Purification of platelet-derived endothelial cell growth inhibitor and its characterization as transforming growth factor-β type 1

In 1986, Brown and Clemmons (Proc. natl Acad. Sci. USA83 (1986) 3321) showed that platelets contain a substance, platelet-derived growth inhibitor (PDGI), that inhibits in vitro endothelial cell replication. Although platelets are rich in transforming grwoth factor (TGF-), PDGI was considered not to be related to TGF-, on the basis of its reported properties (extraction from platelets at neutral pH, binding to heparin-Sepharose). However, we purified PDGI to near homogeneity and showed that on the basis of HPLC retention behavior, in vitro growth inhibitory activities with several cell types, receptor binding, and immunoneutralization of growth inhibitory activity with specific anti-TGF- type 1 antibodies, PDGI is most probably identical with TGF- type 1.     

DanHong Injection inhibits the development of primary abdominal aortic aneurysms in apoE knockout mice

Clinical observations indicate that DanHong Injection （DHI） can increase blood flow and reduce various syndromes in patients with cardiovascular disease. How- ever, it still needs to define the function of DHI and the involved mechanisms in details, such as the protective effect on the development of primary abdominal aortic aneurysms （AAAs）. In this study, we determined whether DHI is able to inhibit AAA in apoE knockout （apoE-/-） mice. Thirty apoE-/- male mice on high-fat diet （0.5 % cholesterol, 21% fat） were randomly divided into two groups and received i.p. injection of saline （100 μL/day） and DHI （100 μL/day）, respectively, for 16 weeks. At the end of experiment, we determined the development of atherosclerosis in en face aorta and aneurysms,pathological morphology of arterial wall, and serum lipid levels. We also determined the expression of monocyte chemoattractant protein-1 （MCP-1）, MMP-2, and MMP-9 mRNA in aortic wall using real-time RT-PCR. Our results indicated that high-fat diet induced the development of AAAs in apoE-/- mice, but the induction was totally blocked by DHI （P 〈 0.01）. The result of staining of abdominal aortic cross sections showed that DHI main- tained the collagen content in arterial wall, thereby pre- venting the animals from the development of AAA. Although DHI had little effect on serum total- and LDL- cholesterol levels, it reduced the expression of MCP-1, MMP-2, and MMP-9 mRNA in aortic wall （P 〈 0.01）. Taken together, our study suggests that DHI can inhibit the high-fat diet-induced AAA formation. The inhibitory effects may be related to the maintenance of the collagen content and inhibition of expression of AAA-related genes. Our study may suggest a new application of DHI in clinics.     

The genomic basis of the Williams – Beuren syndrome

The Williams-Beuren syndrome is a genomic disorder (prevalence: 1/7,500 to 1/20,000), caused by a hemizygous contiguous gene deletion on chromosome 7q11.23. Typical symptoms comprise supravalvular aortic stenosis, mental retardation, overfriendliness and visuospatial impairment. The common deletion sizes range of 1.5–1.8 mega base pairs (Mb), encompassing app. 28 genes. For a few genes, a genotype-phenotype correlation has been established. The best-explored gene within this region is the elastin gene; its haploinsufficiency causes arterial stenosis. The region of the Williams-Beuren syndrome consists of a single copy gene region (~1.2 Mb) flanked by repetitive sequences – Low Copy Repeats (LCR). The deletions arise as a consequence of misalignment of these repetitive sequences during meiosis and a following unequal crossing over due to high similarity of LCRs. This review presents an overview of the Williams-Beuren syndrome region considering the genomic assembly, chromosomal rearrangements and their mechanisms (i.e. deletions, duplications, inversions) and evolutionary and historical aspects. Received 11 July 2008; received after revision 15 October 2008; accepted 16 October 2008     

Genistein inhibits human TNF-α-induced porcine endothelial cell adhesiveness for human monocytes and natural killer cells

Cellular immune response is a major barrier to xenotransplantation. Human tumor necrosis factor-α (hTNF-α) possesses cross-species activity and directly amplifies the immune rejection via the upregulation of adhesion molecules on porcine endothelium. We investigated the role of protein tyrosine phosphorylation in the induction of expression of E-sclectin and vascular cell adhesion molecule-1 (VCAM-1), and the augmentation of adhesion of human peripheral blood monocytes (PBMo) and natural killer cells (PBNK), after rhTNF-α-stimulation of porcine aortic endothelial cells (PAEC) in vitro, rhTNF-α-increased adhesiveness of PAEC for both PBMo and PBNK was dose-dependently reduced by pretreatment of PAEC with the selective protein tyrosine kinase (PTK) inhibitor genistein. The inhibitory effect occurred at the early time of PAEC activation triggered by rhTNF-α, and was completely reversible. PTK activity assay indicated that genistein also suppressed rhTNF-α stimulated activation of protein tyrosine kinases (PTKs) in PAEC in a dose-dependent manner. Flow cytometric analysis showed that genistein inhibited the upregulation of E-selectin and VCAM-1 by rhTNF-α. These results suggest that PTKs may regulate the expression of E-selectin and VCAM-1 on PAEC and the adherence of PBMo and PBNK induced by rhTNF-α. Moreover, dietary genistein, used as an adhesion antagonist, may contribute to managing the cell-mediated rejection in the clinical application.     

采样频率与数据长度对中心动脉波形重建的影响

传递函数法重建CAP(central aortic pressure)多是基于自回归各态历经(auto regressive eXogenous, ARX)模型或傅里叶变换,未考虑采样频率、数据长度.为了研究采样频率和数据长度对重建CAP的影响,基于ARX模型和傅里叶变换,重建CAP并分析误差.结果表明,采样频率100Hz,数据长度大于3s时,基于ARX模型重建CAP效果较好(均方根误差(306.6±80.0)Pa,波形匹配度89%);基于傅里叶变换的算法对采样频率不敏感,数据长度为6s时效果较好(均方根误差(493.3±320.0)Pa,波形匹配度84%).     

胸主动脉夹层动脉瘤腔内隔绝术10例分析

目的:讨论胸主动脉夹层动脉瘤腔内隔绝术的术前注意要点.方法:回顾2004年12月至2008年12月应用带膜支架腔内隔绝术治疗DebakeyⅢ型胸主动脉夹层动脉瘤10例资料.结果:10例患者带膜支架腔内隔绝破口封堵均一次成功.结论:带膜支架腔内隔绝术适应于DebakeyⅢ型胸主动脉夹层动脉瘤,应注意手术时机及胸腹主动脉部成角及内径影响带膜支架的置入.     

雌二醇对体外培养内皮细胞抗氧化活力的影响

雌激素对心血管系统的保护作用,是育龄妇女少患此类疾病的重要原因。本文以体外培养的小牛主动脉内皮细胞为实验材料,考察了雌二醇对血管内皮细胞抗氧化系统的影响。结果表明,０．５μｇ／ｍｌ雌二醇作用内皮细胞后,细胞内ＳＯＤ活性显著增加,与此相对应,细胞内过氧化产物ＭＤＡ的含量显著降低。提示该浓度的雌二醇能够提高细胞内的抗氧化能力,因而可能防止活性氧对内皮细胞的损伤,而这种损伤往往是动脉粥样硬化的开端。０．     

经皮开窗术结合内支架植入术治疗5例Stanford B型主动脉夹层

目的:评价经皮开窗术结合内支架植入术治疗Stanford B型主动脉夹层的疗效.方法:5例Stanford B型主动脉夹层患者均行经皮开窗术及内支架植入术,其中4例加行血管腔内修复术.所有患者术前均并发内脏和(或)下肢缺血症状,术后采用CT血管造影(CTA)定期随访.结果:5例患者血管均成功重建,无明显并发症发生,随访3～25个月,平均14.5个月,5例患者仍存活,缺血症状消失,生活自理.结论:经皮开窗术结合内支架植入术治疗急性期Stanford B型主动脉夹层是一种创伤小、安全性高、疗效显著的方法,加行腔内修复术更能提高其长期疗效.     

中国大鲵心脏及主动脉干的解剖学研究

用血管乳胶色素注射法经中国大鲵动脉干注射后，利用实体显微镜及放大镜对其心脏及血管进行观察、测量及绘图．结果表明：中国大鲵心脏位于体正中线，体腔前部，乌喙骨下方．心脏由心房和心室及静脉窦组成，心房位于体中线偏左，近半圆形，心房尖偏向左后方．心房壁很薄(约0．1mm)，以房间隔将心房分成前后两个腔，分别为前心房和后心房，前心房大于后心房，房间隔上有孔洞．心室位于体中线偏右，近圆形，心室尖偏向右后方，心室壁较厚(约5—10mm)，房室孔处有4个瓣膜．静脉窦位于心脏背面，略呈三角状囊形，壁很薄．主动脉干由动脉圆锥和主动脉弓组成，动脉圆锥位于近心端，稍膨大．主动脉弓位于远心端，分两支，呈Y型．