Objective To investigate the effects of different concentrations of sevoflurane on adhesion and expression of CD24 and CD44v6 in human lung cancer cell line A549.Methods Human lung cancer cell line A549 was obtained from Shanghai Cell Biology Medical Research Institute,Chinese Academy of Sciences and cultured in RPMI1640 culture medium containing 10％ fetal calf serum.The cells were inoculated in 24 well culture plate.After being cultured for 24 h,the cells were randomly divided into 4 groups:control group (group C) and 3 sevoflurane groups exposed to 1.7 ％,3.4 ％ and 5.1％ sevoflurane for 2,4 and 6 h respectively ( groups S1,S2,S3 ).The cells were cultured for another 48 h.Cell adhesion rate was detected by adhesion test and the expression of CD24 and CD44v6 mRNA and protein was determined by RT-PCR and flow cytometry.Results Sevoflurane significantly inhibited the cell adhesion rate and down-regulated CD24 and CD44v6 expression in a concentration and duration of exposure-dependent manner.Conclusion Sevoflurane can inhibit cell adhesion through down-regulation of CD24 and CD44v6 expression.

Asphyxia ; etiology ; Child ; Dysostoses ; complications ; Female ; Humans ; Osteochondrodysplasias ; Thorax ; abnormalities

Many complications occur in the early stage of post-orthotopic liver transplantation, six patients with or the ptopic liver transplantation, mainly contract hemorrhage,renal insufficience,acute host-vs-graftreaction,palmonary infectin,thoracic fluid and oral ulcer.We conclude in order to improver the postoperation survival of the patients it is very important to closely obere the change of patients and early recognize and deal with various complications on the basis of observing and nursing these patients

Objective To evaluate the effect of propofol on invasiveness of human gastric cancer MKN-45 cells.Methods Human gastric cancer cell line MKN-45 were seeded in culture plates.After being cultured for 24 h,the cells were randomly divided into 5 groups(n =12 each):control group (group C),intralipid group (group Ⅰ),4 μg/ml propofol group (group P1),8 μg/ml propofol group (group P2) and 16μg/ml propofol group (group P3).The cells were treated with 10％ intralipid and 4,8 and 16 μg/ml propofol for 24 h in I and P1-3 groups,respectively.The cells were then cultured for another 24 h.The migration of cells was determined by cell scratch test.The invasion of cells was determined by Transwell invasion assay.The expression of RhoA and ROCK1 was detected by Western blot.Results Compared with group C,the cell migration and invasion were significantly decreased,and the expression of RhoA and ROCK1 was down-regulated in P1-3 groups,and no significant changes were found in the parameters mentioned above in group Ⅰ.With the increasing concentrations of propofol,the cell migration and invasion were gradually decreased,and the expression of RhoA and ROCK1 was gradually down-regulated in P1-3 groups.Conclusion Propofol can inhibit the invasiveness of human gastric cancer MKN-45 cells cultured in vitro dose-dependently and inhibition of RhoA/ROCK1 signaling pathway may be involved in the mechanism.

Objective To evaluate the role of interleukin-4 receptor (IL-4R) in renal fibrosis following renal ischemia-reperfusion (I/R) injury in mice.Methods Twelve male wild type BALB/C mice and 12 IL-4Rα gene-knockout mice,aged 8-10 weeks,weighing 20-30 g,were used in the study.The mice of either type were divided into 2 groups (n =6 each) using a random number table:sham operation group (group S) and group I/R.In group I/R,renal I/R was induced by occlusion of the right renal artery for 1 h with atraumatic microclips followed by 2 weeks of reperfusion.The right renal artery was only isolated in group S.At 2 weeks of reperfusion,blood samples were taken from the orbital vein for determination of the concentrations of serum blood urea nitrogen (BUN) and creatinine (Cr).The renal tissues were obtained,and the renal fibrosis area was measured by Sirius Red staining.The expression of fibronectin (FN),collagen Ⅰ (COL-Ⅰ) and α-smooth muscle actin (α-SMA) in renal tissues was detected by immunofluorescence.The expression of signal transducer and activator of transcription 6 (STAT6) and phospho-STAT6 in renal tissues was determined by Western blot.The ratio of phoshop-STAT6 to STAT6 was calculated to reflect the phosphorylation of STAT6.Results Compared with group S of wild type mice,the serum BUN and Cr concentrations and renal fibrosis area were significantly increased,the expression of FN,COL-Ⅰ and α-SMA in renal tissues was significantly up-regulated,and the phosphorylation of STAT6 in renal tissues was significantly increased in group I/R of wild type and IL-4Rα KO mice (P＜0.05).Compared with group I/R of wild type mice,the serum BUN and Cr concentrations and renal fibrosis area were significantly decreased,the expression of FN,COL-Ⅰ and α-SMA in renal tissues was significantly down-regulated,and the phosphorylation of STAT6 in renal tissues was significantly decreased in group I/R of IL-4RαKO mice (P＜0.05).Conclusion The mechanism of renal fibrosis following renal I/R injury is partially related to IL-4R,and IL-4R results in renal fibrosis through promoting activation of STAT6 signaling pathway in mice.

Objective To evaluate the effect about medication compliance for patients with chronic heart failure in outpatients using nursing intervention model based on Omaha system.Methods 100 patients were randomly divided into observation group(50 patients)and control group(50 patients).The two groups of patients were given routine nursing intervention,the observation group also used the Omaha system to develop care programs on this basis, and was given the implementation about continuity of care.Results On the point of the two or three months after the patients were discharged,the AHFKT -V2 questionnaire scores in the observation group[(17.690 ±1.892)points, (20.900 ±2.052)points]were significantly higher than the control group[(14.080 ±2.374)points,(18.450 ± 1.781)points],the differences were statistically significant (t =-8.488,-6.442,all P <0.05).However,the same as the points after the patients were discharged,Morisky questionnaire scores in the observation group[(1.036 ± 0.780)points,(0.487 ±0.260)points]were significantly lower than the control group[(1.54 ±1.182)points, (0.920 ±0.804)points],the differences were statistically significant(t =3.420,4.965,all P <0.05).Conclusion The use of Omaha system to develop the targeted continuity of care,can improve the patients medication compliance.

Objective To investigate the effects of isoflurane and sevonumne on apoptosis and expression of CD44 and CD54 in human lung cancer cell line A549.Methods Human lung cancer A549 cells were obtained from Shanghai Cell Biology Medical Research Institute,Chinese Academy of Sciences,and inoculated in 24 well culture plate.After being cultured for 24 h the cells were randomly divided into 3 groups:group Ⅰ control(group C);group Ⅱ isoflurane (group Iso) and group Ⅲ sevoflurane (group Sev).A 549 cells were exposed to 1.7% isoflurane and 2.5%sevoflurane for 4 h respectively in group Iso and Sev respectively,and were then cultured for another 24 h.Apoptosis and expression of CD44 and CD54 in A549 cells were detected with flow cytometer at 0 (T0),2 h(T1) and 4 h(T2) of and 24 h after(T3) exposure to isoflurane and sevoflurane.Results The percentage of apoptotic cells wag significantly higher at T2 and T3 in group Iso than in group C.The percentage of apoptotic cells was significantly higher at T1,T2 and T3 in group Sev than in group Iso and C.The expression of CD44 and CD54 at T1,T2 and T3 was significantly decreased as compared with the baseline at T0 in group Iso and Sev and was significantly lower in group Iso and Sev than in group C.Conclusion Isoflurane and sevoflurane can induce apoptesis of human lung cancer cell line A549, and sevoflurane is more effective. Isoflurane and sevoflurane can inhibit the expression of CD44 and CD54 of human lung cancer cell line A549.

Objective To investigate the effects of different concentrations of sevoflurane on Survivin expression in human adenocarcinoma cell line A549. Methods A549 cells were obtained from Shanghai Cell Biology Medical Research Institute, Chinese Academy of Sciences and inoculated in 96 well culture plate. After being cultured for 24 h, the cells were randomly divided into 4 groups: Ⅰ , Ⅱ , Ⅲ and Ⅳ groups exposed to 95 % O2 -5 %CO2,1.7%, 3.4% and 5.1% sevoflurane respectively. A549 cells were exposed to sevoflurane for 2, 4 and 6 h respectively and then cultured for another 48 h in Ⅱ , Ⅲ and Ⅳ groups. Proliferation of A549 cells were measured by methyl thiazolyl tetrazolium (MTT) assay, and apoptosis was detected with flow cytometer at 48 h after 2, 4 and 6 h sevoflurane exposure. The expression of Survivin in A549 cells was determined by Western blot analysis at 48h after 4 h sevoflurane exposure. Results The rate of proliferation inhibition and percentage of apoptotic cells were significantly higher while the expression of Survivin was significantly lower in a concentration-dependent manner in Ⅱ , Ⅲ and Ⅳ groups as compared with group Ⅰ . Conclusion Sevoflurane can inhibit proliferation and induce apoptosis of A549 cells by inhibition of Survivin expression.

Objective To explore the role of case based learning (CBL)on Otolaryngology-Head and Neck Surgery teaching. Methods First, correct and high-quailty teaching case was selected. Then, reasonable and precise question was edited. All students needed to prepare their lessons before class and were encouraged to ask question or answer question. And some warnings should be noticed. Result After CBL being implemented, the students received higher clinical grades and more clinical skills. They were more likely to retain their initial interest in or switch their preference to careers in otolaryngology. The supervisor highly appreciated our teaching. Conclusion CBL is feasible in Otolaryngology-Head and Neck Surgery teaching and it should be applied more in future.

Objective To investigate the effects of sevoflurane on inhibition of growth of human lung adenocarcinoma A549 cells by cisplatin and γ ray.Methods The human lung adenocarcinoma cell line A549 was seeded in culture plate.After being cultured for 24 h,the cells were randomly divided into 6 groups (n =6each):control group (group C),sevoflurane group (group S),cisplatin group (group D),cisplatin + sevoflurane group (group DS),γ ray group (group R) and γ ray + sevoflurane group (group RS).A549 cells were exposed to 2.5% sevoflurane for 4 h in group S.Cisplatin with the final concentration of 3 mg/L was added to the culture medium and the cells were then incubated for 4 h in group D.Cisplatin with the final concentration of 3 mg/L was added to the culture medium and the cells were then exposed to 2.5 % sevoflurane for 4 h in group DS.A549 cells were exposed to γ irradiation (2 Gy) for 4 h in group R.A549 cells were exposed to γ irradiation (2Gy) and to 2.5% sevoflurane for 4 h in group RS.The cells were cultured for another 24 h after the end of treatment,the colony formation was detected and the rate of colony formation was calculated by colony formation assay.Proliferation of A549 cells was measured by plate colony formation and MTF assay and the rate of proliferation inhibition was calculated.Cell apoptosis was detected with flow cytometer.The expression of X-linked inhibitor of apoptosis protein (XIAP) and caspase-3 was detected by Western blot.Results Compared with group C,the rate of colony formation was significantly decreased,the rate of proliferation inhibition and percentage of apoptotic cells were increased,XIAP expression was down-regulated and caspase-3 expression was up-regulated in groups S,D,DS,R and RS (P ＜ 0.05).The rate of colony formation was significantly lower,the rate of proliferation inhibition and percentage of apoptotic cells were higher,XIAP expression was lower and caspase-3 expression was higher in group DS than in groups S and D,and in group RS than in groups S and R (P ＜ 0.05).Conclusion Sevoflurane can enhance cisplatin and γ ray-induced inhibition of growth of human lung adenocarcinoma A549 cells,and downregulation of XIAP expression and up-regulation of caspase-3 expression may be involved in the mechanism.