Objective To investigate the clinical features of patients with recurrent epithelial ovarian cancer (EOC),and explore the factors that can prolong the disease-free interval(DFI) after primary treatment.Methods We retrospectively reviewed the medical records of 54 patients with recurrent EOC and analyzed the clinical stage,histological subtypes,primary treatments,DFI,recurrent site,secondary treatment,and the response after secondary treatment.By Mann-Whitney test and T test,factors influent the DFI were analyzed,the relationship between DFI and the response after secondary treatment were analyzed also.Results The mean DFI for all 54 patients was 19.07 months.The DFI of patients received optimal cytoreductive surgery was longer than those received non-optimal cytoreductive surgery [(32 ± 19.10) months vs (18.77 ± 7.80) months,P ＜ 0.01];The DFI of patients with serous,mucous and clear cell tumor was [(20.16 ± 14.63) months,(14.00 ± 4.73) months and (16.67 ± 13.03) months,respectively],suggesting patients with mucous tumor might have shorter DFI.The DFI of patients with low tumor grade was longer than those with high tumor grade [(28.18 ± 16.97) months vs (16.52 ±9.46) months,respectively];The DFI of patients with stage Ⅰ and Ⅱ disease was [(19.60 ± 12.89)months],was compared to the DFI of patients with stage Ⅲ,stage Ⅳ disease,which was [(19.22 ± 12.38) months] and [(11.67 ±5.39) months],respectively.When disease recurred,the most frequent recurrent site was pelvic (50％,n =27),with upper abdominal (29.6％) and lymph node(29.6％) followed.When recurrence was found in lymph node,the most frequent site was pelvic and para-arotic lymph node.In our study,when disease recurred,response of the tumor after the secondary treatment has no relationship with the DFI.Conclusions Patients received optimal cytoreductive surgery,patients with low tumor grade and early stage have longer DFI.Retroperitoneal lymphadenectomy might be chosen during the primary cytoreductive surgery in some selected patients.

Viral infection is the main death cause of infectious diseases in China. The establishment of an animal model to mimic the progression of viral infectious diseases in humans is of great significance to the study of pathogenesis and prevention of viral infectious diseases. As a new animal model established and developed in recent years, tree shrew has showed obvious advantages and potentials compared with other non-human primates and mice which are commonly used as virus-infected animal models. In this paper, the biological advantages of tree shrew as a novel animal model of viral infectious diseases are summarized, including taxonomy, physiology and immunology. In addition, the latest application of tree shrew in the research of many viral infectious diseases such as hepatitis virus, herpes simplex virus, influenza virus and enterovirus infections are compared and summarized.

Currently, there is still no effective curative treatment for the development of late-stage liver fibrosis. Here, we have illustrated that TB001, a dual glucagon-like peptide-1 receptor/glucagon receptor (GLP-1R/GCGR) agonist with higher affinity towards GCGR, could retard the progression of liver fibrosis in various rodent models, with remarkable potency, selectivity, extended half-life and low toxicity. Four types of liver fibrosis animal models which were induced by CCl₄, α-naphthyl-isothiocyanate (ANIT), bile duct ligation (BDL) and Schistosoma japonicum were used in our study. We found that TB001 treatment dose-dependently significantly attenuated liver injury and collagen accumulation in these animal models. In addition to decreased levels of extracellular matrix (ECM) accumulation during hepatic injury, activation of hepatic stellate cells was also inhibited via suppression of TGF-β expression as well as downstream Smad signaling pathways particularly in CCl₄-and S. japonicum-induced liver fibrosis. Moreover, TB001 attenuated liver fibrosis through blocking downstream activation of pro-inflammatory nuclear factor kappa B/NF-kappa-B inhibitor alpha (NFκB/IKBα) pathways as well as c-Jun N-terminal kinase (JNK)-dependent induction of hepatocyte apoptosis. Furthermore, GLP-1R and/or GCGR knock-down results represented GCGR played an important role in ameliorating CCl₄-induced hepatic fibrosis. Therefore, TB001 can be used as a promising therapeutic candidate for the treatment of multiple causes of hepatic fibrosis demonstrated by our extensive pre-clinical evaluation of TB001.