BACKGROUND： Everolimus has no nephrotoxicity and is used to treat patients with post-liver transplant chronic renal insufficiency. The present systematic review was to evaluate the efficacy and safety of everolimus in de novo liver transplant patients.DATA SOURCES： Randomized controlled trials comparing everolimus for de novo liver transplant in Pub Med, the Cochrane Library, and Science Direct published up to March 31, 2014 were searched by two independent reviewers. Mean differences and 95% confidence interval（95% CI） for renal function, relative risk（RR） and 95% CI for treated biopsy-proven acute rejection（t BPAR）, graft loss, death, neoplasms/tumor recurrence, and adverse events were collected. Meta-analyses were performed with Rev Man version 5.10.RESULTS： A total of four randomized controlled trials covering 1119 cases were included. The meta-analyses revealed that compared with standard exposure of calcineurin inhibitors（CNIs）, everolimus combined with reduced CNIs improved creatinine clearance（calculated with the Cockcroft-Gault formula） by 5.13 m L/min at one year（95% CI： 0.42-9.84; P=0.03）, and decreased t BPAR（RR： 0.56; 95% CI： 0.35-0.90; P=0.02）. Everolimus initiation with CNIs elimination improved glomerular filtration rate（GFR, measured with the modification of diet in renal disease formula） of 10.42 m L/min/1.73 m2（95% CI： 3.44-17.41; P〈0.01） one year after treatment, but in-creased t BPAR（RR： 1.71; 95% CI： 1.15-2.53; P〈0.01）. Everolimus decreased the risk of neoplasms/tumor recurrence after liver transplant（RR： 0.60; 95% CI： 0.34-1.03; P=0.06）, but was associated with greater risk of adverse events which resulted in drug discontinuation（RR： 1.98; 95% CI： 1.49-2.64; P〈0.01）. CONCLUSIONS： Early introduction of everolimus combined with low-dose or no CNI in de novo liver transplant significantly improves renal function one year post treatment. Everolimus combined with low-dose CNI decreases the risk of t BPAR one year a
目的：设计人工锌指蛋白（zinc finger protein，ZFP）特异性结合于乙型肝炎病毒x蛋白（hepatitis B virus X protein，HBX）基因启动子，观察zFP在体外对乙型肝炎病毒（hepatitis B virus，HBV）转录的抑制。方法：将pcDNA3．1-ZFP转染入HepG2．2．15细胞24h后，用Western blot检测HBX蛋白的含量：用ELISA和real—time PCR检测上清液中乙型肝炎核心相关抗原（hepatitis B eantigen，HBeAg）和HBV DNA含量，用RT—PCR检测胞内HBV mRNA水平。结果：ZFP可抑制HepG2．2．15细胞中HBX的表达；相比空质粒组，ZFP组细胞培养上清液中HBV DNA拷贝量和HBeAg含量分别下降了51．7％（t=23．079，P=0．000，95％CI=44．98％-58．52％）、33．8％（t=3．887，P=-0．003，95％CI=12．12％～55．48％）；细胞内HBVmRNA也明显减少（t=3．616，P=0．022）。结论：人工设计的可特异性结合于HBX的ZFP可于HepG2．2．15细胞中有效抑制HBV转录。
