Objective To determine the difference of microvessel density(MVD) in each layer and region of abdominal flap. MethodsFlaps were obtained from 60 patients with abdominal operations,10 in each of the regions from I to VI.The vascular endothelial cells were marked with CD34 by immunohistochemistry,and the MVD in each region and layer of the abdominal flaps was determined.Results The vascular net of abdominal flap was divided into five layers: papillary layer of corium,papillary underlayer of corium,papillary deep layer of corium,superficial fascia and deep fascia.The mean MVD of the five layers were 17.80?1.68,9.12?1.84,27.91?2.44,37.18?6.55 and 46.91?7.02,respectively,with significant differences among them(P0.05).Conclusion Anatomic factors may be responsible for the survival of large abdominal flaps.Either of the direct and retrograde motion is feasible in the transplantation.

Objective To investigate the changes of SCD 14, TNF-?, E-SLT and IL-10 level in the process of infection.Methods Serum E-SLT, IL-10, SCD 14 and TNF-? level was measured in 37 patients of abdominal trauma, and in model rabbits with endotoxemia.Results Serum level of SCD 14,TNF-?,E-SLT and IL-10 on the 1st to 3rd day post-op increased significantly in patients suffering from post-op infection 〔(1.61?0.47)??g/ml, (28.63?8.29)?pg/ml,(153.6?48.9)?ng/ml and (38.21?10.87)?pg/ml, compared with control, all P

In this study, nattokinase gene was amplified by PCR using bacillus subtilis chromosomal DNA as template and cloned into expressed vector pBV220. After transforming recombinant plasmid into E.coli HB101, the recombinant strain was yielded. It was proved that expression products was secretive and expression protein was 12% of total cell protein by SDS-PAGE. Optimum culture time and inducing time was determined as 6h and 5h respectively. The plasmid stability studies showed that recombinant plasmid has excellent segregational stability but the structural stability was not good in the host cell.

Dibenzothiophene (DBT) was used as a model compound. A bacteria strain, which can degrade dibenzo-thiophene efficiently, was obtained. This strain was identified as Pseudomonas stutzeris UP-1 according to its morphological, physiological and biochemical characters, and 16S rDNA sequence. The strain exhibits strong degradation capacity of DBT, and the end product of degradation is a kind of soluble compound. After the analysis of product of DBT degradation, it was deduced that the degradation of DBT by Pseudomonas stutzeri UP-1 is in accordance with the Kodama mechanism.

Hirudin (HV) is known as the most potent and specific inhibitor of thrombin. Although hirudin has many advantages , it has the bleeding side effect and this is the great shortage of hiudin for clinical application. In order to alleviate bleeding side effect of hirudin, fusion protein, named as FHV (fusion hirudin linked with FXa recognition peptide) was designed. The fusion protein gene ( fhv) was cloned into plasmid pPIC9K. FHV engineered Pichia pastoris containing high copies was chosen for fermentation and purification at 30 L fermentor scale, finally, FHV with purity of above 97% was obtained. To investigate the function of FHV in vivo, mouse tail thrombosis model was used. In the mice thrombus tail model induced by carrageenan, FHV decreased the length of tail thrombus significantly, similar to that of HV control, and had no obvious effects on the TT, PT and APTT. In conclusion, FHV is constructed and expressed in yeast. FHV fusion proteins is obtained by fermentation and purification. FHV has antithrombotic effects not influencing IT, PT and APTT after administration immediately in animal models. Therefore, FHV is a promising anticoagulant and antithrombotic drug.

Objective To investigate the importance of plasmid-mediated quinolone resistance in the development of quinolone resistance in clinical isolates of gram-negative bacteria.Methods A total of 541 consecutive clinical isolates of gram-negative ba- cilli resistant or intermediate to ciprofloxacin were screened for the qnrA gene by PCR.Conjugation experiments were carried out with azide-resistant E.coli J53 as a recipient.The aac(6')-Ib-cr gene was detected.The mutations in the quinolone-resist- ance-determining region (QRDR) of the gyrA and parC genes were identified in qnrA positive strains.Results qnrA was identi- fied in 7 of the 541 strains.Among the qnrA positive strains,5 were Enterobacter cloacae.No qnrA was detected in nonfer- menters.Quinolone resistance was transferred in 4 of 7 qnrA positive strains.Transconjugants had 12-to 125-fold increases in MIC of ciprofloxacin relative to that of the recipient.Seven strains contained qnrA with a nucleotide sequence identical to that originally reported.Two transconjugants with higher ciprofloxacin MICs contained aac(6')-Ib-cr gene.Mutations occurred in the QRDR of the gyrA and parC genes in 5 PCR-positive clinical strains.Conclusions Transferable plasmid-mediated quinolone resistance associated with qnrA is highly prevalent in clinical strains of Enterobacter spp.aac(6')-Ib-cr gene and mutations in the quinolone targets may co-exist with qnrA,which may contribute to the further increase of resistance to quinolones.

Objective To explore the effects of overexpression of hypoxia inducible factor 1? (HIF 1?) mRNA on vascular endothelial growth factor (VEGF) and novoendotheliasis in venous autografts Methods Wistar rats were randomly divided into two groups with 28 rats in each group A rat experimental model of autogenous vein graft was established by transplanting the right external jugular vein into between the interrupted right common carotid artery The transplanted vein in the experimental group was first immersed into a solution containing recombinant adeno associated virus (rAAV) HIF 1? for 45 minutes Vein grafts and blood simples were taken at 7 or 14 days after transplantation RT PCR, ELISA, immunohistochemistry were used to detected HIF 1? mRNA and VEGF expression Results HIF 1? mRNA and VEGF protein remarkably increased in experimental group, and serum level of E selectin significantly decraesed at day 14 The novoendotheliasis and myo endothelium junction in vein grafts were remodeled at day 14 in the experimental group Conclusion Re establishment of the structure and function of the autograft vein graft endothelium was accelerated by overexpressed HIF 1? mRNA

Objective To study the protective effect and mechanism of ganciclovir(GCV) on acute cerebral injury of mice caused by herpes simplex virus(HCV). Methods Mice model of acute cerebral injury caused by HCV were established, morphological changes in the brain tissue of mouse treated with GCV were observed under the electronic microscope, and the mortality were compared. The HSV - I DNA copies of brain tissue were detected by fluorescent quantitative polymerase chain reaction. Results In the infected model group, there were obvious swelling, karyopyknosis and destruction of the structure in the brain cells, as well as myelin sheath solution and vacuolar degeneration in the mitochondrion and crest were destroyed. There were the virions in the nucleolus. With the GCV treatment, the symptoms were improved, the mortality much lowered, the yields of HSV - I DNA much lower. Conclusions GCV may restrain replication of HSV-Ⅰ effectively and lower the mortality of mice with acute cerebral injury caused by herpes simplex virus significantly.

Objective To investigate the features and significance of pathologic changes in apoptosis of small bowel allograft during acute rejection in rats. Methods All 24 recipients were equally divided into four groups ; group A: nonoperative control; group B: allograft ; group C: isograft, group D: treatment control. The graft samples were harvested on day 3, 5, 7, 10 after transplantation, and subjected to histologic examination . Mucosal thickness, villous height and crypt depth were measured, and apoptotic cells of intestinal mucosa of grafts on day 3,5 and 7 after transplantation were examined. Results The mucosal structure was normal in group A; The degree of the inflammatory infiltrated cells ,intestinal mucosa cell apoptosis and structural injury of mucosa in group B were significantly severe compared with groups C and D. As the post-transplanted time increased, the number of musocal apoptotic cells and the degree of mucosal structural injury were significantly increased. The degree of mucosal structural injury in group C was milder than in group B. A few infiltrated cells and mild edema of mucosa occurred in group D , but no mucosal structural injury was found. Conclusions Inflammatory cell infiltration, mucosal epithelial cell apoptosis and mucosal structural damage are the main pathologic features of small bowel allograft during acute rejection. Dynamic observation of the pathologic changes and cell apoptosis of small bowel graft is of certain value in the diagnosis of acute rejection of small bowel graft and in assessment of the degree of small bowel injury.

Objective To study the effects of nitric oxide (NO) and endothelin-1(ET-1) on cholestasis liver fibrosis. Methods Forty-eight Wistar rats were randomily divided into 3 groups:the control group,the common bile dute ligation(CBDL)group,and the CBDL plus lactulose group.The animals were killed on the 3rd,7th,14th, and 21th days respectively to determine the contents of plasma endotoxin,NO,ET-1, and transaminases(ALT,AST).The degree of hepatic fibrosis was observed by microscopy and the ultrastructural changes of liver were observed by electron microscope. Results After common bile dute ligation,the contents of plasma ET-1 and NO increased significahtly,the plasma endotoxin level also increased and there were positive correlation between the levels of ET-1,and NO and the level of endotoxin.Plasma transaminases also increased greatly compared with those of the control group.The hepatic sinusoidal steonsis and widen Disse space were found.The diameter and number of fenestrate on hepatic sinusoid greatly decreased.Treatment with lactulose could partially alleviate all the pathological changes noted above. Conclusions NO and ET-1 may damage the "liver sieve"to cause the cholestasis liver fibrosis.