Momentum Kick Model Description of the Ridge in (Delta-phi)-(Delta eta) Correlation in pp Collisions at 7 TeV

The near-side ridge structure in the (Delta phi)-(Delta eta) correlation observed by the CMS Collaboration for pp collisions at 7 TeV at LHC can be explained by the momentum kick model in which the ridge particles are medium partons that suffer a collision with the jet and acquire a momentum kick along the jet direction. Similar to the early medium parton momentum distribution obtained in previous analysis for nucleus-nucleus collisions at 0.2 TeV, the early medium parton momentum distribution in pp collisions at 7 TeV exhibits a rapidity plateau as arising from particle production in a flux tube.Comment: Talk presented at Workshop on High-pT Probes of High-Density QCD at the LHC, Palaiseau, May 30-June2, 201

Thermodynamic Geometry and Critical Behavior of Black Holes

Based on the observations that there exists an analogy between the Reissner-Nordstr\"om-anti-de Sitter (RN-AdS) black holes and the van der Waals-Maxwell liquid-gas system, in which a correspondence of variables is $(\phi, q) \leftrightarrow (V,P)$, we study the Ruppeiner geometry, defined as Hessian matrix of black hole entropy with respect to the internal energy (not the mass) of black hole and electric potential (angular velocity), for the RN, Kerr and RN-AdS black holes. It is found that the geometry is curved and the scalar curvature goes to negative infinity at the Davies' phase transition point for the RN and Kerr black holes. Our result for the RN-AdS black holes is also in good agreement with the one about phase transition and its critical behavior in the literature.Comment: Revtex, 18 pages including 4 figure

The phase transition and the Quasi-Normal Modes of black Holes

We reexamined the argument that the quasinormal modes could be a probe of the phase transition of a topological black hole to a hairy configuration by investigating general scalar perturbations. We found further evidence in the quasinormal modes for this phase transition. For the general black hole configurations, we observed that although the quasinormal modes can present us different phases of different configurations, there is no dramatic change in the slope of quasinormal frequencies at the critical point of the phase transition. More detailed studies of quasinormal modes are needed to reveal the subtle behavior of the phase transition.Comment: Revised version, accepted for publication in JHE

Epstein-Barr virus-encoded EBNA1 inhibits the canonical NF-κB pathway in carcinoma cells by inhibiting IKK phosphorylation

Background The Epstein-Barr virus (EBV)-encoded EBNA1 protein is expressed in all EBV-associated tumours, including undifferentiated nasopharyngeal carcinoma (NPC), where it is indispensable for viral replication, genome maintenance and viral gene expression. EBNA1's transcription factor-like functions also extend to influencing the expression of cellular genes involved in pathways commonly dysregulated during oncogenesis, including elevation of AP-1 activity in NPC cell lines resulting in enhancement of angiogenesis in vitro. In this study we sought to extend these observations by examining the role of EBNA1 upon another pathway commonly deregulated during carcinogenesis; namely NF-κB. Results In this report we demonstrate that EBNA1 inhibits the canonical NF-κB pathway in carcinoma lines by inhibiting the phosphorylation of IKKα/β. In agreement with this observation we find a reduction in the phosphorylation of IκBα and reduced phosphorylation and nuclear translocation of p65, resulting in a reduction in the amount of p65 in nuclear NF-κB complexes. Similar effects were also found in carcinoma lines infected with recombinant EBV and in the EBV-positive NPC-derived cell line C666-1. Inhibition of NF-κB was dependent upon regions of EBNA1 essential for gene transactivation whilst the interaction with the deubiquitinating enzyme, USP7, was entirely dispensable. Furthermore, in agreement with EBNA1 inhibiting p65 NF-κB we demonstrate that p65 was exclusively cytoplasmic in 11 out of 11 NPC tumours studied. Conclusions Inhibition of p65 NF-κB in murine and human epidermis results in tissue hyperplasia and the development of squamous cell carcinoma. In line with this, p65 knockout fibroblasts have a transformed phenotype. Inhibition of p65 NF-κB by EBNA1 may therefore contribute to the development of NPC by inducing tissue hyperplasia. Furthermore, inhibition of NF-κB is employed by viruses as an immune evasion strategy which is also closely linked to oncogenesis during persistent viral infection. Our findings therefore further implicate EBNA1 in playing an important role in the pathogenesis of NPC

Reflective imaging improves spatiotemporal resolution and collection efficiency in light sheet microscopy

© The Author(s), 2017. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Nature Communications 8 (2017): 1452, doi:10.1038/s41467-017-01250-8.Light-sheet fluorescence microscopy (LSFM) enables high-speed, high-resolution, and gentle imaging of live specimens over extended periods. Here we describe a technique that improves the spatiotemporal resolution and collection efficiency of LSFM without modifying the underlying microscope. By imaging samples on reflective coverslips, we enable simultaneous collection of four complementary views in 250 ms, doubling speed and improving information content relative to symmetric dual-view LSFM. We also report a modified deconvolution algorithm that removes associated epifluorescence contamination and fuses all views for resolution recovery. Furthermore, we enhance spatial resolution (to <300 nm in all three dimensions) by applying our method to single-view LSFM, permitting simultaneous acquisition of two high-resolution views otherwise difficult to obtain due to steric constraints at high numerical aperture. We demonstrate the broad applicability of our method in a variety of samples, studying mitochondrial, membrane, Golgi, and microtubule dynamics in cells and calcium activity in nematode embryos.This work was supported by the Intramural Research Program of the National Institute of Biomedical Imaging and Bioengineering at the National Institutes of Health. P.L. and H.S. acknowledge summer support from the Marine Biological Laboratory at Woods Hole, through the Whitman- and Fellows- program. P.L. acknowledges support from NIH National Institute of Biomedical Imaging and Bioengineering (NIBIB) of the National Institutes of Health (NIH) under grant number R01EB017293. C.S. acknowledges funding from the National Institute of General Medical Sciences of NIH under Award Number R25GM109439 (Project Title: University of Chicago Initiative for Maximizing Student Development [IMSD]) and NIBIB under grant number T32 EB002103. Partial funding for the computation in this work was provided by NIH grant numbers S10 RRO21039 and P30 CA14599. A.U. and I.R.-S. were supported by the NSF grant number 1607645

Dysregulation of Cell Survival in Diffuse Large B Cell Lymphoma: Mechanisms and Therapeutic Targets

Diffuse large B cell lymphoma (DLBCL) is the most common type of lymphoma worldwide, representing 30–40% of non-Hodgkin lymphomas, and is clinically aggressive. Although more than half of patients with DLBCL are cured by using standard first-line immunochemotherapy, the remaining patients are refractory to the first-line therapy or relapse after complete remission and these patients require novel therapeutic approaches. Understanding the pathogenesis of DLBCL is essential for identifying therapeutic targets to tackle this disease. Cell survival dysregulation, a hallmark of cancer, is a characteristic feature of DLBCL. Intrinsic signaling aberrations, tumor microenvironment dysfunction, and viral factors can all contribute to the cell survival dysregulation in DLBCL. In recent years, several novel drugs that target abnormal cell survival pathways, have been developed and tested in clinical trials of patients with DLBCL. In this review, we discuss cell survival dysregulation, the underlying mechanisms, and how to target abnormal cell survival therapeutically in DLBCL patients

Fecal Contamination of Shallow Tubewells in Bangladesh Inversely Related to Arsenic

The health risks of As exposure due to the installation of millions of shallow tubewells in the Bengal Basin are known, but fecal contamination of shallow aquifers has not systematically been examined. This could be a source of concern in densely populated areas with poor sanitation because the hydraulic travel time from surface water bodies to shallow wells that are low in As was previously shown to be considerably shorter than for shallow wells that are high in As. In this study, 125 tubewells 6−36 m deep were sampled in duplicate for 18 months to quantify the presence of the fecal indicator Escherichia coli. On any given month, E. coli was detected at levels exceeding 1 most probable number per 100 mL in 19−64% of all shallow tubewells, with a higher proportion typically following periods of heavy rainfall. The frequency of E. coli detection averaged over a year was found to increase with population surrounding a well and decrease with the As content of a well, most likely because of downward transport of E. coli associated with local recharge. The health implications of higher fecal contamination of shallow tubewells, to which millions of households in Bangladesh have switched in order to reduce their exposure to As, need to be evaluated