Search

Your search keyword '"Wang, Si-qi"' showing total 421 results
Start Over Author "Wang, Si-qi"
421 results on '"Wang, Si-qi"'

51. Physical exercise rescues cocaine-evoked synaptic deficits in motor cortex

Author

Cheng, Tong, Huang, Xiao-Dan, Hu, Xue-Fei, Wang, Si-Qi, Chen, Kai, Wei, Ji-An, Yan, Lan, So, Kwok-Fai, Yuan, Ti-Fei, and Zhang, Li

Abstract

Drug exposure impairs cortical plasticity and motor learning, which underlies the reduced behavioral flexibility in drug addiction. Physical exercise has been used to prevent relapse in drug rehabilitation program. However, the potential benefits and molecular mechanisms of physical exercise on drug-evoked motor-cortical dysfunctions are unknown. Here we report that 1-week treadmill training restores cocaine-induced synaptic deficits, in the form of improved in vivo spine formation, synaptic transmission, and spontaneous activities of cortical pyramidal neurons, as well as motor-learning ability. The synaptic and behavioral benefits relied on de novoprotein synthesis, which are directed by the activation of the mechanistic target of rapamycin (mTOR)-ribosomal protein S6 pathway. These findings establish synaptic functional restoration and mTOR signaling as the critical mechanism supporting physical exercise training in rehabilitating the addicted brain.

Published
2024
Full Text
View/download PDF

55. Acacetin Alleviates Cardiac Fibrosis via TGF-β1/Smad and AKT/mTOR Signal Pathways in Spontaneous Hypertensive Rats.

Author

Li, Zhi-yi, Lv, Si, Qiao, Jie, Wang, Si-qi, Ji, Fang, Li, Dan, Yan, Jie, Wei, Yan, Wu, Lin, Gao, Changzhen, and Li, Miao-ling

Subjects
HEART fibrosis, CELLULAR signal transduction, HYPERTENSION, ANGIOTENSIN II, EXTRACELLULAR matrix
Abstract

Introduction: Attenuating cardiac fibroblasts activation contributes to reducing excessive extracellular matrix deposition and cardiac structural remodeling in hypertensive hearts. Acacetin plays a protective role in doxorubicin-induced cardiomyopathy and ischemia/reperfusion injury. The aim of this study was to investigate the potential molecular mechanisms underlying the protective role of acacetin on hypertension-induced cardiac fibrosis. Methods: Echocardiography, histopathological methods, and Western blotting techniques were used to evaluate the anti-fibrosis effects in spontaneous hypertensive rat (SHR) which were daily intragastrically administrated with acacetin (10 mg/kg and 20 mg/kg) for 6 weeks. Angiotensin II (Ang II) was used to induce cellular fibrosis in human cardiac fibroblasts (HCFs) in the absence and presence of acacetin treatment for 48 h. Results: Acacetin significantly alleviated hypertension-induced increase in left ventricular (LV) posterior wall thickness and LV mass index in SHR. The expressions of collagen-1, collagen-III, and alpha-smooth muscle actin (α-SMA) were remarkedly decreased after treatment with acacetin (n = 6, p < 0.05). In cultured HCFs, acacetin significantly attenuated Ang II-induced migration and proliferation (n = 6, p < 0.05). Moreover, acacetin substantially inhibited Ang II-induced upregulation of collagen-1 and collagen-III (n = 6, p < 0.05) and downregulated the expression of alpha-SMA in HCFs. Additionally, acacetin decreased the expression of TGF-β1, p-Smad3/Smad3, and p-AKT and p-mTOR but increased the expression of Smad7 (n = 6, p < 0.05). Further studies found that acacetin inhibited TGF-β1 agonist SRI and AKT agonist SC79 caused fibrotic effect. Conclusion: Acacetin inhibits the hypertension-associated cardiac fibrotic processes through regulating TGF-β/Smad3, AKT/mTOR signal transduction pathways. [ABSTRACT FROM AUTHOR]

Published
2023
Full Text
View/download PDF

61. OMA1 maintains the stemness of glioma stem cells by inducing mitochondrial fission/fusion imbalance

Author

Li, Jun jun, primary, Xiong, Cui, additional, Zhu, Kai, additional, Jiang, Cheng, additional, Wang, Min jie, additional, Zhou, Zi jie, additional, Tang, Nan, additional, Wang, Si qi, additional, Shu, Peng wei, additional, Yuan, Hong liang, additional, Xiong, Zhi yong, additional, Li, Jin song, additional, Liang, Tao, additional, Wang, Xuan, additional, and Jiang, Xiao bing, additional

Published
2022
Full Text
View/download PDF

66. Linc01060 suppresses ferroptosis by downregulating SPOP-mediated c-Myc degradation in glioma

Author

Li, Jun Jun, primary, Wang, Qiang Ping, additional, Jiang, Cheng, additional, Wang, Min Jie, additional, Tang, Nan, additional, Zhou, Zi Jie, additional, Zhu, Kai, additional, Cao, Yu, additional, Hu, Guang Fu, additional, Wang, Si Qi, additional, Shu, Peng Wei, additional, Yuan, Hong Liang, additional, Xiong, Zhi Yong, additional, Li, Jin Song, additional, Ouyang, Tao Hui, additional, Liu, Hong Ya, additional, Qiu, Lie Wang, additional, Wang, Xuan, additional, Li, Lin, additional, Hu, Xue Bin, additional, Zhang, Fang Cheng, additional, Zhou, Ying Chun, additional, Zhao, Hong Yang, additional, Rao, Jing, additional, and Jiang, Xiao Bing, additional

Published
2022
Full Text
View/download PDF

69. Flora of Northeast Asia.

Author

Wang, Si-Qi, Dong, Xue-Yun, Ye, Liang, Wang, Hong-Feng, and Ma, Ke-Ping

Subjects
BOTANY, SPECIES distribution, DATA distribution, PHYTOGEOGRAPHY, STATISTICS
Abstract

As a component of the MAP project, the study of the flora in Northeast Asia (comprising Japan, South Korea, North Korea, Northeast China, and Mongolia) convincingly underscores the indispensability of precise and comprehensive diversity data for flora research. Due to variations in the description of flora across different countries in Northeast Asia, it is essential to update our understanding of the region's overall flora using the latest high-quality diversity data. This study employed the most recently published authoritative data from various countries to conduct a statistical analysis of 225 families, 1782 genera, and 10,514 native vascular species and infraspecific taxa in Northeast Asia. Furthermore, species distribution data were incorporated to delineate three gradients in the overall distribution pattern of plant diversity in Northeast Asia. Specifically, Japan (excluding Hokkaido) emerged as the most prolific hotspot for species, followed by the Korean Peninsula and the coastal areas of Northeast China as the second richest hotspots. Conversely, Hokkaido, inland Northeast China, and Mongolia constituted species barren spots. The formation of the diversity gradients is primarily attributed to the effects of latitude and continental gradients, with altitude and topographic factors within the gradients modulating the distribution of species. [ABSTRACT FROM AUTHOR]

Published
2023
Full Text
View/download PDF

70. High-rate performance and super long-cycle stability of Na3V2(PO4)3 cathode material coated by diatomic doped carbon.

Author

Kang, Jia, Zhu, Ling, Teng, Fei-Yang, Wang, Si-Qi, Huang, Yong-Gang, Xiang, Yan-Hong, Chen, Zhe, and Wu, Xian-Wen

Abstract

Copyright of Rare Metals is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2023
Full Text
View/download PDF

76. ABCC9 Is Downregulated and Prone to Microsatellite Instability on ABCC9tetra in Canine Breast Cancer

Author

Hao, Pan, Song, Kai-yue, Wang, Si-qi, Huang, Xiao-jun, Yao, Da-wei, and Yang, De-ji

Subjects
canine breast cancer, General Veterinary, oncogenesis, Veterinary medicine, SF600-1100, Veterinary Science, microsatellite instability, loss of heterozygosity, the adenosine triphosphate binding cassette subfamily C member 9, digestive system diseases, Original Research
Abstract

Tumorigenesis is associated with metabolic abnormalities and genomic instability. Microsatellite mutations, including microsatellite instability (MSI) and loss of heterozygosity (LOH), are associated with the functional impairment of some tumor-related genes. To investigate the role of MSI and LOH in sporadic breast tumors in canines, 22 tumors DNA samples and their adjacent normal tissues were evaluated using polyacrylamide gel electrophoresis and silver staining for 58 microsatellites. Quantitative real-time polymerase chain reaction, promoter methylation analysis and immunohistochemical staining were used to quantify gene expression. The results revealed that a total of 14 tumors (6 benign tumors and 8 breast cancers) exhibited instability as MSI-Low tumors. Most of the microsatellite loci possessed a single occurrence of mutations. The maximum number of MSI mutations on loci was observed in tumors with a lower degree of differentiation. Among the unstable markers, FH2060 (4/22), ABCC9tetra (4/22) and SCN11A (6/22) were high-frequency mutation sites, whereas FH2060 was a high-frequency LOH site (4/22). The ABCC9tetra locus was mutated only in cancerous tissue, although it was excluded by transcription. The corresponding genes and proteins were significantly downregulated in malignant tissues, particularly in tumors with MSI. Furthermore, the promoter methylation results of the adenosine triphosphate binding cassette subfamily C member 9 (ABCC9) showed that there was a high level of methylation in breast tissues, but only one case showed a significant elevation compared with the control. In conclusion, MSI-Low or MSI-Stable is characteristic of most sporadic mammary tumors. Genes associated with tumorigenesis are more likely to develop MSI. ABCC9 protein and transcription abnormalities may be associated with ABCC9tetra instability.

Published
2022

79. Cover Image

Author

Wang, Si‐Qi, primary, Shen, Yue, additional, Li, Jing, additional, Liu, Yun, additional, Cheng, Li‐Sha, additional, Wu, Sheng‐Di, additional, She, Wei‐Min, additional, and Jiang, Wei, additional

Published
2021
Full Text
View/download PDF

93. Paradoxical effects of cellular senescence-inhibited gene involved in hepatocellular carcinoma migration and proliferation by ERK pathway and mesenchymal-like markers

Author

Cheng,Qian, Tong,Tan-jun, Li,Zhao, Hu,Shi-hua, Chen,Ding-bao, Wang,Si-qi, Zhu,Ji-ye, Cheng,Qian, Tong,Tan-jun, Li,Zhao, Hu,Shi-hua, Chen,Ding-bao, Wang,Si-qi, and Zhu,Ji-ye

Abstract

Qian Cheng,1 Tan-jun Tong,2 Zhao Li,1 Shi-hua Hu,1 Ding-bao Chen,1 Si-qi Wang,1 Ji-ye Zhu1 1Peking University Institute of Organ Transplantation, Peking University Center of Liver Cancer Diagnosis and Treatment, Beijing Key Surgical Basic Research Laboratory of Liver Cirrhosis and Liver Cancer, Department of Hepatobiliary Surgery, Peking University People’s Hospital, Beijing, 100044, China; 2Peking University Research Center on Aging, Department of Biochemistry and Molecular Biology, Peking University Health Science Center, Beijing, 100191, China Background: Cellular senescence-inhibited gene (CSIG) strongly prolongs the progression of replicative senescence. However, roles and mechanisms of CSIG in tumor progression have not been studied widely. Methods: Roles of CSIG in migration and proliferation of SMMC7721 and Huh7 cells were analyzed by transwell or cell viability assays, respectively. Tumorigenicity assays were used to study whether CSIG knockdown could affect SMMC7721 proliferation in vivo. Next, Western blotting and RT-PCR were preformed to evaluate the effects of CSIG on P-ERK cascade and epithelial mesenchymal transformation markers. Then, the location and expression of CSIG protein was detected by immunofluorescence and Western blotting, respectively. Finally, the Cancer Genome Atlas dataset was used to analyze CSIG mRNA levels in hepatocellular carcinoma (HCC) and adjacent non-tumor tissues. Results: In this study, we found that CSIG overexpression promoted SMMC7721 cell migration, and CSIG knockdown suppressed tumorigenicity of SMMC7721 cells. In contrast to expectation, CSIG up-regulation could significantly inhibit Huh7 cell growth and migration. CSIG could promote P-ERK activation and levels of mesenchymal-like markers in SMMC7721 cells, whereas CSIG suppressed P-ERK activation and levels of mesenchymal-like markers in Huh7 cells. CSIG protein was located in nucleoli as well as nucleoplasm of SMMC7721 cells, whereas CSIG protein was mainly

Published
2019

Catalog

Books, media, physical & digital resources
See catalog results