3,292 research outputs found

    Neutron Calibration Sources in the Daya Bay Experiment

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    We describe the design and construction of the low rate neutron calibration sources used in the Daya Bay Reactor Anti-neutrino Experiment. Such sources are free of correlated gamma-neutron emission, which is essential in minimizing induced background in the anti-neutrino detector. The design characteristics have been validated in the Daya Bay anti-neutrino detector.Comment: 13 pages, 7 figure

    Automatic Defect Detection for TFT-LCD Array Process Using Quasiconformal Kernel Support Vector Data Description

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    Defect detection has been considered an efficient way to increase the yield rate of panels in thin film transistor liquid crystal display (TFT-LCD) manufacturing. In this study we focus on the array process since it is the first and key process in TFT-LCD manufacturing. Various defects occur in the array process, and some of them could cause great damage to the LCD panels. Thus, how to design a method that can robustly detect defects from the images captured from the surface of LCD panels has become crucial. Previously, support vector data description (SVDD) has been successfully applied to LCD defect detection. However, its generalization performance is limited. In this paper, we propose a novel one-class machine learning method, called quasiconformal kernel SVDD (QK-SVDD) to address this issue. The QK-SVDD can significantly improve generalization performance of the traditional SVDD by introducing the quasiconformal transformation into a predefined kernel. Experimental results, carried out on real LCD images provided by an LCD manufacturer in Taiwan, indicate that the proposed QK-SVDD not only obtains a high defect detection rate of 96%, but also greatly improves generalization performance of SVDD. The improvement has shown to be over 30%. In addition, results also show that the QK-SVDD defect detector is able to accomplish the task of defect detection on an LCD image within 60 ms

    Assembly and Installation of the Daya Bay Antineutrino Detectors

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    The Daya Bay reactor antineutrino experiment is designed to make a precision measurement of the neutrino mixing angle ξ_(13), and recently made the definitive discovery of its non-zero value. It utilizes a set of eight, functionally identical antineutrino detectors to measure the reactor flux and spectrum at baselines of ~ 300–2000 m from the Daya Bay and Ling Ao Nuclear Power Plants. The Daya Bay antineutrino detectors were built in an above-ground facility and deployed side-by-side at three underground experimental sites near and far from the nuclear reactors. This configuration allows the experiment to make a precision measurement of reactor antineutrino disappearance over km-long baselines and reduces relative systematic uncertainties between detectors and nuclear reactors. This paper describes the assembly and installation of the Daya Bay antineutrino detectors

    Comparison of TALE designer transcription factors and the CRISPR/dCas9 in regulation of gene expression by targeting enhancers

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    © The Author(s) 2014. The transcription activator-like effectors (TALEs) and the RNA-guided clustered regularly interspaced short palindromic repeat (CRISPR) associated protein (Cas9) utlil ize distinct molecular mechanisms in targeting site recognition. The two proteins can be modified to carry additional functional domains to regulate expression of genomic loci in mammalian cells. In this study, we have compared the two systems in activation and suppression of the Oct4 and Nanog loci by targeting their enhancers. Although both are able to efficiently activate the luciferase reporters, the CRISPR/dCas9 system is much less potent in activating the endogenous loci and in the application of reprogramming somatic cells to iPS cells. Nevertheless, repression by CRISPR/dCas9 is comparable to or even better than TALE repressors. We demonstrated that dCas9 protein binding results in significant physical interference to binding of native transcription factors at enhancer, less efficient active histone markers induction or recruitment of activating complexes in gene activation. This study thus highlighted the merits and drawbacks of transcription regulation by each system. A combined approach of TALEs and CRISPR/dCas9 should provide an optimized solution to regulate genomic loci and to study genetic elements such as enhancers in biological processes including somatic cell reprogramming and guided differentiation.Link_to_subscribed_fulltex

    Reprogramming to pluripotency using designer TALE transcription factors targeting enhancers

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    The modular DNA recognition code of the transcription-activator-like effectors (TALEs) from plant pathogenic bacterial genus Xanthomonas provides a powerful genetic tool to create designer transcription factors (dTFs) targeting specific DNA sequences for manipulating gene expression. Previous studies have suggested critical roles of enhancers in gene regulation and reprogramming. Here, we report dTF activator targeting the distal enhancer of the Pou5f1 (Oct4) locus induces epigenetic changes, reactivates its expression, and substitutes exogenous OCT4 in reprogramming mouse embryonic fibroblast cells (MEFs) to induced pluripotent stem cells (iPSCs). Similarly, dTF activator targeting a Nanog enhancer activates Nanog expression and reprograms epiblast stem cells (EpiSCs) to iPSCs. Conversely, dTF repressors targeting the same genetic elements inhibit expression of these loci, and effectively block reprogramming. This study indicates that dTFs targeting specific enhancers can be used to study other biological processes such as transdifferentiation or directed differentiation of stem cells. © 2013 The Authors.Link_to_subscribed_fulltex

    Systematics of Stopping and Flow in Au+Au Collisions

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    Excitation functions of flow and stopping observables for the Au+Au system at energies from 40 to 1500 MeV per nucleon are presented. The systematics were obtained by merging the results of the INDRA and FOPI experiments, both performed at the GSI facility. The connection to the nuclear equation of state is discussed.Comment: Contribution to the WCI book "Dynamics and Thermodynamics with Nucleonic Degrees of Freedom

    Gap Junctions Contribute To Ictal/Interictal Genesis In Human Hypothalamic Hamartomas

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    Human hypothalamic hamartoma (HH) is a rare subcortical lesion associated with treatment-resistant epilepsy. Cellular mechanisms responsible for epileptogenesis are unknown. We hypothesized that neuronal gap junctions contribute to epileptogenesis through synchronous activity within the neuron networks in HH tissue. We studied surgically resected HH tissue with Western-blot analysis, immunohistochemistry, electron microscopy, biocytin microinjection of recorded HH neurons, and microelectrode patch clamp recordings with and without pharmacological blockade of gap junctions. Normal human hypothalamus tissue was used as a control. Western blots showed increased expression of both connexin-36 (Cx36) and connexin-43 (Cx43) in HH tissue compared with normal human mammillary body tissue. Immunohistochemistry demonstrated that Cx36 and Cx43 are expressed in HH tissue, but Cx36 was mainly expressed within neuron clusters while Cx43 was mainly expressed outside of neuron clusters. Gap-junction profiles were observed between small HH neurons with electron microscopy. Biocytin injection into single recorded small HH neurons showed labeling of adjacent neurons, which was not observed in the presence of a neuronal gap-junction blocker, mefloquine. Microelectrode field recordings from freshly resected HH slices demonstrated spontaneous ictal/interictal-like discharges in most slices. Bath-application of gap-junction blockers significantly reduced ictal/interictal-like discharges in a concentration-dependent manner, while not affecting the action-potential firing of small gamma-aminobutyric acid (GABA) neurons observed with whole-cell patch-clamp recordings from the same patient\u27s HH tissue. These results suggest that neuronal gap junctions between small GABAergic HH neurons participate in the genesis of epileptic-like discharges. Blockade of gap junctions may be a new therapeutic strategy for controlling seizure activity in HH patients

    Triglyceride-glucose index and the risk of heart failure: Evidence from two large cohorts and a mendelian randomization analysis.

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    The relationship between triglyceride-glucose (TyG) index, an emerging marker of insulin resistance, and the risk of incident heart failure (HF) was unclear. This study thus aimed to investigate this relationship. Subjects without prevalent cardiovascular diseases from the prospective Kailuan cohort (recruited during 2006-2007) and a retrospective cohort of family medicine patients from Hong Kong (recruited during 2000-2003) were followed up until December 31st, 2019 for the outcome of incident HF. Separate adjusted hazard ratios (aHRs) summarizing the relationship between TyG index and HF risk in the two cohorts were combined using a random-effect meta-analysis. Additionally, a two-sample Mendelian randomization (MR) of published genome-wide association study data was performed to assess the causality of observed associations. In total, 95,996 and 19,345 subjects from the Kailuan and Hong Kong cohorts were analyzed, respectively, with 2,726 cases of incident HF in the former and 1,709 in the latter. Subjects in the highest quartile of TyG index had the highest risk of incident HF in both cohorts (Kailuan: aHR 1.23 (95% confidence interval: 1.09-1.39), P<sub>Trend</sub> <0.001; Hong Kong: aHR 1.21 (1.04-1.40), P<sub>Trend</sub> =0.007; both compared with the lowest quartile). Meta-analysis showed similar results (highest versus lowest quartile: HR 1.22 (1.11-1.34), P < 0.001). Findings from MR analysis, which included 47,309 cases and 930,014 controls, supported a causal relationship between higher TyG index and increased risk of HF (odds ratio 1.27 (1.15-1.40), P < 0.001). A higher TyG index is an independent and causal risk factor for incident HF in the general population. URL: https://www.chictr.org.cn ; Unique identifier: ChiCTR-TNRC-11,001,489. [Abstract copyright: © 2022. The Author(s).
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