Objective To investigate the expression of interleukin-6(IL-6),high mobility group protein B1 (HMGB1)and Survivin in patients with gastrointestinal stromal tumors (GISTs)and the relationship between them.Methods 43 patients with GISTs and 30 healthy controls from Jan.2009 to Dec.2012 in Nanchong Central Hospital was enrolled.Expressions of IL-6,HMGB1 and Survivin in serum were assessed with enzyme linked immunosorbent assay(ELISA) and the correlation among IL-6,HMGB1 and Survivin was analyzed.Results The serum levels of IL-6,HMGB1 and Survivin in patients with GISTs((0.61 ±0.05)ng/ml,(3.54 ±0.74) ng/ml,(0.15 ± 0.04)ng/ml,respectively)were higher those that in the healthy controls((0.32 ± 0.03)ng/ml,(1.81 ± 0.06)ng/ml,(0.07 ±0.02)ng/ml,respectively).Among the 43 GISTs,the expressions of IL-6,HMGB1 and Survivin in benign,potentially malignant and malignant group increased gradually.The expressions of IL-6 in each group were (0.55 ± 0.02) ng/ml,(0.59 ± 0.02) ng/ml,(0.64 ± 0.03) ng/ml,respectively,The expressions of HMGB1 in each group were (2.82 ± 0.55) ng/ml,(3.46 ± 0.16) ng/ml,(4.00 ± 0.61) ng/ml,respectively.The expressions of Survivin in each group were (0.10 ± 0.01) ng/ml,(0.15 ± 0.02) ng/ml,(0.18 ± 0.03) ng/ml,respectively.Expressions of IL-6 and HMGB1,IL-6 and Survivin,and HMGB1 and Survivin were positively correlated(r =0.699,P ＜0.05;r =0.774,P ＜0.05;r =0.595,P ＜0.05,respectively).Conclusion The high expression of IL-6,HMGB1 and Survivin may together contribute to the malignancy,invasion and metastasis of GIST.Detection of these three markers may be useful in judging the malignancy degree and predicting the prognosis of GIST.

This study probed into North Sichuan Medical College to explore the problems existing in the cultivation of medical undergraduate, such as the low innovative and practical abilities, lack of pro-fessional knowledge and low level of literacy. Then the study analyzed the causes of the problem from the aspects of students, teachers, external factors and school environment. Basing on the analysis, the study put forward some talent quality promotion measures, such as improving the quality of enrollment, promoting the faculty building, exploration of scientific management of teaching expenditures, strengthening the construc-tion of discipline and curriculum, constructing teaching quality guarantee system and enhancing students' innovative and operative abilities.

Objective To study the effect of CDCA5 silencing on the growth of human breast cancer cell line MDA-MB-435s in vitro and its mechanism.Methods The expression of CDCA5 in breast cancer tissue,the adjacent normal tissue and human breast cancer cell lines MCF-7,MDA-MB-231 and MDA-MB-435s was tested by Western blot.The target sequences of CDCA5 small interfering RNA (siRNA),control siRNA (siRNA-NC) and blank groups were designed.PCR was used to observe the gene silencing effect on CDCA5.The cell viability was measured by MTT assay in siRNA,siRNA-NC and Blank groups.Cell cycle was determined by flow cytometry.Plkl,SA2 and pSA2 protein expression was tested by Western blot.Rssults The expression of CDCA5 was higher in breast cancer tissue than in the adjacent normal tissue.The expression of CDCA5 was higher in human breast cancer cell line MDA-MB-435s than in MCF-7 or MDA-MB-231 cell line.The expression level of CDCA5 was downregulated significantly in siRNA group than other groups.The cell viability was decreased and the cell percentage of G2/M phase was elevated in siRNA group compared with those in siRNA-NC and Blank groups.Inhibition of the CDCA5 gene can suppress the expression of Plk1 and pSA2.Conclusion Silencing CDCA5 expression can effectively inhibit the proliferation of breast cancer cells,whose mechanism may lie in arresting cell cycle in G2/M phase by suppressing CDCA5/Plkl/SA2 signaling pathway.

In recent years, with the continuous studies on tumor metabonomics, more and more results have shown that changes of metabolism play important roles in the occurrence and development of malignant tumor. Carcinogenic factors can destroy the metabolic balance of human body, induce metabolic reprogramming, and then mediate a variety of biological behaviors to partici-pate in the proliferation and invasion of cancer cells. Lipids provide the body with the necessary energy and essential fatty acids, and a variety of lipid molecules and metabolites are involved in cell signal transduction. Lipid metabolism is an important link in the metabolic system of the body, and the relationship between the occurrence and development of pancreatic cancer and lipid metabo-lism is not clear. The purpose of this paper is to reveal the changes of lipid metabolism in pancreatic cancer, summarize some preclinical studies and clinical trials, and deeply explain the research status of abnormal lipid metabolism associated with pancreatic cancer, so as to provide new ideas for the study of pancreatic cancer pathogenesis and accurate treatment.