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简介：Atrialfibrillation(AF),themostcommonlyencoun-teredarrhythmiainclinicalpractice,isassociatedwitha2-foldincreaseintotalcardiovascularmortality[1],aswellasthepotentialforsubstantialmorbidity,includingstroke,congestiveheartfailure,andcardiomyopathy.Itsincidenceandprevalenceareincreasing,anditrepresentsagrowingclinicalandeconomicburden.Owingtorela-tiveinefficacyandside

简介：Gutmicrobiotaexertsasignificantroleinthepathogenesisofthemetabolicsyndrome,asconfirmedbystudiesconductedbothonhumansandanimalmodels.Gutmicrobialcompositionandfunctionsarestronglyinfluencedbydiet.Thiscomplexintestinal'superorganism'seemstoaffecthostmetabolicbalancemodulatingenergyabsorption,gutmotility,appetite,glucoseandlipidmetabolism,aswellashepaticfattystorage.Animpairmentofthefinebalancebetweengutmicrobesandhost’simmunesystemcouldculminateintheintestinaltranslocationofbacterialfragmentsandthedevelopmentof'metabolicendotoxemia',leadingtosystemicinflammationandinsulinresistance.Dietinducedweight-lossandbariatricsurgerypromotesignificantchangesofgutmicrobialcomposition,thatseemtoaffectthesuccess,ortheinefficacy,oftreatmentstrategies.Manipulationofgutmicrobiotathroughtheadministrationofprebioticsorprobioticscouldreduceintestinallowgradeinflammationandimprovegutbarrierintegrity,thus,amelioratingmetabolicbalanceandpromotingweightloss.However,furtherevidenceisneededtobetterunderstandtheirclinicalimpactandtherapeuticuse.

简介：AbstractMetabolic syndrome (MetS) describes a set of risk factors that can eventually lead to the occurrence of cardiovascular and cerebrovascular disease. A detailed understanding of the MetS mechanism will be helpful in developing effective prevention strategies and appropriate intervention tools. In this article, we discuss the relationship between the clinical symptoms of MetS and differences in the gut microbial community compared with healthy individuals, characterized by the proliferation of potentially harmful bacteria and the inhibition of beneficial ones. Interactions between gut microbiota and host metabolism have been shown to be mediated by a number of factors, including inflammation caused by gut barrier defects, short-chain fatty acids metabolism, and bile acid metabolism. However, although we can clearly establish a causal relationship between gut microbial profiles and MetS in animal experiments, the relationship between them is still controversial in humans. Therefore, we need more clinical studies to augment our understanding of how we can manipulate the gut microbiota and address the role of the gut microbiota in the prevention and treatment of MetS.

简介：1.BiochemicalstructureandmolecularactivityofmeldoniumMeldonium(commercialnameMildronate)wasoriginallysynthesizedinthemid-1970sattheInstituteofOrganicSynthesisoftheLatvianSovietSocialistRepublicAcademyofSciences.Thechemicalstructureofthiscompound(3-(2,2,2-

简介：1.TheendocannabinoidsysteminobesityandmetabolicdisordersAsobesityandassociatedmetabolicdisorders,suchastype2diabetesanddyslipidemia,arebecomingoneofthemostserioushealthproblemsworldwide,developmentofeffectivetherapiesisahighpriority.Inthesearchfortreatments,therecentlydiscoveredendocannabinoidsystem(ECS)hasbeguntogarnerattention,andawealthofresearchisnowfocusing

简介：AbstractExcessive consumption of fructose, the sweetest of all naturally occurring carbohydrates, has been linked to worldwide epidemics of metabolic diseases in humans, and it is considered an independent risk factor for cardiovascular diseases. We provide an overview about the features of fructose metabolism, as well as potential mechanisms by which excessive fructose intake is associated with the pathogenesis of metabolic diseases both in humans and rodents. To accomplish this aim, we focus on illuminating the cellular and molecular mechanisms of fructose metabolism as well as its signaling effects on metabolic and cardiovascular homeostasis in health and disease, highlighting the role of carbohydrate-responsive element-binding protein in regulating fructose metabolism.

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简介：Natureisarichsourceofmedicinalplantsandtheirproductsthatareusefulfortreatmentofvariousdiseasesanddisorders.Momordicacharantia,commonlyknownasbittermelonorbittergourd,isoneofsuchplantsknownforitsbiologicalactivitiesusedintraditionalsystemofmedicines.Thisplantiscultivatedinallovertheworld,includingtropicalareasofAsia,Amazon,eastAfrica,andtheCaribbeanandusedasavegetableaswellasfolkmedicine.Allpartsoftheplant,includingthefruit,arecommonlyconsumedandcookedwithdifferentvegetables,stir-fried,stuffedorusedinsmallquantitiesinsoupsorbeanstogiveaslightlybitterflavorandtaste.Theplantisreportedtopossessanti-oxidant,anti-inflammatory,anti-cancer,anti-diabetic,anti-bacterial,anti-obesity,andimmunomodulatoryactivities.Theplantextractinhibitscancercellgrowthbyinducingapoptosis,cellcyclearrest,autophagyandinhibitingcancerstemcells.Theplantisrichinbioactivechemicalconstituentslikecucurbitanetypetriterpenoids,triterpeneglycosides,phenolicacids,flavonoids,essentialoils,saponins,fattyacids,andproteins.Someoftheisolatedcompounds(KuguacinJ,KaravilosideXI,KuguaglycosideC,MomordicosideQ-U,Charantin,α-eleostearicacid)andproteins(α-Momorcharin,RNaseMC2,MAP30)possesspotentbiologicalactivity.Inthepresentreview,wearesummarizingtheanti-oxidant,anti-inflammatory,andanti-canceractivitiesofMomordicacharantiaalongwithashortaccountofimportantchemicalconstituents,providingabasisforestablishingdetailbiologicalactivitiesoftheplantanddevelopingnoveldrugmoleculesbasedontheactivechemicalconstituents.

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简介：当一个非免疫学的机关首先从事了新陈代谢的、滋养的存储和detoxification活动，人的肝通常被察觉。然而，我们现在知道健康的肝也是复杂免疫学的一个地点活动象非造血的房间人口一样由一个多样的有免疫力的房间全部剧目调停了。在疾病得非的肝，新陈代谢并且织物改变功能要求发炎的元素。在有到饮食、微生物引起的产品的常规暴露的联合，这发炎为过多的有免疫力的激活创造潜力。在这复杂微型环境，肝的免疫系统容忍无害的分子当同时对可能的传染代理人仍然保持警惕时，恶意的房间或纸巾损坏。在到由病原体或织物损坏的挑战的适当有免疫力的激活之上，解决发炎的机制是必要的维持肝动态平衡。清除‘的失败；dangerous’；刺激或调整适当地激活的有免疫力的机制导致病理学的发炎和纤维变性，肝硬化和最终的肝失败的进步发展描绘的破坏织物动态平衡。肝的煽动性的机制因此在健康的成年的肝有角色的一个系列；他们是必要的维持织物和机关动态平衡并且dysregulated，肝病理的关键司机与长期的感染，autoimmunity和恶意被联系。在这评论，我们在正常的肝动态平衡探索发炎和煽动性的调停人的变化感觉并且求婚作为一条治疗学的途径肝特定的有免疫力的规定小径指向治疗肝疾病。

简介：Background:Chronicinflammationisanimportantetiologicmechanismformuscleatrophy.Oat-derivedphytochemicalavenanthramides(AVAs)havebeenshowntosuppressinflammatoryresponsesinhumanclinicalstudiesandinseveralcelllinesinvitro,buttheirroleinskeletalmuscleisunclear.TheaimofthisstudywastoinvestigatewhetherAVAtreatmentcanpreventtumornecrosisfactor(TNF)-α-inducedmusclefiberatrophyinC2C12cells.Methods:Wetreated70%confluentcellsfor24hwithAVA.Then,TNF-αwasaddedtocell-culturedmedium.Subsequently,cellswereharvestedatdifferenttimepoints.Thecellswereexaminedusingvariousbiochemicaltechniquesformeasuringprotein,messengerRNAlevels,nuclearbindingactivity,andviability.Fluorescencemicroscopewasusedforanalysisofthemyotubemorphology.Results:CellstreatedwithTNF-asignificantlyincreasednuclearfactorkBactivation,indicatedbyamarkeddecreaseofIkB(p<0.05)anda6.6-foldincreaseinp65-DNAbinding(p<0.01);however,30mmolofAVA-A,-B,and-Ctreatmentreducedthebindingby33%,18%,and19%(p<0.01),respectively,comparedwithcellstreatedwithTNF-awithoutAVA.Theinterleukin-6levelincreasedby2.5fold(p<0.01)withTNF-α,butdecreasedby24%,32%,and28%(p<0.01),respectively,withAVA-A,-B,and-C.Theinterleukin-1blevelalsoshoweda47%increasewithTNF-a(p<0.01),whereasthisincrementwasabolishedinallAVA-treatedcells.Reactiveoxygenspeciesproductionwas1.3-foldhigherintheTNF-α-treatedgroup(p<0.01)butnotintheTNF-α+AVAsgroups.MessengerRNAlevelsofmuscle-specificE3ubiquitinligaseatrogin-1increased23%inTNF-αvs.control(p<0.05)butwasdecreasedby46%,34%,and53%(p<0.01),respectively,withtreatmentofAVA-A,-B,and-C.Moreover,TNF-αtreatmentincreasedthemuscleRINGfinger1messengerRNAlevelby76%(p<0.01);thischangewasabolishedbyAVAs.CellstreatedwithTNF-ademonstratedareducedproliferationcomparedwithcontrolcells(p<0.01)

简介：Medicaltherapyfortype2diabetesmellitusisineffectiveinthelongtermduetotheprogressivenatureofthedisease,whichrequiresincreasingmedicationdosesandpolypharmacy.Conversely,bariatricsurgeryhasemergedasacost-effectivestrategyforobesediabeticindividuals;ithaslowcomplicationratesandresultsindurableweightloss,glycemiccontrolandimprovementsinthequalityoflife,obesity-relatedco-morbidityandoverallsurvival.Thefindingthatglucosehomeostasiscanbeachievedwithaweightloss-independentmechanismimmediatelyafterbariatricsurgery,especiallygastricbypass,hasledtotheparadigmofmetabolicsurgery.However,theprimaryfocusofmetabolicsurgeryisthealterationofthephysio-anatomyofthegastrointestinaltracttoachieveglycemiccontrol,metaboliccontrolandcardio-metabolicriskreduction.Todate,metabolicsurgeryisstillnotwelldefined,asitisusedmostfrequentlyforlessobesepatientswithpoorlycontrolleddiabetes.Themechanismofglycemiccontrolisstillincompletelyunderstood.Publishedresearchfindingsonmetabolicsurgeryarepromising,butmanyaspectsstillneedtobedefined.Thispaperexaminestheproposedmechanismofdiabetesremission,theefficacyofdifferenttypesofmetabolicprocedures,thedurabilityofglucosecontrol,andtherisksandcomplicationsassociatedwiththisprocedure.Weproposeatailoredapproachfortheselectionoftheidealmetabolicprocedurefordifferentgroupsofpatients,consideringtheindicationsandprognosticfactorsfordiabetesremission.

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简介：AbstractMany factors can cause inner ear injury, such as noise exposure, chemicals, viral infection, and radiation. The main pathological manifestations of inner ear injury are local hypoxia-ischemia, micro-trauma, and an increased level of reactive oxygen species and inflammatory mediators. The contribution of the inflammatory response to the mediation of cochlear and vestibular pathologies has received increasing attention in recent years. Aseptic inflammation can devastate audition and balance, which can lead to many typical clinical inner ear diseases. In this review, we will discuss the most pertinent and recent research on inflammatory mechanisms in inner ear injury. We will also discuss the pathophysiology of some common and significant ear diseases, such as sudden sensorineural hearing loss, age-related hearing loss, noise-induced hearing loss, and Meniere’s disease.

简介：前列腺癌症是在人的最普通的恶意之一。以前的研究决定了那雄激素剥夺治疗(ADT)可以被不利新陈代谢的侧面伴随。在这未来的研究，133个人被招募，包括经历了双边的orchiectomy并且在flutamide(ADT组)上的46个前列腺癌症病人，经历了激进的前列腺切除术(non-ADT组)的有前列腺癌症的37个人并且50个正常控制题目(控制组)。所有题目被跟随至少12个月。从基线到3个月，在ADT组的人与另外的二个组相比增加了fasting浆液胰岛素和低密度的脂蛋白的层次(P<；0.05)。没有明显的变化在另外的参数被发现(P>；0.05)。在12个月以后，在ADT组的人增加了腰的层次与另外的二个组相比的圆周，fasting浆液胰岛素和葡萄糖，全部的胆固醇，高密度的脂蛋白和低密度的脂蛋白(P<；0.05)。另外，在ADT组的新陈代谢的症候群的病态率更高(P<；0.05)与另外的二个组相比。通过为有前列腺癌症的人的外科的阉割的ADT可以与不利新陈代谢的变化被联系。治疗的好处应该对这些风险谨慎地被平衡。