Objective To explore whether 5 to -7-day of folic acid supplementation prior to pemetrexed therapy is needed. Methods We retrospectively evaluate the outcomes of non-small cell lung cancer patients received less than the advised folic acid premedication. Seventy patients with Ⅲ-Ⅳ NSCLC were randomly divided into two groups: patients who initiated vitamin supplementation on 7 days before the first dose of pemetrexed (group A) and patients who initiated vitamin supplementation on the day of the first dose of pemetrexed (group B). Results In group A and group B, CR 0 and 0, PR 10 and 8, the response rates of 28.6% and 22.9% were observed, respectively. There was no statistically significant differences between these two groups. No significant differences were observed in the incidence of hematologic and non-hematologic toxicities. Conclusions The initiation of pemetrexed-based chemotherapy does not need to accommodate a vitamin supplementation schedule.

Medical Higher Mathematics,an important fundamental course,is important to improve the students' ability of innovation.According to the characteristics of the students at medical school,and considering the content abstract and the problems difficult to learn and understand,a new teaching model which can focus on absorbing some contents of Pharmacokinetics into Medical Higher Mathematics is dis cussed.At the same time the article discusses how to combine the both courses in three aspects:professional features,the background of the student's knowledge,and teaching method.

The degree of satisfaction of the curriculum is related not only to the degree of the curriculum but also to the degree of the students' development. With the concept of teaching reform micro system engineering, using the SIMPP analysis of the degree of satisfaction of the curriculum, the relevant factors of the students are studied. The results show that, the learning state, learning objec-tives, and the education level of mother affect the students more easily on the curriculum satisfaction. Research shows, in the present curriculum condition, educators should guide the students to study hard, establish a clear and reasonable learning goal, give the students the introduction and analysis of the curriculum, can effectively improve the students on the curriculum satisfaction, enhance the enthusiasm of the study.

The influence extent of students from teachers is related to the teaching effect , which means whether it can successfully promote the study of students and reach the expected teach-ing goal during the teaching process. To have a good teaching effect, guided by the micro-system en-gineering of teaching reform, we used SIMPP to analyze the related factors of the influence of students extent from teachers during the teaching process in TCM colleges and universities. The result shows that the influence extent from teachers is related to not only teachers themselves but students and their self-condition and family backgrounds as well. Going further in researching these factors and the related behavior patterns of influence extent of students from teachers is helpful to making the teach-ing more effective and more targeted.

Objective To investigate the effects of metformin on the proliferation and apoptosis of human oral cancer cell line KB in vitro. Methods Human oral cancer cell line KB was exposed to different doses of metformin (0, 1.25, 2.5, 5, 10, and 20 mmol/L), and the changes in cell viability were detected using MTT assay. Colony formation of the cells was observed following an 8-day metformin exposure. The changes in mitochondrial membrane potential were measured by JC-1 assay, and PI staining was used to observe the cell apoptosis. Western blotting was employed to detect the changes in the protein expressions of GRP78 and activated caspase-3. Results Metformin exposure caused time-and dose-dependent suppression of KB cell proliferation, and exposure to 5 mmol/L metformin for 24, 48 and 72 h resulted in cell survival rates of 68.0%, 36.9%, and 14.5%, respectively. Metformin significantly inhibited KB cell colony formation. Exposure of the cells to increased concentrations of metformin gradually increased the apoptotic rate and decreased mitochondrial membrane potential. Metformin caused an initial up-regulation followed by a down-regulation of GRP78 expression in KB cells and increased the expression of activated caspase-3. Conclusion Metformin can inhibit the proliferation and induce apoptosis of KB cells, the mechanism of which may involve the activation of the mitochondrial apoptotic pathway and endoplasmic reticulum stress.

Objective To investigate the effects of metformin on the proliferation and apoptosis of human oral cancer cell line KB in vitro. Methods Human oral cancer cell line KB was exposed to different doses of metformin (0, 1.25, 2.5, 5, 10, and 20 mmol/L), and the changes in cell viability were detected using MTT assay. Colony formation of the cells was observed following an 8-day metformin exposure. The changes in mitochondrial membrane potential were measured by JC-1 assay, and PI staining was used to observe the cell apoptosis. Western blotting was employed to detect the changes in the protein expressions of GRP78 and activated caspase-3. Results Metformin exposure caused time-and dose-dependent suppression of KB cell proliferation, and exposure to 5 mmol/L metformin for 24, 48 and 72 h resulted in cell survival rates of 68.0%, 36.9%, and 14.5%, respectively. Metformin significantly inhibited KB cell colony formation. Exposure of the cells to increased concentrations of metformin gradually increased the apoptotic rate and decreased mitochondrial membrane potential. Metformin caused an initial up-regulation followed by a down-regulation of GRP78 expression in KB cells and increased the expression of activated caspase-3. Conclusion Metformin can inhibit the proliferation and induce apoptosis of KB cells, the mechanism of which may involve the activation of the mitochondrial apoptotic pathway and endoplasmic reticulum stress.

OBJECTIVETo investigate the effects of metformin on the proliferation and apoptosis of human oral cancer cell line KB in vitro.

METHODSHuman oral cancer cell line KB was exposed to different doses of metformin (0, 1.25, 2.5, 5, 10, and 20 mmol/L), and the changes in cell viability were detected using MTT assay. Colony formation of the cells was observed following an 8-day metformin exposure. The changes in mitochondrial membrane potential were measured by JC-1 assay, and PI staining was used to observe the cell apoptosis. Western blotting was employed to detect the changes in the protein expressions of GRP78 and activated caspase-3.

RESULTSMetformin exposure caused time- and dose-dependent suppression of KB cell proliferation, and exposure to 5 mmol/L metformin for 24, 48 and 72 h resulted in cell survival rates of 68.0%, 36.9%, and 14.5%, respectively. Metformin significantly inhibited KB cell colony formation. Exposure of the cells to increased concentrations of metformin gradually increased the apoptotic rate and decreased mitochondrial membrane potential. Metformin caused an initial up-regulation followed by a down-regulation of GRP78 expression in KB cells and increased the expression of activated caspase-3.

CONCLUSIONMetformin can inhibit the proliferation and induce apoptosis of KB cells, the mechanism of which may involve the activation of the mitochondrial apoptotic pathway and endoplasmic reticulum stress.

Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Cell Proliferation ; drug effects ; Heat-Shock Proteins ; metabolism ; Humans ; KB Cells ; Membrane Potential, Mitochondrial ; drug effects ; Metformin ; pharmacology