切应力作用下联合培养的血管内皮细胞血管假性血友病因子的含量变化

目的：研究切应力对与血管平滑肌细胞联合培养的内皮细胞的抗凝血和粘附的影响。方法：对与平滑肌细胞联合培养的内皮细胞施加生理范围的切应力,用免疫组化及图像分析法检测内皮细胞的血管假性血友病因子（ｖＷＦ）含量。结果：联合培养的内皮细胞ｖＷＦ的变化与切应力大小及作用时间有关,随切应力增大,胞内ｖＷＦ含量逐渐减少,且切应力作用的第１小时减少的最快。结论：生理范围的切应力作用,可能减少与平滑肌细胞联合培养的内皮细胞的ｖＷＦ表达,或促使ｖＷＦ短时释放加快,有利于增强抗凝血功能及内皮细胞的粘附。     

糖尿病大鼠视网膜微血管的重建及某些药物对其的影响

目的：研究糖尿病大鼠视网膜微血管的重建。方法：用链脲佐菌素（ＳＴＺ）诱导ＳＤ大鼠建立糖尿病动物模型,运用视网膜消化铺片和图像分析方法观测糖尿病大鼠视网膜微血管的重建,及非酶糖化抑制剂和活血化瘀中药对其重建的影响。结果：在８周时毛细血管宽度即有显著性变化（Ｐ〈０．０５）,非酶糖化抑制剂和活血化瘀中药治疗组在８～１２周后与糖尿病组有显著性差异（Ｐ〈０．０５）。结论：（１）糖尿病促进了视网膜微血管的形态     

血管内皮生长因子同源体mRNA在原发性肺癌中的表达

目的：探讨血客内皮生长因子（vascular endothelial growth factor,VEGF)在原发性肺癌发生、发展、侵袭和转移等生物学行为中的作用。方法：应用反转录聚合酶链反应技术对34例原发性肺癌患者的癌组织及21例患者的正常肺组织的VEGF mRNA进行检测,统计分析VEGF mRNA的表达与肺癌的淋巴结转移,TNM分期等的关系。结果：VEGF－189mRNA在肺癌组织中的表达（61．8％）显著高于正常肺组织（4．8％,P＜0．01）。VEGF－189 mRNA在有淋巴结转移组的表达（88．2％）显著高于无淋巴结转移组（35．3％）（P＜0．01）。VEGF－189 mRNA的表达在TNMⅠ期与Ⅱ期及Ⅰ期与Ⅲ期之间有显著差异（P＜0．05）。结论：VEGF的结合型同源体VEGF－189 mRNA与原发性肺癌的发生、侵袭和转移等密切相关。     

Effect of prenatal tetrandrine therapy on pulmonary vascular structur al remodeling in the nitrofen-induced CDH rat model

Ｃｏｎｇｅｎｉｔａｌｄｉａｐｈｒａｇｍａｔｉｃｈｅｒｎｉａ (ＣＤＨ)ｒｅｓｕｌｔｓｆｒｏｍｉｎｃｏｍｐｌｅｔｅｄｅｖｅｌｏｐｍｅｎｔｏｆｔｈｅｄｉａｐｈｒａｇｍｉｎｕｔｅｒｏｗｉｔｈｈｅｒｎｉａｔｉｏｎｏｆａｂｄｏｍｉｎａｌｖｉｓｃｅｒａｉｎｔｏｔｈｅｔｈｏｒａｘ Ｓｕｒｇｉｃａｌｒｅｐａｉｒｏｆｔｈｅｈｅｒｎｉａ ,ａｌｔｈｏｕｇｈｎｏｔａｌｗａｙｓｒｏｕｔｉｎｅ ,ｉｓｒｅｌａｔｉｖｅｌｙｕｎｅｖｅｎｔｆｕｌ Ｈｏｗｅｖｅｒ,ｔｈｅｍｏｒｔａｌｉｔｙｒｅｐｏｒｔｅｄｆｏｒｇｒｏｕｐｓｏｆｔｈｏｓｅｈ…     

肿瘤坏死因子α与妊娠高血压综合征发病关系的研究

探讨肿瘤坏死因子α在妊娠高血压综合征发病中的作用。方法对４１例妊高征患者（妊高征组）和１７例正常妊娠妇女（正常妊娠组）进行了下列研究：（１）测定血浆中ＴＮＦα水平,观察胎盘血管内皮细胞的形态学变化;（２）利用其血清对离体培养的脐血管内皮细胞作用,观察其损情表现;（３）利用４００Ｕ／ｍｌ的人重组ＴＮＦα对离体培养的脐血管内皮细胞作用,比较ＴＮＦα和妊娠高征孕妇血清对内皮细胞的损伤作用。结果（１）妊娠     

电针肾俞、膈俞、百会穴对拟血管性痴呆学习记忆障碍小鼠水迷宫实验的影响

目的　观察电针肾俞、膈俞、百会穴对拟血管性痴呆小鼠学习记忆障碍的影响。方法　复制脑缺血再灌注拟血管性痴呆小鼠模型 ,并电针肾俞、膈俞、百会穴 ,分别于术后 7天、15天、30天 ,与药物喜德镇对照 ,采用水迷宫法 ,记录游全程时间、错误次数。结果　造模导致了小鼠学习与记忆能力下降 ,表现为游全程时间延长 ,错误次数增加 ,且随着观察时间的延长 ,这种改变逐渐加重。电针和喜德镇均可使模型小鼠的游全程时间缩短 ,错误次数减少 ,但电针组于 7天和 30天时 ,成绩显著优于药物组。结论　电针肾俞、膈俞、百会穴对模型小鼠学习与记忆能力下降有改善和提高作用     

顺行和逆行取栓对静脉瓣膜及血管壁的影响

目的：比较顺行取栓与逆行取栓在猪腋静脉急性血栓形成对于其瓣膜功能和静脉壁形态的影响。方法：分别结扎猪的腋静脉的近远端,于结扎段内注入凝血酶原,放置６ｈ使形成血栓。随机分配为顺行取栓和逆行取栓组,对血栓段进行取栓。取栓后２４ｈ行取栓静脉插管逆行造影以评估瓣膜功能;切取此段静脉作ＣＤ８＾＋细胞免疫组化和苏木精－伊红（ＨＥ）染色以对比血管内膜及平滑肌的损伤程度。结果：逆行与顺行取栓在所有的例数中都成功地     

氧化低密度脂蛋白、低氧和5-HT对血管平滑肌细胞5-HT2A受体及胞内游离钙的影响

目的　为探讨粥样硬化病变动脉对 5 - HT收缩反应增加的机制 ,观察与粥样硬化有关因子氧化低密度脂蛋白 (ox L DL)、低氧、5 - HT对血管平滑肌细胞 5 - HT2 A受体及其基因表达 ,以及细胞 [Ca2 ]i的效应。方法　分别将大鼠主动脉平滑肌细胞单独以 5 0 μg/ m l ox L DL 培养 8h,2 %低氧处理 2 4和 48h,10 μm ol/ L 5 - HT处理30 min,放射配基结合分析测定 5 - HT2 A受体 ;RT- PCR和 Southern杂交检测受体基因的 m RNA;激光共聚焦扫描显微镜测单个细胞 [Ca2 ]i。结果　经 ox L DL、低氧、 5 - HT处理 ,血管平滑肌细胞 5 - HT2 A受体显著上调 (P<0 .0 1) ;ox L DL及低氧处理的受体基因的 m RNA表达增加 ;ox L DL、低氧处理后 ,5 - HT刺激的血管平滑肌细胞[Ca2 ]i升高幅度显著加大 (P<0 .0 5及 P<0 .0 1)。结论　 ox L DL、低氧、5 - HT引起血管平滑肌细胞 5 - HT2 A受体上调及细胞 [Ca2 ]i增加 ,可能是粥样硬化动脉对 5 - HT收缩反应增强的部分原因。     

Comprehensive genetic screening for vascular Ehlers–Danlos syndrome through an amplification-based next-generation sequencing system

Vascular Ehlers–Danlos syndrome (vEDS) is a hereditary connective tissue disorder (HCTD) characterized by arterial dissection/aneurysm/rupture, sigmoid colon rupture, or uterine rupture. Diagnosis is confirmed by detecting heterozygous variants in COL3A1. This is the largest Asian case series and the first to apply an amplification-based next-generation sequencing through custom panels of causative genes for HCTDs, including a specific method of evaluating copy number variations. Among 429 patients with suspected HCTDs analyzed, 101 were suspected to have vEDS, and 33 of them (32.4%) were found to have COL3A1 variants. Two patients with a clinical diagnosis of Loeys–Dietz syndrome and/or familial thoracic aortic aneurysm and dissection were also found to have COL3A1 variants. Twenty cases (57.1%) had missense variants leading to glycine (Gly) substitutions in the triple helical domain, one (2.9%) had a missense variant leading to non-Gly substitution in this domain, eight (22.9%) had splice site alterations, three (8.6%) had nonsense variants, two (5.7%) had in-frame deletions, and one (2.9%) had a multi-exon deletion, including two deceased patients analyzed with formalin-fixed and paraffin-embedded samples. This is a clinically useful system to detect a wide spectrum of variants from various types of samples.     

Mosaic pathogenic variants in AKT3 cause capillary malformation and undergrowth

Capillary malformations are slow-flow vascular malformations that affect the microcirculation including capillaries and post capillary venules and can be associated with growth differences. Specifically, the association of capillary malformations with undergrowth is a vastly understudied vascular syndrome with few reports of genetic causes including PIK3CA, GNAQ, and GNA11. Recently, a somatic pathogenic variant in AKT3 was identified in one child with a cutaneous vascular syndrome similar to cutis marmorata telangiectatica congenita, undergrowth, and no neurodevelopmental features. Here, we present a male patient with a capillary malformation and undergrowth due to a somatic pathogenic variant in AKT3 to confirm this association. It is essential to consider that mosaic pathogenic variants in AKT3 can cause a wide spectrum of disease. There is a need for future studies focusing on capillary malformations with undergrowth to understand the underlying mechanism.