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A new variant of type II von Willebrand disease with aberrant multimeric structure of plasma but not platelet von Willebrand factor (type IIF) 总被引:2,自引:0,他引:2
A patient with a lifelong bleeding disorder was diagnosed as having Type II von Willebrand disease. The larger multimers of von Willebrand factor were absent from her plasma but present in platelets. A high- resolution electrophoretic technique was used to study the complex structure of individual von Willebrand factor multimers. In normal plasma, each multimer could be resolved into five bands: a more intense central one and four less intense, two moving faster and two slower than the central band. In normal platelets, each multimer could also be resolved into five bands. The central one had a mobility similar to that in plasma, whereas the four satellite bands had a mobility that differed from that of the corresponding plasma bands. In the patient, platelet von Willebrand factor antigen content and ristocetin cofactor activity were normal, and von Willebrand factor showed the same structure of individual multimers as seen in normal platelets. On the other hand, plasma von Willebrand factor antigen and ristocetin cofactor activity were decreased, and the structure of individual von Willebrand factor multimers was different from that of normal plasma and similar to that seen in normal and patient's platelets. After infusion of 1-deamino-8-D-arginine vasopressin, the largest von Willebrand factor multimers, as well as new satellite bands with a mobility similar to those in normal plasma, appeared in the patient plasma, and the levels of von Willebrand factor antigen and ristocetin cofactor activity became normal. Yet no relevant change in the prolonged bleeding time was observed. This new variant of von Willebrand disease, therefore, is characterized by the presence of a dysfunctional von Willebrand factor molecule that exhibits unique structural abnormalities in plasma but appears to be normal in platelets. The designation of Type IIF is proposed for this type of von Willebrand disease in accordance with the terminology that has been previously used. 相似文献
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Afthab Hussain Ahmed Mayel Gharanei Aarondeep Singh Nagra Helen L. Maddock 《Cardiovascular drugs and therapy / sponsored by the International Society of Cardiovascular Pharmacotherapy》2014,28(1):19-32
Purpose
2-CL-IB-MECA, (A3 adenosine receptor agonist)(A3AR) mediated cardioprotection is well documented although the associated intracellular signalling pathways remain unclear. Here we demonstrate a role of the pro-survival signalling pathways MEK1/2-ERK1/2 and PI3K/AKT and their effect on modifying Caspase-3 activity in A3AR mediated cardioprotection.Methods
Isolated perfused rat hearts or primary adult rat cardiac myocytes were subjected to ischaemia/hypoxia and reperfusion/reoxygenation, respectively. 2-CL-IB-MECA (1 nM) was administered at the onset of reperfusion/reoxygenation in the presence and absence of either the PI3K inhibitor Wortmannin (5 nM) or MEK1/2 inhibitor UO126 (10 μM). Heart tissues were harvested for assessment of p-ERK1/2(Thr202/Tyr204) or p-AKT (Ser-473) status or underwent infarct size assessment. Cardiac myocytes underwent flow-cytometric analysis for apoptosis, necrosis, cleaved-caspase 3/p-BAD (Ser-112 and Ser-136) activity post-reoxygenation.Results
2-CL-IB-MECA significantly reduced infarct size compared to non-treated controls, where co-administration with either of the kinase inhibitors abolished the infarct sparing effects. Administration of 2-CL-IB-MECA at reperfusion significantly upregulated the status of p-ERK1/2 and p-AKT compared to time matched controls in a UO126 and Wortmannin sensitive manner respectively. 2-CL-IB-MECA when administered throughout reoxygenation significantly reduced apoptosis, necrosis, cleaved-caspase 3 activity and increased p-BAD (Ser-112) and p-BAD (Ser-136) activity in myocytes subjected to hypoxia/reoxygenation injury. The cytoprotective effect was abolished by co-administration with the kinase inhibitors Wortmannin and/or UO126.Conclusions
We have described the molecular mechanisms associated with A3AR mediated cardioprotection indicating a role for the pro-survival signalling pathways that decrease caspase-3 activity. These observations provide novel insight into the pharmacological effects of A3ARs in ameliorating myocardial ischaemia/reperfusion injury. 相似文献6.
Ram Pyare Singh Sascha Hasan Sherven Sharma Saranpreet Nagra Dean T. Yamaguchi David T.W Wong Bevra H. Hahn Awlad Hossain 《Autoimmunity reviews》2014,13(12):1174-1181
T helper 17 (Th17), a distinct subset of CD4+ T cells with IL-17 as their major cytokine, orchestrate the pathogenesis of inflammatory and autoimmune diseases. Dysregulated Th17 cells contribute to inflammatory and autoimmune diseases. Candidate biologics are in development for targeting IL-17, IL-17 receptors or IL-17 pathways. Several drugs that impact the IL-17 pathway are already in clinical trials for the treatment of autoimmune diseases. In this review we provide evidence for the role of Th17 cells in immune-mediated diseases. An understanding of the role of Th17 in these conditions will provide important insights and unravel novel targets for therapeutic intervention. 相似文献
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目的:在成功分离人皮肤角质形成细胞的基础上,观察表皮生长因子受体在人皮肤角质形成细胞中的表达情况。方法:实验于2006-3/10在北京大学深圳医院中心实验室进行。采用dispase Ⅱ-trypsin两步消化法获取表皮基底层细胞,用小鼠皮肤成纤维母细胞滋养层和黄素腺嘌呤二核苷酸培养液进行培养。小鼠皮肤成纤维母细胞的预处理:向对数生长期的小鼠皮肤成纤维母细胞培养液中加入丝裂霉素C至终浓度为4mg/L,37℃下培养4h,弃去培养液,用D-Hank’s液洗3次,加入浓度为0.25g/L的胰蛋白酶消化,分离出细胞,离心(200g,5min),用黄素腺嘌呤二核苷酸培养液悬浮细胞,计数,以5.0×104/cm2的密度种于培养皿内,37℃、体积分数0.05的CO2培养箱下培养。角质形成细胞的培养:将分离的角质形成细胞悬浮在黄素腺嘌呤二核苷酸培养液中,以2.0×104/cm2的密度接种在前1天经丝裂霉素C处理的小鼠皮肤成纤维母细胞滋养层上,37℃、体积分数0.05的CO2培养箱下培养。24h换液,以后每3d换1次液。采用免疫细胞化学的方法检测表皮生长因子受体的表达,采用复合逆转录聚合酶链反应检测角质形成细胞中表皮生长因子受体mRNA的表达。结果:采用dispaseⅡ消化法分离了真皮和表皮,获得较多的角质形成细胞,可以避免真皮成纤维细胞的污染。人皮肤角质形成细胞在黄素腺嘌呤二核苷酸培养液中培养5d可见明显的集落,约10d可长满单层。免疫细胞化学显示表皮生长因子受体在细胞表面有明显的表达,复合逆转录聚合酶链反应显示表皮生长因子受体mRNA有明显的表达。结论:用小鼠皮肤成纤维母细胞滋养层和黄素腺嘌呤二核苷酸培养液可以较好地培养原代人皮肤角质形成细胞,表皮生长因子受体在细胞表面有明显的表达,这些结果为与表皮生长因子受体相关的皮肤病(如银屑病)的研究奠定了基础。 相似文献
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Bhatty N Gilani AH Nagra SA 《International journal of food sciences and nutrition》2000,51(3):169-174
The study was conducted to determine the nutritional value of mash (Vigna mungo) in raw and cooked forms and as effected by supplementation with different kind of meat, i.e. poultry, mutton and beef at 10, 15 and 20% levels. Nutritional assessment of all mash-containing diets (without or with supplementation) was made by chemical analysis as well as through rat assay. Mash contained 23.83% protein. Cooking resulted in minor changes in nutrients. Mash had 1.79% lysine which was reduced by 35% on cooking. All other amino acids also showed losses during cooking. Protein efficiency ratio (PER) of diet containing raw mash was 1.9% and cooking improved it to 2.8%. True digestibility (TD) also showed a significant improvement. Supplementation of mash with different kinds of meat did not improve the PER significantly over unsupplemented diet containing cooked mash only. TD, however, was improved from 74.89% in cooked to 75.58-87.06% in supplemented diets. Similarly net protein utilization (NPU), as a result of meat supplementation, improved from 43.54% in cooked to 42.88%-51.96%. Higher PER, TD and NPU values were observed in diets containing mash supplemented with 20% level of different meats. 相似文献
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