简介：TheNationalDevelopmentandReformCommissionandtheMinistryofCommercehavejointlypromulgatedNo.24DecreewiththeGuidingCatalogueoftheIndustriesAccessiblebyForeignInvestors(revisedin2004).ItwasputintoeffectonandafterJanuary5,2005.Thecontentsofthecataloguerelatedtothepowerindustryareasfollows.

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简介：BackgroundTheco-administrationofdexrazoxane(DEX)witheachdoseofdoxorubicin(Dox)isanefficientstrategytorelieveDox-inducedcardiotoxicity,however,themechanismsunderlyingthecardioprotectiveeffectofDEXhavenotbeenwellelucidated.MicroRNAs(miRNAs)areendogenous,smallnon-codingRNAsthatnegativelyregulategeneexpressionindiversebiologicalandpathologicalprocesses.TheaimofthepresentstudywastoinvestigatewhetherthecertaincardiacmiRNAswereinvolvedinDOX-inducedcardiotoxicity.MethodsMaleSDratswererandomizedintofivegroups,includingthe4-week(cumulativedose16mg/kg)andthe8-week(cumulativedose32mg/kg)Dox-treatedgroups,andthecorresponding4-weekand8-weekDoxplusDEX-treatedgroupsandthenormalcontrolgroup.Heartfunctionsoftheanimalsweredetectedbyechocardiography.Quantitativereal-timePCRwasusedtodeterminetheexpressionofcardiacremodeling,apoptosis-relatedgenesandmaturemicoRNAsofinterest.ResultsTheechocardiographydetectionshowedthatcardiacremodelingandimpairedheartfunctionwereobservedafter4-weekand8-weekDoxtreatment,andthecardiacremodelinganddecreasedejectionfraction(EF%)andfractionalshortening(FS%)wereefficientlyrescuedinthecorresponding4-weekand8-weekDoxplusDEX-treatedgroups.ThemyocardialexpressionofAnpandCTGFmRNAwassignificantlyupregulatedbyDoxtreatment,buttheupregulationofAnpandCTGFmRNAwasblockedintheDoxplusDEX-treatedgroups.IGF-1mRNAwassignificantlyup-regulatedinratmyocardiuminDoxplusDEX-treatedgroups,withnosignificantchangesofBcl-2andBAXmRNAexpression.MaturemiRNAsdeterminationdemonstratedthatthemyocardialmiR-1and-30eweresignificantlydownregulatedandmiR-21and-208bweresignificantlyup-regulatedinDoxtreatmentgroups,buttheabovemiRNAdysregulationcouldbeefficientlyreversedafterDEXtreatment.ConclusionsDEXcouldtunethemicroRNAsdysregulationinDox-treatedratmyocardium,miRNAsparticipatedinthecardioprotec

简介：AbstractInflammatory bowel disease (IBD) is a non-specific inflammatory disease of the gastrointestinal (GI) tract that is generally accepted to be closely related to intestinal dysbiosis in the host. GI infections contribute a key role in the pathogenesis of IBD; however, although the results of recent clinical studies have revealed an inverse correlation between Helicobacter pylori (H. pylori) infection and IBD, the exact mechanism underlying the development of IBD remains unclear. H. pylori, as a star microorganism, has been a focus for decades, and recent preclinical and real-world studies have demonstrated that H. pylori not only affects the changes in the gastric microbiota and microenvironment but also influences the intestinal microbiota, indicating a potential correlation with IBD. Detailed analysis revealed that H. pylori infection increased the diversity of the intestinal microbiota, reduced the abundance of Bacteroidetes, augmented the abundance of Firmicutes, and produced short-chain fatty acid-producing bacteria such as Akkermansia. All these factors may decrease vulnerability to IBD. Further studies investigating the H. pylori-intestinal microbiota metabolite axis should be performed to understand the mechanism underlying the development of IBD.

简介：OurpreliminarystudiesconfirmedthatanactiveprincipleregionofBuyangHuanwudecoction,comprisingalkaloid,polysaccharide,aglycon,glucosideandvolatileoil,caninducebonemarrowmesenchymalstemcelldifferentiationintoneurons.Mitogen-activatedproteinkinasesignalingwasidentifiedasoneofthekeypathwaysunderlyingthisdifferentiationprocess.Thepresentstudyshowsphosphorylatedextracellularsignal-regulatedproteinkinaseandphosphorylatedp38proteinexpressionwasincreasedafterdifferentiation.Cellularsignalingpathwayblockingagents,PD98059andSB203580,inhibitedextracellularsignal-regulatedproteinkinaseandp38inmitogen-activatedproteinkinasesignalingpathwaysrespectively.mRNAandproteinexpressionoftheneuronalmarker,neuronspecificenolase,andneuralstemcellmarker,nestin,weredecreasedinbonemarrowmesenchymalstemcellsaftertreatmentwiththeactiveprincipleregionofBuyangHuanwudecoction.Experimentalfindingsindicatethat,extracellularsignal-regulatedproteinkinaseandp38inmitogen-activatedproteinkinasesignalingpathwaysparticipateinbonemarrowmesenchymalstemcelldifferentiationintoneuron-likecells,inducedbytheactiveprincipleregionofBuyangHuanwudecoction.