根据某深水桥梁小尺度圆柱形群桩基础施工现场的实测数据,建立承台-群桩-岩土层三维有限元模型,选取线性波理论和Morison方程计算由通航船只引发的波浪力,并在有限元软件中进行加载分析,得到了承台的水平位移时程曲线,在与监测数据对比验证了模型建立合理的基础上,分析了水中自由段桩身的桩端轴力与桩端剪力的变化规律、桩身弯矩的分布规律,及桩身变形特征.结果表明:在波浪力作用下,垂直于波浪传播方向的两排桩,其各项内力指标中,仅桩顶剪力相差较大,工程中需要对承台与桩基的连接予以重视;尽管不同排桩存在波浪的相位差,但各基桩的变形基本保持一致,主要表现为侧弯并沿波浪传播方向作周期性摆动.
与公路隧道相比,城市隧道车流量大,车速低,隧道内环境要求严格,交通量组成也有所不同.通过理论分析对这些因素进行了充分探讨,得出了正常运营工况,怠速及交通阻滞工况下的城市隧道自然通风适用长度,旨在为城市隧道通风方式的判别提供参考.
AIM: To investigate whether neural stem cell-derived exosomes promote the viability and inhibit the apoptosis of neurons under cobalt chloride(CoCl2)-induced hypoxia in vitro.METHODS:The exosomes were isolated based on ultracentrifugation.The exosomal markers,ALG-2-interacting protein X(Alix)and tumor susceptibility gene 101 (TSG101)were identified by Western blot.The shape of exosomes was observed under transmission electron microscope (TEM).The size distributions of exosomes were analyzed by nanoparticle analysis(qNano).The neurons were exposed in CoCl2at different doses(200~600 μmol/L)for 24 h.The exosomes were co-cultured with the neurons pre-treated with CoCl2.The viability and apoptosis of the neurons were measured by CCK-8 assay and TUNEL method.RESULTS: The exosomes released from the neural stem cells expressed exosomal markers Alix and TSG 101.They also displayed a cup-shaped appearance observed under TEM and their sizes were(95.0 ±23.5)nm(n=370).The neuronal viability was sig-nificantly inhibited by CoCl 2in a dose-dependent manner(P<0.05).After treatment with exosomes,the viability of the neuron pre-treated with CoCl2was increased and the apoptotic rate was decreased(P<0.05).CONCLUSION: Neural stem cell-derived exosomes promote the viability and inhibit the apoptosis of rat neurons uneder hypoxia.
提出了一种带朵纠倾掏土孔的既有建筑纠倾新方法,给出了带朵纠倾孔孔壁最大应力的近似计算公式,用数值计算方法验证了近似公式的适用性.新方法相对于传统圆形掏土孔方法能更好地实现建筑纠倾工程的精确可控、快速纠倾、避免过倾.当大孔半径与小朵孔半径之比在1~6范围时,纠倾效果较好.
Objective To investigate the effect of sevoflurane on neuron apoptosis administered after reaching restoration of spontaneous circulation (ROSC) during cardiopulmonary resuscitation (CPR) in rats.Methods The cardiac arrest model was established by ventricular fibrillation.Thirty male Wistar rats were assigned randomly into three groups.Six rats in the sham group were anesthetized and intubated without induction of cardiac arrest.12 rats in the Sevo group were exposed to 2.4% minimal alveolar concentration(1 MAC) of sevoflurane after reaching ROSC for 10 mins.12 rats in the control group received the standard CPR only.24 hours after ROSC,neuro-deficit scoring (NDS) was used to assess the neurological outcome.Then,all the rats were sacrificed with deep anesthesia,mitochondrial injury was observed by electron microscopy.TUNEL assay was used to count the apoptosis neurons ratio.Additionally,the level of Bcl-2,Bax,cytochrome C proteins expression were detected by Western blot.Cleaved caspase-3 expression was evaluated by immunohistochemical staining.Results There were no statistical difference in weight,heart beat,mean arterial pressure (MAP) among the three groups at the beginning of the experiment,and the CPR duration,defibrillation times,epinephrine dosage were not statistically significant between Sevo group and control group.NDS was higher in Sevo group than control group.Less alternation of the mitochondrial ultra-structure under sevoflurane treatment was revealed.The apoptosis neurons ration in Sevo group was markedly reduced [(12 ± 6) % vs.(22-± 8) %,P < 0.01].Furthermore,compared to control group,the ratio of Bcl-2/Baxwas higher in sevo group[(54± 11)% vs.(28 ±9)%,P<0.01],while the expression of cytochrome C,active Cleaved Caspase-3 were lower.Conclusion The administration of sevoflurane after ROSC can inhibit neuronal apoptosis,mitigate neurological function injury partly attributed to the modulation of Bcl-2/Bax expression.
目的:探讨应用甲泼尼龙琥珀酸钠联合无创正压通气(Non-invasive positive pressure ventilation,NPPV)治疗呼吸衰竭的临床研究.方法:选取本院2014年1月-2017年2月收治的急性呼吸衰竭患者98例,按照随机数字表法分为观察组与对照组,每组49例.两组均于入院后进行常规治疗,观察组在常规治疗基础上给予甲泼尼龙琥珀酸钠联合NPPV治疗.比较两组治疗前和治疗24 h收缩压、舒张压、心率、血pH、PaO2、PaCO2、呼吸困难改善时间和平均住院时间.结果:治疗24 h,两组收缩压和舒张压比较,差异均无统计学意义(P>0.05),观察组心率低于对照组(P<0.05);治疗24 h,两组血pH、PaO2水平均增加,而PaCO2水平降低(P<0.05);治疗24 h,观察组血pH、PaO2水平均高于对照组,而PaCO2水平低于对照组(P<0.05);观察组呼吸困难改善时间和平均住院时间均优于对照组(P<0.05).结论:甲泼尼龙琥珀酸钠联合NPPV治疗呼吸衰竭患者效果显著,具有重要研究意义.
目的:了解急诊观察区获得性肺炎(HAP)的发生率和细菌学特点,为急诊观察区HAP的防控提供依据.方法:查阅广西玉林市第一人民医院2015年1月1日-2015年12月30日期间急诊观察区(ED)、呼吸内科(RD)、外科重症监护室(SICU)、内科重症监护室(MICU)院内HAP患者的临床资料,重点关注痰培养、血培养及细菌学报告资料.由三名主治医师根据HAP的诊断标准对每一例患者临床资料进行汇总分析.结果:HAP的发生率急诊观察区显著高于呼吸科、SICU和MICU(P<0.05).急诊观察区细菌培养阳性率仅为6.2%,显著低于其它各科.观察区院内感染的前五位细菌分别为鲍曼不动杆菌(41.57%)、大肠埃希菌(20.22%)、金黄色葡萄球菌(13.48%)、肺炎克雷伯杆菌(8.99%)和铜绿假单泡菌(3.37%),且耐药菌的比例比较高.结论:急诊观察区HAP的发生率高,痰标本细菌培养阳性率低,ESBL和MRSA阳性菌的比例高,应加强对急诊观察区HAP的防控力度.
To investigate the primary neurons autophagy and apoptosis after Oxygen Glucose Deprivation/Re-oxygenation (OGD/R),and to explore the effect of mild hypothermia on autophagy and apoptosis,following methods were used:Primary neurons culture and OGD/R model was established;the neurons were divided into the normal temperature group (37 ℃) and the mild hypothermia group (MH,34 ℃);The cells viability were measured by CCK8;cell apoptosis were measured by TUNEL;The protein expressions of Sirt1,Foxo1,p53,Rab7 and autophagy related genes such as Beclin1,LC3 were detected by western blot at each time point;The neurons autophagy flows were detected through transfection of adenovirus mRFP-GFP-LC3.The primary neuron cultures were successfully developed,and the OGD/R models were established;Western-blot showed that the expressions of Sirt1,P-Foxo1,Rab7,Beclin1 and LC3b/LC3a were gradually reduced,especially at 12 h after OGD/R,P < 0.05;However,the expression of pS3 was increased,P < 0.05;In MH group,the expressions of Sirt1,P-Foxo1,Rab7,Beclin1,LC3b/LC3a were obviously higher than those in NT group,P < 0.05;And the expression of pS3 was obviously lower than that in NT group,P < O.05;in R6 h + MH group,the rate of neuron cells apoptosis were 20% ±6.7%,lower than 56.8% ±7.6% in R6 h + NT group,P <0.05;mRFP-GFP-LC3 adenovirus was transfected into primary neurons,the autophagy flow was detected by fluorescence microscopy.Compared with control group,the autolysosomes were reduced,but autophagosomes were increased after OGD/R,P <0.05;however,compared with NT group,the autophagosomes were reduced and the autolysosomes were increased in MH group,P < 0.05.In conclusion,mild hypothermia therapy could increase the expression of Sirt1,Foxo1,beclin1 and LC3b/LC3a,but decrease the expression of p53,so as to promote autophagy and reduce apoptosis.
AIM: To explore the effect and possible mechanism of type 2 innate lymphoid cell (ILC2) on the development of chronic renal failure (CRF).METHODS: The patients with chronic renal failure (n=36) in the Fist Affiliated Hospital of Sun Yat-sen University from March 2016 to December 2016 were selected, and 32 healthy persons in the same period were enrolled in the study for control.The proportion of ILC2 in the PBMC of CRF patients and healthy controls was detected by flow cytometry, IL-13 concentration in the plasma was measured by ELISA.The isolated PBMCs from the patients and healthy persons were divided into 3 groups (control group, cytokine group, intervention group) and cultured in vitro for 3 days, respespestively, then IL-13 concentration was measured by ELISA.The protein levels of phosphorylated signal transducers and activators of transcription 6 (p-STAT6) in the PBMC of healthy controls before stimulation and after stimulation for 15 min, 30 min, 1 h, 2 h were determined by Western blot.RESULTS: The proportion of ILC2 in the PBMC and the plasma IL-13 concentration of CRF patients was higher than that in the healthy controls (P<0.05).In the culture supernatant in vitro, IL-13 concentration in the 3 subgroups of CRF patients (control group, cytokine group, intervention group) were all higher than that in the healthy controls (P<0.05), both the 2 groups showed a trend that the active IL-13 concentration in cytokine group was higher than that in control group, and that in intervention group was lower than that in cytokine group.The protein levels of p-STAT6 in cytokine stimulated-PBMC with a time dependent manner.CONCLUSION: The percentage of ILC2 in the PBMC is elevated in CRF patients.Furthermore, the ILC2 secret large amount of IL-13 to mediate the polarization of Th2 cells to regulate immunity through activating p-STAT6.
Objective To investigate the effects of enhanced external counterpulsation (EECP)on nitric oxide system in serum in a dog model of cardiac arrest and return of spontaneous circulation (CA-ROSC).Methods Animal models of CA were inducedindogs with alternating current.After ROSC by cardiopulmonary resuscitation (CPR),16 dogs were randomized to either the EECP or control group (n =8 per group)in accordance with the random number table.Each dog of EECP group accepted 3-h EECP from ROSC 1 /4h.Venous serum was separatedat baseline before CA,at ROSC 1 /4h,ROSC 4h,and ROSC 96h, respectively.The serum concentrations of endothelial nitric oxide synthase (eNOS),neuronal nitric oxide synthase (nNOS),inducible nitric oxide synthase (iNOS)and nitric oxide (NO)of each dogs were measured by using enzyme linked immunosorbent assay (ELISA ).Results There was no significant difference in baselinevalues,those of CA modelestablished,serum nNOS between two groups (P >0.05).The mean values of serum NO and eNOSin the EECP groupwere higher than those in the control group at the two points of ROSC4h,96h (P <0.05 or P <0.01).The mean values of serum iNOS in the EECP groupwerelower than those in the control group at the two points of ROSC4h,96h (P <0.05 ).Conclusion EECP can increaseserum NO levelof CA-ROSC dogs,underlying mechanism of which relates to upregulation of serum eNOS and downregulation of serum iNOS.Therefore,EECP can ease the damage ofCA model.
目的:探讨流行性出血热合并急性胰腺炎的早期诊断与治疗方法.方法:报道以急性胰腺炎为首要表现的流行性出血热1例,并检索近年文献进行复习,总结流行性出血热合并急性胰腺炎的临床特点、诊断及治疗方法.结果:共检索到5篇流行性出血热合并胰腺炎的文献,共6例,所有患者均通过临床表现、实验室检查和影像学检查等手段而确诊.其中5例患者予以抑制胰液分泌、抗病毒等对症支持治疗,2例血透治疗,1例腹透治疗,1例患者剖腹探查手术治疗,所有患者均痊愈出院.本文报道病例早期予以抑制胰液分泌、抗感染和对症支持治疗,并行无创呼吸机辅助通气,连续进行CRRT治疗,患者痊愈出院.结论:流行性出血热以急性胰腺炎为首要表现者较少见,容易误诊,但该病进展迅速,预后凶险.临床表现、实验室检查和影像学资料是确诊的主要依据;采取早期抑制胰液分泌、呼吸支持和血液净化等综合治疗手段是治愈患者的关键.
AIM:To investigate the neuroprotective effect of hydrogen sulfide ( H2 S) after cardiopulmonary re-suscitation in rats with cardiac arrest ( CA) , and to explore the effects of H2 S on neuron autophagy.METHODS:The CA model was established through asphyxia.Male Wistar rats were randomly divided into sham group, model group and NaHS group.The levels of beclin-1 and LC3 II/I were measured by Western blot at 2 h, 4 h, 12 h and 24 h after the restoration of spontaneous circulation (ROSC).At 12 h after ROSC, the formation of autophagic vacuole with LC3 dots was deter-mined by immunohistochemical ( IHC) method.The phenomenon of neuron autophagy was observed under transmission electron microscope.The numbers of apoptotic neurons were counted by TUNEL staining at 72 h after ROSC.The neurolo-gic deficit score ( NDS) was used to evaluate the neurologic function after ROSC.RESULTS: The level of beclin-1 was gradually increased in model group, but it was increased and then gradually recovered in NaHS group ( P<0.05 ) .The conversion of LC3 II in the cerebral cortex was the same as beclin-1.The results of IHC showed that LC3-positive nuclei in model group were more than those in NaHS group ( P<0.05) .The number of autophagic vacuole in model group was more than that in NaHS group (P<0.05).The number of the TUNEL-positive cells in model group was more than that in NaHS group (P<0.05).The NDS of the animals in NaHS group after ROSC was lower than that in model group(P<0.05). CONCLUSION:H2 S inhibits neuronal autophagy, decreases apoptosis and improves neurologic function in CA rats after ROSC.
Objective:To observe the impact of therapeutic hypothermia on the apoptosis and autophagy of nerve cells after oxygen and glucose deprivation , thus to clarify the mechanism that therapeutic hypothermia play a protective role on neurons injury through regulating autophagy. Methods: Extraction of cerebral cortex neurons from SPF SD newborn (1d) rats, then to establishing oxygen and glucose deprivation (OGD/R) model. After OGD for 3h, the cell culture plates were put into 34 ℃ or 37 ℃ constant temperature incubator for 6 h or 12 h. Western blot detection of apoptosis protein P53 and protein involved in autophagy including LC3 Ⅱ/Ⅰ, Beclin1,Atg5 and Rab7 expression. The Tunel method was used to detect neuron apoptosis. Results: Primitive cultivation neurons from newborn rats were isolated,cultured and vaccinated in cell plates,sticked to wall well after 4 h. The original generation of neurons after OGD for 3h, were kept in 34℃or 37℃constant temperature incubator for 6 h or 12 h. In 37℃group,the expression of Rab7 gradually reduced, beclin1 expression decreased,LC3Ⅱ/Ⅰratio decreased,Atg5 expression decreased, and P53 protein expression increased significantly, all P<0.05.While the expressions of Rab7,Beclin1,Atg5 in 34℃group were higher than 37℃group, P<0.05. And P53 protein expression was lower than 37℃group, P<0.05. The neuron apoptosis rates were 56.8±3.6%in 37℃group higher than 20±6.7% in control, P < 0.05. Conclusions: The original generation of neurons after oxygen deprivation of oxygen and glucose, neurons autophagy is significantly reduced, apoptosis is increased. Mild hypothermia therapy can promote autophagy,reduce apoptosis.
Objective To evaluate the effect of extracorporeal cardiopulmonary resuscitation (ECPR) and conventional cardiopulmonary resuscitation (CCPR) on survival and neurological function in adult patients with cardiac arrest.Methods The PubMed and Web of Science were searched to collect relevant literature from Jan 1980 to Nov 2015,and two reviewers strictly distinguished the studies,assessed the quality of studies and picked up the valuable data for statistical analysis by using RevMan 5.0.Results A total of 8 studies involving 27 18 patients were included in our review.Of them,462 patients were treated with ECPR and 2 256 patients were cared with CCPR.The meta analysis showed that the survival discharge rate (OR =2.92,95% CI:2.24-3.81,P < 0.01),long-term survival rate (OR =2.97,95% CI:2.11-4.19,P<0.01) and neurological function status (OR=3.50,95%CI:2.36-5.81,P< 0.01) of ECPR (n =182) were better than those of CCPR (n =182).In 4 studies,propensity score matching was used to minimize bias and heterogeneity.The meta analysis also showed that the rate of ROSC,survival discharge rate,long-term survival rate and neurological function status in ECPR were superior over CCPR.Conclusions ECPR would be the excellent measures to improve ROSC rate,survival discharge rate,long-term survival rate and neurological outcome in adult victims with cardiac arrest.
Objective To explore the effects of estrogen on oxidative stress of the lung tissue induced by acute paraquat (PQ) poisoning. Methods Thirty-two male adult New Zealand rabbits were randomly divided into model group and estrogen intervention group, 16 rabbits in each group. The model of lung injury induced by PQ poisoning was reproduced by feeding 16 mg/kg of 20% PQ through gastric tube. The rabbits in estrogen intervention group received intravenous infusion of 5 mg/kg estrogen after PQ challenge for 7 days, and the rabbits in model group received an equal volume of normal saline. Three rabbits in each group were sacrificed at 1, 2 and 3 days respectively after exposure. The lung tissue was harvested, the levels of reactive oxygen species (ROS) was determined by 2',7'-dichlorofluorescin diacetate (DCFH-DA), malondialdehyde (MDA) was determined by thiobarbituric acid (TBA), the mRNA expression of manganese-containing superoxide dismutase (MnSOD) was determined by reverse transcription-polymerase chain reaction (RT-PCR), and adenosine triphosphatase (ATP) content in mitochondrion was determined by enzyme linked immunosorbent assay (ELISA). The pathological changes in lung were observed under light microscopy using hematoxylin and eosin (HE) staining, and the lung injury was evaluated with lung injury score. Results The contents of ROS and MDA in lung within 3 days after PQ poisoning were gradually increased, and MnSOD mRNA expression and ATP content were gradually decreased. Estrogen intervention could significantly reduce the production of ROS and MDA after PQ poisoning [3-day ROS (fluorescence intensity): 161.05±30.04 vs. 188.30±31.80, 3-day MDA (mmol/L): 98.71±0.92 vs. 122.12±1.24], up-regulate MnSOD mRNA expression (integral A value: 3.05±0.90 vs. 1.22±0.24), and increase ATP content in mitochondrion (ng/L: 3.75±0.92 vs. 2.28±0.29) with statistically significant differences (all P < 0.01). In lung tissue after PQ poisoning, congestion, edema, focal pulmonary consolidation, pulmonary interstitial and alveolar space were infiltrated by a large number of neutrophil, alveolar interval were thickened obviously and the above phenomenon were most serious at 3 days after poisoning as shown under optical microscope. Estrogen intervention could significantly improve lung injury as compared with that of model group, and the lung injury score at 3 days was significantly lower than that of model group (11.8±0.7 vs. 13.5±1.0, P < 0.01). Conclusions The oxidative stress indicators in the lung tissue after PQ poisoning were obviously abnormal, the pathological damage was serious with time dependence. The administration of estrogen can reduce acute lung injury after PQ poisoning by reducing the oxidative stress.
Objective To observe the concentration of myocardial glutamate changes after cardiopulmonary resuscitation ( CPR ) by the micro -infiltration techniques and its correlation with cardiac dysfunction.Methods Six adult New Zealand rabbits were implanted the micro-dialysis tubes in the cerebral cortex and myocardium to set up cardiac arrest models.When ventricular fibrillation for 5minutes and then restoration of spontaneous circulation (ROSC), we collected dialysate to detected the glutamate concentration, evaluated the left ventricular systolic function by ultrasound and the cerebral cortex and myocardial cell damage by electron microscopy.Results Before ventricular fibrillation, the concentration of glutamate in the cerebral cortex was (76.07 ±8.50)μmmol/L, but it rapidly increased to (107.70 ±7.17)μmmol/L 30 minutes after ROSC and peaked at (139.62 ±15.64)μmmol/L in 2 hours, then followed by a decline and decreased to ( 68.86 ±3.78 )μmmol/L in 3 hours.The concentration of glutamate in myocardium was (87.26 ±14.14)μmmol/L 30 minutes after ROSC, which was significantly increased compared with before ventricular fibrillation (40.33 ±5.39)μmmol/L ( P<0.001).The trend sustained for 1 hour and then declined gradually.After ROSC for 90 min, the concentration fell to ( 47.82 ±6.72 )μmmol/L.Sixty minutes after ROSC, the value of fractional shortening ( FS ) was ( 39.00 ±1.79 )%, left ventricular ejection fraction ( EF ) was ( 47.00 ± 3.90)%, which were both lower than the baseline of (44.83 ±3.25)%and (53.17 ±4.58)%( P=0.001 and 0.008), respcetively.Four hours after ROSC, we saw the mitochondria of rabbit cortex cells swelling obviously, mitochondria ridge blur or even disappear or blank, formation of apoptotic bodies around nuclear and no apoptotic body formation in myocardial cells. Conclusion After rabbit ventricular fibrillation for 6 min and then ROSC, high concentrations of glutamate may have some correlation with cardiac dysfunction.
The microstructure and inclusions in rare earth treated C-Mn steel were studied, the size distribution of the nuclei in-ducing acicular ferrite nucleation was subjected to statistical analysis, and the formation and growth processes of rare earth inclusions were discussed through quenching the treated samples at different temperatures. It is found that after a small amount of rare earth is added into the C-Mn steel, the inclusion composition changes from MnS ﹢ aluminosilicate to La2 O2 S ﹢ LaAlO3 ﹢ MnS ﹢ alumino-silicates, the inclusion size decreases, and the microstructure converts from martensite ﹢ bainite to ferrite side plate ﹢ acicular ferrite﹢ massive ferrite. The size of effective inclusions inducing acicular ferrite nucleation is mainly concentrated in 1-4μm in the rare earth treated C-Mn steel, they primarily form in liquid steel, but little in the cooling and solidification processes. The rare earth inclu-sions are easy to coalesce and grow up at molten temperature and in the cooling and solidification processes, and MnS can precipitate around the residual rare earth inclusion particles.
目的:了解患者对急诊就诊标准和急诊分诊的认知度,以及对改进分诊制度的意见,为进一步完善分诊系统提供依据。方法自制调查问卷,在某综合性三甲医院急诊室内对急诊患者进行随机抽样调查问卷。结果共发放230份问卷,有效回收率为96.1%。被调查者只有64.3%是因为突发急症来看急诊,53.4%对调查当日候诊时间表示满意,有49.3%认为分诊的主要依据是病情询问凭经验,39.8%表示同意给病情紧急的病人插队先看,有92.3%的被调查者赞成应该根据病情紧急程度不同分不同诊室不同次序就诊,而只有49.7%的被调查者认为分诊时开简单的化验检查可以提高就诊效率。结论相当一部分患者不了解急诊就诊的标准,对急诊分诊的认知度较低。
Objective:To explore the effect on the success rate of diagnosis and treatment of invasive fungal infections by MDRA score and the dynamic changes of PCT. Methods: The clinical data of 32 patients with fungal infection in ICU from Apr 2013 to Apr 2014 were retrospectively analyzed , and the American west virginia university school of medicine were used to establish the fungal infection risk factor scoring system (Multi - diseases Risk Assessment Program, MDRA) rating criteria. The value of MDRA score and the dynamic change of PCT in diagnosis and treatment of invasive fungal infections were observed. Results: The MDRA scores in the 32 cases were greater than 30 score and accorded with the standard of experiential therapy. The effective of antifungal therapy was in the cases with lower PCT value,and ineffective of antifungal treatment was in the cases with higher PCT value. Conclusion:It cannot dogmatic copy the MDRA score standard to diagnosis and treatment the invasive fungal infections,and combine with dynamic PCT level may improve the correct rate of the diagnosis and treatment.
[ ABSTRACT] AIM:To investigate the effects of induced pluripotent stem cells-derived mesenchymal stem cells ( iPSC-MSCs) on cobalt chloride ( CoCl2 )-induced injuries of PC12 cells and its possible mechanism.METHODS:PC12 cells were exposed to CoCl2 to set up a chemical-induced cellular injury model and were cocultured with iPSC-MSCs.The cell viability was tested by CCK-8 assay.The apoptosis was measured by flow cytometry using Annexin V/PI staining.The mitochondrial membrane potential (MMP) was analyzed by flow cytometry using JC-1 staining.Immunofluorescence was employed to observe mitochondrial transfer from iPSC-MSCs to PC12 cells.RESULTS: Apoptosis of PC12 cells was in-creased and MMP of PC12 cells was decreased after exposed to CoCl2 at concentration of 400μmol/L for 24 h.Coculture of PC12 cells with iPSC-MSCs reduced the apoptosis and recovered the MMP of the PC12 cells.Tunneling nanotubes were formed between iPSC-MSCs and PC12 cells, through which the iPSC-MSCs transferred the mitochondria to the PC12 cells. CONCLUSION:iPSC-MSCs protect PC12 cells from CoCl2-induced injuries, which may be associated with the mitochon-drial transfer from iPSC-MSCs to PC12 cells.