本刊计量单位的使用

<正>我刊使用下列计量单位(各类单位中,第一个单位为基本单位):1长度:m,cm,mm,μm,nm,pm,fm;2质量:g,kg,mg,μg,ng,pg;3时间:s,ms,μs,ns,min,h,d;4电流:A,m A,μA,n A;5热力学温度:℃,也可用K;6物质的量:mol,mmol,μmol,nmol,pmol;7频率:Hz,k Hz,MHz,GHz,THz;     

Subject Index

正Aabnormal glucose,lipid metabolism,clinical characteristics,obese,2018043acarbose,metformin,insulin,type 2 diabetes mellitus,2018395acetated ringer's solution,inflammatory,lung tissue,2018309acidic oligosaccharides,P-selectin,pulmonary hypertensive rats,monocrotaline,2018184acquired immune deficiency syndrome,sexual transmitted diseases,2018272     

SUBJECT INDEX

臼今月卜l,5一anhydro一D一glueitol,diabetes mellitus,frue-tosamine,blood glueose,9805612,4一d initrofluorobenzen,eleetrophoresis,arnino aeids,D一norleueine,98036832P glass mieropheres,liver eareinoma,interstitial in-jeetion,hepatie arterial embolisrn,9803158一ehloro一adenosine,aPoptosis,tumor eells eultured,98021199mTc一MDP imaging,hyPerparathyroidism,99mTe-MIBI irnagin拜98040999mTc一MIBI ima套ing,hyperparathyroidism,99mTe-MDP imaging,980409ACA,systemle lupus erythematosus,ANCA,980202…     

本刊计量单位的使用

我刊使用下列计量单位(各类单位中,第一个单位为基本单位):①长度:m,cm,mm,μm,nm,pm,fm;②质量:g,kg,mg,μg,ng,pg;③时间:s,ms,μs,ns,min,h,d;④电流:A,mA,μA,nA;⑤热力学温度:℃,也可用K;⑥物质的量:mol,mmol,μmol,nmol,pmol;⑦频率:Hz,kHz,MHz,GHz,THz;     

Author Index

Ang, Choon Kiat 195 Aronow, Wilbert S. 93 Borlongan, Cesar V. 105, 200 Cardaioli, Paolo 73, 78, 80 Chee, Kok Han 195 Chen, Chen 42 Chen, Jin 144 Chen, Li 227 Chen, Rui 3, 101 Chen, Yundai 137 Cheng, Longxian 175 Cheng, Shujuan 11 Chi, Hongjie 144 Chien, Christopher V. 20 dell’Avvocata, Fabio 78, 80 Ding, Jingdong 220 Ding, Wenhui 42 Deng, Jie 67 Dong, Wei 77 Dou, Kefei 170 Dougherty, Kathy 111 Du, Xiuqing 170 Duthinh, Vuong 148 Fan, Chaomei 170 Fridrich, Viliam 131 Fromm,…     

SUBJECT INDEX

3一d ipropylxathine,8一eyelopentyl一l,adenosine,patehe lanip reehnique,aetion potential,9704495一f luorouraeil.hePatoma,oxalysine,970250一,n lerleukln6,maerophage phagoeytosis,ehemotheraPy,970239sa一reduetase,pseudohermaphroditism,androgen re-eel)tor,9702736一hydroxydopamine,Parkinson disease,ganglioside,dopamlne,9706866一keto一PGFla,hypertension,hyperinsulinemia,妞hromboxane BZ,9702928一eyelo讲。tyl一1,3一dipropylxathine,adenosine,patehe lamp teehnique,aetion Potential,9704499一eis retinoie…     

AVERT:阿托伐他汀与血管重建治疗的对比

作者(a)Mc Cormick LS,Black D,Waters D,Brown WV,Pitt B,及AVERT研究组 (b)Pitt B,Waters D,Brown WV,Van Boven AJ,Schwartz L,Title LM,Eisenberg D,Shurzinske L,Mc Cormick LS,及AVERT研究组 (c)Waters D,Pitt B,Brown WV,Mac Dougall D,Mc Cormick LS,Black D     

Euphorbia neriifolia L.:Review on botany,ethnomedicinal uses,phytochemistry and biological activities

The present review is intended to provide information on botany,ethnomedicinal uses,phytochemistry and biological activities of various parts of Euphorbia neriifolia(E. neriifolia). E. neriifolia has several ethnomedicinal uses. The latex of E. neriifolia is used as laxative,purgative,rubefacient,carminative and expectorant as well as in treatment of whooping cough,gonorrhea,leprosy,asthma,dyspepsia,jaundice,enlargement of the spleen,tumors,stone in the bladder,abdominal troubles and leucoderma. Leaves are brittle,heating,carminative,and good for improving the appetite and treatment of tumors,pains,inflammations,abdominal swellings and bronchial infections. Roots are used as symptomatic treatment of snake bite,scorpion sting and antispasmodic. Various plant parts or whole E. neriifolia extract and its isolates have been reported scientifically using various in-vivo and in-vitro experimental methods for anaesthetic,analgesic,anti-anxiety,anti-convulsant,anti-psychotic,anti-arthritis,anti-carcinogenic,antidiabetic,anti-diarrhoeal,anti-inflammatory,anti-thrombotic,antimicrobial,antioxidant,antiulcer,cytotoxic,death-receptor expression enhancing,dermal irritation,diuretic,hemolytic,immunomodulatory,radioprotective,scorpion venom and wound healing properties. It is reported to have chemical constituents like,neriifolin-S,neriifolin,neriifoliene,euphol,neriifolione,cycloartenol,nerifoliol,lectin,euphonerins A–G,3-O-acetyl-8-O-tigloylingol,taraxerol,antiquorin,etc. Identified chemical constituents are still required to be explored for their advanced isolation techniques and biological activities.     

2004年度《中国人兽共患病杂志》共建合作单位

常务委员单位:南平市第一医院,福建省皮肤病性病防治院委员单位:厦门市同安区医院,莆田市第一医院,上海畜牧兽医站,兰州兽医研究所,山东省疾病预防控制中心,上海市疾病预防控制中心,江门市疾病预防控制中心,广西壮族自治区疾病预防控制中心,珠海市疾病预防控制中心,华南农业大学动物医学院,泉州市卫生防疫站,闽侯县卫生防疫站,晋江市卫生防疫站,南安市医院,福建医科大学附属第二医院,河北科技师范学院成员单位:福建农林大学动物科学院,惠安县卫生防疫站,上杭县卫生防疫站,丰泽区卫生防疫站,龙海市卫生防疫站,福安市卫生防疫站2004年度《中国…     

不典型心绞痛一例

患者.女,70岁,入院前1小时,无诱因,突然出现左半侧头痛,无头晕,无恶心,无眼花耳鸣,无心慌,无胸闷气短,无心前区痛,服用去痛片无效而就诊。入院时查体,血压正常,脉搏80次/分,体温36度,五官端正,左侧太阳穴及风池穴压痛,心肺听诊未见异常,心电图为窦性心律,不完全性右束支传导阻滞,无其他异常变化。患者痛苦,紧张,肌注安定后入睡,2小时后,患者述左耳疼痛,满口牙痛,请五官科医生会诊,未见异常,     

大鼠肝再生增强因子在酵母菌中的表达及生物活性研究

目的构建大鼠肝再生增强因子(rALR)酵母重组表达质粒,在毕赤酵母菌GS115中进行表达.表达产物经超滤方法纯化后在体外进行生物活性研究. 方法以重组质粒pcDNA3.1-rALR为模板,聚合酶链反应(PCR)扩增rALR编码区的DNA,构建重组质粒pPIC9K-rALR,然后电转化至毕赤酵母菌GS115中,在甲醇诱导下进行表达.表达产物经1.5% SDS-PAGE电泳和western blot鉴定后进行超滤纯化.用3H-TdR掺入法检测重组大鼠ALR(rrALR)体外刺激QGY和HepG2人肝癌细胞株和原代大鼠肝细胞的增殖情况. 结果重组质粒经酶切及PCR证实rALR编码区DNA正确插入质粒载体中.重组大鼠ALR被GS115菌以外分泌方式表达,其DNA分子量约为1.5×104,与理论预期值相符,western bolt鉴定发现rrALR能与抗人ALR多克隆抗体发生特异性反应,说明人和大鼠ALR抗原性上存在部分交叉.超滤纯化获得大量高纯度的rrALR.在所测定的剂量范围内,rrALR在体外以剂量依赖方式刺激QGY和HepG2肝癌细胞株增殖,但对原代大鼠肝细胞无刺激增殖作用. 结论 rrALR在毕赤酵母菌GS115中获得分泌性高效表达,rrALR在体外以剂量依赖方式刺激QGY和HepG2肝癌细胞株增殖,但对原代大鼠肝细胞无刺激增殖作用,表明肝癌细胞和正常肝细胞表达的ALR受体不同.人和大鼠ALR在生物学活性和抗原性上存在交叉.     

肝再生增强因子对肝星状细胞基因表达谱的影响

目的将pcDNA3．1（-）．ALR（hALR）和pcDNA3．1（-）分别转染人肝星形细胞（HSC）,筛选在人肝星形细胞中存在表达差异的基因,进一步研究hALR的生物学功能及机制。方法以脂质体技术将pcDNA3．1（-）．ALR和pcDNA3．1（-）分别转染人肝星形细胞系,提取总mRNA,逆转录为cDNA,应用基因表达谱芯片方法分析差异表达的基因。结果在所筛选的4096个基因中,有2个基因表达水平显著上调,25个基因表达水平显著下调。结论hALR对于人肝星形细胞基因表达谱有显著影响,为进一步研究hALR的生物学功能和作用机制提供了线索。     

High expression of human augmenter of liver regeneration in E.coli

ＩＮＴＲＯＤＵＣＴＩＯＮＨｅａｔｓｔａｂｌｅｈｅｐａｔｏｃｙｔｅｓｔｉｍｕｌａｔｏｒｙａｃｔｉｖｉｔｙｈａｓｂｅｅｎｄｅｓｃｒｉｂｅｄｉｎｔｈｅｌｉｖｅｒｏｆｗｅａｎｌｉｎｇｒａｔｓａｎｄｐｉｇｓ．Ｔｈｉｓｇｒｏｗｔｈｆａｃｔｏｒｉｓｃａｌｅｄｈｅ...     

人肝再生增强因子基因组DNA的克隆化与序列分析

目的 克隆人肝再生增强因子（ａｕｇｍｅｎｔｅｒ ｏｆ ｌｉｖｅｒ ｇｅｇｅｎｅｒａｔｉｏｎ,ＡＬＲ）的基因组ＤＮＡ,并进行序列分析。方法 采用人肝再生增强因子ｃＤＮＡ及其编码序列, 核苷酸序列数据库（ＧｅｎＢａｎｋ）以Ｂｌａｓｔ为工具进行核苷酸同源性比较分析,寻找相应的ＡＬＲ基因组ＤＮＡ序列。结果 从ＧｅｎＢａｎｋ核苷酸序列数据库中寻找到ＡＬＲ基因组ＤＮＡ全序列,由１８１３个核苷酸组成。     

人肝再生增强因子基因组DNA的克隆化与序列分析

目的克隆人肝再生增强因子(ALR)的基因组DNA,并进行序列分析。方法采用人肝再生增强因子cDNA及其编码序列,对基因的核苷酸序列数据库(GenBank)以BLAST为工具进行核苷酸序列同源性比较分析,寻找相应的ALR基因组DNA序列。结果从GenBank核苷酸序列数据库中寻找到人ALR基因组DNA全序列,由1813个核苷酸组成。人ALR基因组DNA序列由3段外显示子(exon)组成,分别为18nt,197nt和163nt。基因的编码产物由125个氨基酸残基组成,与小鼠ALR基因组DNA结构类似。基因组DNA定位于染色体的16p13.3位点上。结论克隆了人ALR基因组DNA全序列。     

Unusual resistance of ALR/Lt mouse beta cells to autoimmune destruction: role for beta cell-expressed resistance determinants

Genetic analysis of autoimmune insulin-dependent diabetes mellitus (IDDM) has focused on genes controlling immune functions, with little investigation of innate susceptibility determinants expressed at the level of target beta cells. The Alloxan (AL) Resistant (R) Leiter (Lt) mouse strain, closely related to the IDDM-prone nonobese diabetic (NOD)/Lt strain, demonstrates the importance of such determinants. ALR mice are unusual in their high constitutive expression of molecules associated with dissipation of free-radical stress systemically and at the beta-cell level. ALR islets were found to be remarkably resistant to two different combinations of beta-cytotoxic cytokines (IL-1beta, tumor necrosis factor alpha, and IFN-gamma) that destroyed islets from the related NOD and alloxan-susceptible strains. The close MHC relatedness between the NOD and ALR strains (H2-Kd and H2-Ag7 identical) allowed us to examine whether ALR islet cells could survive autoimmune destruction by NOD-derived Kd-restricted diabetogenic cytotoxic T lymphocyte clones (AI4 and the insulin-reactive G9C8 clones). Both clones killed islet cells from all Kd-expressing strains except ALR. ALR resistance to diabetogenic immune systems was determined in vivo by means of adoptive transfer of the G9C8 clone or by chimerizing lethally irradiated ALR or reciprocal (ALR x NOD)F1 recipients with NOD bone marrow. In all in vivo systems, ALR and F1 female recipients of NOD marrow remained IDDM free; in contrast, all of the NOD recipients became diabetic. In conclusion, the ALR mouse presents a unique opportunity to identify dominant IDDM resistance determinants expressed at the beta cell level.     

mt-Nd2 Allele of the ALR/Lt mouse confers resistance against both chemically induced and autoimmune diabetes

Aims/hypothesis ALR/Lt, a mouse strain with strong resistance to type 1 diabetes, is closely related to autoimmune type 1 diabetes-prone NOD/Lt mice. ALR pancreatic beta cells are resistant to the beta cell toxin alloxan, combinations of cytotoxic cytokines, and diabetogenic NOD T-cell lines. Reciprocal F1 hybrids between either ALR and NOD or ALR and NON/Lt, showed that alloxan resistance was transmitted to F1 progeny only when ALR was the maternal parent. Here we show that the mitochondrial genome (mtDNA) of ALR mice contributes resistance to diabetes.Methods When F1 progeny from reciprocal outcrosses between ALR and NOD were backcrossed to NOD, a four-fold lower frequency of spontaneous type 1 diabetes development occurred when ALR contributed the mtDNA. Because of the apparent interaction between nuclear and mtDNA, the mitochondrial genomes were sequenced.Results An ALR-specific sequence variation in the mt-Nd2 gene producing a leucine to methionine substitution at amino acid residue 276 in the NADH dehydrogenase 2 was discovered. An isoleucine to valine mutation in the mt-Co3 gene encoding COX3 distinguished ALR and NOD from NON and ALS. All four strains were distinguished by variation in a mt-encoded arginyl tRNA polyadenine tract. Shared alleles of mt-Co3 and mt-Tr comparing NOD and ALR allowed for exclusion of these two genes as candidates, implicating the mt-Nd2 variation as a potential ALR-derived type 1 diabetes protective gene.Conclusions/interpretation The unusual resistance of ALR mice to both ROS-mediated and autoimmune type 1 diabete stresses reflects an interaction between the nuclear and mt genomes. The latter contribution is most likely via a single nucleotide polymorphism in mt-Nd2.     

人肝再生增强因子上调细胞周期素B2基因的表达

目的研究人肝再生增强因子(ALR)转基因表达对细胞周期素B2启动子(cyclin B2p)转录的调节作用,从而进一步探讨ALR的生物学作用及机制。方法根据文献确定细胞周期素B2p区域,聚合酶链反应(PCR)扩增细胞周期素B2p,克隆至报告基因表达载体pCAT3-Basic中,构建pCAT3-cyclin B2p报告载体;以该质粒转染肝癌细胞系HepG2细胞系,同时与ALR的真核表达载体pcDNA3．1(-)-ALR共转染HepG2细胞系,用酶联免疫吸附法(ELISA)检测报告基因氯霉素乙酰转移酶(CAT)的表达活性。结果成功构建pCAT3- cyclin B2p报告基因表达载体;pCAT3-cyclin B2p与pcDNA3．1(-)-ALR共转染HepG2细胞系的CAT表达活性是pCAT3-Basic空载体的25．13倍,是pCAT3-cyclin B2p单转染的2．60倍。结论人ALR对细胞周期素B2p基因的转录表达具有反式激活作用。     

肝再生增强因子对细胞周期素依赖性激酶1基因表达的影响

目的研究人肝再生增强因子(ALR)对细胞周期素依赖性激酶1启动子(CDK1p)转录调节的作用,探讨ALR的生物学作用机制。方法根据GenBank中CDK1p序列的分析设计引物,应用聚合酶链反应(PCR)扩增人CDK1基因启动子基因序列,并克隆至真核报告载体pCAT3-Basic中,构建CDK1启动子报告基因表达载体pCAT3-CDK1p,以该质粒转染HepG2细胞系,并同时与pcDNA3.1(-)-ALR共转染HepG2细胞系,用酶联免疫吸附法(ELISA)检测报告基因氯霉素乙酰转移酶(CAT)的表达活性。结果 pCAT3-CDK1p组CAT表达活性明显高于pCAT3-basic组,差异有统计学意义,pCAT3-CDK1p与pcDNA3.1(-)-ALR共转染组的CAT表达活性明显低于pCAT3-CDK1p组,差异有统计学意义。结论 CDK1启动子有顺式激活下游基因的活性,ALR对CDK1基因有下调作用。