Objective To investigate the inhibitory effects of silencing expression ofEZH2 gene on the cell proliferation of human QBC939 cells and its mechanisms. Methods The targeting siRNA was designed and trans-fected into QBC939cells. The expressions of EZH2 mRNA and protein were detected by real-time qPCR and west-ern blotting,respectively. The ability of cellproliferationwas analyzed by MTT assay and plate clone formation assay. Cell apoptosis and cycle percentage weremeasured by flow cytometry. Cell senescence was assessed byβ-galactosi-dase dyeing.The expressions of H3K27me3,P14ARF,P16INK4a,P53,P21 and E2F1 proteinwere determined by West-ern blotting.Results Compared with the control group ,the expressions of mRNAand protein were significantly elevat-ed in experimental group. The ability of cellproliferation in the experiment group was significantly down regulated , which could also cause a rise of G1/S phase ,but not a marked variation of apoptosis rate. Silencing EZH2 would induce a obvious senescence phenotype in QBC939 cells. EZH2-siRNA transferredcould also down-regulate the expressions of H3K27me3 and E2F1 protein,while up-regulating the expressions of P14ARF,P16INK4a,P53 and P21 protein in QBC939 cells.Conclusions Silencing EZH2 could induce a significant inhibition on cell proliferation of QBC939 cells,the mechanism of which may be associated with the senescence pathway regulation.

Objective To investigate the effect of bisdemethoxycurcumin on the proliferation and apoptosis of melanoma B16-F10 cells. Methods The B16-F10 cells were incubated with bisdemethoxycurcumin for 24 h, and MTT assay was used to detect the proliferation of B16-F10 cell. Flow cytometry was used to detect cell cycle and cell apoptosis. A C57BL/6 mouse melanoma model was established to investigate the effect of bisdemethoxycurcumin on the proliferation of melanoma. Expression of BCL-1 in B16-F10 cells and tissues was detected by western blotting assay. Results bisdemethoxycurcumin could significantly inhibit B16-F10 cell proliferation, induce B16-F10 cell apoptosis and block the cell cycle at S phase. The intravenous dosing of bisdemethoxycurcumin could inhibit the growth of melanoma. Bisdemethoxycurcumin could inhibit the expression of BCL-1. Conclusion Bisdemethoxycurcumin can inhibit the proliferation of B16-F10 cell, resulting from its role in promoting cell apoptosis.

The aim of this study was to investigate the effect of Paris saponin I (PS I) on human gastric carcinoma cell growth and apoptosis and to explore the potential mechanisms. The proliferation of SGC7901 cells was monitored by the MTT cell viability assay, while the nuclear morphology of apoptotic cells was assessed by Hoechst 33258 staining. Flow cytometry was performed to analyze the cell cycle progression of propidium iodide (PI)-stained SGC7901 cells and the apoptotic rate of annexin V/PI-stained cells. Western blotting was used to examine the expression of several cell cycle proteins, including cyclin B1 and Cdk1, and the apoptosis-regulated proteins Bcl-2, Bax, cytochrome c, procaspase-9, and procaspase-3. The MTT assay demonstrated that PS I could induce significant dose- and time-dependent inhibition of SGC7901 cell proliferation. Marked morphological changes, including condensation of chromatin, nuclear fragmentation and apoptotic bodies were clearly shown on Hoechst 33258 staining. PSI treatment also resulted in the disruption of the cell cycle at G(2)/M and the induction of apoptosis. Following PSI treatment, the cell cycle-related proteins cyclin B1 and Cdk1 were down-regulated. Expression of the pro-apoptotic protein Bax was increased, while anti-apoptotic protein Bcl-2 decreased. PSI treatment resulted in elevated cytoplasmic cytochrome c and activation of the apoptotic proteases caspase-9 and caspase-3. These data indicate that PS acts as an inhibitor of proli I feration in SGC7901 cells by inducing cell cycle arrest and mitochondria-dependent apoptosis. PSI is a potential therapeutic agent against human gastric carcinoma.

Objective To investigate the effect of silencing Bmi-1 expression in reversing cisplatin resistance in human lung cancer cells and explore the possible mechanisms. Methods Cisplatin-resistant A549/DDP cells with small interference RNA (siRNA)-mediated Bmi-1 expression silencing were examined for cisplatin sensitivity using MTT assay and alterations in cell cycle distribution and apoptosis with flow cytometry, and the changes in cell senescence was assessed using β-galactosidase staining. The protein expressions of Bmi-1, P14ARF, P16INK4a, P53, P21, Rb and ubi-H2AK119 in the cells were determined with Western blotting. Results A549/DDP cells showed significantly higher Bmi-1 expression than A549 cells. After siRNA-mediated Bmi-1 silencing, A549/DDP cells showed significantly enhanced cisplatin sensitivity with an increased IC50 from 40.3± 4.1μmol/L to 18.3 ± 2.8μmol/L (P<0.01) and increased cell percentage in G0/G1 phase from (48.9 ± 2.3)%to (78.7 ± 7.6)%(P<0.01). Silencing Bmi-1 did not cause significant changes in the cell apoptosis rate but induced obvious senescence phenotype in A549/DDP cells with down-regulated expression of ubi-H2AK119 and up-regulated expressions of P14ARF, P16INK4a, P53,P21 and Rb. Conclusion Silencing Bmi-1 by RNA interference can induce cell senescence and resensitize A549/DDP cells to cisplatin possibly by regulating INK4a/ARF/Rb senescence pathway.

Objective: To understand rural students’ perception and satisfaction of the Nutrition Improvement Program for Rural Compulsory Education Students (NIPRCES), and to provide basis for promoting students’ participation in the school feeding program and improving the acceptability of school feeding. Methods: In 3 national pilot counties and 2 local pilot counties of NIPRCES, 1 middle school and 1 primary school were randomly selected. Two classes of 2 364 students from grade 4 to grade 9 were randomly selected and investigated with questionnaires. Results: Students were aware of the policy, with 78.9% of the students reported to be familiar with NIPRCES. The awareness rate of students at the national pilot areas was higher than that in local pilot areas(P<0.05). Students showed positive attitude towards NIPRCES. The median score of students’ understandings of the influence of NIPRCES was 20.0 (18.0, 20.0) points. Students in national pilot areas showed a more positive attitude toward the program than those in local pilot areas(P<0.05). Moderate satisfaction was reported in school feeding, 78.7% of students thought that school provided adequate amount of food, and 60.9% of the students enjoyed the food very much. The main reasons for leftovers were too much in amount(27.4%), repetition of food types (22.8%) and food aversions(9.2%). Conclusion Students are quite aware of NIPRCES and show moderate satisfaction in school feeding. The awareness and satisfaction are relatively higher among students in national pilot areas than those in local pilot areas. Health promoting schools should be established and students and parents should be advocated to take part in the program, health education need to be promoted in schools. Experiences sharing between different places could help improve the quality and acceptability of school feeding program.

Objective To investigate the effect of silencing Bmi-1 expression in reversing cisplatin resistance in human lung cancer cells and explore the possible mechanisms. Methods Cisplatin-resistant A549/DDP cells with small interference RNA (siRNA)-mediated Bmi-1 expression silencing were examined for cisplatin sensitivity using MTT assay and alterations in cell cycle distribution and apoptosis with flow cytometry, and the changes in cell senescence was assessed using β-galactosidase staining. The protein expressions of Bmi-1, P14ARF, P16INK4a, P53, P21, Rb and ubi-H2AK119 in the cells were determined with Western blotting. Results A549/DDP cells showed significantly higher Bmi-1 expression than A549 cells. After siRNA-mediated Bmi-1 silencing, A549/DDP cells showed significantly enhanced cisplatin sensitivity with an increased IC50 from 40.3± 4.1μmol/L to 18.3 ± 2.8μmol/L (P<0.01) and increased cell percentage in G0/G1 phase from (48.9 ± 2.3)%to (78.7 ± 7.6)%(P<0.01). Silencing Bmi-1 did not cause significant changes in the cell apoptosis rate but induced obvious senescence phenotype in A549/DDP cells with down-regulated expression of ubi-H2AK119 and up-regulated expressions of P14ARF, P16INK4a, P53,P21 and Rb. Conclusion Silencing Bmi-1 by RNA interference can induce cell senescence and resensitize A549/DDP cells to cisplatin possibly by regulating INK4a/ARF/Rb senescence pathway.

The aim of this study was to investigate the effect of Paris saponin Ⅰ (PS Ⅰ ) on human gastric carcinoma cell growth and apoptosis and to explore the potential mechanisms.The proliferation of SGC7901 cells was monitored by the MTT cell viability assay,while the nuclear morphology of apoptotic cells was assessed by Hoechst 33258 staining.Flow cytometry was performed to analyze the cell cycle progression of propidium iodide (PI)-stained SGC7901 cells and the apoptotic rate of annexin V/PI-stained cells.Western blotting was used to examine the expression of several cell cycle proteins,including cyclin B1 and Cdkl,and the apoptosis-regulated proteins Bcl-2,Bax,cytochrome c,procaspase-9,and procaspase-3.The MTT assay demonstrated that PSⅠ could induce significant doseand time-dependent inhibition of SGC7901 cell proliferation.Marked morphological changes,including condensation of chromatin,nuclear fragmentation and apoptotic bodies were clearly shown on Hoechst 33258 staining.PSⅠ treatment also resulted in the disruption of the cell cycle at G2/M and the induction of apoptosis.Following PSⅠ treatment,the cell cycle-related proteins cyclin B 1 and Cdk1 were downregulated.Expression of the pro-apoptotic protein Bax was increased,while anti-apoptotic protein Bcl-2decreased.PSⅠ treatment resulted in elevated cytoplasmic cytochrome c and activation of the apoptotic proteases caspase-9 and caspase-3.These data indicate that PSⅠ acts as an inhibitor of proliferation in SGC7901 cells by inducing cell cycle arrest and mitochondria-dependent apoptosis.PSⅠ is a potential therapeutic agent against human gastric carcinoma.

OBJECTIVETo investigate the effect of silencing Bmi-1 expression in reversing cisplatin resistance in human lung cancer cells and explore the possible mechanisms.

METHODSCisplatin-resistant A549/DDP cells with small interference RNA (siRNA)-mediated Bmi-1 expression silencing were examined for cisplatin sensitivity using MTT assay and alterations in cell cycle distribution and apoptosis with flow cytometry, and the changes in cell senescence was assessed using β-galactosidase staining. The protein expressions of Bmi-1, P14(ARF), P16(INK4a), P53, P21, Rb and ubi-H2AK119 in the cells were determined with Western blotting.

RESULTSA549/DDP cells showed significantly higher Bmi-1 expression than A549 cells. After siRNA-mediated Bmi-1 silencing, A549/DDP cells showed significantly enhanced cisplatin sensitivity with an increased IC50 from 40.3±4.1 µmol/L to 18.3±2.8 µmol/L (P<0.01) and increased cell percentage in G0/G1 phase from (48.9±2.3)% to (78.7±7.6)% (P<0.01). Silencing Bmi-1 did not cause significant changes in the cell apoptosis rate but induced obvious senescence phenotype in A549/DDP cells with down-regulated expression of ubi-H2AK119 and up-regulated expressions of P14(ARF), P16(INK4a), P53, P21 and Rb.

CONCLUSIONSilencing Bmi-1 by RNA interference can induce cell senescence and resensitize A549/DDP cells to cisplatin possibly by regulating INK4a/ARF/Rb senescence pathway.

Antineoplastic Agents ; pharmacology ; Apoptosis ; Cell Cycle ; Cell Line, Tumor ; Cisplatin ; pharmacology ; Drug Resistance, Neoplasm ; Gene Silencing ; Humans ; Lung Neoplasms ; genetics ; Polycomb Repressive Complex 1 ; genetics ; RNA, Small Interfering

With the continuous evolution and refinement of the healthcare insurance system,there arises a heightened de-mand for the standardization and efficacy of healthcare insurance management.This paper takes a prominent public hospital in Guangzhou City as a case study to delve into the establishment and enhancement of an intelligent monitoring system for healthcare insurance.Initially,an analysis is conducted from the perspectives of the national,policy,and institutional levels to underscore the imperative and urgency of constructing an intelligent monitoring system for healthcare insurance.Subsequently,a comprehen-sive review of the current research landscape,both domestically and internationally,is presented,highlighting the challenges faced by domestic intelligent auditing systems in terms of their level of intelligence,the sophistication of hospital-level intelligent monitoring,and the standardization of rule libraries.Following this,the paper elaborates on the practical endeavors undertaken by large public hospitals in Guangzhou City regarding the construction and optimization of the intelligent monitoring system for healthcare insurance.This encompasses aspects such as the structure of the intelligent monitoring system,collaborative manage-ment in operational modes,and the standardization of rule libraries.Finally,the paper concludes by summarizing the positive im-pact of these practices on the regulation of medical service behaviors and the enhancement of efficiency in healthcare insurance quality management,while also offering insights into future research directions.

Objective: To investigate drinking behaviors in weekdays and weekends among college students in Hebei Province during spring, and to provide references for propaganda of water drinking. Methods: A total of 156 college students in Hebei Province were selected using simple random sampling method. The survey began in March 2017. 7-day 24hour recording method was applied to record the amount and type of water drinking during for consistent consecutive 7 days, duplicate portion method was used to weigh the food consumed during the consistent consecutive 3 days and to record the water contained in the food. Results: Water intake from food among subjects during weekdays was higher than that among subjects during weekends (1 191 mL vs 1 113 mL, P<0.01). Only 21.9% and 19.9% of subjects consumed sufficient water during weekdays and weekends, according to the recommendation of China on total fluids intake, respectively. The proportion of water intake from staple food among male subjects during weekdays was lower than that during weekends (28.6% vs 31.1%). The proportion of water intake in males from porridge, water intake from soup and vegetables among subjects during weekdays were higher than those among subjects during weekends (6.8% vs 0; 141 mL vs 0 mL; 699 mL vs 647 mL). Water intake from staple food and vegetables among females during weekdays was higher than that during weekends (256 mL vs 210 mL; 559 mL vs 536 mL). There were no statistically differences on plain water, milk and beverages among subjects during weekdays and weekends(P>0.05). Conclusion Water intake from food among college students in Hebei Province during weekdays in spring is higher than that during weekends. There is discrepancy on sources of water intake from food during weekdays and weekends, while no similar difference on sources of drinking water. Proportion of college students without sufficient daily water intake during weekdays and weekends is relatively high which warrants further notice.