Objective To establish a numerical model of adsorption and desorption of CO_2 and to study the influencing factors on the removal system. Method A physical model was expressed by mathematical method, then an isothermal adsorption model for simulating molecular sieve was established. Result The working process of a CO_2 removed device was simulated and its result was analized with the established model.The characteristics of the adsorption and desorption was obtained. Conclusion The model describes the processes correctly, the influencing factors like humidity dimension of the bed are considered simultaneously.It remains to be improved by further experimental corrections.

Objective To investigate the effects of sevoflurane preconditioning on the expression of pulmonary angiotensin converting enzyme (ACE) mRNA in lung tissues during lung ischemia-reperfusion (I/R) in rats.Methods Fifty-four male Sprague-Dawley rats,weighing 250-320 g,were randomly divided into 3 groups (n =18 each):sham operation group (group S),I/R group and sevoflurane preconditioning group (group SP).The animals were anesthetized,tracheostomized and mechanically ventilated.Lung I/R was induced by clamping the left pulmonary hilum for 45 min followed by 120 min reperfusion in groups I/R and SP.While the left pulmonary hilum was only isolated but not ligated in group S.2.1％ sevoflurane was inhaled for 30 min,and lung I/R was induced 10 min after the end of inhalation in group SP.Six rats in each group were chosen at 30,60 and 120 min of reperfusion and sacrificed,lungs were removed for determination of wet/dry lung weight (W/D) ratio,MPO activity (by colorimetric method) and the expression of ACE mRNA (by RT-PCR) and for microscopic examination in lung tissues.Results Compared with group S,the W/D ratio,MPO activity and expression of ACE mRNA were significantly increased in groups I/R and SP (P ＜ 0.05).Compared with group I/R,the W/D ratio,MPO activity and expression of ACE mRNA were significantly decreased in group SP (P ＜ 0.05).Microscopic examination showed that the pathologic changes were significantly attenuated in group SP compared with group I/R.Conclusion Sevoflurane preconditioning can reduce lung I/R injury through downing-regulating the expression of ACE mRNA in rats.

AIM: To investigate the effect of 17?-estradiol(E2) on myocardial hypertrophy induced by endothelin-1(ET-1) and the related mechanism.METHODS: Myocardial cells from neonate rats were cultured in vitro and myocardial hypertrophy model was established with ET-1.The effects of 17?-estradiol on myocardial hypertrophy were observed.The role of ERK1/2 in the effects of 17?-estradiol was also detected.RESULTS: Compared with control group,ET-1 increased cell protein content,cell surface area and -Leucine(-Leu) incorporation.Pretreatment with E2 for 24 h could inhibit the increase in cell protein content,cell surface area and -Leu incorporation induced by ET-1.ET-1 significantly stimulated ERK1/2 activity,which was prevented by pretreatment with E2.Tamoxifen,estradiol receptor antagonist,partially inhibited the effect of E2.The ability of ET-1 to stimulate -Leu incorporation was significantly blocked by PD98059,which could enhance the inhibitory effect of E2 on the increase of -Leu incorporation in cardiomyocytes induced by ET-1.CONCLUSION: E2 can inhibit cardiomyocyte hypertrophy induced by ET-1.This effect is mediated by estrogen receptor.ERK1/2 signal pathway is closely correlated with the inhibitory effect of E2 on cardiomyocyte hypertrophy induced by ET-1.

AIM:To investigate the effect of caveolin-1 and phosphorylation of ERK1/2 on 17?-estradiol (E2) induced inhibition of vascular smooth muscle cells (VSMCs). METHODS:The proliferation in cultured VSMCs was determined by using [3H]-thymidine incorporation. The expressions of caveolin-1,MKP-1 and ERK1/2 phosphorylation were measured by Western blotting. The expression of caveolin-1 mRNA was measured by RT-PCR. RESULTS:Exposed to fetal calf serum (FCS) for 24 h,the increase in proliferation of VSMCs was detected by [3H]-thymidine incorporation. Pretreatment with various concentrations of E2 for 24 h inhibited VSMC proliferation induced by FCS. The results of Western blotting and RT-PCR showed that pretreated with 17?-estradiol for 24 h reserved the decrease in caveolin-1 induced by FCS. Western blotting results further proved that the expression of MKP-1 was significantly increased and the expression of ERK1/2 phosphorylation was decreased after incubated with 17?-estradiol. CONCLUSION:17?-estradiol increases caveolin-1 and MKP-1 expressions,and decreases ERK1/2 phosphorylation,leading to the inhibition of VSMC proliferation.

Objective To develop a portable ventilation device to cool and dehumidify for the astronauts who work or move dressed in spacesuit in the atmospheric environment on the ground.Methods Based on the requirement which the astronauts need when they are dressed in spacesuit on the ground,the overall design project has been brought forward,which expounds the design scheme of DC brushless centrifugal fan,power supply,regulation of blowing rate,intelligent monitor on system parameters,organic light-emitting diode(OLED)display,device configuration,software,and so on.Results The portable device for spacesuit ventilation and heat-regulation,which has been developed,can work stably and safely.It has convenient operation mode and practical human-machine interface.Meanwhile,the device has compact configuration.It is light and portable.Conclusion The portable device for spacesuit ventilation and heat-regulation carry out the portable ventilation and heat-regulation for the astronauts of China dressed in spacesuit dress for the first time.It also fulfils the spacesuit dryness after use and usual maintenance.

[Objective] The aim of the present study was to investigate the role of membrane estrogen receptor (mER) mediated pathway in the proliferation and apoptosis of endothelial progenitor cells (EPCs). [Methods] Bone marrow (BM)-derived EPCs were cultured. The cells were divided into different groups, plus or not plus estrogen receptor blocker (ICI 182,780), PI3K inhibitors (LY294002), and NOS inhibitor (L-NAME) to show the effect of E_2-BSA on EPCs. The proliferation of EPCs was determined by MTT and nitric oxide (NO) release was measured by chromatometry. Apoptotic cell death was determined using the Hochest 33258 staining. The expression of phosphorylated eNOS (p-eNOS) were detected by Western blot. [Results] E_2-BSA could increase EPCs proliferation, and this effect was inhibited by estrogen receptor blocker ICI 182,780, thus indicated that mER-initiated membrane signaling pathways were involved in the action of estrogen on EPCs. E_2-BSA increased nitric oxide production and inhibited apoptosis induced by serum withdrawal, and this effect also inhibited by PI3K inhibitor (LY294002), NOS inhibitor (L-NAME)and estrogen receptor blocker(ICI 182,780), thus indicated that PI3K/Akt/NO pathway was involved the effect of estrogen on EPCs apoptosis. Moreover, E_2-BSA treatment increased phosphorylation of eNOS (p-eNOS). PI3K inhibitors (LY294002) also blocked these effects. [Conclusions] The results of present study suggested that mER mediated EPCs proliferation and apoptosis were related to the PI3K/Akt/eNOS pathway.

AIM: To investigate the effect of caveolin - 1 and phosphorylation of ERK1/2 on 17β - estradiol ( E_2 ) induced inhibition of vascular smooth muscle cells ( VSMCs ). METHODS: The proliferation in cultured VSMCs was determined by using [~3H ] - thymidine incorporation. The expressions of caveolin - 1, MKP -1 and ERK1/2 phosphorylation were measured by Western blotting. The expression of caveolin - 1 mRNA was measured by RT - PCR. RESULTS: Exposed to fetal calf serum ( FCS) for 24 h, the increase in proliferation of VSMCs was detected by [~3H] -thymidine incorporation. Pretreatment with various concentrations of E_2 for 24 h inhibited VSMC proliferation induced by FCS. The results of Western blotting and RT - PCR showed that pretreated with 17β - estradiol for 24 h reserved the decrease in caveolin - 1 induced by FCS. Western blotting results further proved that the expression of MKP - 1 was significantly increased and the expression of ERK1/2 phosphorylation was decreased after incubated with 17β - estradiol. CONCLUSION: 17β -estradiol increases caveolin - 1 and MKP - 1 expressions, and decreases ERK1/2 phosphorylation, leading to the inhibition of VSMC proliferation.

Objective To investigate the effects of remifentanil on lung ischemia-reperfusion (I/R) injury and expression of angiotensin-converting enzyme (ACE) mRNA in rats.Methods Forty pathogen-free adult male Sprague-Dawley rats,weighing 300-350 g,were randomly divided into 5 groups (n =8 each):sham operation group (group S),group I/R and different doses of remifentanil groups (groups R1-R3).Lung I/R was produced by occlusion of the left hilum of lung for 45 min followed by 120 min reperfusion.Remifentanil was infused intravenously at a rate of 0.2,0.6 and 1.2 μg·kg-1 ·min-1 until 120 min of reperfusion after a loading dose of 1 μg/kg at 15 min before occlusion of the left hilum of lung in groups R1,R2 and R3,respectively.The equal volume of normal saline was given in groups S and I/R.The rats were scarified at 120 min of reperfusion and lungs were removed for microscopic examination and determination of wet/dry lung weight ratio (W/D ratio) and the expression of ACE mRNA (by RT-PCR) in the lung tissue.The pathological changes of the lung were scored.Results Compared with group S,the pathological score and W/D ratio were significantly increased and the expression of ACE mRNA was up-regulated in groups I/R,R1 and R2,and the pathological score was significantly increased (P ＜ 0.05),and no significant change was found in W/D ratio and the expression of ACE mRNA in group R3 (P ＞ 0.05).Compared with group I/R,the pathological score and W/D ratio were significantly decreased and the expression of ACE mRNA was down-regulated in groups R2 and R3,and the pathological score and W/D ratio were significantly decreased (P ＜ 0.05) and no significant change was found in the expression of ACE mRNA in group R1 (P ＞0.05).Compared with group R1,the pathological score and W/D ratio were significantly decreased and the expression of ACE mRNA was down-regulated in group R3,and the pathological score and W/D ratio were significantly decreased (P ＜ 0.05) and no significant change was found in the expression of ACE mRNA in group R2 (P ＞ 0.05).The pathological score,W/D ratio and expression of ACE mRNA were significantly lower in groups R3 than in group R2 (P ＜ 0.05).The pathological changes of the lung were significantly reduced in groups R1-R3 as compared with group I/R.Conclusion Remifentanil can attenuate lung I/R injury in rats in a dose-dependent manner and down-regulation of ACE mRNA expression may be involved in the mechanism.

In China,with the development of medicine,more and more clinical researches are increased.However,along with this development,there are still a lot of problems.In order to normalize the management of clinical researches,make the research results reliable and benefit for patients,several strict aspects of management are taken by our hospital,included standardizing the application procedures,introducing the roles of the academic committee and the ethics committee,strengthening the projects management and researchers training,etc.And all these ways promote the good development of clinical researches of our hospital.

Objective To investigate the effects of miR-135a on HOXA10 expression,proliferation and apoptosis of SKOV3 cells.Methods (1) Through computer-aided algorithms,the predicted target gene of miR-135a (HOXA10)were determined.(2) miR-135a mimics,miR-135a inhibitor and negative control were transfected into SKOV3 cells,respectively.Reverse transcription (RT)-PCR,western blot analysis were used to examine the expression levels of HOXA10 at different times (24,48 and 72 hours).(3) A luciferase reporter assay was used to confirm the direct regulation between miR-135a and HOXA10.(4) SKOV3 cells proliferation at different times (24,48 and 72 hours) was detected by methyl thiazolyl tetrazolium(MTT) assay [quantified by absorbance(A)].Western blot was used to examine the expression of apoptosis-associated protein bcl-2,bax and caspase-3 in SKOV3 cells after 48 hours transfection.Results (1) HOXA10 was predicted to be the target gene of miR-135a by computer-aided algorithms.(2) RT-PCR shown that HOXA10 mRNA levels were decreased over time (24,48 and 72 hours) after miR-135a mimics transfectionin SKOV3 cells (0.94 ±0.04 vs 0.78 ±0.03 vs 0.70 ±0.03,P ＜0.05).While,the expression of HOXA10 mRNA was increased over time after miR-135a inhibitor transfection (1.14 ± 0.05 vs 1.16 ±0.03 vs 2.60 ±0.08,P ＜0.05).After transfected with miR-135a mimics or miR-135a inhibitor over 48 and 72 hours,the HOXA10 expression levels in SKOV3 cells were significantly lower or higher than each control group,respectively (all P ＜ 0.01).Western blot analysis of HOXA10 expression in SKOV3 cells confirmed the results of RT-PCR detected.(3) After cotransfection of miR-135a plasmid and pMIR-REPORT luciferase plasmid containing HOXA10,luciferase reporter assays showed that the luciferase activity reduced by 67.8％ (P ＜0.01).(4) MTT showed that SKOV3 cells growth after miR-135a mimics transfection for 48 and 72 hours were significantly lower than those in control group (0.38 ± 0.03 vs 0.52 ± 0.05,0.67 ±0.05 vs 0.75 ± 0.06 ; respectively,all P ＜ 0.05).While,SKOV3 cells transfected with miR-135a inhibitor for 72 hours grew significantly faster than that in control group (0.95 ± 0.05 vs 0.75 ± 0.06,P ＜ 0.01).After miR-135a mimics transfection,the level of bcl-2 protein was significantly lower than that in control group (0.28 ±0.06 vs 0.76 ±0.09,P ＜0.01).The activity of caspase-3 was significantly higher than that in control group (115.0 ± 2.4 vs 95.4 ± 2.1,P ＜ 0.01).While,there was no statistical difference of bax expression (P =0.142).However,after miR-135a inhibitor transfection,the expression level of bcl-2 protein was significantly higher than that in control group (0.92 ± 0.03 vs 0.76 ± 0.09,P =0.037) and the activity of caspase-3 was significantly lower than that in control group (59.5 ± 4.1 vs 95.4 ± 2.1,P ＜ 0.01).There was also no statistical difference of bax expression (P =0.066).Conclusion miR-135a may play an important role in cell proliferation and apoptosis of ovarian cancer cells by regulating HOXA10 and its downstream pathways.