Objective To vie the effect of theophylline on eosinophil (Eos) apoptosis. Methods EDTA-anticoagulated venous blood was obtained from 15 healthy volunteers and pre-incubated with saline or theophylline (10 -4 M) or dexamethasone and rhIL-5(10 -8 M),respectively.The mRNA of bcl-2 and bax were determined by reverse transcriptase polymerase chain reaction(RT-PCR),and their cytoplasm proteins were determined by flo cytometry. Results Analysis revealed that the bax protein express intracellular without any stimulator,but not bcl-2 in protein and mRNA levels.And culturing Eos in the presence of 10 -8 M IL-5 for 24 hours up-regulating bcl-2 mRNA ( P

Objective To explore the narcotic effect of three inhalation induced methods of sevoflurane.Methods According to the different inhalation methods of sevoflurane,60 patients with elective upper abdominal surgery under intubation general anesthesia were divided into group A (vital capacity breathing),group B (tidal volume breathing),and group C (gradually increasing the concentration of sevoflurane),each group 20 cases.The sevoflurane concentration of A group and B group was 9％,which of group C was 4％,and oxygen pipeline was prefilled by oxygen flow(3L/min).The heart rate(HR),mean blood pressure(MAP),diastolic blood pressure(DBP) and systolic blood pressure(SBP) values and the effect of muscle relaxants were observed and recorded at T1 (basic indicators),T2 (eyelash reflex),T3 (before intubation),T4 (intubation time 2 min),T5 (intubation time 4 min),T6 (intubation time 6 min).Results The SBP,DBP,and MAP of group A,B and C at different time points were all inhibited(all P ＜0.05),and the significant inhibitory effect was at time point T3 (all P ＜0.01).There was no close correlation between HR changes and the muscle relaxant effect of group A,B and C at different point(all P ＞ 0.05).Conclusion Three kinds of sevoflurane inhalation induction can lower blood pressure,and they are safe,reliable,and able to be accepted by the patients.

Objective To investigate the effects of muscle relaxant antagonism on patients with residual paralysis in postanesthesia care unit (PACU).Methods The similar patients who were daily accepted into PACU were chosen to make pairs,and were randomly divided into experimental (J; n =26) and control (F; n =26) groups.On arrival to the PACU,the train-of-four ratio (TO-Fr) was assessed using electromyography.When TOFr reached 4,Grour J was given with neostigmine 40 μg/kg and atropine 20 μg/kg; Group F was given with 5ml saline.Extubation was determined with standard clinical criteria.We recorded TOFr,PaO2,PaCO2at the time point of extubation,SpO2 at the time point of left the PACU,the stay time in PACU,the incidence of respiratory dysfunction,and the side effect.Results The TOFr at the time point of extubation in group J (0.96 ± 0.04) was significantly higher than group F (0.92 ±0.06) (P ＜0.05).The stay time in PACU in group J [(26 ±5)min] was significantly less than group F [(33 ±7) min] (P ＜ 0.01).PaO2,PaCO2,extubation time,and SpO2 were no significant difference between two groups (P ＞ 0.05).Two patients in group F had respiratory dysfunction.There was no incidence of postoperative nausea,vomiting,and other side effects in two groups.Conclusions Regular muscle relaxant antagonism lowered the risk of postoperative residual muscle relaxant effect,shortened the PACU residence time,and had no postoperative nausea and vomiting(PONV) and other side effects.

Objective To investigate the effect of dexmedetomidine (Dex) on the apoptosis and respiratory burst of human polymorphonuclear neutrophils (PMN) in vitro. Methods The peripheral venous blood was collected from healthy volunteers. Isolation of PMN was performed by using the discontinuous plasma-Percoll gradient technique. PMN was randomLy divided into four groups: control group and three different concentrations of Dex (1 ng/mL,10 ng/mL,100 ng/mL) groups. PMN was cultured in enriched RPMI-1640 media at 2 × 106/mL for 24 h. The caspase-3 activity, apoptosis rate and respiratory burst of PMN were detected at 2 and 24 h. Results Compared with the control group, the PMN which was treated with three different concentrations of Dex showed no significant difference in caspase-3 activity, apoptosis rate and respiratory burst of PMN after 2 h of incubation. Compared with the control group, 1 ng/mL concentration of Dex did not affect the caspase-3 activity, apoptosis and respiratory burst of PMN cultured for 24 h. However, 10 ng/mL and 100 ng/mL concentrations of Dex promoted the caspase-3 activity, increased apoptosis rate and reduced the respiratory burst of PMN after 24 h of incubation. Compared with 10 ng/mL Dex group, 100 ng/mL concentrations of Dex promoted the caspase-3 activity, increased apoptosis rate and reduced the respiratory burst of PMN after 24 h of incutation. Conclusion Clinically relevant concentration of Dex does not affect apoptosis and respiratory burst of PMN, while high concentration of dexmedetomidine can induce apoptosis of PMN.

ObjectiveTo explore the possible molecular mechanisms of β-elemene combined with cisplatin and heat therapy for killing A549 cell line.MethodsThe protein expressions of Stat3,p21 Waf1/Cip1 and Survivin were detected with Western blot after treatment with β-elemene of different concentrations combined cisplatin and heat therapy.ResultsThe protein expressions of Stat3,and pStat3 and p21Waf1/Cip1 in A549 cell line were enhanced with increasing concentrations,and there was significant difference in the expressions between high and low concentration,but Survivin protein had no change at 37°C.After adding 4 μg/mL cisplatin,the expressions of p21Waf1/ Cip1,Survivin,Stats and pStat3 were reduced at β-elemene of high concentration.At 42°C,there was no significant difference in expression of Stat3 protein at 60 μg/mL elemene,but the expressions of pStat3,p21Waf1/Cip1 and Survivin proteins had sharply declined.When using 15 μg/mL elemene combined with 4 μg/mL cisplatin,the protein expressions of Star3 and pStat3 increased,and Survivin expression decreased.ConclusionsAt temperature of 37°C,β-elemene of high concentration may inhibit growth of A549 cells by higher expression of p21Waf1/Cip1 protein,and mainly by inhibiting expressions of Stat3 and pStat3 and Survivin after combined with cisplatin.At temperature of 42°C,β- elemene of highconcentrationmaypromoteapoptosispossiblythroughinhibition ofStat3 phosphorylation and expression of Survivin protein.β-elemene of low concentration combined with cisplatin leads to synergy killing effect by reducing expression of Survivin protein.

Objective To evaluate the effect of sufentanil postconditioning on myocardial ischemia-reperfusion injury in rats, and to investigate the possible mechanism. Methods Thirty male Sprague-Dawley ratswere randomly divided into 5 groups (n = 6 each): sham group (group S), I/R group (group I/R), low dose of sufentanil postconditioning group (group SL), high dose of sufentanil postconditioning group (group SH) andsufentanil postconditioning plus wortmannin group (group WM). Different drugs were injected before reperfusion: normal saline (NS) and sufentanil 1 μg/kg in group SL, NS and sufentanil 3 μg /kg in group SH, wortmannin 15 μg/kg andsufentanil 1 μg/kgin group WM, and NS in group S and I/R. At the end of reperfusion, artery blood was collected for assessment of plasma cTnI concentration; And the heart was harvested for determination of infarct size (IS) and area at risk (AAR). Results Compared with group S, cTnI concentration was increasedin the rest groups (P< 0.01); Compared with group I/R, cTnI concentration was decreased in group SL, SH and WM, while IS/AAR reduced in group SL and SH (P < 0.01); Compared with group SL, cTnI concentration and IS/AAR were decreased in group SH while increased in group WM (P <0.01). Conclusion Sufentanil postconditioning could attenuate myocardial ischemia-reperfusion injury in rats, and the mechanism involved PI3K related pathway.