2,845 research outputs found

    Tracking continuous gravitational waves from a neutron star at once and twice the spin frequency with a hidden Markov model

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    Searches for continuous gravitational waves from rapidly spinning neutron stars normally assume that the star rotates about one of its principal axes of moment of inertia, and hence the gravitational radiation emits only at twice the spin frequency of the star, 2f∗2f_*. The superfluid interior of a star pinned to the crust along an axis nonaligned with any of its principal axes allows the star to emit gravitational waves at both f∗f_* and 2f∗2f_*, even without free precession, a phenomenon not clearly observed in known pulsars. The dual-harmonic emission mechanism motivates searches combining the two frequency components of a signal to improve signal-to-noise ratio. We describe an economical, semicoherent, dual-harmonic search method, combined with a maximum likelihood coherent matched filter, F-statistic, and improved from an existing hidden Markov model (HMM) tracking scheme to track two frequency components simultaneously. We validate the method and demonstrate its performance through Monte Carlo simulations. We find that for sources emitting gravitational waves at both f∗f_* and 2f∗2f_*, the rate of correctly recovering synthetic signals (i.e., detection efficiency), at a given false alarm probability, can be improved by ∼10\sim 10%-70% by tracking two frequencies simultaneously compared to tracking a single component only. For sources emitting at 2f∗2f_* only, dual-harmonic tracking only leads to minor sensitivity loss, producing ≲10%\lesssim 10\% lower detection efficiency than tracking a single component. In directed continuous-wave searches where f∗f_* is unknown and hence the full frequency band is searched, the computationally efficient HMM tracking algorithm provides an option of conducting both the dual-harmonic search and the conventional single frequency tracking to obtain optimal sensitivity, with a typical run time of ∼103\sim 10^3 core-hr for one year's observation

    The imprint of superradiance on hierarchical black hole mergers

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    Ultralight bosons are a proposed solution to outstanding problems in cosmology and particle physics: they provide a dark-matter candidate while potentially explaining the strong charge-parity problem. If they exist, ultralight bosons can interact with black holes through the superradiant instability. In this work we explore the consequences of this instability on the evolution of hierarchical black holes within dense stellar clusters. By reducing the spin of individual black holes, superradiance reduce the recoil velocity of merging binary black holes, which, in turn, increases the retention fraction of hierarchical merger remnants. We show that the existence of ultralight bosons with mass 2×10−14≲μ/eV≲2×10−13 2\times10^{-14}\lesssim \mu/\textrm{eV} \lesssim2\times10^{-13} would lead to an increased rate of hierarchical black hole mergers in nuclear star clusters. An ultralight boson in this energy range would result in up to ≈60%\approx60\% more present-day nuclear star clusters supporting hierarchical growth. The presence of an ultralight boson can also double the rate of intermediate mass black hole mergers to ≈0.08\approx0.08\,Gpc−3^{-3}\,yr−1^{-1} in the local Universe. These results imply that a select range of ultralight boson mass can have far-reaching consequences for the population of black holes in dense stellar environments. Future studies into black hole cluster populations and the spin distribution of hierarchically formed black holes will test this scenario.Comment: 20 pages, 7 figure

    Tracking continuous gravitational waves from a neutron star at once and twice the spin frequency with a hidden Markov model

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    Searches for continuous gravitational waves from rapidly spinning neutron stars normally assume that the star rotates about one of its principal axes of moment of inertia, and hence the gravitational radiation emits only at twice the spin frequency of the star, 2f⋆. The superfluid interior of a star pinned to the crust along an axis nonaligned with any of its principal axes allows the star to emit gravitational waves at both f⋆ and 2f⋆, even without free precession, a phenomenon not clearly observed in known pulsars. The dual-harmonic emission mechanism motivates searches combining the two frequency components of a signal to improve signal-to-noise ratio. We describe an economical, semicoherent, dual-harmonic search method, combined with a maximum likelihood coherent matched filter, F-statistic, and improved from an existing hidden Markov model (HMM) tracking scheme to track two frequency components simultaneously. We validate the method and demonstrate its performance through Monte Carlo simulations. We find that for sources emitting gravitational waves at both f⋆ and 2f⋆, the rate of correctly recovering synthetic signals (i.e., detection efficiency), at a given false alarm probability, can be improved by ∼10%–70% by tracking two frequencies simultaneously compared to tracking a single component only. For sources emitting at 2f⋆ only, dual-harmonic tracking only leads to minor sensitivity loss, producing ≲10% lower detection efficiency than tracking a single component. In directed continuous-wave searches where f⋆ is unknown and hence the full frequency band is searched, the computationally efficient HMM tracking algorithm provides an option of conducting both the dual-harmonic search and the conventional single frequency tracking to obtain optimal sensitivity, with a typical run time of ∼10^3 core-hr for one year’s observation

    Epstein-Barr Virus BART9 miRNA Modulates LMP1 Levels and Affects Growth Rate of Nasal NK T Cell Lymphomas

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    Nasal NK/T cell lymphomas (NKTCL) are a subset of aggressive Epstein-Barr virus (EBV)-associated non-Hodgkin's lymphomas. The role of EBV in pathogenesis of NKTCL is not clear. Intriguingly, EBV encodes more than 40 microRNAs (miRNA) that are differentially expressed and largely conserved in lymphocryptoviruses. While miRNAs play a critical role in the pathogenesis of cancer, especially lymphomas, the expression and function of EBV transcribed miRNAs in NKTCL are not known. To examine the role of EBV miRNAs in NKTCL, we used microarray profiling and qRT-PCR to identify and validate expression of viral miRNAs in SNK6 and SNT16 cells, which are two independently derived NKTCL cell lines that maintain the type II EBV latency program. All EBV BART miRNAs except BHRF-derived miRNAs were expressed and some of these miRNAs are expressed at higher levels than in nasopharyngeal carcinomas. Modulating the expression of BART9 with antisense RNAs consistently reduced SNK6 and SNT16 proliferation, while antisense RNAs to BARTs-7 and -17-5p affected proliferation only in SNK6 cells. Furthermore, the EBV LMP-1 oncoprotein and transcript levels were repressed when an inhibitor of BART9 miRNA was transfected into SNK6 cells, and overexpression of BART9 miRNA increased LMP-1 protein and mRNA expression. Our data indicate that BART9 is involved in NKTCL proliferation, and one of its mechanisms of action appears to be regulating LMP-1 levels. Our findings may have direct application for improving NKTCL diagnosis and for developing possible novel treatment approaches for this tumor, for which current chemotherapeutic drugs have limited effectiveness

    Atoh1-dependent rhombic lip neurons are required for temporal delay between independent respiratory oscillators in embryonic mice

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    All motor behaviors require precise temporal coordination of different muscle groups. Breathing, for example, involves the sequential activation of numerous muscles hypothesized to be driven by a primary respiratory oscillator, the preBotzinger Complex, and at least one other as-yet unidentified rhythmogenic population. We tested the roles of Atoh1-, Phox2b-, and Dbx1-derived neurons (three groups that have known roles in respiration) in the generation and coordination of respiratory output in embryonic mice. We found that Dbx1-derived neurons are necessary for all respiratory behaviors, whereas independent but coupled respiratory rhythms persist from at least three different motor pools after eliminating or silencing Phox2b-or Atoh1-expressing hindbrain neurons. Without Atoh1 neurons, however, the motor pools become temporally disorganized and coupling between independent respiratory oscillators decreases. We propose Atoh1 neurons tune the sequential activation of independent oscillators essential for the fine control of different muscles during breathing

    Polymorphisms in the SOCS7 gene and glucose homeostasis traits

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    BACKGROUND: SOCS7 is a member of the suppressor of cytokine signaling family of proteins and is expressed in skeletal muscle and islets. SOCS7 deficient mice develop islet hyperplasia in the setting of increased insulin sensitivity and normal glucose tolerance. The objective of this study was to determine if variants in SOCS7 play a role in variation of glucose and insulin levels and the development of type 2 diabetes (T2DM). RESULTS: Five SOCS7 tagging SNPs were genotyped in diabetic and nondiabetic Old Order Amish. A case–control study was performed in T2DM (n = 145) and normal glucose tolerant (n = 358) subjects. Nominal associations were observed with T2DM and the minor alleles for rs8068600 (P = 0.01) and rs8074124 (P = 0.04); however, only rs8068600 remained significant after Bonferroni adjustment for multiple comparisons (P = 0.01). Among nondiabetic Amish (n = 765), no significant associations with glucose or insulin traits including fasting or 2 hour glucose and insulin from the oral glucose tolerance test, insulin or glucose area under the curve, Matsuda Index or HOMA-IR were found for any of the SNPs. CONCLUSION: In conclusion, genetic variants in the SOCS7 gene do not impact variation in glucose homeostasis traits and only minimally impact risk of T2DM in the Old Order Amish. Our study was not able to address whether rare variants that potentially impact gene function might influence T2DM risk

    Reentrant Peak Effect in an anisotropic superconductor 2H-NbSe_2 : Role of disorder

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    The reentrant nature of Peak Effect is established in a single crystal of 2H-NbSe_2 via electrical transport and dc magnetisation studies. The role of disorder on the reentrant branch of PE has been examined in three single crystals with varying levels of quenched random disorder. Increasing disorder presumably shrinks the (H,T) parameter space over which vortex array retains spatial order. Although, the upper branch of the PE curve is somewhat robust, the lower reentrant branch of the same curve is strongly affected by disorder.Comment: 5 Pages of text, 4 figure

    Phosphatidylinositol-4,5 Bisphosphate Produced by PIP5K(gamma) Regulates Gelsolin, Actin Assembly, and Adhesion Strength of N-Cadherin Junctions

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    Phosphoinositides regulate several actin-binding proteins but their role at intercellular adhesions has not been defined. We found that phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) was generated at sites of N-cadherin–mediated intercellular adhesion and was a critical regulator of intercellular adhesion strength. Immunostaining for PI(4,5)P2 or transfection with GFP-PH-PLCδ showed that PI(4,5)P2 was enriched at sites of N-cadherin adhesions and this enrichment required activated Rac1. Isoform-specific immunostaining for type I phosphatidylinositol 4-phosphate 5 kinase (PIP5KI) showed that PIP5KIγ was spatially associated with N-cadherin–Fc beads. Association of PIP5KIγ with N-cadherin adhesions was in part dependent on the activation of RhoA. Transfection with catalytically inactive PIP5KIγ blocked the enrichment of PI(4,5)P2 around beads. Catalytically inactive PIP5KIγ or a cell-permeant peptide that mimics and competes for the PI(4,5)P2-binding region of the actin-binding protein gelsolin inhibited incorporation of actin monomers in response to N-cadherin ligation and reduced intercellular adhesion strength by more than twofold. Gelsolin null fibroblasts transfected with a gelsolin severing mutant containing an intact PI(4,5)P2 binding region, demonstrated intercellular adhesion strength similar to wild-type transfected controls. We conclude that PIP5KIγ-mediated generation of PI(4,5)P2 at sites of N-cadherin contacts regulates intercellular adhesion strength, an effect due in part to PI(4,5)P2-mediated regulation of gelsolin
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