简介：有编码Dermatophagoidespteronyssinus组2的DNA的种痘(Derp2)变应原以前在Derp上显示出它immunologic保护的效果在老鼠的2导致变应原的过敏航线发炎。在现在的学习，我们调查了是否2能施加的DNA疫苗编码Derp在老鼠模型的导致变应原的过敏航线发炎上的治疗学的角色并且在气喘探索了DNA种痘的机制特定变应原的免疫疗法。在由Derp敏化并且质问以后2，BALB/c老鼠与DNA被使免疫疫苗。细胞的渗入的度被获得。在浆液的IgE层次和在BALF的IL-4/lL-13层次被ELISA决定。肺纸巾被组织学的考试估计。在肺的STAT6和NF-B的表情被染色的immunohistochemistry决定。有DNA疫苗的老鼠的种痘禁止了航线发炎和变应原导致的粘蛋白的生产的发展，并且减少了Derp2-specificIgE水平的水平。eosinophii渗入的重要减小和在BALF的IL-4andIL-13的层次在种痘以后被观察。进一步更，DNA种痘在Derp2-immunized老鼠在肺织物禁止了STAT6和NF-Bexpression。这些结果显示DNA疫苗编码Derp2allergen能在我们的老鼠模型被用于导致变应原的过敏航线发炎的治疗。

简介：Severaldrug-resistantvariantshavebeendevelopedbygrowingtheparentalMELcellsinpresenceofcolchicine,adriamycinandvincristinerespectivelywithstepwiseincreasingconcentration.Boththecolchicine-resistantSc9(ColO)andvincristine-resis-tantSc9(VCR5)cellsdisplayedanacceleratedHMBA-inducedcommitmenttoterminalcelldifferentiation,whereastheadriamycin-resistantSC9(A120)showednoaccelerationbutratherasubstantialdelayinHMBA-induceddifferentiation.ThestudiesprovidemorecluesaswellasexperimentalmodelsforfurtherstudyonthemechanismofinduceddifferentiationofMELcells.

简介：AIM:Toestablishtheratmodelofstreptozotocin(STZ)induceddiabeticretinopathy(DR),whichisthemostcommoncauseofvisuallossandblindnessinpatientswithdiabetes,andobservethegeneexpressionofvascularendothelialgrowthfactor(VEGF)anditsreceptorsduringthedevelopmentofDR.METHODS:AratmodelofdiabeteswasestablishedbyintraperitonealinjectionofSTZ.Thediabeticratswerehousedfor2,3and4monthsafterthedevelopmentofdiabetes.Retinalhistopathologicalobservationwasperformed.TheretinalvesselswereobservedbyimmunofluorescencestainingbyCD31.ThemRNAexpressionofVEGF,VEGFreceptor1and2(VEGFR1/2)inratretinawasdetectedbyreversetranscriptionpolymerasechainreaction(RT-PCR)analysis.RESULTS:Retinalhistopathologicalobservationshowedthemorphologicalchangesofinnernuclearlayer(INL)andouternuclearlayer(ONL)atanytime-point,andalsodemonstratedtheincreasednewvesselsatboth3,4monthsafterthedevelopmentofdiabetes.TheCD31stainingresultsshowedthatthenumberofvesselswasincreasedintheretinasofdiabeticratsatboth3and4monthsafterthedevelopmentofdiabetes.Ascomparedtothenormalrats,themRNAexpressionofVEGFwasincreasedinretinasofdiabeticratsat3monthsafterthedevelopmentofdiabetes,whileVEGFR1andVEGFR2mRNAexpressionwasincreasedat2,3and4monthsafterthedevelopmentofdiabetes.CONCLUSION:Takentogether,ourresultsdemonstratedthatDRwasoccurredat3monthsafterthedevelopmentofdiabetes,andthemRNAexpressionofVEGF,VEGFR1andVEGFR2wereincreasedintheprocessofDR.ThepresentstudyfurtherevidencedtheinvolvementofVEGFanditsreceptorsintheprocessofDR.

简介：Aim:ToobservetheapoptoticchangesfollowingexposuretoEMPandtoexplorethepossibleinjurymechanisminNIH-3T3fibroblasts.Methods:FollowingNIH-3T3cellswereexposedtoEMP,theproliferationandviabilityofNIH-3T3fibroblastswereestimatedbyhemacytometerandMTTMeasurements.Apoptoticratewasmeasuredbyflowcytometer.TheimnmohistochemicalSPmethodwasusedtodeterminebcl-2,p53.ThepositivelystainedcellswereanalyzedwithCMIAS-Ⅱimageanalysissystematamagnification400.AlldatawereanalyzedbySPSS8.0software.Results:TheproliferationandviabilityofNIH-3T3cellsweremarkedlyinhibitedandsignificantapoptosiswasinducedfollowingexposuretoEMP.EMPcouldincreasethenumberofnon-adherentcells,thehighestratio(33.9%)ofnon-adherentcellsalsooccurredat6h.TheAs70valueofMTTdecreasedimmediatelyat1h,6hfollowingthecellswereexposedascomparedwiththecontrol(P＜0.05).Thehighestratioofapoptosiswas15.07%at6h,thendecreasedgradually.Down-regulationofbcl-2andup-regulationofp53wereinducedbyEMP(P＜0.05).Conclusions:EMPcouldpromoteapoptosisofNIH-3T3fibroblasts.EMPcouldalsodown-regulatebcl-2levelandup-regulatep53levelinNIH-3T3fibroblasts.Bcl-2andp53genemaytakepartintheprocessofapoptosis.

简介：ＴＢｕｒｎＲｅｓｅａｒｃｈＩｎｓｔｉｔｕｔｅ，ＳｏｕｔｈｗｅｓｔｅｒｎＨｏｓｐｉｔａｌ，ＴｈｉｒｄＭｉｌｉｔａｒｙＭｅｄｉｃａｌＣｏｌｅｇｅ，Ｃｈｏｎｇｑｉｎｇ４０００３８，Ｃｈｉｎａ（ＣｈｉＬＸ，ＹａｎｇＺＣ，ＷａｎｇＸａｎｄＬｉＡ）Ｔｈｉｓｓｔ...

简介：Cisplatin,awidelyusedanticancerdrug,damageshaircellsincochlearorganotypicculturesatlowdoses,butparadoxicallycauseslittledamageathighdosesresultinginaU-shapeddose-responsefunction.Todetermineifthecisplatindose-responsefunctionforvestibularhaircellsfollowsasimilarpattern,wetreatedvestibularorganotypiccultureswithdosesofcisplatinrangingfrom10to1000μM.Vestibularhaircelllesionsprogressivelyincreasedasthedoseofcisplatinincreasedwithmaximumdamageoccurringaround50–100μM,butthelesionsprogressivelydecreasedathigherdosesresultinginlittlehaircelllossat1000μM.TheU-shapeddoseresponsefunctionforcisplatin-treatedvestibularhaircellsincultureappearstoberegulatedbycoppertransporters,Ctr1,ATP7AandATP7B,thatdose-dependentlyregulatetheuptake,sequestrationandextrusionofcisplatin.

简介：ThepresentstudywasdesignedtodeterminetheeffectsofatraditionalChinesemedicine,calledQishenYiqiDroppingPillonchronichypoxia-inducedmyocardialinjury.ToestablisharatchronichypoxiamodeltobeusedintheevaluationofthetherapeuticeffectsoftheQishenYiqiDroppingPill,Sprague-Dawley(SD)ratswererandomlydividedintothreegroups:thecontrol,model,andtreatmentgroups(n=10pergroup).Theanimalswerehousedinaplexiglasscontainer.Thecontrolanimalswereundernormaloxygenconcentrationandthemodelandtreatmentgroupswereexposedtoairandnitrogenfor5weeks.TheratsinthetreatmentgroupwereorallyadministeredtheQishenYiqiDroppingpill(35mg·kg-1·d-1)for5weeks.Afterthetreatment,thecardiacfunctionandmorphologywereanalyzed,andtheexpressionlevelsofhypoxia-induciblefactor1α(HIF-1α)weredeterminedusingWesternblotting.Ourresultsindicatedthatthecardiacfunctionwasimpaired,cellapoptosiswasenhanced,andHIF-1αexpressionwasup-regulatedinthemodelgroup,comparedtothecontrolgroup.ThesechangeswereamelioratedbythetreatmentwiththeQishenYiqiDroppingPill.Inconclusion,QishenYiqiDroppingpillcanamelioratemyocardialinjuryinducedbychronichypoxia,improvecardiacfunction,anddecreasemyocardialcellapoptosis,whichmayprovideabasisforitsclinicaluseforthetreatmentofchroniccardiovasculardiseases

简介：

简介：雄激素缺乏强烈与可勃起的机能障碍(编辑)被联系。不适当的阴茎动脉的血流动是到阴茎海绵体的血流动主要是的编辑的原因从内部pudendal动脉(国际语音学协会)导出的专业之一；然而，没有学习在国际语音学协会功能上评估了雄激素剥夺的效果。我们假设了那阉割损害国际语音学协会反应和结构，在我们的学习贡献编辑，Wistar雄的老鼠，8-week-old，被阉割并且在orchiectomy以后学习了30天。老鼠国际语音学协会的功能、结构的性质是坚定的分别地使用电线和压力肌动描记器系统。蛋白质表示被西方的污点和immunohistochemistry决定。血浆睾丸激素层次用IMMULITE1000免疫分析系统被决定。展出的阉割的老鼠损害了可勃起的功能，由减少的intracavernosal压力/平均数代表了动脉的压力比率。从阉割的老鼠的国际语音学协会展出了减少的phenylephrine-，电场刺激(EFS)导致了收缩并且减少导致醋胆素、导致EFS的vasodilatation。从阉割的老鼠的国际语音学协会展出了减少的内部直径，外部直径，动脉的墙的厚度，和代表性的区域。阉割减少了nNOS和肌动朊表示和增加的骨胶原表示，p38(Thr180/Tyr182)phosphorylation，以及caspase3劈开。在结论，雄激素缺乏与国际语音学协会反应和结构的缺陷被联系并且增加了表明标记的apoptosis。我们的调查结果建议导致缺乏的脉管的机能障碍是的那雄激素包含hypotrophic的一个事件国际语音学协会的脉管的改变。

简介：

简介：AbstractSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced multisystem inflammatory syndrome in children (MIS-C) is a life-threatening illness that has been reported in the United States and Europe. It affects multiple organ systems and often requires patient admission to an intensive care unit. Although some features of MIS-C overlap with Kawasaki disease, MIS-C is more common among older children and adolescents, more often affects cardiovascular and gastrointestinal systems, and more frequently presents with elevated inflammatory markers. Rapid and complete clinical recovery is possible in nearly all patients following immunomodulation therapy. Thus far, MIS-C pathophysiology and long-term prognosis are not sufficiently clear; further studies are needed.

简介：AbstractThis review attempts to unveil the possible mechanisms underlying how gut lymph affects lung and further gives rise to acute respiratory distress syndrome, as well as potential interventional targets under the condition of ischemia-reperfusion injury. We searched electronic databases including PubMed, MEDLINE, Cochrane Central Register of Controlled Trials, Google Scholar, Web of Science, and Embase to identify relevant literatures published up to December 2019. We enrolled the literatures including the Mesh Terms of "gut lymph or intestinal lymph and acute lung injury or acute respiratory distress syndrome." Gut is considered to be the origin of systemic inflammation and the engine of multiple organ distress syndrome in the field of critical care medicine, whereas gut lymph plays a pivotal role in initiation of ischemia-reperfusion injury-induced acute respiratory distress syndrome. In fact, in the having been established pathologic model of sepsis leading to multiple organ dysfunction named by Gut Lymph theory, a variety of literatures showed the position and role of changes in gut lymph components in the initiation of systemic inflammatory response, which allows us to screen out potential intervention targets to pave the way for future clinic and basic research.

简介：瞄准：为了在streptozotocin(STZ)的阴囊的组织每氧化(LPO)和抗氧化剂酶的活动在类脂化合物上检验melatonin治疗的效果，导致了糖尿病的老鼠。方法：26只雄的老鼠随机如下被划分成三个组：组我，控制，非糖尿病的老鼠(n=9)；组II，导致STZ的、未经治疗的糖尿病的老鼠(n=8)；组III，导致STZ，对待melatonin(10mg/kg的剂量。白天)糖尿病的老鼠(n=9)。后面的8星期的melatonin处理，所有老鼠被使麻木然后被打死把睾丸从阴囊移开。结果：作为与组相比我，在老鼠组II的阴囊的纸巾，malondialdehyde(MDA)的增加的层次(P<0.01)并且超级氧化物歧化酶(草皮)(P<0.01)象过氧化氢酶(猫)的减少的层次一样(P<0.01)并且谷胱甘肽过氧化物酶(GSH-Px)(P>0.05)被发现。相反作为与组II相比，在老鼠组III的阴囊的纸巾，MDA的层次减少了(但是这减少不是重要的，P>0.05)并且草皮(P<0.01)象猫一样(P<0.05)增加。GSH-Px没被任何处理影响。Melatonin显著地没影响糖尿病的组的提高的葡萄糖集中。在学习的结束，借助于身体和阴囊的重量在对待melatonin的组和未经治疗的组之间没有有效差量。结论：糖尿病增加氧化应力，melatonin每氧化和力量禁止类脂化合物调整糖尿病的老鼠睾丸的抗氧化剂酶的活动。

简介：瞄准：为了为在肝炎B估计肝的纤维变性决定结缔组织生长因素(CCN2/CTGF)的用途，病毒(HBV)导致了长期的肝疾病(CLD-B)。方法：连接酶的immunosorbent试金被用来与导致HBV的活跃的肝肝硬化和30个健康个人与长期的肝炎B(CHB)和39个病人从107个病人在sera测量CCN2。从有CHB，有导致HBV的肝肝硬化的8个病人和有正常的肝组织学的8个HBV搬运人的31个病人的肝样品为转变生长因素-1(TGF-1)或CCN2mRNA层次由被检验在situ杂交，并且计算机图象分析被执行在肝纸巾测量CCN2mRNA积极的房间的综合最佳的密度(IOD)。组织学的发炎分级和纤维变性阶段被H并且E染色和凡·吉森斯方法评估。结果：分别地，浆液CCN2集中作为与健康个人相比在有CHB或活跃的肝肝硬化的病人更高是4.0褶层或4.9褶层(P<0.01)。在肝纸巾在在sera和CCN2mRNA表示的CCN2的层次之间有好一致性(r=0.87，P<0.01)。在sera的CCN2的层次与CLD-B在病人与组织学的纤维变性阶段的改进被增加(r=0.85，P<0.01)。浆液CCN2是为对肝纤维变性的评价的一个可靠标记，与在操作为从有F1阶段肝纤维变性的病人的分别地，区分的正常的肝控制的0.94或0.85的特征(巨鸟)曲线(AUC)或在温和、重要的纤维变性之间区别的接收装置下面的区域。结论：在有CLD-B的病人的浆液CCN2的察觉可以为对肝的纤维变性的严厉的评价有临床的意义。

简介：

简介：Ithasbeenfoundthatexpressionof15-lipoxygenasc-1(15-LOX-1)anditsmainproduct,13-C-hydroxyoctadecadienoicacid(13-S-HODE),aredecreasedinhumancolorectalandesophagealcancersandthatnonsteroidalanti-inflammatorydrugs(NSAIDs)cantherspeuticallyinduce15-LOC-1expressiontotriggerapoptosisinthosecancercellsindependentlyCOX-2.WefoundthataspecificCOX-2inhibitorSC-236similarlyinduceapoptosisingastriccancercells,althoughthemechanismsoftheseeffectsremaintobedefined.Inthepresentstudy,wetestedwhetherSC-236inducedapoptosisthroughup-regulationof15-LOX-1ingastriccancercells.Wefoundthat,(a)SC-236inhibitedgrowthofgastriccancercellsmainlybyapoptosisinduced;(b)SC-236induced15-LOX-1expressionandincreasedendogenous13-S-HODEproduct,insteadof15-S-HETEduringapoptosisingastriccancercellswithout15-LOX-1expressionbeforetreatmentbySC-236;(c)sc-236didn'teffectexpressionofCOX-1,COX-2,5-LOXand12-LOX;and(d)15-LOX-1inhibitionsuppressedSC-236inducedapoptosis.ThesefindingsdemonstratedthatSC-236inducedapoptosisingastriccancercellsviaup-regulationof25-LOX-1.Theyalsosupporttheconceptthatthelossoftheproapopoticroleof15-LOX-1inepithelialcancersisnotlimitedtohumancolorectalandesophagealcancers.

简介：AbstractBackground:Microglia plays an indispensable role in the pathological process of sleep deprivation (SD). Here, the potential role of microglial CX3C-chemokine receptor 1 (CX3CR1) in modulating the cognition decline during SD was evaluated in terms of microglial neuroinflammation and synaptic pruning. In this study, we aimed to investigat whether the interference in the microglial function by the CX3CR1 knockout affects the CNS’s response to SD.Methods:Middle-aged wild-type (WT) C57BL/6 and CX3CR1-/- mice were either subjected to SD or allowed normal sleep (S) for 8 h to mimic the pathophysiological changes of middle-aged people after staying up all night. After which, behavioral and histological tests were used to explore their different changes.Results:CX3CR1 deficiency prevented SD-induced cognitive impairments, unlike WT groups. Compared with the CX3CR1-/- S group, the CX3CR1-/- SD mice reported a markedly decreased microglia and cellular oncogene fos density in the dentate gyrus (DG), decreased expression of pro-inflammatory cytokines, and decreased microglial phagocytosis-related factors, whereas increased levels of anti-inflammatory cytokines in the hippocampus and a significant increase in the density of spines of the DG were also noted.Conclusions:These findings suggest that CX3CR1 deficiency leads to different cerebral behaviors and responses to SD. The inflammation-attenuating activity and the related modification of synaptic pruning are possible mechanism candidates, which indicate CX3CR1 as a candidate therapeutic target for the prevention of the sleep loss-induced cognitive impairments.

简介：自发的术语劳动在包括cytokine生产和白血球渗入的myometrium与放大煽动性的事件被联系；然而，调整如此的事件的潜在的机制充分没被理解。我们由成长胎儿假设了子宫的墙的那机械段由子宫的myocytes通过各种各样的cytokines的版本便于外部白血球溢出进术语myometrium。人的myometrial房间(hTERT-HM)受到静态的机械段；调节段的媒介被收集并且分析了使用48-plexLuminex试金和ELISA。人的子宫的microvascularendothelial房间(UtMVEC-Myo)的房间粘附分子表示上的调节段的媒介的效果被量的聚合酶链反应(qPCR)和流动cytometry检测；测试leukocyte-endothelial相互作用的功能的试金：到endothelial房间和象THP-1monocytic房间的移植一样的标记calcein的主要人的neutrophils的transendothelial移植的白血球的粘附被萤光计估计。在vitro学习的水流证明机械段(i)直接由hTERT-HM细胞导致多重cytokines和chemokines的分泌物(IL-6，CXCL8，CXCL1，移植禁止的因素(MIF)，VEGF，G-CSF，IL-12p70，bFGF和导出血小板的生长因素子单元B(PDGF-bb)，P<；0.05)；导致段的cytokines(ii)提高白血球粘附到包围的内皮细胞层子宫的微脉管系统由(iii)导致endothelial房间粘附分子的表示并且(iv)指导外部白血球的transendothelial迁居。(vi)抵销Chemokine抗体和用途广泛的chemokine禁止者堵住白血球移植。我们的数据从子宫的血容器为白血球招募提供机械规定的一个证明给myometrium，为白血球建议通常认为的机制在劳动和产后的复杂物期间渗透到子宫。

简介：Pleurotussajorcaju(P。sajorcaju)，一朵可食、无毒的蘑菇，作为抗氧化剂被评估，antitumor，反煽动性并且antihypertensive活动。P。sajorcaju是糖类，饮食的纤维，必要氨基酸，矿物质，维生素B，folic酸和类固醇的好来源。反煽动性，immunomodulatory和止痛活动水并且P的菌丝体的methanolic摘录。sajorcaju被调查(数据没被显示出)。这发现建议那P提取。sajorcaju能对煽动性、自体免疫的疾病被使用。那么，P。为它的antiarthritic活动检验的sajorcaju。植物与水和甲醇镇定、独立提取。为antiarthritic活动500和1000mg

简介：AIM:ToexploretheeffectsofCompoundYi-Zhi(YZC)onlearningandmemorycapacityandfreeradicalmetabolisminD-galactoseinducedmicedementiamodel.METHODS:ThemicedementiamodelwasinducedbyadailyD-galactose0.15g/kgscfor45daysandafter5days'D-galactoseinjection,themiceweretreatedwiththreedosesofYZC