Daniel Gaudet

Université de Montréal, Montréal, Quebec, Canada

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Publications (254)1303.23 Total impact

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    ABSTRACT: Psychiatric conditions contribute the most to global health burden.•Developmental cascades provide a framework for understanding causes and consequences.•Multi-generational design enables studies of virtual health trajectories.•Saguenay Youth Study is a multi-generational and multi-system cohort designed along these lines.
    Developmental Cognitive Neuroscience. 10/2014;
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    ABSTRACT: Prenatal exposure to maternal cigarette smoking (prenatal smoke exposure) had been associated with altered DNA methylation (DNAm) at birth.
    Environmental Health Perspectives 10/2014; · 7.26 Impact Factor
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    ABSTRACT: Background Heterozygous familial hypercholesterolaemia is characterised by low cellular uptake of LDL cholesterol, increased plasma LDL cholesterol concentrations, and premature cardiovascular disease. Despite intensive statin therapy, with or without ezetimibe, many patients are unable to achieve recommended target levels of LDL cholesterol. We investigated the effect of PCSK9 inhibition with evolocumab (AMG 145) on LDL cholesterol in patients with this disorder. Methods This multicentre, randomised, double-blind, placebo-controlled trial was undertaken at 39 sites (most of which were specialised lipid clinics, mainly attached to academic institutions) in Australia, Asia, Europe, New Zealand, North America, and South Africa between Feb 7 and Dec 19, 2013. 331 eligible patients (18–80 years of age), who met clinical criteria for heterozygous familial hypercholesterolaemia and were on stable lipid-lowering therapy for at least 4 weeks, with a fasting LDL cholesterol concentration of 2·6 mmol/L or higher, were randomly allocated in a 2:2:1:1 ratio to receive subcutaneous evolocumab 140 mg every 2 weeks, evolocumab 420 mg monthly, or subcutaneous placebo every 2 weeks or monthly for 12 weeks. Randomisation was computer generated by the study sponsor, implemented by a computerised voice interactive system, and stratified by LDL cholesterol concentration at screening (higher or lower than 4·1 mmol/L) and by baseline ezetimibe use (yes/no). Patients, study personnel, investigators, and Amgen study staff were masked to treatment assignments within dosing frequency groups. The coprimary endpoints were percentage change from baseline in LDL cholesterol at week 12 and at the mean of weeks 10 and 12, analysed by intention-to-treat. This trial is registered with ClinicalTrials.gov, number NCT01763918. Findings Of 415 screened patients, 331 were eligible and were randomly assigned to the four treatment groups: evolocumab 140 mg every 2 weeks (n=111), evolocumab 420 mg monthly (n=110), placebo every 2 weeks (n=55), or placebo monthly (n=55). 329 patients received at least one dose of study drug. Compared with placebo, evolocumab at both dosing schedules led to a significant reduction in mean LDL cholesterol at week 12 (every-2-weeks dose: 59·2% reduction [95% CI 53·4–65·1], monthly dose: 61·3% reduction [53·6–69·0]; both p<0·0001) and at the mean of weeks 10 and 12 (60·2% reduction [95% CI 54·5–65·8] and 65·6% reduction [59·8–71·3]; both p<0·0001). Evolocumab was well tolerated, with rates of adverse events similar to placebo. The most common adverse events occurring more frequently in the evolocumab-treated patients than in the placebo groups were nasopharyngitis (in 19 patients [9%] vs five [5%] in the placebo group) and muscle-related adverse events (ten patients [5%] vs 1 [1%]). Interpretation In patients with heterozygous familial hypercholesterolaemia, evolocumab administered either 140 mg every 2 weeks or 420 mg monthly was well tolerated and yielded similar and rapid 60% reductions in LDL cholesterol compared with placebo. Funding Amgen Inc.
    Lancet. 10/2014;
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    ABSTRACT: Preference for fatty foods is a risk factor for obesity. It is a complex behaviour that involves the brain reward system and is regulated by genetic and environmental factors, such as the opioid receptor mu-1 gene (OPRM1) and prenatal exposure to maternal cigarette smoking (PEMCS). We examined whether OPRM1 and PEMCS interact in influencing fat intake and whether exposure-associated epigenetic modifications of OPRM1 may mediate this gene-environment interaction.
    Journal of psychiatry & neuroscience: JPN 08/2014; 39(4):130263. · 6.24 Impact Factor
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    ABSTRACT: The combination of hypertriglyceridemia (hyperTG) and hyperapobetalipoproteinemia (hyperapoB) is associated with an increased coronary artery disease (CAD) risk. Apolipoprotein (apo) E and lipoprotein lipase (LPL) genes are involved in the catabolism of triglycerides (TG)-rich apoB-containing lipoproteins (VLDL). Several apoE and LPL gene variants affecting CAD risk, plasma TG or apoB concentrations have an allelic frequency of >5% in the general population. This study examined the combined effect of frequent apoE and LPL gene polymorphisms on the expression of hyperTG and hyperapoB. ApoE (E2, E3, and E4) and LPL (D9N, N291S, G188E, and P207L) were genotyped and fasting lipid profiles were assessed among 1,441 French-Canadian subjects. Multivariate analyses were performed to estimate the relationship between apoE and LPL gene variants and the risk of hyperTG (TG>1.7 mmol/l) and hyperapoB (apoB>0.9 g/l). Compared to apoE3 carriers, the apoE4 allele significantly increased the risk of expressing the "hyperTG/hyperapoB" phenotype [odds ratio (OR)=1.95; p=0.014]. This risk was significantly exacerbated (OR=4.69; p=0.017) by the presence of frequent deleterious LPL gene variants in this population. The apoE2 allele was negatively associated with hyperTG/hyperapoB (OR=0.49; p=0.002) in the absence of a deleterious LPL gene variant. These results suggest that epistasis is a phenomenon to consider while assessing the CAD risk associated with gene variants or the effect of frequent alleles on high-risk lipid profiles.
    Journal of endocrinological investigation 07/2014; 30(7):551-7. · 1.65 Impact Factor
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    Nature medicine. 06/2014; 20(6):578-579.
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    ABSTRACT: BACKGROUND: Patients suffering from HoFH are characterized by extreme atherosclerosis progression, leading to premature death. HDL has been shown to exert anti-atherogenic effects. We set out to investigate the effect of infusions of CER-001, an engineered pre-beta HDL mimetic, on atherosclerosis by carotid 3T MRI.
    82nd Congress of the European-Atherosclerosis-Society (EAS), Madrid, SPAIN; 05/2014
  • Journal of Clinical Lipidology 05/2014; 8(3):312. · 3.59 Impact Factor
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    ABSTRACT: Aims: To determine whether placental IGF1R, IGFBP3, INSR and IGF1 DNA methylation and mRNA levels were dysregulated when exposed to maternal impaired glucose tolerance (IGT) and investigate whether the epigenetic profile is associated with feto-placental developmental markers. Patients & methods: The IGT diagnosis was made according to the WHO criteria (IGT: n = 34; normal glucose tolerance [NGT]: n = 106). DNA methylation and mRNA levels were quantified using bisulfite pyrosequencing and qRT-PCR, respectively. Results: IGF1R and IGFBP3 DNA methylation levels were lower in placentas exposed to IGT compared with NGT (-4.3%; p = 0.021 and -2.5%; p = 0.006 respectively) and correlated with 2-h post-oral glucose tolerance test (OGTT) glycemia (r = -0.23; p = 0.010 and r = -0.20; p = 0.028, respectively). IGF1R mRNA levels were associated with newborns' growth markers (e.g., birth weight; r = 0.20; p = 0.032). Conclusion: These results support the growth-promoting role of the IGF system in placental/fetal development and suggest that the IGF1R and IGFBP3 DNA methylation profiles are dysregulated in IGT, potentially affecting the fetal metabolic programming.
    Epigenomics 04/2014; 6(2):193-207. · 2.43 Impact Factor
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    ABSTRACT: Gene polymorphisms associated so far with plasma lipid concentrations explain only a fraction of their heritability, which can reach up to 60%. Recent studies suggest that epigenetic modifications (DNA methylation) could contribute to explain part of this missing heritability. We therefore assessed whether the DNA methylation of key lipoprotein metabolism genes is associated with high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and triglyceride levels in patients with familial hypercholesterolemia (FH). Untreated FH patients (61 men and 37 women) were recruited for the measurement of blood DNA methylation levels at the ABCG1, LIPC, PLTP and SCARB1 gene loci using bisulfite pyrosequencing. ABCG1, LIPC and PLTP DNA methylation was significantly associated with HDL-C, LDL-C and triglyceride levels in a sex-specific manner (all P<0.05). FH subjects with previous history of coronary artery disease (CAD) had higher LIPC DNA methylation levels compared with FH subjects without CAD (P = 0.02). Sex-specific multivariable linear regression models showed that new and previously reported epipolymorphisms (ABCG1-CpGC3, LIPC-CpGA2, mean PLTP-CpGC, LPL-CpGA3, CETP-CpGA2, and CETP-CpGB2) significantly contribute to variations in plasma lipid levels (all P<0.001 in men and P<0.02 in women), independently of traditional predictors such as age, waist circumference, blood pressure, fasting plasma lipids and glucose levels. These results suggest that epigenetic perturbations of key lipoprotein metabolism genes are associated with plasma lipid levels, contribute to the interindividual variability and might partially explain the missing heritability of plasma lipid levels, at least in FH.
    Epigenetics: official journal of the DNA Methylation Society 02/2014; 9(5). · 4.58 Impact Factor
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    ABSTRACT: Aim:ADRB3 DNA hypermethylation was recently associated with dyslipidemia in familial hypercholesterolemia (FH). In this study, we verified whether ADRB3 DNA methylation in blood and visceral adipose tissue (VAT) was associated with obesity and its related complications. Methods: DNA methylation levels were measured in the blood of 61 FH men, and the blood and VAT of 30 severely obese men. Common ADRB3 polymorphisms were genotyped in all subjects. Results: Higher ADRB3 DNA methylation levels were significantly associated with lower low-density lipoprotein cholesterol levels (r = -0.40; p = 0.01) in FH, and with a lower waist-to-hip ratio (r = -0.55; p = 0.01) and higher blood pressure (r = 0.43; p = 0.05) in severely obese men. ADRB3 g.-843C>T and p.W64R polymorphisms were found to be strongly associated (p < 0.001) with ADRB3 DNA methylation and mRNA levels. Conclusion: Although further studies are needed, these results suggest that epigenetic changes at the ADRB3 gene locus might be involved in the development of obesity and its related metabolic complications.
    Epigenomics 02/2014; 6(1):33-43. · 2.43 Impact Factor
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    ABSTRACT: Background: There are important inter-individual variations in the incidence and severity of acute pancreatitis in patients with severe hypertriglyceridemia. Several genes involved in triglyceride-rich lipoprotein metabolism or serine proteases pathways are known to influence the risk of pancreatitis. Aim: To evaluate the association between genes regulating serine proteases, chymotrypsin C (CTRC) and serine peptidase inhibitor kazal type1 (SPINK1), and recurrence of hospitalizations for acute pancreatitis or severe abdominal pain in patients with Lipoprotein Lipase Deficiency (LPLD), a rare and extreme monogenic model of severe hypertriglyceridemia and pancreatitis. Method: The CTRC and SPINK1 genes promoter and coding regions sequencing has been performed in a sample of 38 LPLD adults (22 men and 16 women) and 100 controls (53 men and 47 women). Estimation of the association of CTRC and SPINK1 gene variants or combinations of variants with history of hospitalizations for pancreatitis or acute abdominal pain in LPLD was investigated using non-parametric analyses with correction for multiple testing and logistic regression models controlling for age, gender, family history, and life habits. Results: Gene sequencing followed by genotype-stratified analyses of the CTRC and SPINK1 genes in LPLD and controls revealed a positive association between recurrence of hospitalizations and the rs545634 (CTRC)-rs11319 (SPINK1) combination [OR = 41.4 (CI: 2.0-848.0); p = 0.016]. In all models, a positive family history of pancreatitis was a significant predictor of recurrent hospitalizations independently of the contribution of SPINK1 or CTRC (p < 0.001). Conclusion: These results suggest that a positive family history of pancreatitis and genetic markers in the serine protease pathways could be associated with a risk of recurrent hospitalization for acute pancreatitis in severe hypertriglyceridemia due to LPLD.
    Frontiers in Genetics 01/2014; 5:90.
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    ABSTRACT: Personalized medicine uses various individual characteristics to guide medical decisions. Apolipoprotein (ApoE), the most studied polymorphism in humans, has been associated with several diseases. The purpose of this review is to elucidate the potential role of ApoE polymorphisms in personalized medicine, with a specific focus on neurodegenerative diseases, by giving an overview of its influence on disease risk assessment, diagnosis, prognosis, and therapy. This review is not a systematic inventory of the literature, but rather a summary and discussion of novel, influential and promising works in the field of ApoE research that could be valuable for personalized medicine. Empirical evidence suggests that ApoE genotype informs pre-symptomatic risk for a wide variety of diseases, is valuable for the diagnosis of type III dysbetalipoproteinemia, increases risk of dementia in neurodegenerative diseases, and is associated with a poor prognosis following acute brain damage. ApoE status appears to influence the efficacy of certain drugs, outcome of clinical trials, and might also give insight into disease prevention. Assessing ApoE genotype might therefore help to guide medical decisions in clinical practice.
    Frontiers in Aging Neuroscience 01/2014; 6:154. · 5.20 Impact Factor
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    ABSTRACT: Lipoprotein(a) [Lp(a)] is an independent risk factor for cardiovascular disease, with limited treatment options. This analysis evaluated the effect of a monoclonal antibody to proprotein convertase subtilisin/kexin 9 (PCSK9), alirocumab 150 mg every 2 weeks (Q2W), on Lp(a) levels in pooled data from 3 double-blind, randomized, placebo-controlled phase 2 studies of 8 or 12 weeks duration conducted in patients with hypercholesterolemia on background lipid-lowering therapy (NCT01266876, NCT01288469, NCT01288443). Data were available for 102/108 patients who received alirocumab 150 mg Q2W and 74/77 patients who received placebo. Alirocumab resulted in a significant reduction in Lp(a) from baseline compared with placebo (–30.3% versus –0.3%, p <0.0001). Median percentage Lp(a) reductions in the alirocumab group were of a similar magnitude across a range of baseline Lp(a) levels, resulting in greater absolute reductions in Lp(a) in patients with higher baseline levels. Regression analysis indicated that less than 5% of the variance in the reduction of Lp(a) was explained by the effect of alirocumab on low-density lipoprotein cholesterol (LDL-C). In conclusion, pooled data from 3 phase 2 trials demonstrate substantive reduction in Lp(a) with alirocumab 150 mg Q2W, including patients with baseline Lp(a) >50 mg/dl. Reductions in Lp(a) only weakly correlated with the magnitude of LDL-C lowering.
    The American Journal of Cardiology. 01/2014;
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    ABSTRACT: Placental lipoprotein lipase (LPL) is crucial for placental lipid transfer. Impaired LPL gene expression and activity were reported in pregnancies complicated by gestational diabetes mellitus (GDM) and intra-uterine growth restriction. We hypothesized that placental LPL DNA methylation is altered by maternal metabolic status and could contribute to fetal programming. The objective of this study was thus to assess whether placental LPL DNA methylation is associated with GDM and both maternal and newborn lipid profiles. Placenta biopsies were sampled at delivery from 126 women including 27 women with GDM diagnosed following a post 75 g-oral glucose tolerance test (OGTT) between weeks 24 and 28 of gestation. Placental LPL DNA methylation and expression levels were determined using bisulfite pyrosequencing and quantitative real-time PCR, respectively. DNA methylation levels within LPL proximal promoter region (CpG1) and intron 1 CpG island (CpGs 2 and 3) were lower in placenta of women with GDM. DNA methylation levels at LPL-CpG1 and CpG3 were also negatively correlated with maternal glucose (2-h post OGTT; r=–0.22; P=0.02) and HDL-cholesterol levels (third trimester of pregnancy; r=–0.20; p=0.03), respectively. Moreover, we report correlation between LPL-CpG2 DNA methylation and cord blood lipid profile. DNA methylation levels within intron 1 CpG island explained up to 26% (r⩽–0.51; P<0.001) of placental LPL mRNA expression variance. Overall, we showed that maternal metabolic profile is associated with placental LPL DNA methylation dysregulation. Our results suggest that site-specific LPL epipolymorphisms in the placenta are possibly functional and could potentially be involved in determining the future metabolic health of the newborn.
    J Dev Orig Health Dis. 01/2014; FirstView:1-10.
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    ABSTRACT: Cellular immune responses to adeno-associated viral (AAV) vectors used for gene therapy have been linked to attenuated transgene expression and loss of efficacy. The impact of such cellular immune responses on the clinical efficacy of alipogene tiparvovec (Glybera®, AAV1-LPLS447X, uniQure, Amsterdam, the Netherlands), a gene-therapy consisting of intramuscular administration of a recombinant (r)AAV1 mediating muscle-directed expression of lipoprotein lipase (LPL), was investigated. Five subjects with LPL-deficiency (LPLD) were administered intramuscularly with a dose of 1 x 1012 gc/kg alipogene tiparvovec. All subjects were treated with immune suppression starting shortly before administration of alipogene tiparvovec and maintained until 12 weeks after administration. Systemic antibody and T cell responses against AAV1 and LPLS447X, as well as local cellular immune responses in the injected muscle were investigated in 5 LPLD subjects. Long term transgene expression was demonstrated despite a transient systemic cellular response and a stable humoral immune response against AAV1 capsid protein. Cellular infiltrates were found in 4 of the 5 subjects but were not associated with adverse clinical events or elevation of inflammation markers. Consistent herewith, CD8-positive T cells in the infiltrates lacked cytotoxic potential. Furthermore, FoxP3-positive/CD4-positive T cells were found in the infiltrates suggesting that multiple mechanisms contribute to local tolerance. Systemic and local immune responses induced by intramuscular injection of alipogene tiparvovec have no impact on safety and did not compromise LPL transgene expression. These findings support the use of alipogene tiparvovec in individuals with LPLD and indicate that muscle directed AAV-based gene therapy remains a promising approach for the treatment of human diseases.
    Human gene therapy 12/2013; · 4.20 Impact Factor
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    ABSTRACT: Genealogical analysis has proven a useful method to understand the origins and frequencies of hereditary diseases in many populations. However, this type of analysis has not yet been used for the investigation of drug intolerance among patients suffering from inherited disorders. This study aims to do so, using data from familial hypercholesterolemia (FH) patients receiving high doses of statins. The objective is to measure and compare various genealogical parameters that could shed light on the origins and heritability of muscular intolerance to statins using FH as a model. Analysis was performed on 224 genealogies from 112 FH subjects carrying either the low-density lipoprotein receptor (LDLR) prom_e1 deletion>15 kb (n=28) or c.259T>G (p.Trp87Gly) (n=84) mutations and 112 non-FH controls. Number of ancestors, geographical origins and genetic contribution of founders, inbreeding and kinship coefficients were calculated using the S-Plus-based GENLIB software package. For both mutations, repeated occurrences of the same ancestors are more frequent among the carriers' genealogies than among the controls', but no difference was observed between tolerant and intolerant subjects. Founders who may have introduced both mutations in the population appear with approximately the same frequencies in all genealogies. Kinship coefficients are higher among carriers, with no difference according to statins tolerance. Inbreeding coefficients are slightly lower among >15-kb deletion carriers than among c.259 T>G carriers, but the differences between tolerants and intolerants are not significant. These findings suggest that although muscular intolerance to statins shows a family aggregation, it is not transmitted through the same Mendelian pattern as LDLR mutations.European Journal of Human Genetics advance online publication, 27 November 2013; doi:10.1038/ejhg.2013.270.
    European journal of human genetics: EJHG 11/2013; · 3.56 Impact Factor
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    ABSTRACT: Background: Homozygous familial hypercholesterolemia (HoFH) is a rare genetic disease characterized by markedly elevated LDL-C and high CVD risk. Lomitapide is approved in the US to lower LDL-C as an adjunct to other lipid lowering agents, including apheresis, for adults with HoFH. We report efficacy and safety findings from a long term extension study in patients treated with lomitapide for 2.5-4.5 years. Methods: Following the pivotal 78 week study, eligible patients entered an open label extension phase and continued lomitapide at their maximum tolerated dose. The primary efficacy endpoint was mean % change in LDL-C from baseline to week 126 (~2.5 years). Safety endpoints included assessment of hepatic fat as measured by nuclear magnetic resonance spectroscopy (NMRS), liver function tests, and adverse events (AEs). Results: Nineteen of 23 patients who completed the pivotal study entered the extension study. Follow-up ranged from ~2.5 - 4.5 years. LDL-C levels were reduced by 45.5% at week 126 (356 ± 127 mg /dL vs. 189 ± 120 mg/dL; P <0.001). Similar mean % reductions were observed for Apo B -54%, non-HDL-C -47%, VLDL-C -37%, and triglycerides -53% (median), (P ≤0.006 for all). At any time on study, an LDL-C of ≤ 100 or ≤ 70 mg/dL was achieved by 13 (68%) and 9 (47%) patients, respectively. Median hepatic fat levels were 6.5% at entry to the extension phase and remained stable over 2 years (median 7.7% (range 0.6, 35.2)). Transient aminotransferase elevations >5x ULN occurred in 4 patients; 1 patient had a reversible ALT elevation of 24x ULN following co-prescription of agomelatine and a potent inhibitor of CYP3A4 (clarithromycin); 1 other patient, who use excessive alcohol, was withdrawn due to persistent ALT elevations >5x ULN. No Hy’s law cases were reported. The AE profile in patients who continued on the extension study was similar to the pivotal trial. GI symptoms were the most common AEs,observed in 63% (12/19) of patients in the extension study. One sudden cardiac death occurred in a 58 year old patient with known CAD. Conclusions: Results of the ongoing extension study are consistent with those observed in the pivotal study and demonstrate sustained efficacy and an acceptable longer-term safety profile of lomitapide in patients with HoFH.
    AHA 2013, November 16th-20th, Dallas, TX, Dallas, TX , USA; 11/2013

Publication Stats

6k Citations
1,303.23 Total Impact Points

Institutions

  • 2000–2014
    • Université de Montréal
      • • Department of Medicine
      • • Center for Mathematical Research
      • • Montreal University Health Centre
      Montréal, Quebec, Canada
    • University of Texas at San Antonio
      San Antonio, Texas, United States
  • 2013
    • UniQure
      Amsterdamo, North Holland, Netherlands
    • Hamilton Health Sciences
      Hamilton, Ontario, Canada
  • 2012–2013
    • Université de Sherbrooke
      • Department of Biochemistry
      Sherbrooke, Quebec, Canada
    • SickKids
      Toronto, Ontario, Canada
    • Johns Hopkins University
      Baltimore, Maryland, United States
    • Institut universitaire de cardiologie et de pneumologie de Québec
      Québec, Quebec, Canada
    • University of Toronto
      • Hospital for Sick Children
      Toronto, Ontario, Canada
    • The Clinical Trial Center, LLC
      Jenkintown, Pennsylvania, United States
  • 2007–2013
    • Université du Québec à Montréal
      Montréal, Quebec, Canada
    • Broad Institute of MIT and Harvard
      • Program in Medical and Population Genetics
      Cambridge, MA, United States
  • 1995–2012
    • Centre hospitalier de l'Université de Montréal (CHUM)
      • Département Médecine dentaire
      Montréal, Quebec, Canada
  • 2006–2010
    • McGill University
      • Department of Human Genetics
      Montréal, Quebec, Canada
    • University of Nottingham
      • Brain and Body Centre
      Nottingham, ENG, United Kingdom
  • 1997–2010
    • University of Québec in Chicoutimi
      Saguenay, Quebec, Canada
  • 2000–2008
    • McGill University Health Centre
      Montréal, Quebec, Canada
  • 1997–2007
    • Laval University
      • • Institute of Nutraceuticals and Functional Foods (INAF)
      • • Département de Médecine
      Québec, Quebec, Canada
  • 2004–2006
    • Massachusetts General Hospital
      • • Center for Human Genetic Research
      • • Department of Molecular Biology
      Boston, MA, United States
  • 2005
    • New York State
      New York City, New York, United States
    • Lund University
      • Department of Endocrinology
      Lund, Skane, Sweden
  • 2002
    • Medical College of Wisconsin
      Milwaukee, Wisconsin, United States
  • 2001
    • Massachusetts Institute of Technology
      • Center for Genome Research
      Cambridge, MA, United States
    • Providence University
      臺中市, Taiwan, Taiwan