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Objective@#To investigate lunch supply of public primary school canteens in Zhejiang Province, and to provide a basis for the scientific guidance of school lunch.@*Methods@#During May to Jun. and Sept. to Oct. in 2019, lunch food supply was weighed and recorded and the number of diners in 44 public primary school canteens were summarized. Each investigation lasted for one week.@*Results@#Food was mainly based on the taste of the students (40.91%) in the school canteen. About 45.45% of the schools referred to the Nutrition Guidelines of School Meals for students meals when making recipes in the school canteen. The supplies of cereals, vegetables, fruits, livestock and poultry meat, fish and shrimp, eggs, milk, soybean nuts, vegetable oil and salt were 109.05, 118.01, 0, 63.96, 9.25, 11.31, 0, 10.68, 10.47, 2.54 g. The supply of vegetable oil was basically the same as the recommended amount ( P >0.05). The supplies of energy, protein, calcium, iron, zinc, vitamin A, vitamin B 1, vitamin B 2, vitamin C, dietary fiber were 820.84 kcal, 32.79 g, 164.18 mg, 7.84 mg, 4.71 mg, 23.07 μgRAE, 0.41 mg, 0.35 mg, 20.47 mg, 2.34 g, 37.56% of energy from fat and 48.47% of energy from carbohydrate. The supply of vitamin B 1 was basically the same as the recommended amount ( P >0.05). There were no significant differences in all kinds of food and nutrients between urban and rural primary schools ( P >0.05).@*Conclusion@#Lunch supply is not optimistic in public primary school canteens in Zhejiang Province, with unreasonable structure and fails to agree with current nutritional recommendations. It is suggested that the scientific guidance of students meals should be carried out according to the survey results combined with the characteristics of local diet.
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Objective To investigate the effects of Apollon antisense oligonucleotide (ASODN) on proliferation,apoptosis and drug resistance of human leukemia(K562) cells.Methods Specific phosphorothioate ASODN and missense oligonucleotide (MSODN) of Apollon mRNA were synthesized and transfected into K562 cells following cationic liposome.The proliferation inhibition of K562 cells was assessed by MTT.The apoptosis rate was detected by Annexin V-FITC.The sensitivity of K562 cells to etoposide and vincristine was detected by MTT.Results Apollon antisense oligonucleotide inhibition of K562 cells with the concentration and time increased.ASODN at a final concentration of 600 nmol/L could significantly inhibit the K562 cell proliferation.The apoptosis rate was apparently increased (P ＜ 0.01).Conclusions Apollon ASODN may decrease Apollon gene expression,suppress K562 cells proliferation effectively,and induce significant apoptosis of K562 cells.Apollon ASODN is able to reverse the drug resistance via inhibition of Apollon expression and inducement of apoptosis.
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PURPOSE: Few cells with stem cell characteristics possess capabilities of self-renewal and differentiation, which leads to high tumorigenesis and resistance to standard chemotherapeutic agents. These cells are mostly quiescent, and arrest occurs at the mitotic G0/G1 phase in mitosis. We explored the effects of basic fibroblast growth factor (bFGF) on the MCF-7 cell cycle with CD44+/CD24-. METHODS: Cancer-initiating cells were propagated as mammospheres. The CD44+/CD24- subpopulation was sorted by a fluorescence activating cell sorter-Vantage flow cytometer. A cell cycle analysis was performed with different bFGF concentrations. RESULTS: Differences in the CD44+/CD24- cell proliferation under different bFGF concentrations were observed (p=0.001). When the bFGF concentration was increased, the proportion of CD44+/CD24- at G0/G1 decreased (p=0.023). CONCLUSION: We conclude that bFGF may sustain CD44+/CD24- cell proliferation and could promote cell progression through the G0/G1-->G2/S phase transition.
Subject(s)
Breast Neoplasms , Cell Cycle , Cell Proliferation , Cell Transformation, Neoplastic , Fibroblast Growth Factor 2 , Fibroblast Growth Factors , Fluorescence , MCF-7 Cells , Mitosis , Phase Transition , Stem CellsABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of the expression of the PPAR-gamma gene on the proliferation and glycolysis metabolism of prostate cancer cells.</p><p><b>METHODS</b>Using RNAi, we constructed lowly--expressed shRNA-PPARgamma adenoviruses and transfected them to PC3 prostate cancer cells, with blank vectors as controls. Then we detected the proliferation and apoptosis of the cells, glycolysis metabolism related genes and lactate accumulation by CCK-8 kit, and compared the results between the two groups.</p><p><b>RESULTS</b>Compared with the control group, the PPAR-gamma gene expression was obviously inhibited by RNAi in the PC3 cells, and its protein expression was reduced to (26.00 +/- 4.06)%. The proliferation inhibition rate was (39.5 +/- 4.92)% on the 2nd day, and the apoptosis rate was as high as (21.03 +/- 3.08)%. The glycolysis metabolism related gene products (Myc and Glut-1) were significantly decreased, and the lactate concentration was reduced to 69.71% of that of the controls on the 4th day. There were statistically significant differences in the above findings as compared with the control group (P < 0.01).</p><p><b>CONCLUSION</b>PPAR-gamma gene knockdown is expected to be a new way to treat prostate cancer.</p>