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In order to analyze in depth the release behavior of added flavor components in tobacco matrix using the solid-gas partition coefficient, a PRV-HS-GC-MS method was developed to determine the partition coefficients of monomeric flavors in cut tobacco matrix based on the changing comparison method combined with HS-GC-MS analysis. The partition coefficients (Kcut/air) of six ester flavors in cut tobacco matrix (solid phase) and gas phase were determined by the PRV-HS-GC-MS method. The results showed that: 1) The relative standard deviation (RSD) of Kcut/air of the six ester flavors at 90-110 °C ranged from 0.92% to 9.14%. The developed method was convenient and accurate with good repeatability. 2) The Kcut/air values of the six monomer ester flavors in cut tobacco were negatively correlated with temperature. The prediction equations established on the basis of Kcut/air values in low-temperature regions could predict Kcut/air values that were difficult to determine in high-temperature regions. The relative errors between the actually determined and predicted Kcut/air values at 90-110 °C were between 1.04% and 5.32%, indicating good prediction performance. 3) The Kcut/air values could be used as a parameter for the release performance of monomer flavors in cut tobacco matrix to quantitatively characterize the differences in monomer flavor release behavior, and it provided a new strategy to study the release behavior of tobacco monomer flavors. [ABSTRACT FROM AUTHOR]

The oral deposition of main volatile carbonyls in mainstream smoke of 25 cigarette samples was analyzed by using a smoke oral deposition simulator. The results showed that: 1) All of the intra-and inter-day relative standard deviations of the analytical results of volatile carbonyls were less than 15%, and most of them were less than 10%, which demonstrated that the simulator had a good stability in oral deposition analysis of volatile carbonyls. 2) The oral deposition amounts of different volatile carbonyls from high to low were acetaldehyde, formaldehyde, acetone, propionaldehyde, acrolein, butyraldehyde, crotonaldehyde and 2-butanone, in which the deposition amounts of formaldehyde and acetaldehyde were significantly higher than those of the other volatile carbonyls. The deposition ratios from high to low were formaldehyde, acetaldehyde, propionaldehyde, butyraldehyde, crotonaldehyde, acrolein, acetone and 2-butanone. 3) There were significant negative correlations between smoke oral irritation and the oral deposition amounts of formaldehyde and acetaldehyde with the correlation coefficients of -0.916 and -0.934 respectively, and P values were both less than 0.01. [ABSTRACT FROM AUTHOR]

Since the implementation of the comprehensive housing reform in 1998, the real estate market in China has continued to boom, and the proportion of housing expenditure in residents' income has been increasing, which has an increasingly significant impact on residents' consumption. A regression model is constructed based on the relevant data of urban residents from 1992 to 2019 and the impact of changes in housing expenditures and residential expenditures on household consumption is explored. Meanwhile, time series models of the United States and Japan were constructed for comparative study. The results show that the housing purchase expenditure and residential expenditure in China have a certain degree of crowding-out effect on household consumption; the increase in purchase expenditure in the United States and Japan can stimulate consumption to a certain extent, and the rise in residential expenditure has no significant impact on American household consumption but positive promoting the consumption of Japanese residents. Based on the empirical results, a comparative analysis of the reasons why housing expenditure inhibits household consumption in China is made, and the relevant policy suggestions are put forward in the paper. [ABSTRACT FROM AUTHOR]

In order to construct an Escherichia coli strain with high sensitivity and specificity to detect arsenic ion using fluorescence as reporter, a sensitive strain to arsenic ion was obtained by knocking out the gene arsB that acts as an arsenic efflux pump. The pET28b vector containing arsenite detecting cassette Pars-arsR-egfp was constructed and then transformed into arsB deleted mutant. Measuring conditions of this constructed whole-cell biosensor were optimized and its linear concentration range, limit of detection and specificity were determined. This modified biosensor was much more sensitive than that using wild-type strain as host. The optimal detection range of As³⁺ concentration was 0.013 to 42.71 μmol/L, and the limit concentration of detection was as low as 5.13 nmol/L. Thus we successfully improved the sensitivity of arsenite detecting biosensor by modification of E. coli genome, which may provide useful strategies for development and optimization of microbial sensors to detect heavy metals.

To detect cadmium ions, we constructed a specific microbial sensor and screened detecting cassettes and different fluorescence proteins. Blue fluorescence protein mTagBFP2 was selected as a reporter and a double-promoters model was used in the construction of the fusion reporter vector Pmer::merR-m-Pmer::mTagBFP2-pMD19-T. The reporter vector was then transformed into Escherichia coli MC4100 wild type strain. The medium, incubation time, initial density for induction, and the optimal detection range were determined. The specificity of the biosensor was also checked. The biosensor responded specifically to cadmium irons with low background, and the linear concentration range detection ranged from 0.1 to 75 μmol/L at the initial OD600 = 0.1 with 2 h incubation in IHMM medium. Thus we successfully constructed a specific biosensor to detect cadmium irons and provided useful strategies for development and optimization of microbial sensors to detect heavy metals.

Background: p53 gene is the most commonly mutated gene in lung cancer. p53 mutation results in insensitivity of cells when exposed to chemotherapy. It has been reported that adenovirus-mediated wild-type p53 gene transfection into lung cancer cells can enhance the cytotoxic effect of anti-cancer drugs. The aim of this study is to evaluate the effects of domestic recombinant adenovirus-p53 (Ad-p53, Gendicine) on growth and chemosensitivity of human lung adenocarcinoma cell lines., Methods: Human lung adenocarcinoma cell lines GLC-82 (including mutant p53) and A549 (including wild-type p53) were treated with Ad-p53, cisplatin (DDP) or Ad-p53+DDP respectively. p53 expression was detected by Western blot. The cell growth inhibition was assessed by MTT, and cell cycle and apoptosis were detected by flow cytometry., Results: High-level p53 expression was detected in Ad-p53 infected GLC-82 and A549 cells by Western blot. There was a dose-dependent and time-dependent inhibition of cell proliferation by Ad-p53. After combined treatment with Ad-p53 (100MOI) and DDP (0.5mg/L) for 72h, the growth inhibition rate of A549 cells was 43.13%±0.72%, which was significantly higher than that in Ad-p53 group ( 23.44%±0.54%, P < 0.001) and DDP group (14.17%±1.39%, P < 0.001); and the growth inhibition rate of GLC-82 cells was 63.73%±0.92%, which was significantly higher than that in Ad-p53 group ( 41.51%±0.59%, P < 0.001) and DDP group (56.11%±1.12%, P < 0.001). Combined administration of Ad-p53 and DDP remarkably arrested A549 and GLC-82 cells in G0-G1, and cells in S phase significantly decreased. Meanwhile the apoptotic rate of A549 cells was 28.99%±1.07% in Ad-p53+DDP group, which was significantly higher than that in Ad-p53 group (15.35%±1.31%, P < 0.001) and DDP group (1.74%±0.77%, P < 0.001). The apoptotic rate of GLC-82 cells was 62.98%±2.43% in Ad-p53+DDP group, which was significantly higher than that in Ad-p53 group (20.88%±0.71%, P < 0.001) and DDP group (6.91%±1.52%, P < 0.001)., Conclusions: Ad-p53 (Gendicine) can inhibit the growth of human lung adenocarcinoma cell lines irrespective of the status of endogenous p53 gene. Its combination with DDP may significantly enhance the chemosensitivity of human lung adenocarcinoma cells to DDP.