碳纳米管负载Mo-Co-S基HDS/HDN催化剂的制备及其表征研究

用自行制备的多壁碳纳米管(简写为CNTs)作为载体制备负载型Mo-Co-S催化剂,记为:m%MoiCoj/CNTs(m%为质量百分数),用噻吩加氢脱硫(HDS)和吡咯加氢脱氮(HDN)作为探针反应,XRD、XPS和H2-TPD作为表征手段,考察Co/Mo摩尔比、MoiCoj负载量及Co和Mo的浸渍顺序对所制备催化剂的结构和催化性能的影响.研究结果表明,对于本文自行制备CNTs负载的Mo-Co-S催化剂,最佳的Co/Mo摩尔比为1 3,最适宜的Mo3Co1负载量为~7.2%(质量百分数),Co和Mo的浸渍顺序以“先浸渍Co、经干燥焙烧后浸渍Mo”为佳.与AC负载的参比体系相比,CNTs负载催化剂较易于被还原,工作态催化剂表面具有催化活性的Mo物种(Mo4+)在总负载Mo量中所占份额较高;在另一方面,在HDS/HDN反应条件下,作为载体的CNTs的表面存在着数量更加可观的吸附氢物种,这些活泼氢物种通过“溢流”容易传输至Mo-Co-S催化活性位,于是有助于提高表面加氢反应的速率.以上两方面因素对CNTs负载Mo-Co-S催化剂上高的HDS/HDN反应活性都有重要贡献

解放科学记录： 让数字时代的学术出版为科学服务

本报告是国际科学理事会（International Science Council）发布的&ldquo;Opening the Record of Science: Make Scholarly Publishing Work for Science in the Digital Ear&quot;的中文翻译版（原文请见翻译版中标注）。该报告主要针对科学界及其机构，寻求尽可能建立关于传播科学成果的科学出版系统的原则和优先事项的共同看法，并成为促进积极变化动的行动的前驱。本报告遵循一个鲜明的逻辑：提出一系列作为科学与学术出版运作基础的规范的原则；描述当前出版环境及其进化轨迹；分析这些原则在实践中被遵守的程度；确定在实现这些原则时需要解决的问题，为ISC成员和其他利益相关者随后的讨论和行动提出议题</p

纳米尺寸团簇Ni_nZr_n(n=3～5)的几何结构与成键规律研究

根据化学键理论与拓朴原理 ,设计了团簇 Nin Zrn(n=3～ 5 )的可能几何构型 ,并用从头算方法进行构型优化 .结果表明 :由 Ni Zr组成的团簇原子间的 Zr—Zr和 Zr— Ni键明显较强 ,而 Ni—Ni的成键较弱 ;并发现 Nin Zrn(n=3～ 5 )团簇电子性质与有机烯烃分子等瓣相似 ,原子之间的成键按照强弱相间的规则分

Pregnane X receptor involves in the effect of aflatoxin B1 on necroptosis in human normal L02 liver cells

目的初步探讨孕烷X受体(PXr)对黄曲霉毒素b1(Afb1)诱导肝细胞dnA损伤和坏死性凋亡的影响。方法采用已构建的PXr高表达l02-PXr和空白载体对照l02-P b细胞;实时荧光定量PCr(Q rT-PCr)检测细胞nr1I2和CyP3A4 M rnA水平改变;蛋白免疫印迹(WESTErn blOTTIng)检测细胞内PXr和坏死性凋亡下游效应自噬分子lC3-Ⅰ和lC3-Ⅱ蛋白相对表达含量;双核微核试验(CbMn)检测细胞遗传损伤情况;采用噻唑蓝(MTT)法测定Afb1对细胞活性抑制影响;利用坏死性凋亡抑制剂nEC-1构建坏死性凋亡抑制的细胞模型,验证Afb1诱导的坏死性凋亡的效应。结果与l02-P b细胞相比,l02-PXr细胞nr1I2 M rnA和PXr蛋白显著上调(均P<0.001)。Afb1显著地诱导l02-P b和l02-PXr细胞中CyP3A4 M rnA上调(均P<0.05),在l02-PXr细胞中的效应更为明显。与对照组相比,Afb1在5~30μMOl/l呈剂量反应关系诱导l02-P b和l02-PXr细胞的微核率增高(均P<0.05),l02-PXr细胞更为明显;同时,Afb1明显地诱导两株细胞的核芽率和核桥率,但随Afb1剂量增高都有下降趋势。细胞活性随Afb1浓度(1.875~120μMOl/l)增加呈剂量反应关系抑制(均P<0.05);且相对于l02-P b细胞,l02-PXr细胞对Afb1处理48 H诱导的细胞活性抑制作用更为敏感(P<0.05)。nEC-1可显著性抑制Afb1诱导的l02-PXr细胞活性抑制率(P<0.05),然而却不能降低Afb1诱导l02-P b细胞活性抑制率。此外,Afb1显著性诱导l02-P b和l02-PXr坏死性凋亡下游lC3-Ⅱ的上调(均P<0.05);且与l02-P b细胞相比,nEC-1对Afb1诱导的l02-PXr细胞活性抑制和lC3-Ⅱ上调的抑制效果更为明显(P<0.05)。结论 PXr参与Afb1诱导人肝细胞dnA损伤介导的坏死性凋亡,与PXr促进Afb1诱导CyP3A4基因上调有关。Objective To investigate the effects of pregnane X receptor(PXR) over expression on aflatoxin B1(AFB1)-induced DNA damage and necroptosis in human normal liver L02 cells.Methods The established cells models of stable transfection of over expression PXR(L02-PXR) and null vector p Babe-puro(L02-p B) were used.The background levels of NR1I2 m RNA and PXR protein, and the expression of AFB1-induced CYP3A4 m RNA and LC3-I / LC-3II protein were determined by the real time PCR(q RT-PCR) and Western blotting, respectively.The cytokinesis-block micronucleus(CBMN)assay was adopted to evaluate the genotoxicity.The cell viability inhibition rate was determined by MTT assay, after treatment with different doses of AFB1.The inhibition models of necroptosis were established by treatment with necroptosis inhibitor Nec-1.Results The expression of NR1I2 m RNA and PXR protein in L02-PXR cells were higher than that in L02-p B cells(all P<0.001).The level of CYP3A4 m RNA was significantly up regulated in L02-p B and L02-PXR cells by treatment with AFB1(all P<0.05).Compared with control group(Ctrl), MN frequencies in L02-p B and L02-PXR cells were significantly increased by treatment with AFB1 in a dose-dependent manner(all P <0.05), especially, in L02-PXR cells.Meanwhile, NBD and NBP frequencies were significantly increased by treatment with AFB1.However, AFB1 with a higher dose induced downward trends in frequencies of NBD and NBP.Moreover, the inhibition rate of cell viability was increased after treatment with AFB1(1.875~120 μmol / L) in a dose-dependent manner(all P <0.05); specifically, the inhibitory effects of AFB1-treatment after 48 h were significantly stronger in L02-PXR cells than in L02-p B cells(P <0.05).Interestingly, necroptosis inhibitor Nec-1 could inhibit AFB1-induced cell death in L02-PXR cells(P<0.05).On the contrary, Nec-1 could not prevent L02-p B cells from death by treatment with AFB1.In addition, the expression of necroptotic LC3-II, a classical marker of autophagy, was significantly increased by treatment with AFB1 in two cell lines(all P <0.05).Notably, pre-treatment with Nec-1 was able to block the inducement of necroptotic LC3-II in a more efficiently way in L02-PXR cells than in L02-p B cells(P <0.05).Conclusion PXR involved in the effect of AFB1 on necroptosis by DNA damage mediation in human liver cells;specifically, the up regulation of CYP3A4 gene may relate to the AFB1-induced DNA damage.国家自然科学基金(81172705;81072334); 广东省自然科学基金(S2011020002769); 福建省自然科学基金(2014J01372

Effects of cadmium on promoter methylation and transcriptional level of PPP2R1A gene in hepatocytes

目的分析镉染毒处理肝细胞中蛋白磷酸酶2A(PP2A)-Aα支架亚基基因PPP2r1A启动子区甲基化状态及其转录水平的改变。方法采用永生化人正常肝l02细胞及肝细胞癌HEP g2细胞为研究对象,对其进行以下分组和处理:1低、中和高剂量氯化镉(Cd Cl2)处理组,分别予浓度为20.0、40.0和60.0μMOl/l Cd Cl2处理24 H;2低、中和高剂量5-氮杂-2’-脱氧胞苷(5-AzA-d C)处理组,分别予浓度为2.5、5.0和10.0μMOl/l 5-AzA-d C处理48 H;3 5-AzA-d C组予浓度为5.0μMOl/l的5-AzA-d C处理48 H,Cd Cl2组予浓度为40.0μMOl/l的Cd Cl2处理24 H,(5-AzA-d C+Cd Cl2)组予浓度为5.0μMOl/l的5-AzA-d C预处理48 H后再予浓度为40.0μMOl/l Cd Cl2处理24 H;4 Cd Cl2处理组予浓度为40.0μMOl/l Cd Cl2处理24 H。上述4种分组均设对照组,予等体积生理氯化钠溶液或二甲基亚砜处理。经1~3处理后的细胞采用实时荧光定量聚合酶链反应(PCr)检测PPP2r1A、金属硫蛋白1b(MT1b)和dnA甲基转移酶3A(dnMT3A)的MrnA转录水平(以对照组水平为1.00)。经4处理后的细胞采用亚硫酸氢盐修饰后PCr扩增PPP2r1A启动子区克隆测序检测CP g岛的甲基化情况。结果 l02细胞和HEP g2细胞中,不同剂量Cd Cl2处理组PPP2r1A MrnA转录水平随镉处理剂量增高呈剂量依赖性下降(P0.05)。结论外源化学物Cd Cl2可诱导肝细胞中PPP2r1A转录水平降低,可能与镉能够引起目的基因启动子区甲基化状态改变有关,提示PP2A亚基基因的表观遗传学调控可影响镉诱导的肝细胞功能。Objective To analyze the effects of cadmium on the promoter methylation and transcriptional level of protein phosphatase 2A( PP2A)-Aα supported subunit gene PPP2R1 A gene in hepatocytes.Methods The immortalized human fetal liver cell line L02 and the hepatocellular carcinoma cell line Hep G2 were selected as the research objects: 1 Cells were treated with low-,medium- and high-dose( 20.0,40.0 and 60.0 μmol / L) cadmium chlorid( Cd Cl2) for 24 h.2Cells were treated with low-,medium- and high-dose( 2.5,5.0 and 10.0 μmol / L) 5-aza-2'-deoxycytidine( 5-Aza-d C)for 48 h.3 Cells were given 5.0 μmol / L for 48 h in 5-Aza-d C group,cells were exposed to 40.0 μmol / L Cd Cl2 for 24 h in Cd Cl2 group and cells were exposed to 40.0 μmol / L Cd Cl2 for 24 h after 48 h pretreatment of 5.0 μmol / L 5-Aza-d C in( 5-Aza-d C + Cd Cl2) group.4 Cells were treated with 40.0 μmol/L Cd Cl2 for 24 h in Cd Cl2 group.The above groups were all given the controls with the same volumes of physiological sodium chloride solution or dimethyl sulfoxide.Real-time fluorescent quantitative polymerase chain reaction( PCR) detection was used to detect the mRNA transcriptional levels of PPP2R1 A,Metallothionein 1B( MT1B),DNA methyltransferase 3A( DNMT3A) after treatments 1-3.After treatment4,cloning sequencing was used to detect the Cp G island methylation status of PPP2R1 A promoter after bisulfite sequencing PCR.Results In L02 and Hep G2 cells,the transcriptional levels of PPP2R1 A mRNA in Cd Cl2 group were decreased in a dose-dependent manner( P 0.05).Conclusion It was indicated the Cd Cl2 could lead to the transcription inhibition of PPP2R1 A,and the effect may be related with the change of its promoter methylation status.These data showed epigenetic regulation of PP2 A subunit genes may affect the function of hepatocytes exposed to cadmium.国家自然科学基金(81172705;81072334;81130052); 广东省自然科学基金重点项目(S2011020002769

H_2在K~0-MWCNTs上储存和吸附/脱附特性研究

利用高压容积法辅以卸压升温脱附排水法,测定金属K修饰多壁碳纳米管对H2的吸附储存容量.结果表明,在室温(25℃),7.25MPa实验条件下,x%K0-MWCNTs(x%=30%～35%,质量百分数)对H2的吸附储存容量可达3.80wt%(质量百分数),是相同条件下单纯MWCNTs氢吸附储量的2.5倍;室温下卸至常压的脱附氢量为3.36wt%(占总吸附氢量的～88%),后续升温至673K的脱附氢量为0.41wt%(占总吸附氢量的～11%).利用LRS和H2-TPD-GC/MS等谱学方法对H2/K0-MWCNTs吸附体系的表征研究表明,H2在K0-MWCNTs上吸附存在非解离(即分子态)和解离(即原子态)两种吸附态;在≤723K温度下,H2/K0-MWCNTs体系的脱附产物几乎全为H2气;723K以上高温脱附产物不仅含H2,也含有CH4,C2H4和C2H2等C1/C2-烃

Study of storage and adsorption/desorption characteristics of H-2 on MWCNTs modified by metal potassium

Storage capacity of H-2 in a kind of potassium-modified multiwalled carbon nanotubes, K-0-MWCNTs, was measured by using high-pressure volumetric method combined with desorption water-displacement method. It was experimentally shown that appropriate incorporation of a certain amount of metallic potassium into the MWCNTs could significantly increase the storage capacity of hydrogen. Under conditions of 7.25 MPa and ambient temperature, H-2 uptake of 3.8 wt% could be achieved by the x%K-0-MWCNTs (x%=30%-35%, mass percentage), which was 2.5 times as high as that by the KO-free MWCNTs under the same conditions. It was also indicated that adsorption of 99% of the H2 was reversible, and that 88% of the stored hydrogen (equalling storage capacities of 3.36 wt%) could be desorbed while the pressure was relieved to atmospheric pressure and similar to 11% of the stored hydrogen (equalling storage capacities of 0.41 wt%) was desorbed in the following process of elevating temperature from room temperature to 673 K. The Raman-spectroscopic and TPD-MS/GC investigations of the H-2/K-0-MWCNTs adsorption systems showed that adsorption of H-2 on the MWCNTs could occur in associative and dissociative forms, with the observed v(s)(C-H) for CH2, v(C-H) for CH and v(H-H) for H-2 (a) at 2856, 3228 and 3946 cm(-1), respectively, and that H-2 Was the predominant products desorbed at temperatures lower than 723 K, whereas in addition to H-2, light hydrocarbons such as CH4, C2H4, C2H2, etc. were also involved in the products desorbed at temperatures higher than 723 K

在家系序列数据中同质性检验的连锁研究

全基因组外显子测序数据通常在小家系中收集。单核苷酸多态性（SNP）可以用于连锁分析，但目前只有少量家系进行全基因组测序导致SNP检测功效低。传统连锁分析中假设家系存在同质性（零假设）来寻找LOD值高的区域，备择假设为异质性，即不同家系中疾病基因是否在基因组不同位置。基于此假设的传统连锁分析可能增加检测功效，但对多个易感位点联合作用复杂性状，这个假设有悖常理。因此我们提出颠覆传统假设的新方法：零假设为不同家系中疾病基因存在基因组不同位置上，同质性为备择假设。基于零假设，两个家系中LOD值高的遗传变异出现同一（近似）区域可能性很低。事实上，两个遗传变异出现同一染色体上的概率为50%，进一步缩小范围，出现100bp距离内概率会变得极低。这个令人惊讶的事实是本课题立项依据之一。由此，我们提出检测两个家庭中易感疾病遗传变异发生在同一位置可能性的思路。初步研究表明，我们分析方法较原有方法更为有效

基于全基因组关联研究数据二次分析的肿瘤候选基因变异研究

肿瘤的发生是由遗传因素和环境因素共同作用导致的，且遗传因素往往具有多基因遗传的特征。不同肿瘤的全基因组关联研究（GWAS）表明这些肿瘤的遗传（germline）易感性常见变异（common variant）通常是低外显率的，这些低外显率常见变异的组合效应的揭示对研究肿瘤相关的机理起到重要作用。然而，标准的GWAS数据分析方法并不能检测这种常见变异的组合效应。本研究中，我们将在前期研究工作基础上设计开发新的基于通路的分析方法（pathway-based analysis,PBA），对公开的常见多基因遗传的肿瘤的GWAS数据进行二次深入分析，检测与特定肿瘤相关的通路即候选基因变异的组合效应；并通过网络分析等方法，比较不同肿瘤在关联通路及关联基因变异上的异同；最后以研究结果为依据建立相应的数据库。本研究在基因组学水平上探究肿瘤病因，为肿瘤的实验研究和临床诊断提供依据

中国科学院心理研究所会议论文集

&lt;正&gt;心理疾患(mental disorder),例如精神分裂症(schizophrenia,SZ)、双向情感障碍(bipolar disorder,BD)、重度抑郁症(major depressive disorder,MDD)和注意缺陷多动症(attention deficit hyperactivity disorder,ADHD)等,都是由遗传因素和环境因素共同作用导致。目前,针对心理疾患&nbsp;</p