Search

Your search keyword '"Liu, Tianxiao"' showing total 230 results
Start Over Author "Liu, Tianxiao"
230 results on '"Liu, Tianxiao"'

20. ACS Symposium Series

Author

Xiaoyu Wang, Ruofei Zhang, Hanqing Zhao, Kelong Fan, Yonghua Tang, Youhui Lin, Peng Li, Xuejiao J. Gao, Xingfa Gao, Xuechao Xu, Zhen Zhang, Hengjia Zhu, Jianming Pan, Xiangheng Niu, Shao-Bin He, Meng-Ting Lin, Hao-Hua Deng, Wei Chen, Yu Chong, Cuicui Ge, Bolong Xu, Shanshan Li, Huiyu Liu, Tianxiao M and Xiaoyu Wang, Ruofei Zhang, Hanqing Zhao, Kelong Fan, Yonghua Tang, Youhui Lin, Peng Li, Xuejiao J. Gao, Xingfa Gao, Xuechao Xu, Zhen Zhang, Hengjia Zhu, Jianming Pan, Xiangheng Niu, Shao-Bin He, Meng-Ting Lin, Hao-Hua Deng, Wei Chen, Yu Chong, Cuicui Ge, Bolong Xu, Shanshan Li, Huiyu Liu, Tianxiao M

Published
2022

22. MlrA, an Essential Enzyme for Microcystins and Nodularin on First Step Biodegradation in Microcystin-Degrading Bacteria

Author

Liu, Tianxiao, primary, Kurogo, Narumi, additional, Kodato, Miwa, additional, Fujimoto, Naoshi, additional, Itayama, Tomoaki, additional, Okano, Kunihiro, additional, Utsumi, Motoo, additional, Zhang, Zhenya, additional, Lei, Zhongfang, additional, Yuan, Tian, additional, Maseda, Hideaki, additional, Sugiura, Norio, additional, and Shimizu, Kazuya, additional

Published
2024
Full Text
View/download PDF

25. Eliminating Halogen Vacancies Enables Efficient MACL‐Assisted Formamidine Perovskite Solar Cells.

Author

Liu, Zhiyong, Liu, Tianxiao, Li, Meng, He, Tingwei, Guo, Gaofu, Liu, Pengfei, Chen, Ting, Yang, Jien, Qin, Chaochao, Dai, Xianqi, and Yuan, Mingjian

Subjects
*SOLAR cells, *FORMAMIDINES, *PHOTOVOLTAIC power systems, *PEROVSKITE, *HALOGENS, *CHLORIDE ions, *LEAD
Abstract

Methylammonium chloride (MACl) additive is almost irreplaceable in high‐performance formamidine perovskite photovoltaics. Nevertheless, Some of the problems that can arise from adding MACl are rarely mentioned. Herein, it is proposed for the first time that the addition of MACl would cause the non‐stoichiometric ratio in the perovskite film, resulting in the halogen vacancy. It is demonstrated that the non‐synchronous volatilization of methylamine cations and chloride ions leads to the formation of halogen vacancy defects. To solve this problem, the NH4HCOO is introduced into the perovskite precursor solution to passivate the halogen vacancy. The HCOO− ions have a strong force with lead ions and can fill the halogen vacancy defects. Consequently, the champion devices' power conversion efficiency (PCE) can be improved from 21.23% to 23.72% with negligible hysteresis. And the unencapsulated device can still retain >90% of the initial PCE even operating in N2 atmosphere for over 1200 h. This work illustrates another halogen defect source in the MACl‐assisted formamidine perovskite photovoltaics and provides a new route to obtain high‐performance perovskite solar cells. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

28. Eosinophils improve cardiac function after myocardial infarction

Author

Liu, Jing, Yang, Chongzhe, Liu, Tianxiao, Deng, Zhiyong, Fang, Wenqian, Zhang, Xian, Li, Jie, Huang, Qin, Liu, Conglin, Wang, Yunzhe, Yang, Dafeng, Sukhova, Galina K., Lindholt, Jes S., Diederichsen, Axel, Rasmussen, Lars M., Li, Dazhu, Newton, Gail, Luscinskas, Francis W., Liu, Lijun, Libby, Peter, Wang, Jing, Guo, Junli, and Shi, Guo-Ping

Published
2020
Full Text
View/download PDF

29. Cationic proteins from eosinophils bind bone morphogenetic protein receptors promoting vascular calcification and atherogenesis

Author

Meng, Zhaojie, primary, Zhang, Shuya, additional, Li, Wei, additional, Wang, Yunzhe, additional, Wang, Minjie, additional, Liu, Xin, additional, Liu, Cong-Lin, additional, Liao, Sha, additional, Liu, Tianxiao, additional, Yang, Chongzhe, additional, Lindholt, Jes S, additional, Rasmussen, Lars M, additional, Obel, Lasse M, additional, Stubbe, Jane, additional, Diederichsen, Axel C, additional, Sun, Yong, additional, Chen, Yabing, additional, Yu, Paul B, additional, Libby, Peter, additional, Shi, Guo-Ping, additional, and Guo, Junli, additional

Published
2023
Full Text
View/download PDF

32. Differential roles of eosinophils in cardiovascular disease

Author

Xu, Junyan, Guo, Junli, Liu, Tianxiao, Yang, Chongzhe, Meng, Zhaojie, Libby, Peter, Zhang, Jinying, and Shi, Guo-Ping

Abstract

Eosinophils are essential innate immune cells in allergic responses. Accumulating evidence indicates that eosinophils also participate in the pathogenesis of cardiovascular diseases (CVDs). In clinical studies, high blood eosinophil counts and eosinophil cationic protein levels have been associated with an increased risk of CVD, including myocardial infarction (MI), cardiac hypertrophy, atrial fibrillation, abdominal aortic aneurysm (AAA) and atherosclerosis. However, low blood eosinophil counts have also been reported to be a risk factor for MI, heart failure, aortic dissection, AAA, deep vein thrombosis, pulmonary embolism and ischaemic stroke. Although these conflicting clinical observations remain unexplained, CVD status, timing of eosinophil data collection, and tissue eosinophil phenotypic and functional heterogeneities might account for these discrepancies. Preclinical studies suggest that eosinophils have protective actions in MI, cardiac hypertrophy, heart failure and AAA. By contrast, cationic proteins and platelet-activating factor from eosinophils have been shown to promote vascular smooth muscle cell proliferation, vascular calcification, thrombomodulin inactivation and platelet activation and aggregation, thereby exacerbating atherosclerosis, atrial fibrillation, thrombosis and associated complications. Therefore, eosinophils seem to promote calcification and thrombosis in chronic CVD but are protective in acute cardiovascular settings. In this Review, we summarize the available clinical and preclinical data on the different roles of eosinophils in CVD.

Published
2024
Full Text
View/download PDF

34. Group 2 Innate Lymphoid Cells Protect Mice from Abdominal Aortic Aneurysm Formation via IL5 and Eosinophils

Author

Zhang, Yuanyuan, primary, Liu, Tianxiao, additional, Deng, Zhiyong, additional, Fang, Wenqian, additional, Zhang, Xian, additional, Zhang, Shuya, additional, Wang, Minjie, additional, Luo, Songyuan, additional, Meng, Zhaojie, additional, Liu, Jing, additional, Sukhova, Galina K., additional, Li, Dazhu, additional, McKenzie, Andrew N. J., additional, Libby, Peter, additional, Shi, Guo‐Ping, additional, and Guo, Junli, additional

Published
2023
Full Text
View/download PDF

40. Group 2 innate lymphoid cells protect mouse heart from myocardial infarction injury via interleukin 5, eosinophils, and dendritic cells

Author

Liu, Tianxiao, primary, Meng, Zhaojie, additional, Liu, Jing, additional, Li, Jie, additional, Zhang, Yuanyuan, additional, Deng, Zhiyong, additional, Luo, Songyuan, additional, Wang, Minjie, additional, Huang, Qin, additional, Zhang, Shuya, additional, Fendt, Pauline, additional, Devouassoux, Julie, additional, Li, Dazhu, additional, McKenzie, Andrew Neil James, additional, Nahrendorf, Matthias, additional, Libby, Peter, additional, Guo, Junli, additional, and Shi, Guo-Ping, additional

Published
2022
Full Text
View/download PDF

41. Untyped XQuery Canonization

Author

Travers, Nicolas, Dang Ngoc, Tuyêt Trâm, Liu, Tianxiao, Hutchison, David, editor, Kanade, Takeo, editor, Kittler, Josef, editor, Kleinberg, Jon M., editor, Mattern, Friedemann, editor, Mitchell, John C., editor, Naor, Moni, editor, Nierstrasz, Oscar, editor, Pandu Rangan, C., editor, Steffen, Bernhard, editor, Sudan, Madhu, editor, Terzopoulos, Demetri, editor, Tygar, Doug, editor, Vardi, Moshe Y., editor, Weikum, Gerhard, editor, Chang, Kevin Chen-Chuan, editor, Wang, Wei, editor, Chen, Lei, editor, Ellis, Clarence A., editor, Hsu, Ching-Hsien, editor, Tsoi, Ah Chung, editor, and Wang, Haixun, editor

Published
2007
Full Text
View/download PDF

42. Cost Framework for a Heterogeneous Distributed Semi-structured Environment

Author

Liu, Tianxiao, Dang Ngoc, Tuyêt Trâm, Laurent, Dominique, Hutchison, David, editor, Kanade, Takeo, editor, Kittler, Josef, editor, Kleinberg, Jon M., editor, Mattern, Friedemann, editor, Mitchell, John C., editor, Naor, Moni, editor, Nierstrasz, Oscar, editor, Pandu Rangan, C., editor, Steffen, Bernhard, editor, Sudan, Madhu, editor, Terzopoulos, Demetri, editor, Tygar, Doug, editor, Vardi, Moshe Y., editor, Weikum, Gerhard, editor, Chang, Kevin Chen-Chuan, editor, Wang, Wei, editor, Chen, Lei, editor, Ellis, Clarence A., editor, Hsu, Ching-Hsien, editor, Tsoi, Ah Chung, editor, and Wang, Haixun, editor

Published
2007
Full Text
View/download PDF

43. TGV: A Tree Graph View for Modeling Untyped XQuery

Author

Travers, Nicolas, Ngoc, Tuyêt Trâm Dang, Liu, Tianxiao, Hutchison, David, editor, Kanade, Takeo, editor, Kittler, Josef, editor, Kleinberg, Jon M., editor, Mattern, Friedemann, editor, Mitchell, John C., editor, Naor, Moni, editor, Nierstrasz, Oscar, editor, Pandu Rangan, C., editor, Steffen, Bernhard, editor, Sudan, Madhu, editor, Terzopoulos, Demetri, editor, Tygar, Doug, editor, Vardi, Moshe Y., editor, Weikum, Gerhard, editor, Kotagiri, Ramamohanarao, editor, Krishna, P. Radha, editor, Mohania, Mukesh, editor, and Nantajeewarawat, Ekawit, editor

Published
2007
Full Text
View/download PDF

44. IL18 signaling causes islet β cell development and insulin secretion via different receptors on acinar and β cells

Author

Zhang, Xian, primary, Luo, Songyuan, additional, Wang, Minjie, additional, Huang, Qin, additional, Fang, Wenqian, additional, Li, Jie, additional, Liu, Tianxiao, additional, Zhang, Yuanyuan, additional, Deng, Zhiyong, additional, Liu, Cong-Lin, additional, Guan, Shuling, additional, Ayala, Julio E., additional, Flavell, Richard A., additional, Kulkarni, Rohit N., additional, Libby, Peter, additional, Guo, Junli, additional, Liu, Zhangsuo, additional, and Shi, Guo-Ping, additional

Published
2022
Full Text
View/download PDF

45. Protective Effects of Remimazolam on Cerebral Ischemia/Reperfusion Injury in Rats by Inhibiting of NLRP3 Inflammasome-Dependent Pyroptosis

Author

Shi,Min, Chen,Jing, Liu,Tianxiao, Dai,Weixin, Zhou,Zhan, Chen,Lifei, Xie,Yubo, Shi,Min, Chen,Jing, Liu,Tianxiao, Dai,Weixin, Zhou,Zhan, Chen,Lifei, and Xie,Yubo

Abstract

Min Shi,* Jing Chen,* Tianxiao Liu,* Weixin Dai, Zhan Zhou, Lifei Chen, Yubo Xie Department of Anesthesiology, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yubo Xie, Department of Anesthesiology, The First Affiliated Hospital of Guangxi Medical University, No. 6 Shuang-yong Road, Nanning, 530021, People’s Republic of China, Tel +86 186 7795 8208, Email xybdoctor@163.comIntroduction: Remimazolam is a novel benzodiazepine γ-aminobutyric acid A (GABAa) receptor agonist used for sedation and the induction as well as maintenance of general anesthesia. Previous research proved that anesthetic agents acting on GABAa receptor, such as thiopentone, propofol and midazolam, have protective actions for cerebral ischemia/reperfusion (I/R) injury. We here probed into remimazolam for its protective effect and potential mechanism of action against cerebral I/R injury.Material and Methods: A rat model of middle cerebral artery occlusion (MCAO) with focal transient cerebral I/R injury was established and was given tail vein injection of gradient remimazolam (5, 10, 20 mg/kg) after 2 h of ischemia. Following 24 h of reperfusion, neurological function, brain infarct volume, morphology of cerebral cortical neurons, and expressions of corticocerebral NLRP3, ASC, caspase-1, GSDMD, IL-1β and IL-18 were evaluated.Results: The results showed that remimazolam could effectively improve the neurological dysfunction, reduce the infarct volume and alleviate the damage of cortical neurons after I/R injury. Notably, the expression of NLRP3 inflammasome pathway was down-regulated, suggesting that remimazolam exerted protective actions on I/R injury by suppressing pyroptosis with decreased expression and release of inflammatory factors, and the involvement of the NLRP3 inflammasome pathway might be the core during that process. Overall, our re

Published
2022

47. Group 2 innate lymphoid cells protect mouse heart from myocardial infarction injury via interleukin 5, eosinophils, and dendritic cells.

Author

Liu, Tianxiao, Meng, Zhaojie, Liu, Jing, Li, Jie, Zhang, Yuanyuan, Deng, Zhiyong, Luo, Songyuan, Wang, Minjie, Huang, Qin, Zhang, Shuya, Fendt, Pauline, Devouassoux, Julie, Li, Dazhu, McKenzie, Andrew Neil James, Nahrendorf, Matthias, Libby, Peter, Guo, Junli, and Shi, Guo-Ping

Subjects
*INNATE lymphoid cells, *DENDRITIC cells, *MYOCARDIAL infarction, *EOSINOPHILS, *HEART diseases
Abstract

Aims Group 2 innate lymphoid cells (ILC2s) regulate adaptive and innate immunities. In mouse heart, production of myocardial infarction (MI) increased ILC2 accumulation, suggesting a role for ILC2 in cardiac dysfunction post-MI. Methods and results We produced MI in ILC2-deficeint Rorafl/flIl7rCre/+ mice and in Icosfl-DTR-fl/+Cd4Cre/+ mice that allowed diphtheria toxin-induced ILC2 depletion. Genetic or induced deficiency of ILC2 in mice exacerbated cardiac dysfunction post-MI injury along with increased myocardial accumulation of neutrophils, CD11b+Ly6Chi monocytes, and CD4+ T cells but deficiency of eosinophils (EOS) and dendritic cells (DC). Post-MI hearts from genetic and induced ILC2-deficient mice contained many more apoptotic cells than those of control mice, and Rorafl/flIl7rCre/+ mice showed thinner and larger infarcts and more collagen-I depositions than the Il7rCre/+ mice only at early time points post-MI. Mechanistic studies revealed elevated blood IL5 in Il7rCre/+ mice at 1, 7, and 28 days post-MI. Such increase was blunted in Rorafl/flIl7rCre/+ mice. Administration of recombinant IL5 reversed EOS losses in Rorafl/flIl7rCre/+ mice, but IL5 did not correct the DC loss in these mice. Adoptive transfer of ILC2, EOS, or DC from wild-type mice, but not ILC2 from Il5−/− mice improved post-MI cardiac functions in Rorafl/flIl7rCre/+ recipient mice. EOS are known to protect cardiomyocytes from apoptosis. Here we showed that DC acted like EOS in blocking cardiomyocyte apoptosis. Yet, ILC2 or IL5 alone did not directly affect cardiomyocyte apoptosis or TGF-β (transforming growth factor-β)-induced cardiac fibroblast Smad signalling. Conclusion This study revealed an indirect cardiac reparative role of ILC2 in post-MI hearts via the IL5, EOS, and DC mechanism. [ABSTRACT FROM AUTHOR]

Published
2023
Full Text
View/download PDF

49. Eosinophils protect pressure overload- and β-adrenoreceptor agonist-induced cardiac hypertrophy

Author

Chongzhe, Yang, primary, Li, Jie, additional, Deng, Zhiyong, additional, Luo, Songyuan, additional, Liu, Jing, additional, Fang, Wenqian, additional, Liu, Feng, additional, Liu, Tianxiao, additional, Zhang, Xian, additional, Zhang, Yuanyuan, additional, Meng, Zhaojie, additional, Zhang, Shuya, additional, Luo, Jianfang, additional, Liu, Conglin, additional, Yang, Dafeng, additional, Liu, Lijun, additional, Sukhova, Galina K., additional, Sadybekov, Anastasiia, additional, Katritch, Vsevolod, additional, Libby, Peter, additional, Wang, Jing, additional, Guo, Junli, additional, and Shi, Guo-Ping, additional

Published
2022
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results