Single String Technique for Coronary Bifurcation Stenting: Detailed Technical Evaluation and Feasibility Analysis

ObjectivesThe study aimed to evaluate the adequacy and feasibility of the single string bifurcation stenting technique.BackgroundDouble-stent techniques may be required for complex bifurcations. Currently applied methods all have their morphological or structural limitations with respect to wall coverage, multiple strut layers, and apposition rate.MethodsSingle string is a novel method in which, first, the side branch (SB) stent is deployed with a single stent cell protruding into the main branch (MB). Second, the MB stent is deployed across this protruding stent cell. The procedure is completed by final kissing balloon dilation. The single string technique was first tested in vitro (n = 20) and next applied in patients (n = 11) with complex bifurcation stenoses.ResultsAll procedures were performed successfully, crossing a single stent cell in 100%. Procedure duration was 23.0 ± 7.9 min, and the fluoroscopy time was 9.4 ± 3.5 min. The results were evaluated by optical coherence tomography, showing fully apposed struts in 83.0 ± 9.2% in the bifurcation area. Residual area obstruction in the MB was 6.4 ± 5.6% and 25.0 ± 16.9% in the SB, as evaluated by micro computed tomography. All the human cases were performed successfully with excellent angiographic results: the residual area stenosis was 27 ± 8% and 29 ± 10% in the MB and in the SB, respectively, by 3-dimensional quantitative coronary angiography. No relevant periprocedural enzyme increase was observed. During follow-up (6 ± 4 months), no adverse clinical events (death, myocardial infarction, target vessel revascularization) were noted.ConclusionsThe single string technique for complex bifurcation dilation was shown to be adequate in vitro and feasible in humans, with favorable results in terms of stent overlap, malapposition rate, and low residual obstruction in both the MB and SB.     

Combined Transradial and Transpedal Approach for Femoral Artery Interventions

Objectives

The purpose of this prospective study was to evaluate the acute success and complication rates of combined transradial and transpedal access for femoral artery intervention.

Curcumin attenuates cardiac fibrosis in spontaneously hypertensive rats through PPAR-γ activation

Aim:

To investigate the effects of curcumin (Cur) on cardiac fibrosis in spontaneously hypertensive rats (SHRs) and the mechanisms underlying the anti-fibrotic effect of Cur in rat cardiac fibroblasts (CFs) in vitro.

Methods:

SHRs were orally treated with Cur (100 mg·kg⁻¹·d⁻¹) or Cur (100 mg·kg⁻¹·d⁻¹) plus the PPAR-γ antagonist GW9662 (1 mg·kg⁻¹·d⁻¹) for 12 weeks. Cultured CFs were treated with angiotensin II (Ang II, 0.1 μmol/L) in vitro. The expression of relevant proteins and mRNAs was analyzed using Western blotting and real-time PCR, respectively. The expression and activity of peroxisome proliferator-activated receptor-γ (PPAR-γ) were detected using Western blotting and a DNA-binding assay, respectively.

Results:

Treatment of SHRs with Cur significantly decreased systolic blood pressure, blood Ang II concentration, heart weight/body weight ratio and left ventricle weight/body weight ratio, with concurrently decreased expression of connective tissue growth factor (CTGF), plasminogen activator inhibitor (PAI)-1, collagen III (Col III) and fibronectin (FN), and increased expression and activity of PPAR-γ in the left ventricle. Co-treatment with GW9662 partially abrogated the anti-fibrotic effects of Cur in SHRs. Pretreatment of CFs with Cur (5, 10, 20 μmol/L) dose-dependently inhibited Ang II-induced expression of CTGF, PAI-1, Col III and FN, and increased the expression and binding activity of PPAR-γ. Pretreatment with GW9662 partially reversed anti-fibrotic effects of Cur in vitro. Furthermore, pretreatment of CFs with Cur inhibited Ang II-induced expression of transforming growth factor-β1 (TGF-β1) and phosphorylation of Smad2/3, which were reversed by GW9662.

Conclusion:

Cur attenuates cardiac fibrosis in SHRs and inhibits Ang II-induced production of CTGF, PAI-1 and ECM in CFs in vitro. The crosstalk between PPAR-γ and TGF-β1/Smad2/3 signaling is involved in the anti-fibrotic and anti-proliferative effects of Cur.     

PPARβ/δ及其配体在RAW264.7泡沫细胞模型中的作用

目的研究过氧化物酶体增殖物激活受体（Peroxisome Proliferators-activated Receptor,PPAR）-β/δ及其激动剂GW0742、抑制剂GSK0660在RAW264.7泡沫细胞模型中的作用。方法本研究选用RAW264.7细胞,共分为6组,分别是对照组、LPS组、ox-LDL组、模型组、激动剂组和抑制剂组。实时定量PCR（Real-time Quantitative PCR）用来检测PPARβ/δ和单核细胞趋化蛋白（monocyte chemoattractant protein,MCP）-1 m RNA的水平,蛋白质印迹法（Western Blotting,WB）检测PPARβ/δ和MCP-1蛋白的表达,酶联免疫吸附试验（Enzyme-linked Immunosorbent Assay,ELISA）测定细胞培养液上清中炎症因子肿瘤坏死因子（tumor necrosis factor,TNF）-α,白介素（interleukin,IL）-10和MCP-1的水平。结果对照组、LPS组、ox-LDL组、模型组、激动剂组的PPARβ/δ蛋白质和m RNA水平逐渐增加（P〈0.01）,而抑制剂组PPARβ/δ蛋白质和m RNA水平则明显低于模型组和激动剂组（P〈0.01）。MCP-1蛋白质和m RNA的水平在对照组、ox-LDL组、LPS组、模型组逐渐增加（P〈0.01）,而激动剂组明显降低（P〈0.01）,抑制剂组又有所增加（P〈0.01）。总之,MCP-1的蛋白质和m RNA水平在各组之间差异显著（P〈0.01）。细胞培养液中TNF-α、MCP-1的水平LPS组、ox-LDL组、模型组明显升高（P〈0.01）,而激动剂组明显降低（P〈0.01）,抑制剂组又有所增加（P〈0.01）。而IL-10在激动剂组和抑制剂组则表现出相反的趋势。结论 GW0742可以显著增加PPARβ/δ的表达,降低炎症因子MCP-1、TNF-α的水平,升高IL-10的水平;GSK0660则发挥完全相反的作用。     

PPARβ/δ激动剂GW501516对人角质形成细胞增殖、迁移和粘附的影响

目的:评价过氧化物酶体增殖物激活受体β/δ(PPARβ/δ)的激动剂GW501516对人角质形成细胞(KC)增殖、迁移和粘附的影响。方法:体外培养正常人KC,采用MTT比色法及体外计数法,观察正常人KC在不同浓度GW501516(0,1,5,10,25,50,100 ng/ml)作用下,其增殖、迁移及粘附情况。结果:与对照组比较,GW501516促进KC增殖(P0.01),呈剂量依赖性;GW501516显著促进了KC的迁移(P0.001);细胞粘附性与对照组间无统计学差异(P0.05)。结论:GW501516能够促进人KC增殖和迁移,对KC粘附无影响。     

GW843682X对鼻咽癌细胞周期和凋亡的影响

[目的]研究GW843682X对鼻咽癌5-8F细胞周期和凋亡的影响。[方法]培养鼻咽癌5-8F细胞,0、6.25、12.5、25、50、100、200和400nmol/L的GW843682X处理后,用CCK8试剂检测药物对细胞增殖的影响。分别以0、250,500,1000nmol/L的GW843682X处理5-8F细胞48h后,用PI单染流式细胞仪检测药物对5-8F细胞周期的影响。用Annexin V-FITC双染细胞后,经流式细胞仪检测细胞凋亡的变化。[结果]CCK8比色结果显示,GW843682X能抑制鼻咽癌5-8F细胞的增殖,当药物浓度大于50nmol/L时,细胞增殖显著受抑。细胞周期检测结果显示,与阴性对照组比较,GW843682X增加了G2/M期细胞阻滞,减少了G0/G1期细胞比例（P〈0.05）。细胞凋亡检测结果显示,与对照组相比,随着GW843682X浓度的增加,凋亡细胞所占比例逐渐增大,当药物浓度达到500nmol/L和1000nmol/L时,凋亡细胞所占比例显著增加（P〈0.05）。[结论]GW843682X能够显著抑制鼻咽癌5-8F细胞的增殖,可以诱导细胞阻滞于G2/M期,其诱导5-8F细胞凋亡呈一定的剂量依赖性。     

长骨中超声导波信号的时频特征分析

采用超声导波评价长骨骨质状况已是近几年来的一个研究热点。在应用时频表征方法处理导波实验信号的研究中,选择交叉项抑制效果好的时频表征核函数直接影响到导波信号的分离和提取。提出将Zhao-Atlas-M arks分布(ZAMD)应用于分析长骨中的导波信号,同时与重排光滑伪维格纳维利分布(RSPWVD)的分析结果进行比较,并用图像处理中的骨架求取算法,估计导波平均频率慢度曲线。分析结果表明,ZAMD可较好地去除交叉项干扰,得到较准确的超声导波频散特性曲线,说明ZAMD是分析长骨中超声导波信号的一种较好方法。     

Small conductance calcium-activated potassium channels: From structure to function

The cloning of K_Ca2 channels revealed three subtypes, with each displaying distinct but partially overlapping expression distributions in the mammalian CNS and periphery. Activation of K_Ca2 channels leads to membrane hyperpolarization and inhibition of action potential firing. Block of K_Ca2 channels has been suggested as a novel target for cognitive enhancement, depression, myotonic muscular dystrophy and heart arrhythmias. It is clear however, that blockers selective for individual K_Ca2 channel subtypes would be required to be therapeutically useful. K_Ca2 channel current is blocked by apamin, with the bee venom toxin being unusual in displaying some selectivity between K_Ca2 channel subtypes. This suboptimal selectivity is not sufficient to be therapeutically useful and the toxin has been shown in vivo to have a very narrow therapeutic window. Mutational and molecular modelling studies of the K_Ca2 channels are beginning to determine how selective block might be achieved. Mutagenesis has indicated the importance of the outer pore region and the extracellular loop between transmembrane domains S3 and S4 for block of K_Ca2 current by apamin. Mapping the sequence of transmembrane domains S5, pore helix and S6 onto the crystal structures of KcsA, MthK and Kv1.2 has provided an approximation of the pore structure. This approach has allowed structural modelling of the interactions between toxins and channel, demonstrating that the toxins that show little discrimination between K_Ca2 channel subtypes interact with the outer pore and around the K⁺ selectivity filter. We present the structural modelling of the interaction of apamin and K_Ca2.2, which is superimposed onto the crystal structure of Kv1.2. This has shown that apamin interacts only with the outer pore and does not come into contact with channel's selectivity filter. It is clear that by comparing how different toxins interact with each K_Ca2 channel subtype, a detailed picture will be generated that will aid the development of more specific K_Ca2 channel blockers.     

吡格列酮对家兔局灶性脑缺血再灌注损伤细胞凋亡的影响

目的探讨吡格列酮对脑缺血再灌注损伤家兔细胞凋亡的影响及其机制。方法40只雄性家兔随机分为5组：①假手术组（S组,n=8）;②模型组（M组,n=8）;③吡格列酮组（P组,n=8）;（4）GW9662＋吡格列酮组（GP组,n=8）;（5）DMSO组（D组,n=8）。除S组外,其余各组均通过线栓法建立家兔大脑中动脉阻塞（MCAO）再灌注损伤模型。于术前30min分别给予相应处理。缺血120min再灌注24h后,对家兔进行神经功能评分;HE染色观察病理形态学。TUNEL检测神经细胞凋亡。结果①与S组比较,M组神经功能评分明显增加（P〈0．05）;与M组比较,P组神经功能评分明显降低（P〈0．05）。②与S组比较,M组凋亡细胞明显增加（P〈0．05）;与M组比较,P组凋亡细胞明显降低（P〈0．05）。结论吡格列酮可通过减轻形态学改变、抗神经细胞凋亡,对神经细胞发挥保护作用。