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| 1 | Arterial stiffness and stroke:de-stiffening strategy,a therapeutic target for stroke显示文摘Stroke is the second leading cause of mortality and morbidity worldwide.Early intervention is of great importance in reducing disease burden.Since the conventional risk factors cannot fully account for the pathogenesis of stroke,it is extremely important to detect useful biomarkers of the vascular disorder for appropriate intervention.Arterial stiffness,a newly recognised reliable feature of arterial structure and function,is demonstrated to be associated with stroke onset and serve as an independent predictor of stroke incidence and poststroke functional outcomes.In this review article,different measurements of arterial stiffness,especially pressure wave velocity,were discussed.We explained the association between arterial stiffness and stroke occurrence by discussing the secondary haemodynamic changes.We reviewed clinical data that support the prediction role of arterial stiffness on stroke.Despite the lack of long-term randomised double-blind controlled therapeutic trials,it is high potential to reduce stroke prevalence through a significant reduction of arterial stiffness(which is called de-stiffening therapy).Pharmacological interventions or lifestyle modification that can influence blood pressure,arterial function or structure in either the short or long term are promising de-stiffening therapies.Here,we summarised different de-stiffening strategies including antihypertension drugs,antihyperlipidaemic agents,chemicals that target arterial remodelling and exercise training.Large and well-designed clinical trials on de-stiffening strategy are needed to testify the prevention effect for stroke.Novel techniques such as modern microscopic imaging and reliable animal models would facilitate the mechanistic analyses in pathophysiology,pharmacology and therapeutics. | Yajing Chen Fanxia Shen Jianrong Liu Guo-Yuan Yang | 2017 | Stroke & Vascular Neurology2017，2，2： | 3 |
| 2 | Localization of muscarinic acetylcholine receptor in plant guard cells显示文摘Acetylcholine (ACh), as an important neuro-transmitter in animals, also plays a significant role in various kinds of physiological functions in plants. But relatively little is known about its receptors in plants. A green fluorescence BODIPY FL-labeled ABT, which is a high affinity ligand of muscarinic acetylcholine receptor (mAChR), was used to localize mAChR in plant guard cells. In Vicia faba L. and Pisum sativum L., mAChR was found both on the plasma membrane of guard cells. mAChR may also be distributed on guard cell chloroplast membrane of Vicia faba L. The evidence that mAChR localizes in the guard cells provides a new possible signal transduction pathway in ACh mediated stomata movement. | Fanxia Meng Xin Liu Shuqiu Zhang Chenghou Lou | 2001 | Chinese Science Bulletin2001，46，7： | 2 |
| 3 | Endo thelial progenitor cell transplantation improves long term outcome in mice显示文摘 | Yongfeng Fan Fanxia Shen Tim Frenzel | 2010 | Ann Neurol2010，67，4： | 1 |
| 4 | Angiopoietin- 2 facilitates vascular endothelial growth factor- induced angiogenesis in the mature mouse Brain 显示文摘 | Zhu Yiqiang Lee Chanhung Shen Fanxia | 2005 | Stroke2005，36，7： | 1 |
| 5 | Conserved arginine residue in the membrane-spanning domain of HIV-1 gp41 is required for efficient membrane fusion显示文摘Despite the high mutation rate of HIV-1,the amino acid sequences of the membrane-spanning domain(MSD)of HIV-1 gp41 are well conserved.Arginine residues are rarely found in single membrane-spanning domains,yet an arginine residue,R696(the numbering is based on that of HXB2),is highly conserved in HIV-1 gp41.To examine the role of R696,it was mutated to K,A,I,L,D,E,N,and Q.Most of these substitutions did not affect the expression,processing or surface distribution of the envelope protein(Env).However,a syncytia formation assay showed that the substitution of R696 with amino acid residues other than K,a naturally observed mutation in the gp41 MSD,decreased fusion activity.Substitution with hydrophobic amino acid residues(A,I,and L)resulted in a modest decrease,while substitution with D or E,potentially negatively-charged residues,almost abolished the syncytia formation.All the fusion-defective mutants showed slower kinetics with the cell-based dual split protein(DSP)assay that scores the degree of membrane fusion based on pore formation between fusing cells.Interestingly,the D and E substitutions did show some fusion activity in the DSP assays,suggesting that proteins containing D or E substitutions retained some fusion pore-forming capability.However,nascent pores failed to develop,due probably to impaired activity in the pore enlargement process.Our data show the importance of this conserved arginine residue for efficient membrane fusion. | Yufei Long Fanxia Meng Naoyuki Kondo Aikichi Iwamoto Zene Matsuda | 2011 | Protein & Cell2011，2，5： | 1 |
| 6 | Overexpression of netrin-1 induces neovascularization in the adult mouse brain显示文摘 | Fan Yongfeng Shen Fanxia Chen Yongmei | 2008 | J Cereb Blood Flow Metab2008，28，9： | 1 |
| 7 | MicroRNA-9 Coordinates Proliferation and Migration of Human Embryonic Stem Cell-Derived Neural Progenitors显示文摘 | Celine Delaloy Lei Liu Jin-A Lee Hua Su Fanxia Shen Guo-Yuan Yang William L. Young Kathy N. Ivey Fen-Biao Gao | 2010 | Cell Stem Cell2010，，4： | 1 |
| 8 | Bio‐Inspired, Smart, Multiscale Interfacial Materials显示文摘 | FanXia LeiJiang | 2008 | Mater2008，，15： | 1 |
| 9 | Improvement of crashworthiness behaviour for simplified structural models of aircraft fuselage 显示文摘 | MENG FanXia ZHOU Qing YANG lianLi | 2009 | International Journal of Crashworthiness2009，14，1： | 1 |
| 10 | Angiopoietin - 2 facilitates vascular endothelial growth factor- induced angiogenesis in the mature mouse brain显示文摘 | Zhu Yiqian Lee Chanhung Shen Fanxia | 2005 | Stroke2005，36，7： | 1 |
| 11 | MicroRNA-9 Coordinates Proliferation and Migration of Human Embryonic Stem Cell-Derived Neural Progenitors显示文摘 | Celine Delaloy Lei Liu Jin-A Lee Hua Su Fanxia Shen Guo-Yuan Yang William L. Young Kathy N. Ivey Fen-Biao Gao | 2010 | Cell Stem Cell2010，，4： | 1 |
| 12 | Has the cardiac stem cell controversy settled down?显示文摘Although the human adult heart was considered a terminally differentiated organ and incapable of renewal after injury or with aging for almost a century,recent studies have shown that the heart is capable of new cardiomyocyte | WU MingFu MENG FanXia | 2014 | Science China(Life Sciences)2014，57，9： | 0 |
| 13 | A Distorted Image of Confucius ——on Lin Yutang′s Version of Lunyu(论语)显示文摘Lin Yutang does a great deal in translating and introducing Chinese Classical literature to western countries,yet he also makes many mistakes in the translation and introduction. This essay talks about his three errors. First,he misunderstands the functions of fa(法) in Confueianism. Next,he mistranslates some sayings such as Fafenwangshi(“发愤忘食”), so he distorts the image of Confucius. Last,he doesnot understand the meaning of Sanshierli(“三十而立”)correctly,so that he ignores the important role of li(礼) in Confucius′ whole life. | Qiao Hualin (English Dept.of Pingdingshan Teachers′ College) Chen Fanxia (Foreign Languages College of Henan University,Kaifeng,Henan 467002) | 1999 | 平顶山学院学报1999，0，S1： | 0 |
| 14 | Ketogenic diet alleviates cognitive dysfunction and neuroinflammation in APP/PS1 mice via the Nrf2/HO-1 and NF-κB signaling pathways显示文摘Alzheimer's disease is a progressive neurological disorder characterized by cognitive decline and chronic inflammation within the brain.The ketogenic diet,a widely recognized therapeutic intervention for refractory epilepsy,has recently been proposed as a potential treatment for a variety of neurological diseases,including Alzheimer's disease.However,the efficacy of ketogenic diet in treating Alzheimer's disease and the underlying mechanism remains unclear.The current investigation aimed to explore the effect of ketogenic diet on cognitive function and the underlying biological mechanisms in a mouse model of Alzheimer's disease.Male amyloid precursor protein/presenilin 1(APP/PS1)mice were randomly assigned to either a ketogenic diet or control diet group,and received their respective diets for a duration of 3 months.The findings show that ketogenic diet administration enhanced cognitive function,attenuated amyloid plaque formation and proinflammatory cytokine levels in APP/PS1 mice,and augmented the nuclear factor-erythroid 2-p45 derived factor 2/heme oxygenase-1 signaling pathway while suppressing the nuclear factor-kappa B pathway.Collectively,these data suggest that ketogenic diet may have a therapeutic potential in treating Alzheimer's disease by ameliorating the neurotoxicity associated with Aβ-induced inflammation.This study highlights the urgent need for further research into the use of ketogenic diet as a potential therapy for Alzheimer's disease. | Jingwen Jiang Hong Pan Fanxia Shen Yuyan Tan Shengdi Chen | 2023 | Neural Regeneration Research2023，18，12： | 0 |
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