1.Determination of microvessel density of abdominal flap
lu-de, YANG ; fan, LIU ; de, SHI
Journal of Shanghai Jiaotong University(Medical Science) 2006;0(03):-
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.
2.Research Advances in Molecular Biology of Vascular Restenosis
Jianghua ZHENG ; Yujuan LIU ; De SHI ;
Chinese Journal of Bases and Clinics in General Surgery 2003;0(04):-
Objective To review the research advances in molecular biology of vascular restenosis.Methods The literatures about molecular biology of vascular restenosis were reviewed.Results Current transgenic ways had some advantages and disadvantages. Gene therapy with HSV tk, Rb,p21,p27,p53,c myc, c myb, vascular endothelial growth factor,bFGF,platelet derived growth facfor,nuclear factor ?B and so on inhibited vascular restenosis.Conclusion A better transgenic system and gene combination therapy will be effective to treat vascular restenosis.
4.Effect of vitamin E and fructose 1,6-diphosphate on lipid peroxidation in erythrocytes during artificial total knee replacement
Youhua WANG ; Fan LIU ; Shenghua JIANG ; Defu YU ; De SHI
Chinese Journal of Tissue Engineering Research 2008;12(39):7785-7788
BACKGROUND:Recent studies have demonstrated that surgical trauma leads to lipid peroxidation in erythrocytes.However,injured erythrocytes play an important role in thrombosis following replacement.OBJECTIVE:To evaluate the influence of artificial total knee replacement on the lipid peroxdation in erythrocytes,and the prophylactic treatment of vitamin E and fructose 1,6 diphosphate(FDP)on it.DESIGN,TIME AND SETTING:Contrast clinical study,which was carried out in the Department of Otthopaedics,Affiliated Hospital of Nantong University from January 2003 to June 2006.PARTICIPANTS:Sixty patients with knee osteoarthritis who underwent artificial total knee replacement by anesthesia of epidural block were divided into four groups,including control group,vitamin E group,FDP group and vitamin E+FDP group,with 15 cases in each group.METHODS:Vitamin E was orally taken in the vitamin E group three days before replacement,three times a day,100 mg for each.The administration was performed until the surgical morning.Thirty minutes after the operation,FDP(10 g)was intravenously dripped in the FDP group.Additionally.vitamin E was also orally taken in the vitamin E+FDP group three days before replacement,three times a day,100 mg for each;on the surgical morning,FDP(10 g)was intravenously dripped on the first 30minutes.Blood samples were taken for biochemical determination before and after the operation at 1,3,5,and 7 days.MAIN OUTCOME M[EASURES:Corltents of malonaldehyde(MDA)and cuprum/zincum/superoxide dismutase (Cu-Zn-SOD)in the erythrocytes.RESULTS:MDA level in the vitamin E group and FDP group was significantly higher than that in the vitamin E+FDP group before and 5 and 7 days after replacement(P<0.05);while,Cu-Zn-SOD level was significantly lower(P<0.05).Otherwise,there were no significant differences in vitamin E+FDP group before and after replacement(P>0.05).CONCLUSION:The artificial total knee replacement can enhance lipid peroxidation and decrease antioxygen capability.However,the combination of vitamin E and FDP can prevent and relieve lipid peroxidation and antioxygen capability after replacement.
5.Study on effect of oligochitosan in promoting intestinal absorption of protoberberine alkaloids in extracts from Corydalis saxicola total alkaloids.
Xin-yang LI ; Hui XIE ; Tu-lin LU ; Yue-jiao SHI ; Xing-de ZHANG ; Ting LIU
China Journal of Chinese Materia Medica 2015;40(9):1812-1816
OBJECTIVETo investigate the effect of oligochitosan in promoting intestinal absorption of protoberberine alkaloids in extracts from Corydalis saxicola total alkaloids.
METHODThe in vitro single-pass intestinal perfusion model in rats was established to study the changes in absorption kinetic parameters of dehydrocavidine, berberine hydrochloride and palmatine chloride in C. saxicola total alkaloids after the addition of different concentrations oligochitosan and evaluate the effect of oligochitosan in promoting intestinal absorption of the drugs.
RESULTThe concentration of oligochitosan had different effects on the absorption rate constant (Ka) and apparent permeability coefficient (Peff) of the three active component in rat intestines. Ka and Peff in 0.5% oligochitosan group significantly increased, indicating a stronger effect in promoting the absorption.
CONCLUSIONOligochitosan has a certain effect in promoting the intestinal absorptions of protoberberine alkaloids in C. saxicola total alkaloids.
Animals ; Berberine Alkaloids ; administration & dosage ; pharmacokinetics ; Chitin ; administration & dosage ; analogs & derivatives ; Corydalis ; chemistry ; Drugs, Chinese Herbal ; administration & dosage ; pharmacokinetics ; Intestinal Absorption ; drug effects ; Intestines ; drug effects ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley
6.Research on the mechanism of fluoroquinolone resistance in clinical isolates of Enterococcus faecium
Yu-Bao WANG ; Shi-Duo SONG ; De-Meng LIU ; Wei QI ; Yong-Ming GAO ;
Chinese Journal of Infection and Chemotherapy 2006;0(04):-
Objective To investigate the mechanism of fluoroquinolone resistance in clinical isolates of Enterococcus faecium. Methods The MICs of six fluoroquinolones(norfloxacin,ciprofloxacin,ofloxacin,levofloxacin,gatifloxacin and moxifloxacin) against 35 clinical isolates of E.faecium from eight hospitals in Tianjin were determined by agar dilution method in the absence or presence of multidrug resistance efflux pump inhibitor reserpine.The quinolone-resistance determining region(QRDR)of parC and gyrA were amplified and sequenced.Results No less than twofold decrease in MIC values of the six fluoroquinolones in the presence of reserpine was observed in 35,29,1,0,6 and 2 of the 35 strains of E.faecium respectively.One fluoro- quinolone-susceptible isolate and five fluoroquinolone-resistant isolates were selected randomly to analyze the QRDR of parC and gyrA.All five fluoroquinolone-resistant isolates had single amino acid alteration in both GyrA and ParC.Ser-80 in ParC was substituted by lie(4 isolates)or Arg(1 isolates).Glu-87 in GyrA was replaced by Lys(2 isolates)or Gly(2 isolates). The other one had an Ser-83-to-Ile substitution.The one fluoroquinolone-suseeptible isolate had no alteration in the QRDR of either ParC or GyrA.Conclusions Both target alteration and active efflux are responsible for the resistance to fluoroquinolone in clinical isolates of E.faecium.
7.Cloning , Expression of Human sTNFR1 Gene and the Biological Activity of Its Recombinant Protein
Lei FU ; Shi-Fang PENG ; De-Ming TAN ; Hong-Bo LIU ;
China Biotechnology 2006;0(07):-
Human sTNFR1 (soluble tumor necrosis factor receptor 1) gene was amplified by RT-PCR from Hela cells. A recombinant expression vector of sTNFR1-MBP was constructed in pMAL-c2x, and transformed into E. Coli JM109.It was sequenced and confirmed to be identifical to the sTNFR1 gene in data bank. Recombinant protein sTNFR1-MBP was induced by IPTG and purified by Amylose resin Affinity Chromatography. sTNFR1-MBP was binded to sTNFR1's antibody in Western-blotting. From MTT assays, the results showed that sTNFR1-MBP could effectively block the cytotoxicity mediated by TNF?on QSG7701 cells. Annexin V-FITC staining and flowcytometry were used to observe the recombinant protein's anti-apoptosis capacity and the recombinant protein has marked anti-apoptosis effect in vitro.sTNFR1-MBP had good biological activity and it will be employed in further study.
8.Plasmid-mediated quinolone resistance in clinical isolates of gram-negative bacilli
Xiao-Gang XU ; Shi WU ; Ming-Gui WANG ; Xin-Yu YE ; Yang LIU ; De-Mei ZHU ;
Chinese Journal of Infection and Chemotherapy 2007;0(05):-
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.
9.An experimental study on the removal of thrombi by Fogarty thrombectomy in different time phases
Yi GU ; De SHI ; Yu ZHAO ; Leping YIN ; Chao FENG ; Tong LIU
Chinese Journal of General Surgery 1997;0(06):-
Objective To clarify the effect of Fogarty balloon catheter thrombectomy on venous wall integraty when performed on different time phases.MethodsA murine model of inferior vena caval thrombosis was established. Collagen of venous wall was measured by Van Gieson staining and this was used as the criteria of venous wall injury. The thrombus residue was determined after Fogarty balloon catheter thrombectomy in each individual time phase. Results Collagen deposit in the adventitia of venous wall increased every day,to an amount of (5 902?399) ?m2 on the third day which was significantly different from that of controls (5 333?454) ?m2(P
10.Molecular mechanism of hydroxyurea enhances K562 cell apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand.
Yao-min WU ; Ya-xi ZHANG ; Juan SHI ; Shi-lian LIU ; Yan-xin LIU ; De-xian ZHENG
Acta Academiae Medicinae Sinicae 2012;34(2):146-152
OBJECTIVETo explore the molecular mechanism via which the chemotherapeutic drug hydroxyurea (HU) enhances K562 cell apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).
METHODSChronic myelogenous leukemia-derived K562 and SVT-35 cells were treated with recombinant soluble TRAIL (rsTRAIL) alone or combined with HU for a time course, and the cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-4-sulfophenyl-2H-tetrazolium-phenazine methosulphate assay. Western blot was performed to analyze the activation of apoptosis-related protein kinases and the expression of apoptosis inhibitor molecules.
RESULTSThe survival rates of SVT-35 and K562 cells treated with 1 μg/ml rsTRAIL for 24 hours were 32% and 93%, respectively. HU significantly increased the sensitivity of K562 cells to rsTRAIL cytotoxicity. Combination of rsTRAIL and HU resulted in the phosphorylation of rat sarcoma (RAS), mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MEK), extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase and in the significant reduction of apoptosis-inhibited molecule Fas associated death domain protein-like interleukin-1 beta-convening enzyme inhibitory protein and cellular inhibitor of apoptosis protein-1 in K562 cells.
CONCLUSIONSHU enhanced K562 cell sensitivity to rsTRAIL is mediated by Ras-MEK-ERK signaling pathway. Expression of antiapoptotic proteins cellular Fas associated death domain protein-like interleukin-1 beta-convening enzyme inhibitory protein and cellular inhibitor of apoptosis protein-1 is also down-regulated during this process. These results may through light on the therapeutic study of human chronic myelogenous leukemia.
Apoptosis ; drug effects ; physiology ; CASP8 and FADD-Like Apoptosis Regulating Protein ; metabolism ; Humans ; Hydroxyurea ; pharmacology ; Inhibitor of Apoptosis Proteins ; metabolism ; K562 Cells ; MAP Kinase Signaling System ; TNF-Related Apoptosis-Inducing Ligand ; pharmacology