24 research outputs found

    Neural Multi-network Diffusion towards Social Recommendation

    Full text link
    Graph Neural Networks (GNNs) have been widely applied on a variety of real-world applications, such as social recommendation. However, existing GNN-based models on social recommendation suffer from serious problems of generalization and oversmoothness, because of the underexplored negative sampling method and the direct implanting of the off-the-shelf GNN models. In this paper, we propose a succinct multi-network GNN-based neural model (NeMo) for social recommendation. Compared with the existing methods, the proposed model explores a generative negative sampling strategy, and leverages both the positive and negative user-item interactions for users' interest propagation. The experiments show that NeMo outperforms the state-of-the-art baselines on various real-world benchmark datasets (e.g., by up to 38.8% in terms of NDCG@15)

    Size and shape analysis of error-prone shape data

    Get PDF
    We consider the problem of comparing sizes and shapes of objects when landmark data are prone to measurement error. We show that naive implementation of ordinary Procrustes analysis that ignores measurement error can compromise inference. To account for measurement error, we propose the conditional score method for matching configurations, which guarantees consistent inference under mild model assumptions. The effects of measurement error on inference from naive Procrustes analysis and the performance of the proposed method are illustrated via simulation and application in three real data examples. Supplementary materials for this article are available online

    Participant- and disease-related factors as independent predictors of treatment outcomes in the RESTORE-IMI 2 clinical trial: A multivariable regression analysis

    Get PDF
    BACKGROUND: In the RESTORE-IMI 2 trial, imipenem/cilastatin/relebactam (IMI/REL) was noninferior to piperacillin/tazobactam in treating hospital-acquired bacterial pneumonia/ventilator-associated bacterial pneumonia. This post hoc analysis was conducted to determine independent predictors of efficacy outcomes in the RESTORE-IMI 2 trial, to assist in treatment decision making. METHODS: A stepwise multivariable regression analysis was conducted to identify variables that were independently associated with day 28 all-cause mortality (ACM), favorable clinical response at early follow-up (EFU), and favorable microbiologic response at end of treatment (EOT). The analysis accounted for the number of baseline infecting pathogens and in vitro susceptibility to randomized treatment. RESULTS: Vasopressor use, renal impairment, bacteremia at baseline, and Acute Physiologic Assessment and Chronic Health Evaluation (APACHE) II scores ≥15 were associated with a greater risk of day 28 ACM. A favorable clinical response at EFU was associated with normal renal function, an APACHE II score \u3c15, no vasopressor use, and no bacteremia at baseline. At EOT, a favorable microbiologic response was associated with IMI/REL treatment, normal renal function, no vasopressor use, nonventilated pneumonia at baseline, intensive care unit admission at randomization, monomicrobial infections at baseline, and absence of CONCLUSIONS: This analysis, which accounted for baseline pathogen susceptibility, validated well-recognized patient- and disease-related factors as independent predictors of clinical outcomes. These results lend further support to the noninferiority of IMI/REL to piperacillin/tazobactam and suggests that pathogen eradication may be more likely with IMI/REL. CLINICAL TRIALS REGISTRATION: NCT02493764

    RESTORE-IMI 1: A Multicenter, Randomized, Doubleblind Trial Comparing Efficacy and Safety of Imipenem/Relebactam vs Colistin Plus Imipenem in Patients With Imipenem-nonsusceptible Bacterial Infections

    Get PDF
    Background. The β-lactamase inhibitor relebactam can restore imipenem activity against imipenem-nonsusceptible gram-negative pathogens. We evaluated imipenem/relebactam for treating imipenem-nonsusceptible infections. Methods. Randomized, controlled, double-blind, phase 3 trial. Hospitalized patients with hospital-acquired/ventilatorassociated pneumonia, complicated intraabdominal infection, or complicated urinary tract infection caused by imipenemnonsusceptible (but colistin- and imipenem/relebactam-susceptible) pathogens were randomized 2:1 to 5–21 days imipenem/ relebactam or colistin+imipenem. Primary endpoint: favorable overall response (defined by relevant endpoints for each infection type) in the modified microbiologic intent-to-treat (mMITT) population (qualifying baseline pathogen and ≥1 dose study treatment). Secondary endpoints: clinical response, all-cause mortality, and treatment-emergent nephrotoxicity. Safety analyses included patients with ≥1 dose study treatment. Results. Thirty-one patients received imipenem/relebactam and 16 colistin+imipenem. Among mITT patients (n = 21 imipenem/relebactam, n = 10 colistin+imipenem), 29% had Acute Physiology and Chronic Health Evaluation II scores >15, 23% had creatinine clearance <60 mL/min, and 35% were aged ≥65 years. Qualifying baseline pathogens: Pseudomonas aeruginosa (77%), Klebsiella spp. (16%), other Enterobacteriaceae (6%). Favorable overall response was observed in 71% imipenem/relebactam and 70% colistin+imipenem patients (90% confidence interval [CI] for difference, –27.5, 21.4), day 28 favorable clinical response in 71% and 40% (90% CI, 1.3, 51.5), and 28-day mortality in 10% and 30% (90% CI, –46.4, 6.7), respectively. Serious adverse events (AEs) occurred in 10% of imipenem/relebactam and 31% of colistin+imipenem patients, drug-related AEs in 16% and 31% (no drugrelated deaths), and treatment-emergent nephrotoxicity in 10% and 56% (P = .002), respectively. Conclusions. Imipenem/relebactam is an efficacious and well-tolerated treatment option for carbapenem-nonsusceptible infection

    Correction: PEpiD: A Prostate Epigenetic Database in Mammals

    No full text

    PEpiD: a prostate epigenetic database in mammals.

    Get PDF
    Epigenetic mechanisms play key roles in initiation and progression of prostate cancer by changing gene expression. The Prostate Epigenetic Database (PEpiD: http://wukong.tongji.edu.cn/pepid) archives the three extensively characterized epigenetic mechanisms DNA methylation, histone modification, and microRNA implicated in prostate cancer of human, mouse, and rat. PEpiD uses a distinct color scheme to present the three types of epigenetic data and provides a user-friendly interface for flexible query. The retrieved information includes Refseq ID, gene symbol, gene alias, genomic loci of epigenetic changes, tissue source, experimental method, and supportive references. The change of histone modification (hyper or hypo) and the corresponding gene expression change (up or down) are also indicated. A graphic view of DNA methylation with exon-intron structure and predicted CpG islands is provided as well. Moreover, the prostate-related ENCODE tracks (DNA methylation, histone modifications, chromatin remodelers), and other key transcription factors with reported roles in prostate are displayed in the browser as well. The reversibility of epigenetic aberrations has made them potential markers for diagnosis and prognosis, and targets for treatment of cancers. This curated information will improve our understanding of epigenetic mechanisms of gene regulation in prostate cancer, and serve as an important resource for epigenetic research in prostate cancer

    Correction: PEpiD: A Prostate Epigenetic Database in Mammals

    No full text

    Screen shots showing DNA methylation query by Gene symbol GSTP1 in human.

    No full text
    <p>A, the search form page in which the exclusion relationship between Refseq ID, Gene symbol, and Location is indicated. B, the query result page embedded with the link to track view in UCSC genome browser. C, the details page showing supportive references and DNA methylation loci in a graph.</p

    Number of epigenetic records and genes in PEpiD, with gene numbers in parentheses.

    No full text
    <p>Number of epigenetic records and genes in PEpiD, with gene numbers in parentheses.</p
    corecore