Dihydromyricetin mediates epithelial mesenchymal transformation and regulates the proliferation and apoptosis of esophageal squamous cell carcinoma cells / 中华肿瘤杂志

Objective: To study the effects of dihydromyricetin (DMY) on the proliferation, apoptosis and epithelial mesenchymal transition (EMT) of esophageal squamous cell carcinoma (ESCC) cell KYSE150 and KYSE410. Methods: KYSE150 and KYSE410 cells were treated with different concentrations of DMY (0, 25, 50, 100, 150, 200 μmol/L) for 24 hours. The median inhibition concentration (IC50) values of KYSE150 and KYSE410 were detected by cell counting kit-8 (CCK-8) method. Then 0.5‰ dimethyl sulfoxide (DMSO) was used as control group, dihydromyricetin (DMY), dihydromyricetin and transforming growth factor-β1 (DMY+ TGF-β1), transforming growth factor-β1 (TGF-β1) were used as experimental group. Cell proliferation and apoptosis rates were measured by clonal formation and flow cytometry. Transwell invasion and wound healing assay were used to detect cell invasion and migration. The protein expression levels of Caspase-3, Caspase-9, Bcl-2, Bax, Smad2/3, phosphorylation-Smad2/3 (p-Smad2/3) and Vimentin were detected by western blot. Results: The IC50 values of DMY on KYSE410 and KYSE150 cells were 100.51 and 101.27 μmol/L. The clone formation numbers of KYSE150 and KYSE410 in DMY group [(0.53±0.03) and (0.31±0.03)] were lower than those in DMSO group [(1.00±0.10) and (1.00±0.05), P<0.05]. The apoptosis rates of KYSE150 and KYSE410 cells in DMY group [(1.84±0.22)% and (2.80±0.07)%] were higher than those in DMSO group [(1.00±0.18)% and (1.00±0.07)%, P<0.05]. The invasion numbers of KYSE150 and KYSE410 cells in DMY group [(0.42±0.03) and (0.29±0.05)] were lower than those in DMSO group [(1.00±0.08) and (1.00±0.05), P<0.05]. The migration rates of KYSE150 and KYSE410 cells in DMY group [(0.65±0.14)% and (0.40±0.17)%] were lower than those in DMSO group [(1.00±0.10)% and (1.00±0.08)%, P<0.05]. The clone formation numbers of KYSE150 and KYSE410 in TGF-β1 group [(1.01±0.08) and (0.99±0.25)] were higher than those in DMY+ TGF-β1 group [(0.73±0.10) and (0.58±0.05), P<0.05]. The apoptosis rates of KYSE150 and KYSE410 cells in TGF-β1 group [(0.81±0.14)% and (1.18±0.10)%] were lower than those in DMY+ TGF-β1 group [(1.38±0.22)% and (1.85±0.04)%, P<0.05]. The invasion numbers of KYSE150 and KYSE410 cells in TGF-β1 group [(1.19±0.11) and (1.39±0.11)] were higher than those in DMY+ TGF-β1 group [(0.93±0.09) and (0.93±0.05), P<0.05]. The migration rates of KYSE150 and KYSE410 cells in TGF-β1 group [(1.87±0.19)% and (1.32±0.04)%] were higher than those in DMY+ TGF-β1 group [(0.86±0.16)% and (0.77±0.12)%, P<0.05]. The protein expression levels of Bax, Caspase-3 and Caspase-9 in KYSE150 and KYSE410 cells in DMY group were higher than those in DMSO group, while the protein expression level of Bcl-2 was lower than that in DMSO group (P<0.05). The protein expression levels of p-Smad2/3, Smad2/3 and Vimentin in KYSE150 and KYSE410 cells in DMY group were lower than those in DMSO group (P<0.05). The protein expression levels of Bax, Caspase-3 and Caspase-9 in KYSE150 and KYSE410 cells in TGF-β1 group were lower than those in DMY+ TGF-β1 group, and the protein expression level of Bcl-2 was higher than that in DMY+ TGF-β1 group (P<0.05). The protein expression levels of Bax, Caspase-3 and Caspase-9 in KYSE150 and KYSE410 cells in DMY+ TGF-β1 group were lower than those in DMY group, and the protein expression level of Bcl-2 was higher than that in DMY group (P<0.05). The protein expression levels of p-Smad2/3, Smad2/3 and Vimentin in KYSE150 and KYSE410 cells in TGF-β1 group were higher than those in DMY+ TGF-β1 group (P<0.05). Conclusion: DMY can inhibit the proliferation and EMT of ESCC mediated by TGF-β1 and promote cell apoptosis.

Night Sleep Duration and Risk of Cognitive Impairment in a Chinese Population: A Cross-sectional Study / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>Although sleep is one of the most important health-related behavioral factors, the association between night sleep duration and cognitive impairment has not been fully understood. A cross-sectional study was conducted with a random sample of 2,514 participants (⋝ 40 years of age; 46.6% women) in China to examine the association between night sleep duration and cognitive impairment.</p><p><b>METHODS</b>Night sleep duration was categorized as ⋜ 5, 6, 7, 8, or ⋝ 9 h per night. Cognitive function was measured using the Mini-Mental State Examination. A multivariate regression analysis was used to analyze the association of night sleep duration with cognitive impairment. A total of 122 participants were diagnosed with cognitive impairment.</p><p><b>RESULTS</b>A U-shaped association between night sleep duration and cognitive impairment was found. The odds ratios (95% confidence intervals) of cognitive impairment (with 7 h of daily sleep being considered as the reference) for individuals reporting ⋜ 5, 6, 8, and ⋝ 9 h were 2.14 (1.20-3.83), 1.13 (0.67-1.89), 1.51 (0.82-2.79), and 5.37 (1.62-17.80), respectively (P ⋜ 0.01).</p><p><b>CONCLUSION</b>Short or long night sleep duration was an important sleep-related factor independently associated with cognitive impairment and may be a useful marker for increased risk of cognitive impairment..</p>

Effect of nitric oxide on esophageal cancer cell line TE-1 / 中国医学科学杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the radiosensitizing effect of nitric oxide (NO) combined with radiation on esophageal cancer cell line TE-1.</p><p><b>METHODS</b>Methyl thiazolyl tetrazolium (MTT) assay was used to assess the effects of NO and radiation on TE-1 cells regarding inhibition of cell proliferation. Flow cytometry was used to examine the effect of NO and radiation on cell apoptosis and cycle. Reverse transcription polymerase chine reaction and Western blot were used to evaluete the effect of NO on mRNA and protein expression of manganese superoxide dismutase (MnSOD).</p><p><b>RESULTS</b>NO inhibited the proliferation of TE-1 cells while significantly enhancing their radiosensitivity. The application of NO combined with radiation significantly increased the apoptosis rate and G2/M phase proportion of TE-1 cells, with substantial decreases in the MnSOD mRNA and protein expression levels.</p><p><b>CONCLUSIONS</b>NO reduces the MnSOD mRNA and protein expression levels by affecting TE-1 cell cycle, further inhibiting the apoptosis of esophageal cancer cells and enhancing the killing effect of radiation on esophageal cancer cells.</p>

A case-control study on serum organochlorines residues, genetic polymorphisms of glutathione S-transferase T1 and the risks of breast cancer / 中华流行病学杂志

<p><b>OBJECTIVE</b>To study the potential effect of gene-environment interaction between glutathione S-transferase T1 (GSTT1) and serum organochlorines residues on the risk of breast cancer in women, in China.</p><p><b>METHODS</b>70 newly diagnosed female breast cancer patients and 30 controls from September 2006 to October 2007 were interviewed using the same questionnaire to obtain information regarding exposure to those risks. Organochlorine residues level in serum was measured by gas chromatography (GC). Genotypes of GSTT1 polymorphisms were analyzed by multiplex allele-specific polymerase chain reaction (PCR). Interaction indexes (gamma) were calculated to determine the type of gene-environment interaction.</p><p><b>RESULTS</b>After adjusting the confounding factors, results showed that interaction existed in genetic polymorphisms of GSTT1 and dichlorodiphenyltrichloroethane (DDT)/hexachlorocyclohexane (HCH) residues, with interaction indexes (gamma) value as 1.352 and 1.528.</p><p><b>CONCLUSION</b>Genetic and environmental hazard factors had a co-effect on the development of breast cancer while genetic polymorphisms of GSTT1 and DDT/HCH expressed an interaction to breast cancer.</p>