69 research outputs found

    Learning to Check Contract Inconsistencies

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    Contract consistency is important in ensuring the legal validity of the contract. In many scenarios, a contract is written by filling the blanks in a precompiled form. Due to carelessness, two blanks that should be filled with the same (or different)content may be incorrectly filled with different (or same) content. This will result in the issue of contract inconsistencies, which may severely impair the legal validity of the contract. Traditional methods to address this issue mainly rely on manual contract review, which is labor-intensive and costly. In this work, we formulate a novel Contract Inconsistency Checking (CIC) problem, and design an end-to-end framework, called Pair-wise Blank Resolution (PBR), to solve the CIC problem with high accuracy. Our PBR model contains a novel BlankCoder to address the challenge of modeling meaningless blanks. BlankCoder adopts a two-stage attention mechanism that adequately associates a meaningless blank with its relevant descriptions while avoiding the incorporation of irrelevant context words. Experiments conducted on real-world datasets show the promising performance of our method with a balanced accuracy of 94.05% and an F1 score of 90.90% in the CIC problem.Comment: Accepted by AAAI 202

    DeePMD-kit v2: A software package for Deep Potential models

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    DeePMD-kit is a powerful open-source software package that facilitates molecular dynamics simulations using machine learning potentials (MLP) known as Deep Potential (DP) models. This package, which was released in 2017, has been widely used in the fields of physics, chemistry, biology, and material science for studying atomistic systems. The current version of DeePMD-kit offers numerous advanced features such as DeepPot-SE, attention-based and hybrid descriptors, the ability to fit tensile properties, type embedding, model deviation, Deep Potential - Range Correction (DPRc), Deep Potential Long Range (DPLR), GPU support for customized operators, model compression, non-von Neumann molecular dynamics (NVNMD), and improved usability, including documentation, compiled binary packages, graphical user interfaces (GUI), and application programming interfaces (API). This article presents an overview of the current major version of the DeePMD-kit package, highlighting its features and technical details. Additionally, the article benchmarks the accuracy and efficiency of different models and discusses ongoing developments.Comment: 51 pages, 2 figure

    Kaposi's Sarcoma-Associated Herpesvirus K7 Induces Viral G Protein-Coupled Receptor Degradation and Reduces Its Tumorigenicity

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    The Kaposi's sarcoma-associated herpesvirus (KSHV) genome encodes a G protein-coupled receptor (vGPCR). vGPCR is a ligand-independent, constitutively active signaling molecule that promotes cell growth and proliferation; however, it is not clear how vGPCR is negatively regulated. We report here that the KSHV K7 small membrane protein interacts with vGPCR and induces its degradation, thereby dampening vGPCR signaling. K7 interaction with vGPCR is readily detected in transiently transfected human cells. Mutational analyses reveal that the K7 transmembrane domain is necessary and sufficient for this interaction. Biochemical and confocal microscopy studies indicate that K7 retains vGPCR in the endoplasmic reticulum (ER) and induces vGPCR proteasomeal degradation. Indeed, the knockdown of K7 by shRNA-mediated silencing increases vGPCR protein expression in BCBL-1 cells that are induced for KSHV lytic replication. Interestingly, K7 expression significantly reduces vGPCR tumorigenicity in nude mice. These findings define a viral factor that negatively regulates vGPCR protein expression and reveal a post-translational event that modulates GPCR-dependent transformation and tumorigenicity

    Murine Gamma Herpesvirus 68 Hijacks MAVS and IKKβ to Abrogate NFκB Activation and Antiviral Cytokine Production

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    Upon viral infection, mitochondrial antiviral signaling (MAVS) protein serves as a key adaptor to promote cytokine production. We report here that murine gamma herpesvirus 68 (γHV68), a model virus for oncogenic human gamma herpesviruses, subverts cytokine production via the MAVS adaptor. During early infection, γHV68 hijacks MAVS and IKKβ to induce the site-specific phosphorylation of RelA, a crucial subunit of the transcriptionally active NFκB dimer, which primes RelA for the proteasome-mediated degradation. As such, γHV68 efficiently abrogated NFκB activation and cytokine gene expression. Conversely, uncoupling RelA degradation from γHV68 infection promoted NFκB activation and elevated cytokine production. Loss of MAVS increased cytokine production and immune cell infiltration in the lungs of γHV68-infected mice. Moreover, exogenous expression of the phosphorylation- and degradation-resistant RelA variant restored γHV68-induced cytokine production. Our findings uncover an intricate strategy whereby signaling via the upstream MAVS adaptor is intercepted by a pathogen to nullify the immediate downstream effector, RelA, of the innate immune pathway

    The Ubiquitin/Proteasome System Mediates Entry and Endosomal Trafficking of Kaposi's Sarcoma-Associated Herpesvirus in Endothelial Cells

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    Ubiquitination, a post-translational modification, mediates diverse cellular functions including endocytic transport of molecules. Kaposi's sarcoma-associated herpesvirus (KSHV), an enveloped herpesvirus, enters endothelial cells primarily through clathrin-mediated endocytosis. Whether ubiquitination and proteasome activity regulates KSHV entry and endocytosis remains unknown. We showed that inhibition of proteasome activity reduced KSHV entry into endothelial cells and intracellular trafficking to nuclei, thus preventing KSHV infection of the cells. Three-dimensional (3-D) analyses revealed accumulation of KSHV particles in a cytoplasmic compartment identified as EEA1+ endosomal vesicles upon proteasome inhibition. KSHV particles are colocalized with ubiquitin-binding proteins epsin and eps15. Furthermore, ubiquitination mediates internalization of both KSHV and one of its receptors integrin β1. KSHV particles are colocalized with activated forms of the E3 ligase c-Cbl. Knock-down of c-Cbl or inhibition of its phosphorylation reduced viral entry and intracellular trafficking, resulting in decreased KSHV infectivity. These results demonstrate that ubiquitination mediates internalization of both KSHV and one of its cognate receptors integrin β1, and identify c-Cbl as a potential E3 ligase that facilitates this process

    Pr<sup>3+</sup>-Doped Lithium Niobate and Sodium Niobate with Persistent Luminescence and Mechano-Luminescence Properties

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    In this research, a comprehensive series of Pr3+-doped lithium niobate and sodium niobate materials were obtained at different temperatures via solid-state sintering, and their structures and properties were compared. NaNbO3: 0.75% Pr3+ phosphors were synthesized by sintering at 1150 °C for 2 h and emitted red persistent luminescence for more than 1200 s, peaking at 612 nm under UV excitation, which was a typical long persistent luminescence phenomenon. Furthermore, the sample glowed when pressurized, and a red bright luminescence which lasted for several seconds was visible to the naked eye. This was a typical mechanical luminescence phenomenon of samples under mechanical stress, directly converting mechanical energy into light energy. It was determined that NaNbO3:Pr3+ and LiNbO3:Pr3+ both possess multimode luminescence. Owing to their red long persistent luminescence (LPL) and mechano-luminescence (ML) properties, Pr3+ phosphors can be employed in fields, such as display technologies, stress sensing, structural damage detection, and other complex applications
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