13 research outputs found

    SoK: Training Machine Learning Models over Multiple Sources with Privacy Preservation

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    Nowadays, gathering high-quality training data from multiple data controllers with privacy preservation is a key challenge to train high-quality machine learning models. The potential solutions could dramatically break the barriers among isolated data corpus, and consequently enlarge the range of data available for processing. To this end, both academia researchers and industrial vendors are recently strongly motivated to propose two main-stream folders of solutions: 1) Secure Multi-party Learning (MPL for short); and 2) Federated Learning (FL for short). These two solutions have their advantages and limitations when we evaluate them from privacy preservation, ways of communication, communication overhead, format of data, the accuracy of trained models, and application scenarios. Motivated to demonstrate the research progress and discuss the insights on the future directions, we thoroughly investigate these protocols and frameworks of both MPL and FL. At first, we define the problem of training machine learning models over multiple data sources with privacy-preserving (TMMPP for short). Then, we compare the recent studies of TMMPP from the aspects of the technical routes, parties supported, data partitioning, threat model, and supported machine learning models, to show the advantages and limitations. Next, we introduce the state-of-the-art platforms which support online training over multiple data sources. Finally, we discuss the potential directions to resolve the problem of TMMPP.Comment: 17 pages, 4 figure

    Transcriptomic analysis reveals that enterovirus F strain SWUN-AB001 infection activates JNK/SAPK and p38 MAPK signaling pathways in MDBK cells

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    Abstract Background Enteroviruses (Picornaviridae family) have been widely detected in the feces from cattle with diarrhea. However, the mechanisms responsible for the pathogenicity of enteroviruses in cattle remain unclear. Recently, we isolated a novel EV-F7 strain called SWUN-AB001 from diarrheal yak (Bos grunniens) feces. To explore the pathogenic mechanisms of this novel virus, we used a transcriptomics approach to find genes with differential expression patterns in Madin-Darby bovine kidney (MDBK) cells during infection with SWUN-AB001 over time. Results MDBK cells were sampled at 12 and 24 h post-infection (hpi) to represent the early and late stages of a SWUN-AB001 infection. Compared with the non-infected cells, 19 and 1050 differentially expressed genes (DEGs) were identified at 12 and 24 hpi, respectively. These DEGs were associated with disease, signal transduction, cellular process and cytokine signaling categories. At 24 hpi, the pathway enrichment analysis revealed that signal pathways such as c-Jun NH2-terminal kinase/ stress-activated protein kinase (JNK/SAPK) and mitogen-activated protein kinase (MAPK) pathways and cytokine-cytokine receptor interactions were associated with the interactions occurring between EV-F7 and MDBK cells. Our additional western blot analysis showed that the phosphorylation levels of JNK/SAPK and p38 MAPK proteins increased significantly in the MDBK cells at 24 hpi. The result indicated that infection with EV-F7 could activate JNK/SAPK and p38 MAPK pathways in MDBK cells, and possibly trigger large-scale cytokine production. Conclusion Our transcriptome analysis provides useful initial data towards better understanding of the infection mechanisms used by EV-F7, while highlighting the potential molecular relationships occurring between the virus and the host’s cellular components

    Efficacy and safety of ripretinib in Chinese patients with advanced gastrointestinal stromal tumors: a real-world, multicenter, observational study

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    IntroductionMutations in KIT proto-oncogene, receptor tyrosine kinase (KIT) and platelet-derived growth factor receptor-α (PDGFRA) render the available tyrosine kinase inhibitors (TKI) ineffective in treating advanced gastrointestinal stromal tumors (GIST). Ripretinib, a broad-spectrum switch-control kinase inhibitor, has shown increased efficacy and manageable safety, but real-world evidence remains scarce. This study evaluates the efficacy and safety of ripretinib among Chinese patients in a real-world setting.MethodsAdvanced GIST patients (N=23) receiving ripretinib following progression on previous lines of TKI treatment were enrolled to determine the efficacy [progression-free survival (PFS) and overall survival (OS)]. Safety was assessed by the incidence and severity of adverse events (AEs). All statistical analyses were performed using SPSS version 20.0 and a p-value of <0.05 was considered significant.ResultsThe median PFS (mPFS) of efficacy analysis set (EAS) (N=21) was 7.1 months. mPFS of patients receiving ripretinib following ≤2 lines of previous TKI treatment and ≥3 prior lines of therapy were 7.1 and 9.2 months, respectively. The median OS (mOS) was 12.0 months and shorter interval between the end of the latest TKI and ripretinib therapy was correlated with longer median PFS and OS (p=0.054 and p=0.046), respectively. Alopecia and asthenia were the most common AEs observed.ConclusionCompared to previous lines of TKI in advanced GIST patients, ripretinib showed superior efficacy with clinically manageable AEs. Real-world results are comparable to that of phase III INVICTUS study and its Chinese bridging study. Hence, ripretinib can be used for the clinical management of advanced GIST patients

    Genome-wide association study suggested the PTPRD polymorphisms were associated with weight gain effects of atypical antipsychotic medications

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    Background: Antipsychotic-induced weight gain (AIWG) is a serious concern in therapy with antipsychotic medications. To identify single nucleotide polymorphisms (SNPs) associated with AIWG, we conducted a genome-wide association study (GWAS) for antipsychotic treatment. Methods: The discovery cohort consisted of 534 patients with schizophrenia, who underwent 8-week treatment with antipsychotics and were genotyped using the Illumina Human 610-Quad BeadChip. The independent replication cohort consisted of 547 patients with schizophrenia, treated with similar antipsychotics, and genotyped using the Sequenom MassARRAY platform. Two hundred and thirty-six drug-naive patients treated with risperidone or quetiapine were analyzed independently. Additionally, we conducted pathway and expression analyses using several public bioinformatics databases. Results: After correction for age and gender, the top 2 genome-wide significant SNPs with AIWG were located in the PTPRD gene (protein tyrosine phosphatase, receptor type D, 9p24-p23; rs10977144, P = 9.26E-09; rs10977154, P = 4.53E-08). The third most significant SNP was in the GFPT2 gene (glutamine-fructose-6-phosphate amidotransferase 2, 5q35.3; rs12386481, P = 1.98E-07). These results were validated in the replication cohort (rs10977144, P = 4.30E-03; rs10977154, P = 6.33E-03; rs12386481, P =7.65E-03). These results were also verified in those patients initially exposed to risperidone and quetiapine (rs10977144, P = 1.97E-05; rs10977154, P = 2.04E-05; rs12386481, P = 1.97E-04). Pathway analyses showed that AIWG may involve in multiple pathways related to metabolic processes. Moreover, PTPRD mRNA might be highly expressed in brain regions, and the SNPs (rs10977144, rs1097154) also showed significant expression quantitative trait locus effects. Conclusions: Our findings indicate that PTPRD polymorphisms might modulate AIWG
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