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  • Oxford University Press (OUP)  (14)
  • Li, Yang  (14)
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  • Oxford University Press (OUP)  (14)
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  • 1
    Online Resource
    Online Resource
    C . elegans -based screen identifies lysosome-damaging alkaloids that induce STAT3-dependent lysosomal cell death
    Oxford University Press (OUP) ; 2018
    In:  Protein & Cell Vol. 9, No. 12 ( 2018-12-01), p. 1013-1026
    Details
    In: Protein & Cell, Oxford University Press (OUP), Vol. 9, No. 12 ( 2018-12-01), p. 1013-1026
    Abstract: Lysosomes are degradation and signaling centers within the cell, and their dysfunction impairs a wide variety of cellular processes. To understand the cellular effect of lysosome damage, we screened natural small-molecule compounds that induce lysosomal abnormality using Caenorhabditis elegans (C. elegans) as a model system. A group of vobasinyl-ibogan type bisindole alkaloids (ervachinines A–D) were identified that caused lysosome enlargement in C. elegans macrophage-like cells. Intriguingly, these compounds triggered cell death in the germ line independently of the canonical apoptosis pathway. In mammalian cells, ervachinines A–D induced lysosomal enlargement and damage, leading to leakage of cathepsin proteases, inhibition of autophagosome degradation and necrotic cell death. Further analysis revealed that this ervachinine-induced lysosome damage and lysosomal cell death depended on STAT3 signaling, but not RIP1 or RIP3 signaling. These findings suggest that lysosome-damaging compounds are promising reagents for dissecting signaling mechanisms underlying lysosome homeostasis and lysosome-related human disorders.
    Type of Medium: Online Resource
    ISSN: 1674-800X , 1674-8018
    URL: Article
    DOI: 10.1007/s13238-018-0520-0
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2018
    detail.hit.zdb_id: 2543451-2
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  • 2
    Online Resource
    Online Resource
    Imaging Anatomy and Surface Localization of External Control Device-Targeted Arteries for Noncompressible Torso Hemorrhage
    Oxford University Press (OUP) ; 2022
    In:  Military Medicine Vol. 187, No. 3-4 ( 2022-03-28), p. e343-e350
    Details
    In: Military Medicine, Oxford University Press (OUP), Vol. 187, No. 3-4 ( 2022-03-28), p. e343-e350
    Abstract: External hemorrhage control devices (EHCDs) are effective in reducing the death risk of noncompressible torso hemorrhage (NCTH), but the pressurized area is too large to prevent serious organ damage. This study aims to establish the surface localization strategy of EHCDs based on the anatomical features of NCTH-related arteries through CT images to facilitate the optimal design and application of EHCDs. Methods Two hundred patients who underwent abdominal CT were enrolled. Anatomical parameters such as the length of the common iliac artery (CIA), the external iliac artery (EIA), and the common femoral artery were measured; positional relationships among the EHCD-targeted arteries, umbilicus, anterior superior iliac spine (ASIS), and pubic tubercle (PT) were determined. The accuracy of surface localization was verified by the 3D-printed mannequins of 20 real patients. Results Aortic bifurcation (AB) was 7.5 ± 8.6 mm to the left of the umbilicus. The left CIA (left: 46.6 ± 16.0 mm vs. right: 43.3 ± 15.5 mm, P = .038) and the right EIA (left: 102.6 ± 16.3 mm vs. right: 111.5 ± 18.8 mm, P  & lt; .001) were longer than their counterparts, respectively. The vertical distance between the CIA terminus and the ipsilateral AB–ASIS line was 19.6 ± 8.2 mm, and the left and right perpendicular intersections were located at the upper one-third and one-fourth of the AB–ASIS line, respectively. The length ratio of EIA–ASIS to ASIS–PT was 0.6:1. The predicted point and its actual subpoint were significantly correlated (P ≤ .002), and the vertical distance between the two points was ≤5.5 mm. Conclusion The arterial localization strategy established via anatomical investigation was consistent with the actual situation. The data are necessary for improving EHCD design, precise hemostasis, and EHCD-related collateral injuries. Trial registration: Ratification no. 2019092. Registered November 4, 2020—retrospectively registered, www.chictr.org.cn.
    Type of Medium: Online Resource
    ISSN: 0026-4075 , 1930-613X
    URL: Article
    DOI: 10.1093/milmed/usab050
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 2130577-8
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  • 3
    Online Resource
    Online Resource
    SP009MORTALITY AND COST OF HYPONATREMIA AMONG CHINESE IN-HOSPITAL PATIENTS IN A SINGLE CENTER
    Oxford University Press (OUP) ; 2016
    In:  Nephrology Dialysis Transplantation Vol. 31, No. suppl_1 ( 2016-05), p. i89-i89
    Details
    In: Nephrology Dialysis Transplantation, Oxford University Press (OUP), Vol. 31, No. suppl_1 ( 2016-05), p. i89-i89
    Type of Medium: Online Resource
    ISSN: 1460-2385 , 0931-0509
    URL: Article
    DOI: 10.1093/ndt/gfw155.09
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2016
    detail.hit.zdb_id: 1465709-0
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  • 4
    Online Resource
    Online Resource
    The allosteric gating mechanism of the MthK channel
    Oxford University Press (OUP) ; 2022
    In:  National Science Review Vol. 9, No. 8 ( 2022-09-03)
    Details
    In: National Science Review, Oxford University Press (OUP), Vol. 9, No. 8 ( 2022-09-03)
    Abstract: Allostery is a fundamental element during channel gating in response to an appropriate stimulus by which events occurring at one site are transmitted to distal sites to regulate activity. To address how binding of the first Ca2+ ion at one of the eight chemically identical subunits facilitates the other Ca2+-binding events in MthK, a Ca2+-gated K+ channel containing a conserved ligand-binding RCK domain, we analysed a large collection of MthK structures and performed the corresponding thermodynamic and electrophysiological measurements. These structural and functional studies led us to conclude that the conformations of the Ca2+-binding sites alternate between two quaternary states and exhibit significant differences in Ca2+ affinity. We further propose an allosteric model of the MthK-gating mechanism by which a cascade of structural events connect the initial Ca2+-binding to the final changes of the ring structure that open the ion-conduction pore. This mechanical model reveals the exquisite design that achieves the allosteric gating and could be of general relevance for the action of other ligand-gated ion channels containing the RCK domain.
    Type of Medium: Online Resource
    ISSN: 2095-5138 , 2053-714X
    URL: Article
    DOI: 10.1093/nsr/nwac072
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 2745465-4
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  • 5
    Online Resource
    Online Resource
    WADDINGTON’S LANDSCAPE OF CELL AGING
    Oxford University Press (OUP) ; 2019
    In:  Innovation in Aging Vol. 3, No. Supplement_1 ( 2019-11-08), p. S208-S208
    Details
    In: Innovation in Aging, Oxford University Press (OUP), Vol. 3, No. Supplement_1 ( 2019-11-08), p. S208-S208
    Abstract: Cellular aging is a complex process that involves many interwoven molecular processes. Studies in model organisms have identified many individual genes and factors that have profound effects on lifespan. However, how these genes and factors interact and function collectively to drive the aging process remains unclear. We investigated single-cell aging dynamics throughout the replicative lifespans of S. cerevisiae, and found that isogenic cells diverge towards two aging paths, with distinct phenotypic changes and death forms. We further identified specific molecular pathways driving each aging fate and revealed that these pathways interact and operate dynamically to enable an early-life switch that governs the aging fate decision and the progression towards death. Our work uncovers the interconnected molecular pathways that drives the aging process and opens up the possibility of designing interventions that simultaneously target multiple network nodes, instead of single genes, to more effectively extend the healthspan.
    Type of Medium: Online Resource
    ISSN: 2399-5300
    URL: Article
    DOI: 10.1093/geroni/igz038.755
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 2905697-4
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  • 6
    Online Resource
    Online Resource
    Semi-Parametric Time-to-Event Modelling of Lengths of Hospital Stays
    Oxford University Press (OUP) ; 2022
    In:  Journal of the Royal Statistical Society Series C: Applied Statistics Vol. 71, No. 5 ( 2022-11-01), p. 1623-1647
    Details
    In: Journal of the Royal Statistical Society Series C: Applied Statistics, Oxford University Press (OUP), Vol. 71, No. 5 ( 2022-11-01), p. 1623-1647
    Abstract: Length of stay (LOS) is an essential metric for the quality of hospital care. Published works on LOS analysis have primarily focused on skewed LOS distributions and the influences of patient diagnostic characteristics. Few authors have considered the events that terminate a hospital stay: Both successful discharge and death could end a hospital stay but with completely different implications. Modelling the time to the first occurrence of discharge or death obscures the true nature of LOS. In this research, we propose a structure that simultaneously models the probabilities of discharge and death. The model has a flexible formulation that accounts for both additive and multiplicative effects of factors influencing the occurrence of death and discharge. We present asymptotic properties of the parameter estimates so that valid inference can be performed for the parametric as well as nonparametric model components. Simulation studies confirmed the good finite-sample performance of the proposed method. As the research is motivated by practical issues encountered in LOS analysis, we analysed data from two real clinical studies to showcase the general applicability of the proposed model.
    Type of Medium: Online Resource
    ISSN: 0035-9254 , 1467-9876
    URL: Article
    DOI: 10.1111/rssc.12593
    RVK:
    SA 7810
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 204797-4
    detail.hit.zdb_id: 1482300-7
    detail.hit.zdb_id: 1476894-X
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  • 7
    Online Resource
    Online Resource
    scGNN 2.0: a graph neural network tool for imputation and clustering of single-cell RNA-Seq data
    Oxford University Press (OUP) ; 2022
    In:  Bioinformatics Vol. 38, No. 23 ( 2022-11-30), p. 5322-5325
    Details
    In: Bioinformatics, Oxford University Press (OUP), Vol. 38, No. 23 ( 2022-11-30), p. 5322-5325
    Abstract: Gene expression imputation has been an essential step of the single-cell RNA-Seq data analysis workflow. Among several deep-learning methods, the debut of scGNN gained substantial recognition in 2021 for its superior performance and the ability to produce a cell–cell graph. However, the implementation of scGNN was relatively time-consuming and its performance could still be optimized. Results The implementation of scGNN 2.0 is significantly faster than scGNN thanks to a simplified close-loop architecture. For all eight datasets, cell clustering performance was increased by 85.02% on average in terms of adjusted rand index, and the imputation Median L1 Error was reduced by 67.94% on average. With the built-in visualizations, users can quickly assess the imputation and cell clustering results, compare against benchmarks and interpret the cell–cell interaction. The expanded input and output formats also pave the way for custom workflows that integrate scGNN 2.0 with other scRNA-Seq toolkits on both Python and R platforms. Availability and implementation scGNN 2.0 is implemented in Python (as of version 3.8) with the source code available at https://github.com/OSU-BMBL/scGNN2.0. Supplementary information Supplementary data are available at Bioinformatics online.
    Type of Medium: Online Resource
    ISSN: 1367-4803 , 1367-4811
    URL: Article
    DOI: 10.1093/bioinformatics/btac684
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 1468345-3
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    Radiomics-clinical nomogram for preoperative lymph node metastasis prediction in esophageal carcinoma
    Oxford University Press (OUP) ; 2024
    In:  British Journal of Radiology ( 2024-01-24)
    Details
    In: British Journal of Radiology, Oxford University Press (OUP), ( 2024-01-24)
    Abstract: This research aimed to develop a radiomics-clinical nomogram based on enhanced thin-section CT radiomics and clinical features for the purpose of predicting the presence or absence of metastasis in lymph nodes among patients with resectable esophageal squamous cell carcinoma (ESCC). Methods This study examined the data of 256 patients with ESCC, including 140 cases with lymph node metastasis. Clinical information was gathered for each case, and radiomics features were derived from thin-section contrast-enhanced CT with the help of a 3D slicer. To validate risk factors that are independent of the clinical and radiomics models, least absolute shrinkage and selection operator logistic regression analysis was used. A nomogram pattern was constructed based on the radiomics features and clinical characteristics. The receiver operating characteristic curve and Brier Score were used to evaluate the model's discriminatory ability, the calibration plot to evaluate the model's calibration, and the decision curve analysis to evaluate the model’s clinical utility. The confusion matrix was used to evaluate the applicability of the model. To evaluate the efficacy of the model, 1000 rounds of 5-fold cross-validation were conducted. Results The clinical model identified esophageal wall thickness and clinical T (cT) stage as independent risk factors, whereas the radiomics pattern was built based on 4 radiomics features chosen at random. Area under the curve (AUC) values of 0.684 and 0.701 are observed for the radiomics approach and clinical model, respectively. The AUC of nomogram combining radiomics and clinical features was 0.711. The calibration plot showed good agreement between the incidence of lymph node metastasis predicted by the nomogram and the actual probability of occurrence. The nomogram model displayed acceptable levels of performance. After 1000 rounds of 5-fold cross-validation, the AUC and Brier score had median values of 0.702 (IQR: 0.65, 7.49) and 0.21 (IQR: 0.20, 0.23), respectively. High-risk patients (risk point & gt;110) were found to have an increased risk of lymph node metastasis [odds ratio (OR) = 5.15, 95% CI, 2.95-8.99] based on the risk categorization. Conclusion A successful preoperative prediction performance for metastasis to the lymph nodes among patients with ESCC was demonstrated by the nomogram that incorporated CT radiomics, wall thickness, and cT stage. Advances in knowledge This study demonstrates a novel radiomics-clinical nomogram for lymph node metastasis prediction in ESCC, which helps physicians determine lymph node status preoperatively.
    Type of Medium: Online Resource
    ISSN: 0007-1285 , 1748-880X
    URL: Article
    DOI: 10.1093/bjr/tqae009
    RVK:
    XA 34700
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2024
    detail.hit.zdb_id: 1468548-6
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  • 9
    Online Resource
    Online Resource
    MiR-501-5p regulates CYLD expression and promotes cell proliferation in human hepatocellular carcinoma
    Oxford University Press (OUP) ; 2015
    In:  Japanese Journal of Clinical Oncology Vol. 45, No. 8 ( 2015-08), p. 738-744
    Details
    In: Japanese Journal of Clinical Oncology, Oxford University Press (OUP), Vol. 45, No. 8 ( 2015-08), p. 738-744
    Type of Medium: Online Resource
    ISSN: 0368-2811 , 1465-3621
    URL: Article
    DOI: 10.1093/jjco/hyv063
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2015
    detail.hit.zdb_id: 1494610-5
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  • 10
    Online Resource
    Online Resource
    Glutathione and neodiosmin feedback sustain plant immunity
    Oxford University Press (OUP) ; 2023
    In:  Journal of Experimental Botany Vol. 74, No. 3 ( 2023-02-05), p. 976-990
    Details
    In: Journal of Experimental Botany, Oxford University Press (OUP), Vol. 74, No. 3 ( 2023-02-05), p. 976-990
    Abstract: Plants have evolved a two-layer immune system comprising pattern-triggered immunity (PTI) and effector-triggered immunity (ETI) that is activated in response to pathogen invasion. Microbial patterns and pathogen effectors can be recognized by surface-localized pattern-recognition receptors (PRRs) and intracellularly localized nucleotide-binding leucine-rich repeat receptors (NLRs) to trigger PTI and ETI responses, respectively. At present, the metabolites activated by PTI and ETI and their roles and signalling pathways in plant immunity are not well understood. In this study, metabolomic analysis showed that ETI and PTI induced various flavonoids and amino acids and their derivatives in plants. Interestingly, both glutathione and neodiosmin content were specifically up-regulated by ETI and PTI, respectively, which significantly enhanced plant immunity. Further studies showed that glutathione and neodiosmin failed to induce a plant immune response in which PRRs/co-receptors were mutated. In addition, glutathione-reduced mutant gsh1 analysis showed that GSH1 is also required for PTI and ETI. Finally, we propose a model in which glutathione and neodiosmin are considered signature metabolites induced in the process of ETI and PTI activation in plants and further continuous enhancement of plant immunity in which PRRs/co-receptors are needed. This model is beneficial for an in-depth understanding of the closed-loop mode of the positive feedback regulation of PTI and ETI signals at the metabolic level.
    Type of Medium: Online Resource
    ISSN: 0022-0957 , 1460-2431
    URL: Article
    DOI: 10.1093/jxb/erac442
    RVK:
    WA 15000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 1466717-4
    SSG: 12
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