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124. The Drought-Stress Response of a Drought Resistant Impatiens Processed in PEG-6000 Solution in a Simulation Test

Author

Liao, Xue Lan, Wen, Guo Qin, Liu, Qing Lin, Wu, Xue Yang Li Meng Xi, and Pan, Yuan Zhi

Subjects
Quantitative Biology - Other Quantitative Biology
Abstract

Premise of the Study: Impatiens is a commonly seen garden flower, renowned for its strong adaptability and long history of cultivation. However, seldom has any research touched on its physiological resistance mechanism. In this experiment, the impatiens is selected from those which experienced aerospace mutation and thereafter 12 years of cultivation and breeding. Therefore, it is superior to the non-mutagenized impatiens in terms of drought resistance and demonstrates tremendous differences from the normal impatiens in physiology, which intrigues scholars to search for the underlying reasons . Methods: By reference to Impatiens balsamina L,this experiment uses mutagenized impatiens seeds, processed by PEG-6000 in different solution concentration, to measure the germination rate of impatiens, its relative enzymatic activity and expression differences between gene SoS2 and gene RD29b in the drought lower reaches. Key results: Under simulated drought stress, there is no distinct difference between the mutagenized impatiens and the normal impatiens in terms of germination rate. But by measuring the root tillers and the length, the relative enzymatic activity, MDA, and the expression differences between gene SoS2 and gene RD29b in the drought lower reaches, it is verified that the mutagenized impatiens has more advantages than the normal impatiens, and it Can further cultivate become drought resistance varieties impatiens. Conclusions: In this experiment,which is a positive mutation, the mutagenized impatiens improves drought resistance through radiative mutation. The so obtained impatiens is more pleasing in sight in terms of color and shape and has higher application value in garden virescence., Comment: 19 pages,6 figures,1 table

Published
2016

127. Metabolic reprogramming by PCK1 promotes TCA cataplerosis, oxidative stress and apoptosis in liver cancer cells and suppresses hepatocellular carcinoma

Author

Liu, Meng-Xi, Jin, Lei, Sun, Si-Jia, Liu, Peng, Feng, Xu, Cheng, Zhou-Li, Liu, Wei-Ren, Guan, Kun-Liang, Shi, Ying-Hong, Yuan, Hai-Xin, and Xiong, Yue

Subjects
Cancer, Liver Disease, Digestive Diseases, Rare Diseases, Liver Cancer, Aetiology, 2.1 Biological and endogenous factors, Animals, Apoptosis, Carcinoma, Hepatocellular, Cells, Cultured, Cellular Reprogramming, Citric Acid Cycle, Genes, Tumor Suppressor, Gluconeogenesis, HEK293 Cells, Hep G2 Cells, Humans, Intracellular Signaling Peptides and Proteins, Liver Neoplasms, MCF-7 Cells, Male, Mice, Mice, Inbred ICR, Mice, Nude, Oxidative Stress, Phosphoenolpyruvate Carboxykinase (GTP), Clinical Sciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Phosphoenolpyruvate carboxykinase (PEPCK or PCK) catalyzes the first rate-limiting step in hepatic gluconeogenesis pathway to maintain blood glucose levels. Mammalian cells express two PCK genes, encoding for a cytoplasmic (PCPEK-C or PCK1) and a mitochondrial (PEPCK-M or PCK2) isoforms, respectively. Increased expressions of both PCK genes are found in cancer of several organs, including colon, lung, and skin, and linked to increased anabolic metabolism and cell proliferation. Here, we report that the expressions of both PCK1 and PCK2 genes are downregulated in primary hepatocellular carcinoma (HCC) and low PCK expression was associated with poor prognosis in patients with HCC. Forced expression of either PCK1 or PCK2 in liver cancer cell lines results in severe apoptosis under the condition of glucose deprivation and suppressed liver tumorigenesis in mice. Mechanistically, we show that the pro-apoptotic effect of PCK1 requires its catalytic activity. We demonstrate that forced PCK1 expression in glucose-starved liver cancer cells induced TCA cataplerosis, leading to energy crisis and oxidative stress. Replenishing TCA intermediate α-ketoglutarate or inhibition of reactive oxygen species production blocked the cell death caused by PCK expression. Taken together, our data reveal that PCK1 is detrimental to malignant hepatocytes and suggest activating PCK1 expression as a potential treatment strategy for patients with HCC.

Published
2018

136. Role of intestinal flora in the development of nonalcoholic fatty liver disease in children

Author

Zhang, Jing, primary, Shi, Mengxuan, additional, Zhao, Chunna, additional, Liang, Guangcai, additional, Li, Chuan, additional, Ge, Xiaomeng, additional, Pei, Caixia, additional, Kong, Yawei, additional, Li, Dongdan, additional, Yang, Wenli, additional, Cao, Bingyan, additional, Fu, Libing, additional, Yan, Yinkun, additional, Wu, Jie, additional, Zhou, Jin, additional, Fang, Yongli, additional, Meng, Xi, additional, Li, Yong, additional, and Wang, Liming, additional

Published
2024
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145. A Study of Size Effects of Overview Interfaces on User Performance in Virtual Environments

Author

Chen, Meng-Xi, Chen, Chien-Hsiung, 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, Stephanidis, Constantine, editor, Chen, Jessie Y. C., editor, and Fragomeni, Gino, editor

Published
2020
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146. SEE-LPR: A Semantic Segmentation Based End-to-End System for Unconstrained License Plate Detection and Recognition

Author

Tang, Dongqi, Kong, Hao, Meng, Xi, Liu, Ruo-Ze, Lu, Tong, 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, Ro, Yong Man, editor, Cheng, Wen-Huang, editor, Kim, Junmo, editor, Chu, Wei-Ta, editor, Cui, Peng, editor, Choi, Jung-Woo, editor, Hu, Min-Chun, editor, and De Neve, Wesley, editor

Published
2020
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