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3. Consortium Blockchain Based Anonymous and Trusted Authentication Mechanism for IoT

Author

Su, Tianhong, Li, Wenjing, Liu, Di, Guo, Shaoyong, Ruan, Linna, Angrisani, Leopoldo, Series Editor, Arteaga, Marco, Series Editor, Panigrahi, Bijaya Ketan, Series Editor, Chakraborty, Samarjit, Series Editor, Chen, Jiming, Series Editor, Chen, Shanben, Series Editor, Chen, Tan Kay, Series Editor, Dillmann, Rüdiger, Series Editor, Duan, Haibin, Series Editor, Ferrari, Gianluigi, Series Editor, Ferre, Manuel, Series Editor, Hirche, Sandra, Series Editor, Jabbari, Faryar, Series Editor, Jia, Limin, Series Editor, Kacprzyk, Janusz, Series Editor, Khamis, Alaa, Series Editor, Kroeger, Torsten, Series Editor, Li, Yong, Series Editor, Liang, Qilian, Series Editor, Martín, Ferran, Series Editor, Ming, Tan Cher, Series Editor, Minker, Wolfgang, Series Editor, Misra, Pradeep, Series Editor, Möller, Sebastian, Series Editor, Mukhopadhyay, Subhas, Series Editor, Ning, Cun-Zheng, Series Editor, Nishida, Toyoaki, Series Editor, Oneto, Luca, Series Editor, Pascucci, Federica, Series Editor, Qin, Yong, Series Editor, Seng, Gan Woon, Series Editor, Speidel, Joachim, Series Editor, Veiga, Germano, Series Editor, Wu, Haitao, Series Editor, Zamboni, Walter, Series Editor, Zhang, Junjie James, Series Editor, Sun, Songlin, editor, Hong, Tao, editor, Yu, Peng, editor, and Zou, Jiaqi, editor

Published
2022
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4. A study of the selective pressures on inherited mitochondrial DNA mutations in mitotic cell populations

Author

Su, Tianhong

Subjects
571.6
Abstract

Mitochondrial DNA (mtDNA) mutations accumulate somatically with age in normal individuals causing defects in oxidative phosphorylation (OXPHOS), with no selective pressures promoting their accumulation or removal. mtDNA mutations are also inherited through the germline causing mtDNA disease. In contrast to somatic mutations, they are lost in blood over time, suggesting selective pressure against them. This project aims to further investigate the selective loss of inherited mtDNA point mutations in mitotic tissues, using gastrointestinal epithelium as a model. I have determined the mtDNA mutation load and OXPHOS protein levels in various gastrointestinal segments of patients with the inherited m.3243A > G and m.8344A > G mtDNA mutations. The data shows selective loss of these mutations in the mitotic epithelium, but not the post-mitotic smooth muscle and suggests that the selection occurs in the gastrointestinal stem cells. I have further characterised a mouse model of mitochondrial disease carrying the inherited m.5024C > T mutation and have used them to study potential mechanisms of selective mtDNA mutation loss. These mice show: (1) loss of the m.5024C > T in the mitotic spleen and gastrointestinal epithelium with age but not in the post-mitotic tissues; (2) the rate of mutation loss is related to the rate of epithelial cell turnover; (3) the mutation loss in the intestinal epithelium is consistent with maintained levels of OXPHOS proteins with age, in contrast to the accumulation of cells with OXPHOS defects in aged wild-type mice; (4) significantly upregulated mitochondrial proliferation in the intestinal epithelium. These key findings highlight differences in the selective pressures on inherited and somatic mtDNA mutations in mitotic tissue, and the contrasting tissue-specific dynamics of inherited mtDNA mutations in mitotic and post-mitotic tissues. These findings are important to further the understanding of phenotype development, progression and potential treatment of mtDNA disease, and the effect of mtDNA mutations on ageing stem cell biology.

Published
2019

5. Power Blockchain Guarantee Mechanism Based on Trusted Computing

Author

Yan, Yong, Su, Tianhong, Guo, Shaoyong, Kang, Song, Goos, Gerhard, Founding Editor, Hartmanis, Juris, Founding Editor, Bertino, Elisa, Editorial Board Member, Gao, Wen, Editorial Board Member, Steffen, Bernhard, Editorial Board Member, Woeginger, Gerhard, Editorial Board Member, Yung, Moti, Editorial Board Member, Sun, Xingming, editor, Zhang, Xiaorui, editor, and Xia, Zhihua, editor

Published
2021
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10. N6-Methyladenosine Reader YTHDF1 Promotes Stemness and Therapeutic Resistance in Hepatocellular Carcinoma by Enhancing NOTCH1 Expression

Author

Zhang, Xinyue, primary, Su, Tianhong, additional, Wu, Yifan, additional, Cai, Yuhong, additional, Wang, Lina, additional, Liang, Cong, additional, Zhou, Lei, additional, Wang, Shiyan, additional, Li, Xiao-Xing, additional, Peng, Sui, additional, Kuang, Ming, additional, Yu, Jun, additional, and Xu, Lixia, additional

Published
2024
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13. Cell division can accelerate the loss of a heteroplasmic mitochondrial DNA mutation in a mouse model of mitochondrial disease

Author

Su, Tianhong, primary, Gomes, Tiago MB, additional, Smith, Anna LM, additional, Whitehall, Julia C, additional, Blain, Alasdair P, additional, Simard, Marie-Lune, additional, Scholten, Louisa, additional, Stewart, James B, additional, Turnbull, Doug M, additional, Lawless, Conor, additional, and Greaves, Laura Catherine, additional

Published
2023
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14. Supplementary Figure from Combination Neoantigen-Based Dendritic Cell Vaccination and Adoptive T-Cell Transfer Induces Antitumor Responses Against Recurrence of Hepatocellular Carcinoma

Author

Peng, Sui, primary, Chen, Shuling, primary, Hu, Wei, primary, Mei, Jie, primary, Zeng, Xuezhen, primary, Su, Tianhong, primary, Wang, Wei, primary, Chen, Zebin, primary, Xiao, Han, primary, Zhou, Qian, primary, Li, Bin, primary, Xie, Yubin, primary, Hu, Huanjing, primary, He, Minghui, primary, Han, Yanyan, primary, Tang, Longqing, primary, Ma, Yifan, primary, Li, Xiaoshuang, primary, Zhou, Xiangjun, primary, Dai, Zihao, primary, Liu, Zelong, primary, Tan, Jiehui, primary, Xu, Lixia, primary, Li, Shaoqiang, primary, Shen, Shunli, primary, Li, Dongming, primary, Lai, Jiaming, primary, Peng, Baogang, primary, Peng, Zhenwei, primary, and Kuang, Ming, primary

Published
2023
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15. Data from Combination Neoantigen-Based Dendritic Cell Vaccination and Adoptive T-Cell Transfer Induces Antitumor Responses Against Recurrence of Hepatocellular Carcinoma

Author

Peng, Sui, primary, Chen, Shuling, primary, Hu, Wei, primary, Mei, Jie, primary, Zeng, Xuezhen, primary, Su, Tianhong, primary, Wang, Wei, primary, Chen, Zebin, primary, Xiao, Han, primary, Zhou, Qian, primary, Li, Bin, primary, Xie, Yubin, primary, Hu, Huanjing, primary, He, Minghui, primary, Han, Yanyan, primary, Tang, Longqing, primary, Ma, Yifan, primary, Li, Xiaoshuang, primary, Zhou, Xiangjun, primary, Dai, Zihao, primary, Liu, Zelong, primary, Tan, Jiehui, primary, Xu, Lixia, primary, Li, Shaoqiang, primary, Shen, Shunli, primary, Li, Dongming, primary, Lai, Jiaming, primary, Peng, Baogang, primary, Peng, Zhenwei, primary, and Kuang, Ming, primary

Published
2023
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17. Hypoxia-inducible factor-1α mediates reflux-induced epithelial-mesenchymal plasticity in Barrett’s oesophagus patients

Author

Zhang, Qiuyang, Dunbar, Kerry B, Odze, Robert D, Agoston, Agoston T, Wang, Xuan, Su, Tianhong, Nguyen, Anh D, Zhang, Xi, Spechler, Stuart Jon, and Souza, Rhonda F

Abstract

IntroductionEpithelial-mesenchymal plasticity (EMP), the process through which epithelial cells acquire mesenchymal features, is needed for wound repair but also might contribute to cancer initiation. Earlier, in vitro studies showed that Barrett’s cells exposed to acidic bile salt solutions (ABS) develop EMP. Now, we have (1) induced reflux oesophagitis in Barrett’s oesophagus (BO) patients by stopping proton pump inhibitors (PPIs), (2) assessed their biopsies for EMP and (3) explored molecular pathways underlying reflux-induced EMP in BO cells and spheroids.Methods15 BO patients had endoscopy with biopsies of Barrett’s metaplasia while on PPIs, and 1 and 2 weeks after stopping PPIs; RNA-seq data were assessed for enrichments in hypoxia-inducible factors (HIFs), angiogenesis and EMP pathways. In BO biopsies, cell lines and spheroids, EMP features (motility) and markers (vascular endothelial growth factor (VEGF), ZEB1, miR-200a&b) were evaluated by morphology, migration assays, immunostaining and qPCR; HIF-1α was knocked down with siRNA or shRNA.ResultsAt 1 and/or 2 weeks off PPIs, BO biopsies exhibited EMP features and markers, with significant enrichment for HIF-1α, angiogenesis and EMP pathways. In BO cells, ABS induced HIF-1α activation, which decreased miR-200a&b while increasing VEGF, ZEB1 and motility; HIF-1α knockdown blocked these effects. After ABS treatment, BO spheroids exhibited migratory protrusions showing nuclear HIF-1α, increased VEGF and decreased miR-200a&b.ConclusionsIn BO patients, reflux oesophagitis induces EMP changes associated with increased HIF-1α signalling in Barrett’s metaplasia. In Barrett’s cells, ABS trigger EMP via HIF-1α signalling. Thus, HIF-1α appears to play a key role in mediating reflux-induced EMP that might contribute to cancer in BO.Trial registration numberNCT02579460.

Published
2024
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22. Eliminating METTL1‐mediated accumulation of PMN‐MDSCs prevents hepatocellular carcinoma recurrence after radiofrequency ablation

Author

Zeng, Xuezhen, primary, Liao, Guanrui, additional, Li, Shumin, additional, Liu, Haining, additional, Zhao, Xiao, additional, Li, Shuang, additional, Lei, Kai, additional, Zhu, Shenghua, additional, Chen, Zhihang, additional, Zhao, Yi, additional, Ren, Xuxin, additional, Su, Tianhong, additional, Cheng, Alfred Sze‐Lok, additional, Peng, Sui, additional, Lin, Shuibin, additional, Wang, Ji, additional, Chen, Shuling, additional, and Kuang, Ming, additional

Published
2022
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24. Combination Neoantigen-Based Dendritic Cell Vaccination and Adoptive T-Cell Transfer Induces Antitumor Responses Against Recurrence of Hepatocellular Carcinoma

Author

Peng, Sui, primary, Chen, Shuling, additional, Hu, Wei, additional, Mei, Jie, additional, Zeng, Xuezhen, additional, Su, Tianhong, additional, Wang, Wei, additional, Chen, Zebin, additional, Xiao, Han, additional, Zhou, Qian, additional, Li, Bin, additional, Xie, Yubin, additional, Hu, Huanjing, additional, He, Minghui, additional, Han, Yanyan, additional, Tang, Longqing, additional, Ma, Yifan, additional, Li, Xiaoshuang, additional, Zhou, Xiangjun, additional, Dai, Zihao, additional, Liu, Zelong, additional, Tan, Jiehui, additional, Xu, Lixia, additional, Li, Shaoqiang, additional, Shen, Shunli, additional, Li, Dongming, additional, Lai, Jiaming, additional, Peng, Baogang, additional, Peng, Zhenwei, additional, and Kuang, Ming, additional

Published
2022
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27. Insufficient Radiofrequency Ablation Promotes Hepatocellular Carcinoma Metastasis Through N6‐Methyladenosine mRNA Methylation‐Dependent Mechanism

Author

Su, Tianhong, primary, Huang, Manling, additional, Liao, Junbin, additional, Lin, Shuibin, additional, Yu, Peng, additional, Yang, Jianhua, additional, Cai, Yuhong, additional, Zhu, Shenghua, additional, Xu, Lixia, additional, Peng, Zhenwei, additional, Peng, Sui, additional, Chen, Shuling, additional, and Kuang, Ming, additional

Published
2021
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34. Liver resection versus transarterial chemoembolization for the treatment of intermediate‐stage hepatocellular carcinoma

Author

Chen, Shuling, primary, Jin, Huilin, additional, Dai, Zihao, additional, Wei, Mengchao, additional, Xiao, Han, additional, Su, Tianhong, additional, Li, Bin, additional, Liu, Xin, additional, Wang, Yu, additional, Li, Jiaping, additional, Shen, Shunli, additional, Zhou, Qi, additional, Peng, Baogang, additional, Peng, Zhenwei, additional, and Peng, Sui, additional

Published
2019
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38. Sa1660 - Esophageal Adenocarcinoma (Eac) Exosomes Induce Features of Epithelial Mesenchymal Transition in Non-Neoplastic Barrett's Epithelial Cells: A Potential Mechanism for Carcinogenesis in the Barrett's Metaplasia Surrounding Eacs

Author

Liang, Wei, primary, Zhang, Xi, additional, Huo, Xiaofang, additional, Su, Tianhong, additional, Peng, Sui, additional, Spechler, Stuart J., additional, Souza, Rhonda F., additional, and Zhang, Qiuyang D., additional

Published
2018
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40. Liver Resection Versus Transarterial Chemoembolization for the Treatment of Intermediate-Stage Hepatocellular Carcinoma

Author

Chen, Shuling, primary, Dai, Zihao, additional, Jin, Huilin, additional, Wei, Mengchao, additional, Xiao, Han, additional, Su, Tianhong, additional, Li, Bin, additional, Wang, Yu, additional, Li, Jiaping, additional, Shen, Shunli, additional, Peng, Baogang, additional, Peng, Sui, additional, Peng, Zhenwei, additional, and Kuang, Ming, additional

Published
2018
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41. In Non-Neoplastic Barrett's Epithelial Cells, Acid and Bile Salts Induce Epithelial Mesenchymal Transition (EMT) through a Hif-Mediated Reduction in Microrna-200a and -200b Expression

Author

Su, Tianhong, primary, Zhang, Xi, additional, Yu, Chunhua, additional, Huo, Xiaofang, additional, Pham, Thai, additional, Dunbar, Kerry B., additional, Cheng, Edaire, additional, Bajpai, Manisha, additional, Das, Kiron M., additional, Wang, David H., additional, Spechler, Stuart J., additional, Souza, Rhonda F., additional, and Zhang, Qiuyang D., additional

Published
2017
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48. Correlation between epicardial adipose tissue and myocardial injury in patients with COVID-19.

Author

Su T, Zhong B, Tang C, Qiao S, Feng Y, Peng H, and Gu X

Abstract

Background: Many people infected with COVID-19 develop myocardial injury. Epicardial adipose tissue (EAT) is among the various risk factors contributing to coronary artery disease. However, its correlation with myocardial injury in patients diagnosed with COVID-19 remains uncertain. Methods : We examined myocardial biomarkers in population affected by COVID-19 during the period from December 2022 to January 2023. The patients without myocardial injury were referred to as group A ( n = 152) and those with myocardial injury were referred to as group B ( n = 212). Results: 1) The A group and the B group exhibitedstatistically significant differences in terms of age, TC, CRP, Cr, BUN, LDL-C, IL-6, BNP, LVEF and EAT ( p < 0.05). 2) EAT volumehad a close relationship with IL-6, LDL-C, cTnI, and CRP ( p < 0.05); the corresponding correlation coefficient values were 0.24, 0.21, 0.24, and 0.16. In contrast to those with lower EAT volume, more subjects with a higher volume of EAT had myocardial injury ( p < 0.05). Regression analysis showed that EAT, LDL-C, Age and Cr were established as independent risk variables for myocardial injury in subjects affected by COVID-19. 3) In COVID-19 patients, the likelihood of myocardial injury rised notably as EAT levels increase ( p < 0.001). Addition of EAT to the basic risk model for myocardial injury resulted in improved reclassification. (Net reclassification index: 58.17%, 95% CI: 38.35%, 77.99%, p < 0.001). Conclusion: Patients suffering from COVID-19 with higher volume EAT was prone to follow myocardial injury and EAT was an independent predictor of heart damage in these individuals., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Su, Zhong, Tang, Qiao, Feng, Peng and Gu.)

Published
2024
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49. Single-Cell Studies of Intestinal Stem Cell Heterogeneity During Homeostasis and Regeneration.

Author

Norkin M, Capdevila C, Calderon RI, Su T, Trifas M, Ordóñez-Morán P, and Yan KS

Subjects
Animals, Cell Differentiation genetics, Cell Differentiation physiology, Computational Biology methods, Homeostasis genetics, Homeostasis physiology, Humans, Single-Cell Analysis, Transcriptome genetics, Intestinal Mucosa cytology, Intestinal Mucosa metabolism, Sequence Analysis, RNA methods
Abstract

Single-cell RNA-sequencing (scRNA-seq) provides a unique opportunity to study heterogeneous cell populations within tissues, including the intestinal epithelium, to gain detailed molecular insights into their biology. Many new putative markers of intestinal stem cells and their progeny have been described using single-cell transcriptomics, which has contributed to the identification of novel subpopulations of mature cell types and insight into their developmental trajectories. This approach has revealed tremendous cellular heterogeneity within the intestinal epithelium that is concordant with its diverse and multifaceted functions. We discuss the function of these subpopulations during tissue homeostasis, as well as putative subpopulations with inducible regenerative potential following tissue injury.

Published
2020
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50. [Effect of metformin on colorectal carcinoma in type 2 diabetes mellitus patients: a Markov model analysis].

Author

Su T, Liao B, Dong Y, Peng Z, Zhou Q, Li B, Peng S, and Zhang N

Subjects
Adult, Humans, Prospective Studies, Randomized Controlled Trials as Topic, Retrospective Studies, Colorectal Neoplasms prevention & control, Diabetes Mellitus, Type 2 drug therapy, Hypoglycemic Agents therapeutic use, Metformin therapeutic use
Abstract

Objective: To evaluate the colorectal cancer (CRC) prevention effect of metformin in comparison with that of other T2DM medications from a Markov model perspective., Methods: Literature concerning CRC morbidity of T2DM patients with metformin or other diabetes medications treatment was reviewed in PubMed and Cochrane Library database from September 2010 to December 2016., Inclusion Criteria: (1)enrolled population was adult patients with T2DM but without CRC; (2) any of the parameters applied in our model was reported; (3) randomized clinical trials (RCTs), quasi-randomized trials, prospective or retrospective cohort studies. With CRC morbidity as endpoint, parameters were extracted to construct Markov model to assess CRC morbidity and cumulative tumor-free survival in each group over 11 years' follow-up period. Finally, Monte Carlo analysis was performed to evaluate the influence of parameter instability on the model., Results: Seven literatures were recruited and 10 000 patients were virtually allocated for each arm. In contrast with non-metformin group, T2DM patients treated with metformin had a lower rate of CRC(1.670% vs. 2.146%, P=0.016). Moreover, cumulative tumor-free survival of metformin group was, slightly but significantly, better than that of non-metformin group (10.908 years vs. 10.882 years, P=0.000)., Conclusions: T2DM patients treated with metformin have a lower morbidity of CRC and a better cumulative tumor-free survival than those of non-metformin group. Large scale RCTs are needed to illustrate the role of metformin in the prevention of CRC.

Published
2017

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