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简介:TheeffectoftheadmixturesofAlandSimetalsandB4CandMgAlONcompoundsontheoxidationofMgO/Si3N4compositerefractoryhasbeenstudied,whichisapromisingcarbonfreerefractoryforsteel-makingapplicatlon.Thefourkindsofadmixturescanbeusedasanti-oxidantsforSi3N4,butthemixtureofAlandSiachievedthebestresult.Themixturecannotonlyplaytheroleasantioxidant,butalsoassistthesinteringprocessandhelpformdensesinteringlayer,improvingthepropertyofthecomposite.
简介:Anovertphenotypeofaquaporin-1knockout(AQP1ko)miceisgrowthretardation,suggestingpossibledefectsinbonedevelopmentandmetabolism.Inthepresentstudy,weanalyzedthebonemineraldensity(BMD),bonecalciumandphosphoruscontents,andbonemetabolisminanAQP1komousemodel.TheBMDoffemursinAQP1komicewassignificantlylowerthanthatoflitter-matchedwildtypemiceasmeasuredbydualenergyX-rayabsorptiometry.Consistently,thecontentsofbonetotalcalciumandphosphoruswerealsosignificantlylowerinAQP1komice.ThereducedBMDcausedbyAQP1deficiencymainlyaffectmalemice.Bonemetabolicactivity,asindicatedby99mTc-MDPabsorptionmeasurements,wasremarkablyreducedinAQP1komice.TheseresultsprovidethefirstevidencethatAQP1playanimportantroleinbonestructureandmetabolism.
简介:Notopterygiumincisum(QH)hasbeenusedforthetreatmentofrheumatoidarthritis(RA),andvolatileoilsmaybeitsmainlybioactiveconstituents.ThepresentstudywasdesignedtoanalyzethevolatilecompoundsinQHandtodeterminetheanti-arthriticcapacityofNotopterygiumvolatileoilsandthepotentialmechanismofaction.ThevolatilecompoundsanalysiswasconductedbyGC-MS.Theanti-arthriticcapacitytestofthevolatileoilswasconductedonadjuvant-inducedarthritis(AIA)rats.Theanti-inflammatorypropertywastestedinNOreleasemodelinRAW264.7cells.Endothelialcellswereusedtoevaluatetheanti-proliferativeandanti-tubeformativeeffects.70compoundswereanalyzedbyGC-MSinthevolatileoils.NotopterygiumvolatileoilsweakenedtheratAIAinadose-dependentmanner(2,4,and8gcrudedrug/kg).TheNOproductionbyRAW264.7wasdecreasedbymorethan50%inNotopterygiumvolatileoils(5,15,and45μg·mL-1)pretreatedgroups.NotopterygiumvolatileoilsalsoinhibitedEAhy926cellproliferationandfurtherdelayedEAhy926cellcapillarytubeformationinaconcentration-dependentmanner.Theanti-NOproductive,anti-proliferative,andanti-tubeformativeeffectsofNotopterygiumvolatileoilsstronglysuggestedthatthetherapeuticeffectofQHinAIAmightberelatedtothepotentanti-inflammatoryandanti-angiogeniccapacitiesofthevolatileoils.
简介:Carbon-containingrefiactoriesareeasilyoxidizedathightenperature,thusmakingserviceliferapidlydrop.Theanti-oxidationmethods,suchasimpregnationandaddinganti-oxidatonagents,can'tmeettherequire-mentsofindustry'sdevelopmentandsomespecialcases,Byanalyzingthecharcteristicsofseveraloxidesandnon-oxidesrawmaerials,theoxidationresistantmechanismoftherefractoryanti-oxidationcoatings(RAOC),whichpossessthecharacteristcofself-healingathighttemperature,isdiscussed.
简介:AbstractBackground:Estrogen is involved in the pathophysiological process of benign prostatic hyperplasia (BPH), in which epithelial-mesenchymal transition (EMT) plays an important role. Upregulation of aquaporin (AQP) 5, which is directly activated by estrogen, has been reported to promote EMT in multiple cells. This study aimed to examine the effects of AQP5 on estrogen-induced EMT in the prostate.Methods:Normal prostate (NP) tissue samples without any histopathological changes and BPH tissue samples with pathologically confirmed hyperplasia were obtained. An EMT cell model was subsequently established by adding estradiol (E2) to RWPE-1 cells, after which AQP5 knockdown was performed. Tissue morphological and immunohistochemical features were examined using hematoxylin-eosin and immunohistochemical staining. Western blot analysis was performed to determine the expression of AQPs, estrogen receptors, and EMT-related proteins. Cell proliferation was assessed and supernatants were collected for enzyme-linked immunosorbent assay to determine transforming growth factor-β1 (TGF-β1) concentrations. Immunofluorescence staining was performed to assess protein expressions in RWPE-1 cells.Results:BPH tissues exhibited greater EMT (TGF-β1: 1.362 ± 0.196 vs. 0.107 ± 0.067, P = 0.003; vimentin: 1.581 ± 0.508 vs. 0.221 ± 0.047, P < 0.001; E-cadherin: 0.197 ± 0.188 vs. 1.344 ± 0.088, P < 0.001), higher AQP5 (1.268 ± 0.136 vs. 0.227 ± 0.055, P < 0.001) and estrogen receptor (ER) α (1.250 ± 0.117 vs. 0.329 ± 0.134, P < 0.001) expression but lower ERβ (0.271 ± 0.184 vs. 1.564 ± 0.130, P < 0.001) expression than NP tissues. E2-stimulated cells had higher AQP5 expression (1.298 ± 0.058 vs. 1.085 ± 0.104, P = 0.049), increased cell proliferation (1.510 ± 0.089 vs.1.000 ± 0.038, P < 0.001), and EMT (TGF-β1 concentration: 0.352 ± 0.021 ng/mL vs. 0.125 ± 0.014 ng/mL, P < 0.001; vimentin: 1.641 ± 0.120 vs. 0.188 ± 0.020, P = 0.002; E-cadherin: 0.075 ± 0.030 vs. 0.843 ± 0.046, P < 0.001) than controls. E2-stimulated cells with AQP5 knockdown exhibited decreased EMT (TGF-β1 concentration: 0.223 ± 0.041 ng/mL vs. 0.352 ± 0.021 ng/mL, P= 0.016; vimentin: 0.675 ± 0.056 vs. 1.641 ± 0.120, P = 0.001; E-cadherin: 0.159 ± 0.037 vs. 0.075 ± 0.030, P = 0.040) than E2-stimulated cells with non-related small interfering RNA (siRNA).Conclusion:Our findings suggest that estrogen induces BPH possibly by promoting AQP5 expression. Hence, AQP5 might be a novel target for modulating EMT in prostate epithelial cells.
简介:Syndecan-1(CD138),不可分的膜肝磷脂硫酸盐proteoglycans的一个成员,是为维持正常词法显型的必要矩阵受体。在这研究,我们产生了一只特定的老鼠反人的syndecan-1monoclonal抗体(mAb)4B3并且与可得到的syndecan-1mAb(BB4)由比赛试金识别了它。由4B3染色了,syndecan-1的表示在肿瘤房间线上被检测例如8226,U266,XG-1,XG-2,Daudi和Jurkat。表示也在神经原干细胞上被发现。4B3mAb能禁止XG-1和XG-2增长,这被建立。数据不仅决定4B3mAb是功能的反人的syndecan-1mAb,而且显示syndecan-1可能是珍贵表面抗原并且在肿瘤病理的规定和神经干细胞的区别起一个重要作用。这新奇抗体4B3可以是肿瘤增长/幸存机制的学习的价值并且贡献多样的疾病的诊断和治疗。
简介:AIMTo在透镜调查Aquaporin-1(AQP-1)的角色上皮的房间(LEC)和它的潜在的目标基因。AQP-1明确地在眼睛的LEC被表示并且为透镜动态平衡和透明性维护是重要的。此处,在LEC的AQP-1表示被调查在奔流formation.METHODSLECs与它的潜在的角色联合在房间幸存上评估它的影响是有带AQP-1的lentivirus的transfected小介入RNA(siRNA)。实时聚合酶链反应(PCR)并且西方的弄污被进行从不同的组在LEC检测AQP-1表示。同时,房间数kit-8(CCK-8)试金和流动cytometry被执行测量LEC增长和apoptosis,respectively.RESULTSAQP-1表示显著地在LEC被减少,两个都在mRNA和蛋白质铺平(P<;0.05),在siRNA处理以后。减少的房间生存能力被CCK-8试金与siRNA干扰在LEC检测,与控制房间相比(P<;0.05)。apoptosis率显著地在siRNA干扰以后在房间增加了(P<;0.05).CONCLUSIONThe减少了在规定下面的房间生存能力追随者AQP-1大部分由于它LEC的apoptosis的正式就职。AQP-1减小可能在LEC导致生理的功能的变化,它可能与奔流的出现和发展被联系。
简介:ByusingthegeneralizedPoincaréindextheoremitisprovedthatifthen^2criticalpointsofann-polynomialsystemformaconfigurationoftype(2n-1)-(2n-3)+(2n-5)-…+(-1)^n-1,andthe2n-1outmostanti-saddlesformtheverticesofaconvex(2n-1)-polygon,thenamongthese2n-1anti-saddlesatleastonemustbeanode.
简介:Thepresentstudywasdesignedtoexaminetheanti-hyperuricemicandanti-inflammatoryeffectsandpossiblemechanismsofvaticaffinol,aresveratroltetramerisolatedfromethanolextractsofDipterocarpusalatus,inoxonate-inducedhyperuricemicmice.At1hafter250mg·kg~(-1)potassiumoxonatewasgiven,vaticaffinolat20,40,and60mg·kg~(-1)wasintragastricallyadministeredtohyperuricemicmiceoncedailyforsevenconsecutivedays.Vaticaffinolsignificantlydecreasedserumuricacidlevelsandimprovedkidneyfunctioninhyperuricemicmice.Itinhibitedhepaticactivityofxanthinedehydrogenase(XDH)andxanthineoxidase(XOD),regulatedrenalmRNAandproteinlevelsofuratetransporter1(URAT1),glucosetransporter9(GLUT9),organicaniontransporter1(OAT1),organiccationtransporter1(OCT1),OCT2,organiccation/carnitinetransporter1(OCTN1),andOCTN2inhyperuricemicmice.Moreover,vaticaffinolmarkedlydown-regulatedrenalproteinlevelsofNOD-likereceptor3(NLRP3),apoptosis-associatedspeck-like(ASC),andCaspase-1,resultinginthereductionofinterleukin(IL)-1β,IL-18,IL-6andtumornecrosisfactor-α(TNF-α)levelsinthisanimalmodel.Additionally,HPLCandLC-MSanalysesclearlytestifiedthepresenceofvaticaffinolinthecrudeextract.Theseresultssuggestthatvaticaffinolmaybeusefulforthepreventionandtreatmentofhyperuricemiawithkidneyinflammation.
简介:AbstractThe coronavirus disease 2019 (COVID-19) pandemic was triggered by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a previously unknown strain of coronavirus. To fully understand the consequences and complications of SARS-CoV-2 infections, we have reviewed current literature on coagulation dysfunctions that are related to the disease and vaccination. While COVID-19 is more commonly considered as a respiratory illness, studies indicate that, in addition to respiratory illness, a coagulation dysfunction may develop in individuals after the initial infection, placing them at the risk of developing thrombotic events. Patients who died of COVID-19 had higher levels of D-dimer, a biomarker for blood clot formation and breakdown. Effective treatments for coagulation dysfunctions are critically needed to improve patient survival. On the other hand, antibodies against platelet factor 4 (PF4)/heparin may be found in patients with rare instances of vaccine-induced immunological thrombotic thrombocytopenia (VITT) following vaccination with adenovirus-based vaccines. VITT is characterized by atypical thrombosis and thrombocytopenia, similar to immune-mediated heparin-induced thrombocytopenia (HIT), but with no need for heparin to trigger the immune response. Although both adenovirus-based and mRNA-based vaccines express the Spike protein of SARS-CoV-2, VITT is exclusively related to adenovirus-based vaccines. Due to the resemblance with HIT, the use of heparin is highly discouraged against treating patients with thrombotic thrombocytopenia after SARS-CoV-2 infection or with VITT after vaccination. Intravenous immunoglobulin therapy coupled with anticoagulation is recommended instead. The well-studied anti-PF4 monoclonal antibody RTO, which does not induce pathologic immune complexes in the presence of heparin and has been humanized for a potential treatment modality for HIT, may provide a nonanticoagulant HIT-specific solution to the problem of increased blood coagulation after SARS-CoV-2 infection or the VITT after immunization.
简介:China'sAnti-JapaneseWarWORLDWARⅡ,whichendedhalfacenturyagoinacrushingdefeatforthefascistpowers,wasalife-and-deathstrugglebetw...
简介:Anti-globalizationtrendsareinplayintheUSandWesternEuropewhereelectoratesarerecalcitranttoallowimmigrantsintotheirsocieties,nationalsovereigntyissoughtincertaingeographicareas,andthenationalmoodseekstosuppressnewlyrisingcountries'tradeanddevelopment.ThecontinuationofeconomicdownturninWesterncountriesisreinforcedbytheirinternalwealthgapandexternalcompetition.Ascapitalism'sdemandforprofitisnowbeingcritiquedalongwiththeemergentprofitprospectstobedeliveredbypendingtechnologicalprogress,thetemperofthetimescouldtemporarilyslowdownbutnotreverseglobalization.Timelydiscussionsaboutreformofinternationaleconomicorderandaboutaneffectivenationaldevelopmentmodelshouldseeksustainablesolutionsforhealthy,stableglobalizationanddevelopmentoftheworldeconomy.