Randomized Comparison Between Everolimus-Eluting Bioresorbable Scaffold and Metallic Stent: Multimodality Imaging Through 3 Years

ObjectivesThe aim of this study was to investigate the vascular responses and fates of the scaffold after bioresorbable vascular scaffold (BVS) implantation using multimodality imaging.BackgroundSerial comprehensive image assessments after BVS implantation in the context of a randomized trial have not yet been reported.MethodsIn the ABSORB Japan trial, 400 patients were randomized to a BVS (n = 266) or a cobalt-chromium everolimus-eluting stent (n = 134). Through 3 years, patients underwent serial angiography and intravascular ultrasound or optical coherence tomography (OCT).ResultsLuminal dimension at 3 years was consistently smaller with the BVS than with the cobalt-chromium everolimus-eluting stent (mean angiographic minimal luminal diameter 2.04 ± 0.63 mm vs. 2.40 ± 0.56 mm, mean difference −0.37 mm [95% confidence interval: −0.50 to −0.24 mm]; p < 0.001), mainly because of smaller device area (6.13 ± 2.03 mm² vs. 7.15 ± 2.16 mm², mean difference −1.04 mm² [95% confidence interval: −1.66 to −0.42 mm²]; p < 0.001), and larger neointimal area (2.10 ± 0.61 mm² vs. 1.86 ± 0.64 mm², mean difference 0.24 mm² [95% confidence interval: 0.06 to 0.43 mm²]; p = 0.01) by OCT. BVS-treated vessels did not show previously reported favorable vessel responses, such as positive vessel remodeling, late luminal enlargement, and restoration of vasomotion, although the OCT-based healing score was on average zero (interquartile range: 0.00 to 0.00). At 3 years, intraluminal scaffold dismantling (ISD) was observed in 14% of BVS. On serial OCT, ISD was observed in 6 lesions at 2 years, where the struts had been fully apposed at post-procedure, while ISD was observed in 12 lesions at 3 years, where 8 lesions were free from ISD on 2-year OCT. In 5 cases of very late scaffold thrombosis, strut discontinuities were detected in all 4 cases with available OCT immediately before reintervention.ConclusionsIn this multimodality serial imaging study, luminal dimension at 3 years was smaller with the BVS than with the cobalt-chromium everolimus-eluting stent. ISD, suspected to be one of the mechanisms of very late BVS thrombosis, was observed in a substantial proportion of cases at 3 years, which developed between post-procedure and 2 years and even beyond 2 years. (AVJ-301 Clinical Trial: A Clinical Evaluation of AVJ-301 [Absorb™ BVS] in Japanese Population [ABSORB JAPAN]; NCT01844284)     

Patients with unstable angina pectoris show an increased frequency of the Fc gamma RIIa R131 allele

Patients with Systemic Lupus Erythematosus (SLE) carry an increased risk for the development of coronary artery disease (CAD). The R131 allele of the Fc gamma receptor IIa (FcγRIIa) is associated with SLE incidence and disease severity but also with CAD. Compared to stable angina pectoris (SAP) the unstable angina (UAP), as a manifestation of destabilizing CAD, is associated with increased risk of persistent instability, myocardial infarction, and death. Identification of clinically relevant determinants for unstable angina promises reduction of UAP-associated mortality in patients with SLE. We conducted a clinical study among 553 consecutive patients with stable angina pectoris (n = 330) and unstable angina pectoris (n = 223). All patients were genotyped for a frequent functional variant at position 131 of the mature FcγRIIa. UAP, but not SAP was significantly associated with the R/R131 genotype (P < 0.001). In troponin-negative patients with angina carrying the R/R131 genotype the odds ratio for suffering from UAP was 4.02 (95% confidence interval, 2.52–6.41) compared to those with non-R/R131 genotypes. In a multivariable analysis, the R/R131 genotype independently predicted the risk for development of UAP in a model adjusted for classical atherogenic risk factors. Our data imply that risk stratification of SLE- and other high risk patients with troponin-negative angina could be significantly improved by FcγRIIa genotyping.     

Needle tract seeding of papillary thyroid carcinoma after fine-needle capillary biopsy: A case report

BACKGROUNDFine-needle biopsy is an accurate and cost-efficient tool for the assessment of thyroid nodules. It includes two primary methods: Fine-needle capillary biopsy (FNCB) and fine-needle aspiration biopsy. Needle tract seeding (NTS) is a rare complication of thyroid fine-needle biopsy mainly caused by fine-needle aspiration biopsy rather than FNCB. Here, we present an extremely rare case of a papillary thyroid carcinoma (PTC) patient with FNCB-derived NTS. CASE SUMMARYWe report a 32-year-old woman with PTC who showed subcutaneous NTS 1 year after FNCB and thyroidectomy. NTS was diagnosed based on clinical manifestations, biochemistry indices, and imaging (computed tomography and ultrasound). Pathological identification of PTC metastases consistent with the puncture path is the gold standard for diagnosis. Surgical resection was the main method used to treat the disease. After surgery, thyroid function tests and ultrasound scans were performed every 3-6 mo. To date, no evidence of tumor recurrence has been observed.CONCLUSIONFNCB is a safe procedure as NTS is rare, and can be easily removed surgically with no recurrence. Accordingly, NTS should not limit the usefulness of FNCB.     

沉默热休克蛋白27基因对头颈部鳞状细胞癌细胞生物学行为的影响

目的 观察长效沉默热休克蛋白（Hsp）27基因后头颈部鳞状细胞癌细胞生物学行为的改变。方法 实验分为3组：高滴度pLenti-shRNA-Hsp27慢病毒颗粒长效转染入UM-SCC-22B细胞为实验组（shHsp27组）,常规培养UM-SCC-22B细胞（ctrl组）为空白对照,UM-SCC-22B细胞转染pLenti-shRNA-ctrl慢病毒颗粒（shctrl组）为阴性对照。采用实时荧光定量聚合酶链反应和蛋白质印迹法检测各组中Hsp27的表达,采用MTS细胞增殖实验、细胞划痕实验及Matrigel侵袭实验,观察各组Hsp27表达抑制后UM-SCC-22B细胞的增殖、迁移和侵袭能力的变化。结果 shHsp27组的Hsp27表达明显降低;MTS细胞增殖实验可见,细胞培养24、48 h后,shHsp27组的细胞增殖能力与ctrl组和shctrl组无明显差异;划痕实验表明,划痕产生72 h后,ctrl组细胞迁移能力为shHsp27组的4.38倍;Matrigel侵袭实验显示,ctrl组细胞的体外侵袭能力为shHsp27组的2.03倍。结论 长效转染慢病毒颗粒pLenti-shRNA-Hsp27能够高效、特异地沉默高转移潜能头颈部鳞状细胞癌细胞系UM-SCC-22B的Hsp27基因表达,并能显著抑制其体外侵袭和转移能力。     

植入药物洗脱支架后短期与长期双联抗血小板疗效比较的Meta分析

目的 评价短期（3～6个月）与长期（12个月）双联抗血小板治疗对冠状动脉药物洗脱支架植入后的临床效果。方法 研究病例包括稳定性心绞痛、急性冠脉综合征、无症状心肌缺血,均为原位血管病变。临床观察终点为：全因死亡、心源性死亡、心肌梗死、卒中、支架内血栓形成、靶病变再血管化治疗、严重出血、净不良临床事件（net adverse clinical event）。通过检索Pubmed、中国生物医学文献等中、英文数据库及手工检索,对符合条件的随机对照研究经质量评估、数据提取,进行Meta分析。结果 共计纳入12项随机对照研究。Detsky评分均大于5分。共计25 949个病例,随访率97.9%。两组在全因死亡（OR=0.86,95%CI 0.71～1.05,P=0.14）、心源性死亡（OR=0.94,95% CI 0.70～1.25,P=0.67）、支架血栓形成（OR=1.36,95%CI 0.94～1.98,P=0.11）、卒中（OR=1.01,95%CI 0.71～1.42,P=0.98）、靶病变再血管化（OR=0.121,95%CI 0.94～1.55,P=0.14）及净不良临床事件（OR=0.98,95%CI 0.83～1.14,P=0.75）均无明显差别;短期组随访期间心肌梗死发生率高于长期组（OR=1.27,95%CI 1.02～1.59,P=0.04）,长期组严重出血的比例明显增加（OR=0.69,95%CI 0.50～0.95,P=0.02）。亚洲人群研究结果：长期治疗组全因死亡高于短期组（OR=0.72,95%CI 0.53～0.97,P=0.03）,两组严重出血无明显差别。结论 依据限定的临床观察终点,短期双联抗血小板疗效不劣于长期组;7项亚组人群研究,长期组全因死亡率高,不排除与样本量偏少产生的偏移及（或）人群的个体差异有关,结果还有待进一步验证。此结果可作为临床工作警示,依据患者出血风险及冠状动脉病变结果个体化调整双联抗血小板周期。     

DEK基因RNAi慢病毒表达载体的构建及其功能鉴定

目的：构建DEK基因的RNA干扰（ RNAi）慢病毒表达载体,并对其生物学功能进行初步检测。方法采用RNAi技术,根据DEK基因的序列,确定其有效靶序列,合成DEK基因的Oligo DNA,退火形成双链DNA,将其克隆到经BamHⅠ与EcoRⅠ酶切后的小干扰RNA（ siRNA）表达载体PSIH-H1上,产生PSIH-H1-DEK慢病毒载体,筛选阳性克隆并测序鉴定。与3个包装质粒共转染293T细胞,包装成慢病毒后感染乳腺癌细胞ZR75-1,经嘌呤霉素（ puromycin,puro）筛选2周后,收集部分细胞利用实时聚合酶链反应（ real time-PCR,RT-PCR）和Western印迹分别检验DEK在信使RNA （ mRNA ）和蛋白水平的敲低效果,并通过细胞生长实验检测DEK对人乳腺癌细胞系ZR75-1细胞生长的影响。结果 PCR和DNA测序结果证实,DEK siRNA慢病毒表达载体PSIH-H1-DEK构建成功。 RT-PCR和Western印迹结果显示,构建的DEK siRNA可有效抑制DEK基因的表达,并由此建立了敲低DEK的稳定克隆。生长曲线实验表明, DEK siRNA可抑制人乳腺癌细胞系ZR75-1细胞的生长。结论成功构建了DEK基因的RNAi慢病毒表达载体,感染人乳腺癌细胞系ZR75-1细胞后,有效沉默了ZR75-1细胞中的DEK基因的表达,为进一步研究DEK基因在乳腺癌中的作用奠定基础。     

Atenolol versus the fixed combination of atenolol and nifedipine in stable angina pectoris

One hundred and fourteen patients (94 male) with chronic stableangina who had a positive exercise test after 4 weeks on atenololalone were randomized to receive either atenolol alone or thefixed combination of atenolol and nifedipine slow release formulationfor 4 weeks in a double-blind cross-over manner. Exercise stresstesting (Bruce protocol) at the end of each treatment perioddemonstrated that the time to the onset of pain and occurrenceof 1 mm ST segment depression improved significantly (P <0.05 and P < 0.001 respectively) whilst on the fixed combinationcompared to atenolol alone. In order to achieve sufficient sensitivityin the analysis of the exercise times, novel statistical methodsbased on survival analysis were used. Maximum ST segment depressionwas 0.13 mm less (p < 0.04) while on the fixed combination.The incidence of withdrawals and adverse effects was similaron both treatments.     

弹性髓内钉治疗儿童胫骨干骨折

2010年3月～2013年4月,我院应用弹性髓内钉（elastic stable intramedul-lary nailing,ESIN）治疗35例儿童胫骨干骨折患儿,疗效满意,报道如下。     

Differential loss of natural killer cell activity in patients with acute myocardial infarction and stable angina pectoris

Background: To evaluate the activity of natural killer cells through their inhibitory and activating receptors and quantity in peripheral blood mononuclear cells extracted from patients with acute myocardial infarction, stable angina pectoris and the controls. Methods: 100 patients with myocardial infarction, 100 with stable angina, and 20 healthy volunteers were recruited into the study. 20 randomly chosen people per group were examined for the whole human genome microarray analysis to detect the gene expressions of all 40 inhibitory and activating natural killer cell receptors. Flow cytometry analysis was applied to all 200 patients to measure the quantity of natural killer cells. Results: In myocardial infarction group, the mRNA expressions of six inhibitory receptors KIR2DL2, KIR3DL3, CD94, NKG2A, KLRB1, KLRG1, and eight activating receptors KIR2DS3, KIR2DS5, NKp30, NTB-A, CRACC, CD2, CD7 and CD96 were significantly down-regulated (P<0.05) compared with both angina patients and the controls. There was no statistical difference in receptor expressions between angina patients and control group. The quantity of natural killer cells was significantly decreased in both infarction and angina patients compared with normal range (P<0.001). Conclusions: The significant mRNAs down-regulation of several receptors in myocardial infarction group and reduction in the quantity of natural killer cells in both myocardial infarction and angina patients showed a quantitative loss and dysfunction of natural killer cells in myocardial infarction patients.     

ShcC proteins: Brain aging and beyond

To date, most studies of Shc family of signaling adaptor proteins have been focused on the near-ubiquitously expressed ShcA, indicating its relevance to age-related diseases and longevity. Although the role of the neuronal ShcC protein is much less investigated, accumulated evidence suggests its importance for neuroprotection against such aging-associated conditions as brain ischemia and oxidative stress. Here, we summarize more than decade of studies on the ShcC expression and function in normal brain, age-related brain pathologies and immune disorders with a focus on the interactions of ShcC with signaling proteins/pathways, and the possible implications of these interactions for changes associated with aging.