Objective:By monitoring the lung compliance,oxygenation index(OI),CC16、IL-8 in plasma,observe whether the protective lung ventilation in patients undergoing gynecological laparoscopic surgery can improve the respiratoryw function and reduce lung injury.Methods:40 cases of ASA grade Ⅰ-Ⅱ were selected,and 40 patients were treated by elective laparoscopic radical resection of cervical cancer.The patients were divided into two groups according to the random number table method in 40 cases.Mechanical ventilation in general anesthesia,A group used traditional intermittent positive pressure ventilation mode,tidal volume is set to 10ml/KG (PBW);B group used lung protective ventilation strategy,tidal volume is set to 6ml/KG (PBW) + 5cmH2O PEEP + recruitment manoeuvres.For patients before pneumoperitoneum(T0),2 hours after pneumoperitoneum (T1),4 hours after pneumoperitoneum (T2)MAP,HR,CVP,RR and C were observed.In pneumoperitoneum (T0),2 hours after pneumoperitoneum(T1),4 hours after pneumoperitoneum (T2),2 hours after operation(T3),24 hours after surgery(T4) venous,IL-8,CC16 content detection.Results:Before pneumoperitoneum,two groups of patients with pulmonary compliancethe difference was statistically significant(P ＜0.05).Compared T1 、T2 with T0 in A group and B group,the pulmonary compliance all decreased and there existed significant deference(P＜0.05).Notably,A group decreased evidently(P＜0.05).T0,T1,T3,T4 time points in two groups of patients with oxygenation index,the difference was statistically significant (P ＜ 0.05).Two groups of patients with CC16,IL-8content in T1,T2,T3,T4 time point,the difference was statistically significant (P ＜ 0.05).Conclusions:Lung protective ventilation strategy can improve respiratory function in patients with gynecological laparoscopic surgery,and reduce the incidence of lung injury.

Objective To evaluate the clinical features and prognosis of patients with complete left bundle branch block(CLBBB)following transcatheter device closure of ventricular septal defect(VSD)closure. Methods Clinical feathers of 11 patients with postoperative CLBBB in Department of Pediatric Cardiology,Guangdong General Hospital from January 2011 to December 2013 were collected and reviewed retrospectively. They were treated with dif-ferent protocol based on the appeared time of CLBBB occurrence and clinical symptoms. The patients were followed up, and the prognosis was recorded. Results The median age of 11 patients was 3. 9 years(3. 4 to 17. 5 years old). The median interval of intervention therapy to first attack of CLBBB was 2. 8 months(1 day to 25. 4 months). CLBBB oc-curred within 1 week to 1 month postoperatively in 4 patients,another 1 case suffered from CLBBB between 1 week to 1 month postoperatively,meanwhile 6 cases underwent CLBBB after 6 months postoperatively. The longest term of CLBBB attack postoperatively was 25. 4 months in 1 patient. The electrocardiograms on 5 patients returned to normal by only drug treatment. However,3 patients failed to recover with drug therapy,2 of them undertaken surgical procedure to re-move the occluder associated with VSD repair,1 patient recovered to normal and another converted to incomplete right bundle branch block. One of them refused to undertake surgical procedure and still bothered with persistent CLBBB. Another 3 cases did not receive special treatment due to the later attack of CLBBB(≥6 months)without clinical symp-toms. By the end of observation,the electrocardiogram(ECG)in 4 patients returned to normal,4 patients presented with persistent CLBBB. One patient's ECGs were presented with right bundle branch block. After ECG successfully returning to normal ECG by drug therapy,2 patients relapsed during follow - up,and 1 of them developed to an enlarging left ven-tricle and heart failure which led to death. Conclusions CLBBB may occur in short or long - term after VSD closure. ECG may become normal after early and appropriate treatment postoperatively. Systolic dyssynchrony and cardiac dys-function may be caused by persistent CLBBB. Therefore,patients with CLBBB after VSD closure should be treated ap-propriately without delay,and more frequent and longer follow - ups are required.

Objective To evaluate the clinical efficacy of 5-aminolevulinic acid-photodynamic therapy (ALA-PDT) combined with imiquimod for basal cell carcinoma( BCC).Methods 38 patients with BCC were randomly divided into two groups.ALA-PDT plus imiquimod were given in the treatment group (19 patients) , and the control group(19 patients) were treated with only ALA-PDT.All patients were followed for one year,and the efficacy and relapse rate were observed.Results The cure rate and the recurrence rate of the treatment group was 94.74% ( 18/19) and 5.26% (1/19) .however,those of the control group was 68.42% (13/19) and 31.58% (6/19).There was a statistical difference in the cure rate and recurrence rate between the two groups(x2 =4.37,P <0.05).Conclusion The efficacy and relapse rate of ALA-PDT combined with imiquimod was much better than those of ALA-PDT only in treatment of BCC.

Objective: To observe the effect of extracorporeal shock wave therapy (ESWT) on proliferation, cell cycle and intercellular adhesion molecule-1 (ICAM-1) expression in human umbilical vein endothelial cells (HUVECs). Methods: HUVECs were culturedin vitro at the concentration of (1×105/ml) and the cells were divided into 2 sets of groups:CSWT group, the cells were treated by different energy of (0.03, 0.09, 0.18, 0.24) mJ/mm2 respectively and corresponding Control group, in which the cells had no CSWT. HUVEC proliferation was detected by CCK colorimetric method, cell cycle was measured by lfow cytometry, mRNA and protein expressions of ICAM-1 were examined by RT-PCR and Western blot analysis respectively. Results: Compared with Control group, (0.09 mJ/mm2) CSWT group had promoted HUVECs proliferation,P<0.05 and the other CSWT groups were similar to corresponding Control groups,P>0.05; (0.09 mJ/mm2) CSWT group showed decreased proportion of G0/G1 stage and increased S and G2/M stages, allP<0.05; while (0.03 mJ/mm2) CSWT group only increased the proportion of G2/M stage,P<0.05 and the other CSWT groups were similar to corresponding Control group,P>0.05. Compared with Control group, (0.09 mJ/mm2 ) and (0.03mJ/mm2) CSWT groups showed increased mRNA expression of ICAM-1 (9.27±0.95) vs (1.02±0.27),P<0.001 and (7.08±0.60) vs (1.02±0.27),P<0.01; (0.09 mJ /mm2) CSWT group had elevated protein expression of ICAM-1,P<0.05. Conclusion: ESWT especially at (0.09 mJ/mm2) may accelerate cell cycle transition from G0/G1 stage to S and G2/M stages, promote HUVECs proliferation and increase ICAM-1 expression which may play important roles in ESWT facilitated angiogenesis in vitro.

BACKGROUND:Studies have shown that extracorporeal shock wave therapy is an effective, safe, and non-invasive treatment for ischemic heart disease, which can improve angiogenesis in the ischemic myocardium. OBJECTIVE:To summarize the research advances in promotion of angiogenesis for ischemic myocardium by extracorporeal shock wave therapy. METHODS:A computer-based online search of PubMed database and CNKI database was performed for relevant articles published between 1998 and 2014 with key words of “shock wave, ischemic heart disease, angiogenesis, cytokine, stem cel” in English and Chinese, respectively. Articles related to the promotion of angiogenesis for ischemic cardiovascular disease by extracorporeal shock wave were selected. Repetitive articles were excluded. According to inclusion criteria, 51 literatures were selected in result analysis. RESULTS AND CONCLUSION: Extracorporeal shock wave therapy can improve angiogenesis in the ischemic myocardium by mobilizing proliferation and differentiation of stem cels into vascular endothelial cels, and by enhancing the expression of growth factors such as vascular endothelial growth factor and basic fibroblast growth factor. Moreover, the extracorporeal shock wave therapy can create a local favorable microenvironment for angiogenesis by inhibiting inflammation, oxidative stress and apoptosis and by regulating components of the extracelular matrix. Extracorporeal shock wave therapy plays an important role in the angiogenesis of ischemic myocardium and displays a good clinical prospect in the treatment of ischemic heart disease. However, the specific mechanism requires further studies.

Objective To investigate the imaging features of hepatic epithelioid hemangioendothelioma (EHE) and to improve the level of awareness of this disease.Methods A retrospective analysis was conducted on the CT and MRI findings and the clinical data of 16 patients with liver EHE.The diagnosis was made on specimens obtained by liver biopsy or with operation.Six patients received only CT,6 only MRI,4 both CT and MRI,and 4 with DWI sequence.Results 6 of 16 patients with hepatic EHE had a solitary tumor while the remaining 10 patients had multiple tumors.CT scanning on 10 patients showed a heterogeneous mass with low density.In 4 patients,there were small calcifications in the lesions.The lesions on MRI showed a heterogeneous mass with low signal in T1WI and high signal in T2WI and DWI.In 8 patients,during enhanced scanning,the intrahepatic vein and its branches terminated at the edge of the tumor to form the lollipop sign. On the arterial phase lesions with a diameter ＞ 3 cm showed a centripetal enhancement pattern,which is similar to that of a haemangioma.Lesions with a diameter ＜ 3 cm showed ring enhancement and continuous annular enhancement in the portal venous phase and in the delayed phase.The best observation period for the number of lesions was in the arterial phase.Conclusion Hepatic EHE had certain distinct characteristics on CT and MRI,e.g.the lollipop sign,lesions with small calcification,lesions with a diameter ＞ 3 cm with a centripetal enhancement pattern,and lesions with a diameter ＜ 3 cm with continuous ring enhancement on CT scanning.These radiological features help in the diagnosis of the disease.

Objective To observe the protective effects of soluble Nogo-66 receptor (NgR1 )antagonist (sNgR1-Fc) on cortical axons after cortical infarction in rats,and to study the phenomenon and molecular mechanism of its protective effects on and regeneration of axons.Methods The cortical infarction was induced by photochemistry,termed photothrombotic cortical injury (PCI).Fifteen Sprague Dawley rats were randomly divided into three groups:Sham-operated group,PBS (phosphate buffered solution) group,and s-NgR1-Fc group.In PBS group,PBS was injected into the lateral ventricle of rats; and in sNgR1-Fc group,sNgR1-Fc was injected instead of PBS. The ipsilateral cortex with lesion was harvested for histomorphometry and transmission electron microscope observation 7 days after PCI. Proteins including GTP-RhoA,p-JNK,p-c-JUN and p-ATF-2 were detected by Western blot,as well as Total-J and Total-RhoA.Results The cortical infarction in rats was successfully induced by photochemistry.Compared with sham-operated group,the pathological changes in PBS groups were more serious,including extensive edema or disappearance of axoplasm of fiber without medulla sheath involved and extensive thickening or layer derangement in axoplasm of fiber with medulla sheath involved.These changes were improved significantly after sNgR1-Fc treatment.The levels of GTP-RhoA,p-JNK1,p-JNK2,p-c-JUN and p-ATF-2 in the PBS group were significantly higher than those in the sham-operation group ( P ＜ 0.05 ),whereas the levels of Total-RhoA,Total-JNKl and Total-JNK2 were not different significantly between these two groups (P ＞0.05 ).The sNgR1-Fc treatment up-regulated the levels of these proteins ( P ＜ 0.05 ).Conclusions There is pathological change in axon induced by cerebral hypoxia-ischemia for a long period after cortical infarction.The mechanisms may be associated with RhoA/ROCK/JNK/c-Jun signal way,which is activated by ischemia injury and related to the inhibition of regeneration in axon.Our study shows that NgR1-Fc may inhibit this pathway significantly,and then promote the regeneration of axon partially.

Objective To further prove the multipotentiality of rabbit bone mesenchymal stem cells (MSCs) by inducing it into cardiomyocytes with 5-azacytidine. Methods MSCs from rabbit were abstracted, isolated, cultured. Then MSCs were induced by 5-azacytidine in vitro for 24 hours. After cultured for 4 weeks, MSCs’ differentiation was studied by immunohistochemistry and electron microscopy technique. Results Some of MSCs induced by 5-azacytidine expressed troponinT . Electron microscopy showed myofilaments. Conclusion MSCs which exist in bone marrow are mutipotential stem cells, and they can be induced into cardiomyocytes by 5-azacytidine in vitro.

To explore the dynamic expression and role of Aquaporin5 (AQP5) in lung development and hyperoxia lung injury, gestation 21-day Sprague-Dawley (SD) rats (term=22 days) were randomly assigned to air group and hyperoxia group within 12-24 h after birth. The rats in hyperoxia group were continuously exposed to about 85% oxygen and those in air group to room air. After 1 to 14 days of exposure, total lung RNA was extracted and the expression of AQP5 mRNA was detected by reverse transcription polymerase chain reaction (RT-PCR). Immunohistochemistry and western-blot were used to detect the expression of AQP5 protein. The results showed that the expression of AQP5 in premature rats lung could be detected at various time points after birth, and the positive staining was restricted to the type I alveolar epithelial cells. In air group, the AQP5 expression was detected in a very low level at day 1, but exhibited a persistent increase after birth. Compared with the air group, the expression of AQP5 in hyperoxia group was increased at day 1, and had significant difference in mRNA level (P<0.05), but decreased significantly in mRNA and protein levels after 4 to 14 days (P<0.01 or P<0.05 respectively). It was concluded that AQP5 might play a key role in the alveolar period of premature rats by regulating the lung water balance. Hyperoxia exposure leads to a down-regulation of the AQP5 expression, which may be an important factor for the development of hyperoxia lung injury.

Objective To observe the effects of hyperoxia on Notch 1 receptor of alveolar epithelial type Ⅱ cells (AEC Ⅱ), in a hetcrocellular culture of alveolar epithelial type Ⅱ cells and lung flbroblasts(LF), in order to explore Notch signaling in hyperoxic induced lung injury and thus make theoretical basis for prevention and treatment of a acute/chronie neonatal lung injury. Method Twelve Spragne Dawkey female rats with 200～220 g and 3 Spragne Dawkey male rats with 220～250 g were offered from experimental animal centre of Tongji Medical Colleege, Huazhong University of Science and Technology. The AEC Ⅱ/ LF co-culture system was established successfully. AEC H s from premature rats were randomly assigned to 2 groups: air control group and hyperoxia group. Air control group was kept in room air 50% ml/L CO2 enviromnent at 37°C, while hyperoxia group was exposed to 950 ml/L O2 + 250 ml/L CO2. Immuno-histochemistry was taken to detect Notch 1. Fluorescent quantitafive PCR was used to quantify the Notch 1 mRNA. MTT method was taken to assess cen proliferation viability.Flow eytometry double label method was used to detect cell percentages. Results In hyperoxia group:Notch 1 activation was inhibited, and Notch 1 mRNA decreased to 0.43,0.29,0.11,0.03 fold of control (95% confidence limit). AEC Ⅱ percentage descended predominantly[ 24 h hyperoxia group vs. control group: (68.92±6.88)%vs. (90.35±4.01)%, P =0.006;48 h hyperoxia group vs. control group: (38.03±3.27) vs. (61.47±4.81)%, P =0.000;72 h hyperoxia group vs. control group:(20.13±4.45)% vs. (52.05±3.35)%, P =0.000;96 h hyperoxia group vs. control group:(8.17±1.99)% vs. (52.59±2.93)%, P =0.0001 while that d AECI rised[24 h hyperoxia group vs. contrd group:(0.11±0.03)% vs. (0.01±0.01)%, P=0.006;48h hyperoxia group vs. control gnmp:(49.73±3.45)% vs. (16.13±2.13)%, P =0.000;72 h hyperoxia group vs. control group: (52.43±3.14) % vs. (5.98±0.95) %, P = 0.000;96h hyperorxia group vs. control group:(19.85±3.26)% vs. (29.03±3.16)%, P =0.007]. Comclusions Hyperoxia may inhibit Notch signaling pathway, which can weaken proliferation and disdifferentiation of AEC Ⅱ s. Investigations on how to control Notch signaling will provide fresh thoughts for alveolar epithelium repairing.