激光血管吻合技术研究进展

临床血管吻合常使用缝合、吻合夹或吻合针。缝合法手术成本低、成功率高并且适合各种尺寸的血管,因此使用最为广泛。上述常用方法都会对血管产生损伤,而且手术工作量大。激光血管吻合术提供了一种微创的血管吻合方法。其潜在的优点包括保证吻合口的密闭,增加伤口吻合强度。同时减少手术操作时间、降低感染和流血的可能性,并且术后疤痕少,带有一定美容效果。因此,与传统缝合法等相区别的激光血管吻合技术作为一种新颖的技术受到极大的关注。然而,激光血管吻合术未成为一种临床常用的血管吻合方法,其主要原因有：直接激光照射可对组织产生过度热损伤、组织精准对齐技术难度大、手术成功与否的终点判断比较模糊以及重复性较差等。近年来,随着激光器技术以及材料技术的发展,激光血管吻合术正在逐步走向成熟,有可能作为一种应急性的、微创的血管吻合方法而应用于I临床。     

参芪扶正注射液联合地西他滨对急性髓系白血病患者血清HGF、VEGF与LDH水平的影响

目的:探讨参芪扶正注射液联合地西他滨对急性髓系白血病患者血清肝细胞生长因子(HGF)、血管内皮生长因子(VEGF)与乳酸脱氢酶(LDH)水平的影响。方法:选择2014年8月至2016年8月我院接诊的84例急性髓系白血病患者,通过随机数表法分为观察组(n=42)和对照组(n=42)。对照组给予地西他滨+DA化疗方案(柔红霉素+阿糖胞苷),观察组联合参芪扶正注射液,两组均以21d为1个周期,连续治疗2个周期。比较两组治疗前后血常规、血清HGF、VEGF和LDH水平的变化、临床疗效及不良反应的发生情况。结果:治疗后,两组血常规、血清HGF、VEGF和LDH水平均较治疗前显著改善(P0.05);观察组白细胞计数(WBC)明显低于对照组,血红蛋白(HGB)、血小板计数(PLT)、中性粒细胞计数(NEU)水平明显高于对照组(P0.05);观察组临床疗效总缓解率明显高于对照组(P0.05);观察组恶心呕吐、感染、多汗、出血、心脏毒性发生率均明显低于对照组(P0.05)。结论:应用参芪扶正注射液联合地西他滨治疗急性髓系白血病患者的临床效果显著,有助于降低毒副反应,其内在机制可能和降低血清HGF、VEGF、LDH的水平相关。     

Feasibility of simultaneous measurement of cytosolic calcium and hydrogen peroxide in vascular smooth muscle cells

Interplay between calcium ions (Ca²⁺) and reactive oxygen species (ROS) delicately controls diverse pathophysiological functions of vascular smooth muscle cells (VSMCs). However, details of the Ca²⁺ and ROS signaling network have been hindered by the absence of a method for dual measurement of Ca²⁺ and ROS. Here, a real-time monitoring system for Ca²⁺ and ROS was established using a genetically encoded hydrogen peroxide indicator, HyPer, and a ratiometric Ca²⁺ indicator, fura-2. For the simultaneous detection of fura-2 and HyPer signals, 540 nm emission filter and 500 nm∼ dichroic beamsplitter were combined with conventional exciters. The wide excitation spectrum of HyPer resulted in marginal cross-contamination with fura-2 signal. However, physiological Ca²⁺ transient and hydrogen peroxide were practically measurable in HyPer-expressing, fura-2-loaded VSMCs. Indeed, distinct Ca²⁺ and ROS signals could be successfully detected in serotonin-stimulated VSMCs. The system established in this study is applicable to studies of crosstalk between Ca²⁺ and ROS. [BMB Reports 2013; 46(12): 600-605]     

金川泥炭地两个尺度下苔藓植物间及其与维管植物间的种间关系分析

在金川泥炭地设置1m×1m和25 cm ×25 cm两个尺度的大、小样方进行植被调查,并利用方差比率法、x2检验、Pearson相关分析和Spearman秩相关分析方法,定量分析了9种苔藓植物和30种主要维管植物间的种间关系.偏叶泥炭藓、大泥炭藓和尖叶泥炭藓3种优势苔藓植物彼此呈显著负关联,占领着各自不同的生境;该3种优势苔藓植物同伴生苔藓及维管植物主要呈正相关,形成独特的群落,据此划分出4个生态种组.Spearman秩相关分析表明,大样方741个种对中,正联结种对数占49.53％,明显大于小样方666个种对中的41.14％.样方大小对分析植物个体大小差异悬殊的泥炭地植物群落的种间联结的影响巨大.苔藓与维管植物间以及苔藓植物间的种间联结甚至种间关系应在大、小样方中分别探讨更合适.     

Control of Vascular Permeability by Atrial Natriuretic Peptide via a GEF-H1-dependent Mechanism

Microtubule (MT) dynamics is involved in a variety of cell functions, including control of the endothelial cell (EC) barrier. Release of Rho-specific nucleotide exchange factor GEF-H1 from microtubules activates the Rho pathway of EC permeability. In turn, pathologic vascular leak can be prevented by treatment with atrial natriuretic peptide (ANP). This study investigated a novel mechanism of vascular barrier protection by ANP via modulation of GEF-H1 function. In pulmonary ECs, ANP suppressed thrombin-induced disassembly of peripheral MT and attenuated Rho signaling and cell retraction. ANP effects were mediated by the Rac1 GTPase effector PAK1. Activation of Rac1-PAK1 promoted PAK1 interaction with the Rho activator GEF-H1, inducing phosphorylation of total and MT-bound GEF-H1 and leading to attenuation of Rho-dependent actin remodeling. In vivo, ANP attenuated lung injury caused by excessive mechanical ventilation and TRAP peptide (TRAP/HTV), which was further exacerbated in ANP^−/− mice. The protective effects of ANP against TRAP/HTV-induced lung injury were linked to the increased pool of stabilized MT and inactivation of Rho signaling via ANP-induced, PAK1-dependent inhibitory phosphorylation of GEF-H1. This study demonstrates a novel protective mechanism of ANP against pathologic hyperpermeability and suggests a novel pharmacological intervention for the prevention of increased vascular leak via PAK1-dependent modulation of GEF-H1 activity.     

Endothelin-1 induces the expression of C-reactive protein in rat vascular smooth muscle cells

Numerous studies have shown that both vasoconstrictive peptide endothelin-1 (ET-1) and inflammatory marker C-reactive protein (CRP) are implicated in the inflammatory process of atherosclerosis. The purpose of the present study was to observe effect of ET-1 on CRP production and the molecular mechanisms in rat vascular smooth muscle cells (VSMCs). The results showed that ET-1 was capable of stimulating VSMCs to produce CRP both in protein and in mRNA levels in vitro and in vivo. ET_A receptor antagonist BQ123, but not ET_B receptor antagonist BQ788, inhibited CRP production in VSMCs. In addition, ET-1 was able to elicit reactive oxygen species (ROS) generation and mitogen-activated protein kinase (MAPK) activation, and antioxidant pyrrolidine dithiocarbamate and p38MAPK inhibitor SB203580 inhibited ET-1-induced CRP expression. The results demonstrate that ET-1 induces CPR production in VSMCs via ET_A receptor followed by ROS and MAPK signal pathway, which may contribute to better understanding of the role of ET-1 in inflammatory activation of the vessel wall during atherogenesis.