Search

Your search keyword '"Zhang, Sijia"' showing total 23 results
Start Over Author "Zhang, Sijia" Publisher wiley
23 results on '"Zhang, Sijia"'

2. Origin and evolution of the kiwifruit Y chromosome

Author

Yue, Junyang, primary, Chen, Qinyao, additional, Zhang, Sijia, additional, Lin, Yunzhi, additional, Ren, Wangmei, additional, Li, Bingjie, additional, Wu, Ying, additional, Wang, Yingzhen, additional, Zhou, Yongfeng, additional, and Liu, Yongsheng, additional

Published
2023
Full Text
View/download PDF

6. Lomitapide ameliorates middle cerebral artery occlusion‐induced cerebral ischemia/reperfusion injury by promoting neuronal autophagy and inhibiting microglial migration

Author

Zheng, Yangmin, primary, Hu, Yue, additional, Han, Ziping, additional, Yan, Feng, additional, Zhang, Sijia, additional, Yang, Zhenhong, additional, Zhao, Fangfang, additional, Li, Lingzhi, additional, Fan, Junfen, additional, Wang, Rongliang, additional, and Luo, Yumin, additional

Published
2022
Full Text
View/download PDF

8. The assembly of caprine Y chromosome sequence reveals a unique paternal phylogenetic pattern and improves our understanding of the origin of domestic goat

Author

Xiao, Changyi, primary, Li, Jingjin, additional, Xie, Tanghui, additional, Chen, Jianhai, additional, Zhang, Sijia, additional, Elaksher, Salma Hassan, additional, Jiang, Fan, additional, Jiang, Yaoxin, additional, Zhang, Lu, additional, Zhang, Wei, additional, Xiang, Yue, additional, Wu, Zhenyang, additional, Zhao, Shuhong, additional, and Du, Xiaoyong, additional

Published
2021
Full Text
View/download PDF

9. Simultaneous detection of fetal aneuploidy, de novo FGFR3 mutations and paternally derived β ‐thalassemia by a novel method of noninvasive prenatal testing

Author

Yang, Lin, primary, Wu, Yujing, additional, Hu, Zhiyang, additional, Zhang, Haiping, additional, Pu, Dandan, additional, Yan, Huijuan, additional, Zhang, Sijia, additional, Jiang, Hui, additional, Liu, Qiang, additional, Yuan, Yuying, additional, Zhang, Yanyan, additional, Chen, Fang, additional, Lu, Yanping, additional, Pan, Silin, additional, Lin, Linhua, additional, and Gao, Ya, additional

Published
2021
Full Text
View/download PDF

14. Silencing of microRNA‐494 inhibits the neurotoxic Th1 shift via regulating HDAC2‐STAT4 cascade in ischaemic stroke

Author

Zhao, Haiping, primary, Li, Guangwen, additional, Wang, Rongliang, additional, Tao, Zhen, additional, Ma, Qingfeng, additional, Zhang, Sijia, additional, Han, Ziping, additional, Yan, Feng, additional, Li, Fangfang, additional, Liu, Ping, additional, Ma, Shubei, additional, Ji, Xunming, additional, and Luo, Yumin, additional

Published
2019
Full Text
View/download PDF

19. Modulation of Metal and Insulator States in 2D Ferromagnetic VS2 by van der Waals Interaction Engineering

Author

Guo, Yuqiao, primary, Deng, Haitao, additional, Sun, Xu, additional, Li, Xiuling, additional, Zhao, Jiyin, additional, Wu, Junchi, additional, Chu, Wangsheng, additional, Zhang, Sijia, additional, Pan, Haibin, additional, Zheng, Xusheng, additional, Wu, Xiaojun, additional, Jin, Changqing, additional, Wu, Changzheng, additional, and Xie, Yi, additional

Published
2017
Full Text
View/download PDF

22. Silencing of microRNA-494 inhibits the neurotoxic Th1 shift via regulating HDAC2-STAT4 cascade in ischaemic stroke.

Author

Zhao H, Li G, Wang R, Tao Z, Ma Q, Zhang S, Han Z, Yan F, Li F, Liu P, Ma S, Ji X, and Luo Y

Subjects
Aged, Animals, Antagomirs pharmacology, Female, Histone Deacetylase 2 antagonists & inhibitors, Humans, Ischemic Stroke pathology, Jurkat Cells, Male, Mice, Mice, Inbred C57BL, MicroRNAs antagonists & inhibitors, Middle Aged, STAT4 Transcription Factor antagonists & inhibitors, Th1 Cells drug effects, Th1 Cells pathology, Histone Deacetylase 2 metabolism, Ischemic Stroke metabolism, MicroRNAs metabolism, STAT4 Transcription Factor metabolism, Th1 Cells metabolism
Abstract

Background and Purpose: T helper cell 1 (Th1)-skewed neurotoxicity contributes to the poor outcome of stroke in rodents. Here, we have elucidated the mechanism of the Th1/Th2 shift in acute ischaemic stroke (AIS) patients at hyperacute phase and have looked for a miRNA-based therapeutic target., Experimental Approach: MiR-494 levels in blood from AIS patients and controls were measured by real-time PCR. C57BL/6J mice were subjected to transient middle cerebral artery occlusion, and cortical neurons were subjected to oxygen-glucose deprivation. Luciferase reporter system, chromatin immunoprecipitation sequencing (ChIP-Seq), and ChIP-PCR were used to uncover possible mechanisms., Key Results: In lymphocytes from AIS patients, there was a Th1/Th2 shift and histone deacetylase 2 (HDAC2) was markedly down-regulated. ChIP-seq showed that HDAC2 binding sites were enriched in regulation of Th1 cytokine production, and ChIP-PCR confirmed that HDAC2 binding was changed at the intron of STAT4 and the promoter of T-box transcription factor 21 (T-bet) in lymphocytes from AIS patients. MiR-494 was the most significantly increased miRNA in lymphocytes from AIS patients, and miR-494-3p directly targeted HDAC2. A strong association existed between miR-494 and Th1 cytokines, and neurological deficit as measured by the National Institute of Health Stroke Scale (NIHSS) in AIS patients. In vitro and in vivo experiments showed that antagomir-494 reduced Th1 shift-mediated neuronal and sensorimotor functional damage in the mouse model of ischaemic stroke, via the HDAC2-STAT4 pathway., Conclusion and Implications: We demonstrated that miR-494 inhibition prevented Th1-skewed neurotoxicity through regulation of the HDAC2-STAT4 cascade., (© 2019 The British Pharmacological Society.)

Published
2020
Full Text
View/download PDF

23. Collagen organization regulates stretch-initiated pain-related neuronal signals in vitro: Implications for structure-function relationships in innervated ligaments.

Author

Zhang S, Singh S, and Winkelstein BA

Subjects
Animals, Ganglia, Spinal physiology, In Vitro Techniques, Rats, Zygapophyseal Joint injuries, Extracellular Signal-Regulated MAP Kinases metabolism, Fibrillar Collagens physiology, Neurons physiology, Nociception, Substance P metabolism
Abstract

Injury to the spinal facet capsule, an innervated ligament with heterogeneous collagen organization, produces pain. Although mechanical facet joint trauma activates embedded afferents, it is unclear if, and how, the varied extracellular microstructure of its ligament affects sensory transduction for pain from mechanical inputs. To investigate the effects of macroscopic deformations on afferents in collagen matrices with different organizations, an in vitro neuron-collagen construct (NCC) model was used. NCCs with either randomly organized or parallel aligned collagen fibers were used to mimic the varied microstructure in the facet capsular ligament. Embryonic rat dorsal root ganglia (DRG) were encapsulated in the NCCs; axonal outgrowth was uniform and in all directions in random NCCs, but parallel in aligned NCCs. NCCs underwent uniaxial stretch (0.25 ± 0.06 strain) corresponding to sub-failure facet capsule strains that induce pain. Macroscopic NCC mechanics were measured and axonal expression of phosphorylated extracellular signal-regulated kinase (pERK) and the neurotransmitter substance P (SP) was assayed at 1 day to assess neuronal activation and nociception. Stretch significantly upregulated pERK expression in both random and aligned gels (p < 0.001), with the increase in pERK being significantly higher (p = 0.013) in aligned than in random NCCs. That increase likely relates to the higher peak force (p = 0.025) and stronger axon alignment (p < 0.001) with stretch direction in the aligned NCCs. In contrast, SP expression was greater in stretched NCCs (p < 0.001) regardless of collagen organization. These findings suggest that collagen organization differentially modulates pain-related neuronal signaling and support structural heterogeneity of ligament tissue as mediating sensory function. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:770-777, 2018., (© 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc.)

Published
2018
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results