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2,995 results on '"Zheng, Yue"'

11. Diagnosis, treatment and prevention of severe acute respiratory syndrome coronavirus 2 infection in children: experts’ consensus statement updated for the Omicron variant

Author

Jiang, Rong-Meng, Xie, Zheng-De, Jiang, Yi, Lu, Xiao-Xia, Jin, Run-Ming, Zheng, Yue-Jie, Shang, Yun-Xiao, Xu, Bao-Ping, Liu, Zhi-Sheng, Lu, Gen, Deng, Ji-Kui, Liu, Guang-Hua, Wang, Xiao-Chuan, Wang, Jian-She, Feng, Lu-Zhao, Liu, Wei, Zheng, Yi, Shu, Sai-Nan, Lu, Min, Luo, Wan-Jun, Liu, Miao, Cui, Yu-Xia, Ye, Le-Ping, Shen, A-Dong, Liu, Gang, Gao, Li-Wei, Xiong, Li-Juan, Bai, Yan, Lin, Li-Kai, Wei, Zhuang, Xue, Feng-Xia, Wang, Tian-You, Zhao, Dong-Chi, Shao, Jian-Bo, Ng, Daniel Kwok-keung, Wong, Gary Wing-kin, Zhao, Zheng-Yan, Li, Xing-Wang, Yang, Yong-Hong, and Shen, Kun-Ling

Published
2024
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13. Ammonia-oxidizing bacteria and archaea exhibit differential nitrogen source preferences

Author

Qin, Wei, Wei, Stephany P., Zheng, Yue, Choi, Eunkyung, Li, Xiangpeng, Johnston, Juliet, Wan, Xianhui, Abrahamson, Britt, Flinkstrom, Zachary, Wang, Baozhan, Li, Hanyan, Hou, Lei, Tao, Qing, Chlouber, Wyatt W., Sun, Xin, Wells, Michael, Ngo, Long, Hunt, Kristopher A., Urakawa, Hidetoshi, Tao, Xuanyu, Wang, Dongyu, Yan, Xiaoyuan, Wang, Dazhi, Pan, Chongle, Weber, Peter K., Jiang, Jiandong, Zhou, Jizhong, Zhang, Yao, Stahl, David A., Ward, Bess B., Mayali, Xavier, Martens-Habbena, Willm, and Winkler, Mari-Karoliina H.

Published
2024
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17. CUX1 attenuates the apoptosis of renal tubular epithelial cells induced by contrast media through activating the PI3K/AKT signaling pathway

Author

Rong-Zheng Yue, Jing Wang, Feng Lin, Cong-Jun Li, Bai-Hai Su, and Rui Zeng

Subjects
Renal tubular epithelial cells, Contrast media (CM), PI3K/AKT signaling pathway, CUT-like homeobox 1 (CUX1), Contrast-induced acute kidney injury, Diseases of the genitourinary system. Urology, RC870-923
Abstract

Abstract Objective Contrast media (CM) is a commonly applied drug in medical examination and surgery. However, contrast-induced acute kidney injury (CIAKI) poses a severe threat to human life and health. Notably, the CUT-like homeobox 1 (CUX1) gene shows protective effects in a variety of cells. Therefore, the objective of this study was to provide a new target for the treatment of CIAKI through exploring the role and possible molecular mechanism of CUX1 in CIAKI. Method Blood samples were collected from 20 patients with CIAKI and healthy volunteers. Human kidney 2 (HK-2) cells were incubated with 200 mg/mL iohexol for 6 h to establish a contrast-induced injury model of HK-2 cells. Subsequently, qRT-PCR was used to detect the relative mRNA expression of CUX1; CCK-8 and flow cytometry to assess the proliferation and apoptosis of HK-2 cells; the levels of IL(interleukin)-1β, tumor necrosis factor alpha (TNF-α) and malondialdehyde (MDA) in cells and lactate dehydrogenase (LDH) activity in cell culture supernatant were detect; and western blot to observe the expression levels of CUX1 and the PI3K/AKT signaling pathway related proteins [phosphorylated phosphoinositide 3-kinase (p-PI3K), PI3K, phosphorylated Akt (p-AKT), AKT]. Results CUX1 expression was significantly downregulated in blood samples of patients with CIAKI and contrast-induced HK-2 cells. Contrast media (CM; iohexol) treatment significantly reduced the proliferation of HK-2 cells, promoted apoptosis, stimulated inflammation and oxidative stress that caused cell damage. CUX1 overexpression alleviated cell damage by significantly improving the proliferation level of HK-2 cells induced by CM, inhibiting cell apoptosis, and reducing the level of LDH in culture supernatant and the expression of IL-1β, TNF-α and MDA in cells. CM treatment significantly inhibited the activity of PI3K/AKT signaling pathway activity. Nevertheless, up-regulating CUX1 could activate the PI3K/AKT signaling pathway activity in HK-2 cells induced by CM. Conclusion CUX1 promotes cell proliferation, inhibits apoptosis, and reduces inflammation and oxidative stress in CM-induced HK-2 cells to alleviate CM-induced damage. The mechanism of CUX1 may be correlated with activation of the PI3K/AKT signaling pathway.

Published
2024
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19. PDGFBB facilitates tumorigenesis and malignancy of lung adenocarcinoma associated with PI3K-AKT/MAPK signaling

Author

He Xiu-Ying, Zheng Yue-Xiang, Yang Hui-Si, Yu Hong-Zhou, Xia Qing-Jie, and Wang Ting-Hua

Subjects
Medicine, Science
Abstract

Abstract Lung adenocarcinoma (LUAD) remains one of the most aggressive tumors and the efficacy of conventional treatment has been bleak. Nowadays, gene-targeted therapy has become a new favorite in tumor therapy. Herein, we investigated the effect of platelet derived growth factor BB (PDGFBB) on LUAD. Firstly, PDGFBB was upregulated in LUAD patients and closely linked with poor survival. Furthermore, the expression of PDGFBB and PDGFRα/β in LUAD cells was higher than that in normal lung cells. By loss-of-function with herpes simplex virus (HSV)-PDGFi-shRNA, we found that PDGFBB knockdown caused a significant decrease in proliferation and migration, but evoked apoptosis of LUAD cells in vitro. Conversely, exogenous PDGFBB held adverse effect. Additionally, A549 cells with PDGFBB knockdown had a low probability of tumorigenesis in vivo. Moreover, PDGFBB knockdown restrained the growth of xenografts derived from normal A549 cells. Mechanistically, PDGFBB knockdown suppressed PI3K/AKT and Ras/MAPK signaling, while PDGFBB was the opposite. Therefore, we concluded that PDGFBB might facilitate the tumorigenesis and malignancy of LUAD through its functional downstream nodes—PI3K/AKT and Ras/MAPK signaling, which supported that PDGFBB could serve as a rational therapeutic target for LUAD.

Published
2024
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37. Effect of Cymbopogon martini (Roxb.) Will.Watson essential oil on antioxidant activity, immune and intestinal barrier-related function, and gut microbiota in pigeons infected by Candida albicans

Author

Ting Huang, Zheng-Yue Zhang, Zhi-Lin Qiu, Lin Li, Xian-Xi Liu, Lei Wang, Zi-Ying Wang, Zhi-Peng Li, Geng-Sheng Xiao, and Wei Wang

Subjects
Candida albicans, Cymbopogon martini essential oil, pigeon, antioxidant activity, immune response, intestinal barrier function, Therapeutics. Pharmacology, RM1-950
Abstract

Essential oils are potential alternatives to antibiotics for preventing Candida albicans (C. albicans) infection which is responsible for economic losses in the pigeon industry. Cymbopogon martini essential oil (EO) can inhibit pathogens, particularly fungal pathogens but its potential beneficial effects on C. albicans-infected pigeons remain unclear. Therefore, we investigated the impact of C. martini EO on antioxidant activity, immune response, intestinal barrier function, and intestinal microbiota in C. albicans-infected pigeons. The pigeons were divided into four groups as follows: (1) NC group: C. albicans uninfected/C. martini EO untreated group; (2) PC group: C. albicans infected/C. martini EO untreated group; (3) LPA group: C. albicans infected/1% C. martini EO treated group; and (4) HPA group: C. albicans infected/2% C. martini EO treated group. The pigeons were infected with C. albicans from day of age 35 to 41 and treated with C. martini EO from day of age 42 to 44, with samples collected on day of age 45 for analysis. The results demonstrated that C. martini EO prevented the reduction in the antioxidant enzymes SOD and GSH-Px causes by C. albicans challenge in pigeons. Furthermore, C. martini EO could decrease the relative expression of IL-1β, TGF-β, and IL-8 in the ileum, as well as IL-1β and IL-8 in the crop, while increasing the relative expression of Claudin-1 in the ileum and the crop and Occludin in the ileum in infected pigeons. Although the gut microbiota composition was not significantly affected by C. martini EO, 2% C. martini EO increased the abundance of Alistipes and Pedobacter. In conclusion, the application of 2% C. martini EO not only enhanced the level of antioxidant activity and the expression of genes related to intestinal barrier function but also inhibited inflammatory genes in C. albicans-infected pigeons and increased the abundance of gut bacteria that are resistant to C. albicans.

Published
2024
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