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29 results on '"Ma, Tieliang"'

4. Multi-center verification of the influence of data ratio of training sets on test results of an AI system for detecting early gastric cancer based on the YOLO-v4 algorithm

Author

Jin, Tao, primary, Jiang, Yancai, additional, Mao, Boneng, additional, Wang, Xing, additional, Lu, Bo, additional, Qian, Ji, additional, Zhou, Hutao, additional, Ma, Tieliang, additional, Zhang, Yefei, additional, Li, Sisi, additional, Shi, Yun, additional, and Yao, Zhendong, additional

Published
2022
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9. Effect and mechanism of human gingival mesenchymal stem cell on B cells

Author

Zhang Kai, Chen Keyan, Li Kai, Ma Tieliang, and Gu Jian

Subjects
transforming growth factor, chronic graft-versus-host disease, transplantation immunity, lcsh:R, human peripheral blood mononuclear cell, lcsh:Medicine, b cell, gingival mesenchymal stem cell, t cell, regulatory b cell
Abstract

Objective To investigate the regulating function of human gingival mesenchymal stem cell (GMSC) on the proliferation and differentiation of B cells and its underlying molecular mechanism. Methods GMSC were isolated and B cells were isolated from peripheral blood. GMSC or fibroblasts were co-cultured with B cells in vitro and assigned into the GMSC group and fibroblast group. The proliferation of B cells was detected in two groups. The expression of IgG1 and IgM in the cell supernatants was measured between two groups. The secretion of interleukin (IL)-6, Perforin, interferon (IFN)-γ and tumor necrosis factor (TNF)-α was compared between two groups. The expression levels ofIL-10 and transforming growth factor (TGF)-β in B cells were detected between two groups. The expression of PC-1 in B cells was measured in two groups. The signaling pathway involved with the regulating effect of GMSC on B cell function was investigated. The regulating effect of GMSC on the role of B cells in activating T cell function was assessed. Results Compared with the fibroblast group, the proliferation of B cells was significantly weakened in the GMSC group (P < 0.05). Co-culture of GMSC and B cells significantly inhibited the secretion of IgG1 and IgM from B cells and the secretion ofIL-6, Perforin, IFN-γ and TNF-α (all P < 0.05). Compared with the fibroblast group, the secretion of IL-10 and TGF-βwas significantly higher in the GMSC group (both P < 0.05). The expression level of PC-1 in the GMSC group was significantly down-regulated (P < 0.05). After adding ALK5, an inhibitor of TGF-β receptor, the inhibitory effect of GMSC upon B cells was significantly weakened (P < 0.05). Compared with the fibroblast group, the ability of B cells to activate and proliferate T cells was significantly attenuated in the GMSC group (P < 0.05). Conclusions GMSC can inhibit B cells and their mediated immune responses. The activation of B cells and other related functions can be suppressed through the TGF-β signaling pathway.

Published
2020

17. Synthesis, characterization and antitumor activity of Ln(III) complexes with hydrazone Schiff base derived from 2-acetylpyridine and isonicotinohydrazone

Author

Xie, Jing, primary, Shen, Shanshan, additional, Chen, Ruhua, additional, Xu, Jun, additional, Dong, Kun, additional, Huang, Jiancui, additional, Lu, Qin, additional, Zhu, Wenjiao, additional, Ma, Tieliang, additional, Jia, Lei, additional, Cai, Hongxin, additional, and Zhu, Taofeng, additional

Published
2017
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20. Dexamethasone attenuates bleomycin-induced lung fibrosis in mice through TGF-β, Smad3 and JAK-STAT pathway

Author

Shi, Keyun, Jiang, Jianzhong, Ma, Tieliang, Xie, Jing, Duan, Lirong, Chen, Ruhua, Song, Ping, Yu, Zhixin, Liu, Chao, Zhu, Qin, and Zheng, Jinxu

Subjects
Original Article
Abstract

In order to find the possible mechanism of Dexamethasone (Dex) during curing fibrosis, the bleomycin (BLM)-induced mice model was used. After fibrosis were induced by BLM, histopathological evaluation and RT-PCR were employed to detect the expression of TGF-β1, Smad3 and STAT1. It was found that BLM promoted the development of inflammation, leading to severe pulmonary fibrosis with the increasing of TGF-β1, Smad3 and STAT1. After Dex treatment, the expression of TGF-β1, Smad3 and STAT1 showed a little higher with alleviation of the fibrosis. Thus it is concluded that there is a possible pathway of mouse pulmonary fibrosis model through TGF-β, Smad3 and JAK-STAT pathway.

Published
2014

23. Specific Deletion of Cdh2 in Sertoli Cells Leads to Altered Meiotic Progression and Subfertility of Mice1

Author

Jiang, Xiaohua, primary, Ma, Tieliang, additional, Zhang, Yuanwei, additional, Zhang, Huan, additional, Yin, Shi, additional, Zheng, Wei, additional, Wang, Liu, additional, Wang, Zheng, additional, Khan, Manan, additional, Sheikh, Salma W., additional, Bukhari, Ihtisham, additional, Iqbal, Furhan, additional, Cooke, Howard J., additional, and Shi, Qinghua, additional

Published
2015
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28. Proliferating Cell Nuclear Antigen (PCNA) Regulates Primordial Follicle Assembly by Promoting Apoptosis of Oocytes in Fetal and Neonatal Mouse Ovaries

Author

Xu, Bo, primary, Hua, Juan, additional, Zhang, Yuanwei, additional, Jiang, Xiaohua, additional, Zhang, Huan, additional, Ma, Tieliang, additional, Zheng, Wei, additional, Sun, Rui, additional, Shen, Wei, additional, Sha, Jiahao, additional, Cooke, Howard J., additional, and Shi, Qinghua, additional

Published
2011
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29. Specific Deletion of Cdh2in Sertoli Cells Leads to Altered Meiotic Progression and Subfertility of Mice1

Author

Jiang, Xiaohua, Ma, Tieliang, Zhang, Yuanwei, Zhang, Huan, Yin, Shi, Zheng, Wei, Wang, Liu, Wang, Zheng, Khan, Manan, Sheikh, Salma W., Bukhari, Ihtisham, Iqbal, Furhan, Cooke, Howard J., and Shi, Qinghua

Abstract

CDH2 (cadherin 2, Neural-cadherin, or N-cadherin) is the predominant protein of testicular basal ectoplasmic specializations (basal ES; a testis-specific type of adhesion junction), one of the major cell junctions composing the blood-testis barrier (BTB). The BTB is found between adjacent Sertoli cells in seminiferous tubules, which divides the tubules into basal and adluminal compartments and prevents the deleterious exchange of macromolecules between blood and seminiferous tubules. However, the exact roles of basal ES protein CDH2 in BTB function and spermatogenesis is still unknown. We thus generated mice with Cdh2specifically knocked out in Sertoli cells by crossing Cdh2loxP mice with Amh-Cremice. Cdh2deletion in Sertoli cells did not affect Sertoli cell counts, but led to compromised BTB function, delayed meiotic progression from prophase to metaphase I in testes, increased germ cell apoptosis, sloughing of meiotic cells, and, subsequently, reduced sperm counts in epididymides and subfertility of mice. However, the testes with Cdh2-specific deletion in germ cells did not show any difference from the normal control testes, and phenotypes observed in Sertoli cell and germ cell Cdh2double-knockout mice were indistinguishable from those in mice with Cdh2specifically knocked out only in Sertoli cells. Taken together, our data demonstrate that the adhesion junction component, Cdh2, functions just in Sertoli cells, but not in germ cells during spermatogenesis, and is essential for the integrity of BTB function, its deletion in Sertoli cells would lead to the BTB damage and subsequently meiosis and spermatogenesis failure.

Published
2015
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