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792 results on '"Li, Jingxia"'

203. DANIDA Grantees' Impressions of the IFLA Conference in Glasgow

Author

Nafissatou Bakhoum, Sylvia Ogola, Charles Batambuze, Li Jingxia, Chin Loy Jyoon, and Mac-Anthony Cobblah

Subjects
Operations research, Library science, Sociology, Library and Information Sciences, Information science
Abstract

Extraits des rapports de cinq bibliothecaires des pays en voie de developpement ayant recu la bourse de DANIDA pour participer a la 68eme conference annuelle de l'IFLA (International Federation of Library Associations and Institutions) tenue a Glasgow, Ecosse, 18-24 aout 2002.

Published
2002

204. Metastatic hepatic clear cell carcinoma presenting as lump in the hilum of the lung: a case report and review of the literature

Author

Xun, Qiufen, Li, Yuanyuan, Yang, Huaping, Li, Jingxia, and Hu, Chengping

Subjects
Case Report, respiratory system, respiratory tract diseases
Abstract

We report a case of a 52-year-old Chinese woman with a history of primary hepatic cell carcinoma who presented with chest pain, cough, expectoration and bloody phlegm. Chest computer tomography (CT) revealed a 6.2 cm × 6.8 cm shallow lobulated irregular shaped mass in the hilum of the right lung. Bronchoscopy and CT guided lung biopsy was performed. Histopathological and immunohistochemical examinations of biopsies revealed the diagnosis of lung metastatic hepatic clear cell carcinoma. This case is thought to be extremely rare.

Published
2013

206. Upregulation of SQSTM1/p62 contributes to nickel-induced malignant transformation of human bronchial epithelial cells

Author

Huang, Haishan, primary, Zhu, Junlan, additional, Li, Yang, additional, Zhang, Liping, additional, Gu, Jiayan, additional, Xie, Qipeng, additional, Jin, Honglei, additional, Che, Xun, additional, Li, Jingxia, additional, Huang, Chao, additional, Chen, Lung-Chi, additional, Lyu, Jianxin, additional, Gao, Jimin, additional, and Huang, Chuanshu, additional

Published
2016
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207. XIAP RING domain mediates miR-4295 expression and subsequently inhibiting p63α protein translation and promoting transformation of bladder epithelial cells

Author

Jin, Honglei, primary, Xu, Jiheng, additional, Guo, Xirui, additional, Huang, Haishan, additional, Li, Jingxia, additional, Peng, Minggang, additional, Zhu, Junlan, additional, Tian, Zhongxian, additional, Wu, Xue-Ru, additional, Tang, Moon-Shong, additional, and Huang, Chuanshu, additional

Published
2016
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208. Isorhapontigenin (ISO) Inhibits Invasive Bladder Cancer Formation In Vivo and Human Bladder Cancer Invasion In Vitro by Targeting STAT1/FOXO1 Axis

Author

Jiang, Guosong, primary, Wu, Amy D., additional, Huang, Chao, additional, Gu, Jiayan, additional, Zhang, Liping, additional, Huang, Haishan, additional, Liao, Xin, additional, Li, Jingxia, additional, Zhang, Dongyun, additional, Zeng, Xingruo, additional, Jin, Honglei, additional, Huang, Haojie, additional, and Huang, Chuanshu, additional

Published
2016
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220. XIAP overexpression promotes bladder cancer invasion <italic>in vitro</italic> and lung metastasis <italic>in vivo via</italic> enhancing nucleolin‐mediated Rho‐GDIβ mRNA stability.

Author

Yu, Yonghui, Jin, Honglei, Xu, Jiheng, Gu, Jiayan, Li, Xin, Xie, Qipeng, Huang, Haishan, Li, Jingxia, Tian, Zhongxian, Jiang, Guosong, Chen, Caiyi, He, Feng, Wu, Xue‐Ru, and Huang, Chuanshu

Abstract

Our recent studies demonstrate that X‐linked inhibitor of apoptosis protein (XIAP) is essential for regulating colorectal cancer invasion. Here, we discovered that RhoGDIβ was a key XIAP downstream effector mediating bladder cancer (BC) invasion in vitro and in vivo. We found that both XIAP and RhoGDIβ expressions were consistently elevated in BCs of N‐butyl‐N‐(4‐hydroxybutyl)‐nitrosamine (BBN)‐treated mice in comparison to bladder tissues from vehicle‐treated mice and human BCs in comparison to the paired adjacent normal bladder tissues. Knockdown of XIAP attenuated RhoGDIβ expression and reduced cancer cell invasion, whereas RhoGDIβ expression was attenuated in BBN‐treated urothelium of RING‐deletion knockin mice. Mechanistically, XIAP stabilized RhoGDIβ mRNA by its positively regulating nucleolin mRNA stability via Erks‐dependent manner. Moreover, ectopic expression of GFP‐RhoGDIβ in T24T(shXIAP) cells restored its lung metastasis in nude mice. Our results demonstrate that XIAP‐regulated Erks/nucleolin/RhoGDIβ axis promoted BC invasion and lung metastasis. [ABSTRACT FROM AUTHOR]

Published
2018
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221. Rho GDIβ promotes Sp1/ MMP-2 expression and bladder cancer invasion through perturbing miR-200c-targeted JNK2 protein translation.

Author

Huang, Haishan, Jin, Honglei, Zhao, Huirong, Wang, Jingjing, Li, Xin, Yan, Huiying, Wang, Shuai, Guo, Xirui, Xue, Lei, Li, Jingxia, Peng, Minggang, Wang, Annette, Zhu, Junlan, Wu, Xue ‐ Ru, Chen, Changyan, and Huang, Chuanshu

Abstract

Our most recent studies demonstrate that Rho GDIβ is able to promote human bladder cancer ( BC) invasion and metastasis in an X-link inhibitor of apoptosis protein-dependent fashion accompanied by increased levels of matrix metalloproteinase ( MMP)-2 protein expression. We also found that Rho GDIβ and MMP-2 protein expressions are consistently upregulated in both invasive BC tissues and cell lines. In the present study, we show that knockdown of Rho GDIβ inhibited MMP-2 protein expression accompanied by a reduction of invasion in human BC cells, whereas ectopic expression of Rho GDIβ upregulated MMP-2 protein expression and promoted invasion as well. The mechanistic studies indicated that MMP-2 was upregulated by Rho GDIβ at the transcriptional level by increased specific binding of the transcription factor Sp1 to the mmp-2 promoter region. Further investigation revealed that Rho GDIβ overexpression led to downregulation of miR-200c, whereas miR-200c was able directly to target 3′- UTR of jnk2 mRNA and attenuated JNK2 protein translation, which resulted in attenuation of Sp1 mRNA and protein expression in turn, inhibiting Sp1-dependent mmp-2 transcription. Collectively, our studies demonstrate that Rho GDIβ overexpression inhibits miR-200c abundance, which consequently results in increases of JNK2 protein translation, Sp1 expression, mmp-2 transcription, and BC invasion. These findings, together with our previous results showing X-link inhibitor of apoptosis protein mediating mRNA stabilization of both Rho GDIβ and mmp-2, reveal the nature of the MMP-2 regulatory network, which leads to MMP-2 overexpression and BC invasion. [ABSTRACT FROM AUTHOR]

Published
2017
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222. The bioclimatic features of vernacular architecture in China

Author

Li Jingxia

Subjects
Insolation, Geography, Renewable Energy, Sustainability and the Environment, Environmental protection, business.industry, Vernacular architecture, Environmental resource management, Microclimate, Energy consumption, Architecture, China, business
Abstract

The paper presents an analysis of the form and climatic conditions of two traditional buildings in southern and northern parts of China. The vernacular architecture reflects the principles for contemporary bioclimatic design, such as the choice of location, insolation, weather seasonal protection, etc. It creates wonderful microclimate for the inhabitants. It shows the local traditional architecture as the most adequate and suitable answer to the requirements of enviromental and energy consumption need.

Published
1996

223. Autophagy-mediated Mir6981degradation exhibits CDKN1Bpromotion of PHLPP1 protein translation

Author

Peng, Minggang, Wang, Jingjing, Tian, Zhongxian, Zhang, Dongyun, Jin, Honglei, Liu, Claire, Xu, Jiawei, Li, Jingxia, Hua, Xiaohui, Xu, Jiheng, Huang, Chao, and Huang, Chuanshu

Abstract

ABSTRACTPHLPP1 (PH domain and leucine rich repeat protein phosphatase 1) is a newly identified family of Ser/Thr phosphatases that catalyzes the dephosphorylation of a conserved regulatory motif of the AGC kinases resulting in a tumor suppressive function, while CDKN1B/p27 also acts as a tumor suppressor by regulating cell cycle, senescence, apoptosis, and cell motility. Our most recent studies reveal that CDKN1B is required for PHLPP1 abundance, which contributes to the inhibition of carcinogenic arsenite-induced cell malignant transformation through inhibition of RPS6-mediated Hif1atranslation. However, nothing is known about the mechanisms underlying the crosstalk between these 2 key tumor suppressors in intact cells. Here, for the first time to the best of our knowledge, we show that CDKN1B is able to promote PHLPP1 protein translation by attenuating the abundance of Mir6981, which binds directly to the 5ʹuntranslated region (UTR) of Phlpp1mRNA. Further studies indicate that the attenuation of Mir6981expression is due to macroautophagy/autophagy-mediated degradation of Mir6981in an SQSTM1/p62-dependent fashion. Moreover, we have determined that Sqstm1is upregulated by CDKN1B at the level of transcription viaenhancing SP1 protein stability in an HSP90-depdendent manner. Collectively, our studies prove that: 1) SQSTM1 is a CDKN1B downstream effector responsible for CDKN1B-mediated autophagy; 2) by promoting the autophagy-mediated degradation of Mir6981, CDKN1B exerts a positive regulatory effect on PHLPP1 translation; 3) Mir6981suppresses PHLPP1 translation by binding directly to its mRNA 5ʹ-UTR, rather than classical binding to the 3ʹ-UTR. These findings provide significant insight into understanding the crosstalk between CDKN1B and PHLPP1.Abbreviations:ATG: autophagy related; ACTB: actin beta; BAF: bafilomycin; BECN1: beclin 1; Cdkn1b/p27: cyclin-dependent kinase inhibitor 1B; CHX: cycloheximide; DMEM: dulbecco’s modified eagle medium; FBS: fetal bovine serum; GAPDH: glyceraldehyde −3-phosphate dehydrogenase; Hif1a: hypoxia inducible factor 1, alpha subunit; Hsp90: heat shock protein 90; JUN: Jun proto-oncogene, AP1 transcription factor subunit; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MG132: proteasome inhibitor; Mtor: mechanistic target of rapamycin kinase; Phlpp1: PH domain and leucine rich repeat protein phosphatase 1; Phlpp2: PH domain and leucine rich repeat protein phosphatase 2; Pp2c: protein phosphatase 2 C; RPS6: ribosomal protein S6; Sp1: trans-acting transcription factor 1; Sqstm1/p62: sequestosome 1; TUBA: alpha tubulin; 3ʹ-UTR; 3ʹ-untranslated region; 5ʹ-UTR: 5ʹ-untranslated region.

Published
2019
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224. Ultra-Wideband Remote Chaotic Imaging Radar over Fiber Links

Author

王文珂 Wang Wenke, 刘丽 Liu Li, 张建国 Zhang Jianguo, 李静霞 Li Jingxia, and 王冰洁 Wang Bingjie

Subjects
Electrical and Electronic Engineering, Atomic and Molecular Physics, and Optics, Electronic, Optical and Magnetic Materials
Published
2016

225. IGFBP‑rP1 affects the proliferation, apoptosis and macrophage polarization of endometrial cancer cells by regulating the PI3K/AKT pathway.

Author

Gao, Juan, Suo, Shiqi, Li, Jingxia, Wang, Chunxia, Deng, Ranran, Hu, Yuxia, and Zhang, Chunzheng

Subjects
INSULIN-like growth factor-binding proteins, PI3K/AKT pathway, SERINE/THREONINE kinases, ENDOMETRIAL cancer, CANCER cells, REVERSE transcriptase polymerase chain reaction
Abstract

Insulin-like growth factor binding protein-related protein 1 (IGFBP-rP1) is a potential tumor suppressor gene in a variety of cancers including colorectal cancer and breast cancer. However, its role and the potential mechanism in endometrial carcinoma (EC) are still unclear. The purpose of this study was to explore the effect of IGFBP-rP1 on EC cell proliferation and apoptosis and its underlying mechanism. Western blot analysis and reverse transcription-quantitative PCR were used to assess protein and gene expression levels of IGFBP-rP1 in EC cells. Overexpression of IGFBP-rP1 and/or AKT serine/threonine kinase was used to analyze their effects on cell proliferation and apoptosis of the EC cells. Co-immunoprecipitation and glutathione S transferase pull-down assays were used to analyze the interaction between IGFBP-rP1 and AKT. The expression of IGFBP-rP1 in EC cells was downregulated. Overexpression of IGFBP-rP1 inhibited the proliferation and induced apoptosis of EC cells, which were abolished by the overexpression of AKT. In addition, IGFBP-rP1 directly interacted with AKT to inhibit PI3K/AKT signaling. Additionally, M0 macrophages were induced by EC cells to differentiate into M2 macrophages, which was reversed by IGFBP-rP1. Overexpression of AKT in EC cells abolished the inhibitory effect of IGFBP-rP1 on M2 polarization. IGFBP-rP1 as an oncogenic factor inhibits M2 polarization of TAMs through PI3K/AKT signaling pathway and may be a potentially valuable target for EC therapy. [ABSTRACT FROM AUTHOR]

Published
2023
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226. Low strength static magnetic field inhibits the proliferation, migration, and adhesion of human vascular smooth muscle cells in a restenosis model through mediating integrins β1-FAK, Ca2+ signaling pathway

Author

Yingmei Zhang, Li Jingxia, Jin Yu, Michael Q. Chen, Li-Qiang Song, Wenyi Guo, Guoliang Jia, Haichang Wang, Xuyang Feng, Yan Li, and Weijie Li

Subjects
Integrins, Vascular smooth muscle, Integrin, Myocytes, Smooth Muscle, Biomedical Engineering, Models, Biological, Muscle, Smooth, Vascular, Umbilical Arteries, Focal adhesion, Extracellular matrix, Restenosis, Cell Movement, medicine, Cell Adhesion, Myocyte, Humans, Phosphorylation, Cell Proliferation, biology, Cell growth, Chemistry, Graft Occlusion, Vascular, Adhesion, medicine.disease, Cell biology, Magnetic Fields, Focal Adhesion Kinase 1, Immunology, biology.protein, Oligopeptides
Abstract

The proliferation, migration, and adhesion of vascular smooth muscle cells (VSMCs) and their interactions with extracellular matrix are key features of atherosclerosis and restenosis. Recently, there has been evidence that magnetic fields exert multiple effects on the biological performance of cells and may aid in the treatment of vascular disease. However, the effect of a static magnetic field (SMF) on human VSMCs still remains unknown. In this study, we aimed to determine the effects of low strength SMF on human VSMCs in an in vitro restenosis model. A SMF was established using neodymium-yttrium-iron permanent magnet. Human umbilical artery smooth muscle cells (hUASMCs) were isolated and seeded to a fibronectin-coated plate to form an in vitro restenosis model and then exposed to a vertically oriented field of 5 militesla (mT). MTT, transwell, and adhesion assays were used to demonstrate that the proliferation, migration, and adhesion potential of hUASMCs were significantly decreased after exposure to 5 mT SMF for 48 h compared with a non-treated group. Meanwhile, confocal microscopy analysis was used to demonstrate that integrin β(1) clustering was inhibited by exposure to 5 mT SMF. Furthermore, the phosphorylation of focal adhesion kinase (FAK) was markedly inhibited, and the upregulated cytosolic free calcium had been reversed (p 0.05). However, the biological effects of low strength SMF on hUASMCs could be blocked by the administration of GRGDSP-the blockade of integrins. In conclusion, a low strength SMF can influence the proliferation, migration, and adhesion of VSMCs by inhibiting the clustering of integrin β1, decreasing cytosolic free calcium concentration, and inactivating FAK. With further validation, SMFs may aid in attenuating abnormal VSMCs biological performance and has potential to block atherogenesis and prevent restenosis.

Published
2012

228. PHLPP2 Downregulation Contributes to Lung Carcinogenesis Following B[a]P/B[a]PDE Exposure

Author

Huang, Haishan, primary, Pan, Xiaofu, additional, Jin, Honglei, additional, Li, Yang, additional, Zhang, Lin, additional, Yang, Caili, additional, Liu, Pei, additional, Liu, Ya, additional, Chen, Lili, additional, Li, Jingxia, additional, Zhu, Junlan, additional, Zeng, Xingruo, additional, Fu, Kai, additional, Chen, Guorong, additional, Gao, Jimin, additional, and Huang, Chuanshu, additional

Published
2015
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237. Divergent behaviors and underlying mechanisms of cell migration and invasion in non-metastatic T24 and its metastatic derivative T24T bladder cancer cell lines

Author

Jin, Honglei, primary, Yu, Yonghui, additional, Hu, Young, additional, Lu, Chris, additional, Li, Jingxia, additional, Gu, Jiayan, additional, Zhang, Liping, additional, Huang, Haishan, additional, Zhang, Dongyun, additional, Wu, Xue-Ru, additional, Gao, Jimin, additional, and Huang, Chuanshu, additional

Published
2014
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