106 research outputs found
LongDocFACTScore: Evaluating the Factuality of Long Document Abstractive Summarisation
Maintaining factual consistency is a critical issue in abstractive text
summarisation, however, it cannot be assessed by traditional automatic metrics
used for evaluating text summarisation, such as ROUGE scoring. Recent efforts
have been devoted to developing improved metrics for measuring factual
consistency using pre-trained language models, but these metrics have
restrictive token limits, and are therefore not suitable for evaluating long
document text summarisation. Moreover, there is limited research evaluating
whether existing automatic evaluation metrics are fit for purpose when applied
to long document data sets. In this work, we evaluate the efficacy of automatic
metrics at assessing factual consistency in long document text summarisation
and propose a new evaluation framework LongDocFACTScore. This framework allows
metrics to be extended to any length document. This framework outperforms
existing state-of-the-art metrics in its ability to correlate with human
measures of factuality when used to evaluate long document summarisation data
sets. Furthermore, we show LongDocFACTScore has performance comparable to
state-of-the-art metrics when evaluated against human measures of factual
consistency on short document data sets. We make our code and annotated data
publicly available: https://github.com/jbshp/LongDocFACTScore.Comment: 12 pages, 5 figure
Identity and Counterparthood in a Many Worlds Universe
The Many Worlds Interpretation of quantum mechanics - arguably our most powerfully predictive scientific theory to date - describes a branching Universe composed of an infinite number of quasi-classical macroscopic physical worlds. Though elegant in its straightforward rendering of the mechanics, the Many Worlds Interpretation presents a challenge for understanding identity over time. If we wish to preserve the notion of strict numerical identity, we are faced with the choice between: denying the transitivity of identity; very short-lived lives with near constant death; or accepting that the world is filled with many more individuals than we previously dreamed. In adopting a perdurantist account of identity over time, I argue for this last option. But questions remain about the relationship that branching individuals have to those from whom they’ve split. In this dissertation, I develop a novel account that I call Many Worlds Counterparts. This theory takes its inspiration from Lewis’s Counterpart Theory in offering a modal analysis of de re possibility, but avoids the major challenges that Lewis’s theory faces
Fasting, but not early life stress, increases hypothalamic neuropeptide Y mRNA expression in Japanese quail (Coturnix japonica) chicks.
A light-front coupled-cluster method for the nonperturbative solution of quantum field theories
We propose a new method for the nonperturbative solution of quantum field
theories and illustrate its use in the context of a light-front analog to the
Greenberg--Schweber model. The method is based on light-front quantization and
uses the exponential-operator technique of the many-body coupled-cluster
method. The formulation produces an effective Hamiltonian eigenvalue problem in
the valence Fock sector of the system of interest, combined with nonlinear
integral equations to be solved for the functions that define the effective
Hamiltonian. The method avoids the Fock-space truncations usually used in
nonperturbative light-front Hamiltonian methods and, therefore, does not suffer
from the spectator dependence, Fock-sector dependence, and uncanceled
divergences caused by such truncations.Comment: 11 pages, 4 figures, RevTeX 4.1; expanded description of method and
replaced QED with simpler model for illustratio
The Integration of Optical Stimulation in a Mechanically Dynamic Cell Culture Substrate
A cell culture well with integrated mechanical and optical stimulation is presented. This is achieved by combining dielectric elastomer soft actuators, also known as artificial muscles, and a varifocal micro-electromechanical mirror that couples light from an optical fiber and focuses it onto the transparent cell substrate. The device enables unprecedented control of in vitro cell cultures by allowing the experimenter to tune and synchronize mechanical and optical stimuli, thereby enabling new experimental assays in optogenetics, fluorescent microscopy, or laser stimulation that include dynamic mechanical strain as a controlled input parameter
Combined inverse-forward artificial neural networks for fast and accurate estimation of the diffusion coefficients of cartilage based on multi-physics models
Science CONOPS for Application of SPORT Mission Data to Study Large (~1000km) Ionospheric Plasma Depletions
The Scintillation Prediction Observations Research Task (SPORT) mission is a single 6U CubeSat space weather satellite planned for an October 2022 launch into an ISS-like orbit. The primary purpose of the SPORT mission is to determine the longitudinal effects on equatorial plasma bubble (EPB) growth resulting from the offset dipole magnetic field of the Earth. By combining field and plasma measurements from SPORT with other low-altitude (i.e., alt \u3c 1000 km) spacecraft, it is possible to investigate large-scale (\u3e 1000 km) EPB structures. The types of investigation made possible by measurements from SPORT and other contemporaneous missions include 1) dynamics of depleted magnetic flux tubes; 2) dynamics of field-aligned EPB expansion versus propagation speed; 3) EPB vertical extent; and 4) EPB temporal evolution. To support these investigation types, the respective modes of conjunctions are: 1) simultaneous intersection of a magnetic flux tube; 2) intersection of magnetic flux tube separated in time; 3) Simultaneous Latitude/Longitude position conjunction; and 4) Non-simultaneous latitude/longitude position conjunction. This paper will summarize the SPORT satellite and data used for Science CONOPS to accomplish these objectives
A multi-stage genome-wide association study of bladder cancer identifies multiple susceptibility loci.
We conducted a multi-stage, genome-wide association study of bladder cancer with a primary scan of 591,637 SNPs in 3,532 affected individuals (cases) and 5,120 controls of European descent from five studies followed by a replication strategy, which included 8,382 cases and 48,275 controls from 16 studies. In a combined analysis, we identified three new regions associated with bladder cancer on chromosomes 22q13.1, 19q12 and 2q37.1: rs1014971, (P = 8 × 10⁻¹²) maps to a non-genic region of chromosome 22q13.1, rs8102137 (P = 2 × 10⁻¹¹) on 19q12 maps to CCNE1 and rs11892031 (P = 1 × 10⁻⁷) maps to the UGT1A cluster on 2q37.1. We confirmed four previously identified genome-wide associations on chromosomes 3q28, 4p16.3, 8q24.21 and 8q24.3, validated previous candidate associations for the GSTM1 deletion (P = 4 × 10⁻¹¹) and a tag SNP for NAT2 acetylation status (P = 4 × 10⁻¹¹), and found interactions with smoking in both regions. Our findings on common variants associated with bladder cancer risk should provide new insights into the mechanisms of carcinogenesis
A multi-stage genome-wide association study of bladder cancer identifies multiple susceptibility loci.
We conducted a multi-stage, genome-wide association study of bladder cancer with a primary scan of 591,637 SNPs in 3,532 affected individuals (cases) and 5,120 controls of European descent from five studies followed by a replication strategy, which included 8,382 cases and 48,275 controls from 16 studies. In a combined analysis, we identified three new regions associated with bladder cancer on chromosomes 22q13.1, 19q12 and 2q37.1: rs1014971, (P = 8 × 10⁻¹²) maps to a non-genic region of chromosome 22q13.1, rs8102137 (P = 2 × 10⁻¹¹) on 19q12 maps to CCNE1 and rs11892031 (P = 1 × 10⁻⁷) maps to the UGT1A cluster on 2q37.1. We confirmed four previously identified genome-wide associations on chromosomes 3q28, 4p16.3, 8q24.21 and 8q24.3, validated previous candidate associations for the GSTM1 deletion (P = 4 × 10⁻¹¹) and a tag SNP for NAT2 acetylation status (P = 4 × 10⁻¹¹), and found interactions with smoking in both regions. Our findings on common variants associated with bladder cancer risk should provide new insights into the mechanisms of carcinogenesis
Comparison of Proliferation and Genomic Instability Responses to WRN Silencing in Hematopoietic HL60 and TK6 Cells
BACKGROUND: Werner syndrome (WS) results from defects in the RecQ helicase (WRN) and is characterized by premature aging and accelerated tumorigenesis. Contradictorily, WRN deficient human fibroblasts derived from WS patients show a characteristically slower cell proliferation rate, as do primary fibroblasts and human cancer cell lines with WRN depletion. Previous studies reported that WRN silencing in combination with deficiency in other genes led to significantly accelerated cellular proliferation and tumorigenesis. The aim of the present study was to examine the effects of silencing WRN in p53 deficient HL60 and p53 wild-type TK6 hematopoietic cells, in order to further the understanding of WRN-associated tumorigenesis. METHODOLOGY/PRINCIPAL FINDINGS: We found that silencing WRN accelerated the proliferation of HL60 cells and decreased the cell growth rate of TK6 cells. Loss of WRN increased DNA damage in both cell types as measured by COMET assay, but elicited different responses in each cell line. In HL60 cells, but not in TK6 cells, the loss of WRN led to significant increases in levels of phosphorylated RB and numbers of cells progressing from G1 phase to S phase as shown by cell cycle analysis. Moreover, WRN depletion in HL60 cells led to the hyper-activation of homologous recombination repair via up-regulation of RAD51 and BLM protein levels. This resulted in DNA damage disrepair, apparent by the increased frequencies of both spontaneous and chemically induced structural chromosomal aberrations and sister chromatid exchanges. CONCLUSIONS/SIGNIFICANCE: Together, our data suggest that the effects of WRN silencing on cell proliferation and genomic instability are modulated probably by other genetic factors, including p53, which might play a role in the carcinogenesis induced by WRN deficiency
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