简介：无

简介：无

简介：无

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：AbstractAcute kidney injury (AKI), characterized by acute renal dysfunction, is an increasingly common clinical problem and an important risk factor in the subsequent development of chronic kidney disease (CKD). Regardless of the initial insults, the progression of CKD after AKI involves multiple types of cells, including renal resident cells and immune cells such as macrophages. Recently, the involvements of macrophages in AKI-to-CKD transition have garnered significant attention. Furthermore, substantial progress has also been made in elucidating the pathophysiological functions of macrophages from the acute kidney to repair or fibrosis. In this review, we highlight current knowledge regarding the roles and mechanisms of macrophage activation and phenotypic polarization, and transdifferentiation in the development of AKI-to-CKD transition. In addition, the potential of macrophage-based therapy for preventing AKI-to-CKD transition is also discussed.

简介：无

简介：AbstractNon-alcoholic fatty liver disease (NAFLD) is emerging as the most common chronic liver disease worldwide. It refers to a range of liver conditions affecting people who drink little or no alcohol. NAFLD comprises non-alcoholic fatty liver and non-alcoholic steatohepatitis (NASH), the more aggressive form of NAFLD. NASH is featured by steatosis, lobular inflammation, hepatocyte injury, and various degrees of fibrosis. Although much progress has been made over the past decades, the pathogenic mechanism of NAFLD remains to be fully elucidated. Hepatocyte nuclear factor 4α (HNF4α) is a nuclear hormone receptor that is highly expressed in hepatocytes. Hepatic HNF4α expression is markedly reduced in NAFLD patients and mouse models of NASH. HNF4α has been shown to regulate bile acid, lipid, glucose, and drug metabolism. In this review, we summarize the recent advances in the understanding of the pathogenesis of NAFLD with a focus on the regulation of HNF4α and the role of hepatic HNF4α in NAFLD. Several lines of evidence have shown that hepatic HNF4α plays a key role in the initiation and progression of NAFLD. Recent data suggest that hepatic HNF4α may be a promising target for treatment of NAFLD.

简介：无

简介：无

简介：IL-33/ST2轴在几织物特定的自体免疫的疾病的致病被含有。腹的疾病(CD)是主要基因因素(HLA-DQ2/DQ8)和为危险性的etiologic(饮食的面筋)在被知道的唯一的自体免疫的疾病。我们测量了浆液层次和IL-33和它的受体的坚定的肠的织物表示在病人与的可溶的ST2与疾病活动调查他们的协会的CD。没有CD，IL-33和sST2的浆液和织物层次与在控制病人的那些相比在有CD的病人是显著地更高的。我们证明显著地从大麦和小麦麦胶蛋白质提取的有毒的肽从腹的病人在有教养的外部血mononuclear房间刺激IL-33和ST2的生产，强烈含有在CD的致病的IL-33/ST2轴。在织物和浆液的IL-33和它的受体ST2的高水平反映一个活跃煽动性的状态并且可以为疾病活动代表潜在的biomarker。IL-33/ST2版本，行动的模式，和规定的更好的理解将是关键的开发治疗学指向IL-33/ST2小径到对待CD。

简介：无

简介：Genisteiniseffectiveagainstamyloid-βtoxicity,buttheunderlyingmechanismsareunclear.Wehypothesizedthatgenisteinmayprotectneuronsbyinhibitingthemitochondrialapoptoticpathway,andtherebyplayaroleinthepreventionofAlzheimer'sdisease.AratmodelofAlzheimer'sdiseasewasestablishedbyintraperitonealinjectionofD-galactoseandintracerebralinjectionofamyloid-βpeptide(25–35).Inthegenisteintreatmentgroups,a7-daypretreatmentwithgenistein(10,30,90mg/kg)wasgivenpriortoestablishingAlzheimer'sdiseasemodel,for49consecutivedays.Terminaldeoxyribonucleotidyltransferase-mediateddUTPnickendlabelingassaydemonstratedareductioninapoptosisinthehippocampusofratstreatedwithgenistein.Westernblotanalysisshowedthatexpressionlevelsofcapase-3,Baxandcytochromecweredecreasedcomparedwiththemodelgroup.Furthermore,immunohistochemicalstainingrevealedreductionsincytochromecandBaximmunoreactivityintheserats.MorriswatermazerevealedasubstantialshorteningofescapelatencybygenisteininAlzheimer'sdiseaserats.Thesefindingssuggestthatgenisteindecreasesneuronallossinthehippocampus,andimproveslearningandmemoryability.Theneuroprotectiveeffectsofgenisteinareassociatedwiththeinhibitionofthemitochondrialapoptoticpathway,asshownbyitsabilitytoreducelevelsofcaspase-3,Baxandcytochromec.

简介：DearEditor,Vogt-Koyanagi-Harada(VKH)diseaseisacell-mediatedautoimmunesyndromedirectedagainstmelanocytes.Itisconsideredamultisystemdisordercharacterizedbygranulomatouspanuveitisoftenassociatedwithneurologicandcutaneousmanifestations.Thechoroidisthemainsiteof

简介：AbstractBackground:Due to airway remodeling and emphysematous destruction in the lung, the two classical clinical phenotypes of chronic obstructive pulmonary disease (COPD) are emphysema and bronchiolitis. The present study was designed to investigate the levels of small airway immunoglobulin A (IgA) in COPD with "emphysema phenotype." The study also evaluated the associations between the small airway IgA levels and the severity of disease by the extent of emphysema versus airflow limitation.Methods:Thirty patients (20 with COPD and ten healthy smokers) undergoing lung resection surgery for a solitary peripheral nodule were included. The study was conducted from January 2015 to December 2018 in the Shanxi Dayi Hospital. The presence of small airway IgA expression was determined in the lung by immunohistochemistry. In vivo, Wistar rats were exposed to silica by intratracheal instillation. Rats were sacrificed at 15 and 30 days after exposure of silica (n = 10 for each group). We also evaluated airway IgA from rats.Results:Small airway secretory IgA (sIgA), dimeric IgA (dIgA), and dIgA/sIgA of Global Initiative for Chronic Obstructive Lung Disease grade 1-2 COPD patients showed no difference compared with smoking control subjects (5.15±1.53 vs. 6.03±0.85; 1.94±0.66 vs. 1.67±0.04; 41.69±21.02 vs. 28.44±9.45, all P > 0.05). dIgA/sIgA level in the lung of COPD patients with emphysema showed higher levels than that of COPD patients without emphysema (51.89±24.81 vs. 31.49±9.28, P=0.03). The percentage of low-attenuation area below 950 Hounsfield units was positively correlated with dIgA/sIgA levels (r=0.45, P=0.047), but not associated with the severity of disease by spirometric measurements (forced expiratory volume in the first second %pred, P>0.05). Likewise, in the rat study, significant differences in sIgA, dIgA, dIgA/sIgA, mean linear intercept, mean alveoli number, and mean airway thickness of bronchioles (VV airway, all P < 0.01) were only observed between control rats and those exposed for 30 days. However, in the group exposed for 15 days, although the VV airway was higher than that in normal rats (27.61±2.26 vs. 20.39±1.99, P<0.01), there were no significant differences in IgA and emphysema parameters between the two groups (all P>0.05).Conclusion:Airway IgA concentrations in mild and moderate COPD patients are directly associated with the severity of COPD with "emphysema phenotype" preceding severe airway limitation. This finding suggests that small airway IgA might play an important role in the pathophysiology of COPD, especially emphysema phenotype.

简介：无

简介：BACKGROUND:ResearchesindicatethatpatientswithWilsondisease(WD)haveabnormalskeletalmetabolism,whichisinducedbyvariousfactors.OBJECTIVE:ToprobeintothechangingcharacteristicsofabnormalskeletalmetabolisminWDpatientsandobservetheeffectofdecoppertherapy.DESIGN:Case-contrastandself-controlstudy.SETTING:DepartmentofNeurology,AffiliatedHospitalofNeurologicalInstitute,AnhuiCollegeofTraditionalChineseMedicine.PARTICIPANTS:Atotalof35patientswithWDincluding21malesand14femalesagedfrom10to42yearswiththemeanageof(20±8)yearswereselectedfromDepartmentofNeurology,AffiliatedHospitalofNeurologicalInstitute,AnhuiCollegeofTraditionalChineseMedicinefromSeptember2000toFebruary2001.Allthepatientswereincompliancewiththediagnosticcriteria:historyoffamilyheredity;conesymptomsinvitro,physicalsignorliversymptoms;positiveKayser-Fleischerring;serumcopperprotein＜200mg/LorAcopperoxidase＜0.2;urinecopper＞1.6μmol/24hours;livercopper＞250μg/g(dryweight).Thecontrolgroupwasselectedfrom25casesofhealthindividualsincluding13malesand12femalesagedfrom16to35yearswiththemeanageof(22±6)years.Allpatientswhoparticipatedinthestudywereinformedfirstandconsented.METHODS:Patientsintreatmentgroupweretreatedwithvenousinjectionof1.0gsodiumdimercaptosulfonate,onceadayfortotally6successivedays.Andthen,patientsrestedfor2days.Thisprocedurementionedabovewasregardedasacourse,andthetreatmentlastedfor4-8courses.Beforeandafterinjectionofsodiumdimercaptosulfonate,serumcalcitonin(CT),osteocalcin(BGP),parathyroidhormone(PTH)and1,25-(OH)2VitD3weremeasuredwithradio-immunitymethod:blood,urinecalcium,phosphorumandurinecreatinineweremeasuredwithbiochemicalanalyzer;urinedihydropyrimidinedehydrogenase(DPD)wasdetectedwithenzyme-immunitymethod;bonemineraldensity(BMD)wascheckedattheonethirdfromdistalendofulnaandradiuswithsingle

简介：无

简介：AIM:Toinvestigatewhetherliversteatosisreductionduetoasix-monthdietaryinterventionresultsinsignificantchangesintheconcentrationsoffattyacids.METHODS:Agroupof35Caucasianindividualsdiagnosedwithdifferentlevelsofsteatosiswereprospectivelyenrolledinthepresentstudy.Analysisofthefattyacidprofileswasperformedaccordingtochangesinliversteatosis(liversteatosisreductionbyoneortwodegrees)afterasix-monthdietaryintervention.Thediethelpedreducebodymassinobeseandoverweightpatients,andstabilizebothglycemiaanddyslipidemia.FattyacidswereextractedaccordingtotheFolchmethodandanalyzedbygaschromatography.RESULTS:Thisstudyshowedsignificantchangesinfattyacidprofilesinpatientswhohadreducedliversteatosisbyoneaswellastwodegrees.Areductioninliversteatosisbyonedegreecausedasignificantincreaseinthelevelofthen-3family:eicosapentaenoicacid(P<0.055),docosapentaenoicacid-C22:5(P<0.05)anddocosahexaenoicacid(P<0.05).Areductioninliversteatosisbytwodegreescausedasignificantdecreaseinserumpalmitoleicacid-C16:1(P<0.05).CONCLUSION:Liversteatosisreductionisassociatedwithchangesinfattyacidprofiles,andthesechangesmayreflectanalterationinfattyacidsynthesisandmetabolism.Thesefindingsmayhelpbetterunderstandregressionofnonalcoholicfattyliverdisease.

简介：煽动性的肠疾病(IBD)包括二个实体，Crohn的疾病和ulcerative。两个是有经常的复杂并发症和外科的过程的长期的条件，一个伟人影响病人生命的质量。thiopurine抗代谢物azathioprine和6-mercaptopurine广泛地在IBD病人被使用。当前的指示包括维护治疗，类固醇家属疾病，管闭合，infliximabimmunogenicity的预防和Crohn的疾病复发的预防。令人惊讶地，在最后十年的抑制免疫力的药的宽使用没减少外科的需要，可能因为这些治疗在疾病路线在太迟了的阶段被介绍。immunossupressants的更早的使用现在被一些作者倡导。合理包括：(1)修改现在的治疗学的途径的IBD自然科学的失败，(2)那个azathioprine罐头导致粘膜的愈合的示范，为Crohn的疾病和ulcerative的一个相关预示的因素，并且(3)早immunossupression有的示范很积极的影响在上小儿科，最近诊断的Crohn的疾病病人。我们现在正在等候新研究的结果，诊断了成年Crohn的疾病病人(阿兹台克人学习)，与infliximab(声音的学习)相比澄清azathioprine的贡献，并且在最近表明azathioprine的实用性。

简介：