检索结果-南通市图书馆

国外医学（妇幼保健分册） 2004年第4期15卷 235-236页

作者：冯异田占庄陈伯英复旦大学医学院中西医结合系上海200032

妇女围绝经期的身心健康一直是妇女保健的重要任务。围绝经期异常心理症状尤为突出 ,抑郁症的发病率较高 ,内分泌变化和抑郁症的发病有一定关系。该文从流行病学、影响因素、发病机制和治疗方面综述围绝经期和抑郁症之间的关系。

关键词：围绝经期抑郁症

genetic Analysis of Fruit Body Color in a Hybrid Strain of Flammulina velutipes

在线全文

学校读者我要写书评

暂无评论

食用菌学报 2007年第4期 22-24页

作者： YI Ruirong1,2,CAO Hui1,PAN Yingjie3(1shanghai Biotechnology and Engineering Research center for the Edible Fungi Key Laboratory of Agriculturalgenetics and Breeding of shanghai Institute of Edible Fungi,shanghai Academy of Agricultural Sciences,shanghai 201106,china 2College of Life Sciences,Nanjing Agricultural university,Nanjing,Jiangsu 210095,china3shanghai Fisheries university,shanghai 200090,china)

A series of hybrid Flammulina velutipes dikaryons were obtained by crossing yellow and white *** color of fruit bodies generated from these dikaryons,and the ratio between dark-colored stipe regions and the entire stipe of individual fruit bodies,were *** data suggest that the expression of fruit body color in the hybrid dikaryons was under the control of factors present in both the white and yellow parent monokaryons,and that multiple alleles exist in both white and yellow color-controlling factors.

关键词： Fruit body color Color-controlling factors Flammulina velutipes

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

鲫组织中伊维菌素含量的检测方法

水产学报 2010年第6期34卷 964-971页

作者：彭章晓江敏吴昊何琳杨李上海海洋大学农业部水产种质资源与养殖生态重点开放实验室上海海洋大学水域环境生态上海高校工程研究中心

采用反相高效液相色谱分离、紫外检测器检测,建立了鲫血液、肌肉、肝胰脏、肾脏及性腺组织中伊维菌素(IVM)残留的检测方法。将匀浆后的鲫组织用乙酸乙酯提取,离心后取上清液于45℃下氮气吹干,用甲醇-水(4∶1,V/V)混合液溶解残渣,加正己... 详细信息

采用反相高效液相色谱分离、紫外检测器检测,建立了鲫血液、肌肉、肝胰脏、肾脏及性腺组织中伊维菌素(IVM)残留的检测方法。将匀浆后的鲫组织用乙酸乙酯提取,离心后取上清液于45℃下氮气吹干,用甲醇-水(4∶1,V/V)混合液溶解残渣,加正己烷,漩涡振荡后离心,取下清液经0.22μm的滤膜过滤后,进样20μL进行分析,检测波长为245nm,外标法定量。结果表明:伊维菌素在血浆和肌肉中的检出限分别为7.5μg/L和7.0μg/kg;肌肉、肝胰脏、肾脏及性腺中IVM为0.025～1.00mg/kg,血液中为0.025～1.00mg/L时,色谱峰峰高与浓度呈良好的线性相关。各组织中IVM的平均回收率为(90.09±6.54)%～(97.77±5.91)%,平均批内RSD为(2.55±1.78)%～(3.99±1.55)%,平均批间RSD为(4.18±3.97)%～(6.01±2.54)%。对鲫以0.4mg/kg(药量/体重)剂量单次口灌给药后,用该方法进行残留检测,结果发现:25℃水温条件下,鲫肌肉中伊维菌素的休药期不得少于15d。

关键词：鲫伊维菌素检测高效液相色谱

脂质体介导的c-myc反义硫代寡核苷酸诱导胃癌SGC-7901细胞凋亡

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

复旦学报（医学版） 2002年第1期29卷 26-29页

作者：范钰林庚金钱立平许祖德李华徐康复旦大学附属华山医院消化科上海200040 复旦大学医学院病理学教研室上海200032 南通医学院附属东台医院内窥镜室东台224200

目的　探讨c myc反义硫代寡核苷酸 (antisensephosphorothioateoligodeoxynucleotide ,APSODN)对胃癌SGC 790 1细胞凋亡的影响。方法　人工合成c mycAPSODN ,通过脂质体转染法处理人胃癌细胞系SGC 790 1后 ,于不同时间收集细胞 ,采用Nor... 详细信息

目的　探讨c myc反义硫代寡核苷酸 (antisensephosphorothioateoligodeoxynucleotide ,APSODN)对胃癌SGC 790 1细胞凋亡的影响。方法　人工合成c mycAPSODN ,通过脂质体转染法处理人胃癌细胞系SGC 790 1后 ,于不同时间收集细胞 ,采用Northernblot、Westernblot检测c myc基因mRNA及蛋白表达 ,采用TUNEL方法检测凋亡指数 ,以流式细胞仪检测细胞周期。结果　TUNEL显示c mycAPSODN可诱导胃癌SGC 790 1细胞凋亡 ,并与APSODN的浓度和处理时间有关。流式细胞仪检测显示细胞阻滞于G0 /G1期。结论　c mycAP SODN可诱导胃癌细胞凋亡。

关键词：胃癌细胞 c-myc 反义硫代寡核苷酸脂质体细胞凋亡 SGC-7901细胞 APSODN

Disruption of palladin leads to defects in definitive erythropoiesis by interfering erythroblastic island formation in mouse fetal liver

在线全文

学校读者我要写书评

暂无评论

Disruption of palladin leads to defects in definitive erythr...

中国遗传学会“发育、遗传和疾病”研讨会

作者： Xue-Song Liu~(1,4) Xi-Hua Li~1 Yi Wang~1 Run-Zhe Shu~(1,4) Long Wang~(1-3) Shun-Yuan Lu~(1-3) Hui Kong~3 Yue-E Jin~1 Li-Jun Zhang~1 Jian Fei~3 Sai-Juan Chen~2 Zhu Chen~2 Ming-Min Gu~1 Zhen-Yu Lu~1 Zhu-Gang Wang~(1-3,*) 1 Laboratory of genetic Engineering,Institute of Health Sciences,shanghai Institutes for Biological Sciences,Chinese Academy of Sciences & shanghai Jiao Tong university School of Medicine,shanghai 200025,PR china 2 State Key Laboratory of Medical Genomics,Rui-jin Hospital affiliated to shanghai Jiao Tong university School of Medicine,shanghai 200025,PR china 3 shanghai Research center for Model Organisms,shanghai 201203,PR china 4 Graduate School of Chinese Academy of Sciences,shanghai 200025,PR china.

Palladin was originally found up-regulated with NB4 cell differentiation induced by *** of palladin results in neural tube closure defects,liver herniation and embryonic *** we further report thatpailadinembryos exhibit a significant defect in erythropoiesis,characterized by dramatic reduction in definitive erythrocytes derived from fetal liver but not primitive erythrocytes from yolk *** reduction of erythrocytes is accompanied by increased apoptosis of erythroblasts and partial blockage of erythroid ***,colony forming assay shows no differences between wt and mutant fetal liver or yolk sac in the number and size of colonies *** addition,palladinfetal liver cells can reconstitute hematopoiesis in lethally-irradiated *** data strongly suggest that deficient erythropoiesis in palladin fetal liver is mainly due to compromised erythropoietic *** expected,erythroblastic island in palladin fetal liver was found *** liver cells fail to form erythroblastic island in ***,wt macrophages can form such units with either wt or mutant erythroblasts,while mutant macrophages lose their ability to bind wt or mutant *** data demonstrate that palladin is crucial for definitive erythropoiesis and erythroblastic island formation,and especially,required for normal function ofmacrophages in fetal liver.

关键词： Palladin Fetal liver Erythropoiesis Microenvironment Macrophage.

Etiopathogenesis of Parkinson’s disease:A new beginning?

在线全文

cnki会议

学校读者我要写书评

暂无评论

Etiopathogenesis of Parkinson’s disease:A new beginning?

中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Wei-Dong LE Parkinson''s Disease Research center,Baylor College of Medicine,Institute of Neurology,shanghai Jiao Tong university, School of Medicine,shanghai 20025 china

＜正＞Parkinson’s disease（PD） probably represents a syndrome of different disorders and etiologies converging into a relatively uniform neurodegenerative *** loss of dopaminergic（DAergic） neurons in the substantia nigra（SN） is the pathological hallmark of PD but the mechanisms underlying the loss of DAergic neurons in PD are still poorly understood.A complex interaction of genetic and environmental factors has been thought to play a critical *** on our recent findings in the disease cause and pathogenesis,we postulate that the pathogenic mechanisms may begin much earlier,possibly even in the prenatal *** some patients with PD may be born with fewer than normal number of dopaminergic（and non-dopaminergic） neurons as a result of genetic or other abnormalities sustained during the prenatal or perinatal period,and as a result of the normal age-related neuronal attrition eventually reach the critical threshold（60% or more） of neuronal loss needed for onset of PD to become clinically *** this talk we provide emerging evidence that genetic disruption of normal development,coupled with subsequent environmental factors（the so called "multiple-hit hypothesis"）,plays an important role in the etiopathogenesis of PD.

关键词： Parkinson’s disease etiopathogenesis biomarker genetics environmental factor

SCAP gene polymorphisms decrease the risk of non-alcoholic fatty liver disease in female metabolic syndrome subjectsr

在线全文

cnki会议

学校读者我要写书评

暂无评论

SCAP gene polymorphisms decrease the risk of non-alcoholic f...

第二十一次全国中西医结合肝病学术会议

作者： Shanshan Sun 1,Miao Wang (1,2),Haiyan Song 1,Tao Wu (1,3),Huafeng Wei (1,2),Songhua He 2,Zhaoguo Ding 5,Guang Ji (1,4) 1.Institute of Digestive Disease,Longhua Hospital,shanghai university of Traditional Chinese Medicine, shanghai 200032,china 2.Department of Internal medicine of traditional Chinese Medicine,Longhua Hospital,shanghai university of Traditional Chinese Medicine,shanghai 200032,china 3.center of Chinese medicine therapy and systems biology,shanghai university of Traditional Chinese Medicine, shanghai 201203,china 4.E-institute of shanghai Municipal Education Commission,shanghai university of Traditional Chinese Medicine,shanghai 201203,china 5.Department of Statistics,Uppsala university,Uppsala,Sweden.

Background:The prevalence of Nonalcoholic fatty liver disease(NAFLD)in metabolic syndrome(MS) population is much higher than that in non-MS,NAFLD is recognized as the hepatic additional and specific manifestation of *** variants in the human SREBF-1,SREBF-2 and SCAP genes have been demonstrated to associate with dyslipidemia,meanwhile metabolism of cholesterol and fatty acids plays an important role in the pathogenesis of NAFLD,so we hypothesized that some variants in these genes may be associated with NAFLD. Method:A total of 363 unrelated individuals were enrolled in this study,in which 100 were healthy control subjects and 263 diagnosed as MS(160 complicated with NAFLD,103 without NAFLD).In total,14 tag SNPs of SREBF-1,SREBF-2 and SCAP were chosen for our study. Result:The rs2101247 of SCAP was significantly different between MS+NAFLD group and MS-NAFLD group,but the statistical significance was only observed in *** with the GG genotype, the variant genotypes GA/GG of rs2101247 were associated with a significantly decreased risk for NAFLD(adjusted OR,0.201;95%CI,0.061-0.664;P=0.009/adjusted OR,0.184;95%CI, 0.053-0.640;P=0.008)in female *** neither the lipid levels nor BMI were significant differences among GG,GA and AA genotypes. Conclusion:The present study demonstrates SCAP rs2101247 A allele might decrease the risk of NAFLD in female MS *** studies are warranted to replicate this finding in independent and larger populations.

关键词： genetic polymorphism Nonalcoholic fatty liver disease,SCAP

在线全文

cnki会议

学校读者我要写书评

暂无评论

原发性肝细胞癌的分离分析

复旦学报（医学版） 2002年第4期29卷 272-275页

作者：蔡如琳孟炜陆鸿雁江峰沈福民林文尧姜庆五复旦大学公共卫生学院流行病学教研室上海200032 江苏省海门市卫生防疫站海门226100

目的　对海门市 10 0个原发性肝细胞癌先证者家系的遗传方式进行研究 ,探讨肝癌可能的遗传模式。方法　应用Li Mantel Gart法和SEGRANB软件进行简单分离分析 ,拟合确认概率π ,分离比 p和散发概率x。用PPAP软件进行综合分离分析 ,估计... 详细信息

目的　对海门市 10 0个原发性肝细胞癌先证者家系的遗传方式进行研究 ,探讨肝癌可能的遗传模式。方法　应用Li Mantel Gart法和SEGRANB软件进行简单分离分析 ,拟合确认概率π ,分离比 p和散发概率x。用PPAP软件进行综合分离分析 ,估计原发性肝癌可能的遗传模式。结果　Li Mantel Gart法估计的分离比为0 .10 72 46 38,95 %可信限为 0 .0 432 49～ 0 .139898。应用SEGRANB软件 ,以最大似然法拟合的确认概率为0 .2 30 330 3,分离比为 0 .1134 16 1,散发概率为 0 .46 92 795。结果提示肝癌不符合单基因遗传模式。用PPAP综合分离分析结果提示符合多主基因遗传模式 ,估计的基因频率为 3.0 96 75 1× 10 -2 。结论　原发性肝细胞癌不符合单基因遗传模式 ,伴有一定的散发病例 ,是一种多基因遗传病。

关键词：原发性肝细胞癌分离分析遗传模式

Smad4 is required for the normal organization of the cartilage growth plate

在线全文

学校读者我要写书评

暂无评论

Smad4 is required for the normal organization of the cartila...

中国遗传学会七届一次青年研讨会暨上海高校模式生物E——...

作者： Jishuai Zhang, Xiaohong Tan,Wenlong Li, Youliang Wang, Jian Wang, Xuan Cheng and Xiao Yang (genetic Laboratory of Development and Diseases, Institute of Biotechnology, Beijing 100071 Model animal research center, Nanjing university Model Organism Division, E-insritutes of shanghai Universities, shanghai Second Medical university, P.R.china)

Smad4 is the central intracellular mediator of transforming growth factor-β(TGF-β) signals. To study the role of Smad4 in skeletal development, we introduced a conditional mutation of the gene in chondrocytes using Cre-loxP system. We showed that Smad4 was expressed strongly in prehypertrophic and hypertrophic chondrocytes. The abrogation of Smad4 in chondrocytes resulted in dwarfism with a severely disorganized growth plate characterized by expanded resting zone of chondrocytes, reduced chondrocyte proliferation, accelerated hypertrophic differentiation and ectopic bone collars in perichondrium. Meanwhile, Smad4 mutant mice exhibited decreased expression of molecules in Indian hedgehog/parathyroid hormone-related protein (Ihh/PTHrP) signaling. The cultured mutant metatarsal bones failed to response to both bone morphogenetic protein-2 (BMP-2) and TGF-β1, while the hypertrophic differentiation was largely inhibited by Sonic hedgehog (Shh). These indicated that Ihh/PTHrP inhibited the hypertrophic differentiation of chondrocytes independent of the Smad4 mediated BMP and TGF-P signals. All these data provided the first genetic evidence demonstrating that Smad4 mediated TGF-P signals inhibit the chondrocyte hypertrophic differentiation, and are required for maintaining the normal organization of chondrocytes in the growth plate.

关键词：

Expression of p53, p16 and COX-2 in pancreatic cancer with tissue microarray

在线全文

cnki会议

学校读者我要写书评

暂无评论

Hepatobiliary & Pancreatic Diseases International 2006年第1期5卷 138-142页

作者： Lei Xu, You-Ming Li, Chao-Hui Yu, Lan Li, You-Shi Liu, Bao-Feng Zhang, Jing Fang, Qiong Zhou, Ying Hu and Hen-Jun Gao Department of Gastroenterology, First Affiliated Hospital, Zhejiang university School of Medicine, Hangzhou 310003, china and National Engineering center for Biochip, shanghai 200000, china Department of Gastroenterology First Affiliated Hospital Zhejiang University School of Medicine Hangzhou 310003 China.

BACKGROUND: Pancreatic cancer development and progression is driven by the accumulation of genetic changes. In this study we constructed tissue microarray containing specimens from pancreatic cancer, adjacent non-cancer tissue and normal tissue to survey the expression of p53, p16 and cyclooxyganase-2 (COX-2). METHODS: Tissue microarray containing 337 specimens from different stages of pancreatic cancer, adjacent noncancer tissue and normal tissues was constructed, and the expression of p53, p16 and COX-2 was assayed by immunohistochemistry to consecutive formalin-fixed tissue microarray sections. RESULTS: The expression of p53, p16 and COX-2 was significantly higher in tumorous tissues than in non-tumorons ones. A significant relationship was observed between p53 and COX-2, or p16 and COX-2. But no obvious correlation was seen between p53 and p16 expressions. Logistic regression analysis showed p53 and COX-2 as dependent predictors in pancreatic carcinogenesis, and a reciprocal relationship to neoplastic progression between p53 and COX-2. CONCLUSION: Combination analysis of p53 and COX-2 may be useful in predicting pancreatic carcinogenesis.

关键词： pancreatic cancer tissue microarray p53 p16 cyclooxygenase-2