This paper discusses several problems and improvement method of the WCY-2002 field operation vehicle including the location of the dynamotor,the pothook balance weight of the winch's wire rope,hanging jack's fixture in the operation vehicle's back,the steel-framed structures of the surgery's tent,the power matching of the sterilization trailer and so on.The improvement methods are feasible and have been verified in practical training.

Objective To analyze the clinical and pathological characteristics of 35 hepatocellular carcinoma (HCC) patients with bile duct tumor thrombi (BDTT),and to investigate the expressions of CD133,CD90,EpCAM,CK19,VEGF,and C-kit in the tumor tissues.Methods 35 HCC patients with BDTT out of 943 HCC patients who underwent surgical treatment were studied.The expressions of biomarkers in tissue specimens were determined by immunohistochemistry.35 HCC patients without BDTT were selected using the method of stratified sampling as a control group.Results In 19 of 35 patients,the diameters of the primary tumor were less than 5 cm (range 0 ～ 17 cm,average 6.9 ± 0.7 cm).When compared to the control group,most of the primary tumors were moderately to lowly differentiated (33/35,94％ vs 18/ 35,51％),had incomplete capsules (18/35,51％ vs 3/35,8％) and micro vascular invasion (29/35,83％ vs 7/35,20％).The positive expression rates of CD90,EpCAM,CK19,VEGF,CD133,and C-kit in the group of patients with HCC with BDTT and in the control group were 82.9％,77.1％,71.4％,85.7％,80.0％,80.0％ and 57.1％,54.3％,34.3％,65.7％,54.3％,51.4％,respectively.The 1-,2-,3-year postoperative survival rates of the HCC patients with BDTT were 69％,37％,20％ respectively which were worse than the HCC patients without BDTT (1-,2-,3-year postoperative survival rates were 88％,72％,62％ respectively,P ＜ 0.05).Conclusions The prognosis of HCC patients with BDTT was worse than HCC patients without BDTT.The expressions of liver stem cell biomarkers in the tumor specimens of the group of HCC patients with BDTT were higher than the control group.These findings prompt that this kind of HCC originate from liver stem ceils.

OBJECTIVE: High-fat diet is one of the main risk factors that disrupt the balance of gut microbiota, which eventually will induce colorectal cancer (CRC). Evodiamine (EVO) is a wildly used multifunctional traditional Chinese medicine extract. In this study, we investigated the role of gut microbiota in high-fat diet-propelled CRC and the potential of EVO for CRC chemoprevention. METHODS: Gut microbiota, serum d-lactic acid and endotoxin from 38 patients with colon cancer and 18 healthy subjects were detected by quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay (ELISA). In addition, body mass index, phospho-signal transducer and activator of transcription 3 (p-STAT3) expression in cancer tissues and paracancerous tissues were detected by immunohistochemistry. A mouse intestinal inflammatory tumor model was established by azomethane/sodium dextran sulfate, followed by treatment with EVO and 5-aminosalicylic acid (ASA). Gut microbiota and inflammatory factors were detected by quantitative polymerase chain reaction, while serum d-lactic acid and endotoxin were detected by ELISA. Furthermore, cell proliferation, cell apoptosis, and interleukin (IL)-6/STAT3/P65 pathway were evaluated by 5-ethynyl-2'-deoxyuridine, terminal-deoxynucleotidyl transferase-mediated nick-end labeling, and Western blot assays. RESULTS: In patients with colon cancer, the numbers of Enterococcus faecalis and Escherichia coli were increased, while those of Bifidobacterium, Campylobacter and Lactobacillus were decreased. Serum endotoxin and d-lactic acid levels and p-STAT3 levels were significantly increased. In the mouse model, both EVO and ASA inhibited tumor formation, decreased the proliferation of tumor cells, and induced apoptosis of tumor cells. Compared with the control group, the numbers of E. faecalis and E. coli were decreased, while Bifidobacterium, Campylobacter and Lactobacillus numbers were increased. In the EVO group, serum endotoxin and d-lactic acid levels and inflammatory factors were significantly decreased. Further, the IL6/STAT3/P65 signaling pathway was inhibited in the EVO group. CONCLUSION EVO may inhibit the occurrence of colon cancer by regulating gut microbiota and inhibiting intestinal inflammation. The potential mechanism involves inhibition of the IL6/STAT3/P65 signaling pathway, revealing its potential therapeutic significance in clinical applications.