简介:The2008Wenchuanearthquake,amajorintraplateearthquakewithMw7.9,occurredontheslowlydeformingLongmenshanfault.Tobetterunderstandthecausesofthisdevastatingearthquake,weneedknowledgeoftheregionalstressfieldandtheunderlyinggeodynamicprocesses.Here,wedeterminefocalmechanismsolutions(FMSs)ofthe2008Wenchuanearthquakesequence(WES)usingbothP-wavefirst-motionpolaritydataandSH/Pamplituderatio(AR)data.AsP-wavepolaritiesaremorereliableinformation,theyaregivenpriorityoverSH/PAR,thelatterofwhichareusedonlywhentheformerhaslooseconstraintontheFMSs.Wecollectdatafromthreecategories:(1)permanentstationsdeployedbytheChinaEarthquakeAdministration(CEA);(2)theWesternSichuanPassiveSeismicArray(WSPSA)deployedbyInstituteofGeology,CEA;(3)globalstationsfromIncorporatedResearchInstitutionsforSeismology.Finally,129eventswithmagnitudeoverMs4.0inthe2008WESareidentifiedtohavewell-constrainedFMSs.Amongthem,83arewellconstrainedbyP-wavepolaritiesonlyasshownbyCaietal.(EarthqSci24(1):115–125,2011),andtherestofwhicharenewlyconstrainedbyincorporatingSH/PAR.BasedonthespatialdistributionandFMSsoftheWES,wedrawfollowingconclusions:(1)theprinciplecompressionaldirectionsofmostFMSsoftheWESaresubhorizontal,generallyinagreementwiththeconclusiongivenbyCaietal.(2011)butwithafewmodificationsthatthecompressionaldirectionsareWNW–ESEaroundWenchuanandENE–WSWaroundQingchuan,respectively.ThesubhorizontalcompressionaldirectionalongtheLongmenshanfaultfromSWtoNEseemstohavealeftlateralrotation,whichagreeswellwithregionalstressfieldinvertedbyformerresearchers(e.g.,Xuetal.,ActaSeismolSin30(5),1987;ActaGeophysSin32(6),1989;Cuietal.,SeismolGeol27(2):234–242,2005);(2)theFMSsoftheeventsnotonlyreflectedtheregionalstressstateoftheLongmenshanregion,butalsowereobviouslycontrolledbythefaultstosomeextent,whichwaspointedou
简介:目的通过比较甘松不同提取物对6-羟基多巴胺(6-OHDA)所致人神经母细胞瘤细胞(SH-SY5Y)损伤的保护作用,筛选活性部位并进行成分分析。方法采用体外细胞培养法,建立6-OHDA损伤SH-SY5Y细胞帕金森模型。MTT法检测甘松不同提取部位对6-OHDA诱导损伤的SH-SY5Y细胞活力的影响,计算抑制率;进一步观察细胞形态明确活性提取部位对细胞生长的影响。采用GC-MS技术对该部位进行化学成分分析。结果甘松石油醚、乙酸乙酯、正丁醇及乙醇部位均能抑制6-OHDA所致的SH-SY5Y细胞损伤,提高细胞存活率,其中石油醚部位的保护作用最强,从该部位中分离鉴定出22个成分,主要为倍半萜类化合物。结论甘松不同提取部位对6-OHDA诱导的SH-SY5Y细胞损伤均有一定保护作用,其中石油醚部位活性较强,主要成分为倍半萜类化合物。
简介:摘要目的探讨锌指蛋白580(zinc finger protein 580,ZNF580)在SH-SY5Y细胞系氧糖剥夺(oxygen-glucose deprivation,OGD)模型中的表达情况及其过表达对缺氧缺血神经元凋亡的影响及可能机制。方法研究分两部分:(1)培养人神经母细胞瘤SH-SY5Y细胞系,分为模型组和对照组,模型组建立OGD模型(95% N2、5% CO2、0.1% O2的三气培养箱37 ℃恒温培养6 h),并于OGD后6、12和24 h提取蛋白,利用蛋白质印迹技术定量检测ZNF580的表达情况。(2)慢病毒转染过表达ZNF580对细胞凋亡及半胱氨酸蛋白酶3的活化形式(cleaved caspase-3)表达的影响:取对照组和模型组OGD后24 h的细胞。过表达组细胞首先通过慢病毒转染技术构建过表达ZNF580细胞,再行OGD处理。采用流式细胞技术检测各组细胞凋亡率,采用蛋白质印迹技术检测cleaved caspase-3的表达。采用两独立样本t检验、单因素方差分析及LSD-t两两比较进行统计学分析。结果(1)与对照组(1.00)相比,模型组OGD后6、12及24 h ZNF580相对表达量分别为1.36±0.05、2.12±0.07和1.69±0.05,均显著升高(LSD-t值分别为9.20、28.26和19.21,P值均<0.001)。(2)对照组、模型组、过表达组细胞凋亡率分别为(1.07±0.56)%、(21.51±1.65)%和(3.42±0.93)%,cleaved caspase-3相对表达量分别为1.00、2.47±0.59和1.70±0.25。与对照组相比,模型组的细胞凋亡率及cleaved caspase-3相对表达量升高(LSD-t值分别为21.98和8.17,P值均为0.001);与模型组相比,过表达组的细胞凋亡率及cleaved caspase-3相对表达量降低(LSD-t=19.45,P=0.001;LSD-t=4.28,P=0.005)。结论缺氧缺血可导致ZNF580过表达,ZNF580过表达可能通过抑制cleaved caspase-3表达从而影响其酶解活化来减轻缺氧缺血神经元的凋亡。
简介:摘要目的评价hsa_circ_0025853在人神经母细胞瘤细胞(SK-N-SH细胞)氧糖剥夺/复糖复氧损伤(OGD/R)中的作用。方法传代培养SK-N-SH细胞至对数生长期,采用随机数字表法分为4组(n=40):对照组(C组)、OGD/R组、hsa_circ_0025853过表达组(E组)和hsa_circ_0025853过表达阴性对照组(EV组)。C组细胞在37 ℃、5%CO2正常条件下培养,OGD/R组细胞铺于6孔板或96孔板待完全贴壁后氧糖剥夺16 h后复糖复氧。E组和EV组分别转染hsa_circ_0025853过表达载体或hsa_circ_0025853过表达阴性对照载体后制备OGD/R模型。于复糖复氧4和12 h时,采用qPCR法检测hsa_circ_0025853、线粒体动力相关蛋白1(Drp1)mRNA表达水平;Western blot法检测Drp1表达水平,CCK-8法检测细胞活力,流式细胞术检测细胞凋亡率。结果与C组比较,OGD/R组复糖复氧后细胞活力降低,细胞凋亡率升高,Drp1及其mRNA表达上调,hsa_circ_0025853表达下调(P<0.05);与OGD/R组或EV组比较,E组复糖复氧后细胞活力升高,细胞凋亡率降低,Drp1表达下调,hsa_circ_0025853表达上调(P<0.05),Drp1 mRNA表达差异无统计学意义(P>0.05)。结论hsa_circ_0025853表达下调可促进Drp1表达上调,诱发细胞凋亡,参与SK-N-SH细胞OGD/R的发生机制。
简介:AbstractBackground:The efficacy of entecavir (ETV) add-on peg-interferon therapy compared with ETV monotherapy in treatment-naïve hepatitis B virus (HBV) patients remains controversial. We investigated whether adding peg-interferon to ongoing ETV treatment leads to a better curative effect or not.Methods:All patients have been recruited between August 2013 and January 2015 from the Shanghai Public Health Clinical Center and Zhongshan Hospital (China). Eligible HBV patients (n = 144) were randomly divided (1:1) to receive either ETV monotherapy (n = 70) or peg-interferon add-on therapy from week 26 to 52 (n = 74). Patients were followed-up for at least 2 years. Indexes including hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) seroconversion rate, sustained virologic response, transient elastography value, and histological scores were evaluated every 3 months until the end of the study. The rate of patients with HBsAg loss was defined as the primary endpoint criteria.Results:At week 26, no patient achieved HBsAg seroconversion in either group. At week 52, one patient in the monotherapy group was HBsAg-negative but there was none in the combination therapy group. The monotherapy group showed significantly better liver function recovery results than the combination therapy group. At week 78, one patient in the combination group had HBsAg seroconverted. At week 104, only three patients in the combination therapy group were HBsAg-negative compared with one patient in monotherapy. The mean alanine aminotransferase and aspartate aminotransferase levels and transient elastography values decreased significantly compared with baseline. Both groups showed a favorable decrease in alpha-fetoprotein (monotherapy: 4.5 [2.8, 7.1] vs. 2.2 [1.8, 3.1] ng/mL, P < 0.001; combination therapy: 5.7 [3.0, 18.8] vs. 3.2 [2.0, 4.3] ng/mL, P < 0.001) and an improved result of liver biopsy examination scores. The combination group showed a better improvement in histology compared with the monotherapy group (mean transient elastography value 6.6 [4.9, 9.8] vs. 7.8 [5.4, 11.1] kPa, P = 0.028). But there was no significant difference in HBsAg conversion rate (1.8% [1/56] vs. 4.1% [3/73], P = 0.809) and HBeAg conversion rate (12.5% [7/56] vs. 11.0% [8/73], P = 0.787), as well as HBV-DNA, sustained virologic response (93.2% vs. 98.5%, P = 0.150) between the two groups.Conclusions:Both therapies supported liver function recovery and histology improvement. Combination therapy did not show better anti-viral efficacy in HBsAg or HBeAg seroconversion compared with monotherapy. However, combination therapy played a more positive role in reversing hepatic fibrosis compared with monotherapy.Trial registration:ClinicalTrials.gov: NCT02849132; https://clinicaltrials.gov/ct2/show/NCT02849132
简介:Basedonthecovariantprolongationstructuretechnique,weconstructtheintegrablehigher-orderdeformationsofthe(2+1)-dimensionalHeisenbergferromagnetmodelandobtaintheirsu(2)×R(λ)prolongationstructures.ByassociatingthesedeformedmultidimensionalHeisenbergferromagnetmodelswiththemovingspacecurveinEuclideanspaceandusingtheHasimotofunction,wederivetheirgeometricalequivalentcounterparts,i.e.,higher-order(2+1)-dimensionalnonlinearSchrdingerequations.
简介:摘要目的探讨SH2B1对肺腺癌细胞株LTEP-a-2细胞增殖及运动能力的影响。方法采用RNA干扰技术建立稳定剔除SH2B1的肺腺癌细胞株LTEP-a-2,同时扩增同等滴度的空载病毒(GV-CMV)作对照。并用RT-PCR和WesternBlot方法检测转染效率,在此基础上采用细胞形态及核型分析、MTT法绘制细胞生长曲线、平板集落形成试验分析比较实验转染组、载体对照组细胞生长、凋亡的改变,对细胞的增殖能力进行鉴定;细胞划痕实验分析SH2B1对肺腺癌细胞株LTEP-a-2细胞爬行迁移运动的影响,用Trans-well实验分析SH2B1对肺腺癌细胞株LTEP-a-2细胞侵袭运动的影响。结果RNA干扰技术建立稳定剔除SH2B1的肺腺癌细胞株LTEP-a-2细胞SH2B1表达量明显下降。剔除SH2B1的肺腺癌细胞株LTEP-a-2细胞增殖显著下降(P<0.05)。划痕实验结果显示,实验转染组和载体对照组迁移细胞数目倒置显微镜下10个视野分别为349±121和867±187,实验转染组爬行细胞数目显著低于空载体组,P<0.05;Trans-well实验结果表明,实验转染组和载体对照组细胞透过滤膜的数目分别是129±88和278±107,实验转染组细胞穿过数目显著低于载体对照组,P<0.05。结论SH2B1促进肺腺癌细胞株LTEP-a-2细胞增殖和迁移运动能力。
简介:Ameshlessradialbasisfunction(RBF)collocationmethodbasedontheEringennonlocalelasticitytheoryisdevelopedtocalculatethebandstructuresofternaryandquaternarynanoscalemulti-layeredphononiccrystals(PNCs)withfunctionallygraded(FG)interlayers.Detailedcalculationsareperformedforanti-planetransversewavespropagatinginsuchPNCs.TheinfluencesofFGandhomogeneousinterlayers,componentnumber,nonlocalinterfaceimperfectionsandnanoscalesizeoncut-offfrequencyandbandstructuresareinvestigatedindetail.Numericalresultsshowthatthesefactorshavesignificanteffectsonbandstructuresatthemacroscopicandmicroscopicscales.
简介:【摘要】 目的:探讨不同浓度苦参碱对神经母细胞瘤(NB)SH-SY5Y细胞存活率及凋亡率的影响。方法:MTT法检测SH-SY5Y细胞存活率;FCM法检测细胞凋亡率,检测苦参碱与顺铂对NB细胞株SH-SY5Y存活率的影响。结果:除经ATRA 诱导的顺铂干预组外,各组存活率及凋亡率与对照组比较差异均有统计学意义(P<0.05);未经ATRA诱导的顺铂干预组存活率及凋亡率与经ATRA诱导的顺铂干预组比较差异有统计学意义(P<0.05);苦参碱0.5mg/mL组与经ATRA诱导的顺铂干预组比较,差异无统计学意义(P>0.05)。结论:苦参碱可以抑制神经母细胞瘤SH-SY5Y细胞系增殖、诱导凋亡,可以提高顺铂化疗的敏感性,在本实验范围内浓度越高,抑制增殖、诱导凋亡作用越明显。
简介:摘要目的探讨不同参数的重复磁刺激(rMS)对人神经母细胞瘤细胞系SH-SY5Y细胞生长和分化的影响。方法将不同频率、不同强度和不同脉冲数的rMS作用于体外培养的SH-SY5Y细胞,按照刺激强度设置最大输出强度的15%组、30%组、60%组,按照刺激频率设置0.5 Hz组、1 Hz组、5 Hz组、10 Hz组、20 Hz组,按照脉冲数设置每日800个脉冲组、1600个脉冲组,所有组均rMS干预4 d。应用四甲基偶氮唑盐比色法(MTT)检测细胞活力。采用神经毒素1-甲基-4-苯基吡啶离子(MPP+)诱导SH-SY5Y细胞凋亡,采用全反式维甲酸诱导SH-SY5Y细胞分化,用免疫组化方法观察神经元特异核蛋白表达及表征细胞分化程度。结果在rMS对SH-SY5Y细胞增殖的影响方面,0.5 Hz的rMS抑制SH-SY5Y细胞增殖,10 Hz的rMS促进SH-SY5Y细胞增殖。rMS频率为5 Hz时,最大输出强度15%组和30%组的细胞增殖表现为明显加快(P<0.05)。1600个脉冲组的刺激效果优于800个脉冲组的刺激效果,其中10 Hz的rMS对细胞增殖有明显促进作用(P<0.05)。在rMS对SH-SY5Y细胞凋亡的影响方面,在30%最大输出强度下,0.5 Hz组和10 Hz组细胞凋亡被抑制(P<0.05)。在rMS对SH-SY5Y细胞分化的影响方面,0.5 Hz和10 Hz的rMS均能促进SH-SY5Y细胞向神经元分化。结论rMS能影响SH-SY5Y细胞增殖,表现为低频抑制、高频促进,且影响程度会随着刺激脉冲数的增多而提高。rMS对MPP+诱导的SH-SY5Y细胞凋亡具有保护作用,并能促进全反式维甲酸诱导的SH-SY5Y细胞向神经元分化。
简介:摘要Ras-GTP酶激活蛋白SH3结构域结合蛋白1(Ras-GAP SH3 domain-binding protein,G3BP1)是RNA结合蛋白,通过调控mRNA稳定性和翻译来应对外界刺激,被认为是应激颗粒的成核因子之一。G3BP1在应激颗粒中的作用是目前研究的热点,但除此之外G3BP1在应激颗粒外与RNA的相互作用,调节基因表达的功能也不容忽视。G3BP1与肿瘤发生发展密切相关,包括肿瘤进展、侵袭和转移等。大量研究结果表明,G3BP1可能成为肿瘤治疗的新靶点。本文综述了G3BP1近年来在肿瘤生物学领域取得的重要进展,包括其在肿瘤进展、应激颗粒形成等方面的作用。