Objective? To investigate the mastery of antiplatelet drugs knowledge among coronary heart disease patients with percutaneous coronary intervention (PCI), and to analyze its influencing factors. Methods? From November 2017 to February 2018, we selected 75 PCI patients with routine reexamine of department of cardiology at a classⅢgrade A hospital in Shanghai as subjects by convenience sampling. All of the patients were investigated with the self-designed antiplatelet drugs knowledge questionnaire for coronary heart disease patients with PCI. Results? Among 75 PCI patients, the total score of antiplatelet drugs knowledge among PCI patients was (30.64±6.90) with 54.71% for the scoring rate. Single factor analysis showed that there were statistical differences in the scores of antiplatelet drugs knowledge among PCI patients with different operative time, marital status and monthly incomes (P＜ 0.05). Conclusions? Mastery of antiplatelet drugs knowledge questionnaire among coronary heart disease patients with PCI needs to be improved. Pay attention to the influences of operative time after PCI, marital status and monthly incomes on mastery of antiplatelet drugs knowledge. We should improve the mastery of antiplatelet drugs knowledge by constructing health education evaluation system, strengthening health education and perfecting follow-up system to guide patients to take medicine correctly and regularly, so as to reduce the death risk.

Objectives: To investigate the expression of phosphoserine aminotransferase 1 (PSAT1) in pancreatic cancer tissues, and its potential role in pancreatic cancer. Methods: The expression of PSAT1 in 98 human pancreatic cancer tissues, which were collected from the People＇s Hospital of Guizhou, between July 2013 to July 2017, and the corresponding adjacent normal tissues was analyzed by immunohistochemical staining. Additionally, the relationship between the expression of PSAT1 and the clinicopathological parame-ters, overall survival (OS), and disease-free survival (DFS) of patients with pancreatic cancer was evaluated. The human pancreatic can-cer cell lines, BxPC-3 and SW1990, were transfected with PSAT1-siRNA, to investigate the effect of PSAT1 knockdown on cell prolifera-tion, migration, and invasion. Additionally, we performed Western blot to assess the expression of PI3K/Akt/mTOR-related proteins in PSAT1-knockdown cells. Results: The percentages of PSAT1-positive cells in pancreatic cancer and adjacent non-tumor tissues were 69.4% (68/98) and 5.0% (5/98), respectively, indicating a significantly higher expression of PSAT1 in pancreatic cancer tissues com-pared to adjacent non-tumor tissues (P<0.05). The increased expression of PSAT1 in pancreatic cancer tissues correlated with lymph node metastasis and TNM stage. Kaplan-Meier analysis suggested that a high expression of PSAT1 correlated with a poor OS and DFS compared to a low expression of PSAT1 (P<0.05). Cox regression analysis showed that the expression of PSAT1 is an independent prog-nostic marker for OS and DFS in pancreatic cancer patients (P<0.05, all). Transient transfection of BxPC-3 and SW1990 cells with PSAT1-siRNA markedly reduced the cell proliferation, migration, and invasion abilities of these cells compared to transfection with NC-siRNA (P<0.05). Knockdown of PSAT1 in pancreatic cancer cells also inhibited the expression of p-Akt and p-mTOR (P<0.05). Conclusions: The expression of PSAT1 increases in human pancreatic cancer tissues and cell lines. Additionally, PSAT1 regulates cell proliferation and in-vasion through the PI3K/Akt/mTOR pathway.

Diet is an important environmental factor in the development of inflammatory bowel disease (IBD), and it also represents one of the most promising treatment approaches for IBD. Daily diets usually contain food additives, which are found in many processed foods and even dietary supplements. In recent years, the effects of food additives on human health and intestinal flora have been highly concerned. Here we mainly aim to review the research progress on the potential role of food additives in the pathogenesis of IBD based on bibliometrics.