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：AbstractSevere asthma is "asthma which requires treatment with high dose inhaled corticosteroids (ICS) plus a second controller (and/or systemic corticosteroids) to prevent it from becoming 'uncontrolled’ or which remains 'uncontrolled’ despite this therapy." The state of control was defined by symptoms, exacerbations and the degree of airflow obstruction. Therefore, for the diagnosis of severe asthma, it is important to have evidence for a diagnosis of asthma with an assessment of its severity, followed by a review of comorbidities, risk factors, triggers and an assessment of whether treatment is commensurate with severity, whether the prescribed treatments have been adhered to and whether inhaled therapy has been properly administered. Phenotyping of severe asthma has been introduced with the definition of a severe eosinophilic asthma phenotype characterized by recurrent exacerbations despite being on high dose ICS and sometimes oral corticosteroids, with a high blood eosinophil count and a raised level of nitric oxide in exhaled breath. This phenotype has been associated with a Type-2 (T2) inflammatory profile with expression of interleukin (IL)-4, IL-5, and IL-13. Molecular phenotyping has also revealed non-T2 inflammatory phenotypes such as Type-1 or Type-17 driven phenotypes. Antibody treatments targeted at the T2 targets such as anti-IL5, anti-IL5Rα, and anti-IL4Rα antibodies are now available for treating severe eosinophilic asthma, in addition to anti-immunoglobulin E antibody for severe allergic asthma. No targeted treatments are currently available for non-T2 inflammatory phenotypes. Long-term azithromycin and bronchial thermoplasty may be considered. The future lies with molecular phenotyping of the airway inflammatory process to refine asthma endotypes for precision medicine.

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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：萝卜苍蝇，德莉娅floralis秋天

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：AbstractThe gold standard of cancer diagnosis has long been based on histological characteristics. With the rapid advancement of genetic medicine, such standard algorithm of diagnostic approach is facing a challenge. The genetic findings have been changed from being a "supporting character" into the role of a "main character" . More and more disease diagnosis and classification has to be defined by genetic basis. In this article, we focus on the challenges in the field of pediatric oncology. We cited 2 scenarios where genetic information plays a pivotal role in identifying the underlying pathology. The first scenario is that same genetic mutation can lead to variable clinical phenotypes, this includes EWSR1-PATZ1 fusion related neoplasms; BCOR neoplasms; and GATA-2 deficiency related immunodeficiency and myelodysplastic syndrome. Another scenario is relatively more common that is the same clinical and histopathological phenotype with different underlying genotypes. The genotypes actually impact on the treatment response and outcome. We used medulloblastoma as an example. In fact, we can also find similar scenario in many pediatric cancers such as Ewing sarcoma, ependymoma, etc. The essence of this article is to remind clinicians of the rapid development in genetic medicine and it has been reshaping the landscape of the modern disease classification and therapeutic approach. In the near future, it may even lead to a paradigm shift in our disease diagnostic algorithm.

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：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。

简介：Hormonereplacementtherapy(HRT)isinuseformorethanahalfofcentury,butthequestionofindicationsandidealcandidatesforHRTremainsunclear.Postmenopausalwomenareapopulationwiththeincreasingrisksforcardiovasculardiseaseswhicharethemaincauseofdeathinthisgroup.Declineinoestrogenconcentrations

简介：Thetraceamines(TAs)areafamilyofendogenousamineswithstructural,metabolic,physiologicalandpharmacologicalsimilaritiestoclassicalmonoamineneurotransmitters.TheTAfamilyincludestyramine,octopamine,β-phenylethylamine(PEA),andtryptamine(Figure1).Theirpresencehasbeenwell

简介：AbstractChronic obstructive pulmonary disease (COPD) is a heterogeneous disease characteristic of small airway inflammation, obstruction, and emphysema. It is well known that spirometry alone cannot differentiate each separate component. Computed tomography (CT) is widely used to determine the extent of emphysema and small airway involvement in COPD. Compared with the pulmonary function test, small airway CT phenotypes can accurately reflect disease severity in patients with COPD, which is conducive to improving the prognosis of this disease. CT measurement of central airway morphology has been applied in clinical, epidemiologic, and genetic investigations as an inference of the presence and severity of small airway disease. This review will focus on presenting the current knowledge and methodologies in chest CT that aid in identifying discrete COPD phenotypes.