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1.
经络—神经—内分泌—免疫网络   总被引:6,自引:0,他引:6  
张燕华 《华西医学》1998,13(3):316-317
本文阐述了经络系统和神经—内分泌—免疫网络的联系,对经络—神经—内分泌—免疫网络的结构体系进行了具体的分析,从经络—神经—内分泌—免疫网络调节的角度对针灸调节免疫的机理进行了深入的研究,为针灸免疫学基本理论的建立奠定了基础  相似文献   

2.
目的 建立2-氯-4-硝基苯-β-D-半乳糖-麦芽二糖苷(GalG2-CNP)作底物测定淀粉酶的方法。方法 用连续监测法对pH值,Km值及最适底物浓度等反应条件进行实验研究,并对建立的方法进行评价。结果 用双试剂连续监测法;试剂Ⅰ:含KSCN 200mmol/L,CaCl26.7mmol/L,NaCl400mmol/L;试剂Ⅱ:含GalG2-CNP20mmol/L;均用pH6.0 50mmol/L MES缓冲液。线性范围达1200U/L批内CV=2.77%,批间CV=3.56%,与参考方法(BPS-G7)有良好的相关性。结论 本法操作简便,结果准确,可用于常规分析。  相似文献   

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4.
目的 建立简便,灵敏,试剂稳定性好的2-(8′-羟基喹啉-5′-磺酸-7′-偶氮)-变色酸(8Q5SAC)血清镁测定法,方法 用国内合成的8Q5SAC作显色剂,EGTA掩蔽钙,在甘氨酸-NaOH缓冲体系中以分光光度法测定血清镁。结果 该法线性0~3mmol/L,平均回收率98.1%,变异系数1.92%~2.98%,与Calmagite法对照,r=0.996,P〉0.2;与MTB法对照,r=0.98  相似文献   

5.
根据作者来稿中经常疏漏问题,特请作者注意以下两点:1、参考文献一般限10条以内。未公开发表的资料请勿引用。著录格式如下(含标点):[期刊]序号作者.论文题.刊名,出版年,卷号(期号):起—止页.[专著]序号作者.书名.版本(第一版可略).出版地:出版者,出版年.起—止页.作者不超过3位时,全部列出;超过3位时,只列出3位,后面加等字或相应外文,作者  相似文献   

6.
Peutz——Jeghers综合征(色素沉着——胃肠道多发性息肉症候群),是一种先天性疾病。国内1958年葛氏及钟氏首先各报告1例(可能为同1病例,均为张××,女,18岁,广东梅县人,侨居印尼)。此后相继报告,1984年刘氏收集57份国内资料159例及其本人9例共计168例作了综述报道。近几年来,我院收治4例,现报告讨论如下。病例报告例1 黄某,女,21岁,广东东莞县人,住院号00619。因间歇性腹痛,吐咖啡色液约400毫升,并有头晕、心悸于1979年6月9日入院。于12岁时因有肠阻塞征行剖腹探查术,术后诊断未明。  相似文献   

7.
根据作者来稿中经常疏漏问题,特请作者注意以下两点:1、参考文献一般限10条以内。未公开以表的资料请勿引用。著录格式如下(含标点):  相似文献   

8.
目的:建立2-(8‘-羟基喹啉-5’-磺酸-7’-偶氮)-变色酸(8Q5SAC)血清钙测定法。方法 以8Q5SAC作显色剂,8-羟基喹啉掩蔽镁,在三乙酸胺缓冲介质中以分光光度法测定血清钙。结果:方法学线性范围0-4.5mmol/L,平均回收率100.85%,批内CV0.84% ̄1.24%,批间CV1.52% ̄1.56%,与OCPC法对照,r=0.995,P〉0.5,与MTB法对照,r=0.989,  相似文献   

9.
目的 建立灵敏度高、选择性好的2-(8′-羟基喹啉-5′磺酸-7′-偶氮)-鸾以酸(简称8Q5SAC)血清钙络合解离测定法。方法 在甘氨酸-NaOH缓冲介质中,8Q5SAC与钙、镁等金属离子络合显色,加入EGTA使8Q5SAC与钙解离,以测定吸光度的下降值分析血清钙。对反应条件、方法性能进行系统研究。结果 该法线性0 ̄5mmol/L,平均回收率99.3%,变异系数0.56% ̄1.81%。与邻甲酚酞  相似文献   

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11.
目的分析中国广东籍人β纤维蛋白原G/A455(βFBG455G/A)基因多态性,计算各型的基因频率,测定不同基因型人血浆纤维蛋白原(FBG)水平,探讨该基因多态性与基因表达的相关性。方法应用聚合酶链反应限制性酶切分析方法,分析210名广东籍人DNA样品的βFBG455G/A多态性,比浊法测定其中92名血浆FBG水平。结果βFBG455A/A纯合子8名,基因型频率为0.038;βFBG455G/G野生型108名,基因型频率为0.514;βFBG455G/A杂合子94名,基因型频率为0448。A等位基因频率为0.262。46名G/A型血浆FBG水平为(2.18±0.24)g/L,42名G/G型为(2.03±0.25)g/L,两组比较差异有显著性(P<0.01)。结论中国广东籍人群中βFBG455A等位基因频率比欧洲一些国家高(P<0.01)。G/A型血浆FBG水平比G/G型高(P<0.01)。提示该基因位点多态性与血浆FBG的表达有一定相关。  相似文献   

12.
目的调查156名广东汉族健康人纤维蛋白原(Fg)β-455G/A、-148C/T、448G/A基因多态性频率分布、连锁不平衡关系及与血浆Fg水平的关系。方法用限制性片段长度多态性(RFLP)分析方法和比浊法检测血浆Fg水平。结果等位基因A^-455、T-148和A^448的频率分别是为0.276,0.285及0.272。156人中3个多态性位点G^-455、C^-148和G^448或A^-455、  相似文献   

13.
A common mutation (G-455--> A) in the promoter region of the beta-fibrinogen gene has been associated with elevated plasma fibrinogen levels. Whether fibrinogen genotype affects plasma fibrinogen levels and risk of ischemic heart disease in the general population has not been studied. We investigated the association between fibrinogen genotype, plasma fibrinogen levels, and ischemic heart disease in a general population sample (n = 9,127). The A-allele (relative frequency, 0.20) was associated with elevated plasma fibrinogen levels in both genders (P < 0.001). While the effect of the A-allele on fibrinogen level was additive in men, the effect was dominant in postmenopausal women. The A-allele raising effect appeared to be two- to threefold greater in individuals with ischemic heart disease than in those without. An increase of 1 SD in plasma fibrinogen increased the odds ratio for ischemic heart disease by approximately 20% (P < 0.01 for women and < 0.005 for men). However, the frequency of the A-allele was similar in those with and without ischemic heart disease, and genotype was not a predictor of disease. These results demonstrate that the (G-455--> A) mutation in the promoter region of the beta-fibrinogen gene is associated with an increase in plasma fibrinogen in both genders in the general population. This increase does not appear to cause ischemic heart disease.  相似文献   

14.
目的分析纤维蛋白原(FIB)3个紧密连锁不平衡基因位点BβG/A-455、C/T-148、G/A+448基因多态性及血浆FIB水平与缺血性脑血管病的相关性。方法以我院2010年2月至2012年2月收治的缺血性脑血管病患者89例为病例组,以同期在我院健康体检的50例为对照组,检测两组血浆FIB水平,使用多聚酶链式反应-限制性片段长度多态性(PCR-RFLP)技术测定BβG/A-455、C/T-148、G/A+448基因片段。结果缺血性脑血管病患者中,FIB基因型分布、BβA-455、T-148、A+448等位基因频率与对照组比较差异有统计学意义(P0.05)。两组血浆FIB水平比较差异有统计学意义(P0.01),病例组高于对照组。A、T等位基因携带者与非携带者血浆FIB水平比较差异有统计学意义(缺血性脑血管病患者组,P0.01;对照组,P0.05),携带者高于非携带者。结论 FIB 3个紧密连锁不平衡基因位点BβG/A-455、C/T-148、G/A+448基因多态性及血浆FIB水平与缺血性脑血管病呈明显的正相关,BβG/A-455、C/T-148、G/A+448基因多态性可能是缺血性脑血管病的遗传易感因素。  相似文献   

15.
β-纤维蛋白原-455 G/A基因多态性与脑梗死的关系   总被引:1,自引:0,他引:1  
目的:探讨β-纤维蛋白原-455 G/A(-βFg-455G/A)基因多态性与中国东北地区汉族脑梗死发病(CI)的关系。方法:应用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)方法,检测脑梗死组(CI组)72例和对照组69例-βFg-455G/A基因的多态性,并测定其血浆纤维蛋白原(Fg)的含量。结果:经χ2检验,各基因型频率和等位基因频率在两组间均无显著性差异(P>0.05);CI组血浆Fg水平(2.70±1.05 g/L)和对照组(2.62±0.51 g/L)比较差异无显著性意义(P>0.05)。结论:本研究未发现-βFg-455G/A基因多态性与脑梗死之间存在相关关系。  相似文献   

16.
纤维蛋白原基因多态性与缺血性心脑血管病的关系   总被引:19,自引:0,他引:19  
目的:调查健康人、心肌梗死患者及脑梗死患者的纤维蛋白原(Fg)β-455G/A、-148C/T、448G/A基因多态性频率分布、Fg分子反应性及与血浆Fg水平的关系。方法:用限制性片段长度多态性分析基因频率分布,用计算机辅助的纤维蛋白单体聚合反应分析方法和Clauss法分析血浆Fg水平。结果:等位基因-455A、-148T和448A在正常人中的频率分别是0.185,0.194及0.192;在心肌梗死患者中的频率分别是0.295,0.318及0.307;在脑梗死患者中的频率分别是0.177,0.193及0.182。心肌梗死患者中-455A、-148T和448A的频率比健康人明显升高。3个多态性位点-455G、-148C和448G或-455A、-148T和448A分别紧密连锁,符合率超过98%。心脑血管病患者的Fg功能明显增高且与Fg水平相关。3个多态性位点不同基因型组血浆Fg水平差异无显著性。结论:3对等位基因紧密连锁不平衡,不同基因型组血浆Fg水平差异无显著性,心肌梗死患者中-455A、-148T和448A的频率比健康人明显升高。提示Fgβ-455G/A、-148C/T和448G/A三种基因多态性与血浆Fg水平无关,而与心肌梗死的发病相关。心脑血管病患者不仅Fg功能明显增高,且与Fg水平相关。  相似文献   

17.
目的分析β纤维蛋白原(FGB)基因启动子区-455 bp位点多态性与新疆哈萨克族冠心病(CHD)的关系。方法采用聚合酶链式反应-限制性片段长度多态性分析法检测新疆哈萨克族220例CHD患者和200例正常对照者的FGB基因启动子区-455 bp位点多态性,并测定血浆纤维蛋白原(Fg)水平。结果①CHD组GA/AA基因型及A等位基因含量均高于对照组,差异有统计学意义(P均<0.05);②CHD组各基因型的Fg水平均高于对照组同种基因型,在CHD和对照组中,不同基因型Fg水平,以AA基因型为最高,GG基因型为最低,组间比较差异均有统计学意义(P<0.05)。结论β纤维蛋白原基因启动子区-455 bp位点多态性与新疆哈萨克族CHD有关,A等位基因是CHD的易感危险因素,可能通过影响Fg水平与CHD产生联系。  相似文献   

18.
Summary.  Background: Confounding by common causes and reverse causation have been proposed as explanations for the association between high fibrinogen levels and cardiovascular disease. Genetic variants can alter fibrinogen characteristics and are not subject to these problems. Objectives: To determine the fibrinogen plasma levels for genotypic variants in fibrinogen-Aα (FGA Thr312Ala) and fibrinogen-Bβ (FGB − 455G/A), and whether these variants are associated with arterial thrombosis. Methods: Fibrinogen genotypes were determined in a population-based case–control study including women aged 18–50 years; 218 cases with myocardial infarction, 192 cases with ischemic stroke, and 769 healthy controls. Fibrinogen levels were determined in the control population. Results: The FGB − 455G/A variant increased plasma fibrinogen levels, whereas the FGA Thr312Ala variant lowered plasma fibrinogen levels, albeit to a modest extent. The risk of ischemic stroke was altered when the homozygote minor allele was compared with the homozygote major allele. The FGA Thr312Ala single-nucleotide polymorphism (SNP) was associated with a decrease in risk [odds ratio (OR) 0.43; 95% confidence interval (CI) 0.21–0.87], whereas the FGB − 455G/A SNP might have increased the risk (OR 1.76; 95% CI  0.7–4.03). The risk of myocardial infarction was not altered for either SNP (FGA Thr312Ala, OR 0.98, 95% CI  0.40–2.40; FGB − 455G/A, OR 0.98, 95% CI  0.40–2.40). Conclusions: With the genetic variations as markers of plasma fibrinogen levels alterations, thereby ruling out confounding and reverse causation, our results suggest that plasma fibrinogen levels could play a more pronounced role as risk factors for ischemic stroke than for myocardial infarction.  相似文献   

19.
BACKGROUND: Previous genotype-phenotype association studies of fibrinogen have been limited by incomplete knowledge of genomic sequence variation within and between major ethnic groups in FGB, FGA, and FGG. METHODS: We characterized the linkage disequilibrium patterns and haplotype structure across the human fibrinogen gene locus in European- and African-American populations. We analyzed the association between common polymorphisms in the fibrinogen genes and circulating levels of both 'functional' fibrinogen (measured by the Clauss clotting rate method) and total fibrinogen (measured by immunonephelometry) in a large, multi-center, bi-racial cohort of young US adults. RESULTS: A common haplotype tagged by the A minor allele of the well-studied FGB-455 G/A promoter polymorphism (FGB 1437) was confirmed to be strongly associated with increased plasma fibrinogen levels. Two non-coding variants specific to African-American chromosomes, FGA 3845 A and FGG 5729 G, were each associated with lower plasma fibrinogen levels. In European-Americans, a common haplotype tagged by FGA Thr312Ala and several other variant alleles across the fibrinogen gene locus was strongly associated with decreased fibrinogen levels as measured by functional assay, but not by immunoassay. Overall, common polymorphisms within the three fibrinogen genes explain < 2% of the variability in plasma fibrinogen concentration. CONCLUSIONS: In young adults, fibrinogen multi-locus genotypes are associated with plasma fibrinogen levels. The specific single nucleotide polymorphism and haplotype patterns for these associations differ according to population and also according to phenotypic assay. It is likely that a substantial proportion of the heritable component of plasma fibrinogen concentration is due to genetic variation outside the three fibrinogen genes.  相似文献   

20.
G-455A polymorphism of the fibrinogen beta gene and deep vein thrombosis   总被引:11,自引:0,他引:11  
BACKGROUND: Elevated fibrinogen levels have been linked to increased risk for deep venous thrombosis, although it is not clear whether fibrinogen is causal or rather a marker for the presence of other risk factors. A common G/A polymorphism in the gene for the fibrinogen beta-chain (FGB G-455A) is associated with elevated fibrinogen levels. The present study was designed to analyze the role of this genetic marker for deep venous thrombosis. MATERIALS AND METHODS: We performed a case-control study including 307 patients with documented deep venous thrombosis and 316 control subjects. beta-fibrinogen genotypes were determined by allele-specific polymerase chain reaction. RESULTS: GG, GA and AA genotype frequencies were similar among the patients (53.1%, 41.0, 5.9) and controls (51.6%, 42.1, 6.3; P = 0.92). Fibrinogen levels of the patients (median 3.72 g l-1; range 1.93-11.6) did not differ significantly from those of the controls (3.76; 2.17-9.99). Carriers of the homozygous AA genotype had significantly higher fibrinogen levels than noncarriers (patients: 5.32 vs. 3.59; P = 0.024; controls: 6.29 vs. 3.72; P = 0.048). CONCLUSION: Our data suggest that the fibrinogen-elevating FGB G-455A gene polymorphism is not linked to an increased risk for deep venous thrombosis.  相似文献   

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