Objective To study the characteristics of respiratory impedance in patients with chronic obstructive pulmonary disease (COPD),obstructive sleep apnea hypopnea syndrome (OSAHS).Methods The respiratory impedance were measured by Impulse Oscillometry(IOS) technique and polysomnography(PSG) were done synchronously in 11 COPD patients,15 OSAHS patients,4 overlap syndrome patients(COPD+OSAHS) and 10 control group. Results Zrs、R5、Rc and RP in COPD group,OSAHS group and COPD+OSAHS group were higer than those in contml group.Zrs、R5、R5-20、Fres.Rc and Rp in COPD group and COPD+OSAHS group were significantly higerthan those in OSAHS group.R20 and Rc in OSAHS group were higher than those in COPD group and control group (P<0.05).Rc in OSAHS group was still significantly higher than that in COPD group (P<0.05). The level of sleep efficiency was positive correlated with FEVl/pre% of COPD(r=0.632),while the levels of rouse frequence (r=-0.672),time of SaO2 <90% (-0.868) and ODI (-0.846) were negative correlated with FEVl/pre% of COPD.Condusion For OSAHS patients, there is some dysfunction in peripheral airway tract;For COPD patients,ODI and time of SaO2<90% are good index for the severity of disease.

Background and purpose:Over-expression of Hypoxia-inducible factor-1? in tumors was known to be associated with resistance to radiation,chemotherapy and with the more malignant tumor phenotypes relative to increased invasiveness,metastatic potential.Furthermore,research has shown that HIF-1? over-expression is associated with aberrant P53 accumulation in human tumors.So we investigated the significance of HIF-1? expression and the relationships among expression of HIF-1?,P53 and P-gp in gastric carcinoma.Methods:The expressions of HIF-1?,P53 and P-gp were investigated by immunohistochemistry in 74 specimens of gastric carcinoma.Results:The positive percentage of P53 protein was higher in the group with HIF-1? positive than the one with HIF-1? negative(70.45% vs 30.0%).The positive rate of P-gp protein was also higher in HIF-1? positive group than in HIF-1? negative group(61.36% vs 36.67%),The positive expression of HIF-1? was significantly related to expression of P-53 and P-gp(r_(s)=0.372,0.256).The positive rate of P-gp protein was higher in P53 positive group than in P53 negative group.Spearman rank correlation test showed a positive correlation between P53 expression and P-gp(r_(s)=0.0283,P

Objective To address the correlation between self-efficacy and quality of life in patients after coronary artery bypass graft. Methods A total of 88 patients in our hospital were investigated by using general data questionnaire, Barnason self-efficacy scale and concise health questionnaire ( MOS-SF 36 ) at 2 weeks, 6 weeks and 3 months after coronary artery bypass graft. Results The self-efficacy scores were (42. 8 ± 5. 4) at 2 weeks after operation, (44. 5 ± 4. 2) at 6 weeks after operation and (47. 6 ± 5. 6) at 3 months after operation, and the scores of quality of life were (73. 7 ± 11. 4) at 2 weeks after operation, (85. 9 ± 10. 6) at 6 weeks afteroperationand(93.9±16.2)at3monthsafteroperation(F=3.452,P<0.05). Afteroperation,theself-efficacy increase gradually, and the difference was statistically significant. The scores of quality of life were (73. 7 ± 11. 4) at 2 weeks, (85. 9 ± 10. 6) at 6 weeks, and (93. 9 ± 16. 2) at 3 months after operation, and there was a positive correlation between self-efficacy and quality of life ( r=0. 411, 0. 447, 0. 307,respectively;P<0. 01). Conclusions The quality of life and self-efficacy of patients after coronary artery bypass surgery are improved, and the two are positively correlated. Nursing staff should be based on principles of self-efficacy theory to strengthen the nursing work which may improve the patient′s self-efficacy and the quality of life.

Objective:To investigate the expression of Per2 mRNA, HDAC1 mRNA and E-cadherin mRNA in esophageal cancer cells and their significance.Methods:The experimental study was conducted. Human normal esophageal epithelial cells as the control group and human esophageal cancer cell line KYSE-150 cells as the experimental group were cultured in vitro to logarithmic growth stage. Observation indicators: (1) the proliferation of cells; (2) the migration and invasion of cells; (3) the expression of Per2 mRNA, HDAC1 mRNA, and E-cadherin mRNA in cells of initial physiological state; (4) the expression of Per2 mRNA, HDAC1 mRNA, and E-cadherin mRNA after cells were treated with Per2-agonists or inhibitors; (5) the expression of Per2 mRNA and E-cadherin mRNA after cells were treated with HDAC1 inhibitors. Measurement data with normal distribution were represented as Mean± SD, the t test was used for comparison within groups and the t test or ANCOVA were used for comparison between groups. Results:(1) The proliferation of cells: the cell proliferation of the experimental group and control group were 0.90%±0.14% and 0.52%±0.08%, with a significant difference between the two groups ( t=5.166, P<0.05). (2) The migration and invasion of cells: the numbers of cell migration and invasion for the experimental group were 173±41 and 86±27, versus 50±15 and 21±9 for the control group, with significant differences between the two groups ( t=6.274, 5.153, P<0.05). (3) The expression of Per2 mRNA, HDAC1 mRNA, and E-cadherin mRNA in cells of initial physiological state: the expression of Per2 mRNA, HDAC1 mRNA, and E-cadherin mRNA in cells of initial physiological state for the experimental group was 11.7±2.7, 20.4±6.6, and 12.4±2.5, respectively, versus 2.4±0.5, 8.5±2.2, and 27.3±4.5 for the control group, with significant differences between the two groups ( t=5.782, 2.982, -5.034, P<0.05). (4) The expression of Per2 mRNA, HDAC1 mRNA, and E-cadherin mRNA after cells were treated with Per2-agonists or inhibitors: after cells were treated with Per2-agonists, the expression of Per2 mRNA, HDAC1 mRNA, and E-cadherin mRNA were 13.1±2.2, 22.4±6.2, 16.6±4.2 for the experimental group, and 9.9±3.1, 18.4±5.6, 15.3±2.3 for the control group, respectively. There was no significant difference in the expression of Per2 mRNA, HDAC1 mRNA, or E-cadherin mRNA of the experimental group between cells being treated with and without Per2-agonists ( t=-4.300, 10.087, -4.187, P>0.05). There were significant differences in the expression of Per2 mRNA, HDAC1 mRNA, and E-cadherin mRNA of the control group between cells being treated with and without Per2-agonists ( t=-4.846, 3.501, 9.294, P<0.05). There was no significant difference in the expression of Per2 mRNA or E-cadherin mRNA between the experimental group and control group after cells were treated with Per2-agonists ( F=1.000, 7.582, P>0.05), while there was a significant difference in the expression of HDAC1 mRNA between the two groups ( F=1.724, P<0.05). After cells were treated with Per2-inhibitors, the expression of Per2 mRNA, HDAC1 mRNA, and E-cadherin mRNA were 4.1±1.7, 7.5±2.2, 22.8±4.2 for the experimental group, and 3.1±0.9, 9.3±3.2, 28.4±5.8 for the control group, respectively. There were significant differences in the expression of Per2 mRNA, HDAC1 mRNA, and E-cadherin mRNA of the experimental group between cells being treated with and without Per2-inhibitors ( t=12.124, 5.105, -10.245, P<0.05). There was no significant difference in the expression of Per2 mRNA, HDAC1 mRNA, or E-cadherin mRNA of the control group between cells being treated with and without Per2-inhibitors ( t=-2.815, 1.568, -1.439, P>0.05). There were significant differences in the expression of Per2 mRNA and E-cadherin mRNA after cells were treated with Per2-inhibitors between the experimental group and control group ( F=22.965, 82.134, P<0.05), while there was no significant difference in the expressions of HDAC1 mRNA between the two groups ( F=6.416, P>0.05). (5) The expression of Per2 mRNA and E-cadherin mRNA after cells were treated with HDAC1 inhibitors: after cells were treated with HDAC1 inhibitors, the expression of Per2 mRNA and E-cadherin mRNA were 13.4±3.5, 24.2±3.4 for the experimental group, and 3.1±1.2, 26.8±5.2 for the control group, respectively. There was no significant difference in the expression of Per2 mRNA of the experimental group between cells being treated with and without HDAC1-inhibitors ( t=-3.959, P>0.05). There was a significant difference in the expression of E-cadherin mRNA of the experimental group between cells being treated with and without HDAC1-inhibitors ( t=-21.977, P<0.05). There was no significant difference in the expression of Per2 mRNA or E-cadherin mRNA of the control group between cells being treated with and without HDAC1-inhibitors ( t=-1.440, 1.058, P>0.05). After cells were treated with HDAC1-inhibitors, there was no significant difference in the expressions of Per2 mRNA between the experimental group and control group ( F=2.004, P>0.05), while there was a significant difference in the expression of E-cadherin mRNA between the two groups ( F=325.800, P<0.05). Conclusions:Human esophageal cancer cells have an elevated expression of Per2 mRNA and HDAC1 mRNA, and a reduced expression of E-cadherin mRNA. The overexpression of Per2 mRNA may activate the expression of downstream targeting protein HDAC1, and inhibit the expression of cell surface E-cadherin mRNA.