Yong Chen

University of Science and Technology of China, Luchow, Anhui Sheng, China

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Publications (21)68.69 Total impact

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    ABSTRACT: ArfGAP With Coiled-Coil, Ankyrin Repeat And PH Domains 4 (ACAP4) is an ADP-ribosylation factor 6 (ARF6) GTPase-activating protein essential for EGF-elicited cell migration. However, how ACAP4 regulates membrane dynamics and curvature in response to EGF stimulation is unknown. Here, we show that phosphorylation of the N-terminal region of ACAP4, named the Bin, Amphiphysin, and RSV161/167 (BAR) domain, at Tyr34 is necessary for EGF-elicited membrane remodeling. Domain structure analysis demonstrates that the BAR domain regulates membrane curvature. EGF stimulation of cells causes phosphorylation of ACAP4 at Tyr34, which subsequently promotes ACAP4 homodimer curvature. The phospho-mimicking mutant of ACAP4 demonstrates lipid-binding activity and tubulation in vitro, and ARF6 enrichment at the membrane is associated with ruffles of EGF-stimulated cells. Expression of the phospho-mimicking ACAP4 mutant promotes ARF6-dependent cell migration. Thus, the results present a previously undefined mechanism by which EGF-elicited phosphorylation of the BAR domain controls ACAP4 molecular plasticity and plasma membrane dynamics during cell migration.
    Proceedings of the National Academy of Sciences 06/2013; · 9.74 Impact Factor
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    ABSTRACT: To evaluate the one year effect of modified Roux-en-Y gastric bypass (RYGP) in the treatment of non-obese type 2 diabetes and to investigate the reasonable indications for surgery. Totally 72 patients diagnosed as type 2 diabetes underwent RYGP from May 2009 to June 2010. There were 45 male and 27 female patients, with an average age of (47 ± 10) years. Preoperative body mass index (BMI) of the patients was 18.69 to 31.22 kg/m(2), average (26 ± 4) kg/m(2). The follow-up data included fasting plasma glucose (FPG), 2 h plasma glucose after oral glucose challenge (2hPG), weight, BMI and medication usage in 1, 3, 6 and 12 months postoperative; hemoglobin A1c (HbA1c), fasting C-peptide (C-P), fasting serum insulin (Fins) and homeostasis model assessment of insulin resistance index (HOMA-IR) in 6 and 12 months postoperative, respectively. Compared with the preoperative, FPG, 2hPG, weight and BMI in 1, 3, 6 and 12 months after surgery were improved (t = 7.014 to 10.254, P = 0.000), while HbA1c, C-P and HOMA-IR in 6 and 12 months after surgery were improved (t = 1.782 to 7.789, P = 0.000 to 0.103) and there was no significant difference in Fins (P > 0.05). The rates of complete remission in 1, 3, 6 and 12 months after surgery were gradually improved to 22.2%, 27.8%, 36.1% and 60.6%, respectively, and the rate of remission in 1 year was 94.3%. The complete remission of 1 year after surgery was associated with normal C-P, insulin antibody and oral antidiabetic drugs (χ(2) = 11.730, P = 0.003; χ(2) = 7.131, P = 0.028;χ(2) = 6.149, P = 0.046). Modified RYGP is safely and effectively in the treatment of no-obese type 2 diabetes patients. The function of islet cells is significantly improved after operation. Especially for the patients of whom C-P is normal, insulin antibody is negative before surgery, the rate of complete remission after 1 year is better.
    Zhonghua wai ke za zhi [Chinese journal of surgery] 10/2012; 50(10):879-82.
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    ABSTRACT: ARF6 GTPase is an important regulator of membrane trafficking and actin-based cytoskeleton dynamics active at the leading edge of migrating cells. The integrin family heterodimeric transmembrane proteins serve as major receptors for extracellular matrix proteins, which play essential roles in cell adhesion and migration. Our recent proteomic analyses of ARF6 effectors have identified a novel ARF6 GTPase-activating protein, ACAP4, essential for EGF-induced cell migration. However, molecular mechanisms underlying ACAP4-mediated cell migration have remained elusive. Here, we show that ACAP4 regulates integrin β1 dynamics during EGF-stimulated cell migration by interaction with Grb2. Our biochemical study shows that EGF stimulation induces phosphorylation of tyrosine 733, which enables ACAP4 to bind Grb2. This interaction of ACAP4 with Grb2 regulates integrin β1 recycling to the plasma membrane. Importantly, knockdown of ACAP4 by siRNA or overexpression of ACAP4 decreased recycling of integrin β1 to the plasma membrane and reduced integrin-mediated cell migration. Taken together, these results suggest a novel function for ACAP4 in the regulation of cell migration through controlling integrin β1 dynamics.
    Journal of Biological Chemistry 12/2011; 286(51):43735-47. · 4.65 Impact Factor
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    ABSTRACT: ARF6 GTPase is an important regulator of membrane trafficking and actin-based cytoskeleton dynamics active at the leading edge of migrating cells. The integrin family heterodimeric transmembrane proteins serve as major receptors for extracellular matrix proteins, which play essential roles in cell adhesion and migration. Our recent proteomic analyses of ARF6 effectors have identified a novel ARF6 GTPase-activating protein, ACAP4, essential for EGF-induced cell migration. However, molecular mechanisms underlying ACAP4-mediated cell migration has remained elusive. Here we show that ACAP4 regulates integrin β1 dynamics during EGF-stimulated cell migration by interaction with Grb2. Our biochemical study shows that EGF stimulation induces phosphorylation of tyrosine 733 which enables ACAP4 to bind Grb2. This interaction of ACAP4 with Grb2 regulates integrin β1 recycling to the plasma membrane. Importantly, knockdown of ACAP4 by siRNA or overexpression of ACAP4 decreased recycling of integrin β1 to the plasma membrane and reduced integrin-mediated cell migration. Taken together, these results suggest a novel function for ACAP4 in the regulation of cell migration through controlling integrin β1 dynamics.
    Journal of Biological Chemistry 10/2011; · 4.65 Impact Factor
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    ABSTRACT: During progression of hepatocellular carcinoma, multiple genetic and epigenetic alterations act to posttranslationally modulate the function of proteins that promote cancer invasion and metastasis. To define such abnormalities that contribute to liver cancer metastasis, we carried out a proteomic comparison of primary hepatocellular carcinoma and samples of intravascular thrombi from the same patient. Mass spectrometric analyses of the liver cancer samples revealed a series of acidic phospho-isotypes associated with the intravascular thrombi samples. In particular, we found that Thr567 hyperphosphorylation of the cytoskeletal protein ezrin was tightly correlated to an invasive phenotype of clinical hepatocellular carcinomas and to poor outcomes in tumor xenograft assays. Using phospho-mimicking mutants, we showed that ezrin phosphorylation at Thr567 promoted in vitro invasion by hepatocarcinoma cells. Phospho-mimicking mutant ezrinT567D, but not the nonphosphorylatable mutant ezrinT567A, stimulated formation of membrane ruffles, suggesting that Thr567 phosphorylation promotes cytoskeletal-membrane remodeling. Importantly, inhibition of Rho kinase, either by Y27632 or RNA interference, resulted in inhibition of Thr567 phosphorylation and a blockade to cell invasion, implicating Rho kinase-ezrin signaling in hepatocellular carcinoma cell invasion. Our findings suggest a strategy to reduce liver tumor metastasis by blocking Rho kinase-mediated phosphorylation of ezrin.
    Cancer Research 03/2011; 71(5):1721-9. · 8.65 Impact Factor
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    ABSTRACT: This study was designed to evaluate the protective effect of cyclosporin A (CsA) on brain injury in rats with acute necrotic pancreatitis (ANP) in order to provide a scientific basis for the use of the drug in treating brain injury caused by pancreatitis. The rats were divided into a sham group, an ANP group and an ANP+CsA group. The ANP model was induced by administering 5% sodium taurocholate through the biliopancreatic duct. Five minutes before the preparation of the ANP model, 1 ml of CsA (10mg/kg) was injected in a clinically used pharmaceutical formulation (Sandimmun) via the dorsal vein of the penis. Twelve hours after the model was established, samples were taken from the rats in all groups for measurement of appropriate indexes. The serum levels of pro-inflammatory tumor necrosis factor-alpha (TNF-alpha), interleukin 1beta (IL-1beta), and anti-inflammatory interleukin 10 (IL-10) were determined by ELISA. The pancreatic mRNA expressions of these cytokines were evaluated by RT-PCR. Brain water content was tested by the dry-wet method, and brain malondialdehyde (MDA) content was detected by the chemical colorimetry method. Both the serum levels and the pancreatic tissue mRNA expression of TNF-alpha and IL-1beta, as well as the brain water content and brain MDA content, were significantly increased in the ANP group. CsA treatment noticeably reduced both the serum levels and the pancreatic mRNA expression of TNF-alpha and IL-1beta and decreased brain water and MDA contents. In contrast to the pro-inflammatory cytokines, the serum levels and the pancreatic tissue mRNA expression of IL-10 were markedly increased by the injection of CsA. CsA could alleviate acute pancreatitis-associated brain injury.
    Life sciences 07/2010; 87(1-2):64-8. · 2.56 Impact Factor
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    ABSTRACT: ARF6 GTPase is a conserved regulator of membrane trafficking and actin-based cytoskeleton dynamics at the leading edge of migrating cells. A key determinant of ARF6 function is the lifetime of the GTP-bound active state, which is orchestrated by GTPase-activating protein (GAP) and GTP-GDP exchanging factor. However, very little is known about the molecular mechanisms underlying ARF6-mediated cell migration. To systematically analyze proteins that regulate ARF6 activity during cell migration, we performed a proteomic analysis of proteins selectively bound to active ARF6 using mass spectrometry and identified a novel ARF6-specific GAP, ACAP4. ACAP4 encodes 903 amino acids and contains two coiled coils, one pleckstrin homology domain, one GAP motif, and two ankyrin repeats. Our biochemical characterization demonstrated that ACAP4 has a phosphatidylinositol 4,5-bisphosphate-dependent GAP activity specific for ARF6. The co-localization of ACAP4 with ARF6 occurred in ruffling membranes formed upon AIF(4) and epidermal growth factor stimulation. ACAP4 overexpression limited the recruitment of ARF6 to the membrane ruffles in the absence of epidermal growth factor stimulation. Expression of GTP hydrolysis-resistant ARF6(Q67L) resulted in accumulations of ACAP4 and ARF6 in the cytoplasmic membrane, suggesting that GTP hydrolysis is required for the ARF6-dependent membrane remodeling. Significantly the depletion of ACAP4 by small interfering RNA or inhibition of ARF6 GTP hydrolysis by overexpressing GAP-deficient ACAP4 suppressed ARF6-dependent cell migration in wound healing, demonstrating the importance of ACAP4 in cell migration. Thus, our study sheds new light on the biological function of ARF6-mediated cell migration.
    Molecular &amp Cellular Proteomics 09/2006; 5(8):1437-49. · 7.25 Impact Factor
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    ABSTRACT: High levels of adenosine accumulate in hypoxic tissues during the rapid growth of tumors, suggesting activation of adenosine receptors may facilitate tumor progress. The relevance of adenosine receptors to hepatocellular carcinoma (HCC), in particular the adenosine A(2b) receptor (A(2b)), is not yet fully understood. The aim of this study was to assess whether A(2b) was differentially expressed in normal and cancerous tissues and evaluate the clinicopathological correlation of A(2b) level in HCC. Expression of A(2b) in tumor cells was investigated by immunohistochemical staining. Protein analysis was done by Western blotting and evaluation of A(2b) mRNA expression levels utilized quantitative real-time PCR analysis of tissue samples of 64 hepatocellular carcinomas and in their paired adjacent normal tissues. Western blot data suggested that A(2b) was expressed predominantly in the cell membrane and cytoplasm of tumor cells and that the intensity of A(2b) protein expression was consistently higher in HCC than in adjacent normal tissues. Levels of A(2b) mRNA in HCC were significantly higher than in adjacent tissues, as measured by real-time PCR (P<0.001). With regard to venous invasion, satellite lesions and advanced pathologic Tumor-Node-Metastasis (pTNM) stage, the A(2b) level tended to be higher than that seen in negative cases (P<0.05). Our findings demonstrate that A(2b) expression is up-regulated in HCC, the expression level of A(2b) is correlated to tumor progression in HCC, and suggest that A(2b) may be a novel target for HCC therapeutic strategy.
    Hepatology Research 09/2006; 36(1):56-60. · 2.07 Impact Factor
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    ABSTRACT: The ezrin-radixin-moesin proteins provide a regulated linkage between membrane proteins and the cortical cytoskeleton, and also participate in signal-transduction pathways. Ezrin is localized to the apical membrane of parietal cells and couples the cAMP-dependent protein kinase activation cascade to the regulated HCl secretion in gastric parietal cells. Our recent studies have mapped the PKA-mediated phosphorylation site to Ser(66) and established its functional role in parietal cell activation [R. Zhou et al., Characterization of protein kinase A-mediated phosphorylation of ezrin in gastric parietal cell activation, J. Biol. Chem. 278 (2003) 35651-35659], but the underlying basis for this regulation is not known. Here, we provide the first evidence that PKA-mediated phosphorylation of Ser(66)regulates the interaction of ezrin with WWOX, a WW domain-containing protein. Our biochemical study reveals that ezrin directly binds to the first WW domain of WWOX via its C-terminal tyrosine-containing polyproline sequence (470)PPPPPPVY(477). Mutational analyses further demonstrate that tyrosine(477) is essential for the ezrin-WWOX interaction. In addition, our study shows that PKA-mediated phosphorylation of ezrin is essential and sufficient for the apical localization of WWOX protein as disruption of ezrin-WWOX interaction eliminated the apical localization of WWOX. Finally, our study demonstrates the essential role of ezrin-WWOX interaction in the apical membrane remodeling associated with H,K-ATPase recruitment. Taken together, these results define a novel molecular mechanism underlying phospho-regulation of ezrin function by PKA in parietal cell activation.
    Biochemical and Biophysical Research Communications 04/2006; 341(3):784-91. · 2.41 Impact Factor
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    ABSTRACT: The goal of this study was to examine the efficacy of liver-targeted gene delivery by chitosan-DNA nanoparticles through retrograde intrabiliary infusion (RII). The transfection efficiency of chitosan-DNA nanoparticles, as compared with PEI-DNA nanoparticles or naked DNA, was evaluated in Wistar rats by infusion into the common bile duct, portal vein, or tail vein. Chitosan-DNA nanoparticles administrated through the portal vein or tail vein did not produce detectable luciferase expression. In contrast, rats that received chitosan-DNA nanoparticles showed more than 500 times higher luciferase expression in the liver 3 days after RII; and transgene expression levels decreased gradually over 14 days. Luciferase expression in the kidney, lung, spleen, and heart was negligible compared with that in the liver. RII of chitosan-DNA nanoparticles did not yield significant toxicity and damage to the liver and biliary tree as evidenced by liver function analysis and histopathological examination. Luciferase expression by RII of PEI-DNA nanoparticles was 17-fold lower than that of chitosan-DNA nanoparticles on day 3, but it increased slightly over time. These results suggest that RII is a promising routine to achieve liver-targeted gene delivery by non-viral nanoparticles; and both gene carrier characteristics and mode of administration significantly influence gene delivery efficiency.
    International Journal of Nanomedicine 02/2006; 1(4):507-22. · 3.46 Impact Factor
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    ABSTRACT: Different strategies have been proposed to increase and prolong liver-targeted transgene expression using non-viral vectors. Hepatic Kupffer cells (KCs) are known to eliminate a large proportion of i.v.-injected vector particles and contribute to innate immune responses following viral and non-viral vector administration. Recently, we have shown that KCs play an important role in limiting gene transfer in hepatocytes by DNA nanoparticles or naked DNA1. Transient depletion of KCs by clodronate liposomes, for example, enhances transgene expression in the liver by 14,510-, 100- and 2,020-fold in rats received intrabiliary infusion of PEI/DNA nanoparticles, chitosan/DNA nanoparticles and naked DNA, respectively. To better understand the mechanism of this phenomenon, in this study we selectively blocked the activity of transcriptional factor NK-κB in KCs using NF-κB/decoy/ODN liposomes 24 hours prior to intrabiliary infusion of plasmid DNA. Sequences of the double-stranded phosphorothioate ODNs used as NF-κB decoy were 5′-CCTTGAAGGGATTTCCCTCC-3′ and 3′-GGAACTTCCCTAAAGGGAGG-5′ (consensus sequences are underlined)2. This pretreatment yielded more than 200-fold higher gene expression than non-treatment group. We also inhibited TNF-α, one of the major proinflammatory cytokines secreted by KCs upon activation, by pentoxifylline 30 min before intrabiliary infusion of DNA nanoparticles or naked DNA. This pretreatment increased luciferase expression by more than 60-fold for the naked DNA group, and about 12-fold for the chitosan/DNA nanoparticle and PEI/DNA nanoparticle groups. While this suggests the inhibitory role of TNF-α in vivo, its role in transfection of primary rat hepatocytes in vitro was not as obvious. Instead, the in vitro transfection was clearly inhibited by a conditioned medium containing cytokines released by KCs upon activation by LPS. Taken together, this study showed that, following intrabiliary infusion of DNA nanoparticles or naked DNA, proinflammatory cytokines secreted by activated KCs may act collectively to reduce or inhibit the transgene expression in hepatocytes. This reduction in transgene expression might be related to the inactivation of CMV promoter involving KC-released cytokines such as TNF-α and IFN-γ. In summary, this study suggests that, in addition to sequestration, proinflammatory cytokines secreted by activated KCs play an important role in modulating transgene expression in the liver. (See Figure)
    Molecular Therapy 01/2005; 11. · 7.04 Impact Factor
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    ABSTRACT: Control laws that are based on the nonlinear inverse dynamics (NID) of the aircraft offer the potential for providing improved levels of performance over conventional flight control designs. The NID and its application in the flight control during windshear penetration are introduced here. With the employment of a real engineering windshear model and NID, a low-altitude windshear penetration flight control law is designed. The simulative calculation results indicated that the NID control logic works effectively in the trajectory control of the aircraft during the penetration of windshear.
    Aircraft Engineering and Aerospace Technology 11/2004; 76(6):592-599. · 0.08 Impact Factor
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    ABSTRACT: To construct pEGFP-hepatocyte growth factor (HGF) expression vector, the to detect its expression in transfected human hepatocytes, and to investigate the influence of autocrine HGF expression on the proliferative potential and cytoprotective effects in human hepatocytes. Human HGF cDNA was ligated to the pEGFP vector. Recombinant plasmid was transfected into human hepatocyte line QZG with liposome. Expression of HGF protein was observed by fluorescence microscopy and immunohistochemistry. Hepatic cells were collected 24, 48, and 72 h after transfection to detect the number of ((3)H)-TdR uptake in DNA. DNA synthesis was observed by using PCNA stain immunohistochemistry. Acute liver cell damage was induced by carbon tetrachloride. Cytoprotective effect was observed by examining the survival rate of hepatocytes and leakage of intracellular alanine transaminase (ALT) and potassium ions. HGF identification of pEGFP-HGF by enzyme digestion showed that HGF fragment was cloned into BamH I and Sal I sites of pEGFP-N3. Expression of GFP in transfected hepatocytes was observed with fluorescence microscopy. The ((3)H)-TdR uptake became 7 times as many as in the control group 96 h after transfection. After HGF transfection, the survival rate of hepatocytes poisoned by CCl(4) significantly increased (83% vs 61%, P<0.05), and the leakage of intracellular alanine transaminase and potassium ions decreased (586 nkat/L vs 1 089 nkat/L, P<0.01; and 5.59 mmol/L vs 6.02 mmol/L, P<0.01 respectively). Culture of transfected hepatic cells promoted the proliferation of other non-transfected cells. Transfected HGF is expressed in hepatic cells and has the activity of promoting cell division and protecting hepatic cells against poisoning.
    World Journal of Gastroenterology 11/2004; 10(19):2827-30. · 2.55 Impact Factor
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    ABSTRACT: Chromosome segregation in mitosis is orchestrated by the kinetochore and spindle microtubules stemming from two centrosomes. Our recent studies demonstrated the importance of Nek2A in faithful chromosome segregation during mitosis. Here, we report that Nek2A regulates the function of numatrin in mitosis. The biochemical interaction between Nek2A and numatrin in mitotic cells was revealed by a set of reciprocal immunoprecipitation experiments using Nek2A and numatrin antibodies, respectively. The interaction is validated by a pull-down assay using recombinant Nek2A and numatrin proteins. Moreover, our immunofluorescence studies demonstrate that numatrin becomes centrosome-associated as the cell enters into mitosis and depart from the centrosome after sister chromatid separation in anaphase. The co-localization of numatrin and Nek2A to the centrosome suggests their interaction with and involvement in centrosome function. Indeed, elimination of Nek2A kinase by siRNA diminished its association with the centrosome. Furthermore, we show that numatrin is phosphorylated by wild type but not kinase-death Nek2A. Our studies suggest that the Nek2A kinase cascade is essential for the localization of numatrin to the centrosome.
    FEBS Letters 10/2004; 575(1-3):112-8. · 3.58 Impact Factor
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    ABSTRACT: To set up a stand for surgical classification of pancreatic duct stone and evaluate the benefits of different management according to the classification. Retrospectively analysis the diagnosis and prognosis of different management of 33 cases pancreatic duct stones to establish a new standard of classification and strategy of management of pancreatic duct stone. According to the results of imaging examination (B-US, CT, ERCP) and finding during surgery, pancreatic duct stone can be classified into four different types: Type I: The stones mainly located in the head of pancreas. Endoscopic pancreas drainage and remove of stones is the first line choice of treatment. If it fail the Whipple procedure should be applied. Type II, The stones mainly located in the body of pancreas. It can be treated by Pusetow procedure. Type III, The stones mainly located in the tail of pancreas. The resection of the tail of pancreas or combined with spleenectomy was recommended for the management of this type stones. Type IV, The stones can be found from the head to tail of the main duct of pancreas. The Pusetow-Gillesby procedure or dividing of the neck of pancreas removing stones from both ends of pancreatic duct and reconstructed by two ends pancreatic duct-ileostomy in Roux-en-Y fashion are the choice of management. The invadulaized strategy of the management based upon correct diagnosis and classification play the most important role in the treatment of pancreatic duct stone.
    Zhonghua wai ke za zhi [Chinese journal of surgery] 05/2004; 42(7):417-20.
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    ABSTRACT: Molecular Therapy (2004) 9, S136–S137; doi: 10.1016/j.ymthe.2004.06.284 357. Selective Depletion of Kupffer Cells Leads to Enhanced Transgene Expression in Rat Liver Following Intraductal Infusion of Naked DNA and DNA Nanoparticles Hui Dai1,2, Xuan Jiang1, Weiseng Lim1, Xuesong Jiang1, Yong Chen2, Hai-Quan Mao1,3 and Kam W. Leong1,41Division of Johns Hopkins in Singapore, Singapore, Singapore2Department of Hepatobiliary Surgery, Xijing Hospital, The Fourth Military Medical University, Xian, China3Department of Materials Science and Engineering, Johns Hopkins University, Baltimore, MD4Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, MD
    Molecular Therapy 04/2004; · 7.04 Impact Factor
  • Aircraft engineering and aerospace technology 01/2004; 76(6):592-599. · 0.44 Impact Factor
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    ABSTRACT: To evaluate the efficacy of adenovirus mediated fibroblast growth factor (FGF) receptor gene transfer in inhibition of accelerated graft arteriosclerosis (AGA) in rat aorta transplantation model. The PCR product of rat sFGFR-1 cDNA was cloned into pCMV1-flag vector, then flag-sFGFR was cloned into pAdvs6a to construct recombinant vector pAv3flag-sFGFR1. The abdominal aorta was injected with buffer containing 5 x 10(9) pfu Adv3-sFGFR-1 and then resected in 30 DA rats. A section of abdominal aorta was resected in 30 PVG rats and the abdominal aorta of DA rats was transplanted. Av3-Nall and normal saline of the same volume were injected into the abdominal aortae of and rats as experimental controls and blank controls. Six rats were killed 5, 30, 60, and 90 days after the operation respectively. The transplanted aorta was harvested. RT-PCR was performed to detect the expression of sFGFR-1 gene with pCMV-Flag-sFGFR1 cDNA as positive control and the abdominal aorta RNA of non-transfected rats as negative control. Immunohistochemistry and HE staning were used to detect the localization and expression of sFGFR-1, and the morphology and cytology of the transplanted vessels. A construct encoding the FGFR1 ectodomain produced secreted sFGFR1 protein, which bound [(125)I]FGF-2 with high affinity and specificity, and inhibited FGF-2 stimulated 3T3 fibroblast proliferation in vitro. Gene transfer of sFGFR1 into rat aortic grafts, using an adenoviral vector, resulted in expression of sFGFR1 protein in endothelium and adventitia. Neointimal formation 60 and 90 days after transplantation was inhibited (P = 0.013) in aortic allograft transduced with sFGFR1, compared to allograft transduced with Null virus and saline. FGFs play a causal role in the development of AGA in the rat aortic transplant model and postulate that targeted interruption of FGF function could similarly reduce neointimal formation in transplant setting.
    Zhonghua yi xue za zhi 10/2003; 83(18):1607-10.
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    ABSTRACT: To assess the value of argon supper-cryosurgery for 42 patients with middle and late stage liver cancer. Forty-two patients who had received argon supper-cryosurgery were analyzed retrospectively in terms of their clinical characteristics as well as the performance of argon supper-cryosurgery. All patients were ameliorated in symptoms shortly after the operation, including pain alleviation, psyche straightening up, alpha-fetoprotein descending or recovery. Jaundice occurred in 1 patient and intraabdominal hemorrhage in 2. The levels of aspartate transaminase and alanine transaminase in all patients were elevated 1 month after the operation, and normalized after protective therapy of the liver. No operative death was noted. Cold and heat reversed therapy of argon supper-cryosurgery can drastically destroy tumor tissue, especially the tumors which are too large to resect or close to the large vessels. It is applicable to increase the operative rate, decrease the operative death rate, and enlarge the therapeutic scope.
    Hepatobiliary & pancreatic diseases international: HBPD INT 09/2003; 2(3):354-7. · 1.26 Impact Factor
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    ABSTRACT: To develop a surgical model of acute hepatic failure. Hepatectomy was performed in rats according to the method described by Higgins and Anderson. Ninety percent liver resection (removing the left lateral, median, and right lateral lobes) (n=7) and 95% liver resection leaving only half of the caudate lobe (n=13) were performed. Hypoglycemia was corrected by giving 20% glucose in the drinking water, coupled with repeated intraperitoneal injection of 5% glucose adapted to glycemia. While the survival rate, alanine transaminase (ALT) and bilirubin were observed. 95% liver resection decreased survival rates of the rats from 86% (90% liver resection) to 23% (P<0.05), and increased bilirubin levels (4.04+/-2.84 mg/dL vs. 1.25+/-1.85 mg/dL [90% liver resection]). 95% liver resection is a good rat model for acute hepatic failure.
    Hepatobiliary & pancreatic diseases international: HBPD INT 08/2003; 2(3):423-5. · 1.26 Impact Factor

Publication Stats

105 Citations
68.69 Total Impact Points

Institutions

  • 2004–2013
    • University of Science and Technology of China
      • School of Life Sciences
      Luchow, Anhui Sheng, China
    • Beijing University of Aeronautics and Astronautics (Beihang University)
      Peping, Beijing, China
  • 2003–2012
    • Fourth Military Medical University
      • Department of Hepatobiliary Surgery
      Xi’an, Liaoning, China