目的:探究过氧化物酶(peroxidase,PXDN)在卵巢癌中的功能和潜在的作用机制.方法:通过癌症基因组图谱(The Cancer Genome Atlas,TCGA)数据库和Kaplan-Meier Plotter数据库分析PXDN在卵巢癌组织中的表达情况,以及与患者预后的关系.采用免疫组织化学法检测79例浆液性卵巢癌及137例良性卵巢囊肿组织中PXDN的表达情况,并分析与临床病理参数的相关性.使用特异性针对PXDN基因的siRNA沉默卵巢癌SKOV3和OV15细胞中PXDN蛋白的表达,用CCK-8法、平板克隆形成实验、Transwell小室法和划痕愈合实验检测沉默PXDN基因表达对SKOV3和OV15细胞增殖和迁移功能的影响.采用特异性针对PXDN基因的shRNA沉默SKOV3细胞中PXDN蛋白的表达,再用转化生长因子β(transforming growth factor-β,TGF-β) (10 ng/mL)处理PXDN沉默后的SKOV3细胞;通过蛋白质印迹法检测上皮-间质转化相关标志物E-钙黏蛋白(E-cadherin)和纤维连接蛋白(fibronectin,FN)的表达水平以及TGF-β3信号通路中Snail1、Smad2、Smad3、Smad4以及磷酸化Smad2和Smad3蛋白的表达水平.结果:相较良性卵巢组织,卵巢癌组织中PXDN表达显著增高(P＜0.001),并且PXDN高表达与卵巢癌预后不良相关(P＜0.001).沉默PXDN表达可抑制卵巢癌细胞的增殖和迁移(P值均＜ 0.001).沉默PXDN表达后再用TGF-β处理SKOV3细胞,E-cadherin蛋白的表达水平明显上调,而FN蛋白的表达水平下调(P值均＜0.01),Smad2和Smad3的表达水平没有明显变化,Snail1、Smad4以及磷酸化Smad2和Smad3蛋白的表达水平均明显下调(P值均＜ 0.01),沉默PXDN表达可逆转TGF-β诱导的上皮-间质转化的发生.结论:PXDN可能通过TGF-β/Smad通路调控卵巢癌上皮-间质转化的发生.

目的 探讨微绒毛包涵体病(microvillus inclusion disease,MVID)患儿临床表型与基因型的关系,以提高对MVID的认识.方法 2017年4月,1例MVID患儿在南方医科大学珠江医院新生儿科住院治疗,2017年6月采用二代测序法对患儿及其父母进行基因测序,采用一代测序方法对患儿胞兄进行定点突变检测.回顾性分析患儿临床表现、治疗、预后及家系基因测序结果.结果 患儿女,胎儿期提示肠管扩张,生后第2天开始出现腹泻,为黄绿色黏液样便,合并多种电解质紊乱及代谢性酸中毒.基因测序结果显示,患儿STX3基因无义突变,突变位点为c.424C>T和c.739C>T,分别遗传自表型正常的父母.患儿胞兄8岁,表型正常,测序结果显示有STX3基因的1个杂合突变,位点为c.424C>T(p.R142),突变来源于表型正常的母亲.该突变为国内首次报道.结论 STX3基因分析有助于微绒毛包涵体病的诊断.

目的 研究围绝经期女性骨量下降现况,揭示骨量下降的饮食相关因素.方法 因腰部酸痛就诊的围绝经期女性共计385例.使用双能X线骨密度仪测定骨密度.采用自行设计的问卷进行饮食因素等方面的资料收集.应用x2检验、秩和检验和多因素logistic回归进行资料分析.结果 围绝经期女性总的骨量下降发生率为40.4％(骨量减少和骨质疏松发生率分别为26.1％和14.3％),且随年龄增长呈现逐渐升高的趋势(P<0.001).饮食因素中,乳制品和红茶可能是保护因素,而腌熏食物可能是危险因素.结论 围绝经期女性存在随年龄增长而发生的骨量下降,且与饮食因素密切相关.在健康宣传中,应提倡围绝经期女性早期食用乳制品,适当饮用红茶,减少腌熏饮食,从而延缓骨量下降,预防骨质疏松性骨折发生.

目的 探讨婴幼儿Kasabach-Merritt综合征(Kasabach-Merritt syndrome,KMS)的临床特征及治疗方法,为临床提供参考.方法 2013年1月至2016年12月,南方医科大学珠江医院儿科中心共收治8例婴幼儿KMS患儿.采用回顾性分析的方法,记录8例患儿的病史、临床表现、辅助检查结果、治疗方案及疗效等相关资料,并随访患儿预后.结果 8例患儿中,血管瘤分布分别为:颌下3例,下肢2例,内脏器官3例(肝脏、胰腺和肠系膜各1例).6例患儿经药物综合治疗(糖皮质激素、α-2b干扰素、雷帕霉素和长春新碱等单药或联合治疗)后,瘤体缩小变软、颜色变淡,其中肠系膜和胰腺血管瘤患儿在药物治疗前分别因危及生命的瘤体内大出血和器官压迫接受缩瘤手术.血小板完全恢复正常的时间为4～30天,凝血功能完全恢复正常的时间为2～50天,瘤体完全消失的时间为1～2年.2例患儿因经济原因放弃治疗后死亡.存活的6例患儿随诊2年均治愈,身高、体重和器官功能均良好.结论 婴幼儿KMS病情危重、进展迅速,糖皮质激素、长春新碱和雷帕霉素等联合治疗可快速控制出血症状,改善预后.对于发生危及生命的大出血、巨大血管瘤压迫重要器官的患儿,可考虑手术治疗以快速减少瘤体面积从而缓解出血.

1临床资料 患儿,男,2天,因“气促1天”于2017-06-11由广州市某妇幼保健院转入我院.患儿系G2P1,胎龄41周.患儿母亲孕早期无特殊用药史及特殊疾病史,孕期定期在外院产检未见明显异常.于2017年06月07日发现胎动减少,外院胎监提示异常,因“可疑宫内窘迫”于2017-06-09在广州市某妇幼保健院经剖腹产出生,出生时否认窒息抢救史,Apgar评分均为10分,羊水Ⅰ度污染,胎盘未见异常,脐带无绕颈,体重2.82kg.生后2小时反复出现低血糖,波动在1.8-2.9mmol/L,予开奶及静脉补糖下血糖可维持正常.2017-06-11患儿出现低热,热峰37.8℃,伴气促、发绀,经吸氧后症状可缓解.家属为求进一步治疗遂转入我科.

目的 分析2例Wiskott-Aldrich综合征(Wiskott-Aldrich syndrome,WAS)患儿的临床资料和基因测序结果,探讨其诊治方法,以提高对本病的认识.方法 对南方医科大学附属珠江医收治的2例WAS患儿的临床特点、实验室检查结果、治疗经过进行回顾性分析.利用Sanger测序方法检测患儿及其部分家庭成员的WAS基因,分析其家系特征.结果 2例患儿分别于2月龄和1月龄起病,以皮肤瘀点瘀斑、血便及湿疹起病,多次发生呼吸道及消化道感染.血常规提示血小板减少、血小板体积小;免疫功能检测提示IgG、IgM及IgA水平正常或减低、CD4+/CD8+T细胞比值升高;骨髓形态学提示巨核细胞成熟障碍.其中1例淋巴细胞扫描电镜示细胞表面绒毛消失、呈皱折状.WAS基因测序分析:病例1患儿为c.IVS3-7T>G,其母亲和姐姐为携带者;病例2患儿为c.1057_1058delAC(p.P341fsX493),其母亲及二姐为携带者,其大姐及表姐基因检测结果正常.两例患儿在确诊WAS前均误诊为免疫性血小板减少症,并反复使用糖皮质激素治疗,效果不佳.确诊WAS后给予定期输注人免疫球蛋白支持治疗,其中病例2患儿行异基因造血干细胞移植术(HSCT).分别随访至患儿9岁7个月、7岁10个月,两例患儿均存活,病例1患儿随访期间发生EB病毒感染及多次溶血性贫血,病例2患儿无病生存.结论 对于出生后早期罹患血小板减少伴湿疹和感染,且激素和IVIG治疗效果不佳的男性患儿,需要警惕患WAS的可能.基因检测是确诊WAS的金标准.定期免疫球蛋白输注是重要的支持治疗手段.HSCT是目前有效的治疗手段.

早期婴儿型癫痫性脑病(early infantile epileptic encephalopathy,EIEE)是指 1 组在婴幼儿期起病的难治性癫痫,由于频繁的癫痫发作或发作间期癫痫样放电可导致严重认知和行为障碍,同时基因突变本身也可导致患儿精神运动发育迟缓[1].迄今为止,已发现 57 个基因与 EIEE 有关(http://www. omim.org/),见 表 1. 其 中 包 括 STXBP1、SCN8A、SLC25A22、KCNT1、KCNQ2、CDKL5、ST3GAL3、SCN1A 和 TBC1D24 等基因,覆盖神经元离子通道、神经递质合成释放、膜受体、转运蛋白、细胞代谢、以及神经元前体细胞增殖、迁移、分化、突触发生和修剪等多个方面[2].目前研究最多的是离子通道类基因和神经递质受体类基因.最常见的癫痫脑病是 Ohtahara 综合征、West 综合征、Lennox-Gastaut 综 合 征、Dravet 综 合 征、早 期 肌 阵 挛 脑病 等[3]. 已有报道表明,ARX、CDKL5、MAGI2、SCN1A 和 MC4R 等基因可致 West 综合征[4];Na+通道基因(如 SCN1A、SCN2A、SCN8A 等)及其他基因(如 PCDH19、GABRG2、CHD2 等)可致 Dravet 综合征[5].现就 EIEE 最新基因研究进行综述.

Objectives To explore the calcium signaling mechanism of STIM1 in breast cancer cells. Meth-ods After SiRNA interruption, Western blot and Transwell were used to measure protein expression of STIM1 and cell migration in MDA-MB-231 cells respectively. The relationship between STIM1 and SOCE calcium signaling were analysed by Laser confocal microscopy. Western blots were used to measure protein expression of FAK after si-lence STIM1. Results The numbers of cells without STIM1 were significantly lower than those cells with STIM1 by Transwell assay. STIM1 mediated SOCE in MDA-MB-231. Blocking SOCE might inhibite cells migration. Si-lence STIM1 did not affect the expression or activation of FAK in MDA-MB-231 cells. Conclusion STIM1 influ-ences cell migration through SOCE pathway in breast cancer cells, which is independent on the expression or activa-tion of FAK.

Objective To examine the effects of p38 mitogen-activated protein kinase (MAPK) inhibitor on the behavioral response to zebrafish larvae after hypoxia/reoxygenation brain injury and to identify whether the protective effect is mediated by inhibiting apoptosis and protein,and mRNA related to apoptosis.Methods The 5-day post-fertilization zebrafish larvae were randomly assigned to 3 groups:control group,model group and intervention group.Fishes in the intervention group were separated into 3 subgroups according to p38 MAPK inhibitor concentration (5,10,20 μmol/L).The activity levels of the larvae were analyzed by using quantization mode of ZebraLab software,swimming distance and moving speed were recorded.Terminal transferase dUTP nick end labeling (TUNEL) assays of brain assays were performed.The protein levels of phosphorylation of p38 MAPK,apoptosis related proteins of B-cell lymphoma-2 (Bcl-2),Bcl-2 associated X protein(Bax) and Caspase-3 were determined by Western blot.The mRNA expressions of Bcl-2,Bax,and caspase-3 were also analyzed by reverse transcription-quantitative PCR (RT-qPCR).Results The activity movement analysis of the intervention group 2 and 3 demonstrated a significantly increase in the swimming distance compared with the model group(P ＜ 0.05).After irradiation under strong light,all groups showed dramatically increasing in the moving speed.After removal of strong light,a significant decrease in moving speed was found in the control group and intervention group 2 and intervention group 3.The TUNEL assay showed that apoptosis index decreased in the intervention group (21.7 ±2.0,12.8 ± 1.9,17.7 ±2.6) compared with model group (46.8 ±5.3) (all P ＜0.01).Western blot assays demonstrated a significant increase protein level of phosphorylation of p38 MAPK after hypoxia and reoxygenation,and the inhibitor reduced the p-p38 MAPK expression.Compared with the model group,p38 MAPK inhibitor increased the protein and mRNA expression level of Bcl-2,whereas reduced the Bax and caspase-3 expression in the brain.Conclusions Under the influences of p38 MAPK inhibitor,zebrafish larvae improved the behavioral changes after hypoxia-induced brain injury.The inhibitor (10 μmol/L) optimally reduces hypoxia-induced apoptosis in brain by up-regulating Bcl-2,down-regulating Bax/caspase-3 protein and their mRNA level.

Objective To investigate the expression of endoplasmic reticulum stress - related factors, glucose - regulated protein 78(GRP78)and growth arrest and DNA damage - inducible protein 34( GADD34)and neuronal apoptosis in the brain of zebrafish larvae after hypoxia/ reoxygenation brain injury,and the neuroprotective role of Taurine. Methods The 5 day post - fertilization zebrafish larvae were randomly assigned to 3 groups:control group, hypoxia/ reoxygenation model group(model group)and Taurine treatment group(Taurine group). According to the dif-ferent time points for observation,each group was subdivided into 5 subgroups(1 h,3 h,6 h,24 h,48 h)with 100 ze-brafish larvae each. The pathological changes in the brain tissues and cell apoptosis were detected by fluorescence ter-minal deoxynucleotidyltransferase - mediated dUTP nick end - labeling( TUNEL). The expression of GRP78 and GADD34 mRNA in the brain of zebrafish larvae were detected by real - time quantitative reverse transcription PCR (qRT - PCR). The changes in GRP78 and GADD34 protein were detected by Western blot. Results (1)TUNEL:apoptosis index(AI)was increased after hypoxia/ reoxygenation,and reached the peak at 3 h in model group,the AI in Taurine group was decreased compared with that in the model group at the same time point(1 h:22. 83 ± 1. 80 vs 30. 18 ± 1. 81,3 h:23. 22 ± 2. 46 vs 42. 97 ± 4. 01,6 h:16. 80 ± 1. 69 vs 22. 97 ± 1. 91,all P ﹤ 0. 05).(2)qRT -PCR:the expression of GRP78 and GADD34 mRNA was increased at 1 h after hypoxia/ reoxygenation,and reached the peak at 3 h in the model group,the expression in Taurine group was decreased compared with that in the model group at the same time point(GRP78 mRNA:1 h:2. 35 ± 0. 13 vs 5. 36 ± 0. 35,3 h:3. 08 ± 0. 33 vs 4. 27 ± 0. 52,6 h:1. 57 ± 0. 12 vs 3. 00 ± 0. 13,all P ﹤ 0. 05;GADD34 mRNA:1 h:5. 14 ± 0. 55 vs 7. 45 ± 0. 67,3 h:2. 79 ± 0. 58 vs 5. 83 ± 0. 51,6 h:1. 79 ± 0. 22 vs 3. 67 ± 0. 30,all P ﹤ 0. 05).(3)Western blot:the expression of GRP78 and GADD34 pro-tein was increased at 1 h,reached the peak at 6 h,but it was decreased in Taurine group(GRP78 protein:1 h:1. 12 ± 0. 11 vs 1. 37 ± 0. 13,3 h:0. 79 ± 0. 11 vs 1. 25 ± 0. 10,6 h:0. 55 ± 0. 10 vs 1. 52 ± 0. 14,all P ﹤ 0. 05;GADD34 pro-tein:1 h:0. 92 ± 0. 11 vs 1. 11 ± 0. 13,3 h:0. 96 ± 0. 11 vs 1. 52 ± 0. 09,6 h:0. 76 ± 0. 05 vs 1. 89 ± 0. 06,all P ﹤0. 05).(4)The expression of GRP78 and GADD34 protein was positively correlated with AI in the model group(r =0. 53,0. 56 respectively,all P ﹤ 0. 05). Conclusion One of neuroprotective mechanisms of Taurine against hypoxia/reoxygenation brain injury may down - regulate GRP78 and GADD34 expression.

目的:总结婴幼儿公民逝世后器官捐赠(DCD)来源单侧供肾成人肾移植的临床效果.方法:回顾分析26例婴幼儿DCD供肾用于成人单侧肾移植的临床资料.分析受者术后血肌酐、表皮生长因子受体(eGFR)、移植肾长径的变化情况;1年内人/肾存活率;术后并发症等.结果:婴幼儿供者年龄为8个月~5岁,并获取的26个肾脏均以单肾移植入成人受者体内,术后1年内eGFR由(27.80±15.27)[mL/(min·1.73 m2)]增高至(67.76±10.48)[mL/(min·1.73 m2)];术后1年内肾脏长径由(7.52±0.39)cm增长至(11.17±1.12)cm;术后1年人/肾存活率为100%/92.3%.发生移植肾功能恢复延迟(DGF)5例(19.23%);术后发生移植肾动脉瘤1例(3.85%),予介入动脉扩张和支架植入治疗无效予以切除肾脏;尿漏1例(3.85%),保守治疗无效予开腹探查并放置双J管后治愈;肺部感染4例(15.38%),1例为细菌感染,予抗感染治疗后好转,3例为真菌感染,但未需行呼吸机辅助治疗,均予抗真菌治疗后好转;其余受者至今未见明显异常.结论:婴幼儿是DCD的重要潜在捐赠者,通过严格维护供体及器官的质量,结合良好的手术技巧与完善的术后管理等,是可以实现婴幼儿供肾成人单肾移植的.

Objective To explore the effect of docosahexaenoic acid (DHA) on long-term learning and memory disorders and potential mechanism in rats after hypoxic ischemic brain damage. Methods Sixty neonatal 7-day-old SD rats were ramdonly divided into three groups: group S (sham operation+vehicle treatment), group C (hypoxic-ischemic brain damage [HIBD]+vehicle treatment) and group D (HIBD+DHA treatment). After left common carotid artery was isolated and ligated for 2.5 h, rats of group C and group D were put into a condition which oxygen concentration was about 8%for 2 h;rats in the group S were only isolated the left carotid artery, without ligation or hypoxia treatment;rats in the group D were intraperitoneally injected DHA of 15 mg/kg after modeling, and rats in the group S and group C were intraperitoneally injected equivalent volume of vehcle, once a day for 10 consecutive days. The pathomorphology changes of the hypocampal CA1 area, and marginal division of striatum were observed by Nissl staining 48 h after modling; the apoptosis cells were measured by TUNEL;immunohistochemical method was used to detect the expressions of Bax and Caspase-3 positive cells in the two brain areas. Morris water maza test was used to evaluate the long-term lerning and momory functions of 2-month-old rats, and the expressions of N-methyl-D-aspartate receptor 1 (NMDAR1)&nbsp;positive cells were detected by immunohistochemical method. Results The pathomorphology damage was significantly improved, the expressions of Bax and Caspase-3 positive cells and the neuron apoptosis in hypocampal CA1 areas and marginal division of striatum in group D were all signficantly decreased as compared with those in the group C (P<0.05). Rats in group D had significantly decreased escape latency as compared with those in group C in Morris water maze test (P<0.05), and the expression of NMDAR1 positive cells in the two brain areas of group D was significantly increased as compared with that in the group C (P<0.05). Conclusion DHA has the ameliorative effect on long-term learning and memory disorders after hypoxic ischemic brain damage in rats, which may be associated with inhibitory action of cell apoptosis at early phase and up-regulation of expression of NMDA1 at the late phase.

Docosahexaenoic acid( DHA) is a n-3 polyunsaturated fatty acid which were mainly found in fish oil supplements and algae. In human, DHA mainly exists in the brain, it plays an important role in nervous system and shows potential clinical application value. This article reviewed the influence of DHA on regulating neurotransmitter pathways,synaptic transmission and signal transduction,to give references for further clinical application of DHA.

ObjectivesTo investigate the expression of glucose regulated protein 78 (GRP78), CCAAT/enhancer binding protein homologous protein (CHOP) and cysteine asparate protease-12 (caspase-12) and neuronal apoptosis in the brain of zebraifsh larvae after hypoxia reperfusion, and the neuroprotective effect of taurine.Methods Five day old post-fertilization zebraifsh larvae were randomly assigned into 3 groups, control group, hypoxia reperfusion group (model group) and taurine group, and the taurine group was further divided into 3 subgroups according to different concentrations (1 mmol/L, 5 mmol/L, 10 mmol/L) with 100 zebraifsh larvae each. The behavior, recovery time and median survival time of those zebraifsh larvae after hypoxia with 1h reperfusion were observed and recorded. The pathological changes and apoptosis of neurons were detected by Nissl staining and terminal deoxynucleotidyltransferase-mediated dUTP nick end-labeling. The expression of GRP78, CHOP and caspase-12 in the brain of zebrafish larvae were detected by Western blot.Results Compared with the model group, the recovery time was shortened, the median survival time was extended, the Nissl stained neurons was increased and the apoptotic neurons were decreased in the taurine groups. GRP78, CHOP and caspase-12 were expressed in model group and taurine group. The expression of GRP78, CHOP and caspase-12 was much lower in taurine group than in model group.Conclusions Hypoxia reperfusion may induce endoplasmic reticulum stress and taurine may be neuroprotective against hypoxia reperfusion by down-regulating GRP78, CHOP and caspase-12.

Many factors,especially perinatal asphyxia,can lead to varying degrees of hypoxia brain injury in fetus or newborns within perinatal period.So far,the mechanisms of neonatal cerebral damage caused by hypoxia during the perinatal period have not been clearly demonstrated,and there have no effective drugs or therapeutic methods to improve hypoxia-induced cerebral damage.This review focuses on the recent progress of zebrafish as a model organism of using in research of hypoxia brain injury,including the anatomic and behavior basis,model making,research strategies and the advantages of neurotrophic drug screening.The application of zebrish in the research of neonatal hypoxic brain injury is promising,and may provide a new tool as research in finding out the therapy strategies of hypoxic-ischemic encephalopathy.

新生儿缺血缺氧性脑病(hypoxic-ischemic encephalopathy,HIE)是新生儿在生后短期内诊断出的由于脑内供血供氧不足导致的缺氧缺血性脑损伤.在发达国家,HIE在足月儿中的发病率约为1.5/1000[1],其中15％～ 20％在新生儿期死亡,存活者25％～30％可能留有远期神经发育后遗症,严重威胁新生儿的生命及健康,给家庭和社会造成巨大的负担[2].

在过去的40年里,因为技术和设备精密程度的进步,对液体和血流控制精密性提高,持续肾替代疗法(continuous renal replacement therapy,CRRT)已经成为儿童急性肾损伤(acute kidney injury,AKI)的重要治疗方法[1-2].与传统透析方法相比,CRRT用于危重和情况不稳定患儿时,可靠性更高,更易于操作,清除细胞外溶质和液体功能更稳定,效率更高.由于CRRT清除溶质和调节细胞外液体量是缓慢持续的,这对难以耐受液体量和溶质浓度突然改变的危重症患儿更有利.CRRT已经成为危重症合并AKI患儿治疗的优选治疗模式.当然,目前的CRRT技术是在成人实践的基础上发展起来的,儿童与成人CRRT还是有重要区别的,例如因为血液总量的缘故,小婴儿尤其是体重＜3.0kg的新生儿,CRRT通常需要预充全血;根据体重改变参数;用于儿童特有疾病如先天性遗传代谢病.本文对CRRT原理不再赘述,就近年来与儿童使用CRRT相关的一些问题进行综述.

Objective To establish a model of HIF1α and VEGF over-expression in glioma cells. Methods By MTT and fluorescence microscope, effects of hypoxia (1% O2) on proliferation and apoptosis were investigated in U87 cells. Western blot was used to detect HIF1α expression after hypoxia. By real-time RT-PCR and ELISA, VEGF mRNA and protein secretion were detected respectively. Results Hoechst staining showed that hypoxia for 24 h or 48 h did not cause cell apoptosis. Hypoxia for 24 h slightly inhibited cell proliferation (decrease by 3.23%, P <0.01) and for 48 h inhibited cell proliferation by 22.53% (P <0.001). Hypoxia for 2 h and 4 h increased expression of HIF-1α (P <0.01). VEGF was substantially induced by hypoxia for 10 h (P <0.01). Meanwhile, VEGF protein secretion was found to increase after hypoxia for 24 h (P <0.01). Conclusions 1%O2 simulates hypoxic microenvironment in glioma and induces over-expression of HIF1α and VEGF.

Objective To investigate whether TRPC1 was involved in VEGF expression induced by hypoxia in U87 MG cells.Methods RT-PCR and calcium image technique were used to observe the TRPC subtypes existed in U87 cells.RNAi,real-time RT-PCR,western blot and ELISA technique were used to observe effects of TRPC1 on hypoxia-induced VEGF gene expression and secretion.Results TRPC1,TRPC3,TRPC4 and TRPC5 were found expressed in U87 cell.Calcium concentration of U-87 cells was increased by OAG(agonist of TRPC),OAG-induced calcium concentration rise was attenuated by 2-APB(antagonist of TRPC).TRPC1 mRNA were reduced to 64%,39% and 36% respectively by the chemical synthesis of siRNA-1,siRNA-2,siRNA-3(P < 0.01);TRPC1 protein were reduced to 48%,29%,33% respectively by the chemical synthesis of siRNA-1,siRNA-2,siRNA-3(P < 0.01).Hypoxia enhanced VEGF gene up-regulation was restrained by siRNA-2 and siRNA-3(P < 0.01);VEGF gene expression in Hypoxia U87 cell was restrained too(P < 0.01).Conclusion U87 glioma cells express the functional TRPC channels;TRPC1 participates the VEGF expression induced by hypoxia.

人类血红蛋白在个体发育不同阶段有种类和数量上的变化,这些变化使红细胞功能得以很好地适应各时期的生理需要.珠蛋白肽链编码基因的选择性表达决定血红蛋白合成的种类和数量.