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| 1 | A Tracing Algorithm of Thevenin Equivalent Parameters for Power Systems With Large Disturbance显示文摘 | SUN huadong CHEN Shuyong CHANG Xiaopeng LIN Weifang | 2012 | 中国电机工程学报2012，32，22： | 5 |
| 2 | The electrochemical behavior of PbSO 4 with different structures on Pb显示文摘 | Yonglang Guo Lin Niu Shuyong Zhang Shenhao Chen | 2000 | Journal of Power Sources2000，，1： | 1 |
| 3 | Preemptive analgesic effects of low-dose ketamine on growth-associated protein expression in dorsal root ganglion of chronic constriction injury model rats显示文摘BACKGROUND: Ketamine is a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonists and plays an important role in the treatment of pain. OBJECTIVE: To analyze the preemptive analgesic effects of different doses of ketamine on growth-associated protein-43 (GAP-43) expression in dorsal root ganglion in a rat model of chronic sciatic nerve constricted injury, and to study the differences between high-dose and low-dose ketamine DESIGN: Randomized controlled animal study. SETTING: Medical College of Shantou University. MATERIALS: Thirty-five adult male Sprague Dawley rats were provided by the Experimental Animal Center of Guangzhou University of Traditional Chinese Medicine. Ketamine hydrochloride injection was provided by Hengrui Pharmaceutical Co., Ltd., Jiangsu. METHODS: This study was performed at the Immunological Laboratory, Medical College of Shantou University from September to December 2006. Model of chronic sciatic nerve constricted injury: after anesthesia, the right sciatic nerve was exposed and ligated 1-cm distal to the ischiadic tuberosity with a No. 3-0 cat gut suture. Grouping and intervention: 35 rats were randomly divided into 4 groups: normal control group (n = 5), chronic constriction injury (CCI) group (n = 10), low-dose ketamine group (n = 10), and high-dose ketamine group (n = 10). Rats in the normal control group did not undergo any surgery or drug intervention. Rats in the CCI group received intraperitoneal injection of saline (1 mL), and their sciatic nerves were ligated after 10 minutes. Rats in the low-dose ketamine group underwent intraperitoneal injection of ketamine (25 mg/kg) 10 minutes prior to ligation of sciatic nerve; while, rats in the high-dose ketamine group were given intraperitoneal injection of ketamine (50 mg/kg) 10 minutes prior to ligation of sciatic nerve. On the third and the seventh days after surgery, dorsal root ganglion were resected from the sciatic nerve and cut into sections. MAIN OUTCOME MEASURES: GAP-43 expression in dorsal root ganglion was detected by immunohistochemistry and image analysis system, as well as semi-quantitative analysis. RESULTS: Thirty-five Sprague Dawley rats were included in the final analysis. Qualitative analysis: GAP-43 expression in the CCI group was higher than in the normal control group. Quantitative analysis: after three post-operative days, GAP-43 expression in the CCI group was significantly higher than in the normal control group (t = 22.919, 7.319, P < 0.05). GAP-43 expression in the low-dose and high-dose ketamine group was significantly lower than in the CCI group (t = 11.166, 26.474, P < 0.05). After seven postoperative days, GAP-43 expression in the low-dose and high-dose ketamine groups was significantly lower than in the CCI group (t = 2.382, 5.016, P < 0.05). CONCLUSION: Preoperative administration of ketamine inhibited the increased GAP-43 expression in dorsal root ganglion during neuropathic pain. | Shuyong Lin Chen Wang | 2008 | Neural Regeneration Research2008，3，4： | 1 |
| 4 | Targeting LncRNA LLNLR-299G3.1 with antisense oligonucleotide inhibits malignancy of esophageal squamous cell carcinoma cells in vitro and in vivo显示文摘Accumulating evidence has indicated that long non-coding RNAs(lncRNAs)play critical roles in the development and progression of cancers,including esophageal squamous cell carcinoma(ESCC).However,the mechanisms of lncRNAs in ESCC are still incompletely understood and therapeutic attempts for in vivo targeting cancer-associated lncRNA remain a challenge.By RNA-sequencing analysis,we identified that LLNLR-299G3.1 was a novel ESCC-associated lncRNA.LLNLR-299G3.1 was up-regulated in ESCC tissues and cells and promoted ESCC cell proliferation and invasion.Silencing of LLNLR-299G3.1 with ASO(antisense oligonucleotide)resulted in opposite effects.Mechanistically,LLNLR-299G3.1 bound to cancerassociated RNA binding proteins and regulated the expression of cancer-related genes,including OSM,TNFRSF4,HRH3,and SSTR3.ChIRP-seq(chromatin isolation by RNA purification and sequencing)revealed that these genes contained enriched chromatin binding sites for LLNLR-299G3.1.Rescue experiments confirmed that the effects of LLNLR-299G3.1 on ESCC cell proliferation were dependent on interaction with HRH3 and TNFRSF4.Therapeutically,intravenous delivery of placental chondroitin sulfate A binding peptide-coated nanoparticles containing antisense oligonucleotide(pICSA-BP-ANPs)strongly inhibited ESCC tumor growth and significantly improved animal survival in vivo.Overall,our results suggest that LLNLR-299G3.1 promotes ESCC malignancy through regulating gene-chromatin interactions and targeting ESCC by pICSA-BP-ANPs may be an effective strategy for the treatment of lncRNA-associated ESCC. | LI TIAN YONGYI HUANG BAOZHEN ZHANG YI SONG LIN YANG QIANQIAN CHEN ZHENG WANG YILING WANG QIHAN HE WENHAN YANG SHUYONG YU TIANYU LU ZICHEN LIU KAIPING GAO XIUJUN FAN JIAN SONG RIHONG ZHAI | 2023 | Oncology Research2023，31，4： | 0 |
| 5 | BRSK2 in pancreatic β cells promotes hyperinsulinemia-coupled insulin resistance and its genetic variants are associated with human type 2 diabetes显示文摘Brain-specific serine/threonine-protein kinase 2(BRSK2)plays critical roles in insulin secretion andβ-cell biology.However,whether BRSK2 is associated with human type 2 diabetes mellitus(T2DM)has not been determined.Here,we report that BRSK2 genetic variants are closely related to worsening glucose metabolism due to hyperinsulinemia and insulin resistance in the Chinese population.BRSK2 protein levels are significantly elevated inβcells from T2DM patients and high-fat diet(HFD)-fed mice due to enhanced protein stability.Mice with inducibleβ-cell-specific Brsk2 knockout(βKO)exhibit normal metabolism with a high potential for insulin secretion under chow-diet conditions.Moreover,βKO mice are protected from HFD-induced hyperinsulinemia,obesity,insulin resistance,and glucose intolerance.Conversely,gain-of-function BRSK2 in matureβcells reversibly triggers hyperglycemia due toβ-cell hypersecretion-coupled insulin resistance.Mechanistically,BRSK2 senses lipid signals and induces basal insulin secretion in a kinase-dependent manner.The enhanced basal insulin secretion drives insulin resistance andβ-cell exhaustion and thus the onset of T2DM in mice fed an HFD or with gain-of-function BRSK2 inβcells.These findings reveal that BRSK2 links hyperinsulinemia to systematic insulin resistance via interplay betweenβcells and insulin-sensitive tissues in the populations carrying human genetic variants or under nutrient-overload conditions. | Rufeng Xu Kaiyuan Wang Zhengjian Yao Yan Zhang Li Jin Jing Pang Yuncai Zhou Kai Wang Dechen Liu Yaqin Zhang Peng Sun Fuqiang Wang Xiaoai Chang Tengli Liu Shusen Wang Yalin Zhang Shuyong Lin Cheng Hu Yunxia Zhu Xiao Han | 2023 | Journal of Molecular Cell Biology2023，15，5： | 0 |
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