Coordinated Reasoning for Cross-Lingual Knowledge Graph Alignment

Existing entity alignment methods mainly vary on the choices of encoding the knowledge graph, but they typically use the same decoding method, which independently chooses the local optimal match for each source entity. This decoding method may not only cause the "many-to-one" problem but also neglect the coordinated nature of this task, that is, each alignment decision may highly correlate to the other decisions. In this paper, we introduce two coordinated reasoning methods, i.e., the Easy-to-Hard decoding strategy and joint entity alignment algorithm. Specifically, the Easy-to-Hard strategy first retrieves the model-confident alignments from the predicted results and then incorporates them as additional knowledge to resolve the remaining model-uncertain alignments. To achieve this, we further propose an enhanced alignment model that is built on the current state-of-the-art baseline. In addition, to address the many-to-one problem, we propose to jointly predict entity alignments so that the one-to-one constraint can be naturally incorporated into the alignment prediction. Experimental results show that our model achieves the state-of-the-art performance and our reasoning methods can also significantly improve existing baselines.Comment: in AAAI 202

The source localization technique based on improved functional beamforming using a virtual array

Beamforming have become a popular technique to identify sound source. The most common application is conventional beamforming, but it has low resolution and requires a large number of microphones at low frequency. To overcome this problem, an improved functional beamforming method based on “virtual array” and the relative spectral matrix is introduced. Firstly, the relative complex pressures of the sound field can be acquired by “virtual array” with one scanning microphone and a fixed reference microphone. Thereby, a relative spectral matrix of the relative complex pressures measured can be obtained. Then the improved functional beamforming method with order v is developed based on the relative spectral matrix. And the resolution of the improved method can be modified by increased the number of order v. but it also can be improved by changing virtual microphones. This property allows widening the scope of this interesting beamforming method

A novel approach to inhibit HIV-1 infection and enhance lysis of HIV by a targeted activator of complement

<p>Abstract</p> <p>Background</p> <p>The complement system is one of the most potent weapons of innate immunity. It is not only a mechanism for direct protection against invading pathogens but it also interacts with the adaptive immunity to optimize the pathogen-specific humoral and cellular defense cascades in the body. Complement-mediated lysis of HIV is inefficient but the presence of HIV particles results in complement activation by the generation of many C3-fragments, such as C3dg and C3d. It has been demonstrated that activation of complement can enhance HIV infection through the binding of special complement receptor type 2 expression on the surface of mature B cells and follicular dendritic cells.</p> <p>Presentation of the hypothesis</p> <p>Previous studies have proven that the complement-mediated antibody-dependent enhancement of HIV infection is mediated by the association of complement receptor type 2 bound to the C3 fragment and deposited on the surface of HIV virions. Thus, we hypothesize that a new activator of complement, consisting of a target domain (C3-binding region of complement receptor type 2) linked to a complement-activating human IgG1 Fc domain (CR2-Fc), can target and amplify complement deposition on HIV virions and enhance the efficiency of HIV lysis.</p> <p>Testing the hypothesis</p> <p>Our hypothesis was tested using cell-free HIV-1 virions cultivated <it>in vitro </it>and assessment of virus opsonization was performed by incubating appropriate dilutions of virus with medium containing normal human serum and purified CR2-Fc proteins. As a control group, viruses were incubated with normal human serum under the same conditions. Virus neutralization assays were used to estimate the degree of CR2-Fc-enhanced lysis of HIV compared to untreated virus.</p> <p>Implications of the hypothesis</p> <p>The targeted complement activator, CR2-Fc, can be used as a novel approach to HIV therapy by abrogating the complement-enhanced HIV infection of cells.</p

Rheumatoid Arthritis and Risk of Atrial Fibrillation: Results from Pooled Cohort Studies and Mendelian Randomization Analysis

Observational research has indicated that individuals diagnosed with rheumatoid arthritis (RA) have an elevated likelihood of developing atrial fibrillation (AF). Herein, we performed meta-analysis and Mendelian randomization (MR) analysis to explore the correlation and potential causal relationship between RA and AF. We searched PubMed, Embase, and Web of Science for cohort studies comparing AF risk among participants with and without RA. Quantitative synthesis of the adjusted risk ratio (RR) or hazard ratio was performed with the random-effects model. RA and AF were studied with two-sample MR analysis with the random-effects inverse variance weighted method. Patients with RA had a higher risk of AF than participants without RA [RR = 1.32, 95% confidence interval (CI): 1.23–1.43, P < 0.0001]. Genetically predicted RA was not associated with a significantly elevated risk of AF (odds ratio = 1.009, 95% CI: 0.986–1.032, P = 0.449). After adjustment for confounding factors in multifactorial MR, RA and AF still showed no correlation. Sensitivity analyses yielded similar results, thus indicating the robustness of the causal association. Overall, RA was associated with elevated risk of AF in our meta-analysis. However, genetically predicted RA may not be causal

Improved algorithm of three-dimensional beamforming based on spatial cross-array

Three-dimensional beamforming based on microphone array signal processing is the expansion of traditional 2D beamforming. However, its identification accuracy is often badly reduced by the effect of grating lobes and side lobes. To overcome this problem, a method called the hybrid method beamforming (HMB) combining functional generalized inverse beamforming with multiplicative filter of spatial cross-array is proposed. In this method, the statistically optimal processing and iterated generalized inverse beamforming with regularized matrix function are utilized to obtain initial result. Then the high order function is applied to filter the output. Subsequently, a novel non-uniform spatial cross-array optimized by genetic algorithm is used to obtain sound pressure distribution. The array consists of three orthogonal sub-arrays. Mutual cancellation is realized by computing respectively with data of sub-arrays and multiplying together. With fewer microphones, the result of the improved method can be obtained with a higher spatial resolution. The proposed method is verified by the simulation and the source localization test in a room. Compared with the conventional frequency domain beamforming (FDBF) algorithm and statistically optimal array processing (SOAP) beamforming, the performance of the proposed method is significantly improved in terms of resolution of the acoustic source

A new therapeutic strategy for lung tissue injury induced by influenza with CR2 targeting complement inhibitior

<p>Abstract</p> <p>Background</p> <p>Influenza is a respiratory disease that seriously threatens human health. In fact, influenza virus itself does not make critical contribution to mortality induced by influenza, but "cytokine storm" produced by the excessive immune response triggered by the virus can result in inflammatory reaction of lung tissues and fatal lung tissue injury, and thus increase influenza mortality. Therefore, besides antiviral drugs, immunosuppression drugs should also be included in infection treatment.</p> <p>Presentation of the hypothesis</p> <p>Complement is the center of inflammatory reaction. If complement system is over activated, the body will have strong inflammatory reaction or tissue injury, resulting in pathological process. Many studies have proved that, inflammatory injury of lung tissues caused by influenza virus is closely related to complement activation. Therefore, inhibiting complement activation can significantly reduce inflammatory injury in lung tissues. As complement is both a physiological defense and pathological damage medium, systematic inhibition may result in side effects including infection. Therefore, we design targeting complement inhibitors for complement activation sites, i.e. with CR2 as targeting vector, complement inhibitors like CD59 and Crry are targeted to inflammatory sites to specially inhibit the complement activation in local injury, thus local inflammatory reaction is inhibited.</p> <p>Testing the hypothesis</p> <p>CR2-CD59 and CR2-Crry targeting complement inhibitors are fusion-expressed, and their biological activity is examined via in <it>vivo </it>and in vitro tests. CR2 targeting complement inhibitors are used to treat mouse influenza viral pneumonia model, with PBS treatment group as the control. The survival and lung tissue injury of the mice is observed and the effect of CR2 targeting complement inhibitors on pneumonia induced by influenza virus is evaluated.</p> <p>Implications of the hypothesis</p> <p>CR2 targeting complement inhibitors are expected to be ideal drugs for viral pneumonia.</p

A new treatment for neurogenic inflammation caused by EV71 with CR2-targeted complement inhibitor

BACKGROUND: Enterovirus 71 (EV71), one of the most important neurotropic EVs, has caused death and long-term neurological sequelae in hundreds of thousands of young children in the Asia-Pacific region in the past decade. The neurological diseases are attributed to infection by EV71 inducing an extensive peripheral and central nervous system (CNS) inflammatory response with abnormal cytokine production and lymphocyte depletion induced by EV71 infection. In the absence of specific antiviral agents or vaccines, an effective immunosuppressive strategy would be valuable to alleviate the severity of the local inflammation induced by EV71 infection. PRESENTATION OF THE HYPOTHESIS: The complement system plays a pivotal role in the inflammatory response. Inappropriate or excessive activation of the complement system results in a severe inflammatory reaction or numerous pathological injuries. Previous studies have revealed that EV71 infection can induce complement activation and an inflammatory response of the CNS. CR2-targeted complement inhibition has been proved to be a potential therapeutic strategy for many diseases, such as influenza virus-induced lung tissue injury, postischemic cerebral injury and spinal cord injury. In this paper, a mouse model is proposed to test whether a recombinant fusion protein consisting of CR2 and a region of Crry (CR2-Crry) is able to specifically inhibit the local complement activation induced by EV71 infection, and to observe whether this treatment strategy can alleviate or even cure the neurogenic inflammation. TESTING THE HYPOTHESIS: CR2-Crry is expressed in CHO cells, and its biological activity is determined by complement inhibition assays. 7-day-old ICR mice are inoculated intracranially with EV71 to duplicate the neurological symptoms. The mice are then divided into two groups, in one of which the mice are treated with CR2-Crry targeted complement inhibitor, and in the other with phosphate-buffered saline. A group of mice deficient in complement C3, the breakdown products of which bind to CR2, are also infected with EV71 virus. The potential bioavailability and efficacy of the targeted complement inhibitor are evaluated by histology, immunofluorescence staining and radiolabeling. IMPLICATIONS OF THE HYPOTHESIS: CR2-Crry-mediated targeting complement inhibition will alleviate the local inflammation and provide an effective treatment for the severe neurological diseases associated with EV71 infection

A novel trifunctional IgG-like bispecific antibody to inhibit HIV-1 infection and enhance lysis of HIV by targeting activation of complement

BACKGROUND: The complement system is not only a key component of innate immunity but also provides a first line of defense against invading pathogens, especially for viral pathogens. Human immunodeficiency virus (HIV), however, possesses several mechanisms to evade complement-mediated lysis (CoML) and exploit the complement system to enhance viral infectivity. Responsible for this intrinsic resistance against complement-mediated virolysis are complement regulatory membrane proteins derived from the host cell that inherently downregulates complement activation at several stages of the cascade. In addition, HIV is protected from complement-mediated lysis by binding soluble factor H (fH) through the viral envelope proteins, gp120 and gp41. Whereas inhibition of complement activity is the desired outcome in the vast majority of therapeutic approaches, there is a broader potential for complement-mediated inhibition of HIV by complement local stimulation. PRESENTATION OF THE HYPOTHESIS: Our previous studies have proven that the complement-mediated antibody-dependent enhancement of HIV infection is mediated by the association of complement receptor type 2 bound to the C3 fragment and deposited on the surface of HIV virions. Thus, we hypothesize that another new activator of complement, consisting of two dsFv (against gp120 and against C3d respectively) linked to a complement-activating human IgG1 Fc domain ((anti-gp120 × anti-C3d)-Fc), can not only target and amplify complement activation on HIV virions for enhancing the efficiency of HIV lysis, but also reduce the infectivity of HIV through blocking the gp120 and C3d on the surface of HIV. TESTING THE HYPOTHESIS: Our hypothesis was tested using cell-free HIV-1 virions cultivated in vitro and assessment of virus opsonization was performed by incubating appropriate dilutions of virus with medium containing normal human serum and purified (anti-gp120 × anti-C3d)-Fc proteins. As a control group, viruses were incubated with normal human serum under the same conditions. Virus neutralization assays were used to estimate the degree of (anti-gp120 × anti-C3d)-Fc lysis of HIV compared to untreated virus. IMPLICATIONS OF THE HYPOTHESIS: The targeted complement activator, (anti-gp120 × anti-C3d)-Fc, can be used as a novel approach to HIV therapy by abrogating the complement-enhanced HIV infection of cells