目的 探讨钾通道四聚化结构域5(KCTD5)对胰腺癌细胞的生物学行为的影响.方法 生物信息学检测KCTD5在胰腺癌中184例mRNA及211例蛋白质中的表达水平,观察KCTD5的表达对胰腺癌患者预后的影响,进一步对数据库中所得数据进行单因素Cox回归分析.定量聚合酶链反应(qPCR)、蛋白免疫印迹法检测KCTD5在胰腺癌细胞株中的表达水平.转染KCTD5小干扰RNA至SW1990胰腺癌细胞中,分为si-NC、si-KCTD5-1、si-KCTD5-2组.细胞计数实验(CCK-8)实验检测细胞增殖能力;Transwell实验检测转染后胰腺癌细胞迁移及侵袭能力.结果 生物信息学结果表明KCTD5在胰腺癌中的mRNA及蛋白表达水平显著高于正常组织;单因素分析及生存分析结果表明KCTD5可作为胰腺癌患者一种独立危险因素;qPCR结果表明KCTD5在正常人胰腺导管上皮细胞HPDE中的表达水平为1.10±0.18,在胰腺癌细胞株中的表达水平分别为SW1990(2.44±0.19)、PANC-1(1.65±0.15)、ASPC-1(2.15±0.12),KCTD5 在胰腺癌细胞株中的表达水平明显升高(t=12.84,5.76,12.16,P 均＜0.05);转染后,CCK-8 实验表明 72 h 后 si-KCTD5-1、si-KCTD5-2、si-KCTD5-3 组吸光度值分别为 2.93±0.88、1.76±0.97、3.03±0.99,明显低于对照组(4.20±1.02,t=2.31、4.25、2.02,P 均＜0.05);降低 KCTD5 表达后 Transwell 实验中胰腺癌细胞的迁移能力和侵袭能力明显降低.结论 胰腺癌中表达升高的KCTD5可促进胰腺癌细胞的增殖、迁移和侵袭能力,降低其表达后胰腺癌细胞上述能力降低.

目的 利用轧塞酸二钠(Gd-EOB-DTPA)增强核磁共振成像(MRI)肝胆期的结节强化程度预测肝细胞癌(HCC)靶向联合免疫治疗的效果.方法 回顾性收集2020年1月至2022年1月河南省人民医院诊断为HCC,且在靶向联合免疫治疗前行钆塞酸二钠增强MRI检查的53例患者信息,利用影像处理软件测量107个肝内结节的信号强度,计算肝胆期相对强化比(RER),并比较高强化和低强化HCC结节间的每个结节体积增加20％的时间(TTNP).根据实体肿瘤免疫疗效评价标准(iRECIST),比较肝胆期高强化的HCC结节患者和低强化的HCC结节患者的无进展生存期(PFS)和客观缓解率(ORR)与疾病控制率(DCR)等.结果 高强化HCC结节患者的中位PFS为3.4 个月[95％置信区间(CI):2.5-4.3,n=21),ORR 为 14.3％(3/21),DCR 为 47.5％(10/21).低强化 HCC 结节患者的中位 PFS 为 6.8 个月(95％CI:6.2-7.3,n=32),ORR 为 37.5％(12/32),DCR为75.0％(24/32);进展型高强化HCC结节(n=23)的中位TTNP为2.3个月(95％CI:2.0-2.6),低强化 HCC 结节(n=62)的中位 TTNP 为 6.1 个月(95％CI:5.0～7.2).结论 Gd-EOB-DTPA增强MRI肝胆期肝内HCC结节的强化程度与结节TTNP、PFS、DCR明显相关.

目的 研究益气养心中药联合西药治疗慢性心力衰竭(心衰)的临床疗效及安全性.方法 检索自建库至2020年5月31日发表与益气养心中药联合西药治疗慢性心衰的临床随机对照试验(RCT)相关文献,通过RevMan 5.3、Stata 14.0软件进行统计处理.结果 该研究纳入14个RCT共1706例患者,其中治疗组(T)、对照组(C)均为853例,文献质量不高.Meta分析结果显示,在慢性心衰常规西药治疗基础上加用益气养心中药后,治疗组较对照组显著提高了患者临床有效率、改善脑钠肽(BNP)及心脏功能指标.临床有效率(RR=1.18,95％CI:1.07～1.29,P=0.0005)、BNP(MD=-200.96,95％CI:-335.30～-66.63,P=0.003)、左室射血分数(MD=8.22,95％CI:4.45～11.99,P<0.0001)、左室收缩末期内径(MD=-2.70,95％CI:-3.63～-1.76,P<0.00001)、左室舒张末期内径(MD=-2.60,95％CI:-4.69～-0.52,P=0.01)差异均有统计学意义.结论 益气养心中药与西药联合,提高了慢性心衰患者的临床疗效、改善心功能指标、降低BNP水平.

Objective:To detect the expression of GINS complex subunit 4 (GINS4) protein in hepatocellular carcinoma tissues and observe its effect on the invasion and proliferation of hepatocellular carcinoma cells.Methods:From September 2019 to December 2020 in our hospital, 60 patients with hepatocellular carcinoma were collected during surgery and hepatocellular carcinoma tissues and corresponding para-cancerous tissue specimens were selected as the observation group and the control group. Real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) and Western blotting was used to detect the expression of GINS4 in hepatocellular carcinoma tissues, use specific short hairpin RNA (shRNA) to construct low-expressing stable hepatocellular carcinoma cell lines, and divide them into experimental groups (shRNA group) and the control group (NC group); Transwell tested its ability to invade HepG2 cells; colony formation test and cell counting kit (CCK-8) test tested its proliferation ability on HepG2 cells. Comparison between groups is by paired sample t test. Results:RT-qPCR showed that the expression of GINS4 in hepatocellular carcinoma tissues (2.89±0.11) was higher than that in adjacent tissues (1.34±0.15), and the difference was statistically significant ( t=8.56, P<0.01). Western blot showed that the expression of GINS4 in hepatocellular carcinoma tissue was (1.54±0.76) times higher than that in adjacent tissues, and the difference was statistically significant ( t=2.67, P<0.05). After shRNA transfection of HepG2 cells, GINS4 in the experimental group The expression level was (1.88±0.34) times lower than that of the control group, and the difference was statistically significant ( t=7.43, P<0.05); the Transwell experiment showed that the number of perforated cells in the experimental group was (56.33±3.51) compared with the control group (90.42±1.53) cells were significantly reduced, and the difference was statistically significant ( t=3.34, P<0.01); the colony formation experiment showed that the number of cell clusters in the experimental group (83.33±7.37) was significantly less than that in the control group (345.00±16.64). The difference was statistically significant ( t=15.28, P<0.01); CCK-8 experiment showed that the 3 d absorbance of the experimental group was (1.43±0.11) lower than that of the control group (2.15±0.15), and the difference was statistically significant ( t=6.52, P<0.001). Conclusion:The expression of GINS4 in hepatocellular carcinoma tissues is higher than that in adjacent tissues. Reducing the expression of GINS4 can significantly inhibit the invasion and proliferation of hepatocellular carcinoma cells.

Objective:To investigate the application of nano-fluorescent probes in hepatocellular carcinoma (HCC) blood supply molecular imaging in rats and pave the foundation of double blood supply treatment in HCC.Methods:The HCC models of 12 rats were established by diethylnitrosamine (DEN) chemical induction. After 15 weeks, the magnetic resonance imaging (MRI) and pathological findings were observed. Different nano-fluorescent probes were applied through hepatic artery and portal vein to observe the blood supply molecular images of HCC tissues.Results:A total of 4 rats died at 13-14 weeks, with a survival rate of 66.67% at 15 weeks and the tumor formation rate of 100%. The pathological sections were consistent with the signs of HCC. The arterial 1, 1′-dioctadecy1-3, 3, 3′, 3′-tetramethylindocarbocyanine perchlorate (DiI) fluorescence intensity in tumor of molecular fluorescence imaging [(2.99±0.41)×10 7] was significantly greater than the surrounding liver tissue [(1.06±0.22)×10 7, t=-9.410, P<0.05]; and fluorescence intensity of Alexa fluor 647 in tumor of portal vein [(1.30±0.29)×10 7] was significantly weaker than that of peripheral liver tissue [(2.76±0.38)×10 7, t=7.480, P<0.05]. The slide scan showed that arterial blood supply in tumor tissue was higher than the surrounding liver tissue, and the portal vein blood supply was found in the parenchyma and surrounding areas of the liver tumor. Conclusion:The DEN induction is a mature and stable method to establish the HCC model, and the nano-fluorescent probe can observe the double blood supply for HCC in the microscopic level.