简介:【 摘要 】 目的:研究 胃癌组织中 VEGF-A 、 ADD1 与临床病理特征的相关性 。 方法: 选择 2019 年 6 月至 2020 年 1 月来我院进行治疗的 80 例胃癌患者开展本次研究,选择患者的肿瘤组织作为研究的实验组,选择距离肿瘤组织大于 1.5 厘米远的正常组织作为本研究的对比组。分别观察胃癌患者肿瘤组织、癌旁正常组织中的 VEGF-A、 ADD1 表达水平。 结果: VEGF-A胃癌组织与中的高表达率显著高于癌旁正常组织,比较 P<0.05 ; ADD1 在胃癌组织中的高表达率显著高于癌旁正常组织,比较 P<0.05 。 VEGF-A表达主要与 肿瘤不同位置存在差异性,对比有统计学意义( P<0.05 )。与患者的淋巴结转移、浸润深、组织分化程度、 TNM 分期、性别、年龄等不存在相关性,无统计学意义( P>0.05 ); ADD1 表达与胃癌患者的淋巴结转移、浸润深、组织分化程度、 TNM 分期等存在统计学意义( P<0.05 ),与患者的肿瘤不同位置、性别、年龄无统计学意义( P>0.05 )。 VEGF-A、 ADD1 在胃癌组织中的表达呈现出正相关。 结论: VEGF-A、 ADD1 在胃癌组织中的表达呈现出正相关。提示了 VEGF-A、 ADD1 表达和胃癌患者的预后存在相关性。
简介:摘要:烘丝机是烟草制丝线上的重要设备,其加工性能和质量将直接影响卷烟的内在质量和风格特征,烘丝机内风速也直接影响卷烟内质。本文通过对现在常用的风速仪研究,找到 SH6型薄板式烘丝机最适合的风速测量方式,并通过风速值反映烘丝的排潮等性能,保证烘丝机高效稳定运行。
简介:摘要目的评价hsa_circ_0025853在人神经母细胞瘤细胞(SK-N-SH细胞)氧糖剥夺/复糖复氧损伤(OGD/R)中的作用。方法传代培养SK-N-SH细胞至对数生长期,采用随机数字表法分为4组(n=40):对照组(C组)、OGD/R组、hsa_circ_0025853过表达组(E组)和hsa_circ_0025853过表达阴性对照组(EV组)。C组细胞在37 ℃、5%CO2正常条件下培养,OGD/R组细胞铺于6孔板或96孔板待完全贴壁后氧糖剥夺16 h后复糖复氧。E组和EV组分别转染hsa_circ_0025853过表达载体或hsa_circ_0025853过表达阴性对照载体后制备OGD/R模型。于复糖复氧4和12 h时,采用qPCR法检测hsa_circ_0025853、线粒体动力相关蛋白1(Drp1)mRNA表达水平;Western blot法检测Drp1表达水平,CCK-8法检测细胞活力,流式细胞术检测细胞凋亡率。结果与C组比较,OGD/R组复糖复氧后细胞活力降低,细胞凋亡率升高,Drp1及其mRNA表达上调,hsa_circ_0025853表达下调(P<0.05);与OGD/R组或EV组比较,E组复糖复氧后细胞活力升高,细胞凋亡率降低,Drp1表达下调,hsa_circ_0025853表达上调(P<0.05),Drp1 mRNA表达差异无统计学意义(P>0.05)。结论hsa_circ_0025853表达下调可促进Drp1表达上调,诱发细胞凋亡,参与SK-N-SH细胞OGD/R的发生机制。
简介:AbstractBackground:The efficacy of entecavir (ETV) add-on peg-interferon therapy compared with ETV monotherapy in treatment-naïve hepatitis B virus (HBV) patients remains controversial. We investigated whether adding peg-interferon to ongoing ETV treatment leads to a better curative effect or not.Methods:All patients have been recruited between August 2013 and January 2015 from the Shanghai Public Health Clinical Center and Zhongshan Hospital (China). Eligible HBV patients (n = 144) were randomly divided (1:1) to receive either ETV monotherapy (n = 70) or peg-interferon add-on therapy from week 26 to 52 (n = 74). Patients were followed-up for at least 2 years. Indexes including hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) seroconversion rate, sustained virologic response, transient elastography value, and histological scores were evaluated every 3 months until the end of the study. The rate of patients with HBsAg loss was defined as the primary endpoint criteria.Results:At week 26, no patient achieved HBsAg seroconversion in either group. At week 52, one patient in the monotherapy group was HBsAg-negative but there was none in the combination therapy group. The monotherapy group showed significantly better liver function recovery results than the combination therapy group. At week 78, one patient in the combination group had HBsAg seroconverted. At week 104, only three patients in the combination therapy group were HBsAg-negative compared with one patient in monotherapy. The mean alanine aminotransferase and aspartate aminotransferase levels and transient elastography values decreased significantly compared with baseline. Both groups showed a favorable decrease in alpha-fetoprotein (monotherapy: 4.5 [2.8, 7.1] vs. 2.2 [1.8, 3.1] ng/mL, P < 0.001; combination therapy: 5.7 [3.0, 18.8] vs. 3.2 [2.0, 4.3] ng/mL, P < 0.001) and an improved result of liver biopsy examination scores. The combination group showed a better improvement in histology compared with the monotherapy group (mean transient elastography value 6.6 [4.9, 9.8] vs. 7.8 [5.4, 11.1] kPa, P = 0.028). But there was no significant difference in HBsAg conversion rate (1.8% [1/56] vs. 4.1% [3/73], P = 0.809) and HBeAg conversion rate (12.5% [7/56] vs. 11.0% [8/73], P = 0.787), as well as HBV-DNA, sustained virologic response (93.2% vs. 98.5%, P = 0.150) between the two groups.Conclusions:Both therapies supported liver function recovery and histology improvement. Combination therapy did not show better anti-viral efficacy in HBsAg or HBeAg seroconversion compared with monotherapy. However, combination therapy played a more positive role in reversing hepatic fibrosis compared with monotherapy.Trial registration:ClinicalTrials.gov: NCT02849132; https://clinicaltrials.gov/ct2/show/NCT02849132
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