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Your search keyword '"Van Huyen, J. -p. Duong"' showing total 14 results
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14 results on '"Van Huyen, J. -p. Duong"'

1. The Banff 2017 Kidney Meeting Report: Revised diagnostic criteria for chronic active T cell–mediated rejection, antibody‐mediated rejection, and prospects for integrative endpoints for next‐generation clinical trials

Author

Haas, M., Loupy, A., Lefaucheur, C., Roufosse, C., Glotz, D., Seron, D., Nankivell, B. J., Halloran, P. F., Colvin, R. B., Akalin, Enver, Alachkar, N., Bagnasco, S., Bouatou, Y., Becker, J. U., Cornell, L. D., van Huyen, J. P. Duong, Gibson, I. W., Kraus, Edward S., Mannon, R. B., Naesens, M., Nickeleit, V., Nickerson, P., Segev, D. L., Singh, H. K., Stegall, M., Randhawa, P., Racusen, L., Solez, K., and Mengel, M.

Published
2018
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10. Therapeutic effect of fucoidan-stimulated endothelial colony-forming cells in peripheral ischemia

Author

Sarlon, G., Zemani, F., David, L., Van Huyen, J. -p. Duong, Dizier, B., Grelac, F., Colliec-jouault, Sylvia, Galy-fauroux, Isabelle, Bruneval, P., Fischer, Anne-marie, Emmerich, J., Boisson-vidal, Catherine, Sarlon, G., Zemani, F., David, L., Van Huyen, J. -p. Duong, Dizier, B., Grelac, F., Colliec-jouault, Sylvia, Galy-fauroux, Isabelle, Bruneval, P., Fischer, Anne-marie, Emmerich, J., and Boisson-vidal, Catherine

Abstract

Background: Fucoidan, an antithrombotic polysaccharide, can induce endothelial colony-forming cells (ECFC) to adopt an angiogenic phenotype in vitro. Objectives: We evaluated the effect of fucoidan on vasculogenesis induced by ECFC in vivo. Methods: We used a murine hindlimb ischemia model to probe the synergic role of fucoidan-treatment and ECFC infusion during tissue repair. Results: We found that exposure of ECFC to fucoidan prior to their intravenous injection improved residual muscle blood flow and increased collateral vessel formation. Necrosis of ischemic tissue was significantly reduced on day 14, to 12.1% of the gastronecmius cross-sectional surface area compared with 40.1% in animals injected with untreated-ECFC. ECFC stimulation with fucoidan caused a rapid increase in cell adhesion to activated endothelium in flow conditions, and enhanced transendothelial extravasation. Fucoidan-stimulated ECFC were resistant to shear stresses of up to 21 dyn cm-2. Direct binding assays showed strong interaction of fucoidan with displaceable binding sites on the ECFC membrane. Bolus intramuscular administration of fucoidan 1 day after surgery reduces rhabdomyolysis. Mice injected with fucoidan (15 mg kg-1) had significantly lower mean serum creatine phosphokinase (CPK) activity than control animals. This CPK reduction was correlated with muscle preservation against necrosis (P < 0.001). Conclusions: Fucoidan greatly increases ECFC-mediated angiogenesis in vivo. Its angiogenic effect would be due in part to its transportation to the ischemic site and its release after displacement by proteoglycans present in the extracellular matrix. The use of ECFC and fucoidan together, will be an efficient angiogenesis strategy to provide therapeutic neovascularization.

Published
2012
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11. Spatiotemporal distribution of insulin-like growth factor receptors during nephrogenesis in fetuses from normal and diabetic rats.

Author

Van Huyen, J.-P. Duong, Amri, K., Bélair, M.-F., Vilar, J., Merlet-Bénichou, C., Bruneval, P., and Lelièvre -Pégorier, M.

Subjects
*HYPERGLYCEMIA, *HYPOGLYCEMIC agents, *PEOPLE with diabetes, *INSULIN receptors, *BLOOD sugar, *IMMUNOSUPPRESSIVE agents
Abstract

Exposure to hyperglycemia in utero impairs rat nephrogenesis. The effect of maternal diabetes on insulin-like growth factors and their receptors in the fetal kidney is associated with an increase in both mRNA and protein of the insulin-like growth factor II/mannose 6-phosphate receptor. However, this receptor has never been localized in the fetal kidney. The spatial and temporal distribution of the three insulin-like growth factor receptors (insulin-like growth factor I receptor, insulin-like growth factor II/mannose 6-phosphate receptor and insulin receptor) in rat metanephros during both normal and streptozotocin-induced diabetic renal development was investigated using in situ hybridization and immunohistochemistry. All receptors were found in the fetal kidney from the start of nephrogenesis. Insulin-like growth factor I receptor expression was ubiquitous and continuously present during metanephric development. Insulin receptor expression was developmentally regulated during kidney maturation with an enhanced expression in proximal tubules at the late stages of development. Insulin-like growth factor II/mannose 6-phosphate receptor expression was ubiquitous in the early stages of development and was dramatically decreased at the late stages of normal kidney development. Insulin receptor and insulin-like growth factor I receptor expressions were unchanged in diabetic metanephroi. Although the spatial expression of insulin-like growth factor II/mannose 6-phosphate receptor was unaffected by hyperglycemia, its expression was not downregulated in the mesenchyme of the nephrogenic zone of diabetic fetuses on gestational day 20. This study suggests a crucial role of insulin-like growth factor II/mannose 6-phosphate receptor in the pathogenesis of the impaired nephrogenesis in fetuses of diabetic mothers. [ABSTRACT FROM AUTHOR]

Published
2003
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12. Inflammatory Cell Burden and Phenotype in Endomyocardial Biopsies With Antibody‐Mediated Rejection (AMR): A Multicenter Pilot Study From the AECVP

Author

Fedrigo, M., Leone, O., Burke, M. M., Rice, A., Toquet, C., Vernerey, D., Frigo, A.‐C., Guillemain, R., Pattier, S., Smith, J., Lota, A., Potena, L., Bontadini, A., Ceccarelli, C., Poli, F., Feltrin, G., Gerosa, G., Manzan, E., Thiene, G., Bruneval, P., Angelini, A., and Van Huyen, J.‐P. Duong

Abstract

In this multicenter study, the authors evaluate the endomyocardial biopsy inflammatory burden and its phenotype, and show that it is a constant feature during antibody‐mediated rejection in heart transplantation.

Published
2015
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13. Very Late Heart Transplant Rejection Is Associated with Microvascular Injury, Complement Deposition and Progression to Cardiac Allograft Vasculopathy

Author

Loupy, A., Cazes, A., Guillemain, R., Amrein, C., Hedjoudje, A., Tible, M., Pezzella, V., Fabiani, J. N., Suberbielle, C., Nochy, D., Hill, G. S., Empana, J. P., Jouven, X., Bruneval, P., and Van Huyen, J. P. Duong

Abstract

In heart transplants, the significance of very late rejection (after 7 years post‐transplant, VLR) detected by routine endomyocardial biopsies (EMB) remains uncertain. Here, we assessed the prevalence, histopathological and immunological phenotype, and outcome of VLR in clinically stable patients. Between 1985 and 2009, 10 662 protocol EMB were performed at our institution in 398 consecutive heart transplants recipients. Among the 196 patients with >7‐year follow‐up, 20 (10.2%) presented subclinical ≥3A/2R‐ISHLT rejection. The VLR group was compared to a matched control group of patients without rejection. All biopsies were stained for C4d/C3d/CD68 with sera screened for the presence of donor‐specific antibodies (DSAs). In addition to cellular infiltrates with myocyte damage, 60% of VLR patients had evidence of intravascular macrophages. C4d and/or C3d‐capillary deposition was found in 55% VLR EMB. All cases of VLR associated with microcirculation injury had DSAs (mean DSAmax−MFI = 1751 ± 583). This entity was absent from the control group (p < 0.0001). Finally, after a similar follow‐up postreference EMB of 6.4 ± 1 years, the mean of CAV grade was 0.76 ± 0.18 in the control group compared to 2.06 ± 0.26 in the VLR group respectively, p = 0.001). There was no difference in patient survival between study and control groups. In conclusion, VLR is frequently associated with complement‐cascade activation, microvascular injury and DSA, suggesting an antibody‐mediated process. VLR is associated with a dramatic progression to severe CAV in long‐term follow‐up.

Published
2011
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