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5,117 results on '"Yin, Xin"'

161. Improving prediction of the terrestrial water storage anomalies during the GRACE and GRACE-FO gap with Bayesian convolutional neural networks

Author

Mo, Shaoxing, Zhong, Yulong, Shi, Xiaoqing, Feng, Wei, Yin, Xin, and Wu, Jichun

Subjects
Physics - Atmospheric and Oceanic Physics, Computer Science - Machine Learning
Abstract

The Gravity Recovery and Climate Experiment (GRACE) satellite and its successor GRACE Follow-On (GRACE-FO) provide valuable and accurate observations of terrestrial water storage anomalies (TWSAs) at a global scale. However, there is an approximately one-year observation gap of TWSAs between GRACE and GRACE-FO. This poses a challenge for practical applications, as discontinuity in the TWSA observations may introduce significant biases and uncertainties in the hydrological model predictions and consequently mislead decision making. To tackle this challenge, a Bayesian convolutional neural network (BCNN) driven by climatic data is proposed in this study to bridge this gap at a global scale. Enhanced by integrating recent advances in deep learning, including the attention mechanisms and the residual and dense connections, BCNN can automatically and efficiently extract important features for TWSA predictions from multi-source input data. The predicted TWSAs are compared to the hydrological model outputs and three recent TWSA prediction products. The comparison suggests the superior performance of BCNN in providing improved predictions of TWSAs during the gap in particular in the relatively arid regions. The BCNN's ability to identify the extreme dry and wet events during the gap period is further discussed and comprehensively demonstrated by comparing with the precipitation anomalies, drought index, ground/surface water levels. Results indicate that BCNN is capable of offering a reliable solution to maintain the TWSA data continuity and quantify the impacts of climate extremes during the gap., Comment: 27 pages, 13 figures

Published
2021
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166. 4 Combinations of immune checkpoint inhibitors with fractionated radiotherapy or DNA damage response agents leads to improved anti-tumour responses and modulates the tumour immune microenvironment

Author

Emily Wright, Stewart Brown, Lorraine Mooney, Charlotte Bell, Nick Moore, Theoni Katopodi, Yin Xin Ho, Lyndsey Hanson, Amy Cantrell, Jane Kendrew, Pablo Binder, Tobias Bunday, Paul Farrington, and Shannon Sharman

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Published
2023
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167. Functional landscape of SARS-CoV-2 cellular restriction

Author

Martin-Sancho, Laura, Lewinski, Mary K, Pache, Lars, Stoneham, Charlotte A, Yin, Xin, Becker, Mark E, Pratt, Dexter, Churas, Christopher, Rosenthal, Sara B, Liu, Sophie, Weston, Stuart, De Jesus, Paul D, O'Neill, Alan M, Gounder, Anshu P, Nguyen, Courtney, Pu, Yuan, Curry, Heather M, Oom, Aaron L, Miorin, Lisa, Rodriguez-Frandsen, Ariel, Zheng, Fan, Wu, Chunxiang, Xiong, Yong, Urbanowski, Matthew, Shaw, Megan L, Chang, Max W, Benner, Christopher, Hope, Thomas J, Frieman, Matthew B, García-Sastre, Adolfo, Ideker, Trey, Hultquist, Judd F, Guatelli, John, and Chanda, Sumit K

Subjects
Biological Sciences, Bioinformatics and Computational Biology, Vaccine Related, Lung, Pneumonia, Infectious Diseases, Biodefense, Pneumonia & Influenza, Prevention, Genetics, Emerging Infectious Diseases, 2.1 Biological and endogenous factors, Aetiology, Infection, Good Health and Well Being, Animals, Antigens, CD, Binding Sites, Cell Line, Tumor, Chlorocebus aethiops, Endoplasmic Reticulum, GPI-Linked Proteins, Gene Expression Regulation, Golgi Apparatus, HEK293 Cells, Host-Pathogen Interactions, Humans, Immunity, Innate, Interferon Regulatory Factors, Interferon Type I, Molecular Docking Simulation, Protein Binding, Protein Conformation, alpha-Helical, Protein Conformation, beta-Strand, Protein Interaction Domains and Motifs, SARS-CoV-2, Signal Transduction, Vero Cells, Viral Proteins, Virus Internalization, Virus Release, Virus Replication, BST2, ISG, Orf7a, innate immunity, interferon, viral evasion, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

A deficient interferon (IFN) response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been implicated as a determinant of severe coronavirus disease 2019 (COVID-19). To identify the molecular effectors that govern IFN control of SARS-CoV-2 infection, we conducted a large-scale gain-of-function analysis that evaluated the impact of human IFN-stimulated genes (ISGs) on viral replication. A limited subset of ISGs were found to control viral infection, including endosomal factors inhibiting viral entry, RNA binding proteins suppressing viral RNA synthesis, and a highly enriched cluster of endoplasmic reticulum (ER)/Golgi-resident ISGs inhibiting viral assembly/egress. These included broad-acting antiviral ISGs and eight ISGs that specifically inhibited SARS-CoV-2 and SARS-CoV-1 replication. Among the broad-acting ISGs was BST2/tetherin, which impeded viral release and is antagonized by SARS-CoV-2 Orf7a protein. Overall, these data illuminate a set of ISGs that underlie innate immune control of SARS-CoV-2/SARS-CoV-1 infection, which will facilitate the understanding of host determinants that impact disease severity and offer potential therapeutic strategies for COVID-19.

Published
2021

189. Mechanism of LINC00601 in regulating sensitivity of hepatocellular carcinoma cells to oxaliplatin chemotherapy

Author

HU Keshu, LIU Wenfeng, ZHANG Feng, QUAN Bing, YIN Xin

Subjects
hepatocellular carcinoma, long non-coding rna, oxaliplatin, chemotherapy resistance, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Background and purpose: Hepatocellular carcinoma (HCC) is still one of the most prevalent malignancies in China and throughout the world, while most of these patients are in intermediate or advanced stage when diagnosed. The resistance of advanced HCC to chemotherapy or interventional therapy is one of the crucial factors significantly limiting the survival and prognosis of patients. However, the molecular mechanisms involved have not been fully clarified. We previously found that the long non-coding RNA LINC00601 was highly expressed in oxaliplatin resistant HCC cells. This study aimed to explore the role and specific mechanism of LINC00601 in regulating the sensitivity of HCC cells to oxaliplatin chemotherapy, to provide a novel target to identify proper candidates for oxaliplatin chemotherapy, and the theoretical basis for the treatment of patients with advanced HCC. Methods: Human HCC cell line MHCC-97H and Hep-3B were induced to establish oxaliplatin resistant cell lines 97H-OXR and 3B-OXR by long-term low-dose oxaliplatin treatment in vitro. Real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) was used to detect the expression of LINC00601 in cell lines. Cell counting kit-8 (CCK-8) assay was performed to detect the effect of LINC00601 gene silencing or overexpression on the sensitivity of HCC cells to oxaliplatin treatment. Flow cytometry and Western blot experiments were conducted to detect the alteration of cell apoptosis. Finally, Western blot and immunofluorescence staining were applied to explore the nuclear translocation of growth arrest and DNA damage-inducible protein 45α (GADD45A), and RNA pull-down together with RNA immunoprecipitation (RIP) experiments were carried out to validate the combination of LINC00601 and GADD45A. Results: Compared with the control cells, LINC00601 expression level was significantly increased in oxaliplatin resistant cells. Both induced-oxaliplatin-resistant cells and LINC00601-overexpressed MHCC-97H cells were observed to be less sensitive to oxaliplatin administration. On the contrary, the down-regulation of LINC00601 expression in oxaliplatin resistant cells significantly increased the sensitivity to oxaliplatin treatment. Meanwhile, upregulated expression of LINC00601 inhibited the apoptosis level of HCC cell lines after oxaliplatin treatment, which was consistent with the sensitivity levels of different cell lines to oxaliplatin as above. In addition, the overexpression of LINC00601 reduced the nuclear translocation of GADD45A and the expression of GADD45A in the nucleus. Furthermore, the combination of LINC00601 and GADD45A was observed. Conclusion: LINC00601 might regulate the apoptotic progress of cells after oxaliplatin chemotherapy by interfering with the nuclear translocation of GADD45A, which eventually lead to the resistance to oxaliplatin.

Published
2023
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