Epidemiological surveys have shown that the incidence of type 2 diabetes mellitus (T2DM) and malignancies is rapidly increasing worldwide and has become a major disease that threatens human life. In this study, we quantitatively analyzed the proteome of tumor tissues and adjacent normal tissues from six patients withT2DM combined with colorectal cancer (CRC) and eight non-diabetic CRC, focusing on the effect of T2DM on tumor tissues. We analyzed the functional enrichment of differentially expressed proteins (DEPs) using clusterProfiler in R and the expression level of protein tyrosine phosphatase non-receptor type 11 (PTPN11) and other key proteins in the TIMER and GEPIA2 databases. The HPA database was used to validate PTPN11 protein expression. The correlation between PTPN11 expression and clinicopathological features was analyzed by UALCAN database. The impact of PTPN11 on clinical prognosis was evaluated utilizing Kaplan-Meier Plotter. The correlation between PTPN11 expression and tumor-infiltrated immune cells was investigated via TIMER and TISIDB databases. Gene set enrichment analysis (GSEA) was performed to examined the pathway of PTPN11 enrichment in CRC using data from The Cancer Genome Atlas (TCGA) database. Furthermore, small interfering (si) RNA was used to knock down PTPN11 in CRC cell line SW480. Western blot analysis was used to detect PTPN11 expression in tissue samples or cells and the effect of PTPN11 knockdown on key proteins related to PI3K/AKT and cell cycle pathway in SW480 cells. Cell proliferation and wound healing assays were used to detect the effects of cell proliferation and migration after knockdown of PTPN11 or treatment with high glucose. We found that metabolic pathways such as oxidative phosphorylation, glycolysis/gluconeogenesis, and insulin secretion were significantly enriched in tumor tissues from diabetic patients compared to non-diabetic patients. In addition, PTPN11, a marker gene associated with T2DM and CRC, were mined in diabetic tumor tissues. PTPN11 showed high expression in diabetic tumor tissues compared to normal tissues. High PTPN11 expression predicted poor prognosis in CRC. PTPN11 expression was strongly associated with immune infiltrating cells in CRC. GSEA analysis revealed that PTPN11 was enriched in cancer-related pathways. Western blotting analysis indicated that PTPN11 knockdown reduced the protein levels of p-PI3K, p-AKT, CDK1 and CYCLIN D, without altering PI3K and AKT protein levels. Cell proliferation and wound healing data showed that PTPN11 and high glucose could increase the proliferation and migration ability. These findings showed that PTPN11 may be a potential key biomarker for CRC in patients with diabetes, which will provide new potential targets for future intervention of T2DM complicated with CRC.

Objective To study the sleep improvement function of DHA-PC. Methods The mice were randomly divided into control,vehicle,DHA + Lecithin( 60 + 200 mg / kg) and DHA-PC( 50,100,200 mg / kg) groups. Ten mice were enrolled in each group. The mice of control were administered with normal food,the vehicle group was orally given normal saline at the dosage of 0. 2 ml /10 g,while both DHA-PC and DHA + Lecithin were orally given corresponding drugs at the dosage of 0. 2 ml /10 g. All the groups were treated for 30 days except control group. The direct sleep-inducing test,the test of lengthening sleep time induced by pentobarbital sodium,the test of pentobarbital sodium subthreshold-hypnosis and the test of barbital sodium sleep latency were conducted to observe the inductive effect of DHA-PC. Results Neither the effect on mice body mass nor directly-induced sleep was observed. DHA-PC( 50,100,and 200 mg / kg) could prolong sleep time to( 56. 2 ± 13. 7),( 57. 9 ± 25. 4) and( 64. 1 ± 18. 4) min,respectively,compared to vehicle( 32. 9 ± 10. 8) min( P 0. 05). DHA + Lecithin could not prolong sleep time( 38. 6 ± 11. 7) min compared to( 32. 9 ± 10. 8) min of vehicle. There was significant difference compared with DHA-PC at the dosage of 200 mg / kg( 64. 1 ± 18. 4) min( P 0. 05). DHA-PC( 200 mg/kg) enhanced pentobarbital sodium subthreshold-hypnosis( 70%) compared to vehicle( 10%)( P 0. 05),so did DHA + Lecithin( 60%) compared to vehicle( 10%)( P 0. 05). Both DHA-PC( 200 mg / kg) [( 22. 9 ± 4. 1) min ]and DHA + Lecithin [( 19. 5 ± 2. 7) min ]could shorten sleep latency compared to vehicle( 31. 3 ± 6. 9) min( P 0. 01),and the sleep latency of DHA + Lecithin( 19. 5 ± 2. 7) min was shorter than that of DHA-PC( 50,100 mg / kg). Conclusion DHA-PC has some effect some sleep improvement in mice.

Objective To study the sleep improvement function of DHA +Lecithin.Methods By measur-ing the direct sleep time ,the sleep time that induced by pentobarbital sodium ,the sleep incidence rate of sudbissociative dose and the latency time that induced by barbital sodium ,it could observe the mice sleep improvement function .Results Each dose group had no significant difference on the mice weight and direct inducing sleep .DHA could shorten the la-tency time that induced by barbital sodium (P<0.05).DHA+Lecithin could increase the sleep incidence rate of sud-bissociative dose(P<0.05) and shorten the latency time that induced by barbital sodium (P<0.05).Conclusion DHA+Lecithin can improve the mice sleep time .

目的 观察硫辛酰维格列汀对2型糖尿病大鼠血糖的影响.方法 选用雄性Wistar大鼠,高脂高糖饲料喂养4周后小剂量注射链脲佐菌素建立2型糖尿病模型,随机将大鼠分为正常对照组、糖尿病模型组、胰岛素糖尿病组、硫辛酰维格列汀糖尿病组.分别测定给药后0、0.5、1、2、3、4、5、6、7、8、9、10、12、24h的血糖变化.结果 注射链脲佐菌素72h后造模大鼠血糖均明显高于注射前(P＜0.05)和正常对照组(P＜0.05).与正常对照组和糖尿病模型组相比,胰岛素糖尿病组在注射胰岛素后0.5～4h,血糖变化差异有统计学意义(P＜0.05);硫辛酰维格列汀糖尿病组在灌胃给药3～10h,血糖变化差异有统计学意义(P＜0.05).结论 硫辛酰维格列汀和胰岛素有不同程度的降血糖作用,相比胰岛素,硫辛酰维格列汀降糖作用更加持久.