117 research outputs found

    Improving Distantly-Supervised Named Entity Recognition with Self-Collaborative Denoising Learning

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    Distantly supervised named entity recognition (DS-NER) efficiently reduces labor costs but meanwhile intrinsically suffers from the label noise due to the strong assumption of distant supervision. Typically, the wrongly labeled instances comprise numbers of incomplete and inaccurate annotation noise, while most prior denoising works are only concerned with one kind of noise and fail to fully explore useful information in the whole training set. To address this issue, we propose a robust learning paradigm named Self-Collaborative Denoising Learning (SCDL), which jointly trains two teacher-student networks in a mutually-beneficial manner to iteratively perform noisy label refinery. Each network is designed to exploit reliable labels via self denoising, and two networks communicate with each other to explore unreliable annotations by collaborative denoising. Extensive experimental results on five real-world datasets demonstrate that SCDL is superior to state-of-the-art DS-NER denoising methods.Comment: EMNLP (12 pages, 4 figures, 6 tables

    Reliability Analysis of Vision Transformers

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    Vision Transformers (ViTs) that leverage self-attention mechanism have shown superior performance on many classical vision tasks compared to convolutional neural networks (CNNs) and gain increasing popularity recently. Existing ViTs works mainly optimize performance and accuracy, but ViTs reliability issues induced by soft errors in large-scale VLSI designs have generally been overlooked. In this work, we mainly study the reliability of ViTs and investigate the vulnerability from different architecture granularities ranging from models, layers, modules, and patches for the first time. The investigation reveals that ViTs with the self-attention mechanism are generally more resilient on linear computing including general matrix-matrix multiplication (GEMM) and full connection (FC) and show a relatively even vulnerability distribution across the patches. ViTs involve more fragile non-linear computing such as softmax and GELU compared to typical CNNs. With the above observations, we propose a lightweight block-wise algorithm-based fault tolerance (LB-ABFT) approach to protect the linear computing implemented with distinct sizes of GEMM and apply a range-based protection scheme to mitigate soft errors in non-linear computing. According to our experiments, the proposed fault-tolerant approaches enhance ViTs accuracy significantly with minor computing overhead in presence of various soft errors

    Exploring Winograd Convolution for Cost-effective Neural Network Fault Tolerance

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    Winograd is generally utilized to optimize convolution performance and computational efficiency because of the reduced multiplication operations, but the reliability issues brought by winograd are usually overlooked. In this work, we observe the great potential of winograd convolution in improving neural network (NN) fault tolerance. Based on the observation, we evaluate winograd convolution fault tolerance comprehensively from different granularities ranging from models, layers, and operation types for the first time. Then, we explore the use of inherent fault tolerance of winograd convolution for cost-effective NN protection against soft errors. Specifically, we mainly investigate how winograd convolution can be effectively incorporated with classical fault-tolerant design approaches including triple modular redundancy (TMR), fault-aware retraining, and constrained activation functions. According to our experiments, winograd convolution can reduce the fault-tolerant design overhead by 55.77\% on average without any accuracy loss compared to standard convolution, and further reduce the computing overhead by 17.24\% when the inherent fault tolerance of winograd convolution is considered. When it is applied on fault-tolerant neural networks enhanced with fault-aware retraining and constrained activation functions, the resulting model accuracy generally shows significant improvement in presence of various faults

    Analysis of Large Phenotypic Variability of EEC and SHFM4 Syndromes Caused by K193E Mutation of the TP63 Gene

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    EEC (ectrodactyly, ectodermal dysplasia, clefting; OMIM 604292) is an autosomal dominant developmental disorder resulting mainly from pathogenic mutations of the DNA-binding domain (DBD) of the TP63 gene. In this study, we showed that K193E mutation in nine affected individuals of a four-generation kindred with a large degree of phenotypic variability causes four different syndromes or TP63-related disorders: EEC, Ectrodactyly-ectodermal dysplasia (EE), isolated ectodermal dysplasia, and isolated Split Hand/Foot Malformation type 4 (SHFM4). Genotype-phenotype and DBD structural modeling analysis showed that the K193-located loop L2-A is associated with R280 through hydrogen bonding interactions, while R280 mutations also often cause large phenotypic variability of EEC and SHFM4. Thus, we speculate that K193 and several other DBD mutation-associated syndromes may share similar pathogenic mechanisms, particularly in the case of the same mutation with different phenotypes. Our study and others also suggest that the phenotypic variability of EEC is attributed, at least partially, to genetic and/or epigenetic modifiers

    Direct and indirect effects of climate on richness drive the latitudinal diversity gradient in forest trees

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    Data accessibility statement: Full census data are available upon reasonable request from the ForestGEO data portal, http://ctfs.si.edu/datarequest/ We thank Margie Mayfield, three anonymous reviewers and Jacob Weiner for constructive comments on the manuscript. This study was financially supported by the National Key R&D Program of China (2017YFC0506100), the National Natural Science Foundation of China (31622014 and 31570426), and the Fundamental Research Funds for the Central Universities (17lgzd24) to CC. XW was supported by the Strategic Priority Research Program of the Chinese Academy of Sciences (XDB3103). DS was supported by the Czech Science Foundation (grant no. 16-26369S). Yves Rosseel provided us valuable suggestions on using the lavaan package conducting SEM analyses. Funding and citation information for each forest plot is available in the Supplementary Information Text 1.Peer reviewedPostprin

    Inferring causal molecular networks: empirical assessment through a community-based effort

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    Inferring molecular networks is a central challenge in computational biology. However, it has remained unclear whether causal, rather than merely correlational, relationships can be effectively inferred in complex biological settings. Here we describe the HPN-DREAM network inference challenge that focused on learning causal influences in signaling networks. We used phosphoprotein data from cancer cell lines as well as in silico data from a nonlinear dynamical model. Using the phosphoprotein data, we scored more than 2,000 networks submitted by challenge participants. The networks spanned 32 biological contexts and were scored in terms of causal validity with respect to unseen interventional data. A number of approaches were effective and incorporating known biology was generally advantageous. Additional sub-challenges considered time-course prediction and visualization. Our results constitute the most comprehensive assessment of causal network inference in a mammalian setting carried out to date and suggest that learning causal relationships may be feasible in complex settings such as disease states. Furthermore, our scoring approach provides a practical way to empirically assess the causal validity of inferred molecular networks

    Inferring causal molecular networks: empirical assessment through a community-based effort

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    It remains unclear whether causal, rather than merely correlational, relationships in molecular networks can be inferred in complex biological settings. Here we describe the HPN-DREAM network inference challenge, which focused on learning causal influences in signaling networks. We used phosphoprotein data from cancer cell lines as well as in silico data from a nonlinear dynamical model. Using the phosphoprotein data, we scored more than 2,000 networks submitted by challenge participants. The networks spanned 32 biological contexts and were scored in terms of causal validity with respect to unseen interventional data. A number of approaches were effective, and incorporating known biology was generally advantageous. Additional sub-challenges considered time-course prediction and visualization. Our results suggest that learning causal relationships may be feasible in complex settings such as disease states. Furthermore, our scoring approach provides a practical way to empirically assess inferred molecular networks in a causal sense
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