简介：Serioushearingandbalanceimpairmentscanoccurasaresultoflossofhaircellsrelatedtoaging,environmentalstresses(suchasnoisesexposure)orexposuretochemotherapeuticdrugs(suchascisplatinandaminoglycosideantibiotics).Becausealargeportionofhearingimpairmentinvolveslossofhaircells,regenerationorreplacementofthesecellsisapossiblealternativetoprostheticdevices1.Researchershavepaidhotattentiontothestudyofinnerearhaircellregenerationforhearingrestorationformanyyears.Besidestheimportantfunctionofhaircells,therearemanyothercontributorsessentialfornormalhearing.Haircellregenerationisoneoftheessentialstepsfortotalhearingrecovery,butnottheonlyone.Inthisarticle,wewillreviewtheprogressesinresearchonhearingloss,stemcellapplicationandhearingrestoration.

简介：介绍进散开张肌图象(DTI)的Rician噪音能在追踪的张肌计算和纤维以后带严肃的影响。减少Rician噪音的效果，我们建议认为基于小浪的散开方法降噪多信道的打的散开加权(DW)图象。当保存质地和边时，介绍变光滑的策略，在小浪领域利用各向异性的非线性的散开，成功地移开噪音。为了评估份量上，在为介绍进DW图象，peak-to-peaksignal-to-noise比率(PSNR)和signal-to-mean的Rician噪音的财务的介绍方法的效率摆平错误比率(SMSE)度量标准被采用。基于合成、真实的数据，我们计算了明显的散开系数(模数转换器)并且追踪了纤维。我们做了在介绍模型，波浪收缩和调整非线性的散开变光滑方法之间的比较。所有实验结果证明份量上并且视觉上介绍过滤器的更好的表演。

简介：Brachialplexusinjuryisfrequentlyinducedbyinjuries,accidentsorbirthtrauma.Upperlimbfunctionmaybepartiallyortotallylostafterinjury,orleftpermanentlydisabled.Withthedevelopmentofvariousmedicaltechnologies,differenttypesofinterventionsareused,buttheireffectivenessiswideranging.Manyrepairmethodshavephasiccharacteristics,i.e.,repairsaredoneindifferentphases.Thisstudyexploredresearchprogressandhottopicmethodsforprotectionafterbrachialplexusinjury,byanalyzing1,797articlesconcerningtherepairofbrachialplexusinjuries,publishedbetween2004and2013andindexedbytheScienceCitationIndexdatabase.Resultsrevealedthattherearemanymethodsusedtorepairbrachialplexusinjury,andtheireffectsarevaried.Interventionmethodsincludenervetransfersurgery,electricalstimulation,celltransplantation,neurotrophicfactortherapyanddrugtreatment.Therapeuticmethodsinthisfieldchangeaccordingtothehottopicofresearch.

简介：Thebraincontrolsvirtuallyallbodyfunctions,bothinternallyandininteractionwiththeexternalenvironment.Asthebasicbodyanatomyofallvertebrateshasabilateralsymmetry,structuresandfunctionsofvertebratebrainsarealsoorganizedaccordingtothisfundamentalanatomicalprincipletomeetallsensory,motor,andinternalrequirementsofbodycontrol.Consequently,particularpartsorfunctionsofthebodyarecontrolledbyparticularbrainstructures.Formammalswhosebrainsonlyhaveaverylimitedcapacityto

简介：Objectives:Facialnerveaberrationisthemosttroublesomesituationincongenitalmalformationsofmiddleear.Theaimofourstudyistoinvestigateitsimagingandclinicalfeaturesaswellasrelevantchoiceofsurgicaltechniquesforhearingimprovement.Methods:Aretrospectivestudyinvolvingreviewofclinicaldataof227patients(256ears)withcongenitalmiddleearanomalywasundertaken,includingpreoperativecomputedtomography(CT)data,surgicalrecordsandvideos.Results:Aberrationinvolvingintratemporalfacialnervewasfoundin82/256ears(32.03%)withcongenitalmiddleearanomaly.Themostcommonformsofaberrationincludedoverhangingovertheovalwindow(50/82ears,60.98%),bifurcation(3/82ears,3.66%)andtransverseoverthepromontory(3/82ears,3.66%),countingfor68.29%(56/82)ofthecaseswithfacialnerveaberration.Concomitantstapesmalformationwasfoundin76/82ears(92.68%)andatresiaorstenosisoftheovalwindowin27/82ears(32.93%).In9/82ears(10.98%)bothstapesandovalwindowwasabsent.Electivesurgeriesforthepurposeofhearingimprovementincludedstapodotomy+pistonimplantation,labyrinthotomy,labyrinthotomy+totalossicularreplacementprosthesis(TORP)implantationandVibrantSoundbridge(VSB)implantation.Conclusion:Themajorityoffacialnerveaberrationincongenitalmalformationofmiddleearinvolvesdisplacementoffacialnerve,inadditiontoconcomitantmalformationsofthestapesand/orovalwindow,whichmayinfluencethechoiceofsurgeryforhearingimprovement.VSBimplantationmaybeconsideredasausefuloption.

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简介：AbstractBackground:Autophagy of alveolar macrophages is a crucial process in ischemia/reperfusion injury-induced acute lung injury (ALI). Bone marrow-derived mesenchymal stem cells (BM-MSCs) are multipotent cells with the potential for repairing injured sites and regulating autophagy. This study was to investigate the influence of BM-MSCs on autophagy of macrophages in the oxygen-glucose deprivation/restoration (OGD/R) microenvironment and to explore the potential mechanism.Methods:We established a co-culture system of macrophages (RAW264.7) with BM-MSCs under OGD/R conditions in vitro. RAW264.7 cells were transfected with recombinant adenovirus (Ad-mCherry-GFP-LC3B) and autophagic status of RAW264.7 cells was observed under a fluorescence microscope. Autophagy-related proteins light chain 3 (LC3)-I, LC3-II, and p62 in RAW264.7 cells were detected by Western blotting. We used microarray expression analysis to identify the differently expressed genes between OGD/R treated macrophages and macrophages co-culture with BM-MSCs. We investigated the gene heme oxygenase-1 (HO-1), which is downstream of the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signaling pathway.Results:The ratio of LC3-II/LC3-I of OGD/R treated RAW264.7 cells was increased (1.27 ± 0.20 vs. 0.44 ± 0.08, t = 6.67, P < 0.05), while the expression of p62 was decreased (0.77 ± 0.04 vs. 0.95 ± 0.10, t = 2.90, P < 0.05), and PI3K (0.40 ± 0.06 vs. 0.63 ± 0.10, t = 3.42, P < 0.05) and p-Akt/Akt ratio was also decreased (0.39 ± 0.02 vs. 0.58 ± 0.03, t = 9.13, P < 0.05). BM-MSCs reduced the LC3-II/LC3-I ratio of OGD/R treated RAW264.7 cells (0.68 ± 0.14 vs. 1.27 ± 0.20, t = 4.12, P < 0.05), up-regulated p62 expression (1.10 ± 0.20 vs. 0.77 ± 0.04, t = 2.80, P < 0.05), and up-regulated PI3K (0.54 ± 0.05 vs. 0.40 ± 0.06, t = 3.11, P < 0.05) and p-Akt/Akt ratios (0.52 ± 0.05 vs. 0.39 ± 0.02, t = 9.13, P < 0.05). A whole-genome microarray assay screened the differentially expressed gene HO-1, which is downstream of the PI3K/Akt signaling pathway, and the alteration of HO-1 mRNA and protein expression was consistent with the data on PI3K/Akt pathway.Conclusions:Our results suggest the existence of the PI3K/Akt/HO-1 signaling pathway in RAW264.7 cells under OGD/R circumstances in vitro, revealing the mechanism underlying BM-MSC-mediated regulation of autophagy and enriching the understanding of potential therapeutic targets for the treatment of ALI.