Objective To investigate the role of ischemic postconditioning(I-post) on intestinal mucosa in rats with ischemia-reperfusion (I/R) injury.Methods By using rat model of intestine I/R injury,32 male Sprague-Dawley rats were randomly divided into 4 groups: sham-operation group(S),I/R group(I/R),ischemic preconditioning group(IPC),and ischemic postconditioning group(I-post),respectively.The contents of malondialdehyde(MDA), the activity of superoxidase dismutase(SOD),and the activity of myeloperoxidase(MPO) in intestinal mucosa were measured respectively.The status of intestinal mucosa cellular apoptosis was detected by TdT-mediated dUTP-biotin nick end labeling(TUNEL).Chiu's count was used to assess the changes in intestinal pathological morphology.Results The content of MDA and activity of MPO were significantly reduced and the activity of SOD was enhanced in IPC group and I-post group compared with I/R group.There was obvious cellular apoptosis after reperfusion,and the apoptotic index in I-post group and IPC group was significantly lower than that in I/R group.Conclusion Ischemic postconditioning can result in protection against intestinal mucosa with I/R injury,which may be related to reducing the production of oxygen free radicals,maintaining the activities of antioxidant systems,and reducing intestinal mucosa cellular apoptosis.

Objective To investigate the effects of ischemic postconditioning (I-post) on intestinal mucosa mitochondrion after ischemia-reperfusion (IR) injury in rat intestine.Methods By using rat model of intestine IR injury,male Sprague-Dawley rats were divided into 4 groups:sham-operation group (S),IR group (IR),ischemic preconditioning group (IPC),and I-post group.Intestinal mucosa mitochondrial ultrastructural changes were observed by using transmission electron microscope (TEM).Mucosal cellular mitochondrial respiration function was studied by measuring the mitochondrial dehydrogenase-dependent reduction of MTT to its formazan derivative,and intestinal mucosal mitochondrial membrane potential was detected by confocal laser scanning microscopy.Results Compared with that in IR group,the injury of mitochondrion in I-post group and IPC group began to recover.The mitochondrial respiratory function and the mitochondrial membrane potential were significantly improved in I-post group and IPC group (P0.05).Conclusion The mechanism of ischemic postconditioning against IR injury of intestine in rats is partly related to maintaining the mitochondrial ultrastructural changes and respiratory function and improving mitochondrial membrane potential.

Objective Study the effect of induced differentiation of abscisic acid (ABA) on human HCC cell line SMMC-7221.Methods Cultured SMMC-7221 cells were treated separately with RPMI-1640 culture medium, HMBA and ABA with different concentrations. Firstly, the appropriate concentration of ABA which inhibits SMMC-7221 cell proliferation was selected with the modified MTT method. Then electron microscopy was performed to observe the changes of microstructure. The cell cycle was analyzed by flow cytometry. Results Apart from 4?10 -4mmol/L concentration of ABA, the others could inhibit the cell proliferation. The inhibition rate increased with the time prolonging and the concentration increasing. The effect was most obvious with 4?10 -3mmol/L ABA. At this concentration the cells were arrested in G0/ G1 phase (P

Objective To investigate the application of prenatal ultrasonograpy in diagnosis of fetal heart disease during the medium-term and terminal pregnancy,and to avoid misdiagnosis.Methods The prenatal ultrasonographic screening was conducted in 7020 pregnant women with medium-term and terminal pregnancy.All confirmed and suspicious cases of fetal heart disease were observed by echocardiography once 4 weeks until postnatal sixth month to 1 year while normal cases was traced at the intervals of 8 weeks.All the cases were confirmed by autopsy or surgery while part of them were confirmed by postnatal angiocardiography before surgery.The reasons of misdiagnosis were analyzed.Results In fifty-three cases of fetal cardiovascular abnormality,43 cases were found,2 cases were misdiagnosis while 8 cases were missed diagnosis.2 cases of misdiagnosis included 1 case of pulmonary valve stenosis and 1 case of tetralogy of Fallot.8 cases of miss diagnosis included 2 cases of inferior vena cava in ectopic drainage and 6 cases of ventricular septal defect (defect diameter ＜ 5 mm).The accuracy rate of diagnosis of fetal heart disease was 81.1 ％ by echocardiography.Conclusions Using high frequency probe,image zoom,enhancing the detection of vein-atrium connection and the structure of right ventricular outflow with pulmonary artery are important factors to avoid missed diagnosis and incomplete diagnosis.

Objective To investigate the application of transthoracic echocardiography (TTE) and 320-row CT in diagnosis of complex congenital heart disease(CCHD).Methods A retrospective analysis was performed in 68 patients with CCHD,which contained the echocardiographic apprarance,320-row CT and surgical outcoming.All of malformations were divided into three groups:intracardiac group,heart-large vascular connecting group and extracardiac group.Results One hundred and eighty-four malformations were comfirmed by surgery in the 68 cases.The misdiagnosis and missed diagnosis rate of CT and TTE:for the intracardiac anomalies were 12％ (11/93),1％ (1/93) respectively (P ＜ 0.05),for the heart-large vascular connecting malformation were 4％ (2/49),6％ (3/49) respectively (P ＞ 0.05),and for the extracardiac anomalies were 2％(1/42),19％(8/42) respectively (P ＜0.05),for the total anomalies were 8％(14/184),7％ (12/184) respectively (P ＞0.05).While it was 1％ (2/184) in diagnosis of total anomalies by both CT and TTE.Conclusions Both 320-row CT and TTE have their own advantages and shortcomings in the diagnosis of CCHD.Joint application of two methods could reduce the rate of misdiagnosis and missed diagnosis of CCHD.

Objective The aim of this study is to demonstrate the pathological characteristics about two types of pancreati‐tis ,providing new thinking about the mechanism of severe acute pancreatitis .Methods Thirty male Sprague‐Dawley rats were ran‐domly divided into three equal groups :sham‐operated (SO ,n=10) group ,mild acute pancreatitis (MAP ,n=10)) group and severe acute pancreatitis (SAP ,n=10) group ,all the rats were killed after 12 h of building model .Under the microscope ,we detected the pathological changes of pancreas ,liver ,lung and small intestine .The ultrastructure of pancreas ,liver ,lung and small intestine tissue were observed by transmission electron microscope .Results In SAP group ,congestion ,edema ,inflammatory cell infiltration ,lea‐king of blood componedts ,vascular endothelial injury and thrombosis of microcirculation were obviously observed .There is no ap‐parent pathological changes in the MAP group except the edema of pancreas .Conclusion Hemorrhage and necrosis are the main pathological characteristics in SAP rats ,has essential difference with MAP .These pathological characteristics provides us a new thinking for further study about the mechanism of SAP .

Objective To investigate the effect of caspases-3 on doxepin-induced apoptosis in rat neurons.Methods The PC12 cells seeded in culture plates were randomly divided into 4 groups (n =10 each) using a random number table:normal control group (group C);doxepin group (group D);caspase-3 inhibitor Z-DEVD-FMK group (group Z);doxepin + Z-DEVD-FMK group (group DZ).In group C,the cells were continuously incubated for 24 h.In group D,doxepin was added with the final concentration of 120 μmol/L,and the cells were continuously incubated for 24 h.In group Z,Z-DEVD-FMK was added with the final concentration of 10 μmol/L,and the cells were continuously incubated for 24 h.In group DZ,doxepin and Z-DEVD-FMK with the final concentrations of 120 and 10 μmol/L,respectively,were added,and the cells were continuously incubated for 24 h.After 24 h of incubation,the cell viability was detected by methyl thiazolyl tetrazolium assay,the cell morphology was observed under inverted microscope,and the neuronal apoptosis was measured by flow cytometry.Apoptosis rate was calculated.Results Compared with group C,the cell viability was significantly decreased,and apoptosis rate was increased in D and DZ groups (P＜0.01),and no significant change was found in the parameters mentioned above in group Z (P ＞ 0.05).Compared with group D,the cell viability was significantly increased,and apoptosis rate was decreased in group DZ (P＜ 0.01).The morphological changes were significantly mitigated in group DZ as compared with group D.Conclusion Caspases-3 may mediate doxepin-induced apoptosis in rat neurons.

【Objective】 To understand the antigen profile and antibody frequency of Wr^a in voluntary blood donors in Shaanxi province. 【Methods】 Wr^a antigen and antibody screening as well as blood group typing and antibody identification were performed by serological tests and confirmed by genetic testing. 【Results】 The incidence of Wr^a antigen in 7 490 voluntary blood donors was 0.013%(1/7 490), and the frequency of anti-Wr^a in 729 voluntary blood donors was 0.823%(6/729). 【Conclusion】 This study explored the polymorphism of Wr^a antigen and antibodies in blood donors, which is informative in the risk assessment of blood transfusion and the screening and identification of respective antibodies.

Objective: To explore the impact of PI3K-Akt-eNOS signaling on atrial fibrillation inducibility in diabetic rats. Method: Eight-week-old male diabetic rats were randomized assigned into GK group, IGF group and L-NAME group (n=8 each) which respectively received normal saline (NS), insulin like growth factor (IGF-1) or L-NAME+IGF-1 through tail vein daily for 4 weeks. Eight 8-week-old male homologous Wister-Kyoto(WKY) rats treated with intravenous NS served as control group (WKY group). Blood glucose was measured once per week. The left atrial diameter (LAD) was measured by echocardiography, the atrial electrical parameters, including the P-wave duration, the atrial effective refractory period (AERP) and its dispersion (AERP-d), the incidence and the duration of atrial fibrillation induced by atrial burst pacing, were evaluated by electro-physiological instrument at 4 weeks post various treatments. Rats were then sacrificed, left atrial (LA) cell morphology was determined on HE stained sections, LA interstitial collagen was determined on Masson stained sections. The protein expression of phosphatidylinositol 3-kinase (PI3K) and phosphate endothelial nitric oxide synthase (p-eNOS) were detected by Western blot. Results: (1) At the beginning of the study, the random blood glucose (GLU) level was significantly higher and LAD was large in GK, IGF and L-NAME groups than in WKY group;after 4 weeks, GLU level and LAD dimension of IGF group were lower than GK and L-NAME groups (P<0.01 or 0.05). (2) One rat in L-NAME group died during operation. Four weeks later, the incidence of atrial fibrillation in GK group, IGF group, L-NAME group and WKY group was 7/8, 2/8, 6/7 and 3/8. The median duration of atrial fibrillation in GK group, IGF group, L-NAME group and WKY group was 11.9(9.3, 13.1), 0(0, 1.8), 11.5(4.4, 12.0), and 0(0, 3.0) s. Compare with WKY group, the P-wave duration and PR interval were significantly longer, AERP-d, incidence, and duration of atrial fibrillation were significantly higher in GK group (P<0.01), these changed were significantly reversed in IGF group compared to GK and L-NAME groups (all P<0.01). Heart rate and AERP were similar among the 4 groups on (P>0.05). (3) Four weeks later, the CSA and CVF of LA were significantly larger in GK group than in WKY group (P<0.01), which were significantly reversed in IGF group (P<0.01 vs. GK group), and the beneficial effects of IGF disappeared by co-treatment with L-NAME (P<0.01 vs. IGF group). (4) Four weeks later, compare with WKY group, the protein expression of PI3K (P<0.01) and p-eNOS (P<0.05) of LA were significantly downregulated in GK group, which could be significantly upregulated by IGF (P<0.01 and 0.05 vs. GK group), these effects diminished by co-treatment with L-NAME (P<0.01 or 0.05 vs. IGF group). Conclusion Increased atrial fibrillation susceptibility in diabetic rat is linked with structural and electrical remodeling in LA, possibly mediated through downregulated PI3K-Akt-eNOS signaling.

BACKGROUND:Bone marrow mesenchymal stem cel s transplantation can inhibit experimental emphysema inflammatory reaction and apoptosis, and has been experimental y confirmed to treat severe lung function impairment. OBJECTIVE:To explore the inhibitory effects of bone marrow mesenchymal stem cel s transplantation via different ways on inflammatory reaction and apoptosis due to experimental emphysema. METHODS:Female Wistar rats were randomly divided into control group, intravenous group and endotracheal group fol owing model establishment using fumigation plus intratracheal instil ation of porcine pancreatic elastase. In the latter two groups, bone marrow mesenchymal stem cel s from male rats were injected via the tail vein and the trachea, respectively. In the control group, rats were given PBS via he tail vein and trachea. At 14 days after transplantation, pathological changes of rat lung tissues were observed, cel apoptotic index in alveolar wal cel s and tumor necrosis factorαlevel in the bronchoalveolar lavage fluid were detected. RESULTS AND CONCLUSION:Compared with the control group, in the intravenous and endotracheal groups,the pathological changes of lung tissues were relieved, tumor necrosis factorαlevel and apoptosis index were reduced significantly (P<0.01);but there were no differences between the intravenous and endotracheal groups (P>0.05). These findings indicate that bone marrow mesenchymal stem cel s transplantation via the tail vein and trachea both can exert obvious therapeutic effects on emphysema. Moreover, cel transplantation via the tail vein is more convenient and easier than that via the trachea in the treatment of emphysema.