简介：AbstractType 1 diabetes (T1D) results from dysfunction of pancreatic islets β cells. Recent studies supported that endoplasmic reticulum (ER) stress takes an important role in pancreatic β cell excessive loss, resulting in T1D. Here, we aimed to review the relationship between ER stress and T1D. Additionally, we also reviewed the potential mechanisms underlying ER stress mediated T1D. Studies have shown that severe ER stress is directly involved in the pancreatic β cells destruction and pathogenesis of T1D. ER stress plays a key part in pancreatic β cells and T1D, which will help in developing new effective therapeutics for T1D.

简介：它一致地被看了那oncoproteinp28GANK，它是在人的hepatocellular癌(HCC)的overexpressed，在HCC的tumorigenesis起一个关键作用。然而，内在的机制仍然保持不清楚。这里，我们证明p28GANK在endoplasmic蜂窝胃导致的HCC房间禁止apoptosis(嗯)应力。在期间嗯应力，p28GANK提高展开的蛋白质反应，支持嗯从翻译压抑的恢复，并且从而便于房间的能力应付压力条件。而且，p28GANKupregulates调整葡萄糖的蛋白质78(GRP78)，一把钥匙嗯女伴蛋白质，它随后提高合拢能力的ER并且支持恢复从嗯应力。我们也证明p28GANK增加p38激活mitogen的蛋白质kinase和Aktphosphorylation，并且禁止原子因素kappaB(NF-B)激活在下面嗯强调upregulation，它接着贡献GRP78。一起拿，我们的结果显示p28GANK禁止嗯在HCC房间的导致压力的apoptosis，至少部分地，由提高适应反应和GRP78表示。我们建议p28GANK在ER压力条件下面为HCC前进有潜在的含意。

简介：Brainischemicstrokeistheleadingcauseoflong-lastinginjury,disability,anddeathinadults.Althoughthebrainrepresentsonlyabout2%ofthetotalbodymass,itconsumesalmost20%ofthebody’soxygen.Asaresult,braincellsareextremelysensitivetohypoxia.Oncecerebralischemiaoccurs,thecoreofthe

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简介：Centralnervoussystem(CNS)injuriescausedbycerebrovascularpathologies(e.g.,stroke)ormechanicalcontusions(e.g.,traumaticbraininjury)disrupttheblood-brainbarrier(BBB)thatprotectstheCNSmicroenvironmentfromadirectcontactwithbloodsubstancesandcells.Theinitialneuraldamagecausedbythetraumaandtheischemicprocess

简介：ActivinA,amemberofthetransforminggrowthfactor-betasuperfamily,playsaneuroprotectiveroleinmultipleneurologicaldiseases.Endoplasmicreticulum(ER)stress-mediatedapoptoticandautophagiccelldeathisimplicatedinawiderangeofdiseases,includingcerebralischemiaandneurodegenerativediseases.ThapsigarginwasusedtoinducePC12celldeath,andActivinAwasusedforintervention.OurresultsshowedthatActivinAsignificantlyinhibitedmorphologicalchangesinthapsigargin-inducedapoptoticcells,andtheexpressionofapoptosis-associatedproteins[cleaved-caspase-12,C/EBPhomologousprotein(CHOP)andcleaved-caspase-3]andbiomarkersofautophagy(Beclin-1andlightchain3),anddownregulatedtheexpressionofthapsigargin-inducedERstress-associatedproteins[inositolrequiringenzyme-1(IRE1),tumornecrosisfactorreceptor-associatedfactor2(TRAF2),apoptosissignal-regulatingkinase1(ASK1),c-JunN-terminalkinase(JNK)andp38].Theinhibitionofthapsigargin-inducedcelldeathwasconcentration-dependent.ThesefindingssuggestthatadministrationofActivinAprotectsPC12cellsagainstERstress-mediatedapoptoticandautophagiccelldeathbyinhibitingtheactivationoftheIRE1-TRAF2-ASK1-JNK/p38cascade.

简介：1-methyl-4-phenylpyridiniumion(MPP+)inducesendoplasmicreticulumstressandactivatescaspase-12inPC12cells,leadingtoneuronalapoptosis.However,theunderlyingmolecularmechanismremainsunknown.Thepresentstudyinvestigatedtheregulatoryeffectsofnervegrowthfactor(Aktactivator)andlithiumchloride(glycogensynthasekinase-3βinhibitor)ontheendoplasmicreticulumstresssignalingpathway.TheresultsrevealedthatMPP+inducedexpressionofBipandC/EBPhomologousprotein.TheupregulationofBipandC/EBPhomologousprotein,aswellasthedecreasedpro-caspase-12levelinducedbyMPP+wereinhibitedbypretreatmentofthenervegrowthfactororlithiumchloride.Theseresultssuggestthatthephosphatidylinositol3kinase-Akt-glycogensynthasekinase-3βpathwayisinvolvedinMPP+-inducedendoplasmicreticulumstress.

简介：ThelocalCa^2+releasefromtheheterogeneouslydistributedendoplasmicreticulum(ER)calciumstorehasacriticalroleincalciumhomeostasisandcellularfunction.However;singlefluorescentproteinbasedERcalciumprobesexperiencechallengesinquantifyingtheERcalciumstoreindifferinglivecells,andintensity-basedmeasurementsmakeitdifficulttodetectlocalcalciummicrodomainsintheER.Here,wedevelopedageneticallyencodedratiometricERcalciumindicator[GCEPIA1-SNAPer]thatcandetectthereal-timeERcalciumstoreandlocalcalciummicrodomainsinlivecells.GCEPIA1-SNAPerwaslocatedinthelumenoftheERandshowedalinear;reversibleandrapidresponsetochangesintheERcalciumstore.TheGCEPIA1-SNAPerprobeeffectivelymonitoredthedepletionoftheERcalciumstorebyTGorstarvationtreatment,andthrough让suseweidentifiedheterogeneouslydistributedcalciummicrodomainsintheERwhichwerecorrelatedw让hthedistributionofSTIM1clustersuponERcalciumstoredepletion.Lastly,GCEPIA1-SNAPercanbeusedtodetecttheERcalciumstorebyhigh-throughputflowcytometryandconferstheabilitytostudythefunctionofcalciummicrodomainsoftheER.

简介：AbstractMitochondrial injury and endoplasmic reticulum (ER) stress are considered to be the key mechanisms of renal ischemia-reperfusion (I/R) injury. Mitochondria are membrane-bound organelles that form close physical contact with a specific domain of the ER, known as mitochondrial-associated membranes. The close physical contact between them is mainly restrained by ER-mitochondria tethering complexes, which can play an important role in mitochondrial damage, ER stress, lipid homeostasis, and cell death. Several ER-mitochondria tethering complex components are involved in the process of renal I/R injury. A better understanding of the physical and functional interaction between ER and mitochondria is helpful to further clarify the mechanism of renal I/R injury and provide potential therapeutic targets. In this review, we aim to describe the structure of the tethering complex and elucidate its pivotal role in renal I/R injury by summarizing its role in many important mechanisms, such as mitophagy, mitochondrial fission, mitochondrial fusion, apoptosis and necrosis, ER stress, mitochondrial substance transport, and lipid metabolism.

简介：Angiogenesis在出生后的生命期间在胚胎的脉管的树的发展以及处于几个正常、病理学的条件起一个基本作用。Bloodsupply，由neovascularization建立了，在愈合弯屈期间为histogenesis是必要的以及变长的手足在骨胳的损伤sequalae的治疗广泛地适用。Butlittle注意对这个区域被给予了。这评论试图在机械应力下面总结angiogenesis规定，在愈合的创伤中的angiogenesis的过程和angiogenesis，特别地与紧张压力原则联合。

简介：Undertheconditionthatallthestresscomponentsatacrack-tiparethefunctionsofθonly,makinguseofequilibriumequationsandhydrostaticstress-dependentyieldcondition,inthispaper,wederivethegenerallyanalyticalexpressionsofthehydrostaticstress-dependentperfectly-plasticstressfieldsatastationaryplane-stresscrack-tip.Applyingthesegenerallyanalyticalexpressionstotheconcretecracks,theanalyticalexpressionsofhydrostaticstress-dependentperfectly-plasticstressfieldsatthetipsofmodeⅠandmodeⅡcracksareobtained.

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简介：铁人王进喜同志生前有一句铮铮名言：“井没压力不出油，人无压力轻飘飘。”人需要压力来产生动力，但压力过大又会使人萎靡不振。西方有句谚语这样说：“最后一棵草会压垮骆驼背。”如何把压力减少到一个适当的程度呢？

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简介：客观：当在骨头织物工程(TE)和有钛蜂窝胃的公山羊的mandible的部分缺点的修理的脚手架增强了，调查使用自然poritos的可行性。方法：有在大约50%-65%的尺寸和孔的190-230μm的一个毛孔的自然poritos被塑造进小粒的形状5公里x5公里x在尺寸的5尼姑。扩展的自体同源的公山羊的髓间充质的干细胞被recombinant导致人的形态基因的protein-2(rhBMP2)到改进osteoblastic显型。然后，髓导出造骨细胞在4x10~7/ml的密度被播种进poritos并且在培植以前在vitro孵化了48个小时。然后，osteoblasticcells/poritos建筑群被植入进mandible的缺点，缺点被钛蜂窝胃增强。poritos的培植独自扮演了著名计算机生产厂商他控制。骨头新生被估计4，8，在用roentgenographicanalysis和组织学的观察的培植以后的16个星期在16个星期以后被做。结果：新骨头能是observedhistologically在表面上并且在在在cell-seedinggroup的所有标本的自然珊瑚的毛孔，而在控制组没有在构造的中心的成骨过程的证据。结果证明新骨头接枝16个星期成功地在培植以后被恢复。结论：当与髓移植的支架材料由TE方法导出造骨细胞，这研究建议使用多孔的珊瑚的可行性。借助于钛蜂窝胃加强，mandible的缺点能成功地被恢复。它显示出在诊所为骨头缺点的重建使用这个方法的潜力。

简介：随着生活节奏的加快，形态迥异的压力接踵而来：生存压力、升学压力、工作压力等，这一切无不困扰着我们的生活与学习。对于压力你又了解多少呢？你又有什么样的妙招儿对付它呢？现在的你正承受着什么样的压力？本文以假日压力为例，帮你认识并缓解压力。一起加入到减压的队伍中来吧!

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简介：Thereare13papersinthisspecialissueonstressfield,crustaldeformationandseismicity.ThegreatWenchuanearthquakeisagrievousdisaster,butChinesescientistsaretryingtolearnmorefromtheeventinordertounderstandbetterthephysicsofearthquakesfor

简介：Ithasbeenwellrecognizedthat,duetoanisotropicpackingstructureofgranularmaterial,thetruestressinaspecimenisdifferentfromtheappliedstress.However,veryfewresearcheffortshavebeenfocusedonquantifyingtherelationshipbetweenthetruestressandappliedstress.Inthispaper,wederiveanexplicitrelationshipamongappliedstresstensor,material-fabrictensor,andforce-fabrictensor;andweproposearelationshipbetweenthetruestresstensorandtheappliedstresstensor.Thevalidityofthisderivedrelationshipisexaminedbyusingthediscreteelementsimulationresultsforgranularmaterialunderbiaxialandtriaxialloadingconditions.