Autophagy is an important physiological process in eukaryotic cells and is contributive to normal update of cellular components.When the body is in hunger state,autophagy can not only produce amino acid and ATP through degrading proteins to provide conditions for cell survival,but also remove the damaged organelles to maintain the normal functions of cells.The abnormal functions of autophagy are closely related to the formation and development of tumors,and the degree which is too high or too low both can inhibit tumors.It has been found that autophagy is regulated by many kinds of molecules,and the results are different.So in-depth studies on the mechanisms of these autophagy-related molecules will become a starting point for further understanding the autophagy and a sally port for treating tumors.

AimTo study the effects of aspirin (Asp) and verapamil(Ver)alone or in combination on mesenteric microcirculation of rats. MethodsAcute microcirculation disturbance(AMD) was produced by highmolecular weight dextran(Mr 480, 000) 360 mg· kg-1 iv. Arteriol and venul blood flow velocity and diameter (ABFV, VBFV, AD, VD) and blood flow state(BFS) were observed by intravital microcirculation method. Results Asp 2.5, 5 mg · kg-i, Ver 0.3, 0.6 mg · kg-1,Asp+ Ver(1 + 0.15), (2. 5+ 0. 3) mg· kg-1 iv significant increase ABFV by 11.1%, 31.3%, 18.7%,19.5%, 26.5%, 37.3%, VBFV by 12.5%, 5.7%, 2.5%, 3.7%, 30%, 34.7%,AD by 4.3%, 17.9%, 31.5%, 35%, 20%, 38.1% and VDby 2.2%,4.2%, 25%, 31.5%,5.8%,23.5%espectively, and got a raise in the number of capillaries and a marked improvement of BFS. Asp + Ver(1+0.15, 2.5+0.3) mg · kg-1 iv could reverse AMD. Conclusion Asp is superior to Ver in the increase of BFV, but Ver is superior to Asp in expansion of blood vessel. Asp in combination with Ver produces marked synergistic action and protection againist AMD.

BACKGROUND:Previous studies have suggested that the risks for coronary atherosclerotic plaque progression and in-stent restenosis are increased in patients with coronary heart disease combined with type 2 diabetes. OBJECTIVE:To explore the predictive factors for in-stent late loss and non-culprit coronary lesion progression in patients with type 2 diabetes mel itus. METHODS:A total of 399 stenting patients were enrol ed, including 179 diabetic patients and 220 non-diabetic patients. The clinical materials, angiography parameters and biochemical markers were col ected. The difference between the two groups was compared, and also we conducted subgroup analysis in the diabetic patients. Low-density lipoprotein cholesterol, hemoglobin A1c, fibrinogen and high-sensitivity C-reactive protein were detected at days 3, 120, 210 and 360 after stenting. RESULTS AND CONCLUSION:Compared with non-diabetic patients, the stent length (P=0.18) was longer and the stent diameter (P=0.002) was smal er in the diabetic patients. The minimal lumen diameters of post-procedure and fol ow-up angiography in the diabetic group were significantly decreased (P=0.001, P=0), and the diabetic patients also showed severe coronary artery stenosis instantly and within the fol ow-up after stenting (P=0.038, P=0.004). The fol ow-up angiography showed that the diabetic patients had more late loss and restenosis (P=0, P=0.097). Furthermore, in the subgroup analysis of diabetic patients, the levels of hemoglobin A1c, fibrinogen and high-sensitivity C-reactive protein were significantly increased in the patients with restenosis and non-culprit lesion progression. These findings indicate that diabetic patients appear to have the higher incidence of restenosis and non-culprit lesion progression. Moreover, hemoglobin A1c, fibrinogen and high-sensitivity C-reactive protein are effective predictors for in-stent late loss and non-culprit coronary lesion progression.