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简介：几份临床的报告证实那胃的萎缩是限于成年病人的一个病理不仅。在儿科，它最经常与Hpylori感染而是这联合被描述细菌不似乎是在孩子的这个肿瘤前状态的唯一的病因学的因素。因为他们系统地没在上面的胃肠的内视镜检查法期间被寻求，在孩子的胃的萎缩和肠的组织变形的频率是未知的。childrenosgastropathies的特定的组织学的分类的缺乏为病理学家使他们的诊断困难。迄今为止基于我们的知识，我们认为详细，描述是必要的这损害的自然功课在童年期间。靠近、延长的临床、内视镜的后续为有胃的萎缩的孩子是重要的。

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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：MemorylossandmentalconfusionarethefirstovertsignsofAlzheimer'sDisease,anincurableandfatalbrainailment.Butscientistsarestartingtofindevidenceofthediseaselongbeforesymptomsappear.

简介：AbstractBackground:Sleep disorders are common but under-researched symptoms in patients with multiple system atrophy (MSA). We investigated the frequency and factors associated with sleep-related symptoms in patients with MSA and the impact of sleep disturbances on disease severity.Methods:This cross-sectional study involved 165 patients with MSA. Three sleep-related symptoms, namely Parkinson’s disease (PD)-related sleep problems (PD-SP), excessive daytime sleepiness (EDS), and rapid eye movement sleep behavior disorder (RBD), were evaluated using the PD Sleep Scale-2 (PDSS-2), Epworth Sleepiness Scale (ESS), and RBD Screening Questionnaire (RBDSQ), respectively. Disease severity was evaluated using the Unified MSA Rating Scale (UMSARS).Results:The frequency of PD-SP (PDSS-2 score of ≥18), EDS (ESS score of ≥10), and RBD (RBDSQ score of ≥5) in patients with MSA was 18.8%, 27.3%, and 49.7%, respectively. The frequency of coexistence of all three sleep-related symptoms was 7.3%. Compared with the cerebellar subtype of MSA (MSA-C), the parkinsonism subtype of MSA (MSA-P) was associated with a higher frequency of PD-SP and EDS, but not of RBD. Binary logistic regression revealed that the MSA-P subtype, a higher total UMSARS score, and anxiety were associated with PD-SP; that male sex, a higher total UMSARS score, the MSA-P subtype, and fatigue were associated with EDS; and that male sex, a higher total UMSARS score, and autonomic onset were associated with RBD in patients with MSA. Stepwise linear regression showed that the number of sleep-related symptoms (PD-SP, EDS, and RBD), disease duration, depression, fatigue, and total Montreal Cognitive Assessment score were predictors of disease severity in patients with MSA.Conclusions:Sleep-related disorders were associated with both MSA subtypes and the severity of disease in patients with MSA, indicating that sleep disorders may reflect the distribution and degree of dopaminergic/non-dopaminergic neuron degeneration in MSA.

简介：Background:Apreviousstudyhasreporteda50%reductionindisuseatrophyofthequadricepsduringthefirst14daysafteranteriorcruciateligament(ACL)reconstruction.Afollow-uptrialisneededtoconfirmthesepromisingresults.ThepresentstudyaimstoinvestigatetheeffectofanocclusionstimulusonquadricepsatrophyafterACLreconstruction.Methods:Atotalof24subjectsparticipatedinthestudy.Theywererandomizedintotwogroups.Startingthe2nddayaftersurgery,theocclusiongroupreceivedanocclusionstimulusfor5min,followedbyremovaloftheocclusivepressurefor3min.Thiswasrepeatedfivetimesinonetrainingsession,twicedaily.Duringtheperiodofocclusivestimulus,thesubjectsperformed20lowloadexercisesforthequadriceps.Thecontrolgroupfollowedthesameexerciseprotocol,butwithouttheocclusionstimulus.Changesinquadricepsanatomicalcrosssectionarea(ACSA)weremeasuredusingaxialmagneticresonance(MR)imagesat40%and50%ofthelengthofthefemur.Results:BothgroupshadasignificantreductionofquadricepsACSAfrom2daysbeforesurgeryto16daysaftersurgery.Duringtheinterventionperiod,theocclusiongrouplost13.8%±1.1%(mean±SEM)andthecontrolgrouplost13.1%±1.0%oftheirquadricepsACSA,respectively.Therewasnosignificantdifferencebetweentheocclusionandcontrolgroupswithregardstoatrophyofthequadricepsmuscles.Conclusion:Inconflictwithotherstudiesusingasimilarprotocol,applicationofbloodflowrestrictionthefirst14daysafterACLreconstructiondidnotreducequadricepsACSAmuscleatrophymeasuredbyMRinapopulationofathletes.

简介：AbstractBackground:Insufficient cerebral perfusion is suggested to play a role in the development of Alzheimer disease (AD). However, there is a lack of direct evidence indicating whether hypoperfusion causes or aggravates AD pathology. We investigated the effect of chronic cerebral hypoperfusion on AD-related pathology in humans.Methods:We enrolled a group of cognitively normal patients (median age: 64 years) with unilateral chronic cerebral hypoperfusion. Regions of interest with the most pronounced hypoperfusion changes were chosen in the hypoperfused region and were then mirrored in the contralateral hemisphere to create a control region with normal perfusion. 11C-Pittsburgh compound-positron emission tomography standard uptake ratios and brain atrophy indices were calculated from the computed tomography images of each patient.Results:The median age of the 10 participants, consisting of 4 males and 6 females, was 64 years (47-76 years). We found that there were no differences in standard uptake ratios of the cortex (volume of interest [VOI]: P = 0.721, region of interest [ROI]: P = 0.241) and grey/white ratio (VOI: P = 0.333, ROI: P = 0.445) and brain atrophy indices (Bicaudate, Bifrontal, Evans, Cella, Cella media, and Ventricular index, P > 0.05) between the hypoperfused regions and contralateral normally perfused regions in patients with unilateral chronic cerebral hypoperfusion.Conclusion:Our findings suggest that chronic hypoperfusion due to large vessel stenosis may not directly induce cerebral β-amyloid deposition and neurodegeneration in humans.

简介：Purpose:Theobjectiveofthepresentstudywastodeterminewhetheradenervatedmuscleextract(DmEx)couldstimulatesatellitecellresponseindenervatedmuscle.Methods:Wistarratsweredividedinto4groups:normalrats,normalratstreatedwithDmEx,denervatedrats,anddenervatedratstreatedwithDmEx.Thesoleusmuscleswereexaminedusingimmunohistochemicaltechniquesforproliferatingcellnuclearantigen,desmin,andmyogenicdifferentiationantigen(MyoD),andelectronmicroscopywasusedforanalysisofthesatellitecells.Results:Theresultsindicatethatwhiledenervationcausesactivationofsatellitecells,DmExalsoinducesmyogenicdifferentiationofcellslocalizedintheinterstitialspaceandtheformationofnewmusclefibers.AlthoughDmExhadasimilareffectinnatureoninnervatedanddenervatedmuscles,thisresponsewasofgreatermagnitudeindenervatedvs.intactmuscles.Conclusion:OurstudyshowsthattreatmentofdenervatedratswithDmExpotentiatesthemyogenicresponseinatrophicdenervatedmuscles.

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