Nutritional knowledge, attitudes and dietary behaviors of teachers and students in a medical college in Beijing and their influencing factors / 北京大学学报(医学版)

OBJECTIVE@#To investigate nutritional knowledge, attitudes and dietary behaviors of teachers and students in a medical college in Beijing and their influencine factors, and to provide evidence for nutrition education and promotion.@*METHODS@#The subjects of this study were teachers, as well as first-year and second-year graduate students, and first-year to third-year undergraduate students. The teachers and students were respectively sampled by stratified cluster sampling with equal proportion. t-test or ANOVA was used to compare the means between the groups, and multiple linear regression was used to analyze the influencing factors of knowledge, attitude and practice (KAP) score.@*RESULTS@#The average score of nutrition knowledge was 5.7±1.5. The knowledge rate of nutrition was 57.3%. The average score of nutritional attitudes was 8.3±3.0. The mean nutritional behavior score was 5.1±2.0. The average nutritional KAP score was 19.1±4.6, with the teachers 19.9±5.2 higher than the students 18.9±4.5; the female 19.5±4.5 higher than the male 18.4±4.5; All the differences were statistically significant (P < 0.05). The scores of nutritional attitudes, nutritional behavior and total KAP scores of doctoral students were significantly higher than those of the undergraduate and postgraduate students (P < 0.01).@*CONCLUSION@#The nutrition attitudes of teachers and students is relatively correct, the nutrition knowledge needs to be further strengthened, and there are some unreasonable aspects in the nutrition behaviors. Gender, identity and degree are the main influencing factors of the nutrition score of knowledge, attitudes and behaviors. It is necessary to carry out nutritional education in schools to improve the nutrition knowledge of teachers and students, correct bad eating habits, and promote the construction of healthy China action.

Experimental study of the function of nuclear factor-κB-dependent epithelial to mesenchymal transition in pancreatic cancer cells under hypoxic conditions / 中华外科杂志

<p><b>OBJECTIVE</b>To investigate the function of nuclear factor (NF)-κB in the epithelial to mesenchymal transition induced by hypoxia in pancreatic cancer cells.</p><p><b>METHODS</b>For cultured pancreatic cancer cells (BxPC-3 and Panc-1) under hypoxic and normoxic conditions, the differences in the morphology were observed by optical microscope. The expression of markers of epithelial and mesenchymal phenotypes, E-cadherin, vimentin and N-cadherin, were determined by Western blot. NF-κB P65 activity was measured by electrophoretic mobility shift assay. Invasion and gemcitabine resistance of pancreatic cancer cells were evaluated in matrigel invasion assay and cell counting kit-8 assay. Both molecular and pharmacologic means of inhibiting NF-κB P65 were used in these hypoxic cells and then the above resulting phenotypes were compared with those of the control-treated cells.</p><p><b>RESULTS</b>After cultured pancreatic cancer cells under hypoxic conditions for 48 h, normoxic cells exhibited a polygonal shape and formed tight clusters of cells, whereas hypoxic cells took on an elongated, fibroblastoid morphology associated with a more highly invasive character and resistance to gemcitabine; hypoxic cells exhibited an suppression of E-cadherin and increase in vimentin and N-cadherin expression. NF-κB P65 activity was elevated in hypoxic cells. On the contrary, on molecular or pharmacologic inhibition of NF-κB P65, hypoxic cells regained expression of E-cadherin, lost expression of N-cadherin, and reversed their highly invasive and drug resistant phenotype.</p><p><b>CONCLUSIONS</b>Pancreatic cancer cells underwent epithelial to mesenchymal transition exposed to hypoxia, exhibited highly invasive and drug resistant phenotype. Inhibition of NF-κB P65 under hypoxic conditions, pancreatic cancer cells regained expression of E-cadherin, lost expression of N-cadherin, and reversed their highly invasive and drug resistant phenotype.</p>

Experimental study of the function and mechanism combining dihydroartemisinin and gemcitabine in treating pancreatic cancer / 中华外科杂志

<p><b>OBJECTIVE</b>To investigate the anti-tumor activity of combined gemcitabine with dihydroartemisinin, and the mechanism of the anti-tumor effect of gemcitabine enhanced by dihydroartemisinin on pancreatic cancer.</p><p><b>METHODS</b>For cultured cells, cell growth was determined by the MTT assay and apoptosis was evaluated by flow cytometry analysis and confocal laser scanning microscope stained with Annexin V-FITC/PI. The nuclear extract for determining NF-kappaB DNA-binding activity was analyzed by EMSA, while nuclear P65 and its downstream gene expression was determined by Western blot assay. BxPC-3 cells were injected subcutaneously into nude mice to establish pancreatic xenograft tumors and the tumor volume was monitored after exposure to agents. TUNEL assay was used to assess tumor cell apoptosis in tumor tissue.</p><p><b>RESULTS</b>After combination of gemcitabine and dihydroartemisinin treatment, the proliferative inhibition rates of pancreatic cancer cells BxPC-3 and Panc-1 reached up to (81.1 +/- 3.9)% and (76.5 +/- 3.3)%, and the apoptosis rates were up to (53.6 +/- 3.8)% and (48.3 +/- 4.3)%, the differences were significantly (P < 0.01) compared with gemcitabine [(24.8 +/- 2.9)% and (21.8 +/- 3.5)%]. All the treatment groups inhibited the growth of pancreatic xenograft tumors in nude mice. The tumor volume and apoptosis index were (262 +/- 37) mm(3) and (50 +/- 4)% respectively in the combined treatment, compared to those of [(384 +/- 56) mm(3) and (25 +/- 3)%] in gemcitabine, the differences were significantly (P < 0.05). EMSA showed that gemcitabine alone obviously enhanced its DNA-binding activity compared to control. However, dihydroartemisinin significantly reduced its DNA-binding activity, so that abrogated the inducing effect of gemcitabine on NF-kappaB activation. Western blot assay indicated that dihydroartemisinin downregulated expression of nuclear P65, and combined treatment not only downregulated the expression of Cyclin D1, Bcl-xL and Bcl-2 while upregulated Bax, thus reduced the Bcl-2/Bax ratio, but also increased the caspase-3 activation, all of which increased apoptosis in both BxPC-3 and Panc-1 cells.</p><p><b>CONCLUSION</b>Dihydroartemisinin significantly abrogated the inducing effect of gemcitabine on NF-kappaB activation and downregulated the expression of NF-kappaB targeted gene products, which may be one possible mechanism by which dihydroartemisinin augments the anti-tumor effect of gemcitabine on pancreatic cancer.</p>

An experimental study of gemcitabine inducing pancreatic cancer cell apoptosis potentiated by nuclear factor-kappa B P65 siRNA / 中华外科杂志

<p><b>OBJECTIVE</b>To investigate the effect and mechanism of NF-kappaB P65 gene silencing by small interference RNA on the apoptosis of human pancreatic cancer cells induced by gemcitabine in vitro and in vivo.</p><p><b>METHODS</b>Human pancreatic cancer cells (BxPC-3 and PANC-1) were cultured and respectively divided into five groups: blank control group, negative control siRNA group, gemcitabine group, NF-kappaB P65 siRNA group and gemcitabine + P65 siRNA group. The ability of cell proliferation was analyzed by MTT; the expression of NF-kappaB P65 and the apoptosis related proteins were examined by Western blot assay; the apoptosis was evaluated by the flow cytometry and laser scanning confocal microscopy analysis stained with Annexin V-FITC/PI; the DNA binding activity of NF-kappaB was examined by electrophoretic mobility shift assay. BxPC-3 cells were injected subcutaneously into nude mice to establish pancreatic xenograft tumors. The tumor volume was monitored and TUNEL assay was used to assess the apoptosis index in tumor tissue after treatment.</p><p><b>RESULTS</b>At 72 h after transfection, the combination with gemcitabine and p65 siRNA significantly decreased the cell viability index (P < 0.05), and down-regulated the expression of Bcl-2 and procaspase-3 and up-regulated the expression of Bax compared with other groups. The combined treatment significantly increased the rate of apoptosis compared with other groups (P < 0.05). EMSA assay indicated that the DNA binding activity of NF-kappaB significantly decreased in NF-kappaB P65 siRNA group and gemcitabine+P65 siRNA group compared with Control group. The combined therapy inhibited the growth of pancreatic xenograft tumors by apoptosis induction in nude mice (P < 0.01).</p><p><b>CONCLUSIONS</b>The effect of gemcitabine inducing cell apoptosis may be potentiated through inhibiting the DNA binding activity of NF-kappaB and regulating the expression of apoptosis related proteins by NF-kappaB P65 siRNA, which can activate the mitochondria apoptosis pathway in pancreatic cancer in vitro and in vivo.</p>