Surgical Technique Notes of Arterial Vascular Reconstruction During Kidney Transplantation: Personal Experience and Literature Review

Background

Arterial vascular anomalies in patients undergoing kidney transplantation (KT) are correlated with a higher incidence of early surgical complications, potentially causing graft loss. Arterial reconstruction allows patients to overcome these surgical challenges, thus minimizing the risk of poor outcomes. The aim of the present study is to retrospectively investigate the safety and effectiveness of the multiple arterial reconstruction technique with a Teflon patch in case of an unavailable aortic patch: to do so, surgical complications, graft function, and patient survival were evaluated.

Profilin 1, negatively regulated by microRNA-19a-3p,serves as a tumor suppressor in human hepatocellular carcinoma

Profilin 1 (PFN1) is a critical actin-regulatory protein; however, its functional role in hepatocellular carcinoma (HCC) progression remains to be further elucidated. In the present study, we observed that the expression levels of PFN1 were significantly decreased in HCC tissues and cell lines. Low PFN1 expression was significantly correlated with aggressive clinicopathological characteristics and poor prognosis of HCC patients. Further in vitro experiments demonstrated that overexpression of PFN1 remarkably inhibited the proliferation, migration, invasion and EMT of HCC cells. Moreover, we also found that PFN1 was a direct target gene of miR-19a-3p, and in HCC tissues, and there was a significantly inverse correlation between PFN1 mRNA and miR-19a-3p expression. Collectively, our results showed that PFN1 functions as a tumor suppressor in HCC, and might serve as a diagnostic and therapeutic target for HCC patients.     

miR-200、 miR -155及血管新生因子与复发性流产的相关性分析

目的 研究miR-200、miR-155及血管新生因子与原因不明复发性流产(unexplained recurrent spontaneousabortion,URSA)的相关性分析。 方法 选择2015年3月—2018年1月在青岛市妇女儿童医院妇产科就诊的URSA患者作为URSA组、要求终止妊娠的正常早孕患者作为对照组,检测绒毛组织中微小RNA(microRNA, miR)miR-200、miR-155、血管内皮生长因子(vascular endothelial growth factor,VEGF)、可溶性FMS样酪氨酸激酶1(soluble FMS like tyrosine kinase-1,sFlt-1)的表达量及血清中VEGF、sFlt-1的含量,对miR-200、miR-155靶向结合VEGF、sFlt-1进行生物信息学分析。 结果 URSA组的绒毛组织中miR-200(1.78±0.32 vs. 0.91±0.15)、sFlt-1(1.87±0.35 vs. 1.06±0.21)的相对表达量及血清中sFlt-1的含量[(12.39±2.31)ng/ml vs. (6.51±0.95)ng/ml]均高于对照组,差异有统计学意义(均P<0.05)。绒毛组织中miR-155相对表达量(0.60±0.10 vs. 0.93±0.16)、VEGF mRNA相对表达量(0.59±0.09 vs. 1.02±0.16)及蛋白表达量(0.62±0.07 vs. 1.04±0.18)、血清中VEGF的含量[(601.25±94.39)ng/ml vs. (935.12±132.47)ng/ml]低于对照组,差异有统计学意义(均P<0.05);URSA组患者绒毛组织中miR-200的表达量与血清中VEGF的含量、绒毛组织中VEGF的表达量均呈负相关,绒毛组织中miR-155的表达量与血清中sFlt-1的含量和绒毛组织中sFlt-1的表达量均呈负相关;miR-200、miR-155分别靶向结合VEGF、sFlt-1基因的3’UTR。 结论 miR-200表达增多、miR-155表达减少与URSA发生有关,miR-200靶向VEGF、miR-155靶向sFlt-1是介导该过程的可能机制。     

Sister chromatid exchanges in patients with retinoblastoma

Spontaneous and mitomycin C(MMC)-induced sisyer chromatid exchanges were studied in 11 patients with retinoblastoma and 7 normal controls. Spontaneous rates were similar in patients and in controls. The MMC-induced rate was found to be significantly higher in bilaterally affected patients than in controls. It is suggested that this increase may be due to a DNA repair deficiency. However, it is not possible to clarify wether this abnormality is associated with the retinoblastoma gene or with another factor acting on the degree of expressivity of the disease in gene carriers.     

miR-499 rs3746444多态性抑制宫颈癌细胞的增殖作用及分子机制

目的探讨miR-499 rs3746444多态性与宫颈癌临床特征相关性及对宫颈癌细胞增殖的影响作用与机制。方法应用病例对照研究方法,选取2012年6月至2018年12月于内蒙古自治区人民医院就诊的宫颈癌病人857例作为实验组,同期873例健康志愿者作为对照组,两组年龄均在23~62岁,采用TaqMan探针法对rs3746444位点的多态性进行基因分型;构建包含pGL3-Sox63'UTR和miR-499的GG或AA的海肾荧光素酶载体(Renilla luciferase vector)于prl-sV40质粒中,并采用lipo2000转染人宫颈上皮永生化细胞H8和人宫颈癌细胞系:腺癌样SiHa、上皮样HeLa和C33A,CCK-8法检测细胞增殖;双荧光素报告基因检测法分析Frefly和Renilla荧光素酶活性;Western blot检测Hela和SiHa细胞Cyclin D1、CyclinE、CDK4、CDK6和Sox6蛋白表达。结果AG和GG基因型宫颈癌发生风险分别是AA基因型个体的1.09倍和2.41倍,携带G等位基因的个体患宫颈癌的风险是AA基因型个体的1.28倍,GG基因型宫颈癌患者III期及以上的比例显著高于AA基因型。GG表型肿瘤高度分化比例明显高于AA表型组,rs3746444不同基因型对正常宫颈H8细胞的增殖无显著影响。miR-499 GG+Sox6-3'UTR处理组Hela、C33A和SiHa细胞72 h时OD450显著低于miR-499 AA+Sox6-3'UTR组,且高于Sox6-3'UTR组(P<0.05)。miR-499 GG+Sox6-3'UTR处理组Hela和SiHa细胞Cyclin D1、CyclinE、CDK4和CDK6显著高于miR-499 AA+Sox6-3'UTR组,低于Sox6-3'UTR组(P<0.05)。与miR-499 AA+Sox6-3'UTR处理组相比,miR-499 GG+Sox6-3'UTR处理组Sox6的表达水平增加(P<0.05),且均低于Sox6-3'UTR对照组(P<0.05)。结论miR-499的rs3746444突变(A>G)与宫颈癌肿瘤生长和分化程度密切相关,其通过上调Sox6介导的CyclinD1高表达具有明显的促进宫颈癌细胞生长增殖作用。     

Hemodynamic differences between carvedilol and labetalol in the cutaneous circulation

The effects of labetalol and carvedilol on local cutaneous microvascular perfusion and calculated local cutaneous microvascular resistance were investigated in anesthetized rats at submaximal doses that produced equivalent reductions in blood pressure and heart rate. Labetalol decreased cutaneous perfusion (– 25% ± 3%) without significantly affecting cutaneous vascular resistance ( – 6% ± 3%). In marked contrast, carvedilol dramatically increased cutaneous perfusion ( + 64% ± 9%) and significantly reduced cutaneous vascular resistance ( – 57% ± 3%). These results suggest that carvedilol and labetalol possess differences in the mechanisms by which they produce vasodilation in vivo.     

胰腺导管腺癌中microRNA-21与TGF-β1信号通路相关

目的：对胰腺导管腺癌样本进行基因分析,筛选与胰腺导管腺癌相关的microRNA(miRNA),并初步分析目标miRNA与胰腺癌转化生长因子-β1(TGF-β1)信号通路的相关性。方法：收集在海南省中医院住院的胰腺导管癌患者术前外周静脉血血清标本19份,健康体检人群的外周静脉血血清标本21份作为非胰腺导管癌对照组。利用GCBI(Gene-Cloud Biotechnology Information)数据平台筛选与胰腺导管腺癌样本有关的基因并对其进行生物信息学分析,将筛选出的基因作为研究对象,用real-time PCR和蛋白质印迹法验证该基因在胰腺导管腺癌中的表达。通过改变胰腺导管腺癌细胞中该基因的表达水平观察其与TGF-β1之间的关系。结果：通过聚类分析和基因功能富集分析筛选出miRNA-21为胰腺导管癌相关基因。MiRNA-21在胰腺导管腺癌患者体内高表达。在miRNA-21过表达的PANC-1细胞中,TGF-β1表达受到抑制;但当miRNA-21的表达受到抑制时,TGF-β1的表达明显上升。结论：MiRNA-21在胰腺导管腺癌患者体内高表达,可调控TGF-β1的表达,从而参与胰腺导管腺癌的发生发展。     

MiR-30a-5p通过泛素水解酶22抑制人宫颈癌细胞上皮-间质转化功能

【目的】研究microRNA-30a-5p（miR-30a-5p）对人宫颈癌Hela细胞上皮-间质转化功能的影响及其相关机制。【方法】宫颈癌Hela细胞株分别转染目的mir的模拟物和阴性对照模拟物,分别以30a-5p组、NC组命名并标记细胞。同时,以未经过处理的Hela细胞作为对照（Control组）。分别用逆转录-聚合酶链反应法检测各组宫颈癌细胞的miR-30a-5p含量。Transwell实验检测3组细胞迁移能力和侵袭能力。Western-blot法检测3组细胞神经-钙粘素（N-cadherin）、α-连环蛋白（α-Catenin）和泛素水解酶22（USP22）表达水平。运用生物信息学方法预测miR-30a-5p的靶基因。采用Western blot法检测USP22过表达对miR-30a-5p抑制EMT的拮抗作用。双荧光素酶实验检测miR-30a-5p与USP22的关系。建立皮下移植瘤模型观察miR-30a-5p的体内作用。【结果】30a-5p组宫颈癌细胞miR-30a-5p的表达水平明显上调,表达水平为Control组的853.82（862.26~843.11）倍（P＜0.01）。30a-5p组侵袭细胞数量8.17（8.32~8.03）明显低于Control组（P＜0.01）。30a-5p组细胞N-cadherin蛋白的细胞内含量明显下降,α-Catenin蛋白的细胞内含量明显上升,USP22蛋白表达量明显降低。合并USP22过表达处理的30a-5p组宫颈癌细胞中N-cadherin蛋白表达量明显升高,α-Catenin蛋白表达量明显降低。双荧光素酶检验结果显示USP22为miR-30a-5p的下游靶基因（P＜0.01）。30a-5p组皮下移植瘤明显小于Control组（P＜0.01）。与Control组肿瘤组织相比,30a-5p组肿瘤组织miR-30a-5p的相对含量升高,USP22蛋白含量降低,N-cadherin蛋白的含量降低,α-Catenin蛋白含量升高。【结论】miR-30a-5p在宫颈癌Hela细胞中,可能通过靶向识别下游靶基因USP22,进而抑制其翻译。最终实现对宫颈癌细胞EMT过程的抑制。     

Quaking and miR-155 interactions in inflammation and leukemogenesis

Quaking (QKI) is a tumor-suppressor gene encoding a conserved RNA-binding protein, whose expression is downregulated in several solid tumors. Here we report that QKI plays an important role in the immune response and suppression of leukemogenesis. We show that the expression of Qki is reduced in lipopolysaccharide (LPS)-challenged macrophages, suggesting that Qki is a key regulator of LPS signaling pathway. Furthermore, LPS-induced downregulation of Qki expression is miR-155-dependent. Qki overexpression impairs LPS-induced phosphorylation of JNK and particularly p38 MAPKs, in addition to increasing the production of anti-inflammatory cytokine IL-10. In contrast, Qki ablation decreases Fas expression and the rate of Caspase3/7 activity, while increasing the levels of IL-1α, IL-1β and IL-6, and p38 phosphorylation. Similarly, the p38 pathway is also a target of QKI activity in chronic lymphocytic leukemia (CLL)-derived MEC2 cells. Finally, B-CLL patients show lower levels of QKI expression compared with B cells from healthy donor, and Qki is similarily downregulated with the progression of leukemia in Eμ-miR-155 transgenic mice. Altogether, these data implicate QKI in the pathophysiology of inflammation and oncogenesis where miR-155 is involved.     

miR-155反义寡核苷酸转染对人大肠癌Lovo细胞侵袭的影响

目的探讨miR-155对人大肠癌细胞侵袭能力的影响。方法大肠癌Lovo细胞分为3组：脂质体介导反义miR-155（AS-miR-155）组、无义寡脱氧核苷酸（ODN）组和对照组。测定荧光素酶活性验证3组细胞中miR-155的表达,采用Matrigel基质生长试验检测细胞生长情况,以Transwe Ⅱ方法检测细胞的侵袭力,结果与对照组和无义ODN组比较,转染AS-miR-155组Lovo细胞miR-2l表达水平降低;Matrigel基质生长试验显示,转染AS-miR-155组Lovo细胞体外培养克隆平均直径较小,Transwe Ⅱ细胞侵袭试验显示转染AS-miR-155组穿膜细胞数较少。结论 miR-2l高表达可促进Lovo大肠癌细胞侵袭生长,提示miR-155可以作为基因治疗大肠癌的候选靶点。