Objective To investigate the actual cost and benefit of stoma nursing at present as a reference for the improvement of stoma care cost management program. Methods A cross sectional study was carried out in gastrointestinal surgery of a tertiary- level hospital in southwestern China from April 2014 to December 2014. The consumption of intestinal stoma care work, the average monthly income/average monthly working hours ratio and other indicators of stoma care nurse specialist were measured by the step cost allocation method, to investigate the actually cost of a single stoma care service which colostomy patients had received and analyze the gap between actually costs and charge standard of Sichuan Province. Results The directly human cost of stoma care expenses were (22.33 ± 3.66) yuan; working fee expenses were (4.18 ± 0.68) yuan;administrative expenses were (1.87 ± 1.32 ) yuan; research and education expenses were (1.87 ± 1.32 ) yuan; the total cost of investment was (29.14 ± 4.76) yuan, which was much higher than the current charge standard of Chengdu Bureau of Commodity Prices (t=119.50, P <0.05). Conclusions There is a difference between the actual cost and charge standard of stoma care. The situation of low pay to labor is not in line with economic laws, and not conducive to the future development of stoma care speciality.

Objective To explore the effect of several cytokines, including interferon-γ, interleukin-10 and interlekin-4, on promoter activity of human BAFF (B-cell activating factor belonging to tumor necrosis factor family) gene. Methods A construct of phBAFF 1.02 containing sequence form -1349 bp to -329 bp of human BAFF gene, linking with chloramphenicol acetyltransferase (CAT) as reporter gene, was transiently transfected into human HL-60 cells, a kind of myeloid tumor cell lines. The cells were subsequently treated with IFN-γ, IL-10 and IL-4, and the CAT activity was assessed 24 hours after stimulation with each cytokines. Results IFN-γ of 5 ng/ml, IL-10 of 100 ng/ml could increase the CAT activity of phBAFF 1.02 to 4.18 and 2.13 folds respectively compared to the control. IL-4 at 100 ng/ml had no effect on promoter activity of human BAFF gene. Combination of IFN-γ, IL-10 and IL-4 could increase the CAT activity of phBAFF 1.02 to 3.41 and 1.58 folds respectively compared with controls. Conclusion IFN-γ and IL-10 can increase the promoter activity of human BAFF gene. IL-4 treatment can not affect the CAT activity driven by BAFF promoter. However, IL-4 can decrease the upregulating effect of IFN-γ and IL-10 on phBAFF1.02. These provide essential evidence for future study on the interaction mechanism of cytokines and BAFF in autoimmune diseases.

Objective To explore the effect of IFN-γ, IL-10 and IL-4 on B cell activating factor (BAFF) expression in human HL-60 cells, a kind of myeloid tumor cell lines, and its possible regulation mechanism. Methods Cultured human HL-60 cells were treated with IFN-γ, IL-10 and IL-4 for 1-3 days. The expression of membrane-bound BAFF on HL-60 cells was examined by flow cytometry, the amount of soluble BAFF was detected by ELISA assay, and the level of BAFF mRNA was tested by real-time PCR method. A functional 1021 bp fragment of the 5'-tlanking region of the human BAFF gene (-1349 to -329 bp) was cloned and investigated with serial 5'-deletion. The 5'-deleted promoters were recombinated with chloramphenicol acetyltransferase (CAT) as reporter gene. These five recombinant plasmids were transiently transfected to HL-60 cells with liposomal transfectian method. Promoters activities were determined by CAT reporter gene assay(CAT-ELISA) in those transfected cells treated with different cytokines. Results The results showed that the expression of membrane-bound BAFF, soluble BAFF and BAFF mRNA in human HL-60 cells were significantly elevated (P ＜ 0. 05) after incubated with IFN-γ and IL-10. In addition, IFN-γ and IL-10 showed significantly (P ＜ 0. 05) increased effects on promoter activity in human BAFF gane. And the cytokines-responsive sequences were located between -929 and -719 bp of the BAFF promoter region. Conclusion The enhancement of IFN-γ and IL-10 on BAFF expression and synthesis were regnla-ted by promoter activation. Our in vitro studies also raise the possibility to investigate the mechanisms regula-ting BAFF expression in other tumor cells of myeloid origin under pathological circumstances.

AIM: To investigate the expression of microRNA-375 (miR-375) in hepatocellular carcinoma (HCC) and to analyze the target genes and signaling pathways regulated by miR-375.METHODS: The expression of miR-375 was examined at tissue microarray of HCC by in situ hybridization.The whole human genome chip and bioinforma-tics analysis were applied to screen out the differential expression genes and signaling pathways in 4 HCC cell lines trans-fected with miR-375 mimic.RESULTS:In situ hybridization showed the expression of miR-375 in HCC tissues were obvi-ously higher than that in tumor-adjacent tissues (P<0.05).There were 20 co-upregulated genes and 17 co-downregulated genes in all 4 cell lines.Bioinformatic analysis showed that there were 54 signaling pathways related to up-regulated genes and 48 signaling pathways related to down-regulated genes in all 4 cell lines.CONCLUSION: miR-375 may play a key role in the pathological process of HCC.The bioinformatic analysis is able to screen the target genes and signaling pathways regulated by miR-375 and to provide an explicit direction for further mechanism research on HCC.

The effects of over-expression of ANXA10 gene on proliferation and apoptosis of hepato-cellular carcinoma cell line HepG2 were elucidated. The human ANXA10 gene was subcloned into the lentiviral vector, PGC-FU, to generate the lentiviral expression vector, PGC-FU-ANXA10. The corrected ANXA10 was confirmed by endoenzyme digestion, and sequencing. Recombinant lentiviruses were produced by 293T cells following the co-transfection of PGC-FU-ANXA10 with the packaging plasmids pHelper1.0 and pHelper2.0. The resulting recombinant lentiviruses carrying ANXA10 were then used to infect human embryonic kidney epithelial cells, and lentiviral particles were produced. The ANXA10 expression in 293T cells was detected by using fluorescent microscope and Western blotting. HepG2 cells were infected, and divided into PGC-Fu-ANXA10 group, PGC-Fu group and HepG2 cell group. The changes of ANXA10 mRNA and protein expression were detected by using RT-PCR and Western blotting respectively. Flow cytometry and MTT assay were performed to examine the changes in cell apoptosis and proliferation respectively. The recombinant PGC-FU-ANXA10 vector was successfully constructed, the ANXA10 protein was detected by using Western blotting, and virus titer was 2×10(8) TU/mL. The recombinant lentiviruses were effectively infected into HepG2 cells in vitro and the infection efficiency was 70%. At 72 h after infection, the ANXA10 mRNA and protein expression levels in PGC-Fu-ANXA10 group were significantly higher than in PGC-Fu group and HepG2 cell group (P<0.05); the in vitro growth inhibition rate of HepG2 cells in PGC-Fu-ANXA10 group was 24.65%, significantly higher than that in PGC-Fu group and HepG2 cell group (P<0.05), but there was no significant difference between PGC-Fu group and HepG2 cell group; the apoptosis rate in PGC-Fu-ANXA10 group, PGC-Fu group and HepG2 cell group was (51.92±1.41)%, (19.00±1.12)% and (3.59±0.89)% respectively. The apoptosis rate in PGC-Fu-ANXA10 group was significantly higher than in PGC-Fu group and HepG2 cell group (P<0.05). The recombinant lentiviruses PGC-FU-ANXA10 were constructed successfully and infected into HepG2 cells. The overexpression of ANXA10 gene can significantly inhibit proliferation and promote apoptosis of HepG2 cells in vitro.

The effects of over-expression of ANXA10 gene on proliferation and apoptosis of hepato-cellular carcinoma cell line HepG2 were elucidated. The human ANXA10 gene was subcloned into the lentiviral vector, PGC-FU, to generate the lentiviral expression vector, PGC-FU-ANXA10. The corrected ANXA10 was confirmed by endoenzyme digestion, and sequencing. Recombinant lentiviruses were produced by 293T cells following the co-transfection of PGC-FU-ANXA10 with the packaging plasmids pHelper1.0 and pHelper2.0. The resulting recombinant lentiviruses carrying ANXA10 were then used to infect human embryonic kidney epithelial cells, and lentiviral particles were produced. The ANXA10 expression in 293T cells was detected by using fluorescent microscope and Western blotting. HepG2 cells were infected, and divided into PGC-Fu-ANXA10 group, PGC-Fu group and HepG2 cell group. The changes of ANXA10 mRNA and protein expression were detected by using RT-PCR and Western blotting respectively. Flow cytometry and MTT assay were performed to examine the changes in cell apoptosis and proliferation respectively. The recombinant PGC-FU-ANXA10 vector was successfully constructed, the ANXA10 protein was detected by using Western blotting, and virus titer was 2×10(8) TU/mL. The recombinant lentiviruses were effectively infected into HepG2 cells in vitro and the infection efficiency was 70%. At 72 h after infection, the ANXA10 mRNA and protein expression levels in PGC-Fu-ANXA10 group were significantly higher than in PGC-Fu group and HepG2 cell group (P<0.05); the in vitro growth inhibition rate of HepG2 cells in PGC-Fu-ANXA10 group was 24.65%, significantly higher than that in PGC-Fu group and HepG2 cell group (P<0.05), but there was no significant difference between PGC-Fu group and HepG2 cell group; the apoptosis rate in PGC-Fu-ANXA10 group, PGC-Fu group and HepG2 cell group was (51.92±1.41)%, (19.00±1.12)% and (3.59±0.89)% respectively. The apoptosis rate in PGC-Fu-ANXA10 group was significantly higher than in PGC-Fu group and HepG2 cell group (P<0.05). The recombinant lentiviruses PGC-FU-ANXA10 were constructed successfully and infected into HepG2 cells. The overexpression of ANXA10 gene can significantly inhibit proliferation and promote apoptosis of HepG2 cells in vitro.
Annexins ; genetics ; Apoptosis ; genetics ; Carcinoma, Hepatocellular ; genetics ; Cell Line, Tumor ; Cell Proliferation ; Hep G2 Cells ; Humans ; Liver Neoplasms ; genetics

Objective:To explore the relationship between blood urea nitrogen to creatinine ratio and frailty in the elderly aged ≥65 years in 8 longevity areas in China.Methods:Participants were recruited from the Healthy Aging and Biomarkers Cohort Study. Based on baseline information about blood urea nitrogen and risk for frailty obtained at follow-up of the participants, blood urea nitrogen to creatinine ratio was classified according to quintiles, Cox proportional hazard regression models were used to analyze the association between blood urea nitrogen to creatinine ratio and frailty.Results:A total of 1 562 participants aged (81.0±17.0) years were included, in whom 814 (52.1%) were men, and 258 frailty events occurred during a mean follow-up of (3.73±1.43) years. Cox proportional hazards model showed that after adjusting for relevant confounders, compared with the participants in the lowest quintile group ( Q1), the risk for frailty decreased by 36%, 44%, and 40% in the participants in the third quintile group ( Q3), the fourth quintile group ( Q4) and the highest quintile group ( Q5) respectively [hazard ratio ( HR)=0.64, 95% CI: 0.43-0.94; HR=0.56, 95% CI: 0.38-0.84; HR=0.60, 95% CI: 0.41-0.88]. The risk for frailty decreased by 20% for every unit standard deviation increase in blood urea nitrogen to creatinine ratio ( HR=0.80, 95% CI: 0.70-0.91). Moreover, blood urea nitrogen to creatinine ratio and the risk for frailty showed a nearly linear dose-response relationship. Conclusions:The increase in blood urea nitrogen to creatinine ratio was associated with higher risk for frailty. Maintaining high blood urea nitrogen to creatinine ratio is important for the prevention of frailty in the elderly.

Objective To explore the application disturbance coefficient (DC) value of noninvasive brain edema monitoring in patients after traumatic brain injury.Methods A total of 54 cerebral injury patients were performed by non-invasive brain edema monitoring from June to November 2016.The essential information,DC,intracranial pressure (ICP),and 6-month-later glasgow outcome score (GOS) were collected.Results DC was negatively correlated with ICP (r=-0.779 5,P＜0.01),and it was positively correlated with glasgow coma scale (GCS) and GOS (r=0.667 5,P＜0.01;r=0.630 6,P＜0.01).The mean of DC with good prognosis patients was 106.99±4.09,and that of the poor prognosis patients was85.26±4.45,the difference was statistically significant (P＜0.05).Conclusion DC has a good clinical application value.

Objective:To investigate the association between oxygen saturation (SpO 2) and risk of 3-year all-cause mortality among Chinese older adults aged 65 or over. Methods:The participants were enrolled from Healthy Aging and Biomarkers Cohort Study in year of 2012 to 2014 in 9 longevity areas in China. In this prospective cohort study, 2 287 participants aged 65 or over were enrolled. Data on SpO 2 and body measurements were collected at baseline in 2012, and data on survival outcome and time of mortality were collected at the follow-up in 2014. Participants were divided into two groups according to whether SpO 2 was abnormal (SpO 2<94% was defined as abnormal). Results:The 2 287 participants were (86.5±12.2) years old, 1 006 were males (44.0%), and 315 (13.8%) were abnormal in SpO 2. During follow-up in 2014, 452 were died, 1 434 were survived, and 401 were lost to follow-up. The all-cause mortality rate was 19.8%, and the follow-up rate was 82.5%. The mortality rate of SpO 2 in normal group was 21.1%, and that of abnormal group was 41.6% ( P<0.001). After adjusting for confounding factors, compared to participants with normal SpO 2, participants with abnormal SpO 2 had increased risk of all-cause mortality with HR (95% CI) of 1.62 (1.31-2.02); HR (95 % CI) was 1.49 (0.98-2.26) for males and 1.71 (1.30-2.26) for females in abnormal SpO 2group, respectively; HR (95% CI) was 2.70 (0.98-7.44) for aged 65-79 years old, 1.22 (0.63-2.38) for aged 80-89 years old, and 1.72 (1.35-2.19) for aged over 90 years old in abnormal SpO 2 group, respectively. Conclusion:Abnormal SpO 2 was responsible for increased risk of 3-year all-cause mortality among Chinese elderly adults.