Professor of Surgery, Beth Israel Deaconess Medical Center
Nephrology
Dr. Christiane J. Ferran, MD
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Christiane J. Ferran practices Nephrology. She studied medicine at St Joseph's University Medical School. Christiane J. Ferran, MD is a published doctor as well. She has 100 publications published. The latest was: Membrane-associated lymphotoxin on natural killer cells activates endothelial cells via an NF-kappaB-dependent pathway.
Publications
- Cytotoxicity associated with electrospun polyvinyl alcohol.
- Bidirectional crosstalk between periventricular endothelial cells and neural progenitor cells promotes the formation of a neurovascular unit.
- A20 promotes liver regeneration by decreasing SOCS3 expression to enhance IL-6/STAT3 proliferative signals.
- The C-terminal domain of A1/Bfl-1 regulates its anti-inflammatory function in human endothelial cells.
- Temporal network based analysis of cell specific vein graft transcriptome defines key pathways and hub genes in implantation injury.
- Molecular biomarkers of vascular dysfunction in obstructive sleep apnea.
- Adenovirus-mediated gene transfer of A20 in murine islets inhibits Fas-induced apoptosis.
- A20 and BCL proteins exert a broad and complementary cytoprotective effect in endothelial cells via blockade of NF-kappaB and NFAT.
- The BH4 domain of A1, an anti-apoptotic bcl family gene, is necessary and sufficient for its antiinflammatory function in endothelial cells.
- Overexpression of A20 in endothelial cells of vascularized grafts creates a protective barrier against TNF- and FAS-mediated apoptosis.
- A20 inhibits cytokine-induced apoptosis and nuclear factor kappaB-dependent gene activation in islets.
- Barriers to xenotransplantation.
- Overexpression of A1, an NF-kappaB-inducible anti-apoptotic bcl gene, inhibits endothelial cell activation.
- A novel function for A20 in smooth muscle cells: inhibition of activation and proliferation.
- Adenovirus-mediated gene transfer of the anti-apoptotic protein A20 in rodent islets inhibits IL-1 beta-induced NO release.
- Bcl-2 and Bcl-XL serve an anti-inflammatory function in endothelial cells through inhibition of NF-kappaB.
- Membrane-associated lymphotoxin on natural killer cells activates endothelial cells via an NF-kappaB-dependent pathway.
- Adenovirus-mediated expression of a dominant negative mutant of p65/RelA inhibits proinflammatory gene expression in endothelial cells without sensitizing to apoptosis.
- A20 inhibits NF-kappaB activation in endothelial cells without sensitizing to tumor necrosis factor-mediated apoptosis.
- Henoch-Schönlein purpura as clinical presentation of a myelodysplastic syndrome.
- Xenotransplantation: progress toward clinical development.
- Protective genes expressed in endothelial cells: a regulatory response to injury.
- Modification of vascular responses in xenotransplantation: inflammation and apoptosis.
- Expression of a negative dominant mutant of human p55 tumor necrosis factor-receptor inhibits TNF and monocyte-induced activation in porcine aortic endothelial cells.
- A20 expression inhibits endothelial cell activation.
- Adenovirus-mediated gene transfer of A20 renders endothelial cells resistant to activation: a means of evaluating the role of endothelial cell activation in xenograft ...
- Accommodation of xenografts: expression of "protective genes" in endothelial and smooth muscle cells.
- Human monocytes activate porcine endothelial cells, resulting in increased E-selectin, interleukin-8, monocyte chemotactic protein-1, and plasminogen activator inhibit...
- Accommodation of vascularized xenografts: expression of "protective genes" by donor endothelial cells in a host Th2 cytokine environment.
- Delayed xenograft rejection.
- Genetic engineering of endothelial cells to ameliorate xenograft rejection.
- A20 blocks endothelial cell activation through a NF-kappaB-dependent mechanism.
- Xenotransplantation: a possible solution to the shortage of donor organs.
- Expression of a truncated form of the human p55 TNF-receptor in bovine aortic endothelial cells renders them resistant to human TNF.
- In vivo anti-CD3-driven cell activation. Cellular source of induced tumor necrosis factor, interleukin-1 beta, and interleukin-6.
- [Monoclonal antibodies. Diagnostic and therapeutic use and prospects for the future].
- [T lymphocyte activation induced in vivo in different strains of mice after injection of anti-CD3 antibodies: prevention by an anti- TNF antibody].
- Anti-tumor necrosis factor modulates anti-CD3-triggered T cell cytokine gene expression in vivo.
- In vivo T cell activation properties of anti-T cell monoclonal antibodies.
- Xenotransplantation: problems and approaches.
- Xenotransplantation: endothelial cell activation and beyond.
- Endothelial cell activation and thromboregulation during xenograft rejection.
- Implications of de novo ELAM-1 and VCAM-1 expression in human cardiac allograft rejection.
- Inhibition of NF-kappa B by pyrrolidine dithiocarbamate blocks endothelial cell activation.
- [Life-expectancy in the acute leukaemias (author''s transl)].
- [Variations in the toxicity of cadmium in relation to the possibility of controlling the environmental status by motor activity in the rat].
- [Variations in blood lactic acid and glucose levels in the rabbit after infusion of isoprenaline with or without prior infusion of minaprine].
- [Effects of minaprine hydrochloride on changes in body weight, blood pressure and cerebral amine concentrations induced by unavoidable planter electric shock].
- [Effect of piracetam on metabolic stages in the rat brain].
- Assay of cerebral catecholamines, serotonin and their metabolites in experimental hemorrhagic shock in rats.
- Action of certain pharmacological associations on the level of cerebral biogenic amines and some metabolites in the curative treatment of hemorrhagic shock in rats.
- [Effect of minaprine on arterial pressure and levels of cerebral amines in spontaneously hypertensive rats].
- [T lymphocyte activation induced in vivo by the first injection of OKT3 monoclonal antibodies].
- Deletion analysis of sucrose metabolic genes from a Salmonella plasmid cloned in Escherichia coli K12.
- Systemic reaction to the anti-T-cell monoclonal antibody OKT3 in relation to serum levels of tumor necrosis factor and interferon-gamma [corrected].
- The natural history of inherited renal diseases.
- In-vivo anti-CD3 treatment of autoimmune patients.
- In vivo T lymphocyte activation induced in mice following the injection of anti-CD3 monoclonal antibody.
- Cytokine-related syndrome following injection of anti-CD3 monoclonal antibody: further evidence for transient in vivo T cell activation.
- In vivo use of OKT3: main issues for the monitoring of treated patients.
- Immunological follow-up of renal allograft recipients treated with the BMA 031 (anti-TCR) monoclonal antibody.
- In vivo cell activation following OKT3 administration. Systemic cytokine release and modulation by corticosteroids.
- Clinical applications of anti-T-cell monoclonal antibodies.
- Corticosteroid inhibition of the OKT3-induced cytokine-related syndrome--dosage and kinetics prerequisites.
- Plasmid-mediated sucrose metabolism in Escherichia coli: characterization of scrY, the structural gene for a phosphoenolpyruvate-dependent sucrose phosphotransferase s...
- The anti-CD3-induced syndrome: a consequence of massive in vivo cell activation.
- [Acute clinical syndrome associated with OKT3 administration. Prevention by single injection of an anti-human TNF monoclonal antibody].
- Cascade modulation by anti-tumor necrosis factor monoclonal antibody of interferon-gamma, interleukin 3 and interleukin 6 release after triggering of the CD3/T cell re...
- Anti-TNF abrogates the cytokine-related anti-CD3 induced syndrome.
- Inter-mouse strain differences in the in vivo anti-CD3 induced cytokine release.
- Reduction of morbidity and cytokine release in anti-CD3 MoAb-treated mice by corticosteroids.
- Evidence that antihuman tumor necrosis factor monoclonal antibody prevents OKT3-induced acute syndrome.
- [Granulocyte transfusion. Its efficacy as a complementary treatment of infections in the granulocytopenic patient (author''s transl)].
- [Biochemical and neurophysiological study of various fish toxins].
- The universal NF-kappaB inhibitor a20 protects from transplant vasculopathy by differentially affecting apoptosis in endothelial and smooth muscle cells.
- Epstein-Barr virus infection is associated with endothelial Bcl-2 expression in transplant liver allografts.
- Induction of protective genes leads to islet survival and function.
- Hepatocyte growth factor preferentially activates the anti-inflammatory arm of NF-κB signaling to induce A20 and protect renal proximal tubular epithelial cells from i...
- A20 modulates lipid metabolism and energy production to promote liver regeneration.
- O-glycosylation regulates ubiquitination and degradation of the anti-inflammatory protein A20 to accelerate atherosclerosis in diabetic ApoE-null mice.
- Endothelial cells are susceptible to rapid siRNA transfection and gene silencing ex vivo.
- Endothelium-dependent coronary vasodilatation requires NADPH oxidase-derived reactive oxygen species.
- A20 inhibits post-angioplasty restenosis by blocking macrophage trafficking and decreasing adventitial neovascularization.
- A20 protects mice from lethal liver ischemia/reperfusion injury by increasing peroxisome proliferator-activated receptor-alpha expression.
- Mechanism of purinergic activation of endothelial nitric oxide synthase in endothelial cells.
- TNFalpha-induced macrophage death via caspase-dependent and independent pathways.
- MARCKS silencing differentially affects human vascular smooth muscle and endothelial cell phenotypes to inhibit neointimal hyperplasia in saphenous vein.
- Comparison of gene silencing in human vascular cells using small interfering RNAs.
- A novel function for cadherin 11/osteoblast-cadherin in vascular smooth muscle cells: modulation of cell migration and proliferation.
- A20 protects mice from D-galactosamine/lipopolysaccharide acute toxic lethal hepatitis.
- Increased expression of antioxidant and antiapoptotic genes in islets that may contribute to beta-cell survival during chronic hyperglycemia.
- A20 protects from CD40-CD40 ligand-mediated endothelial cell activation and apoptosis.
- Genetic engineering of a suboptimal islet graft with A20 preserves beta cell mass and function.
- Expression of A20 in the vessel wall of rat-kidney allografts correlates with protection from transplant arteriosclerosis.
- The graft unveils its secrets: provocative therapeutic leads to protected vascularized allografts.
- Expression of protective genes in human renal allografts: a regulatory response to injury associated with graft rejection.
- Protective genes in the vessel wall: Modulators of graft survival and function.
- A20, a modulator of smooth muscle cell proliferation and apoptosis, prevents and induces regression of neointimal hyperplasia.
- Valsartan improves resting skin blood flow in type 2 diabetic patients and reduces poly(adenosine diphosphate-ribose) polymerase activation.
Doctors Specialties
- Nephrology
Accepted Insurances
Education
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Beth Israel Deaconess Medical Center -
St Joseph's University Medical School
Hospital
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Beth Israel Deaconess Medical Center
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