Valérie Deckert

University of Burgundy, Dijon, Bourgogne, France

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Publications (45)263.53 Total impact

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    ABSTRACT: Quantitation of plasma lipopolysaccharides (LPS) might be used to document Gram(-) bacterial infection. In the present work, LPS-derived 3-hydroxymyristate was extracted from plasma samples with an organic solvent, separated by reversed phase HPLC and quantitated by tandem mass spectrometry (HPLC-MS/MS). This mass assay was combined with the limulus amebocyte lysate (LAL) bioassay to monitor neutralisation of LPS activity in biological samples. The described HPLC-MS/MS method is a reliable, practical, accurate, and sensitive tool to quantitate LPS. The combination of the LAL and HPLC-MS/MS analyses provided new evidence for the intrinsic capacity of plasma lipoproteins and phospholipid transfer protein to neutralize the activity of LPS. In a subset of patients with Systemic Inflammatory Response Syndrome (SIRS), with documented infection but with a negative plasma LAL test, significant amounts of LPS were measured by the HPLC-MS/MS method. Patients with the highest plasma LPS concentration were more severely ill. HPLC-MS/MS is a relevant method to quantitate endotoxin in a sample, to assess the efficacy of LPS neutralization, and to evaluate the proinflammatory potential of LPS in vivo. Copyright © 2015, The American Society for Biochemistry and Molecular Biology.
    The Journal of Lipid Research 05/2015; 56(7). DOI:10.1194/jlr.D059725 · 4.73 Impact Factor
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    ABSTRACT: Systemic inflammatory response syndrome and sepsis frequently occur after cardiac surgery with cardiopulmonary bypass. The aim of the present study was to investigate whether preoperative cholesterol levels can predict sepsis onset and postoperative complications in patients undergoing cardiac surgery with cardiopulmonary bypass. Prospective observational study. Surgical ICU of a French university hospital. Two hundred and seventeen consecutive patients older than 18 years admitted for planned cardiac surgery with cardiopulmonary bypass. Measurements of plasma blood lipids and inflammation markers before anesthesia induction (baseline), at cardiopulmonary bypass start, at cardiopulmonary bypass end, and 3 and 24 hours after cardiac surgery. Outcomes were compared in systemic inflammatory response syndrome patients with sepsis (n = 15), systemic inflammatory response syndrome patients without sepsis (n = 95), and non-systemic inflammatory response syndrome patients (n = 107). A gradual decrease in plasma cholesterol concentration occurred during surgery with cardiopulmonary bypass but was no longer present after correction for hemodilution. Corrected cholesterol levels were significantly lower at baseline in sepsis patients than in other subgroups, and it remained lower in the sepsis group during and after cardiopulmonary bypass. With regard to sepsis, the discriminatory power of baseline cholesterol was fairly good as indicated by receiver operating characteristic curve analysis (area under the curve, 0.78; 95% CI, 0.72-0.84). The frequency of sepsis progressively decreased with increasing baseline cholesterol level quintiles (18.6% and 0% in the bottom and top quintiles, respectively, p = 0.005). In multivariate analysis, baseline cholesterol levels and cardiopulmonary bypass duration were significant and independent determinants of the 3-hour postcardiopulmonary bypass increase in concentrations of procalcitonin and interleukin-8, but not of interleukin-6. Low cholesterol levels before elective cardiac surgery with cardiopulmonary bypass may be a simple biomarker for the early identification of patients with a high risk of sepsis.
    Critical care medicine 01/2014; 42(5). DOI:10.1097/CCM.0000000000000165 · 6.15 Impact Factor
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    ABSTRACT: Lipopolysaccharides (LPS) or endotoxins are amphipathic, pro-inflammatory components of the outer membrane of Gram-negative bacteria. In the host, LPS can trigger a systemic inflammatory response syndrome. To bring insight into in vivo tissue distribution and cellular uptake of LPS, dual labeling was performed with a bimodal molecular probe designed for fluorescence and nuclear imaging. LPS were labeled with DOTA-Bodipy-NCS, and pro-inflammatory properties were controlled after each labeling step. LPS were then radiolabeled with In-111 and subsequently injected intravenously into wild-type, C57B16 mice, and their in vivo behavior was followed by single photon emission computed tomography coupled with X-ray computed tomography (SPECT-CT) and fluorescence microscopy. Time course of liver uptake of radiolabeled LPS (In-111-DOTA-Bodipy-LPS) was visualized over a 24-h period in the whole animal by SPECT-CT. In complementary histological analyses with fluorescent microscopy, the bulk of injected In-111-DOTA-Bodipy-LPS was found to localize early within the liver. Serum kinetics of unlabeled and DOTA-Bodipy-labeled LPS in mouse plasma were similar as ascertained by direct quantitation of beta-hydroxymyristate, and DOTA-Bodipy-LPS was found to retain the potent, pro-inflammatory property of the unlabeled molecule as assessed by serum cytokine assays. It is concluded that the dual labeling process, involving the formation of covalent bonds between a DOTA-Bodipy-NCS probe and LPS molecules is relevant for imaging and kinetic analysis of LPS biodistribution, both in vivo and ex vivo. Data of the present study come in direct and visual support of a lipopolysaccharide transport through which pro-inflammatory LPS can be transported from the periphery to the liver for detoxification. The In-111-DOTA-Bodipy-LPS probe arises here as a relevant tool to identify key components of LPS detoxification in vivo.
    ACS Chemical Biology 12/2013; 9(3). DOI:10.1021/cb400779j · 5.36 Impact Factor
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    ABSTRACT: Lipopolysaccharides (LPS) of the cell wall of Gram (-) bacteria trigger inflammation, which is associated with marked changes in glucose metabolism. Hyperglycemia is frequently observed during bacterial infection and it is a marker of a poor clinical outcome in critically ill patients. The aim of the present study was to investigate the effect of an acute injection or continuous infusion of LPS on experimentally-induced hyperglycemia in wild-type and genetically-engineered mice. The acute injection of a single dose of LPS produced an increase in glucose disposal and glucose-stimulated insulin secretion (GSIS). Continuous infusion of LPS through mini-osmotic pumps was also associated with increased GSIS. Finally, manipulation of LPS detoxification by knocking out the plasma phospholipid transfer protein (PLTP) led to increased glucose disposal and GSIS. Overall, glucose tolerance and GSIS tests supported the hypothesis that mice treated with LPS develop glucose-induced hyperinsulinemia. The effects of LPS on glucose metabolism were significantly altered as a result of either the accumulation or antagonism of glucagon-like peptide 1 (GLP1). Complementary studies in wild-type and GLP1-R knockout mice further implicated the GLP1R-dependent pathway in mediating the LPS-mediated changes in glucose metabolism. Hence, enhanced GLP1 secretion and action underlies the development of glucose-mediated hyperinsulinemia associated with endotoxemia.
    Diabetes 11/2013; 63(2). DOI:10.2337/db13-0903 · 8.47 Impact Factor
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    ABSTRACT: Plasma phospholipid transfer protein (PLTP) increases the circulating levels of proatherogenic lipoproteins, accelerates blood coagulation, and modulates inflammation. The role of PLTP in the development of abdominal aortic aneurysm (AAA) was investigated by using either a combination of mechanical and elastase injury at one site of mouse aorta (elastase model) or continuous infusion of angiotensin II in hyperlipidemic ApoE-knockout mice (Ang II model). With the elastase model, complete PLTP deficiency was associated with a significantly lower incidence and a lesser degree of AAA expansion. With the Ang II model, findings were consistent with those in the elastase model, with a lower severity grade in PLTP-deficient mice, an intermediate phenotype in PLTP-deficient heterozygotes, and a blunted effect of the PLTP-deficient trait when restricted to bone marrow-derived immune cells. The protective effect of whole-body PLTP deficiency in AAA was illustrated further by a lesser degree of adventitia expansion, reduced elastin degradation, fewer recruited macrophages, and less smooth muscle cell depletion in PLTP-deficient than in wild-type mice, as evident from comparative microscopic analysis of aorta sections. Finally, cumulative evidence supports the association of PLTP deficiency with reduced expression and activity levels of matrix metalloproteinases, known to degrade elastin and collagen. We conclude that PLTP can play a significant role in the pathophysiology of AAA.
    American Journal Of Pathology 07/2013; 10(3). DOI:10.1016/j.ajpath.2013.05.018 · 4.60 Impact Factor
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    ABSTRACT: Context:PCSK9 (proprotein convertase subtilisin kexin type 9) is a secreted protease that modulates cholesterol homeostasis by decreasing low-density lipoprotein receptor expression. Low levels of plasma lipoproteins are related to severity of illness and survival in patients of intensive care units (ICU).Objective:The aim of the study was to investigate the regulation of plasma PCSK9 and its association with plasma lipid parameters and clinical markers of severity during critical illness.Design and Patients:The plasma biobank from the previously published HYPOLYTE prospective study was used to measure PCSK9 concentrations by ELISA at days 0 and 8 in 111 patients admitted to surgical ICU for severe multiple trauma. Patients were randomly assigned to hydrocortisone therapy or placebo.Results:Plasma PCSK9 levels were increased by 2-fold between days 0 and 8 (231 ± 116 vs 481 ± 227 ng/ml; P = .0001). Hydrocortisone therapy did not alter PCSK9 concentrations (451 ± 216 vs 511 ± 239 ng/ml in placebo group; P = .33). PCSK9 was positively associated with low-density lipoprotein-cholesterol (Pearson coefficient, 0.26; P = .007) at day 0, but not at day 8. At day 8, an inverse correlation was found between PCSK9 and high-density lipoprotein-cholesterol (β = -653; P = .004). Although baseline PCSK9 concentrations were not associated to severity scores, PCSK9 values at day 8 were related to injury severity score (β = 6.17; P = .0007), length of stay in ICU (β = 6.14; P = .0001), and duration of both mechanical ventilation (β = 8.26; P = .0001) and norepinephrine infusion (β = 18.57; P = .015).Conclusions:Plasma PCSK9 appears as a late biomarker of illness severity in patients with severe multiple trauma.
    The Journal of Clinical Endocrinology and Metabolism 02/2013; 98(4). DOI:10.1210/jc.2012-4236 · 6.31 Impact Factor
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    ABSTRACT: Oxidative stress is recognized as one of the earliest and most intense pathological processes in Alzheimer's disease (AD), and the antioxidant vitamin E has been shown to efficiently prevent amyloid plaque formation and neurodegeneration. Plasma phospholipid transfer protein (PLTP) plays a major role in vitamin E transfers in vivo, and PLTP deficiency in mice is associated with reduced brain vitamin E levels. To determine the impact of PLTP on amyloid pathology in vivo, we analyzed the vulnerability of PLTP-deficient (PLTP-KO) mice to the toxic effects induced by intracerebroventricular injection of oligomeric amyloid-β(25-35) (Aβ(25-35)) peptide, a nontransgenic model of AD. Under basal conditions, PLTP-KO mice showed increased cerebral oxidative stress, increased brain Aβ(1-42) levels, and a lower expression of the synaptic function marker synaptophysin, as compared to wild-type mice. This PLTP-deficient phenotype was associated with increased memory impairment one week after Aβ(25-35) peptide injection. Restoration of brain vitamin E levels in PLTP-KO mice through a chronic dietary supplementation prevented Aβ(25-35)-induced memory deficits and reduced cerebral oxidative stress and toxicity. We conclude that PLTP, through its ability to deliver vitamin E to the brain, constitutes an endogenous neuroprotective agent. Increasing PLTP activity may offer a new way to develop neuroprotective therapies.Neuropsychopharmacology accepted article preview online, 3 December 2012; doi:10.1038/npp.2012.247.
    Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology 12/2012; 38(5). DOI:10.1038/npp.2012.247 · 7.83 Impact Factor
  • 59ème Congrès de la SFMBCB; 05/2012
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    ABSTRACT: The goal of this study was to determine the impact of the nuclear receptor constitutive androstane receptor (CAR) on lipoprotein metabolism and atherosclerosis in hyperlipidemic mice. Low-density lipoprotein receptor-deficient (Ldlr(-/-)) and apolipoprotein E-deficient (ApoE(-/-)) mice fed a Western-type diet were treated weekly with the Car agonist 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) or the vehicle only for 8 weeks. In Ldlr(-/-) mice, treatment with TCPOBOP induced a decrease in plasma triglyceride and intermediate-density lipoprotein/low-density lipoprotein cholesterol levels (≈30% decrease in both cases after 2 months, P<0.01). These mice also showed a significant reduction in the production of very-low-density lipoproteins associated with a decrease in hepatic triglyceride content and the repression of several genes involved in lipogenesis. TCPOBOP treatment also induced a marked increase in the very-low-density lipoprotein receptor in the liver, which probably contributed to the decrease in intermediate-density lipoprotein/low-density lipoprotein levels. Atherosclerotic lesions in the aortic valves of TCPOBOP-treated Ldlr(-/-) mice were also reduced (-60%, P<0.001). In ApoE(-/-) mice, which lack the physiological apoE ligand for the very-low-density lipoprotein receptor, the effect of TCPOBOP on plasma cholesterol levels and the development of atherosclerotic lesions was markedly attenuated. CAR is a potential target in the prevention and treatment of hypercholesterolemia and atherosclerosis.
    Arteriosclerosis Thrombosis and Vascular Biology 07/2011; 31(10):2232-9. DOI:10.1161/ATVBAHA.110.222497 · 5.53 Impact Factor
  • Atherosclerosis Supplements 06/2011; 12(1):78-78. DOI:10.1016/S1567-5688(11)70365-8 · 9.67 Impact Factor
  • Atherosclerosis Supplements 06/2011; 12(1):184-184. DOI:10.1016/S1567-5688(11)70880-7 · 9.67 Impact Factor
  • Atherosclerosis Supplements 06/2011; 12(1):95-96. DOI:10.1016/S1567-5688(11)70449-4 · 9.67 Impact Factor
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    ABSTRACT: Plasma phospholipid transfer protein (PLTP) is involved in intravascular lipoprotein metabolism. PLTP is known to act through 2 main mechanisms: by remodeling high-density lipoproteins (HDL) and by increasing apolipoprotein (apo) B-containing lipoproteins. The aim of this study was to generate a new model of human PLTP transgenic (HuPLTPTg) rabbit and to determine whether PLTP expression modulates atherosclerosis in this species that, unlike humans and mice, displays naturally very low PLTP activity. In HuPLTPTg rabbits, the human PLTP cDNA was placed under the control of the human eF1-α gene promoter, resulting in a widespread tissue expression pattern and in increased plasma PLTP. The HuPLTPTg rabbits showed a significant increase in the cholesterol content of the plasma apoB-containing lipoprotein fractions, with a more severe trait when animals were fed a cholesterol-rich diet. In contrast, HDL cholesterol level was not modified in HuPLTPTg rabbits. Formation of aortic fatty streaks was increased in hypercholesterolemic HuPLTPTg animals as compared with nontransgenic littermates. Human PLTP expression in HuPLTPTg rabbit worsens atherosclerosis as a result of increased levels of atherogenic apoB-containing lipoproteins but not of alterations in their antioxidative protection or in cholesterol content of plasma HDL.
    Arteriosclerosis Thrombosis and Vascular Biology 03/2011; 31(4):766-74. DOI:10.1161/ATVBAHA.110.215756 · 5.53 Impact Factor
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    ABSTRACT: Earlier in vitro studies suggested a putative role for the plasma phospholipid transfer protein (PLTP) in the modulation of blood coagulation. The effect of PLTP expression on blood coagulation under both basal and oxidative stress conditions was compared here in wild-type and PLTP-deficient (PLTP-/-) mice. Under basal conditions, PLTP deficiency was associated with an extended tail bleeding time despite a significant depletion of vascular α-tocopherol content and an impairment of endothelial function. When acute oxidative stress was generated in vivo in the brain vasculature, the steady state levels of oxidized lipid derivatives, the extent of blood vessel occlusion, and the volume of ischemic lesions were more severe in wild-type than in PLTP-/- mice. In addition to its recognized hyperlipidemic, proinflammatory, and proatherogenic properties, PLTP increases blood coagulation and worsens the extent of ischemic lesions in response to acute oxidative stress. Thus, PLTP arises here as a cardiovascular risk factor for the late thrombotic events occurring in the acute phase of atherosclerosis.
    Arteriosclerosis Thrombosis and Vascular Biology 12/2010; 30(12):2452-7. DOI:10.1161/ATVBAHA.110.207654 · 5.53 Impact Factor
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    ABSTRACT: Hexaacyl lipopolysaccharide (LPS) aggregates in aqueous media, but its partially deacylated lipid A moiety forms monomers with weaker toxicity. Because plasma phospholipid transfer protein (PLTP) transfers hexaacyl LPS, its impact on metabolism and biological activity of triacyl lipid A in mice was addressed. Triacyl lipid A bound readily to plasma high-density lipoproteins (HDLs) when active PLTP was expressed [HDL-associated lipid A after 4.5 h: 59.1+/-16.0% of total in wild-type (WT) vs. 32.5+/-10.3% in PLTP-deficient mice, P<0.05]. In the opposite to hexaacyl LPS, plasma residence time of lipid A was extended by PLTP, and proinflammatory cytokines were produced in higher amounts in WT than PLTP(-/-) mice (remaining lipid A after 8 h: 53+/-12 vs. 35+/-7%, and IL6 concentration after 4.5 h: 45.5+/-5.9 vs. 14.6+/-7.8 ng/ml, respectively; P<0.05 in all cases). After 1 wk, onset of B16-induced melanoma was observed in only 30% of lipid A-treated WT mice, whereas >80% of the untreated WT, untreated PLTP-deficient, or lipid A-treated PLTP-deficient animals bore tumors (P<0.05 in all cases). It is concluded that PLTP is essential in mediating the association of triacyl lipid A with lipoproteins, leading to extension of its residence time and to magnification of its proinflammatory and anticancer properties.
    The FASEB Journal 04/2010; 24(9):3544-54. DOI:10.1096/fj.09-152876 · 5.48 Impact Factor
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    ABSTRACT: The nuclear hormone receptor constitutive androstane receptor (CAR, NR1I3) regulates detoxification of xenobiotics and endogenous molecules, and has been shown to be involved in the metabolism of hepatic bile acids and cholesterol. The goal of this study was to address potential effects of CAR on the metabolism of HDL particles, key components in the reverse transport of cholesterol to the liver. Wild-type (WT) mice, transgenic mice expressing human apolipoprotein A-I (HuAITg), and CAR-deficient (CAR(-/-)) mice were treated with the specific CAR agonist 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP). CAR activation decreased HDL cholesterol and plasma apolipoprotein A-I (apoA-I) levels in both WT and HuAITg mice, but not CAR(-/-) mice. Both mouse apoA-I and human apoA-I were decreased by more than 40% after TCPOBOP treatment, and kinetic studies revealed that the production rate of HDL is reduced in TCPOBOP-treated WT mice. In transient transfections, TCPOBOP-activated CAR decreased the activity of the human apoA-I promoter. Although loss of CAR function did not alter HDL levels in normal chow-fed mice, HDL cholesterol, apoA-I concentration, and apoA-I mRNA levels were increased in CAR(-/-) mice relative to WT mice when both were fed a high-fat diet. We conclude that CAR activation in mice induces a pronounced decrease in circulating levels of plasma HDL, at least in part through downregulation of apoA-I gene expression.
    The Journal of Lipid Research 09/2008; 49(8):1682-91. DOI:10.1194/jlr.M700374-JLR200 · 4.73 Impact Factor
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    ABSTRACT: Lipopolysaccharides (LPS) are components of Gram-negative bacteria. The cellular response from the host to LPS is mediated through stepwise interactions involving the lipopolysaccharide-binding protein (LBP), CD14, and MD-2, which produces the rearrangement of TLR4. In addition to LBP, the lipid transfer/lipopolysaccharide-binding protein gene family includes the phospholipid transfer protein (PLTP). Here we show that the intravascular redistribution of LPS from the plasma lipoprotein-free fraction toward circulating lipoproteins is delayed in PLTP-deficient mice. In agreement with earlier in vitro studies, which predicted the neutralization of the endotoxic properties of LPS when associated with lipoproteins, significant increases in the plasma concentration of proinflammatory cytokines were found in PLTP-deficient as compared with wild type mice. Similar inflammatory damage occurred in tissues from wild type and PLTP-deficient mice 24 h after one single intraperitoneal injection of LPS but with a more severe accumulation of red blood cells in glomeruli of LPS-injected PLTP-deficient mice. Complementary ex vivo experiments on isolated splenocytes from wild type and PLTP-deficient mice further supported the ability of cell-derived PLTP to prevent LPS-mediated inflammation and cytotoxicity when combined with lipoprotein acceptors. Finally, PLTP deficiency in mice led to a significant increase in LPS-induced mortality. It is concluded that increasing circulating levels of PLTP may constitute a new and promising strategy in preventing endotoxic shock.
    Journal of Biological Chemistry 08/2008; 283(27):18702-10. DOI:10.1074/jbc.M802802200 · 4.57 Impact Factor
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    ABSTRACT: Phospholipid transfer protein (PLTP) is a multifunctional, extracellular lipid transport protein that plays a major role in lipoprotein metabolism and atherosclerosis. Recent in vivo studies suggested that unlike systemic PLTP, macrophage-derived PLTP would be antiatherogenic. The present study aimed at characterizing the atheroprotective properties of macrophage-derived PLTP. Peritoneal macrophages were isolated from PLTP-deficient and wild-type mice and their biochemical characteristics were compared. It is shown that macrophages isolated from PLTP-deficient mice have increased basal cholesterol content and accumulate more cholesterol in the presence of LDL compared with wild-type cells. Cholesterol parameters in macrophages of PLTP-deficient mice were normalized by dietary alpha-tocopherol supplementation. The antiatherogenic properties of macrophage-derived PLTP are related at least in part to its ability to reduce cholesterol accumulation in macrophages through changes in the alpha-tocopherol content and oxidative status of the cells.
    Arteriosclerosis Thrombosis and Vascular Biology 12/2007; 27(11):2407-12. DOI:10.1161/ATVBAHA.107.151753 · 5.53 Impact Factor
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    ABSTRACT: Our aim was to characterize cholesteryl ester transfer protein (CETP) activity in the early phase of acute myocardial infarction (MI). Cholesteryl ester transfer protein catalyzes the transfer of cholesteryl esters from high-density lipoprotein (HDL) donors to apolipoprotein B-containing lipoprotein acceptors. The CETP concentration, lipid profiles, and the rate of cholesteryl ester transfer (CET) from a tracer dose of radiolabeled HDL toward endogenous lipoproteins were determined within 24 h after symptom onset. Among 347 patients with first MI, CETP concentration, triglycerides, and non-HDL-cholesterol increased across tertiles of the CET rate, whereas HDL-cholesterol, HDL, and LDL sizes decreased gradually. Among lipoprotein donors and acceptors, the best predictors of the CET rate were HDL2b and non-HDL-cholesterol, respectively. Mean age at first MI was 8.5 years lower in the patients from the highest CET tertile than in those in the lowest CET tertile. Diagonal stratification according to both non-HDL-cholesterol and HDL2b tertiles revealed that patients in the highest CET group were 18 years younger than patients in the lowest CET group. Parameters of the high CETP mass/high non-HDL-cholesterol/low HDL2b triad were independently associated with the CET rate. In patients with acute MI, high CET rates are characterized by the presence of the high CETP mass/high non-HDL-cholesterol/low HDL2b triad. The association of high CET rates with young age at first MI lends support to a significant contribution of CETP to the accelerated progression of disease among asymptomatic patients.
    Journal of the American College of Cardiology 12/2007; 50(20):1948-55. DOI:10.1016/j.jacc.2007.06.052 · 15.34 Impact Factor

Publication Stats

957 Citations
263.53 Total Impact Points


  • 2006–2014
    • University of Burgundy
      Dijon, Bourgogne, France
  • 2011
    • ДЗ "Дніпропетровська медична академія"
      Yekaterinoslav, Dnipropetrovsk, Ukraine
  • 2008
    • Baylor College of Medicine
      • Department of Molecular & Cellular Biology
      Houston, Texas, United States
  • 2007
    • Unité Inserm U1077
      Caen, Lower Normandy, France
  • 2004
    • Columbia University
      New York, New York, United States
  • 2002
    • Leiden University
      Leyden, South Holland, Netherlands
  • 1997
    • CHRU de Strasbourg
      Strasburg, Alsace, France