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| 1 | Inhibiting effect of antisense oligonucleotides phosphorthioate on gene expression of TIMP-1 in rat liver fibrosis显示文摘AIM To observe the inhibition of antisenseoligonucleotides (asON) phosphorthioate to thetissue inhibitors metalloproteinase-1 (TIMP-1)gene and protein expression in the liver tissue ofimmunologically induced hepatic fibrosis rats.The possibility of reversing hepatic fibrosisthrough gene therapy was observed.METHODS Human serum albumin (HSA) wasused to attack rats, as hepatic fibrosis model, inwhich asONs were used to block the gene andprotein expressing TIMP-1. According to theanalysis of modulator, structure protein, codingseries of TIMP-1 genome, we designed fourdifferent asONs. These asONs were injected intothe hepatic fibrosis models through coccygealvein. The results was observed by RT-PCR formeasuring TIMP-1 mRNA expression,immunohistochemistry and in situ hybridizationfor collagen Ⅰ, Ⅲ, special staining of collagenfiber, and electron microscopic examination.RESULTS Hepatic fibrosis could last within 363days in our modified model. The expressinglevel of TIMP-1 was high during hepatic fibrosisprocess. It has been proved by theimmunohistochemical and the electronmicroscopic examination that the asONphosphorthioate of TIMP-1 could exactly expressin vivo. The effect of colchicine wasdemonstrated to inhibit the expressing level ofmRNA and the content of collagen Ⅰ, Ⅲ in theliver of experimental hepatic fibrosis rats.However, the electron microscopy research andthe pathologic grading of hepatic fibrosisshowed that there was no significant differencebetween the treatment group and the modelgroup (P>0.05).CONCLUSION The experimental rat model ofhepatic fibrosis is one of the preferable modelsto estimate the curative effect of anti-hepaticfibrosis drugs. The asON phosphorthioate ofTIMP-1 could block the gene and proteinexpression of TIMP-1 in the liver of experimentalhepatic fibrosis rats at the mRNA level. It ispossible to reverse hepatic fibrosis, and it isexpected to study a new drug of anti-hepaticfibrosis on the genetic level. Colchicine has verylimited therapeutic effect on hepatic fibrosis,furthermore, its toxicity and side effects areobvious. | Qing He Nie Yong Qian Cheng Yu Mei Xie Yong Xing Zhou Yi Zhan Cao The Center of Infectious Disease Diagnosis and Treatment of PLA,Tangdu Hospital,Forth Military Medical University,Xi’an 710038,Shaanxi Province,ChinaDr,Qing He Nie graduated from Qinghai Medical College as a doctor in 1983,got master degree at Beijing 302 Army Hospital in 1993,got doctor degree at the Third Military Medical University in 1998,engaged in postdoctoral research at the Fourth Military Medical University from 1998 to 2000,now an associate professor,specialized in clinical and experimental research of infectious diseases,had more than 90 papers published,coauthor of ten books,first author of one book. | 2001 | World Journal of Gastroenterology2001，7，3： | 73 |
| 2 | CRISPR-Cas12a has both cis- and trans-cleavage activities on single-stranded DNA显示文摘 | Shi-Yuan Li Qiu-Xiang Cheng Jia-Kun Liu Xiao-Qun Nie Guo-Ping Zhao Jin Wang | 2018 | Cell Research2018，28，4： | 41 |
| 3 | PTEN-L is a novel protein phosphatase for ubiquitin dephosphorylation to inhibit PINK1-Parkin-mediated mitophagy显示文摘Mitophagy 是为损坏线粒体的特定的消除的选择 autophagy 的一种重要类型。(PINK1 )导致 PTEN 的通常认为的 kinase 蛋白质 1 催化 ubiquitin (Ub ) 的 phosphorylation 在 PINK1-Parkin-mediated mitophagy 的发作起一个关键作用。(PTEN-L ) 磷酸酶和 tensin 相当或相同的事物(PTEN ) 长是 PTEN 的最新识别的 isoform,与到它的 N 终点的 173 氨基酸的增加。这里,我们报导 PTEN-L 是经由它对 phosphorylated ubiquitin 的蛋白质磷酸酶活动的 mitophagy 的一个新奇否定管理者。我们发现 PTEN-L 在外部 mitochondrial 膜(OMM ) 本地化,而 PTEN-L 的删除支持, PTEN-L 的 overexpression 禁止, mitophagy 由各种各样的损坏线粒体的代理人导致了。机械学地, PTEN-L 能够有效地阻止 Parkin mitochondrial translocation,减少 Parkin phosphorylation,维持它的关上的不活跃的符合构造,并且禁止它的 E3 ligase 活动。更重要地, PTEN-L 在 vivo 减少 phosphorylated ubiquitin (pSer65-Ub ) 的水平,并且在 vitro,磷酸酶试金经由它的蛋白质磷酸酶活动证实那 PTEN-L dephosphorylates pSer65-Ub,独立于它的类脂化合物磷酸酶功能。一起拿,我们的调查结果为 ubiquitin 作为蛋白质磷酸酶表明 PTEN-L 的新奇功能,它抵抗在 mitophagy 正式就职和 mitophagy 的最终的抑制导致前馈控制机制的阻塞的调停 PINK1 的 ubiquitin phosphorylation。因此,理解 PTEN-L 的这新奇功能在控制 mitophagy 的分子的难题提供一关键错过片,在包括象 Parkinsons 那样的 neurodegenerative 混乱的许多重要人的疾病的一个批评过程疾病。 | Liming Wang Yik-Lam Cho Yancheng Tang Jigang Wang Jung-Eun Park Yajun Wu Chunxin Wang Yan Tong Ritu Chawla Jianbin Zhang Yin Shi Shuo Deng Guang Lu Yihua Wu Hayden Weng-Siong Tan Pornteera Pawijit Grace Gui-Yin Lim Hui-Ying Chan Jingzi Zhang Lei Fang Hanry Yu Yih-Cherng Liou Mallilankaraman Karthik Boon-Huat Bay Kah-Leong Lim Siu-Kwan Sze Celestial T. Yap Han-Ming Shen | 2018 | Cell Research2018，28，8： | 25 |
| 4 | MiRNA-133a is involved in the regulation of postmenopausal osteoporosis through promoting osteoclast differentiation显示文摘然而,在绝经后的骨质疏松症的进步和发展的 miR-133a 的重要角色被报导了内在的机制还不是清楚的。在这研究, qRT-PCR 分析被执行在从绝经后的骨质疏松症病人(PMOP ) 和健康控制孤立的浆液估计 miR-133 表示。骨头矿物质密度(BMD ) 被双精力的 X 光检查 absorptiometry (DXA ) 在腰部的脊骨测量。结果证明 miR-133a 是显著地 upregulated 并且否定地在绝经后的 osteoporotic 女人的浆液与腰部的脊骨 BMD 相关。miR-133a 模仿, miR-133a 禁止者,和相应控制分别地是进 RAW264.7 和 THP-1 房间的 transfected。陷井积极的房间被数, NFATc1, c-Fos 和陷井的蛋白质表示被西方的污点分析检测。我们发现 MiR-133a 在 osteoclastogenesis 期间是 upregulated,并且 miR-133a 的 overexpression 支持了 RAW264.7 和 THP-1 房间的导致 RANKL 的区别进骨破折,而 miR-133a 击倒显示出颠倒的结果。在里面在 vivo 实验,老鼠是双边地 ovariectomized (OVX ) 并且与 antagomiR-133a 或 antagoNC 注射了,并且为分别地为 ELISA,微计算断层摄影术(CT ) 和骨头 histomorphology 分析收集浆液和腰部的脊骨被牺牲。它被发现那,在 OVX 老鼠, miR-133a 击倒在浆液改变了 osteoclastogenesis 相关的因素的层次并且增加了腰部的脊骨 BMD 并且改变了骨头 histomorphology。一起, miRNA-133a 通过支持骨破折区别涉及绝经后的骨质疏松症的规定。 | Zhongqi Li Wenzhi Zhang Yan Huang | 2018 | Acta Biochimica et Biophysica Sinica2018，50，3： | 24 |
| 5 | Ginkgolide B promotes the proliferation and differentiation of neural stem cells following cerebral ischemia/reperfusion injury,both in vivo and in vitro显示文摘Neural stem cells have great potential for the development of novel therapies for nervous system diseases.However,the proliferation of endogenous neural stem cells following brain ischemia is insufficient for central nervous system self-repair.Ginkgolide B has a robust neuroprotective effect.In this study,we investigated the cell and molecular mechanisms underlying the neuroprotective effect of ginkgolide B on focal cerebral ischemia/reperfusion injury in vitro and in vivo.Neural stem cells were treated with 20,40 and 60 mg/L ginkgolide B in vitro.Immunofluorescence staining was used to assess cellular expression of neuron-specific enolase,glial fibrillary acid protein and suppressor of cytokine signaling 2.After treatment with 40 and 60 mg/L ginkgolide B,cells were large,with long processes.Moreover,the proportions of neuron-specific enolase-,glial fibrillary acid protein-and suppressor of cytokine signaling 2-positive cells increased.A rat model of cerebral ischemia/reperfusion injury was established by middle cerebral artery occlusion.Six hours after ischemia,ginkgolide B(20 mg/kg) was intraperitoneally injected,once a day.Zea Longa's method was used to assess neurological function.Immunohistochemistry was performed to evaluate the proportion of nestin-,neuron-specific enolase-and glial fibrillary acid protein-positive cells.Real-time quantitative polymerase chain reaction was used to measure m RNA expression of brain-derived neurotrophic factor and epidermal growth factor.Western blot assay was used to analyze the expression levels of brain-derived neurotrophic factor and suppressor of cytokine signaling 2.Ginkgolide B decreased the neurological deficit score,increased the proportion of nestin-,neuron-specific enolase-and glial fibrillary acid protein-positive cells,increased the m RNA expression of brain-derived neurotrophic factor and epidermal growth factor,and increased the expression levels of brain-derived neurotrophic factor and suppressor of cytokine signaling 2 in the ischemic penumbra.Together,the in vivo and in vitro findings suggest that ginkgolide B improves neurological function by promoting the proliferation and differentiation of neural stem cells in rats with cerebral ischemia/reperfusion injury. | Pei-Dong Zheng Rajneesh Mungur Heng-Jun Zhou Muhammad Hassan Sheng-Nan Jiang Jie-Sheng Zheng | 2018 | Neural Regeneration Research2018，13，7： | 21 |
| 6 | Polyubiquitin chain-induced p62 phase separation drives autophagic cargo segregation显示文摘错误褶层蛋白质能被选择 autophagy 降级。占优势的看法由 autophagosomes 是标注 ubiquitin 的错误褶层蛋白质被支架蛋白质 p62 装配进总数,并且总数然后被吞没并且降级。这里,我们报导 p62 在在 photobleaching 以后有象高球状,经历熔化的能力,和恢复那样的像液体的性质的 vivo 形成微滴。Recombinant p62 不在 vitro 经历阶段分离;然而,补充说到 p62 的 K63 polyubiquitin 链导致 p62 阶段分离,它导致高度分子的重量 ubiquitin 的丰富在 p62 微滴发信号。从 p62 / 房间与 cytosol 混合 recombinant p62 也以一种 polyubiquitination 依赖的方式导致 p62 阶段分离。机械学地, p62 阶段分离依赖于 p62 聚合,在 p62 和 ubiquitin 之间的相互作用,和 polyubiquitin 链的原子价。而且, p62 阶段分离能被象 phosphorylation 那样的 translational 以后修正调整。最后,我们证明在 p62 的联系疾病的变化能影响阶段分离。我们建议那 polyubiquitin 导致链的 p62 阶段分离运动 autophagic 货物集中和分离。 | Daxiao Sun Rongbo Wu Jingxiang Zheng Pilong Li Li YU | 2018 | Cell Research2018，28，4： | 21 |
| 7 | Loss of canonical Wnt signaling is involved in the pathogenesis of Alzheimer's disease显示文摘Alzheimer's disease(AD) is the most common form of dementia in the older population, however, the precise cause of the disease is unknown. The neuropathology is characterized by the presence of aggregates formed by amyloid-β(Aβ) peptide and phosphorylated tau; which is accompanied by progressive impairment of memory. Diverse signaling pathways are linked to AD, and among these the Wnt signaling pathway is becoming increasingly relevant, since it plays essential roles in the adult brain. Initially, Wnt signaling activation was proposed as a neuroprotective mechanism against Aβ toxicity. Later, it was reported that it participates in tau phosphorylation and processes of learning and memory. Interestingly, in the last years we demonstrated that Wnt signaling is fundamental in amyloid precursor protein(APP) processing and that Wnt dysfunction results in Aβ production and aggregation in vitro. Recent in vivo studies reported that loss of canonical Wnt signaling exacerbates amyloid deposition in a transgenic(Tg) mouse model of AD. Finally, we showed that inhibition of Wnt signaling in a Tg mouse previously at the appearance of AD signs, resulted in memory loss, tau phosphorylation and Aβ formation and aggregation; indicating that Wnt dysfunction accelerated the onset of AD. More importantly, Wnt signaling loss promoted cognitive impairment, tau phosphorylation and Aβ1–42 production in the hippocampus of wild-type(WT) mice, contributing to the development of an Alzheimer's-like neurophatology. Therefore, in this review we highlight the importance of Wnt/β-catenin signaling dysfunction in the onset of AD and propose that the loss of canonical Wnt signaling is a triggering factor of AD. | Cheril Tapia-Rojas Nibaldo C.Inestrosa | 2018 | Neural Regeneration Research2018，13，10： | 21 |
| 8 | Diterpene ginkgolides protect against cerebral ischemia/reperfusion damage in rats by activating Nrf2 and CREB through PI3K/Akt signaling显示文摘Diterpene ginkgolides meglumine 注射(DGMI ) 是白果树 biloba L 的一篇治疗学的摘录,它在中国被用于服的 ischemic 击的处理。Ginkgolides A, B 和 C 是 DGMI 的主要部件。这研究被设计在 vivo 并且在 vitro 对 ischemic 击调查 DGMI 部件的 neuroprotective 效果。尖锐服的 ischemic 损害被中间的服的动脉(MCA ) 的吸藏为 24 h 灌注跟随的 1.5 h 在老鼠导致。老鼠与 DGMI 被对待(1, 3 和 10 mg/kg, iv ) 在在灌注以后的灌注和 12 h 的发作。DGMI 的管理显著地减少了神经病学的赤字获得的老鼠,减少的大脑梗塞卷,和导致的蛋白质 kinase B (Akt ) phosphorylation,它推动了原子 factor-erythroid 2-related 的原子 translocation 因素 2 (Nrf2 ) 并且幸存的 phosphorylation 规章的蛋白质周期的安培应答的元素绑定蛋白质(CREB ) 。Nrf2 激活导致了下游的蛋白质 heme oxygenase-1 (HO-1 ) 的表示。另外, PC12 房间在 vitro 受到氧葡萄糖 deprivation/reperfusion ( OGD/R ),有 DGMI ( 1 , 10 和 20 g/mL )的处理或 ginkgolides A , B 或 C (为各个的 10 mol/L )显著地减少了 PC12 房间死亡并且增加了 Akt 的 phosphorylation , Nrf2 的原子 translocation 和 CREB 的激活。Nrf2 和 CREB 的激活能被合作处理与 phosphoinositide-3-kinase (PI3K ) 颠倒禁止者 LY294002。这些观察建议 ginkgolides 充当激活表明小径的 Akt/Nrf2 和 Akt/CREB 的新奇外来的管理者,免于服的 ischemia/reperfusion (I/R ) 在 vivo 并且在 vitro 的损坏。 | Wen ZHANG Jun-ke SONG Rong YAN Li LI Zhi-yong XIAO Wen-xia ZHOU Zhen-zhong WANG Wei XIAO Guan-hua DU | 2018 | Acta Pharmacologica Sinica2018，39，8： | 20 |
| 9 | Inhibition of KLF7-Targeting Micro RNA 146b Promotes Sciatic Nerve Regeneration显示文摘A previous study has indicated that Krüppel-like factor 7(KLF7), a transcription factor that stimulates Schwann cell(SC) proliferation and axonal regeneration after peripheral nerve injury, is a promising therapeutic transcription factor in nerve injury. We aimed to identify whether inhibition of micro RNA-146 b(mi R-146 b)affected SC proliferation, migration, and myelinated axon regeneration following sciatic nerve injury by regulating its direct target KLF7. SCs were transfected with mi RNA lentivirus, mi RNA inhibitor lentivirus, or KLF7 si RNA lentivirus in vitro. The expression of mi R146 b and KLF7,as well as SC proliferation and migration, were subsequently evaluated. In vivo, an acellular nerve allograft(ANA) followed by injection of GFP control vector or a lentiviral vector encoding an mi R-146 b inhibitor was used to assess the repair potential in a model of sciatic nerve gap. mi R-146 b directly targeted KLF7 by binding to the 30-UTR, suppressing KLF7. Up-regulation of mi R-146 b and KLF7 knockdown significantly reduced the proliferation and migration of SCs, whereas silencing mi R-146 b resulted in increased proliferation and migration. KLF7 protein was localized in SCs in which mi R-146 b was expressed in vivo.Similarly, 4 weeks after the ANA, anti-mi R-146 b increased KLF7 and its target gene nerve growth factor cascade, promoting axonal outgrowth. Closer analysis revealed improved nerve conduction and sciatic function index score, and enhanced expression of neurofilaments, P0(anti-peripheral myelin), and myelinated axon regeneration. Our findings provide new insight into the regulation of KLF7 by mi R-146 b during peripheral nerve regeneration and suggest a potential therapeutic strategy for peripheral nerve injury. | Wen-Yuan Li Wei-Ting Zhang Yong-Xia Cheng Yan-Cui Liu Feng-Guo Zhai Ping Sun Hui-Ting Li Ling-Xiao Deng Xiao-Feng Zhu Ying Wang | 2018 | Neuroscience Bulletin2018，34，3： | 19 |
| 10 | Suppression of m6A reader Ythdf2 promotes hematopoietic stem cell expansion显示文摘 | Zhenrui Li Pengxu Qian Wanqing Shao Hailing Shi Xi C. He Madelaine Gogol Zulin Yu Yongfu Wang Meijie Qi Yunfei Zhu John M. Perry Kai Zhang Fang Tao Kun Zhou Deqing Hu Yingli Han Chongbei Zhao Richard Alexander Hanzhang Xu Shiyuan Chen Allison Peak Kathyrn Hall Michael Peterson Anoja Perera Jeffrey S. Haug Tari Parmely Hua Li Bin Shen Julia Zeitlinger Chuan He Linheng Li | 2018 | Cell Research2018，28，9： | 18 |
| 11 | The emerging role and targetability of the TCA cycle in cancer metabolism显示文摘tricarboxylic 酸(TCA ) 周期是为在房间的氧化 phosphorylation 的一条中央线路,并且完成他们的 bioenergetic, biosynthetic,和氧化还原作用平衡要求。尽管有癌症房间绕过的早教义 TCA 骑车并且首先利用氧气的 glycolysis,新兴的证据表明那某些癌症房间,特别那些与 deregulated oncogene 和肿瘤 suppressor 表示,为精力重重地依靠 TCA 周期生产和大分子合成。作为地进步,在 tumorigenesis 和使用小分子禁止者使不安的潜力的异常 TCA 周期功能的重要性为癌症治疗的提高的周期功能开始演变。在这评论,我们关于在燃料上喂周期, oncogenes 的效果和肿瘤 suppressors 的燃料总结当前的知识,周期酶的周期用法,普通基因改变和解除管制,和为指向 TCA 的潜在的治疗学的机会在癌症房间骑车。用先进技术并且在 vivo 模型有机体研究的申请,是我们的希望这个以前俯看的生物化学的中心学习将提供新鲜卓见进癌症新陈代谢和 tumorigenesis,随后在各种各样的癌症为治疗学的干预揭示危险打字。 | Nicole M. Anderson Patrick Mucka Joseph G. Kern Hui Feng | 2018 | Protein & Cell2018，9，2： | 17 |
| 12 | Scutellarin protects oxygen/glucose-deprived astrocytes and reduces focal cerebral ischemic injury显示文摘Scutellarin, a bioactive flavone isolated from Scutellaria baicalensis, has anti-inflammatory, anti-neurotoxic, anti-apoptotic and anti-oxidative effects and has been used to treat cardiovascular and cerebrovascular diseases in China. However, the mechanisms by which scutellarin mediates neuroprotection in cerebral ischemia remain unclear. The interaction between scutellarin and nicotinamide adenine dinucleotide phosphate oxidase 2(NOX2) was assessed by molecular docking study, which showed that scutellarin selectively binds to NOX2 with high affinity. Cultures of primary astrocytes isolated from the cerebral cortex of neonatal Sprague-Dawley rats were pretreated with 2, 10 or 50 μM scutellarin for 30 minutes. The astrocytes were then subjected to oxygen/glucose deprivation by incubation for 2 hours in glucose-free Dulbecco's modified Eagle's medium in a 95% N2/5% CO_2 incubator, followed by simulated reperfusion for 22 hours. Cell viability was assessed by cell counting kit-8 assay. Expression levels of NOX2, connexin 43 and caspase-3 were assessed by western blot assay. Reactive oxygen species were measured spectrophotometrically. Pretreatment with 10 or 50 μM scutellarin substantially increased viability, reduced the expression of NOX2 and caspase-3, increased the expression of connexin 43, and diminished the levels of reactive oxygen species in astrocytes subjected to ischemia-reperfusion. We also assessed the effects of scutellarin in vivo in the rat transient middle cerebral artery occlusion model of cerebral ischemia-reperfusion injury. Rats were given intraperitoneal injection of 100 mg/kg scutellarin 2 hours before surgery. The Bederson scale was used to assess neurological deficit, and 2,3,5-triphenyltetrazolium chloride staining was used to measure infarct size. Western blot assay was used to assess expression of NOX2 and connexin 43 in brain tissue. Enzyme-linked immunosorbent assay was used to detect 8-hydroxydeoxyguanosine(8-OHd G), 4-hydroxy-2-nonenal(4-HNE) and 3-nitrotyrosin(3-NT) in brain tissue. Immunofluorescence double staining was used to determine the co-expression of caspase-3 and Neu N. Pretreatment with scutellarin improved the neurological function of rats with focal cerebral ischemia, reduced infarct size, diminished the expression of NOX2, reduced levels of 8-OHd G, 4-HNE and 3-NT, and reduced the number of cells co-expressing caspase-3 and Neu N in the injured brain tissue. Furthermore, we examined the effect of the NOX2 inhibitor apocynin. Apocynin substantially increased connexin 43 expression in vivo and in vitro. Collectively, our findings suggest that scutellarin protects against ischemic injury in vitro and in vivo by downregulating NOX2, upregulating connexin 43, decreasing oxidative damage, and reducing apoptotic cell death. | Jing-Bo Sun Yan Li Ye-Feng Cai Yan Huang Shu Liu Patrick KK Yeung Min-Zhen Deng Guang-Shun Sun Prince LM Zilundu Qian-Sheng Hu Rui-Xin An Li-Hua Zhou Li-Xin Wang Xiao Cheng | 2018 | Neural Regeneration Research2018，13，8： | 16 |
| 13 | Basic and Clinical Evidence of an Alternative Method to Produce Vivo Nanofat显示文摘 | Hong-Sen Bi Chen Zhang Fang-Fei Nie Bo-Lin Pan E Xiao | 2018 | Chinese Medical Journal2018，，5： | 14 |
| 14 | In vivo theranostics with near-infraredemitting carbon dots—highly efficient photothermal therapy based on passive targeting after intravenous administration显示文摘Carbon dots that exhibit near-infrared fluorescence(NIR CDs)are considered emerging nanomaterials for advanced biomedical applications with low toxicity and superior photostability and targeting compared to currently used photoluminescence agents.Despite progress in the synthesis of NIR CDs,there remains a key obstacle to using them as an in vivo theranostic agent.This work demonstrates that the newly developed sulfur and nitrogen codoped NIR CDs are highly efficient in photothermal therapy(PTT)in mouse models(conversion efficiency of 59%)and can be readily visualized by photoluminescence and photoacoustic imaging.The real theranostic potential of NIR CDs is enhanced by their unique biodistribution and targeting.Contrary to all other nanomaterials that have been tested in biomedicine,they are excreted through the body’s renal filtration system.Moreover,after intravenous injection,NIR CDs are accumulated in tumor tissue via passive targeting,without any active species such as antibodies.Due to their accumulation in tumor tissue without the need for intratumor injection,high photothermal conversion,excellent optical and photoacoustic imaging performance,and renal excretion,the developed CDs are suitable for transfer to clinical biomedical practice. | Xin Bao Ye Yuan Jingqin Chen Bohan Zhang Di Li Ding Zhou Pengtao Jing Guiying Xu Yingli Wang Kateřina Holá Dezhen Shen Changfeng Wu Liang Song Chengbo Liu Radek Zbořil Songnan Qu | 2018 | Light(Science & Applications)2018，7，1： | 13 |
| 15 | 支持科研和学术发现的语义网应用实例研究显示文摘针对当前语义网技术在支持科研创新方面的发展,比较两个支持科学研究和学术发现的工具——哈佛大学信息搜索引擎Harvard Catalyst和语义网探索的科学家网络VIVO,包括两者在信息组织方式、系统架构、系统实现关键技术、数据来源、实现的功能等方面的差异,分析VIVO所具有的特色以及存在的问题,讨论当前语义网应用在支持科学研究上具有的特点。 | 黄金霞 | 2011 | 图书情报工作2011，55，11： | 12 |
| 16 | A combination of astragaloside I, levistilide A and calycosin exerts anti-liver fibrosis effects in vitro and in vivo显示文摘肝纤维变性是源于各种各样的长期的肝疾病的细胞外的矩阵蛋白质的过多的累积。肝的星形的房间(HSC ) 在肝纤维变性的致病起一个必要作用。Danggui 唐步学(DBT ) 是中国传统的药的一个经典公式。我们以前证明 DBT 能改善在老鼠的肝纤维变性。然而,在肝纤维变性的处理的 DBT 的 bioactive 部件仍然保持未知。在这研究,我们在人的肝的星形的房间线 LX-2 从 DBT 评估了 14 成分,并且发现了那 astragaloside 我(A) , levistilide A (L) 和 calycosin (C) 在 LX-2 房间和 TGF-1-activated LX-2 房间上生产了 synergistic 增长抑制。因此,我们准备了他们的混合物,并且作为 ALC 公式说出这联合。用高内容的屏蔽和西方的污点试金,我们表明 ALC 公式显著地减少了 -SMA 和骨胶原的表示我在 LX-2 房间。在里面 ALC 公式的 vivo 反纤维变性效果在通过 dimethylnitrosamine 的注射建立的 C57BL/6 老鼠在一个肝纤维变性模型被评估(DMN 2 mg/kg, ip ) 为 4 个星期。在第三个星期内,好与 ALC 公式被注射(astragaloside 我 44.21 mg/kg 每天, levistilide A 6 mg/kg 每天和 calycosin 3.45 mg/kg 每天;ip ) 或 sorafenib,积极控制药(6 mg/kg 每天, ip ) 为 2 个星期。我们发现了显著地减少的骨胶原免职, hydroxyproline (忧郁) 内容和 -SMA 表示与模型鼠标相比在肝纸巾铺平的 ALC 公式的那个政府。在结论,现在的学习第一次表明我, levistilide A 和 calycosin 可以是的那 astragaloside 在 DBT 的 3 个主要 bioactive 部件;他们的联合在 vitro 并且在 vivo 施加反肝纤维变性效果。 | Tao GUO Zu-long LIu Qiang ZHAO Zhi-min ZHAO Cheng-hai LIU | 2018 | Acta Pharmacologica Sinica2018，39，9： | 11 |
| 17 | Endothelial progenitor cell-conditioned medium promotes angiogenesis and is neuroprotective after spinal cord injury显示文摘Endothelial progenitor cells secrete a variety of growth factors that inhibit inflammation, promote angiogenesis and exert neuroprotective effects. Therefore, in this study, we investigated whether endothelial progenitor cell-conditioned medium might have therapeutic effectiveness for the treatment of spinal cord injury using both in vitro and in vivo experiments. After primary culture of bone marrow-derived macrophages, lipopolysaccharide stimulation was used to classically activate macrophages to their proinflammatory phenotype. These cells were then treated with endothelial progenitor cell-conditioned medium or control medium. Polymerase chain reaction was used to determine mR NA expression levels of related inflammatory factors. Afterwards, primary cultures of rat spinal cord neuronal cells were prepared and treated with H_2O_2 and either endothelial progenitor cell-conditioned medium or control medium. Hoechst 33258 and propidium iodide staining were used to calculate the proportion of neurons undergoing apoptosis. Aortic ring assay was performed to assess the effect of endothelial progenitor cell-conditioned medium on angiogenesis. Compared with control medium, endothelial progenitor cell-conditioned medium mitigated the macrophage inflammatory response at the spinal cord injury site, suppressed apoptosis, and promoted angiogenesis. Next, we used a rat model of spinal cord injury to examine the effects of the endothelial progenitor cell-conditioned medium in vivo. The rats were randomly administered intraperitoneal injection of PBS, control medium or endothelial progenitor cell-conditioned medium, once a day, for 6 consecutive weeks. Immunohistochemistry was used to observe neuronal morphology. Terminal deoxynucleotidyl transferase-mediated d UTP nick-end labeling assay was performed to detect the proportion of apoptotic neurons in the gray matter. The Basso, Beattie and Bresnahan Locomotor Rating Scale was used to evaluate the recovery of motor function of the bilateral hind limbs after spinal cord injury. Compared with the other two groups, the number of axons was increased, cavities in the spinal cord were decreased, the proportion of apoptotic neurons in the gray matter was reduced, and the Basso, Beattie and Bresnahan score was higher in the endothelial progenitor cell-conditioned medium group. Taken together, the in vivo and in vitro results suggest that endothelial progenitor cell-conditioned medium suppresses inflammation, promotes angiogenesis, provides neuroprotection, and promotes functional recovery after spinal cord injury. | Tao Wang Xiao Fang Zong-Sheng Yin | 2018 | Neural Regeneration Research2018，13，5： | 11 |
| 18 | Pharmacokinetic Studies of Factor VIII in Chinese Boys with Severe Hemophilia A: A Single-Center Study显示文摘 | Zhen-Ping Chen Pei-jing Li Gang Li Ling Tang Ying-Zi Zhen Xin-Yi Wu Xiao-Ling Cheng Koon Hung Luke Victor S Blanchette Man-Chiu Poon Qiu-Lan Ding Run-Hui Wu | 2018 | Chinese Medical Journal2018，，15： | 11 |
| 19 | Effective and persistent antitumor activity of HER2-directed CAR-T cells against gastric cancer cells in vitro and xenotransplanted tumors in vivo显示文摘 | Yanjing Song Chuan Tong Yao Wang Yunhe Gao Hanren Dai Yelei Guo Xudong Zhao Yi Wang Zizheng Wang Weidong Han Lin Chen | 2018 | Protein & Cell2018，9，10： | 11 |
| 20 | Clinical Outcomes of Ex Vivo Liver Resection and Liver Autotransplantation for Hepatic Alveolar Echinococcosis显示文摘The effectiveness of liver autotransplantation for patients with partial hepatic alveolar echinococcosis was analyzed.We retrospectively studied 6 patients with hepatic alveolar echinococcosis who underwent liver autotransplantation in our hospital from 2008 to 2010.We also summarized the surgical indications of liver autotransplantation for hepatic alveolar echinococcosis and our experience in the management of postoperative complications of liver autotransplantation.Of 6 patients,5 achieved good curative results,and one died of multiple organ failure caused by portal vein thrombosis.Main complications included postoperative bleeding,bile leak and small-for-size liver graft syndrome.Liver autotransplantation offers a new approach to cure hepatic alveolar echinococcosis with non-resectable lesions.It could be the most effective method to cure intractable hepatic alveolar echinococcosis if correct handling in operation and proper prevention of complications are performed.But the long-term outcomes are still needed to be confirmed in longer follow-up. | 王海 刘巧玉 王昭明 张峰 李相成 王学浩 | 2012 | Journal of Huazhong University of Science and Technology(Medical Sciences)2012，32，4： | 11 |
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