The long non-coding (lnc)RNA cancer susceptibility 11 (CASC11) promotes gastric cancer, however its role in other diseases is unknown. The present study demonstrated upregulation of lncRNA CASC11 and microRNA (miR)-21 in hepatocellular carcinoma (HCC). Furthermore, the expression of CASC11 was positively correlated with that of miR-21 in HCC tumors. Moreover, overexpression of lncRNA CASC11 led to upregulation of miR-21 in HCC cells, whereas overexpression of miR-21 had no effect on CASC11 levels. The levels of lncRNA CASC11 and miR-21 were found to be upregulated in the plasma of patients with HCC during chemotherapy. In vitro cell experiments demonstrated upregulation of lncRNA CASC11 in HCC cells treated with carboplatin. Additionally, overexpression of lncRNA CASC11 promoted, whereas its knockdown inhibited the viability of HCC cells following carboplatin treatment. Finally, overexpression of miR-21 ameliorated the effects of lncRNA CASC11 knockdown on cell viability. Thus, these findings suggest that upregulation of lncRNA CASC11 is involved in the development of chemoresistance to carboplatin in patients with HCC, via the upregulation of miR-21.

目的 探讨化滞柔肝颗粒联合硫普罗宁片治疗非酒精性脂肪肝的临床疗效.方法 选取2016年6月-2018年6月在青岛市第六人民医院进行治疗的100例非酒精性脂肪肝患者作为研究对象,根据用药的不同将患者分为对照组(50例)和治疗组(50例).对照组患者口服硫普罗宁片,2片/次,3次/d;治疗组患者在对照组治疗的基础上口服化滞柔肝颗粒,1袋/次,3次/d.两组均治疗8周.观察两组患者的临床疗效,同时比较两组治疗前后的血脂水平、肝功能指标和血清学指标.结果 治疗后,对照组总有效率为82.00％,显著低于治疗组的96.00％,两组比较差异具有统计学意义(P＜0.05).治疗后,两组总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)水平均明显降低,高密度脂蛋白胆固醇(HDL-C)水平显著增高(P＜0.05);治疗后,治疗组血脂水平显著优于对照组(P＜0.05).治疗后,两组丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)和γ-谷氨酰转肽酶(γ-GT)水平均明显降低(P＜0.05);治疗后,治疗组肝功能指标显著低于对照组(P＜0.05).治疗后,两组瘦素(LEP)、摄食抑制因子-1(NSF-1)、成纤维细胞生长因子-21 (FGF-21)、硫氧还蛋白相互作用蛋白(TXNIP)、低氧诱导因子-1α (HIF-1α)水平均显著降低(P＜0.05);治疗后,治疗组血清学指标显著低于对照组(P＜0.05).结论 化滞柔肝颗粒联合硫普罗宁片治疗非酒精性脂肪肝疗效确切,可改善患者肝功能,降低血脂和血清因子水平,具有一定的临床应用价值.

Astragaloside IV (AS-IV) in improving liver cirrhosis injury in rats and its effect on the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mechanistic target of rapamycin (mTOR) signaling pathway were observed. Rat model of liver cirrhosis was induced by injection of carbon tetrachloride (CCl4). A total of 36 Sprague-Dawley (SD) rats were randomly divided into three groups: the normal control group (n=10), the model control group (n=13), and the AS-IV group (n=13). The normal control group was injected with olive oil and given carboxymethyl cellulose (CMC)-Na (10 ml/kg/day), the model control group was given CMC-Na (10 ml/kg/day), and the AS-IV group underwent intragastric administration of AS-IV (20 ml/kg/day). The content of alanine transaminase (ALT) and aspartate transaminase (AST) of rats was detected. The levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and IL-1β in serum were detected via enzyme-linked immunosorbent assay (ELISA). Hematoxylin and eosin (H&E) staining was applied to observe morphological changes in liver tissues. The expression of collagens in liver tissues was detected via Masson's trichrome staining. Additionally, the expression of proteins in liver tissues was detected via western blotting. Compared with those in the blank group, the levels of AST, ALT, TNF-α, IL-6 and IL-1β were higher, the expression level of collagens in liver tissues was increased, and the expression ratios of phosphorylated (p)-PI3K/PI3K, p-Akt/Akt and p-mTOR/mTOR proteins were increased in the model group. Compared with the model group, AS-IV could significantly decrease the content of AST, ALT, TNF-α, IL-6 and IL-β in serum of rats, obviously inhibit the expression of collagens in liver tissues and decrease the expression ratios of p-PI3K/PI3K, p-Akt/Akt and p-mTOR/mTOR proteins in liver tissues. AS-IV can inhibit the inflammatory response so as to reduce the expression of collagens, and its mechanism may play a key role by inhibiting the PI3K/Akt/mTOR signaling pathway.

Association between the expression of nuclear factor κB (NF-κB) and the drug resistance of hepatoma cells was investigated. HepG-2 cells and HepG2/ADM cells were cultured, respectively. The morphology and status of the two groups of cells were observed by cell white light. The immunofluorescence by NF-κB and MDR1 staining on HepG-2 cells and HepG2/ADM cells, respectively, was applied and the fluorescence expression in the two groups of cells was observed. RT-qPCR was used to detect the expression of NF-κB and MDR1 mRNA, the NF-κB and MDR1 protein expression was detected by western blot analysis. The results of cell white illumination showed that the structure of HepG-2 and HepG2/ADM cells was complete and the cell morphology was normal, and there was no significant difference, and could be used for comparative study. Immunofluorescence staining showed that the expression of NF-κB and MDR1 in HepG-2 cells was very low, while the expression of NF-κB and MDR1 in HepG2/ADM cells was increased significantly. The RT-qPCR results showed that NF-κB and MDR1 mRNA expression in HepG-2 cells was very low, while NF-κB and MDR1 mRNA expression in HepG-2/ADM cells was significantly increased, and western blot results showed that NF-κB and MDR1 protein expression in HepG-2 cells was very low, while NF-κB and MDR1 protein expression in HepG-2/ADM cells was increased significantly. The results of variance analysis showed that there was significant difference in the expression of the control group and paeonol group (P<0.01). In conclusion, the expression of NF-κB in the drug-resistant cells of liver cancer is closely related to the resistance-related gene MDR1. This result may provide a new solution for the drug resistance of liver cancer.

Objective To explore characteristics of serum HBV genotype of HBsAg positive patients with primary hepatocellular carcinoma (PHC). Methods Total of 97 cases of HBsAg positive patients with PHC were detected by HBV genotype. Results In 97 cases, there are 38 cases (39.1%) with genotype B and 54 cases (55.7%) with genotype C. There are 33 HBeAg positive cases (35.9%) in 92 cases of HBV genotype B and C. Conclusions HBV genotype C is mainly in HBsAg positive patients with primary hepatocellular carcinoma and most of them are HBeAg negative and have history of chronic hepatitis B.

慢性丙型肝炎(CHC)患者经规范抗病毒治疗后约40％的患者可出现持久的丙型肝炎病毒清除.近年研究发现宿主IL-28B基因多态性与抗丙型肝炎病毒治疗的效果相关.现就IL-28B基因多态性在慢性丙型肝炎抗病毒治疗中的价值做简要综述.

Objective The aim of this study was to assess the association between HBVDNA in serum and PBMCs in chronic hepatitis B patients treated with Ente- cavir.Methods 73 cases of chronic hepatitis B patients were randomly divided into treatment group( 38 cases) and control group( 35 cases) ,treatment group received entecavir 0.5 mg/day treatment 48 weeks.HBVDNA in serum and PBMCs were assessed at baseline,during treatment( weeks 4,12,24and 48) .Results Serum HBVD-NA negative rates were respectively 31.57% ,81.58% ,94.74% and 97.37% at weeks 4,12,24 and 48 after treatment,HBVDNA in PBMCs negative rates were 10. 52% 、42.12% 、57.89% 、76.32% in treatment group,respectively.The difference between HBVDNA negative rate in serum and PBMCs in treatment group and control group was significant( P 0.005) .Conclusion HBVDNA in serum and PBMCs was significantly inhibited in chronic hepatitis B patients treated with Entecavir,but HB-VDNA in PBMCs negative rate was lower than Serum HBVDNA negative rate.

目的:研究恩替卡韦治疗HBeAg阳性慢性乙型肝炎期间PBMC中HBV DNA水平与HBeAg血清转换率的相关性.方法:77例HBeAg阳性慢性乙型肝炎患者,随机分为对照组(40例)和治疗组(37例),治疗组给予恩替卡韦0.5 mg/d治疗＞48周,于治疗的0、4、12、24、48周时分别测定乙型肝炎病毒血清标志物、血清及PBMC中HBV DNA水平.结果:治疗48周时治疗组血清及PBMC中HBV DNA阴转率均显著高于对照组,治疗组初始治疗前患者PBMC中HBV DNA阳性率为78.4％,随治疗疗程的延长血清及PBMC中HBV DNA阳性率降低.治疗组初始治疗时PBMC中HBV DNA阴性的患者治疗48周时E抗原血清转换率高于初始治疗时PBMC中HBV DNA阳性的患者(P＜0.05).结论:恩替卡韦对血清及PBMC中HBV DNA均有明显的抑制作用；PBMC中HBV DNA阴转对预测HBeAg血清转换有一定价值.

重度黄疸肝炎多见于淤胆型肝炎、慢性重度肝炎、重型肝炎,病程进展快,预后差,治疗困难.我们在联用思美泰、凯时治疗重度黄疸型肝炎的过程中取得了较满意的疗效,现报告如下:

随着药学技术的日新月异,药物研究已进入制剂创新时代,新型的给药系统,如缓释和控释制剂等越来越备受人们的青睐,其巨大的市场潜力,广阔的发展前景,推动着我国医药产业的迅猛发展.

我院1996～2002年6月共收治流行性出血热(EHF)162例,其中32例后证实为其他疾病,32例中有6例为白血病,占病例总数3.73%,现报告如下.

目的以清热解毒、健脾化湿的纯天然中草药制剂乙肝散,治疗慢乙肝36例观察效果.方法通过治疗前后临床症状、体征及肝功能恢复比较,及乙肝病毒标志物为指标.结果HBeAg转阴率为52.9%.HBV-DNA阴转率47.62%.结论证实乙肝散对改善症状,及肝功能恢复有明显的效果.表明乙肝散具有抑制乙肝病毒复制的作用.

肾综合征出血热(HFRS)合并高血糖的报道较多,而少有合并低血糖的报道.1996～1997年,我们收治14例HFRS合并顽固性低血糖患者,现报告并分析如下.