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434 results on '"Su, Zijian"'

3. Assessing MgO/Al2O3 Effect on Limonitic Laterite Sintering Process

Author

Tu, Yikang, Zhang, Yuanbo, Su, Zijian, Peng, Zhiwei, editor, Zhang, Mingming, editor, Li, Jian, editor, Li, Bowen, editor, Monteiro, Sergio Neves, editor, Soman, Rajiv, editor, Hwang, Jiann-Yang, editor, Kalay, Yunus Eren, editor, Escobedo-Diaz, Juan P., editor, Carpenter, John S., editor, Brown, Andrew D., editor, and Ikhmayies, Shadia, editor

Published
2024
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7. Lian-Mei-Yin formula alleviates diet-induced hepatic steatosis by suppressing Yap1/FOXM1 pathway-dependent lipid synthesis

Author

Zhang Peiguang, Cao Jieqiong, Liang Xujing, Su Zijian, Zhang Bihui, Wang Zhenyu, Xie Junye, Chen Gengrui, Chen Xue, Zhang Jinting, Feng Yanxian, Xu Qin, Song Jianping, Hong An, Chen Xiaojia, and Zhang Yibo

Subjects
non-alcoholic fatty liver disease, traditional Chinese medicine, Lian-Mei-Yin, Yap1, Foxm1, Biochemistry, QD415-436, Genetics, QH426-470
Abstract

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, with a global prevalence of 25%. Patients with NAFLD are more likely to suffer from advanced liver disease, cardiovascular disease, or type II diabetes. However, unfortunately, there is still a shortage of FDA-approved therapeutic agents for NAFLD. Lian-Mei-Yin (LMY) is a traditional Chinese medicine formula used for decades to treat liver disorders. It has recently been applied to type II diabetes which is closely related to insulin resistance. Given that NAFLD is another disease involved in insulin resistance, we hypothesize that LMY might be a promising formula for NAFLD therapy. Herein, we verify that the LMY formula effectively reduces hepatic steatosis in diet-induced zebrafish and NAFLD model mice in a time- and dose-dependent manner. Mechanistically, LMY suppresses Yap1-mediated Foxm1 activation, which is crucial for the occurrence and development of NAFLD. Consequently, lipogenesis is ameliorated by LMY administration. In summary, the LMY formula alleviates diet-induced NAFLD in zebrafish and mice by inhibiting Yap1/Foxm1 signaling-mediated NAFLD pathology.

Published
2024
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21. CH02 peptide promotes ex vivo expansion of umbilical cord blood-derived CD34+ hematopoietic stem/progenitor cells

Author

Yang Yiqi, Zhang Bihui, Xie Junye, Li Jingsheng, Liu Jia, Liu Rongzhan, Zhang Linhao, Zhang Jinting, Su Zijian, Li Fu, Zhang Leisheng, Hong An, and Chen Xiaojia

Subjects
CH02 peptide, umbilical cord blood, CD34+ hematopoietic stem/progenitor cell, Fms-like tyrosine kinase receptor 3, wound healing, Biochemistry, QD415-436, Genetics, QH426-470
Abstract

Umbilical cord blood (UCB) is an advantageous source for hematopoietic stem/progenitor cell (HSPC) transplantation, yet the current strategies for large-scale and cost-effective UCB-HSPC preparation are still unavailable. To overcome these obstacles, we systematically evaluate the feasibility of our newly identified CH02 peptide for ex vivo expansion of CD34+ UCB-HSPCs. We herein report that the CH02 peptide is specifically enriched in HSPC proliferation via activating the FLT3 signaling. Notably, the CH02-based cocktails are adequate for boosting 12-fold ex vivo expansion of UCB-HSPCs. Meanwhile, CH02-preconditioned UCB-HSPCs manifest preferable efficacy upon wound healing in diabetic mice via bidirectional orchestration of proinflammatory and anti-inflammatory factors. Together, our data indicate the advantages of the CH02-based strategy for ex vivo expansion of CD34+ UCB-HSPCs, which will provide new strategies for further development of large-scale HSPC preparation for clinical purposes.

Published
2023
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31. A cyclic peptide retards the proliferation of DU145 prostate cancer cells in vitro and in vivo through inhibition of FGFR2

Author

Zhang, Yibo, Ouyang, Man, Wang, Hailong, Zhang, Bihui, Guang, Wenhua, Liu, Ruiwu, Li, Xiaocen, Shih, Tsung‐Chieh, Li, Zhixin, Cao, Jieqiong, Meng, Qiling, Su, Zijian, Ye, Jinshao, Liu, Feng, Hong, An, and Chen, Xiaojia

Subjects
Cancer, Biotechnology, Urologic Diseases, cancer therapy, cyclic peptide, fibroblast growth factor receptor 2, peptide drug
Abstract

In malignancies, fibroblast growth factor receptors (FGFRs) signaling is reinforced through overexpression of fibroblast growth factors (FGFs) or their receptors. FGFR2 has been proposed as a target for cancer therapy, because both the expression and activation of FGFR2 are boosted in various malignant carcinomas. Although several chemicals have been designed against FGFR2, they did not exhibit enough specificity and might bring potential accumulated toxicity. In this study, we developed an epitope peptide (P5) and its cyclic derivative (DcP5) based on the structure of FGF2 to limit the activation of FGFR2. The anticancer activities of P5 and DcP5 were examined in vitro and in vivo. Our results demonstrated that P5 significantly inhibited the cell proliferation in FGFR2-dependent manner in DU145 cells and retarded tumor growth in DU145 xenograft model with negligible toxicity toward normal organs. Further investigations found that the Gln4 and Glu6 residues of P5 bind to FGFR2 to abolish its activation. Moreover, we developed the P5 cyclic derivative, DcP5, which achieved reinforced stability and anticancer activity in vivo. Our findings suggest P5 and its cyclic derivative DcP5 as potential candidates for anticancer therapy.

Published
2020

48. Preparation of Refractory Materials by Co-sintering of Ferronickel Slag and Ferrochromium Slag: Thermodynamic Analysis

Author

Gu, Foquan, Zhang, Yuanbo, Peng, Zhiwei, Tang, Huimin, Su, Zijian, Jiang, Tao, Anderson, Corby, editor, Goodall, Graeme, editor, Gostu, Sumedh, editor, Gregurek, Dean, editor, Lundström, Mari, editor, Meskers, Christina, editor, Nicol, Stuart, editor, Peuraniemi, Esa, editor, Tesfaye, Fiseha, editor, Tripathy, Prabhat K., editor, Wang, Shijie, editor, and Zhang, Yuanbo, editor

Published
2021
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