Daniel Gaudet

Université du Québec à Montréal, Montréal, Quebec, Canada

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Publications (346)1751.04 Total impact

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    ABSTRACT: Familial chylomicronemia syndrome (FCS) is a rare lipid disease caused by complete lipoprotein lipase (LPL) deficiency resulting in fasting chylomicronemia and severe hypertriglyceridemia. Inhibition of diacylglycerol acyltransferase 1 (DGAT1), which mediates chylomicron triglyceride (TG) synthesis, is an attractive strategy to reduce TG levels in FCS. In this study we assessed the safety, tolerability and TG-lowering efficacy of the DGAT1 inhibitor pradigastat in patients with FCS. Six FCS patients were enrolled in an open-label clinical study. Following a 1-week very low fat diet run-in period patients underwent baseline lipid assessments, including a low fat meal tolerance test. Patients then underwent three consecutive 21 day treatment periods (pradigastat at 20, 40 & 10 mg, respectively). Treatment periods were separated by washout periods of ≥4 weeks. Fasting TG levels were assessed weekly through the treatment periods. Postprandial TGs, ApoB48 and lipoprotein lipid content were also monitored. Following once daily oral dosing, steady-state exposure was reached by Day 14. There was an approximately dose proportional increase in pradigastat exposure at studied doses. Pradigastat was associated with a 41% (20 mg) and 70% (40 mg) reduction in fasting triglyceride over 21 days of treatment. The reduction in fasting TG was almost entirely accounted for by a reduction in chylomicron TG. Pradigastat treatment also led to substantial reductions in postprandial TG as well as apo48 (both fasting and postprandial). Pradigastat was safe and well tolerated, with only mild, transient gastrointestinal adverse events. The novel DGAT1 inhibitor pradigastat substantially reduces plasma TG levels in FCS patients, and may be a promising new treatment for this orphan disease. Trial registration ClinicalTrials.gov identifier NCT01146522.
    Lipids in Health and Disease 12/2015; 14(1). DOI:10.1186/s12944-015-0006-5 · 2.22 Impact Factor
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    ABSTRACT: Background Excess visceral fat is a major risk factor for hypertension. Enhanced blood pressure (BP) reactivity and delayed BP recovery from physical and mental challenges predict future hypertension.Objectives Determine whether visceral fat is associated with higher BP reactivity and delayed BP recovery from physical and mental challenges during adolescence.Methods In a community-based sample of 283 male and 308 female adolescents, we measured visceral fat with magnetic resonance imaging, total body fat with bioimpedance, and beat-by-beat BP with a Finometer at rest and during physical (10-min standing) and mental (2-min math stress) challenges.ResultsMales vs. females showed greater BP reactivity and no differences in BP recovery from either type of challenges. Visceral fat was positively associated with BP reactivity to standing up only and in males only (+8.4 ± 3.6 mmHg per 1 log cm3 of visceral fat, P = 0.008), and this association was independent of total body fat. No association was seen between visceral fat and BP recovery from either type of challenge in either sex. All these associations were independent of age, puberty stage, height and initial BP.Conclusions Adolescent males vs. females demonstrate greater BP reactivity but similar BP recovery from physical and mental challenges. Excess visceral fat enhances BP reactivity to physical but not mental challenges in males only.
    Pediatric Obesity 10/2015; 10(5). DOI:10.1111/ijpo.12068 · 4.57 Impact Factor
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    ABSTRACT: Apolipoprotein C-III (APOC3) is a key regulator of plasma triglyceride levels. Elevated triglyceride levels are associated with a risk of adverse cardiovascular events and pancreatitis. ISIS 304801 is a second-generation antisense inhibitor of APOC3 synthesis. We conducted a randomized, double-blind, placebo-controlled, dose-ranging, phase 2 study to evaluate ISIS 304801 in untreated patients with fasting triglyceride levels between 350 mg per deciliter (4.0 mmol per liter) and 2000 mg per deciliter (22.6 mmol per liter) (ISIS 304801 monotherapy cohort), as well as in patients receiving stable fibrate therapy who had fasting triglyceride levels between 225 mg per deciliter (2.5 mmol per liter) and 2000 mg per deciliter (ISIS 304801-fibrate cohort). Eligible patients were randomly assigned to receive either ISIS 304801, at doses ranging from 100 to 300 mg, or placebo, once weekly for 13 weeks. The primary outcome was the percentage change in APOC3 level from baseline. A total of 57 patients were treated in the ISIS 304801 monotherapy cohort (41 received active agent, and 16 received placebo), and 28 patients were treated in the ISIS 304801-fibrate cohort (20 received active agent, and 8 received placebo). The mean (±SD) baseline triglyceride levels in the two cohorts were 581±291 mg per deciliter (6.6±3.3 mmol per liter) and 376±188 mg per deciliter (4.2±2.1 mmol per liter), respectively. Treatment with ISIS 304801 resulted in dose-dependent and prolonged decreases in plasma APOC3 levels when the drug was administered as a single agent (decreases of 40.0±32.0% in the 100-mg group, 63.8±22.3% in the 200-mg group, and 79.6±9.3% in the 300-mg group, vs. an increase of 4.2±41.7% in the placebo group) and when it was administered as an add-on to fibrates (decreases of 60.2±12.5% in the 200-mg group and 70.9±13.0% in the 300-mg group, vs. a decrease of 2.2±25.2% in the placebo group). Concordant reductions of 31.3 to 70.9% were observed in triglyceride levels. No safety concerns were identified in this short-term study. We found that treatment with ISIS 304801 was associated with significant lowering of triglyceride levels, among patients with a broad range of baseline levels, through selective antisense inhibition of APOC3 synthesis. (Funded by Isis Pharmaceuticals; ClinicalTrials.gov number, NCT01529424.).
    New England Journal of Medicine 07/2015; 373(5):438-47. DOI:10.1056/NEJMoa1400283 · 55.87 Impact Factor
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    ABSTRACT: DNA methylation may contribute to the etiology of complex genetic disorders through its impact on genome integrity and gene expression; it is modulated by DNA-sequence variants, named methylation quantitative-trait loci (meQTLs). Most meQTLs influence methylation of a few CpG dinucleotides within short genomic regions (<3kb). Here we identified a layered genetic control of DNA methylation at numerous CpGs across a long 300-kb genomic region. This control involved a single long-range meQTL and multiple local meQTLs. The long-range meQTL explained up to 75% of variance in methylation of CpGs located over extended areas of the 300-kb region. The meQTL was identified in four samples (p=2.8x10(-17), p=3.1x10(-31), 4.0x10(-71), 5.2x10(-199)), comprising a total of 2,796 individuals. The long-range meQTL was strongly associated not only with DNA methylation but also with mRNA expression of several genes within the 300-kb region (p=7.1x10(-18)-1.0x10(-123)). The associations of the meQTL with gene expression became attenuated when adjusted for DNA methylation (causal inference test: p=2.4×10(-13)-7.1×10(-20)), indicating coordinated regulation of DNA methylation and gene expression. Further, the long-range meQTL was found to be in linkage disequilibrium with the most replicated locus of multiple sclerosis, a disease affecting primarily the brain white matter. In middle-aged adults free of the disease, we observed that the risk allele was associated with subtle structural properties of the brain white matter found in multiple sclerosis (p=0.02). In summary, we identified a long-range meQTL that controls methylation and expression of several genes and may be involved in increasing brain vulnerability to multiple sclerosis. © The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
    Human Molecular Genetics 07/2015; DOI:10.1093/hmg/ddv294 · 6.39 Impact Factor
  • Atherosclerosis 07/2015; 241(1):e26. DOI:10.1016/j.atherosclerosis.2015.04.100 · 3.99 Impact Factor
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    ABSTRACT: Despite current standard-of-care, many patients at high cardiovascular disease (CVD) risk still have elevated low-density lipoprotein cholesterol (LDL-C). Alirocumab is a fully human monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9). To compare LDL-C-lowering efficacy of adding alirocumab vs other common lipid-lowering strategies. Design, Patients, Interventions: Patients (n=355) with CVD and LDL-C levels ≥70 mg/dL, or CVD risk factors and LDL-C ≥100 mg/dL, on baseline atorvastatin 20 or 40 mg, were randomized to: (1) add-on alirocumab 75 mg every 2 weeks (Q2W) subcutaneously; (2) add-on ezetimibe 10 mg/day; (3) double atorvastatin dose; (4) for atorvastatin 40 mg regimen only, switch to rosuvastatin 40 mg. For patients not achieving protocol-defined LDL-C goals, alirocumab dose was increased (blinded) at week 12 to 150 mg Q2W. Primary endpoint was % change in calculated LDL-C from baseline to 24 weeks (intent-to-treat). Among atorvastatin 20 and 40 mg regimens respectively, add-on alirocumab reduced LDL-C levels by 44.1% and 54.0% (p<0.001 vs all comparators); add-on ezetimibe, 20.5% and 22.6%; doubling of atorvastatin dose, 5.0% and 4.8%; and switching atorvastatin 40 mg to rosuvastatin 40 mg, 21.4%. Most alirocumab-treated patients (87.2% and 84.6%) achieved their LDL-C goals. Most alirocumab-treated patients (86%) maintained their 75 mg Q2W regimen. Treatment-emergent adverse events occurred in 65.4% of alirocumab patients, vs 64.4% ezetimibe and 63.8% double atorvastatin/switch to rosuvastatin (data pooled). Adding alirocumab to atorvastatin provided significantly greater LDL-C reductions vs adding ezetimibe, doubling atorvastatin dose, or switching to rosuvastatin, and enabled greater LDL-C goal achievement.
    The Journal of Clinical Endocrinology and Metabolism 06/2015; 100(8):jc20151520. DOI:10.1210/jc.2015-1520 · 6.21 Impact Factor
  • Pancreatology 06/2015; 15(3):S53-S54. DOI:10.1016/j.pan.2015.05.212 · 2.84 Impact Factor
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    ABSTRACT: Background and objectives • Homozygous familial hypercholesterolemia (HoFH) is a rare genetic condition characterized by markedly elevated low-density lipoprotein cholesterol (LDL-C) levels, inadequate response to conventional drug therapy and premature-onset cardiovascular disease.1 • HoFH is most commonly caused by the occurrence of two LDL–receptor (LDL-R) gene (LDLR) mutations but can also be caused by mutations in other genes which directly or indirectly affect the LDL-C/LDL-R pathway, including the genes encoding apolipoprotein B (APOB) and proprotein convertase subtilisin/kexin type 9 (PCSK9), and LDL-receptor adapter protein 1 (LDLRAP1) (Figure 1).1 • The genotype and clinical phenotype of HoFH patients varies, and depending on the type of mutations, patients can present with untreated LDL-C levels as low as 4.4 mmol/L.1, 2 • To further explore the variability of HoFH, we examined the phenotype, genotype and baseline-treated LDL-C levels in a cohort of patients with genetically confirmed HoFH enrolled in a clinical trial.
    ISA 2015 - 17th International Symposium on Atherosclerosis, Netherlands, Amsterdam; 05/2015
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    ABSTRACT: Homozygous familial hypercholesterolemia features a wide range of LDL-C levels Abstract nr. 389 Author Stefanutti , Claudia, ‘Sapienza’ University of Rome, Rome, Italy Co-author(s) - Blom , Dirk Co-author(s) - Averna , Maurizio Co-author(s) - Meagher , Emma Co-author(s) - Theron , Hendrik du toit Co-author(s) - Marais , David Co-author(s) - Hegele , Robert Co-author(s) - Sirtori , Cesare Co-author(s) - Shah , Prediman Co-author(s) - Gaudet , Daniel Co-author(s) - Vigna , Giovanni Co-author(s) - Du Plessis , Anne Co-author(s) - Bloedon , LeAnne Co-author(s) - Rader , Daniel Co-author(s) - Cuchel , Marina Topic Dyslipidemia; Lipids, Lipoproteins and Apolipoproteins Keywords Familial Hypercholesterolemia,Genetics,Hypolipidemic Drugs,LDL Objectives: Homozygous familial hypercholesterolemia (HoFH) is a rare genetic disease characterized by highly elevated LDL-C levels, limited response to conventional lipid-lowering therapies, and increased risk of premature CVD. Severe atherosclerosis may develop before the age of 30. Traditionally, HoFH has been diagnosed according to untreated plasma LDL-C levels >500mg/dL; or treated levels ≥300mg/dL. More recently, studies suggest that the range of LDL-C levels in HoFH may be more variable. To explore this, we analyzed baseline LDL-C levels in a group of treated clinical trial subjects with genetically confirmed HoFH. Methods: Baseline characteristics of 29 HoFH patients from a multinational Phase 3 study were collected. All subjects were ≥18 years and met the diagnosis of HoFH based on: untreated TC >500 mg/dL and both parents with documented untreated TC >250mg/dL; documented genetic mutations of genes known to affect LDLR functionality; or skin fibroblast LDLR activity <20% normal. Results: All patients had confirmed mutations in both alleles of LDLR (n=28) or LDLRAP1 (n=1) gene. Age range was 18-55 years. Nearly all patients (93%) had a history of CVD: CABG, 35%; coronary angioplasty, 10%; aortic valve replacement, 10%; mitral valve replacement/repair, 10%. Therapy included statins (93%; 76% with ezetimibe) and apheresis (62%). Treated LDL-C levels were in the range 152-564mg/dL; 38% had LDL-C <300mg/dL and 14% <200mg/dL (Table). There were no differences in LDL-C levels between subjects who were receiving apheresis treatment and those who were not. Conclusion: Consistent with other recent studies, this analysis provides additional evidence of the heterogeneity of on-treatment LDL-C values in patients with genetically defined HoFH. Diagnosis of HoFH should not rely solely on treated LDL-C >300 mg/dL, but should also include other clinical or genetic factors. Table of baseline characteristics Subdivision 3. Clinical Studies Presentation Preference Electronic poster presentation
    17th triennial congress of the International Atherosclerosis Society, Netherlands, Amsterdam; 05/2015
  • Journal of Clinical Lipidology 05/2015; 9(3):449-450. DOI:10.1016/j.jacl.2015.03.065 · 3.90 Impact Factor
  • Journal of Clinical Lipidology 05/2015; 9(3):450. DOI:10.1016/j.jacl.2015.03.066 · 3.90 Impact Factor
  • Journal of Clinical Lipidology 05/2015; 9(3):454-455. DOI:10.1016/j.jacl.2015.03.073 · 3.90 Impact Factor
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    ABSTRACT: (EN): The invention relates to traceable metallic products, methods of uses and methods of making same. The metallic products may be made traceable for integrity purposes, identification purposes, counterfeit avoidance and the like. The invention also relates to metallic supports for nanostorage of various compounds and samples. (FR): L'invention concerne des produits métalliques traçables, des procédés d'utilisation et des procédés de fabrication de ceuxci. Ces produits métalliques peuvent être rendus traçables à des fins d'intégrité, d'identification, de lutte contre la contrefaçon et analogue. L'invention concerne également des supports métalliques pour le nanostockage de divers composés et échantillons.
    Ref. No: WO/2015/054778, Year: 04/2015
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    ABSTRACT: Objective: Hypertension and osteoporosis are age-related health risks differentially expressed in men and women. Here we have analysed their prevalence in a randomly selected cross-sectional cohort [CARTaGENE (CaG) of Quebec, Canada and explored their existing relationships along with height, arterial stiffness and bone fractures. Methods: The principal cohort CaG included 20 007 individuals of age 40–70 years. Participants were subjected to an extensive phenotyping and a questionnaire of medical history and habits. Results: We determined the differences in height of participants and their relation to hypertension status and sex in this cohort and validated it in two other cohorts (The Canadian Heart Health Study and a family cohort from the Saguenay Lac Saint-Jean, a region of Quebec). In all three cohorts, we found that at younger age individuals with hypertension are taller than normotensive individuals, but they have a shorter stature at an older age compared with normotensive individuals. In CaG, we observed that hypertension, low bone mineral density (BMD) and arterial stiffness are strongly associated with height when adjusted for antihypertensive medications (P < 0.0001). Fractures are the net outcome of low BMD, and a significant association is observed (odds ratio = 2.34, confidence interval = 2.12–2.57); this relation was stronger in hypertensive individuals compared with normotensive individuals particularly in younger hypertensive individuals. In addition, we observed that increased arterial stiffness was significantly correlated with a low BMD in both men and women at all ages. Conclusion: Shorter stature in elderly, low BMD and fractures correlated with increased arterial stiffness and hypertension. We propose that hypertension and osteoporosis share components of accelerated aging.
    Journal of Hypertension 04/2015; 33(4):727-735. DOI:10.1097/HJH.0000000000000475 · 4.72 Impact Factor
  • Journal of the American College of Cardiology 03/2015; 65(10):A1370. DOI:10.1016/S0735-1097(15)61370-5 · 16.50 Impact Factor
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    ABSTRACT: Objective Lomitapide (a microsomal triglyceride transfer protein inhibitor) is an adjunctive treatment for homozygous familial hypercholesterolaemia (HoFH), a rare genetic condition characterised by elevated low-density lipoprotein-cholesterol (LDL-C), and premature, severe, accelerated atherosclerosis. Standard of care for HoFH includes lipid-lowering drugs and lipoprotein apheresis. We conducted a post-hoc analysis using data from a pivotal Phase 3 study to assess whether concomitant apheresis affected the lipid-lowering efficacy of lomitapide Methods Existing lipid-lowering therapy, including apheresis, was to remain stable from Week –6 to Week 26. Lomitapide dose was escalated on the basis of individual safety/tolerability from 5 mg to a maximum of 60 mg a day. The primary endpoint was mean percent change in LDL-C from baseline to Week 26 (efficacy phase), after which patients remained on lomitapide through Week 78 for safety assessment and further evaluation of efficacy. During this latter period, apheresis could be adjusted. We analysed the potential impact of apheresis on LDL-C reductions in patients receiving lomitapide Results Of the 29 patients that entered the efficacy phase, 18 (62%) were receiving apheresis at baseline. Twenty-three patients (13 receiving apheresis) completed the Week-26 evaluation. Of the six patients who discontinued in the first 26 weeks, five were receiving apheresis. There were no significant differences in percent change from baseline of LDL-C at Week 26 in patients treated (–48%) and not treated (–55%) with apheresis (p=0.545). Lp(a) levels did not change in either group Conclusion The LDL-C lowering efficacy of lomitapide is independent of lipoprotein apheresis
    Atherosclerosis 03/2015; 240(2). DOI:10.1016/j.atherosclerosis.2015.03.014 · 3.99 Impact Factor
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    ABSTRACT: To assess whether DNA methylation is associated with coronary artery disease (CAD). An epigenome-wide analysis has been performed on leucocytes from familial hypercholesterolemic (FH) men with (n = 6) or without CAD (n = 6). The results were replicated in an extended sample of FH men (n = 61) and in non-FH men (n = 100) for two of the top differentially methylated loci. FH men with CAD had significantly more hypomethylated and hypermethylated loci and showed less DNA methylation level variability compared with men without CAD (p < 0.001). Moreover, COL14A1 and MMP9 DNA methylation levels were associated with CAD, age of onset of CAD or CAD risk factors. These results suggest that epigenome-wide changes are associated with CAD occurrence in men.
    Epigenomics 02/2015; 7(1):17-34. DOI:10.2217/epi.14.64 · 4.65 Impact Factor
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    ABSTRACT: Patients with homozygous familial hypercholesterolemia (HoFH) are at extremely elevated risk for early cardiovascular disease because of exposure to elevated low-density lipoprotein cholesterol (LDL-C) plasma levels from birth. Lowering LDL-C by statin therapy is the cornerstone for cardiovascular disease prevention, but the residual risk in HoFH remains high, emphasizing the need for additional therapies. In the present study, we evaluated the effect of serial infusions with CER-001, a recombinant human apolipoprotein A-I (apoA-I)-containing high-density lipoprotein-mimetic particle, on carotid artery wall dimensions in patients with HoFH. Twenty-three patients (mean age 39.4 ± 13.5 years, mean LDL-C 214.2 ± 81.5 mg/dL) with genetically confirmed homozygosity or compound heterozygosity for LDLR, APOB, PCSK9, or LDLRAP1 mutations received 12 biweekly infusions with CER-001 (8 mg/kg). Before and 1 hour after the first infusion, lipid values were measured. Magnetic resonance imaging (3-T magnetic resonance imaging) scans of the carotid arteries were acquired at baseline and after 24 weeks to assess changes in artery wall dimensions. After CER-001 infusion, apoA-I increased from 114.8 ± 20.7 mg/dL to 129.3 ± 23.0 mg/dL. After 24 weeks, mean vessel wall area (primary end point) decreased from 17.23 to 16.75 mm(2) (P = .008). A trend toward reduction of mean vessel wall thickness was observed (0.75 mm at baseline and 0.74 mm at follow-up, P = .0835). In HoFH, 12 biweekly infusions with an apoA-I-containing high-density lipoprotein-mimetic particle resulted in a significant reduction in carotid mean vessel wall area, implying that CER-001 may reverse atherogenic changes in the arterial wall on top of maximal low-density lipoprotein-lowering therapy. This finding supports further clinical evaluation of apoA-I-containing particles in patients with HoFH. Copyright © 2015 Mosby, Inc. All rights reserved.
    American heart journal 01/2015; 169(5). DOI:10.1016/j.ahj.2015.01.008 · 4.46 Impact Factor
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    ABSTRACT: Adolescents who exhibit exaggerated blood pressure (BP) reactivity to physical and mental challenges are at increased risk of developing hypertension in adulthood. BP at rest and in response to challenges is higher in males than females, beginning in early adolescence. CYP17A1 is one of the well-established gene loci of adult hypertension. Here, we investigated whether this gene locus is associated with elevated BP at rest and in response to physical (active standing) and mental (math stress) challenges in adolescence. We studied 496 male and 532 female adolescents (age 12-18 years) who were recruited from a genetic founder population. Our results showed that the variant of CYP17A1 rs10786718 was associated with enhanced BP reactivity to the mental but not physical challenge and in males but not females. In males, BP increase in response to math stress was higher in major versus minor allele homozygotes by 7.6 mm Hg (P = 8.3 × 10(-6)). Resting BP was not associated with the CYP17A1 variant in either sex. These results suggest that, in adolescent males but not females, CYP17A1 enhances BP reactivity to mental stress. Whether this effect contributes to the higher prevalence of hypertension in males than females later in life remains to be determined.
    International Journal of Hypertension 01/2015; 2015:734586. DOI:10.1155/2015/734586
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Publication Stats

8k Citations
1,751.04 Total Impact Points


  • 2009–2015
    • Université du Québec à Montréal
      Montréal, Quebec, Canada
  • 2001–2015
    • Université de Montréal
      • Department of Medicine
      Montréal, Quebec, Canada
  • 2014
    • AVACO AG, Switzerland
      Basel-Landschaft, Switzerland
    • Centre hospitalier affilié universitaire de Québec (CHA)
      Quebec City, Quebec, Canada
  • 2013
    • Université de Sherbrooke
      Sherbrooke, Quebec, Canada
  • 1997–2013
    • University of Québec in Chicoutimi
      • Department of Health Sciences
      Saguenay, Quebec, Canada
  • 2010
    • University of Nottingham
      • Brain and Body Centre
      Nottigham, England, United Kingdom
  • 2007
    • University of Helsinki
      Helsinki, Uusimaa, Finland
  • 2006
    • Institute of Heart Sciences
      Valladolid, Castille and León, Spain
  • 1997–2006
    • Laval University
      • Department of Food and Nutrition Sciences
      Quebec City, Quebec, Canada
  • 2005
    • University of Amsterdam
      Amsterdamo, North Holland, Netherlands
    • New York State
      New York City, New York, United States
  • 2002–2004
    • Philadelphia ZOO
      Filadelfia, Pennsylvania, United States
  • 2003
    • University of Toronto
      Toronto, Ontario, Canada
    • Children's Hospital of Eastern Ontario
      Ottawa, Ontario, Canada
  • 2001–2002
    • Medical College of Wisconsin
      • Department of Medicine
      Milwaukee, Wisconsin, United States
  • 2000–2001
    • Centre hospitalier de l'Université de Montréal (CHUM)
      Montréal, Quebec, Canada
    • University of Texas at San Antonio
      San Antonio, Texas, United States