Objective Implement etimicin polymethylmethacrylat (PMMA) bone cement implantation treatment for the postoperative patients suitable with intramedullary infection after open fracture surgery,and observe the efficacy,provide new ideas for clinical treatment.Methods Selected 60 patients in Second People's Hospital of Kunshan from Jan.2009 to Dec.2016 whose infection was confined to the fracture caused by trauma after the internal fixation.Thirty cases of etimicin bone cement implantation were treated group,30 cases of CEMEX GEN antibiotic bone cement (containing gentamicin) implantation were control group.The internal fixation was taken out of 9 cases of autogenous PMMA bone graft with bone cement cover in the treatment group,debrided and taken first phase of bone grafting internal fixation combined with etimicin PMMA bone cement,21 patients with direct bone cement filling underwent surgery to remove the internal fixation devices,debridement cavity filling etimicin bone cement.Six months later when the infection was controlled,the second phase of autogenous bone graft fixation was done.Ten cases of autogenous bone graft with bone cement cover in the control group,debrided and taken first phaes of bone grafting internal fixation combined with CEMEX GEN antibiotic bone cement (containing gentamicin).Twenty patients with direct bone cement filling underwent surgery to remove the internal fixation devices,debridement cavity filling CEMEX GEN antibiotic bone cement (containing gcntamicin).Six months later when the infection was controlled,the second phase of autogenous bone graft fixation was done.SPSS 19.0 software was used for statistical analysis.The t test was used for measurement data,and the counting data were checked by chi-square.Results The pathogens were mainly staphylococcus aureus and coagulase-negative staphylococci.Thirty-seven strains of pathogenic bacteria were detected with MIC ≤ 2 mg/L in the treatment group,which was in the safe and effective drug concentration range of etimicin(MIC ≤ 12 mg/L).Thirty strains of pathogenic bacteria were detected with MIC ≤ 8 mg/L in the control group,which was in the safe and effective drug concentration range of gentamicin(MIC ≤ 12 mg/L).The average follow-up period of the treatment group was 11.2 months (range 8 to 24 months),29 cases were controlled.The average follow-up period of the control group was 15.6 months (range 6-35 months),24 cases were controlled.The difference of infection control rate between treatment group and control group was statistically significant (x2 =4.043,P =0.044).Conclusion The complete debridement,a lot of washing,and etimicin bone cement implantation can effectively control the infection after the internal fixation of fracture and reduce the recurrence,which can be used in clinical practice.

Objective To evaluate the expression of mitochondrial fission factor (MFF) and its biological effects in the progression of hepatocellular carcinoma (HCC).Methods ①Quantitative real-time PCR (qPCR),Western blotting and immunohistochemistry analysis were used to detect the expression levels of MFF in HCC tumor tissues and cell lines.②The effect of MFF knockdown on proliferation of HCC cells was analyzed by methyl thiazolyl tetrazolium (MrTT) and colony formation assays in siCtrl,si-MFF#1,si-MFF#2 groups.③The effect of MFF knockdown on apoptosis of HCC cells was analyzed by apoptosis assay with Annexin Ⅴ-FITC and PI.Results ①The MFF expression was higher in tumor tissues compared with tumor-adjacent normal tissues [mRNA level M(QR):0.292 (0.443) vs.0.235(0.333),Z=-4.166,P＜0.001;protein level M(QR):5.414 (4.545) vs.3.120 (3.955),Z =-3.961,P ＜ 0.001)].The MFF expression was higher in HCC cell lines compared with normal liver cell line.②RNA interference-mediated knockdown of MFF inhibited proliferation of HCC cells (siCtrl vs.si-MFF#1:5.29 ± 0.34 vs.3.34 ± 0.37,P =0.014;siCtrl vs.si-MFF#2:5.29 ± 0.34 vs.3.09 ± 0.40,P =0.010).RNA interference-mediated knockdown of MFF inhibited colony formation of HCC cells (siCtrl vs.si-MFF#1:95.35 ± 21.20 vs.37.56 ± 10.61,P =0.003;siCtrl vs.si-MFF#2:95.35 ± 21.20 vs.41.23 ± 10.82,P =0.004).③RNA interference-mediated knockdown of MFF induced apoptosis of HCC cells (siCtrl vs.si-MFF#1:9.56％ ± 1.70％ vs.20.08％ ± 2.03％,P ＜ 0.001;siCtrl vs.si-MFF#2:9.56％ ± 1.70％ vs.21.14％ ± 1.38％,P ＜ 0.001).Conclusion MFF is overexpressed in HCC,which accelerates cell proliferation and suppresses apoptosis,indicating that MFF can serve as a potential oncogene and drug target in HCC treatment.

Objective: To explore the function and molecular mechanism of Timeless in promoting hepatocellular carcinoma (HCC) growth. Methods: The expression of Timeless in HCC and paracancer tissues were analyzed by using the public data of HCC. Timeless was overexpressed in MHCC97L cells and silenced in MHCC97H cells, respectively, and the expression of Timeless and its downstream molecules were detected by real-time PCR and western blot. The effects of Timeless on cell glycolysis, oxidative phosphorylation and proliferation were detected by the glucose uptake experiment, lactic acid detection experiment, the extracellular fluid pH detection experiment, cell oxygen consumption test and cell viability assay, respectively. Results: The level of Timeless in HCC tissue was significantly higher than that of paracancer tissue (P<0.05). The relative cellular glucose uptake levels in the groups of Timeless knockdown, including siTimeless-1 and siTimeless-2 group were 0.510±0.119 and 0.508±0.099, respectively, significantly different from that of control group (P<0.05); The relative cellular uptake level of Timeless overexpressed group was 1.953±0.324, significantly different from that of vector transfected group (P<0.05). The relative levels of lactic acid production in the siTimeless-1 and siTimeless-2 group were 0.579±0.096 and 0.550±0.120, respectively, significantly different from that of control group (P<0.05); The relative production level of lactic acid in the Timeless overexpressed group was 1.463±0.179, significantly different that of vector transfected group (P<0.05). The extracellular pH values of siTimeless-1 and siTimeless-2 group were 7.390±0.035 and 7.370±0.060, respectively, significantly different from that of control group (P<0.05); the extracellular pH value of Timeless overexpressed group was 7.130±0.031, significantly different than vector transfected group (P<0.05). Oxygen consumption rate of siTimeless-1 and siTimeless-2 group were 3.686±0.389 and 3.955±0.431, respectively, significantly higher than 1.690±0.297 of control group (P<0.05); Oxygen consumption rate of Timeless overexpressed group was 1.302±0.336, significantly lower than 3.185±0.262 of vector transfected group (P<0.05) Timeless inhibited the expression of p53. The cell glucose uptake, lactic acid production, the pH of extracellular culture medium and cell oxygen consumption of control group were not significantly different from that of Timeless and p53 co-silenced group [(si-Timeless+sip53) group] (P>0.05); the glucose uptake, the production of lactic acid, the pH of the extracellular culture medium and the oxygen consumption of Timeless co-transfected with p53 (Timeless+p53) group were not significantly different from those of vector transfected group (P>0.05). Timeless promoted the proliferation of HCC cells through inhibiting the expression of p53. Conclusion Timeless promotes reprogramming of glucose metabolism and proliferation of HCC cells by inhibiting the p53-dependent signaling pathway.

Objective: To investigate the methods for qualitative pathological assessment of dynamic changes in liver fibrosis/cirrhosis after antiviral therapy in patients with chronic hepatitis B (CHB), since antiviral therapy can partially reverse liver fibrosis and cirrhosis caused by hepatitis B and semi-quantitative, rather than qualitative, pathological assessment is often used for the research on liver fibrosis regression. Methods: Previously untreated CHB patients with liver fibrosis and cirrhosis were enrolled, and liver biopsy was performed before treatment and at 78 weeks after the antiviral therapy based on entecavir. The follow-up assessment was performed once every half a year. Based on the proportion of different types of fibrous septum, we put forward the new qualitative criteria called P-I-R classification (predominantly progressive, predominantly regressive, and indeterminate) for evaluating dynamic changes in liver fibrosis. This classification or Ishak fibrosis stage was used to evaluate the change in liver fibrosis after treatment and Ishak liver inflammation score was used to evaluate the change in liver inflammation after treatment. Results: A total of 112 CHB patients who underwent liver biopsy before and after treatment were enrolled, and among these patients, 71 with an Ishak stage of ≥3 and qualified results of live biopsy were included in the final analysis. Based on the P-I-R classification, 58% (41/71) were classified as predominantly progressive, 29% (21/71) were classified as indeterminate, and 13% (9/71) were classified as predominantly regressive; there were no significant differences between the three groups in alanine aminotransferase, aspartate aminotransferase, albumin, HBeAg positive rate, HBV DNA, and liver stiffness (P < 0.05). After treatment, the proportion of predominantly progressive, indeterminate, or predominantly regressive patients changed to 11% (8/71), 11% (8/71), and 78% (55/71), respectively. Among the 35 patients who had no change in Ishak stage after treatment, 72% (25/35) were classified as predominantly regressive and had certain reductions in the Laennec score, percentage of collagen area, and liver stiffness. Conclusion This new P-I-R classification can be used to assess the dynamic changes in liver fibrosis after antiviral therapy in CHB patients.