Objective To investigate the expression of RECK and MMP-9 in pancreatic cancer and to explore the relationship between RECK, MMP-9 expression and the clinicopathological characteristics.Methods PV6000 immunohistochemical method was used to detect the expression of RECK and MMP-9 in 28 cases of pancreatic cancer and 10 cases of normal pancreatic tissue. All the statistical analyses were performed by using SPSS 13.0 statistical software to determine the relationship between RECK, MMP-9 expression and the clinicopathological characteristics. Results The overall positive rate of RECK espression was 46.43% (13/28)in pancreatic cancer, which was significantly lower than that in normal pancreatic tissue (90%, 9/10). The positive rate of RECK espression in Ⅰ + Ⅱ clinical stage (75.0% ,9/12) was significantly higher than that in Ⅲ + Ⅳ stage (25.0%, 4/16 P < 0.05 ). The positive rate of RECK expression in cases without distant metastases (60.0%, 12/60) was significantly higher than that in cases with distant metastasis (12.5%, 1/8,P<0.05). The overall positive rate of MMP-9 was 75% (21/28) in pancreatic cancer, and 20% (2/10) in normal pancreatic tissue. The comparison between these two groups indicated a significant difference (P <0.01 ). The positive rate of MMP-9 in Ⅰ + Ⅱ clinical stage(50.0% ,6/12) was significantly lower than that in Ⅲ + Ⅳ stage (93.8,15/16, P < 0.05). The positive rate of MMP-9 in well differentiation group(33.3%,1/3 ) was significantly lower than that in poor differentiation group ( 100%, 12/12 ,P < 0. 01 ). The expressionof RECK was negatively correlated with the expression of MMP-9 ( r = - 0. 536, P < 0.01 ). Conclusions RECK is lowly expressed in pancreatic cancer, but MMP-9 is highly expressed. RECK and MMP-9 may serve as important markers in the evaluation of tumor stage.

This study aims to investigate the effects of fibroblast growth factor 21 (FGF-21) on learning and memory abilities and antioxidant capacity of D-galactose-induced aging mice. Kunming mice (37.1 +/- 0.62) g were randomly divided into normal control group, model group and FGF-21 high, medium and low dose groups (n = 8). Each group was injected in cervical part subcutaneously with D-galactose 180 mg x kg(-1) x d(-1) once a day for 8 weeks. At the same time, FGF-21-treated mice were administered with FGF-21 by giving subcutaneous injection in cervical part at the daily doses of 5, 2 and 1 mg x kg(-1) x d(-1). The normal control group was given with normal saline by subcutaneous injection in cervical part. At seventh week of the experiment, the learning and memory abilities of mice were determined by water maze and jumping stand tests. At the end of the experiment, the mice were sacrificed and the cells damage of hippocampus was observed by HE staining in each group. Reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and total antioxidant capacity (T-AOC) in the brain of mice were determined. The results showed that different doses of FGF-21 could reduce the time reaching the end (P < 0.01 or P < 0.05) and the number of touching blind side (P < 0.01 or P < 0.05) in the water maze comparing with the model group. It could also prolong the latency time (P < 0.05) and decrease the number of errors (P < 0.01 or P < 0.05) in the step down test. The result of HE staining showed that FGF-21 could significantly reduce brain cell damage in the hippocampus. The ROS and MDA levels of three different doses FGF-21 treatment group reduced significantly than that of the model group [(5.58 +/- 1.07), (7.78 +/- 1.92), (9.03 +/- 1.77) vs (12.75 +/- 2.02) pmol (DCF) x min(-1) x mg(-1), P < 0.01 or P < 0.05], [(2.92 +/- 0.71), (4.21 +/- 0.81), (4.41 +/- 0.97) vs (5.62 +/- 0.63) nmol x mg(-1) (protein), P < 0.01]. Comparing with the model group, the activities of SOD, GPx, CAT and T-AOC of the three different doses FGF-21 treatment groups were also improved in a dose-dependent manner. This study demonstrates that FGF-21 can ameliorate learning and memory abilities of D-galactose induced aging mice, improve the antioxidant abilities in brain tissue and delay brain aging. This finding provides a theoretical support for clinical application of FGF-21 as a novel therapeutics for preventing aging.

Objective To summarize and analyze the dynamic change of HBsAg levels in patients with chronic Hepatitis B (CHB) after receiving nucleos(t)ide analogues (NAs) as antiviral treatment.Methods Patients who were performed quantitative Hepatitis B surface antigen(qHBsAg) from July 30, 2012 to December 30,2016 in Peking Union Medical College Hospital were retrospectively enrolled.qHBsAg, HBV DNA, HBeAg were collected and analyzed at baseline and at 192-week follow-up every 24 weeks.qHBsAg and HBeAg were assessed with chemiluminesent microparticle immuno assay(CMIA).HBV DNA was assessed with PCR and COBAS Amplicor.Results 60 patients were included.Patients in HBeAg-positive group had higher HBV DNA than that in HBeAg-negative group (P<0.05)at baseline and the two groups both were under detection limit after 48 weeks.BaselineqHBsAg in HBeAg positive-group and negative-group were (3.43±0.73) log10 IU/mL, (3.08±0.47) log10 IU/mL respectively.qHBsAg in HBeAg-positive group was higher than that in HBeAg negative-group on all follow-ups(P<0.05) except 48weeks.However on 168 weeks and 192 weeks, difference between the two groups was statistically significant(P<0.05).In HBeAg-positive group,quantitative HBeAg dropped significantly during antiviral treatment.Conclusions HBV replication can be suppressed in the process of long-term NAs treatment in CHB patients.However qHBsAg decline is not so obvious, which indicates that HBsAg cleavence is difficult,and long-term NAs therapy is still necessary.