Figure
First clinical evaluation of a novel capacitive ECG system in patients with acute myocardial infarction
Electron-Spin Excitation Coupling in an Electron Doped Copper Oxide Superconductor
High-temperature (high-Tc) superconductivity in the copper oxides arises from
electron or hole doping of their antiferromagnetic (AF) insulating parent
compounds. The evolution of the AF phase with doping and its spatial
coexistence with superconductivity are governed by the nature of charge and
spin correlations and provide clues to the mechanism of high-Tc
superconductivity. Here we use a combined neutron scattering and scanning
tunneling spectroscopy (STS) to study the Tc evolution of electron-doped
superconducting Pr0.88LaCe0.12CuO4-delta obtained through the oxygen annealing
process. We find that spin excitations detected by neutron scattering have two
distinct modes that evolve with Tc in a remarkably similar fashion to the
electron tunneling modes in STS. These results demonstrate that
antiferromagnetism and superconductivity compete locally and coexist spatially
on nanometer length scales, and the dominant electron-boson coupling at low
energies originates from the electron-spin excitations.Comment: 30 pages, 12 figures, supplementary information include
Widespread Expression of BORIS/CTCFL in Normal and Cancer Cells
BORIS (CTCFL) is the paralog of CTCF (CCCTC-binding factor; NM_006565), a ubiquitously expressed DNA-binding protein with diverse roles in gene expression and chromatin organisation. BORIS and CTCF have virtually identical zinc finger domains, yet display major differences in their respective C- and N-terminal regions. Unlike CTCF, BORIS expression has been reported only in the testis and certain malignancies, leading to its classification as a “cancer-testis” antigen. However, the expression pattern of BORIS is both a significant and unresolved question in the field of DNA binding proteins. Here, we identify BORIS in the cytoplasm and nucleus of a wide range of normal and cancer cells. We compare the localization of CTCF and BORIS in the nucleus and demonstrate enrichment of BORIS within the nucleolus, inside the nucleolin core structure and adjacent to fibrillarin in the dense fibrillar component. In contrast, CTCF is not enriched in the nucleolus. Live imaging of cells transiently transfected with GFP tagged BORIS confirmed the nucleolar accumulation of BORIS. While BORIS transcript levels are low compared to CTCF, its protein levels are readily detectable. These findings show that BORIS expression is more widespread than previously believed, and suggest a role for BORIS in nucleolar function
Internet-based medical education: a realist review of what works, for whom and in what circumstances
http://creativecommons.org/licenses/by/2.0
Cryptosporidium Priming Is More Effective than Vaccine for Protection against Cryptosporidiosis in a Murine Protein Malnutrition Model
Cryptosporidium is a major cause of severe diarrhea, especially in malnourished children. Using a murine model of C. parvum oocyst challenge that recapitulates clinical features of severe cryptosporidiosis during malnutrition, we interrogated the effect of protein malnutrition (PM) on primary and secondary responses to C. parvum challenge, and tested the differential ability of mucosal priming strategies to overcome the PM-induced susceptibility. We determined that while PM fundamentally alters systemic and mucosal primary immune responses to Cryptosporidium, priming with C. parvum (106 oocysts) provides robust protective immunity against re-challenge despite ongoing PM. C. parvum priming restores mucosal Th1-type effectors (CD3+CD8+CD103+ T-cells) and cytokines (IFNγ, and IL12p40) that otherwise decrease with ongoing PM. Vaccination strategies with Cryptosporidium antigens expressed in the S. Typhi vector 908htr, however, do not enhance Th1-type responses to C. parvum challenge during PM, even though vaccination strongly boosts immunity in challenged fully nourished hosts. Remote non-specific exposures to the attenuated S. Typhi vector alone or the TLR9 agonist CpG ODN-1668 can partially attenuate C. parvum severity during PM, but neither as effectively as viable C. parvum priming. We conclude that although PM interferes with basal and vaccine-boosted immune responses to C. parvum, sustained reductions in disease severity are possible through mucosal activators of host defenses, and specifically C. parvum priming can elicit impressively robust Th1-type protective immunity despite ongoing protein malnutrition. These findings add insight into potential correlates of Cryptosporidium immunity and future vaccine strategies in malnourished children
Modulation of enhancer looping and differential gene targeting by Epstein-Barr virus transcription factors directs cellular reprogramming
Epstein-Barr virus (EBV) epigenetically reprogrammes B-lymphocytes to drive immortalization and facilitate viral persistence. Host-cell transcription is perturbed principally through the actions of EBV EBNA 2, 3A, 3B and 3C, with cellular genes deregulated by specific combinations of these EBNAs through unknown mechanisms. Comparing human genome binding by these viral transcription factors, we discovered that 25% of binding sites were shared by EBNA 2 and the EBNA 3s and were located predominantly in enhancers. Moreover, 80% of potential EBNA 3A, 3B or 3C target genes were also targeted by EBNA 2, implicating extensive interplay between EBNA 2 and 3 proteins in cellular reprogramming. Investigating shared enhancer sites neighbouring two new targets (WEE1 and CTBP2) we discovered that EBNA 3 proteins repress transcription by modulating enhancer-promoter loop formation to establish repressive chromatin hubs or prevent assembly of active hubs. Re-ChIP analysis revealed that EBNA 2 and 3 proteins do not bind simultaneously at shared sites but compete for binding thereby modulating enhancer-promoter interactions. At an EBNA 3-only intergenic enhancer site between ADAM28 and ADAMDEC1 EBNA 3C was also able to independently direct epigenetic repression of both genes through enhancer-promoter looping. Significantly, studying shared or unique EBNA 3 binding sites at WEE1, CTBP2, ITGAL (LFA-1 alpha chain), BCL2L11 (Bim) and the ADAMs, we also discovered that different sets of EBNA 3 proteins bind regulatory elements in a gene and cell-type specific manner. Binding profiles correlated with the effects of individual EBNA 3 proteins on the expression of these genes, providing a molecular basis for the targeting of different sets of cellular genes by the EBNA 3s. Our results therefore highlight the influence of the genomic and cellular context in determining the specificity of gene deregulation by EBV and provide a paradigm for host-cell reprogramming through modulation of enhancer-promoter interactions by viral transcription factors
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