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1.
胰腺癌中FXYD6蛋白的表达及临床意义   总被引:1,自引:0,他引:1  
目的:探讨FXYD6蛋白在胰腺癌中的表达及临床意义.方法:应用免疫组化法检测FXYD6蛋白在胰腺癌中的表达,并分析其与临床病理因素的关系.结果:47例胰腺癌病例中,FXYD6蛋白阳性表达42例,阳性表达率为89.34%,而正常胰腺组织中不表达或低表达,两组相比有显著性差异(X2=10.863l,P=0.0125).按FXYD6蛋白表达程度将47例胰腺癌病例分为高表达组和低表达组,两组年龄、性别、肿瘤大小及远处转移之间的差异无统计学意义,而肿瘤分化程度(X=11.562,P=0.0031)、淋巴转移(X2=4.1947,P=0.0406)、TNM分期(X2=9.5995,P=0.0223).间的差异有显著统计学意义,肿瘤分化程度低、出现淋巴转移、TNM分期为Ⅲ.Ⅳ期的胰腺癌组织中FXYD6蛋白表达明显增高.Spearman等级相关分析显示,FXYD6蛋白表达程度与肿瘤大小(r=0.2991)、分化程度(r=0.6980)、淋巴转移(r=0.4971)、远处转移相关(r=0.4967).结论:FXYD6蛋白在胰腺癌发病机制中发挥重要作用.  相似文献   

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目的探讨自发性高血压大鼠新的高血压相关基因。方法从自发性高血压大鼠(Spontaneously Hypertensive Rats,SHR)和正常血压大鼠(Wistar-Kyoto,WKY)阻力血管(肠系膜动脉第二、三级分支)和肾脏组织中提取总RNA,利用含10000个大鼠基因的芯片检测两组大鼠mRNA表达水平,找出差异表达的基因,并经RT-PCR和定量RT-PCR初步筛选出高血压新的相关基因。结果从基因芯片的检测结果发现在SHR组中19个基因表达下调,另外19个基因表达上调,其中涉及细胞周期,直接参与代谢的酶,细胞信号转导及核转录因子等基因。选择部分已知的、并可能有功能的代表基因用RT-PCR验证,结果发现FXYD5基因在SHR明显下调,定量RT-PCR验证示FXYD5基因的表达水平在SHR组比WKY组明显下调14.8倍(P<0.01)。结论从基因芯片的结果证明了SHR和WKY不同的遗传异质性。FXYD家族的FXYD5可能与高血压的形成有关,深入研究FXYD5基因及其功能为进一步了解高血压病的分子机制提供新的思路和线索。  相似文献   

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<正>FXYD基因蛋白是指一类有离子通道或离子通道调节作用的小分子单跨膜蛋白,和钠钾泵(也称Na+-K+-ATP酶,钠钾转运体)的结构功能密切相关[1]。高血压病(primary hypertension,PH)是以动脉血压持续升高为主要表现,影响全球近1/3人口的健康,由多种因素导致,具有高度遗传异质性的复杂疾病[2],是脑卒中、冠心病、慢性肾脏疾病、栓塞和血管破裂等多  相似文献   

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自发性高血压大鼠FXYD5基因的实验研究   总被引:2,自引:0,他引:2  
目的 探讨自发性高血压大鼠新的高血压相关基因.方法 从自发性高血压大鼠(Spontaneously Hypertensive Rats,SHR)和正常血压大鼠(Wistar-Kyoto,WKY)阻力血管(肠系膜动脉第二、三级分支)和肾脏组织中提取总RNA,利用含10 000个大鼠基因的芯片检测两组大鼠mRNA表达水平,找出差异表达的基因,并经RT-PCR和定量RT-PCR初步筛选出高血压新的相关基因.结果 从基因芯片的检测结果发现在SHR组中19个基因表达下调,另外19个基因表达上调,其中涉及细胞周期,直接参与代谢的酶,细胞信号转导及核转录因子等基因.选择部分已知的、并可能有功能的代表基因用RT-PCR验证,结果发现FXYD5基因在SHR明显下调,定量RT-PCR验证示FXYD5基因的表达水平在SHR组比WKY组明显下调14.8倍(P<0.01).结论 从基因芯片的结果证明了SHR和WKY不同的遗传异质性.FXYD家族的FXYD5可能与高血压的形成有关,深入研究FXYD5基因及其功能为进一步了解高血压病的分子机制提供新的思路和线索.  相似文献   

5.
目的构建FXYD6蛋白功能区(FXYD6-ex)的原核表达质粒,并诱导FXYD6-ex在原核细胞中表达与纯化,以进一步研究FXYD6功能。方法用全长FXYD6 cDNA扩增FXYD6-ex,扩增产物插入克隆质粒载体pMD18-T Simple并用限制性内切酶酶切,将目的片段插入以限制性内切酶切后的表达质粒载体pET28a(+)中,经PCR电泳和测序证实后转化宿主大肠杆菌Rossetta,异丙基-β-8-D硫代半乳糖(IPTG)诱导重组蛋白表达,镍柱纯化重组蛋白,十二烷基硫酸钠—聚丙烯酰胺(SDS-PAGE)凝胶和Western blot检测鉴定蛋白表达及纯化情况。结果成功构建pET28a(+)-FXYD6-ex大肠杆菌表达载体,并实现该蛋白在大肠杆菌中的高表达,分离纯化的产物纯度达90%。结论本研究成功对FXYD6-ex进行原核表达及纯化;此为后续制备该蛋白抗体库及进一步研究其具体功能奠定了良好基础。  相似文献   

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In 2011, a Shiga toxin (Stx) type 2a-producing enteroaggregative E. coli (EAEC) strain of serotype O104:H4 caused a large lethal outbreak in Northern Europe. Until recently, the pathogenic mechanisms explaining the high virulence of the strain have remained unclear. Our laboratories have shown that EAEC genes encoded on the pAA virulence plasmid, particularly the AggR-regulated AAF/I fimbriae, enhance inflammation and enable the outbreak strain to both adhere to epithelial cells and translocate Stx2a across the intestinal epithelium, possibly explaining the high incidence of the life threatening post-diarrheal sequelae of hemolytic uremic syndrome. Epidemiologic evidence supports a model of EAEC pathogenesis comprising the concerted action of multiple virulence factors along with induction of inflammation. Here, we suggest a model for the pathogenesis of the O104:H4 outbreak strain that includes contributions from EAEC alone, but incorporating additional injury induced by Stx2a.  相似文献   

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56岁妇女因胆囊结石入院。术后第4天发生麻痹性肠梗阻,静脉输注PGF_(2α)(8ug/min)。输注开始后15分钟突然主诉压迫样胸痛,Ⅱ、ⅢaVF,V_5和V_6导联ST段压低和T波倒置。停止输注PGF_(2α)并舌下含服硝酸甘油之后症状缓解,心电图恢复正常。一个月后进行心导管检查。静脉输注PGF_(2α)  相似文献   

12.
Two siblings of consanguineous parents presented in infancy with failure to thrive, mild coarsening of facies, visceromegaly and corneal opacities. One showed reduced hepatic -galactosidase activity suggesting a GM1-gangliosidosis variant. Both patients developed progressive coarsening of facies, slow neurological deterioration, macular cherry-red spots and punctate cataracts over the first decade. Urine screening with thin layer chromatography revealed abnormal excretion of two slow-moving oligosaccharide bands and leukocyte and fibroblast neuraminidase activity was grossly reduced. The mother, phenotypically normal, showed levels of neuraminidase compatible with heterozygosity.These patients have primary neuraminidase deficiency. The clinical and biochemical variables are reviewed.  相似文献   

13.
目的 以干扰素α 2a(IFNα 2a ,罗荛愫 ,罗氏 )为对照 ,评估聚乙二醇干扰素α 2a(FEG IFNα 2a ,派罗欣 ,罗氏 )治疗中国慢性丙型肝炎的效果及其安全性和耐受性。方法 采用随机、开放和对照的多中心临床试验设计 ,将 2 0 8例慢性丙型肝炎患者随机分为PEG IFNα 2a组 (10 6例 )和IFNα 2a组 (10 2例 ) ,两组治疗前HCVRNA、基因型等临床资料具有可比性 ,以病毒学应答和生化应答作为疗效的主要评价指标。同时观察患者药物治疗后的不良反应。结果 PEG IFNα 2a组持续性病毒应答率 (SVR)显著高于IFNα 2a组 (分别是 4 1.5 1%和 16 .6 7% ,P <0 .0 0 0 1)。PEG IFNα 2a治疗HCV基因 1型和非基因 1型的SVR显著高于IFNα 2a组 (P =0 .0 0 3) ,PEG IFNα 2a治疗高病毒载量慢性丙型肝炎的SVR明显高于IFNα 2a组 (P =0 .0 0 0 3) ,但是低病毒载量的SVR两组之间差异无显著性 (P =0 .0 5 9)。PEG IFNα 2a与IFNα 2a有相似的不良反应 ,不良反应间差异无显著性 ,两组患者均无发生不良事件。结论 PEG IFNα 2a对慢性丙型肝炎患者的疗效优于传统干扰素IFNα 2a ,在中国慢性丙型肝炎人群中具有较好的安全性和耐受性。  相似文献   

14.
Selective COX-2 inhibitors: a promise unfulfilled?   总被引:4,自引:0,他引:4  
  相似文献   

15.
Cross-sectionally, higher weight is associated with higher blood pressure levels; prospectively, baseline weight and weight gain predict higher blood pressure. The loss of weight is frequently associated with a decrease in blood pressure. These findings suggest that weight gain may pathophysiologically contribute to blood pressure elevation. In this review, we present data to indicate that the reverse is also true; persons of equal weight who had higher initial blood pressures gain more weight in the future. We also propose a plausible hypothesis to explain this reverse relationship. Both the blood pressure elevation and the gain of weight may reflect a primary increase in sympathetic tone. It is well known that in a milieu of increased sympathetic tone, the beta-adrenergic responsiveness decreases. Sympathetic overactivity and decreased cardiovascular beta-adrenergic responsiveness have been described in hypertension. beta-Adrenergic receptors mediate increases in energy expenditure. If these metabolic receptors were downregulated in hypertension, the ability of hypertensive patients to dissipate calories would decrease and they would gain more weight. The possible relationship of decreased beta-adrenergic responsiveness to weight in hypertension can be experimentally tested. Such research may contribute to an explanation of why patients with hypertension can rarely lose weight. An understanding of this pathophysiological relationship may open new avenues for therapeutic interventions.  相似文献   

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1临床资料 1.1一般资料我科在2001年-2002年收治慢性乙型肝炎的住院患者,诊断符合2000年西安会议病毒性肝炎防治方案标准[1].其中30例均HBsAg、HBeAg及HBVDNA阳性,为抗病毒适应证;ALT治疗前均在100~150U/L之间,TBIL阴性或<30μmol/L.按入院次序随机分2组治疗.第1组:15例,男12例,女3例.接受干扰素α-2a(迪恩安)600万U治疗,诱导期1/d,连用2周,后改为1/2d,应用10周,再改为1/3d,肌注6个月为1疗程.第2组:15例,男9例,女6例,年龄均在25~50岁,接受干扰素α-2a(迪恩安)300万U治疗,方法同上,2组对比疗效.  相似文献   

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We report here the hematological and molecular features of a novel δ-globin chain variant found in a Southern Thai woman. Her complete blood count was as follows: red blood cell (RBC) count 5.90?×?1012/L, hemoglobin concentration (Hb) 12.6?g/dL, packed cell volume (PCV) 0.41?L/L, mean corpuscular volume (MCV) 69.5 fL, mean corpuscular Hb (MCH) 21.4?pg, mean corpuscular Hb concentration (MCHC) 30.7?g/dL and RBC distribution width (RDW) 13.1%. The blood smear demonstrated microcytic hypochromic RBCs suggestive of thalassemia trait. Hemoglobin analysis identified Hb A2?+?Hb A2-Kiriwong (2.4%) and Hb F (0.1%) on high performance liquid chromatography (HPLC). To characterize the α-thalassemia (α-thal) genotype, common α-thal-1 and α-thal-2 alleles were characterized by multiplex gap-polymerase chain reaction (gap-PCR). The results revealed homozygous α-thal-2 (–α3.7/–α3.7) in this case. DNA sequencing showed the presence of a novel δ-globin gene mutation [δ77(EF1)His→Arg; HBD: c.233A>G] that we named Hb A2-Kiriwong for the village from where the proband lived. In summary, the presence of microcytic hypochromic RBCs in this case was likely the result of the homozygous –α3.7 (rightward) deletion and was not affected by this Hb A2 variant.  相似文献   

20.
聚乙二醇干扰素-α2a治疗乙型肝炎病毒感染   总被引:1,自引:0,他引:1  
W Graham 《传染病信息》2005,18(Z1):38-43
1乙型肝炎概况 大多数国家都已推荐采用乙型肝炎(乙肝)疫苗进行广泛性免疫预防,但乙肝仍然是一个严重的全球问题.目前,全世界大约有3.6亿慢性乙型肝炎(慢乙肝)患者,其中大多数患者在亚洲,然而这种疾病在全球各地都有发生.  相似文献   

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