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病理基因
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  pathological gene
     BACKGROUND:Researches find that Alzheimer disease(AD) may relate with the pathological gene in chromosome; However,the relationship between Apolipoprotein E(ApoE) gene that located on No. 19 chromosome and the onset of AD and vascular dementia (VD) is still not clear.
     背景:研究发现阿尔茨海默病与染色体的病理基因可能有关,而位于19号染色体上ApoE基因与阿尔茨海默病及血管性痴呆发病的关系仍不确切。
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  “病理基因”译为未确定词的双语例句
     Clinic Study of Peutz-Jeghers Syndrome and the Screen and Annotation of Its Related Genes
     黑斑息肉综合征临床诊治及相关病理基因筛选研究
短句来源
     Objective The model that the rats are filled by thyroxin are examined , their cardic muscle structure , ultrastructure, physiology structure, hormone level, cell gene and pathology gene are inspected through biochemistry, electron microscope , super liquid chromatogram and RT-PCR .
     目的 通过采用灌胃法诱导建立甲亢大鼠合并心脏病变的模型,运用生化、电镜、高效液相色谱法、逆转录多聚酶链法(RT-PCR),检测高甲状腺素水平下,大鼠心肌结构、超微结构、生理功能、激素水平、细胞因子、病理基因,确定造模的可靠性。 使用复方甲亢片、纯中药、甲巯咪唑等进行干预,比较三种药物的疗效,从而得出结论。
短句来源
     Although environmental factor has an important role we should not neglect the genetic predisposition in its etiology. The disease may be caused by the combination of these two factors exceeding certain threshold intensity. Thus using“Inheritance-iodine deficiency”to interpret the etiopathogenesis of endemic cretinism is appropriate.
     分析结果认为:地方性克汀病是一种多基因遗传疾病,其遗传度为48%,这表明影响发病的环境因素起着比较重要的作用,而遗传因素更不能忽视,病理基因乃是本病发生的物质基础,两者结合超过了一定的强度或阈值,就会发生地方性克汀病,因此,本病用“遗传—缺碘”这一病因来解释比较恰当。
短句来源
     Objective:To show the expression of pathogenesis associated genes in placentae with pregnancy-induced hypertension syndrome(PIHS).
     目的研究与细胞因子信号转导等相关的病理基因在妊娠高血压综合征(妊高征)胎盘组织中的表达变化。
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  相似匹配句对
     4 new genes were obtained.
     U基因
短句来源
     DESIGN:A case controlled genetic and pathological analysis.
     设计:临床、病理基因分析对照研究。
短句来源
     Clinicopathological Implication of O~(6)-methylguanine-DNA-methyltransferase Gene Expression in Gastric Carcinoma
     胃癌MGMT基因表达的临床病理意义
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     The Gene of All Fears
     害怕的基因
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     Pathological examination proved that E.
     病理证实E .
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  pathological gene
These patients are probably carriers of the pathological gene responsible for the disease.
      


It has been already established that the person with erythrocyte glucose-6-phosphate dehydrogenase deficiency is liable to develop favism. It is generally accepted that the heterozygote does not develop the disease. In order to detect heterozy-got.es, the writer has used three methods (namely MR-microhistochemical elution test, MR-mierophotometric test, and glutathione stability test), and found that the MR-microhistochemical elution test is most sensitive, detecting heterozygotes in 92%. Moreover, there are...

It has been already established that the person with erythrocyte glucose-6-phosphate dehydrogenase deficiency is liable to develop favism. It is generally accepted that the heterozygote does not develop the disease. In order to detect heterozy-got.es, the writer has used three methods (namely MR-microhistochemical elution test, MR-mierophotometric test, and glutathione stability test), and found that the MR-microhistochemical elution test is most sensitive, detecting heterozygotes in 92%. Moreover, there are 17 females with history of favism 10 out of 17 females with history of favism are found to be heterozygotes. This indicates clearly that heterozygotes are liable to suffer the disease after ingestion of fava beans.In addition, according to the degree of expressivity shown by the microhistoche-mical elution method, the heterozygotes can be devided into three types: the reactive, the intermediate, and the non-reactive. Out of 44 cases of heterozygote, there are 29 cases of reactive type (65.9%), evidently being more than the other two types. Among 11 cases of heterozygotes with history of favism, there are 10 reactive including the intermediate. This illustrates that the occurrence of favism is more or less related to the degree of expressivity. Therefore, the reactive and intermediate types should be included as an object of prophylactic measures.

蚕豆病是进食蚕豆后引起的一种急性溶血性疾病。己经查明,红细胞中缺乏6-磷酸葡萄糖脱氢酶是对蚕豆敏感的主要原因。这种酶缺乏是按伴性不完全显性规律遗传的。一般认为,携带此病理基因的杂合子不发病。本文探讨鉴定杂合子较敏感的方法,并研究杂合子是否发病。在比较了高铁血红蛋白还原试验微量洗脱法、微量比色法和谷胱甘肽稳定性试验后认为,前法较后二法敏感。 用上述三种方法检查了17例有蚕豆病史的女性,证明其中10例为杂合子,6例为纯合子。说明杂合子可以发病。若将杂合子按微量洗脱法显示的表现度分为三型:即反应型、中间型和非反应型,则有患病史的杂合子绝大多数属于反应型及中间型(11例中之10例)。说明杂合子是否发病与其表现度有关。故建议在预防工作中,将此二型列入预防对象。

In studying the genetic factors of endemic cretinism, we used four approaches. 1. Inbreeding investigation. The rate of population inbreeding was 13.14%. Average inbreeding coefficient was 82.13_x10~(-4). The rate of inbreeding in patients with cretinism accounted for 17.35%. 2. Chromosome analysis. Diploid in 19 healthy subjects was 97.72%. In 74 cretin cases, diploid was found in 93.82%. The karyotype in one of those was 47, XXX. 3. Dermatoglyphic studies in 16 patients with cretinism revealed expansion of...

In studying the genetic factors of endemic cretinism, we used four approaches. 1. Inbreeding investigation. The rate of population inbreeding was 13.14%. Average inbreeding coefficient was 82.13_x10~(-4). The rate of inbreeding in patients with cretinism accounted for 17.35%. 2. Chromosome analysis. Diploid in 19 healthy subjects was 97.72%. In 74 cretin cases, diploid was found in 93.82%. The karyotype in one of those was 47, XXX. 3. Dermatoglyphic studies in 16 patients with cretinism revealed expansion of atd angle, abnormal palmar flexion crease and fibular loop or proximal arch of hallucal area was found higher than healthy subjects. As the hallucal arch rises, atd angle expands. 4. Pedigree analysis. The incidence of cousins of patients with cretinism was 3.15%-highest among grandfather-mother-and older brother-younger sister. In cousins of every degree, first degree cousins had the highest incidence. If parents had normal phenotype, their children’s incidence was 86.21%. If one of the parents had cretinism, their children’s incidence was 13.79%. We consider endemic cretinism is a disease with polygenic inheritance. Its heritability is 48%. Although environmental factor has an important role we should not neglect the genetic predisposition in its etiology. The disease may be caused by the combination of these two factors exceeding certain threshold intensity. Thus using“Inheritance-iodine deficiency”to interpret the etiopathogenesis of endemic cretinism is appropriate.

为了探讨地方性克汀病的遗传因素,本文通过:(1)近亲婚配的调查,群体近亲婚配率为13.14%,平均近交系数82.13×10~(-4),克汀病患者近亲婚配率为17.35%;(2)染色体检查,19例正常人二倍体占97.72%,74例克汀病患者二倍体占93.82%,其中1例为47,XXX:(3)克汀病手、足皮纹学16项指标的研究,atd角增大,异常掌屈纹和拇趾球部纹的腓箕形、近弓形出现率高于正常人,拇趾弓形纹出现率增高,足apd角增大;(4)家系调查,克汀病亲属患病率为3.15%,其中以祖父母和兄妹患病率最高,在各级亲属中,一级亲属患病率最高,父母双亲表现型正常,子女患病率为86.21%;双亲之一为患者,子女患病率为13.79%。分析结果认为:地方性克汀病是一种多基因遗传疾病,其遗传度为48%,这表明影响发病的环境因素起着比较重要的作用,而遗传因素更不能忽视,病理基因乃是本病发生的物质基础,两者结合超过了一定的强度或阈值,就会发生地方性克汀病,因此,本病用“遗传—缺碘”这一病因来解释比较恰当。

Objective:To study the phenotype and genotype of a thrombophilia family.Methods:Antigens and activities of protein C,antithrombin Ⅲ,protein S,plasminogen and activated protein C resistance were assayed in 13 members from four generations of the family.Results:TypeⅠ protein C deficiency was revealed in 5 members including the 3 members with deep vein thrombosis.All the exons and intron/exon junctions of the protein C gene were amplified by PCR.No abnormal band was found in SSCP assay.DNA sequencing identified...

Objective:To study the phenotype and genotype of a thrombophilia family.Methods:Antigens and activities of protein C,antithrombin Ⅲ,protein S,plasminogen and activated protein C resistance were assayed in 13 members from four generations of the family.Results:TypeⅠ protein C deficiency was revealed in 5 members including the 3 members with deep vein thrombosis.All the exons and intron/exon junctions of the protein C gene were amplified by PCR.No abnormal band was found in SSCP assay.DNA sequencing identified a novel mutation 3444C→A in exon Ⅵ of protein C gene leading to His134Asn.This mutation erased a Hph Ⅰ site.PCR/HphⅠ analysis demonstrated that 6 members including 5 protein C deficiency members had the same mutations.Conclusion:His134Asn is a novel mutation causing type Ⅰ protein C deficiency. 

目的:研究一家族性血栓病相关病因的表型及基因型。方法:先证者、其母、二兄分别在35,19,33岁起无明显诱因患反复性下肢深静脉血栓(DVT)。对其四代13个家庭成员的抗凝血酶Ⅲ、蛋白C(PC)、蛋白S(PS)、纤溶酶原的抗原和活性及活化的PC抗性等进行检测。结果:该家族5个成员患有Ⅰ型杂合子PC缺乏症(PC抗原和活性降低50%左右)。PC基因各外显子及外显子、内含子连接区聚合酶链反应-单链构象多态性(PCR-SSCP)未发现明显的异常带;亚克隆后测序发现PC的第Ⅵ外显子3444C→A导致134His→Asn变异,这是国外尚未报道的新突变,被命名为PC长沙。此突变使限制性内切酶HphⅠ位点丧失,用PCR/HphⅠ进行家系分析,证实了6个家系成员(包括5个PC缺乏者)具有同样的突变。结论:His134Asn是此家族PC缺乏所致DVT的密切相关病理基因型。

 
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