Objective To establish a novel liver and lung metastatic tumor model in nude mice by splenic inoculation of hilar cholangiocarcinoma cell line.Methods Human hilar cholangiocarcinoma cell line(FPH-0201) cells was established and cultured with a fresh human hilar cholangiocarcinoma specimen.The spleen of 7 nude mice was injected with 0.1ml of hilar cholangiocarcinoma cell suspension(1.5?10~7 cell).The tumor appearing time,tumor local and metastatic formation rate,histological,morphological and ultrastructure of metastatic tumor cell were observed.The sub-cell line was obtained by cutture of metastatic specimen,and sub-cell line cells were again injected into the lower pole of the spleen and metastatic tumor formation rate was observed again.Results The overall local tumor formation rate in spleen was 100%,and metastatic tumor formation rate was 14.3%.The sub-cell line cells that were re-inoculated in mice spleen,had a metastatic tumor formation rate of 100%.Morphological observation of metastatic tumor showed the common features of cholangiocarcinoma.Chromosome number showed a variation of 18~44.Conclusions The hilar cholagiocarcinoma metastatic tumor model that was established in this laboratomy had characteristics compatible with malignant tumor and had all the biological characteristics of human hilar cholagiocarcinoma.

To investigate the effects of TGF?antisense oligodexynucleotides(ASODN) and EGFR ASODN on human rectal carcinoma cell line HR8348. Cationic liposome, lipofectamine, were selected as delivery vector HR8348 cells were treated with ASODN in vitro. HR8348 cells with or without pretreatment were inoculated into nude mice. The proliferation and DNA synthesis of HR8348 cells treated with TGF-? ASODN and EGFR ASODN were greatly inhibited, and tumorigenic rate was also greatly reduced. TGF-? ASODN and EGFR ASODN could inhibit the proliferation of human colon cancer cell line in vitro as well as in vivo, the results implicate. The potential value in colorectal cancer gene therapy.

Objective To observe the characteristic, mechanisms and the change of pathophysiology about thoracic explosive injury from an explosive device. Methods Seventy-three millimetres prefabricated steel-ball bomb was used to be the center of explosion. According to the distance from each group to the center of explosion, 30 sheep were randomly divided into 5 groups. The injuries of thoracic wall, lung and surrounding organs were observed from fragments and blast wave. Results The mortality of thoracic explosive injury on the ground testing was 56.7%.Most of fragment wounds were blind wound. The track of wounds was often complicated and curved. The major associated injuries were myocardial contusion, splenic-hepatic rupture and gastric-enteric rupture. There were much severe pulmonary hemorrhage and lung edema. The parameters of trauma were well correlated with the severity of thoracic injury.　Conclusion The parameters of trauma were well correlated with the severity of thoracic injury. The characteristic of thoracic injury from explosive device was more complicated and severe.

Objective　To study the effect of gadolinium chl oride hexahydrate (GDCL3) on the structure and lipid peroxide (LPO) of rat hep atocellular mitochondria during liver cold ischemia storage. 　Methods　Forty Wistar rats were randomized into 8 gr oups ( 5 in each group). Group 1～4 served as control. The other 4 groups were p retreated with GDCL3 (7mg/kg). The ultrastructures of hepatocellular mitocho ndria were observed by electron microscope and LPO of hepatocellular mitochondri a were investigated. 　Results　LPO o f hepatocellular mitochondria in group 1h, 2h, 3h pretreated with GDCL3 for 1、 2、 3 h were 1.0±0.3、1.7±0.2、2.0±1.0, LPO was suppressed sign ificantly compared with control group (2.2±1.0、2.8±1.0、3.5±1.0、 P<0.05). With time prclonging of liver storage, the damage of hepatocellular mitochondria ultrastructure became more severe and LPO of hepatocellular mitoch ondria increased significantly. Pretreated with GDCL3, the damage of hepatocel lular mitochondria ultrastructures were lessened and the elevation of LPO was s uppressed significantly (1 hour、 2 hours、3 hours，P<0.05). 　Conclusion　Mitochondria damage is one of the sensitive characters of liver cold ischemia injury, GDCL3 inhibits rat hepatoc ellular injury during liver cold ischemia storage.

Objective:To investigate the correlation between ankle-brachial index(ABI)and intracranial atherosclerosis in patients with ischemic stroke.MetlaTds:qhe ABI of 73 patients with ischemic stroke were detected using vascular Doppler ultrasound;head magnetic resonance angiography(MkA)was performed using a 1.5 T magnetic resonance imahing system,and the extent of intracranial artery stenosis was graded.The correlation between ABI and the grade of intracranial artery stenosis in patieras with ischemic stroke was analyzed.Results:The ABI in patients without intracranial artery stenosis(n=38)was significantly higher than those with intracranial artery stenosis(n=35)(0.975±0.114 vs 0.837±0.096,P<0.001).The ABI was significantly negatively correlated with the extent of intracranial artery stenosis(r=-0.736,P=0.001).Conclusions:The ABI was negatively correlated with the extent of intracranial artery stcnosis.It can he used as a preliminary screening means of intracranial atherosclerosis.

OBJECTIVE:To establish a method for content determination of cyproheptadine hydrochloride in fuyan cream.METHODS:Ultraviolet spectophotometry was applied to determine the contents of cyprohepatadine hydrochloride as well as its adjuvant as two coexisting components without isolation and extraction,the wavelengths were286nm and258nm res_ pectively,linear regression and simultaneous equations were used to analyze the results.RESULTS:Cyproheptadine hydrochlor_ ide and its adjuvant showed good linear relationship in the range of2.52～25.2and2.5022～25.022?g/ml respectively,the average recovery of cyproheptadine hydrochloride was98.61%(RSD=1.08%).CONCLUSION:The present method is simple,convenient,reproducible and reliable,which is suitable for rapid determination for fuyan cream.

Objective To study the effect of adaptive support ventilation (ASV) in treatment of severe asthma.Methods Forty-nine cases of severe asthma were divided into ASV group (25 cases) and control group (24 cases,tradition mechanical ventilation).The arterial blood gas,respiratory dynamics,mechanical ventilation time,hospital stay and thorax barotrauma was compared between two groups.Results The arterial blood gas and respiratory dynamics was improved after mechanical ventilation compared with that before mechanical ventilation in two groups,and there was significant difference (P ＜ 0.05 or ＜ 0.01).The airway peak voltage,lung dynamic compliance and platform pressure after mechanical ventilation of 2,12 and 24 h in ASV group was better than that in control group[2 h:(33 ± 12) cm H2O(1 cm H2O =0.098kPa) vs.(37 ± 11) cm H2O,(16 ± 9) ml/cm H2O vs.(17 ± 10) ml/cm H2O,(27 ± 6) cm H2O vs.(30 ±12) cm H2O; 12 h:(23 ± 12) cm H2O vs.(25 ± 11) cm H2O,(28 ± 6) ml/cm H2O vs.(23 ± 10) ml/cm H2O,(20 ±6) cm H2O vs.(25 ±4) cm H2O; 24 h:(18 ± 12) cm H2O vs.(20 ± 11) cm H2O,(32 ±9)ml/cm H2O vs.(28 ± 10) ml/cm H2O,(12 ±7) cm H2O vs.(16 ±7) cm H2O],and there was significant difference(P＜ 0.05 or ＜ 0.01).The mechanical ventilation time and hospital stay in ASV group was shorter than that in control group [(46 ± 8) h vs.(56 ± 6) h,(7 ± 2) d vs.(10 ± 3) d],and there was significant difference (P＜ 0.01).The thorax barotrauma was not observed in ASV group; 3 cases showed subcutaneous emphysema and 2 cases showed pneumothorax in control group.Conclusions ASV mode could decrease airway peak voltage and platform pressure,improve arterial blood gas and lung dynamic compliance,shorten mechanical ventilation time and hospital stay.It is safe and effective for patients with severe asthma.

Objective To investigate the changes of coagulation function and blood rheology in acute exacerbation of chronic obstructive pulmonary disease (AECOPD) and effects of depside salt from salvia miltiorrhiza.Methods The patients with AECOPD were randomly divided into depside salt from salvia miltiorrhiza anticoagulation group (45 patients) and conventional treatment group (45 patients).At the same time 50 normal were choosed as control group (50 patients).On the 14th day after treatment,4 indexes of coagulation,D-dimer and of blood rheology in depside salt from salvia miltiorrhiza anticoagulation group and conventional treatment group were determine and compared with those of normal control group.Results The levels of Fbg (4.6 ± 0.7) g/L and D-dimer (1.58 ± 1.13) mg/L were significantly different between depside salt from salvia miltiorrhiza anticoagulation group and normal controls.After depside salt from salvia miltiorrhiza anticoagulation,The levels of FbgFbg (3.3 ± 1.2) g/L and D-dimer (0.48 ± 0.36)mg/L were decreased significantly (P ＜ 0.01).The 1 evels of Fbg (3.3 ± 1.2) g/L and D-dimer (0.48 ± 0.36)mg/L were decreased significantly in depside salt from salvia miltiorrhiza anticoagulation group compared with those in Conventional treatment group (P ＜ 0.01).But PT,APTT and TT level were not significantly different in three groups (P ＜0.05).After treatment,hemodynamic indexes:whole blood high shearing viscosity (4.76 ± 1.35)mPa.S,low shearing viscosity (8.69 ± 2.36) mPa.S plasma viscosity (2.32 ± 0.26) mPa.S and hematocrit (40.3 ± 2.38)％ in depside salt from salvia miltiorrhiza anticoagulation group indicated significant differences compared to those in Conventional treatment group[(5.50.3 ± 1.34) mPa.S,(12.30 ± 2.30) mPa.S,(2.32 ± 0.26) mPa.S,(47.89 ± 3.13)％)] (P ＜ 0.01).Conclusion Patients with in AECOPD have hypercoagulable state.depside salt from salvia miltiorrhiza could improved hypercoagulable state in acute exacerbation of chronic obstructive pulmonary disease and decrease blood viscosity.

Objective To investigate the factor related to atherosclerosis of carotid artery. Methods Carotid arteries of 142 conscious patients with cerebral infarction (CI) and 78 without cerebrovascular disease (NCVD) were detected with color Doppler ultrasonography. Results Atherosclerotic plaques were found in 64.8% (92/142) patients with CI, and in 28.0% (22/78) NCVD patients (P<0.01). Logistic regression analysis showed that incidence of atherosclerotic plaques correlated with age, hypertension, and diabetes mellitus (P<0.01). Conclusion Formation of atherosclerotic plaques is a risk factor to CI, and related with age, hypertension, and diabetes mellitus.

BACKGROUND:Cytochrome P450 ( CYP) epoxygenases metabolize arachidonic acids ( AA) to form epoxyeicosatrienoic acids
(EETs), which exert beneficial roles in the treatment of cardiovascular diseases , but little is known about its role on adventitial remo-deling.METHODS:We used C57BL/6J mice in vivo and primary rat adventitial fibroblasts ( AFs) in vitro treated with angiotensin II (Ang II) to investigate the effects of CYP2J2 gene delivery and exogenous EETs administration on adventitial remodeling .RESULTS:CYP/sEH system was found to exist in human adventitia , and involved in adventitial remodeling process .Exogenous EETs administra-tion significantly inhibited Ang II-induced AFs activation , characterized by differentiation , proliferation, migration, and collagen syn-thesis.These protective effects were partially reversed by PPARγantagonist GW9662 pretreatment or SOCS3 siRNA transfection.EETs suppressed Ang II-induced IκBαphosphorylation , subsequent NF-κB nuclear translocation via PPARγdependent signaling pathway in AFs.Additionally, EETs reduced Ang II-induced JAK2, STAT3 phosphorylation and subsequent phosphor-STAT3 nuclear transloca-tion, which were mediated by SOCS3 induction but independent of PPARγactivation.Furthermore, rAAV-CYP2J2 gene delivery re-duced vessel wall thickening , AFs differentiation , proliferation and collagen deposition in aortic adventitia induced by Ang II infusion , which were mediated by NF-κB and SOCS3/JAK/STAT signaling pathways in blood pressure-dependent and -independent manners , re-spectively.CONCLUSION:We concluded that CYP2J2 overexpression attenuated Ang II-induced adventitial remodeling via PPARγ-dependent NF-κB and PPARγ-independent SOCS 3/JAK/STAT inflammatory signaling pathways .