Objective:To explore causes of complicated acute lung injury (ALI) after percutaneous coronary interven-tion (PCI) .Methods:According to blood gas analysis and chest imaging examination ,a total of 175 patients under-going PCI were divided into ALI group (n=62) and non-ALI group (n=113) .High performance liquid chromatog-raphy was used to measure plasma concentrations of epinephrine (E) and norepinephrine (NE) during perioperative period .Plasma levels of interleukin-6 (IL-6) and procalcitonin (PCT) and chest CT imaging changes were meas-ured .Fluorescent immunoassay was used to measure plasma level of brain natriuretic peptide (BNP) to assess impact of cardiac function on ALI .Results:Compared with non-ALI group on 1d after PCI ,there were significant rise in plasma levels of NE [ (2.51 ± 0.31) nmol/L vs .(6.91 ± 0.39) nmol/L] and E [ (1.23 ± 0.11) nmol/L vs .(6.03 ± 0.37) nmol/L] ,P<0.01 all;and significant rise in plasma levels of IL-6 [ (119.81 ± 17.23) pg/ml vs .(252.28 ± 34.23) pg/ml] ,PCT [ (0.88 ± 0.01) pg/ml vs .(4.99 ± 0.87) pg/ml] and BNP [ (927.82 ± 89.72) pg/ml vs . (3936.55 ± 131.78) pg/ml] in ALI group (P<0.01 all) .Chest CT indicated that lung tissue inflammation was seri-ous .Conclusion:In patients undergoing percutaneous coronary intervention ,complicated acute lung injury is related to hyperactive sympathetic activity ,postoperative inflammation and heart function status etc .

Objective To investigate the effects of propofol on the whole-cell excitatory postsynaptic currents (EPSC) and spontaneous excitatory postsynaptic current (sEPSC) in hippocampal CAl neurons.Methods Wistar rats (13-19 days old) weighing 40-60 g were decapitated and the hippocampi were immediately removed and placed in 0-4℃ artificial CSF aerated with 95% O2 and 5% CO2 . The hippocampi were sliced (400 ?m thick) . EPSCs were recorded in hippocampal CA1 neurons by stimulating the Schaffer collateral / commissural pathway. The 50 slices were divided into 5 groups (n = 10 each): group Ⅰ intralipid-1; group Ⅱ propofol-1; group Ⅲ SR95531 + propofol; group Ⅳ intralipid-2 and group Ⅴ propofol-2. In group Ⅰ, Ⅱ and Ⅲ after EPSCs were recorded for 10 min, 10% intralipid 90 ?l, 1% propofol 90 ?l (final concentration was 100 ?mol?L-1 and SR95531 10 ?mol?L-1 + propofol 100 ?mol?L-1 were added to the perfusate and again EPSCs were recorded for 40min. The changes in amplitude of EPSC were analyzed. In group Ⅳ and Ⅴ after the cell membrane was perforated and being stabilized for 10-15 min 10% intralipid 90 ?l and 1 % propofol (100 ?mol?L-1) was added to the perfusate and sEPSCs were recorded without stimulation. The holding potential was - 70 mV. Results Intralipid didn't affect EPSC but propfol 100 ?mol?L-1 reduced EPSC to 47.7% of the baseline value. SR95531 could reverse the effect of propofol on EPSCs. The frequency, amplitude and decay time of sEPSC in group propofol-2 were reduced to 31. 9% , 70. 9% and 50. 7% of those in group Ⅳ (intralipid-2) (P

Objective To observe the characteristics of macular optical coherence tomography (OCT) changes before and after silicone oil removal in patients who had undergone pars plana vitrectomy with silicone oil tamponade for macula-off rhegmatogenous retinal detachment (RRD).Methods Thirty-nine eyes that underwent silicone oil removal were enrolled in this retrospective study.The patients included 24 males and 15 females,with an average age of (53.05±4.03) years,the duration of silicone oil tamponade ranged from 3 to 7 months.Best-corrected visual acuity,intraocular pressure,slit lamp microscope and prelens,indirect ophthalmoscopy and fourier domain OCT were measured for all patients before and at months 1,3 and 6 after silicone oil removal.The macular microstructure were observed before and after silicone oil removal.Results Submacular fluid was detected in 6 eyes (15.38％),at the last time of follow-up,submacular fluid resolved completely in 2 eyes with disrupted ellipsoid zone,and resolved partly in 2 eyes.Disrupted ellipsoid zone were observed before silicone oil removal in 16 eyes (41.02％),6 eyes showed simultaneous disrupted ellipsoid zone and disrupted external limiting membrane,and there were 2 eyes that external limiting membrane was not identified,at the last time of follow-up,disrupted ellipsoid zone restored in 2 eyes and the extent of disrupted ellipsoid zone became reduced in 4 eyes.Cystoids macular edema were found in 2 eyes (5.12％),it resolved completely in 1 eye and resolved partly in 1 eye at the last time of follow-up.Macular epiretinal membrane was detected in 10 eyes (25.64％),and macular epiretinal membrane was found before silicone oil removal in 5 eyes,at the last time of follow-up,the membrane became thickened in 2 eye;5 eyes developed macular epiretinal membrane after silicone oil removal,at the last time of follow-up,the membrane became thickened in 1 eye.Secondary macular hole were noted in 2 eyes.Microcystic macular changes were observed in 9 eyes (23.07％),it was observed in 7 eyes before silicone oil removal,and was observed in 2 eyes after silicone oil removal,at the last time of follow-up,the cysts reduced in 1 eye.Conclusion Submacular fluid,disrupted ellipsoid zone and microcystic macular are the main macular ultrastructural changes that developed in patients with RRD before and after silicone oil removal.

0.05 ) ; propofol 500 /?mol?L-1 had dual effects : in 2/3 cells EPSCs were reduced to 67.5 % of the basiline values ( P

0.05). The EPSCs 10-40 min after LFS were 40.8% of the baseline (propofol group), 45.4% of the baseline (corticosterone group) and 25.4% of the baseline (propofol + corticosterone group) respectively, significantly lower than that in group Ⅰ and Ⅱ ( P

Objective To evaluate the effect of dexmedetomidine on the activity of glycogen synthase kinase-3 beta (GSK-3β) during propofol-induced apoptosis in hippocampal nerve cells of newborn rats.Methods Sixty male 7-day-old Sprague-Dawley rats,weighing 10-15 g,were divided into 6 groups (n=10 each) using a random number table:normal saline group (group NS),fat emulsion group (group F),propofol group (group P) and different doses of dexmedetomindine groups (group D25,group D50 and group D75).Normal saline and fat emulsion 100 μl were injected intraperitoneally in group NS and group F,respectively.In group P,propofol 50 mg/kg was intraperitoneally injected,and an increment of propofol 50 mg/kg was added after righting reflex completely recovered,with the total amount of 100 mg/kg.In group D25,group D50 and group D75,dexmedetomidine 25,50 and 75 μg/kg were intraperitoneally injected,respectively,and 30 min later propofol 100 mg/kg was administered.At 2 h after emergence,the rats were sacrificed,their brains were removed for determination of apoptosis in hippocampal nerve cells (by TUNEL),and the hippocampi were isolated for detection of the expression of GSK-3β and phosphorylated GSK-3β (p-GSK-3β) by Western blot analysis.The apoptosis index (AI) and ratio of p-GSK-3β/GSK-3β were calculated.Results Compared with group NS,AI was significantly increased,the expression of p-GSK-3β was down-regulated,and the p-GSK-3β/GSK-3β ratio was decreased in P,D25,D50 and D75 groups (P＜0.05).Compared with group P,AI was significantly decreased,the expression of p-GSK-3β was up-regulated,and the p-GSK-3β/GSK-3β ratio was increased in D25,D50 and D75 groups (P＜0.05).Compared with group D25,AI was significantly decreased (P＜0.05),and no significant change was found in the expression of p-GSK-3β or ratio of p-GSK-3β/GSK-3β in D50 and D75 groups (P＞0.05).Compared with group D50,AI was significantly decreased (P＜0.05),and no significant change was found in the expression of p-GSK-3β or ratio of p-GSK-3β/GSK-3β in group D75 (P＞0.05).Conclusion The mechanism by which dexmedetomidine attenuates propofol-induced apoptosis in hippocampal nerve cells may be related to inhibition of GSK-3β activity in newborn rats.

Objective To evaluate the effects of dexmedetomidine on the expression of phosphor-cAMP response element binding protein (p-CREB) in isoloated hippocampal neurons of fetal rats.Methods SpragueDawley rats on 16-18 days of gestation were sacrificed and the fetal rats were obtained.The hippocampi of fetal rats were isolated and hippocampal neurons were seeded in culture medium for 8 days.The cells were then divided into 4 groups (n =12 each) using a random number table:control group (group C),dexmedetomidine 0.001 μmol/L group (group D1),dexmedetomidine 0.010 μmol/L group (group D2),and dexmedetomidine 0.100μmol/L group (group D3).In D1.3 groups,dexmedetomidine with the final concentrations of 0.001 μmol/L,0.010 μmol/L,and 0.100 μmol/L was added to the culture medium,respectively,and then the cells were incubated for 3.5 h.The apoptosis in hippocampal neurons was detected by flow cytometry.The expression of p-CREB in hippocampal neurons was determined by RT-PCR and Western blot.Results Compared with group C,apoptosis rate was significantly decreased and the expression of p-CREB was up-regulated in D1.3 groups.Conclusion Dexmedetomidine inhibits apoptosis in isolated hippocampal neurons of fetal rats by up-regulating the expression of p-CREB.

Objective To evaluate the effects of propofol on apoptosis in the hippocampal neurons of fetal rats in vitro.Methods The isolated hippocampal neurons were seeded into 96-well plates or 24-well plates at a density of 5 × 104 cells/ml.The cells were randomly divided into 5 groups (n =18 each) using a random number table:control group (group C),in tralipid group (group Ⅰ) and propofol 1,10,100 μmol/L groups (P1-3 groups).In group Ⅰ,10％ intralipid was added to the culture media until the final concentration reached 100 μmol/L.In groups P1-3,propofol was added to the culture media until the final concentration reached 1,10 and 100 μmol/L,respectively,and the cells were then incubated for 3 h.The cell apoptosis was assessed by flow cytometry.The expression of Bcl-2 mRNA and caspase-3 mRNA was detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR).The expression of Bcl-2 and actived-caspase-3 protein was determined by Western blot analysis.The apoptosis rate was calculated.Results Compared with group C,the apoptosis rate was significantly increased,the expression of Bcl-2 mRNA and protein was down-regulated,and the expression of caspase-3 mRNA and actived-caspase-3 protein was up-regulated in P1-3 groups (P ＜ 0.05).There was no significant difference in the parameters mentioned above between group Ⅰ and group C (P ＞ 0.05).Conclusion Propofol induces apoptosis in isolated hippocampal neurons by inhibiting Bcl-2 expression and enhancing caspase-3 activity in fetal rats.

Objective Methods To explore the value of VEGF levels in serum and pleural effusion for diagnosis of benign and malignant tumors, and evaluate clinical value of VEGF-A, C, D in malignant pleural effusion.Methods Serum and pleural effusion of 34 cases patients with lung cancer were collected in our hospital, the application of ELISA method for the detection of VEGF level in serum and pleural effusion in patients with lung cancer and with benign pleural effusion.VEGF-A, C, D levels were detected.Results VEGF levels in serum and pleural effusion in malignant group were significantly higher than those in benign group(P<0.05).In addition, patients with lung cancer before initial treatment, the VEGF levels in serum and pleural effusion of distant metastasis group were significantly higher than those of without distant metastasis group(P<0.05).There was a correlation between the level of VEGF and the malignant pleural effusion(r=0.878, P<0.05).No correlation existed between VEGF level and benign pleural effusion.The content of sVEGF-A in serum had no statistical difference in cancer group and benign group.Effusion supernatants of pVEGF-A content in lung cancer group were higher than those in benign effusion group(P<0.05).pVEGF-A and sVEGF-A levels were similar in benign effusion group. Effusion supernatants pVEGF-A in malignant group was higher than that in benign effusion group(P<0.05).pVEGF-A was significantly higher than that of sVEGF-A in malignant effusion(P<0.05).Serum VEGF-C, VEGF-D content had no significant difference between cancer group and benign group. pVEGF-C, pVEGF-D content had no significant difference between cancer group and benign group.Conclusion Level of VEGF in serum and pleural effusion detection would help to diagnose and differentially diagnose benign and malignant pleural effusion.Effusion VEGF-A is different in benign and malignant effusion, which may become benign and malignant effusion tumor markers.

Objective To evaluate the effects of propofol on the intracellular calcium ion concentration ([Ca2+ ]i) and nuclear factor kappa B (NF-κB) activity in hippocampal neurons of fetal rats in vitro .Methods Ten pregnant Sprague-Dawley rats at 16-18 days of gestation ,were sacrificed and the fetal rats were taken out from the abdominal cavity .The hippocampal neurons of the fetal rats were isolated and seeded in culture plates .After being cultured for 9 days ,the neurons were divided into 7 groups ( n=12 each ) using a random number table :control group (C group) ,intralipid group (I group) and propofol 0.1 ,1 ,10 ,100 ,1 000 μmol/L groups (P1-5 groups) .In group I ,10% intralipid was added to the culture media until the final concentration reached 100μmol/L .In P1-5 groups ,propofol was added to the culture media until the final concentration reached 0.1 ,1 ,10 , 100 and 1 000μmol/L ,respectively .The cells were then incubated for 3 h .The [Ca2+ ]i and cellular morphology of hippocampal neurons were examined by laser scanning confocal microscopy before incubation with propofol and within 10 min after the end of incubation with propofol .The expression of NF-κB protein in the nucleus was detected at 7 days after the end of incubation with propofol by Western blot analysis to reflect NF-κB activity . Results Propofol increased [Ca2+ ]i in P2-4 groups ,while decreased [Ca2+ ]i in group P5 ( P<0.05 ) .Compared with group C ,the activity of NF-κB was significantly decreased in P1-5 groups ( P<0.05 ) ,while no significant change was found in C and I groups ( P>0.05 ) .The structure of hippocampal neurons was normal in C ,I and P1 groups .The branchings of axons and dendrites in hippocampal neurons were significantly decreased in P 2-4 groups , while the structure of hippocampal neurons became fuzzy , the cell membrane was destroyed and the axons and dendrites were not seen in group P5 .Conclusion Propofol can produce neurotoxic effects on hippocampal neurons of fetal rats by changing the [Ca2+ ]i and promoting NF-κB activation in vitro .