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| 1 | 体外缺氧诱导子痫前期滋养细胞模型优化及代谢组学鉴定显示文摘目的:探讨滋养细胞体外缺氧不同处理方法模拟子痫前期模型的优化研究。方法:HTR8/SVneo滋养细胞分别在1%O2(缺氧环境)和21%O2(常氧环境)培养箱中培养1 h(记为H1、N1)或2 h(记为H2、N2),缺氧1 h后复氧1 h(记为H1R1)和缺氧2 h后复氧2 h(记为H2R2),H1R1后再缺氧1 h(记为H1R1H1),H2R2后再缺氧2 h(记为H2R2H2),H1R12个循环(记为H1R1H1R1)和H2R22个循环(记为H2R2H2R2),缺氧2 h后复氧6 h(记为H2R6),持续缺氧24 h,以及持续常氧4 h(记为N4)、8 h(记为N8)和24 h(记为Normoxia),然后提取蛋白以Western blot检测腺苷酸活化蛋白激酶(AMP-activated protein kinase,AMPK)磷酸化水平,以验证各组处理对于诱导滋养细胞能量应激的效果;HTR8/SVneo滋养细胞在常氧或者缺氧环境培养24 h后经气相质谱技术(gas chromatography mass spectrum,GS-MS)进行细胞代谢组学分析,以验证AMPK磷酸化水平上调是否与滋养细胞代谢组变化具有一致性。结果:缺氧组AMPK的活性(1.615±0.111)明显高于常氧组(1.000±0.107)和缺氧复氧组(1.277±0.113);缺氧时显著增加的代谢物有4-甲基-2-戊酮酸(log22.597为1.377)、水合乙醛酸(log22.483为1.312)、组氨酸(log21.188为0.248)、苯丙氨酸(log21.262为0.335)、缬氨酸(log21.518为0.602)、正亮氨酸(log21.519为0.603)、乙酰丝氨酸(log21.691为0.758)、丝氨酸(log21.783为0.834)、半胱氨酸(log21.851为0.889)、蛋氨酸(log22.072为1.051)、鸟氨酸(log22.251为1.170)等;而棕榈反油酸(log20.127为-2.983)、11,14,17-廿碳三烯酸(log20.334为-1.583)、二十四单烯酸(log20.600为-0.738)、共轭亚油酸(log20.680为-0.557)、顺式十八碳烯酸(log20.711为-0.492)、9-十七碳烯酸(log20.782为-0.355)、二十二碳六烯酸(log20.829为-0.271)、二十碳五烯酸(log20.841为-0.250)、芥酸(log20.844为-0.244)、二十二碳五烯酸(log20.898为-0.156)、柠檬酸(log20.279为-1.842)、苹果酸(log20.208为-2.264)、琥珀酸(log20.254为-1.980)、顺乌头酸(log20.260为-1.946)、β-柠檬酸-左旋谷氨酸(log20.093为-3.430)、β-丙氨酸(log20.139为-2.851)、胱硫醚(log20.267为-1.904)、顺式-4-羟脯氨酸(log20.500为-1.000)等在缺氧时显著降低。代谢途径结果分析显示缺氧时滋养细胞中核苷酸代谢[log2(1.811、1.149)分别为0.857、0.201]、能量代谢[log2(1.510、1.173、1.149)分别为0.595、0.230、0.201]、维生素代谢[log2(1.045、1.052、1.125)分别为0.064、0.073、0.170]、氨基酸代谢[log2(1.245、1.020、1.027、1.123、1.127、1.076)分别为0.316、0.028、0.039、0.167、0.173、0.106]、信号转导(log21.046为0.065)、蛋白翻译(log21.026为0.037)等途径被激活,而碳水化合物[log2(0.857、0.857、0.799)分别为-0.222、-0.222、-0.323]、脂肪酸[log2(0.944、0.912、0.826)分别为-0.083、-0.133、-0.276]、内分泌代谢[log2(0.885、0.799、0.799)分别为-0.176、-0.323、-0.323]和其他第二代谢物生物合成[log2(0.947、0.871、0.743)分别为-0.079、-0.199、-0.428]等代谢途径显著受到抑制。结论:单纯缺氧模型更适合用于子痫前期病理生理机制的体外研究。 | 杨晓涛 韩顶立 Philip N.Baker 漆洪波 童超 杨竹 | 2017 | 重庆医科大学学报2017，42，8： | 10 |
| 2 | 慢性砷暴露对小鼠脑和血清代谢组学的影响显示文摘目的观察慢性砷暴露对小鼠皮层及血清代谢组学的影响,探讨其神经毒性机制。方法将12只C57BL/6J三周龄雄鼠,按体质量随机分为2组,暴露组饮用含50 mg/L亚砷酸钠水12周,对照组饮用蒸馏水。暴露结束后,采用氢化物发生一原子荧光光谱法测定脑砷含量;气相色谱/质谱联用法(GC/MS)对砷暴露组和对照组小鼠皮层和血清进行代谢组学研究,运用主成分分析法(PCA)分析比较两组代谢产物的差异,两样本t检验筛选两组间差异性代谢产物,利用代谢途径在线分析工具查找其影响的相关代谢途径。结果砷暴露组脑砷含量高于对照组,差异具有统计学意义(P<0.05);砷暴露组大脑皮层中苯丙氨酸、酪氨酸、组氨酸、赖氨酸和柠檬酸含量升高,血清中丝氨酸、甘氨酸、脯氨酸、天门冬氨酸及谷氨酸含量升高,而α-酮戊二酸含量下降。PCA分析显示暴露组与对照组小鼠皮层和血清代谢特征存在差异,差异具有统计学意义(P<0.05)。结论慢性砷暴露可通过干扰皮层和血清氨基酸类代谢和三羧酸循环,导致神经递质合成障碍以及干扰能量代谢而影响中枢神经系统功能。 | 代华 夏茵茵 Ting-Li Han Philip N.Baker 唐旭 张瑞源 杜航 蔡同建 程淑群 | 2016 | 南方医科大学学报2016，36，9： | 6 |
| 3 | 妊娠糖尿病抑制胎盘AKT-mTOR及SIRT1信号通路显示文摘目的:探讨AKT-mTOR信号通路与SIRT1在妊娠期糖尿病(gestational diabetes mellitus,GDM)编程胎儿生长发育中的作用。方法:收集重庆医科大学附属第一医院2014年12月至2015年6月分娩的15例GDM和15例正常产妇的胎盘组织,应用Western blot检测胎盘中AKT-mTOR磷酸化水平与SIRT1的表达水平。以人绒毛外滋养细胞(HTR8/SVneo)体外培养,分为空白对照组、渗透对照组和高糖组。各组处理后使用Western blot检测AKT-mTOR总蛋白和磷酸化水平,以及SIRT1的表达水平,应用流式细胞术(flow cytometry)检测各组的凋亡率。db/+杂合雌鼠妊娠至18.5 d处死后,取其胎盘组织,对其进行基因型鉴定后,选取野生型子代胎盘为GDM组,C57雌鼠胎盘组织为正常对照组,每组各6只。然后应用Western blot检测胎盘组织中AKT-mTOR信号通路。结果:AKT及其下游mTOR磷酸化水平在GDM胎盘中的表达明显低于正常胎盘(0.347±0.031 vs.1.000±0.175,P=0.004;0.465±0.045 vs.1.000±0.098,P=0.000)。同样,GDM组的SIRT1的表达水平也明显低于正常组(0.682±0.055 vs.1.000±0.127,P=0.044);在细胞模型中,经高糖处理后,AKT-mTOR磷酸化水平明显降低(0.512±0.056 vs.1.103±0.111,P=0.023;0.262±0.091 vs.1.153±0.057,P=0.001),而SIRT1的表达同样明显降低(0.472±0.034 vs.1.013±0.098,P=0.040)。高糖组的细胞凋亡率明显升高(14.550±1.624 vs.9.547±0.685,P=0.032)。在动物模型中,GDM组的AKT-mTOR磷酸化水平明显降低(0.527±0.080 vs 1.000±0.055,P=0.003;0.418±0.059 vs.1.000±0.084,P=0.001)。结论:宫内高血糖环境可能通过抑制胎盘AKT-mTOR信号通路,从而编程子代的发育轨迹。 | 张莉 余昕烊 徐萍 Philip N.Baker 漆洪波 童超 张华 | 2017 | 重庆医科大学学报2017，42，8： | 4 |
| 4 | 结核分枝杆菌H37Ra FadD3基因克隆与表达研究显示文摘为探索FadD3在结核分枝杆菌胆固醇分解代谢中的作用,从结核分枝杆菌H37Ra的全基因组中克隆了FadD3基因,并在大肠杆菌BL21中表达.根据NCBI公布的结核分枝杆菌全基因组序列设计一对引物,PCR扩增FadD3基因.PCR扩增产物与克隆载体pGEM3Zf(+)进行拼接,得到重组基因FadD3-pGEM3Zf(+),再转化到大肠杆菌DH5ɑ得到克隆.PCR检测阳性克隆,再与表达载体pYUB28b拼接,得到重组质粒FadD3-pYUB28b.阳性重组质粒亚克隆到大肠杆菌BL21宿主菌进行自体诱导表达.经过表型筛选及鉴定分析,已成功构建了重组表达质粒FadD3-pYUB28b.SDS-PAGE和Western blotting证实,重组基因FadD3-pYUB28b在大肠杆菌BL21中有表达产物.实验结果表明,以pYUB28b为表达载体,FadD3重组基因在大肠杆菌表达体系于温度分别为18,28℃有包涵体形式的表达蛋白,在37℃无表达产物. | 袁方 陈元晓 Stephanie Dawes Edward N.Baker | 2014 | 云南大学学报(自然科学版)2014，36，4： | 4 |
| 5 | The metabolic role of LncZBTB39-1:2 in the trophoblast mobility of preeclampsia显示文摘Preeclampsia is characterized by new onset of hypertension and proteinuria after 20 weeks’gestation and is a leading cause of maternal and neonatal morbidity and mortality.The pathogenesis of preeclampsia is often associated with aberrant trophoblast function that leads to shallow placental implantation.However,the exact underlying mechanisms remain unclear.Placental LncZBTB39-1:2 expression level was investigated in 20 healthy placentae and 20 placentae with preeclampsia using qRT-PCR,and the metabolic profile of trophoblasts overexpressing LncZBTB39-1:2 in vitro was analysed using gas chromatography-mass spectrometry(GCeMS).In this study,we found that the expression of LncZBTB39-1:2 was significantly higher in preeclamptic placentae than in healthy placentae.Our metabolomics results have shown that tricarboxylic acid cycle intermediates and metabolites related to carbohydrate metabolism were decreased with the overexpression of LncZBTB39-1:2 in HTR8/SVneo cells.These findings were validated by detecting a lower level of intracellular ATP in HTR8/Vneo cells.Furthermore,the migration of HTR8/SVneo cells was compromised when cells were transfected with a plasmid encompassing LncZBTB39-1:2 overexpression.From these results,we conclude that abnormal levels of LncZBTB39-1:2 expression might lead to aberrant conditions in HTR-8/SVneo trophoblast cells.Aberrant conditions might be associated with dysregulated trophoblast migration and subsequent failure of uterine spiral artery remodelling,a pathogenesis recognised as a contributing factor in the aetiology of preeclampsia. | Yamin Liu Ting-Li Han Xiaofang Luo Yuxiang Bai Xuehai Chen Wei Peng Xi Xiong Philip N.Baker Chao Tong Hongbo Qi | 2018 | Genes & Diseases2018，5，3： | 3 |
| 6 | Innovative use of strategic energy design tools in building design in China显示文摘This paper expresses the importance of the use of strategic energy design tool in building design in China. The features of this kind of tool have been illustrated. The reliability, user friendliness, and usability are the most important characteristic of the early design software. This paper introduces an integrated energy design tool - LT Europe, which is widely used in the UK architectural practice and European. The climate data for Beijing has been produced from Meteonorm and integrated into LT Europe. A case study has been performed and the comparisons have been made by applying the Chinese old and new building energy regulations. It has been demonstrated that LT Europe software can be used for Chinese building energy design at the early stage by creating the local proper climate data. | LIBaizhan R.Yao N.Baker K.Steemers | 2003 | Journal of Chongqing University2003，2，U10： | 2 |
| 7 | Luminescent Carbon Nanodots: Emergent Nanolights显示文摘 | Sheila?N.Baker Gary?A.Baker | 2010 | Angewandte Chemie International Edition2010，，38： | 1 |
| 8 | 苯并[a]芘暴露大鼠的皮层代谢组学研究显示文摘目的基于气相色谱/质谱联用技术(GC/MS)的代谢组学方法,分析苯并[a]芘(B[a]P)暴露后大鼠皮层内源性小分子代谢物的变化,研究其神经毒性机制。方法将五日龄SD大鼠随机分为对照组和B[a]P暴露组(2 mg/kg),连续灌胃染毒7周以构建B[a]P暴露模型。染毒结束后,Morris水迷宫(MWM)测定大鼠的空间学习能力;电镜观察皮层神经元超微结构;GC/MS检测皮层代谢谱,结合偏最小二乘法判别分析(PLS-DA)和两独立样本t检验分析筛选两组间的差异代谢物,Cytoscape软件分析与差异代谢物相关的代谢通路。结果与对照组相比,B[a]P暴露大鼠出现较长的逃避潜伏期(P<0.05)、较短的目标象限停留时间(P<0.05);与对照组相比,B[a]P暴露大鼠出现突触间隙增宽、突触后膜增厚以及胞浆肿胀;两组大鼠的皮层中存在18个差异代谢物(VIP>1,P<0.05),分析差异代谢物得到9条与B[a]P神经毒性机制相关的通路,这些通路涉及氨基酸代谢、三羧酸循环以及维生素B3(烟酸和烟酰胺)代谢。结论 B[a]P可干扰机体的正常代谢,其神经毒性机制可能与氨基酸类代谢紊乱、三羧酸循环紊乱以及维生素代谢紊乱等有关。 | 王晶 李春林 白璐璐 唐强虎 张瑞源 Ting-Li Han 郭玉明 Philip N.Baker 夏茵茵 涂白杰 | 2018 | 南方医科大学学报2018，38，2： | 1 |
| 9 | Rodents on a high-fat diet born to mothers with gestational diabetes exhibit sex-specific lipidomic changes in reproductive organs显示文摘Maternal gestatonal diabetes mellitus(GDM)and offspring high-fat diet(HFD)have been shown to have sex-specific detrimental effects on the health of the offspring.Maternal GDM combined with an offspring HFD alters the lipidomic profiles of offspring reproductive organs with sex hormones and increases insulin signaling,resulting in offspring obesity and diabetes.The pre-pregnancy maternal GDM mice model is established by feeding maternal C57BL/6 mice and their offspring are fed with either a HFD or a low-fat diet(LFD).Testis,ovary and liver are collected from offspring at 20 weeks of age.The lipidomic profiles of the testis and ovary are characterized using gas chromatography-mass spectrometry.Male offspring following a HFD have elevated body weight.In reproductive organs and hormones,male offspring from GDM mothers have decreased testes weights and testosterone levels,while female offspring from GDM mothers show increased ovary weights and estrogen levels.Maternal GDM aggravates the effects of an offspring HFD in male offspring on the AKT pathway,while increasing the risk of developing inflammation when expose to a HFD in female offspring liver.Testes are prone to the effect of maternal GDM,whereas ovarian metabolite profiles are upregulated in maternal GDM and downregulated in offspring following an HFD.Maternal GDM and an offspring HFD have different metabolic effects on offspring reproductive organs,and PUFAs may protect against detrimental outcomes in the offspring,such as obesity and diabetes. | Andi Wang Baiyu Luo Zhu Chen Yinyin Xia Chang Chen Hongbo Qi Philip N.Baker Richard Saffery Ting-Li Han Hua Zhang | 2022 | Acta Biochimica et Biophysica Sinica2022，54，5： | 0 |
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