中文摘要：

为与血壅滞症候群联系并且包含了在 hypertension.MethodsThis 学习探索血壅滞症候群的基因机制的 mRNAs 的 ObjectiveTo 屏幕与 Qi 缺乏， Qi 停滞，冷保留和热保留与高血压和血壅滞病人组织，包括那些；象没有血壅滞和健康个人的高血压的病人一样。人的脐的静脉 endothelial 房间与血壅滞症候群与这些健康个人和病人的 sera 是 co 有教养的。全部的 RNA 从这些房间被提取并且由一个高产量的定序方法(Solexa ) 和数字基因表示估计了。差别在这六个组之中表示了基因用与血联系的整个染色体序列，和 mRNAs 被比较识别的壅滞症候群。在基因使用和基因本体论功能的差别被分析。，显著地充实的基因和他们的小径被决定是网络相互作用，并且编码了蛋白质。基因身份被即时聚合酶链 reactions.ResultsCompared 与在血壅滞组，的 sera 有教养的房间证实在健康个人并且非血壅滞组的 sera 的那些文化显示出 11 和 301 差别，分别地在壅滞相关的基因。作为在血壅滞和健康的组之间不同识别的基因包括了激活抄写因素 4，激活抄写因素 3， DNA 损坏可诱导的抄写因素 3， Tribbles 相当或相同的事物 3， CCAAT/enhancer 有约束力的蛋白质 -- ，并且 6 月 proto-oncogene (6 月) 。小径和蛋白质相互作用网络分析证明这些基因与 endoplasmic 蜂窝胃应力被联系。在有血壅滞和 Qi 缺乏， Qi 停滞，热保留，和冷保留的病人的 sera 有教养的房间与在有另外的类型血壅滞症候群的病人的 sera 有教养的房间相比。比较在 28,28,34 ，和 32 特定的基因的表示显示出差别，在高血压的血壅滞症候群的 respectively.ConclusionThe 致病与 endoplasmic 蜂窝胃应力有关并且包含激活的抄写因素的微分表示 4 ，激活抄写因素 3 ，DNA损坏可诱导的抄写因素 3 ， Tribbles 相当或相同的事物 3 ， CCAAT/enhancer 有约束力的蛋白质--，?

英文摘要：

OBJECTIVE： To screen for m RNAs associated with blood stasis syndrome and to explore the genetic mechanisms of blood stasis syndrome in hypertension.METHODS： This study involved groups of patients with hypertension and blood stasis, including those with Qi deficiency, Qi stagnation, cold retention and heat retention; as well as hypertensive patients without blood stasis and healthy individuals.Human umbilical vein endothelial cells were co-cultured with the sera of these healthy individuals and patients with blood stasis syndrome. Total RNA was extracted from these cells and assessed by a high-throughput sequencing method（Solexa） and digital gene expression. Differentially expressed genes among these six groups were compared using whole genome sequences, and m RNAs associated with blood stasis syndrome identified. Differences in gene use and gene ontology function were an-alyzed. Genes enriched significantly and their pathways were determined, as were network interactions, and encoded proteins. Gene identities were confirmed by real-time polymerase chain reactions.RESULTS： Compared with cells cultured in sera of the blood stasis groups, those culture in sera of healthy individuals and of the non-blood stasis group showed 11 and 301 differences, respectively in stasis-related genes. Genes identified as differing between the blood stasis and healthy groups included activating transcription factor 4, activating transcription factor 3, DNA-damage inducible transcription factor 3, Tribbles homolog 3, CCAAT/enhancer binding protein-β, and Jun proto-oncogene（JUN）. Pathway and protein interaction network analyses showed that these genes were associated with endoplasmic reticulum stress. Cells cultured in sera of patients with blood stasis and Qi deficiency,Qi stagnation, heat retention, and cold retention were compared with cells cultured in sera of patients with the other types blood stasis syndrome.The comparison showed differences in expression of 28, 28, 34, and 32 specific genes, respectively.CONCLUSI