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简介：InChina,thereisnotoneschoolthatdoesnottakeEnglishteachingseriously.Thereisnotonestu-dentwhodoesnotwanttolearnEnglishwell.How-ever,notmanylearnerswhosucceedinEnglishlearning,communicatefluentlyinbothoralorwrit-tenEnglish,andmuchfewerreachahighlevelinhighschoolyears.Therefore,whenweencounteredahighschoolEnglishloverwhoreachedaveryhighlevelofEnglish,ourinterestinknowinghernatural-lygrew.

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简介：Beingavisually-impaired(VI)studentattendingmainstreamclassesposesachallengetothemconsideringthelimitationpresentedbytheirlimitedvision.Thisphenomenologicalstudytriedtoexplorethesedifficultiesandidentifythedifferentcopingskillsthathelpedtheminpursuingtheirschooling.ItwasfoundoutthatVIstudentsdevelopedacertainadaptivemechanismthatenablesthemtosurvivetheiracademicjourney.Theirdifficultytaughtthemtoinnovatethemselvestobecomeaccustomedtothegrowingdemandofsocietyforthemtobeequallycompetitiveandproductiveindividualthatdoesnotconsidertheirdifficultiesashindrance.ItwasfoundoutthatVIstudentswhoareinthemainstreamclasseshaveastrongersocio-academicadaptabilitywhichenablesthemtorelatethemselvestotheirmainstreamcounterpartsandtoexcelintheiracademics.Thestudyrevealedthattheirsocialadaptationinvolvesstrongspiritualfoundation,self-confidence,self-motivation,senseofbelongingness,andbettersupportsystemfromfamiliesandfriends.Ontheotherhand,theiracademicadaptationincludestechnology,effectiveteacheraides,innovativestrategies,andmaterialsfortheblind.Whenallthiscomponentsareconsidered,thereisanassurancethatVIstudentsattendingmainstreamclassescanfinishtheirschooling.

简介：Theuseofspeckle-trackingechocardiography(STE)isbecominganincreasinglyusefultoolintheevaluationofmyocardialdisease.STEsoftwarecantrackthemotionofthespecularpatterncreatedbytheinterferenceofultrasoundwiththemyofibersoftheheartandprovideaquantitativemeanstoevaluatesubtlechangesinventricularfunctionthatoftenoccurbeforechangesinventricularejectionfractionareobserved.STEismostoftenusedtomeasurethechangeinshape(strain)ofmyocardialsegmentsinthecircumferential,radial,andlongitudinaldirections.Invariousdiseases,includingcoronaryarterydisease,aorticstenosis,andmitralregurgitation,deficitsinlongitudinalstrainappeartooccurearlierthandeficitsinothermeasuresofstrainorinejectionfraction.ConsiderationofSTEmeasuresofleftventricularcontractionhasthepotentialtosignificantlyaffectclinicalmanagementandoutcomesofischemicandvalvularheartdiseasegiventheabilitytoseparatethosewithasymptomaticdiseasewhomaybenefitfromearlierinterventionsthancurrentguidelinesmaysuggest.

简介：AbstractBackground:Fibroblast-like synoviocytes (FLSs), resident mesenchymal cells of synovial joints, play an important role in the pathogenesis of rheumatoid arthritis (RA). Dickkopf-1 (DKK-1) has been proposed to be a master regulator of bone remodeling in inflammatory arthritis. Here, potential impairation on the activity of FLSs derived from RA to small interfering RNAs (siRNAs) targeting DKK-1 was investigated.Methods:siRNAs targeting DKK-1 were transfected into FLSs of patients with RA. Interleukin (IL)-1β, IL-6, IL-8, matrix metalloproteinase (MMP) 2, MMP3, MMP9, transforming growth factor (TGF)-β1, TGF-β2 and monocyte chemoattractant protein (MCP)-1 levels in the cell culture supernatant were detected by enzyme-linked immunosorbent assay (ELISA). Invasion assay and 3H incorporation assay were utilized to investigate the effects of siRNAs targeting DKK-1 on FLSs invasion and cell proliferation, respectively. Western blotting was performed to analyze the expression of nuclear factor (NF)-κB, interleukin-1 receptor-associated kinase (IRAK)1, extracellular regulated protein kinases (ERK)1, Jun N-terminal kinase (JNK) and β-catenin in FLSs.Results:DKK-1 targeting siRNAs inhibited the expression of DKK-1 in FLSs (P < 0.01). siRNAs induced a significant reduction of the levels of IL-6, IL-8, MMP2, MMP3 and MMP9 in FLSs compared to the control group (P < 0.05). DKK-1 targeting siRNAs inhibited the proliferation and invasion of FLSs (P < 0.05). Important molecules of pro-inflammatory signaling in FLSs, including IRAK1 and ERK1, were decreased by the inhibition of DKK-1 in FLSs. In contrast, β-catenin, a pivotal downstream molecule of the Wnt signaling pathway was increased.Conclusions:By inhibiting DKK-1, we were able to inhibit the proliferation, invasion and pro-inflammatory cytokine secretion of FLSs derived from RA, which was mediated by the ERK or the IRAK-1 signaling pathway. These data indicate the application of DKK-1 silencing could be a potential therapeutic approach to RA.

简介：TheNationalUniversityCorporationTsukubaUniversityofTechnology(NTUT)istheonlyinstituteofhighereducationforthehearingandthevisuallyimpairedinJapan.Inouruniversity,hearingorvisuallyimpairedstudentsarestudyingtobetechniciansaftertheygraduate,towardsocialindependence.Frompreviousexperienceofhighereducationforstudentswithdisabilities,effectsareincreasedwhenmodelingisusedbytheteachersinvolvedinprofessionaleducation.IntheMechanicalEngineeringCourse,weareusingmodeling,tomatchthedrawingandshapeforbeginningstudents.Itincludessupportforenhancingone’sview,andhowtodrawouttheabilityofmechanicalengineeringstudentsforthebasics.ForstudentstostudyMechanicalDesignandDrawing,ModelingofGearPump,JackandGlobeValveareeasilyshownthroughdrawingsandtheoperationofeachmechanismthroughsampledrawingsinthetextbook.Itispossibletomakeanopportunitytothinkaboutthemachinemechanism.Itwillbeshownbystudents’works.Theassemblingofthemodeltriggerstheneedforformaccuracybymakingafunction,andimprovesthequalityoflearning.Itispossiblethatathree-dimensionalmoldingmachinecanbeproducedthroughexperientiallearningbythemodel,andmodelingwiththedimensionnumericaldata.Moreover,itisalsoembodiedinathree-dimensionalmodelingwhichresultsintheimageprocessingprogrammingcreated.Confirmingtheimprovementoftheprogramthroughtheshapewiththequality.IntheDepartmentofSyntheticDesign,studentshavechancestorealizeandself-evaluatefromthedesignofthelampshadewithacomplicatedshape.IntheFacultyofHealthSciencefromDepartmentofHealth,highqualityteachingofvisually-impairedstudentsthroughtheuseofbonemodelteachingmaterialshasbecomepossibleinthemedical-relatedcourses.

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简介：ObjectivesEndothelialdysfunctionistheearliestmarkerforatherosclerosisandplayskeyroleinthepathogenesisofcardiovasculardiseases.Thepresentstudywasperformedtoevaluateeffectofagingonarterialelasticitybyusingpulsewaveformanalysisandinvestigatewhetherthechangesinarterialelasticitycanbeusedasanon-invasivemeasureforearlydetectionofendothelialdysfunction.MethodsUsingmodifiedWindkesselmodelofthecirculationandpulsewaveformanalysis,C1largearteryandC2smallarteryelasticityindicesof204normalhealthysubjects(age15-80years)weremeasured.Amongthemtwenty-fourmalehealthysubjectsweredividedintoboththeyoung(age20-30years,n=12)andelderly(age60-70years,n=12)groups.Wedeliveredacethycholine(Ach),anendotheliumdependentvasodilator,andsodiumnitroprusside(SNP),anendothelium-independentvasodilator,todermalvesselsoftheforearmusingiontophoresis,respectively,andmeasuredbasalandpeakbloodflowusinglaserdopplerfluximetry.ResultsC1largearteryandC2smallarteryelasticityindiceswerereducedwithadvancingage.C1largearteryandC2smallarteryelasticityindiceswerenegativelycorrelatedwithage(r=-0.628,p＜0.001;r=-0.595,p＜0.001).Basalbloodflowwassimilarbetweentheyoungandelderlygroups(14.58±3.4vs13.52±3.41PU,p=NS).PeakbloodflowinducedbyAchwassignificantlyreducedintheelderlygroupcomparedwiththeyounggroup(83.4±11.9vs93.75±10.87PU,p＜0.05).However,peakbloodflowinducedbySNPwassimilarinthetwogroups(119.17±16.76vs128.33±21.29PU,p=NS).Ach-inducedpeakbloodflowcorrelatedpositivelywithC1largearteryandC2smallarteryelasticityindices(r=0.56,p＜0.01;r=0.53,p＜0.01).ConclusionsAdvancingageleadstoimpairedarteryelasticityandendothelialdysfunction.Reducedarterialelasticityis,inparallel,associatedwithdiminishedendothelium-dependentvasodilation.Itisconcludedthata

简介：Complicationsaremorefrequentinelderlypatientswithcoronaryheartdisease(CHD),suchasimpairedglucosetoleranceandconstipations.Itisalwaysdifficulttocurethesecomplicationsinclinicalpractice.Inthiscasewehadsuccessfullycuredaneighty-threeyearsoldmanwithCHDcomplicatingimpairedglucosetoleranceandconstipationbyintegratedChinese-Westernmedicine.

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简介：氮的氧化物(没有)在neurodegeneration的提升被含有。然而，很少对在之间的关系被知道没有并且在neurodegenerative的神经干细胞(NSC)的自强或区别能力疾病。在这研究，我们调查了效果不，在在一个动物的NSC的自强上，为Niemann精选的模型打C(NPC)疾病。我们发现没有生产显著地从NPC1缺乏的老鼠(NPC1-/-)在NSC被增加，它显示出减少的NSC自强。nestin积极的房间的数字和neurospheres的尺寸显著地两个都被减少。没有synthase(NOS)的表达式在与野类型的neurospheres相比从NPC1-/-鼠标的大脑导出的neurospheres被增加。肝糖synthasekinase-3beta(GSK3beta)和caspase-3的不调停的激活也从NPC1-/-老鼠在NSC被观察。从NPC1-/-老鼠的NSC的自强能力被一个NOS禁止者恢复，L名字，它导致了GSK3beta和caspase-3的抑制。另外，NSC的区别能力部分被恢复并且Fluoro碧玉的数字C积极的堕落神经原被减少。这些数据建议那生产过剩不，在NPC，疾病损害了NSC的自强。没有生产的控制可能为NPC疾病的处理是关键的。

简介：AbstractObjective:To investigate the possible regulatory mechanism of corticotropin-releasing hormone (CRH), urocortin (UCN), and Wolfram syndrome 1 (WFS1) in 17α-ethynylestradiol (EE)-induced intrahepatic cholestasis pregnant rats and its ischemia reperfusion (IR) model.Methods:Pregnant rats (n=60) were randomly divided into four experimental groups by random number table (Control, EE, IR, and EE-IR groups),and were studied on the 17th, 19th, and 21st gestational days (GD) (n=5 in each group at the indicated time). Growth and development indicators of fetal rats among these four groups were recorded. Enzyme-linked immunosorbent assay was employed to detect CRH, UCN, and WFS1 levels in maternal sera. Western blotting and real-time polymerase chain reaction were used to quantify placental protein and placental mRNA levels of CRH, UCN, and WFS1. Multivariate analysis of variance and least significant difference test were used to establish the group and individual comparisons.Results:A significant difference was found in placenta weight (F=8.10, P<0.05), fetal rat weight (F=40.86, P<0.05), fetal rat length (F=61.61, P<0.05), and fetal rat tail length (F=55.63, P<0.05) among four groups on the 17th ,19th , and 21st GD.What’s more, the overall differences of maternal serum UCN levels among Control, EE, IR, and EE-IR groups were significant (F=2.48, P<0.05). Expression of WFS1 mRNA in the EE-IR group was significantly increased and higher than Control (0.46±0.15 vs. 0.24±0.09, P<0.05), EE (0.46±0.15 vs. 0.17±0.04, P>0.05), and IR (0.46±0.15 vs. 0.22±0.15, P>0.05) groups at 19th GD, indicating that endoplasmic reticulum stress may be activated. However, the expression of CRH (0.42±0.05 vs. 0.58±0.12, P<0.05), UCN (0.43±0.01 vs. 0.47±0.16, P>0.05), and WFS1 (0.57±0.07 vs. 0.74±0.12, P>0.05) protein in the EE-IR group was subsided compared to the IR group at 17th GD.Conclusion:Fetal rat growth restriction was found in the EE-induced intrahepatic cholestasis model. This study revealed that significant changes in the maternal sera level of UCN , placental level of WFS1 mRNA and placental levels of CRH, UCN, and WFS1 protein in chronic versus acute stress in a rat model of pregnancy. This suggests an impaired compensatory vasodilatory effect mediated by these factors at gene transcription and protein translation levels, following acute hypoxia stress in EE-induced intrahepatic cholestasis in pregnant rats.