A Comprehensive Study of the Association between LEPR Gene rs1137101 Variant and Risk of Digestive System Cancers.

Objective: The leptin receptor, encoded by the LEPR gene, is involved in tumorigenesis. A potential functional variant of LEPR, rs1137101 (Gln223Arg), has been extensively investigated for its contribution to the risk of digestive system (DS) cancers, but results remain conflicting rather than conclusive. Here, we performed a case-control study and subsequent meta-analysis to examine the association between rs1137101 and DS cancer risk. Methods: A total of 1,727 patients with cancer (gastric/liver/colorectal: 460/480/787) and 800 healthy controls were recruited. Genotyping of rs1137101 was conducted using a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay and confirmed using Sanger sequencing. Twenty-four eligible studies were included in the meta-analysis. Results: After Bonferroni correction, the case-control study revealed that rs1137101 was significantly associated with the risk of liver cancer in the Hubei Chinese population. The meta-analysis suggested that rs1137101 is significantly associated with the risk of overall DS, gastric, and liver cancer in the Chinese population. Conclusion: The LEPR rs1137101 variant may be a genetic biomarker for susceptibility to DS cancers (especially liver and gastric cancer) in the Chinese population.

[Studies on the propagation characteristics of duck plague virulent virus in duck embryo fibroblasts].

The propagation characteristics of virulent duck plague virus (DPV) in duck embryo fibroblast (DEF) were studied by the method of light microscopy observation of DEF cell culture monolayer, electron microscopy observation of infected DEF cell culture, real-time PCR detecting virus propagation. The results demonstrated that on duck embryo fibroblast a number of plaques were formed by DPV 42 h postinfection. Electron microscopy of the ultrathin section of infected duck embryo fibroblasts demonstrated that the nucleic acid of DPV was round in shape with diameter of 35-45 nm and was often in a cluster in the nucleus of DEF. The nucleocapsid of DPV was round in shape with diameter of 90-100 nm and could be observed both in nucleus and cytoplasm of DEF. The mature DPV which had the structures of envelop and tegument was spherical in shape with diameter of 150-300 nm and was located in cytoplasmic vacuoles. DPV penetrated the DEF cell membrane by direct fusion between the viral envelop and the plasma membrane. Progeny viral nucleic acid was produced in the nucleus and the assembled nucleocapsids obtained the structure of tegument in the cytoplasm and obtained the structure of envelop by budding into the cytoplasmic vesicles. The mature DPV particles were released out of the cell through exocytosis of the cytoplasmic vesicles. Detection of DPV by real-time PCR demonstrated that virus in DEF began its obvious propagation 10 h postinfection and virus amount tended to increase until 30 h postinfection. DPV began to be released into the supernatant 22 h postinfection and the DPV amount peaked 50 h postinfection, when the virus content in DEF and supernatant both underwent approximately 10(3) fold increase. DPV mainly existed in the DEF and the virus content in DEF was 10(2)-10(3) fold than the supernatant.