Abraham Aviv

Rutgers, The State University of New Jersey, Нью-Брансуик, New Jersey, United States

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Publications (226)1332.93 Total impact

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    ABSTRACT: Evidence for an association of leukocyte telomere length (LTL) with cognitive function, predominantly in older adults, is inconsistent. No report has examined the association of LTL dynamics (age-specific LTL and its attrition rate) with cognitive function. We aimed to examine the association of LTL dynamics over 13 years in young adulthood with cognitive function in midlife. 497 individuals who had LTL measured at ages 28-32 and 41-46 years were assessed at ages 48-52 for global cognitive function and its five specific component domains with a NeuroTrax computerized test battery. Multivariable regression and logistic models were applied for cognition treated as a continuous and categorical variable, respectively. We found that LTL attrition (adjusted for sex, baseline LTL and potential confounders including socioeconomic variables) was inversely associated with global cognition (standardized β = -.119, p = .004) and its component domains: information processing speed (β = -.102, p = .024), visual-spatial function (β = -.102, p = .017) and memory (β = -.093, p = .045), but less so for the attention and executive domains. The multivariable-adjusted odds ratio for low global cognition comparing the upper versus lower thirds of LTL attrition was 2.12 (95 % CI 1.11-4.08, p for trend = .023). There was no association of baseline or follow-up LTL with cognition. No effect modification was evident for sex, smoking or inflammatory markers. In conclusion, faster LTL attrition in young adulthood was associated with poorer global and domain-specific cognitive function in midlife, suggesting that more rapid LTL attrition may be predictive of cognitive aging in healthy young adults.
    European Journal of Epidemiology 06/2015; DOI:10.1007/s10654-015-0051-4 · 5.15 Impact Factor
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    ABSTRACT: Telomere length, a highly heritable trait, is longer in offspring of older fathers. This perplexing feature has been attributed to the longer telomeres in sperm of older men and it might be an 'epigenetic' mechanism through which paternal age plays a role in telomere length regulation in humans. Based on two independent (discovery and replication) twin studies, comprising 889 twin pairs, we show an increase in the resemblance of leukocyte telomere length between dizygotic twins of older fathers, which is not seen in monozygotic twins. This phenomenon might result from a paternal age-dependent germ stem cell selection process, whereby the selected stem cells have longer telomeres, are more homogenous with respect to telomere length, and share resistance to aging. © 2015 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
    Aging cell 04/2015; DOI:10.1111/acel.12334 · 5.94 Impact Factor
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    ABSTRACT: Patients with histories of myocardial infarction display shortened leukocyte telomere length (LTL), but conflicting findings have been reported on the relation between LTL and subclinical coronary artery atherosclerosis, as expressed by coronary artery calcium (CAC). The aim of this study was to examine the relation between LTL, measured by Southern blots, and CAC in 3,169 participants in the National Heart, Lung, and Blood Institute Family Heart Study. Participants consisted of 2,556 whites, 613 blacks, 1,790 women, and 1,379 men. The odds of having CAC ≥100 for the shortest LTL tertile versus the longest LTL tertile were 1.95 (95% confidence interval [CI] 1.28 to 3.16) in white men and 1.76 (95% CI 1.18 to 2.45) in white women, after adjusting for multiple covariates of CAC. The corresponding odds ratios for blacks were 1.53 (95% CI 0.67 to 3.50) and 0.87 (95% CI 0.37 to 2.00). Significance levels of tests for trend across LTL tertiles were p = 0.002 in white men, p = 0.006 in white women, p = 0.32 in black men, and p = 0.74 in black women. The associations, or lack of associations, were independent of C-reactive protein levels and other risk factors for CAC. As previously shown in other studies, whites displayed shorter LTLs than blacks (p <0.0001). In conclusion, the higher the coronary artery atherosclerotic burden in whites, the shorter the LTL. This LTL-atherosclerosis connection is not found in blacks. The mechanisms for the racial difference in LTL, CAC, and their interrelations do not seem to be related to inflammation and merit further research. Copyright © 2015 Elsevier Inc. All rights reserved.
    The American Journal of Cardiology 04/2015; DOI:10.1016/j.amjcard.2015.03.060 · 3.43 Impact Factor
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    Abraham Aviv, Jeremy D Kark, Ezra Susser
    Epidemiology (Cambridge, Mass.) 03/2015; 26(3). DOI:10.1097/EDE.0000000000000280 · 6.18 Impact Factor
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    ABSTRACT: Leucocyte telomere length (LTL) is a complex trait associated with ageing and longevity. LTL dynamics are defined by LTL and its age-dependent attrition. Strong, but indirect evidence suggests that LTL at birth and its attrition during childhood largely explains interindividual LTL variation among adults. A number of studies have estimated the heritability of LTL, but none has assessed the heritability of age-dependent LTL attrition. We examined the heritability of LTL dynamics based on a longitudinal evaluation (an average follow-up of 12 years) in 355 monozygotic and 297 dizygotic same-sex twins (aged 19-64 years at baseline). Heritability of LTL at baseline was estimated at 64% (95% CI 39% to 83%) with 22% (95% CI 6% to 49%) of shared environmental effects. Heritability of age-dependent LTL attrition rate was estimated at 28% (95% CI 16% to 44%). Individually unique environmental factors, estimated at 72% (95% CI 56% to 84%) affected LTL attrition rate with no indication of shared environmental effects. This is the first study that estimated heritability of LTL and also its age-dependent attrition. As LTL attrition is much slower in adults than in children and given that having a long or a short LTL is largely determined before adulthood, our findings suggest that heritability and early life environment are the main determinants of LTL throughout the human life course. Thus, insights into factors that influence LTL at birth and its dynamics during childhood are crucial for understanding the role of telomere genetics in human ageing and longevity. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
    Journal of Medical Genetics 03/2015; 52(5). DOI:10.1136/jmedgenet-2014-102736 · 5.64 Impact Factor
  • Steven C Hunt, Jeremy D Kark, Abraham Aviv
    Circulation Cardiovascular Genetics 02/2015; 8(1):4-7. DOI:10.1161/CIRCGENETICS.114.000964 · 5.34 Impact Factor
  • American Journal of Obstetrics and Gynecology 01/2015; 212(1):S39. DOI:10.1016/j.ajog.2014.10.102 · 3.97 Impact Factor
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    ABSTRACT: Leucocyte telomere length (LTL), which is fashioned by multiple genes, has been linked to a host of human diseases, including sporadic melanoma. A number of genes associated with LTL have already been identified through genome-wide association studies. The main aim of this study was to establish whether DCAF4 (DDB1 and CUL4-associated factor 4) is associated with LTL. In addition, using ingenuity pathway analysis (IPA), we examined whether LTL-associated genes in the general population might partially explain the inherently longer LTL in patients with sporadic melanoma, the risk for which is increased with ultraviolet radiation (UVR). Genome-wide association (GWA) meta-analysis and de novo genotyping of 20 022 individuals revealed a novel association (p=6.4×10(-10)) between LTL and rs2535913, which lies within DCAF4. Notably, eQTL analysis showed that rs2535913 is associated with decline in DCAF4 expressions in both lymphoblastoid cells and sun-exposed skin (p=4.1×10(-3) and 2×10(-3), respectively). Moreover, IPA revealed that LTL-associated genes, derived from GWA meta-analysis (N=9190), are over-represented among genes engaged in melanoma pathways. Meeting increasingly stringent p value thresholds (p<0.05, <0.01, <0.005, <0.001) in the LTL-GWA meta-analysis, these genes were jointly over-represented for melanoma at p values ranging from 1.97×10(-169) to 3.42×10(-24). We uncovered a new locus associated with LTL in the general population. We also provided preliminary findings that suggest a link of LTL through genetic mechanisms with UVR and melanoma in the general population. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
    Journal of Medical Genetics 01/2015; 52(3). DOI:10.1136/jmedgenet-2014-102681 · 5.64 Impact Factor
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    ABSTRACT: Naevus count is the strongest risk factor for melanoma. Body Mass Index (BMI) has been linked to melanoma risk. In this study, we investigate the link between naevus count and height, weight and bone mineral density (BMD) in the TwinsUK cohort (N = 2119). In addition we adjusted for leucocyte telomere length (LTL) as LTL is linked to both BMD and naevus count. Naevus count was positively associated with height (p = 0.001) but not with weight (p = 0.187) despite adjusting for age and twin relatedness. This suggests that the previously reported melanoma association with BMI may be explained by height alone. Further adjustment for LTL did not affect the significance of the association between height and naevus count so LTL does not fully explain these results. BMD was associated with naevus count at the spine (coeff 18.9, p = 0.01), hip (coeff = 18.9, p = 0.03) and forearm (coeff = 32.7, p = 0.06) despite adjusting for age, twin relatedness, weight, height and LTL. This large study in healthy individuals shows that growth via height, probably in early life, and bone mass are risk factors for melanoma via increased naevus count. The link between these two phenotypes may possibly be explained by telomere biology, differentiation genes from the neural crests but also other yet unknown factors which may influence both bones and melanocytes biology.
    PLoS ONE 01/2015; 10(1):e0116863. DOI:10.1371/journal.pone.0116863 · 3.53 Impact Factor
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    ABSTRACT: Disruption of telomere maintenance pathways leads to accelerated entry into cellular senescence, a stable proliferative arrest that promotes aging-associated disorders in some mammals. The budding yeast CST complex, comprising Cdc13, Stn1, and Ctc1, is critical for telomere replication, length regulation, and end protection. Although mammalian homologues of CST have been identified recently, their role and function for telomere maintenance in normal somatic human cells are still incompletely understood. Here, we characterize the function of human Stn1 in cultured human fibroblasts and demonstrate its critical role in telomere replication, length regulation, and function. In the absence of high telomerase activity, shRNA-mediated knockdown of hStn1 resulted in aberrant and fragile telomeric structures, stochastic telomere attrition, increased telomere erosion rates, telomere dysfunction, and consequently accelerated entry into cellular senescence. Oxidative stress augmented the defects caused by Stn1 knockdown leading to almost immediate cessation of cell proliferation. In contrast, overexpression of hTERT suppressed some of the defects caused by hStn1 knockdown suggesting that telomerase can partially compensate for hStn1 loss. Our findings reveal a critical role for human Stn1 in telomere length maintenance and function, supporting the model that efficient replication of telomeric repeats is critical for long-term viability of normal somatic mammalian cells. © 2014 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
    Aging cell 11/2014; 14(3). DOI:10.1111/acel.12289 · 5.94 Impact Factor
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    ABSTRACT: CXCL12 encodes stromal cell-derived factor 1 α (SDF-1), which binds to the receptor encoded by CXCR4. Variation at the CXCL12 locus is associated with coronary artery disease and endothelial progenitor cell numbers, whereas variation at the CXCR4 locus is associated with leukocyte telomere length, which has been shown to be associated with coronary artery disease. Therefore, we examined the relationships of plasma SDF-1 levels to cardiovascular disease (CVD)-related outcomes, risk factors, leukocyte telomere length, and endothelial progenitor cells.
    Arteriosclerosis Thrombosis and Vascular Biology 07/2014; 34(9). DOI:10.1161/ATVBAHA.114.303579 · 5.53 Impact Factor
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    ABSTRACT: Background: In eutherian mammals and in humans, the female fetus may be masculinized while sharing the intra-uterine environment with a male fetus. Telomere length (TL), as expressed in leukocytes, is heritable and is longer in women than in men. The main determinant of leukocyte TL (LTL) is LTL at birth. However, LTL is modified by age dependent attrition. Methods: We studied LTL dynamics (LTL and its attrition) in adult same-sex(monozygotic, n=268; dizygotic, n=308) twins and opposite-sex (n=144) twins. LTL was measured by Southern blots of the terminal restriction fragments. Results: We observed that in same-sex (both monozygotic and dizygotic) twins, as reported in singletons, LTL was longer in females than in males [estimate ± standard error (SE):163 ± 63 bp, P<0.01]. However, in opposite-sex twins, female LTL was indistinguishable from that of males (-31 ± 52 bp, P=0.6), whereas male LTL was not affected. Findings were similar when the comparison was restricted to opposite-sex and same-sex dizygotic twins (females relative to males: same-sex: 188 ± 90 bp, P<0.05; other-sex: -32 ± 64 bp, P=0.6). Conclusions: These findings are compatible with masculinization of the female fetus in opposite-sex twins. They suggest that the sex difference in LTL, seen in the general population, is largely determined in utero, perhaps by the intrauterine hormonal environment. Further studies in newborn twins are warranted to test this thesis.
    International Journal of Epidemiology 07/2014; DOI:10.1093/ije/dyu146 · 9.20 Impact Factor
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    ABSTRACT: Shortening of telomeres, the protective structures at the ends of eukaryotic chromosomes, is associated with age-related pathologies. Telomere length is influenced by DNA integrity and DNA and histone methylation. Folate plays a role in providing precursors for nucleotides and methyl groups for methylation reactions and has the potential to influence telomere length. We determined the association between leukocyte telomere length and long-term plasma folate status (mean of 4 years) in Framingham Offspring Study (n = 1,044, females = 52.1 %, mean age 59 years) using data from samples collected before and after folic acid fortification. Leukocyte telomere length was determined by Southern analysis and fasting plasma folate concentration using microbiological assay. There was no significant positive association between long-term plasma folate and leukocyte telomere length among the Framingham Offspring Study participants perhaps due to their adequate folate status. While the leukocyte telomere length in the second quintile of plasma folate was longer than that in the first quintile, the difference was not statistically significant. The leukocyte telomere length of the individuals in the fifth quintile of plasma folate was shorter than that of those in the second quintile by 180 bp (P < 0.01). There was a linear decrease in leukocyte telomere length with higher plasma folate concentrations in the upper four quintiles of plasma folate (P for trend = 0.001). Multivitamin use was associated with shorter telomeres in this cohort (P = 0.015). High plasma folate status possibly resulting from high folic acid intake may interfere with the role of folate in maintaining telomere integrity.
    European Journal of Nutrition 05/2014; 54(2). DOI:10.1007/s00394-014-0704-1 · 3.84 Impact Factor
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    ABSTRACT: Telomeres play a key role in replicative ageing and undergo age-dependent attrition in vivo. Here, we report a novel method, TelSeq, to measure average telomere length from whole genome or exome shotgun sequence data. In 260 leukocyte samples, we show that TelSeq results correlate with Southern blot measurements of the mean length of terminal restriction fragments (mTRFs) and display age-dependent attrition comparably well as mTRFs.
    Nucleic Acids Research 03/2014; 42(9). DOI:10.1093/nar/gku181 · 9.11 Impact Factor
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    ABSTRACT: Introduction. Fatigue is often present in older adults with no identified underlying cause. The accruing burden of oxidative stress and inflammation might be underlying factors of fatigue. We therefore hypothesized that leukocyte telomere length (LTL) is relatively short in older adults who experience fatigue. Materials and Methods. We assessed 439 older nondisabled Danish twins. LTL was measured using Southern blots of terminal restriction fragments. Fatigue was measured by the Mob-T Scale based on questions on whether the respondents felt fatigued after performing six mobility items. Results. LTL was significantly associated with fatigue (P = 0.023), showing an increase of 0.038 kb/fatigue score unit. Aging-related diseases and mental health did not explain the association, while lifestyle factors slightly attenuated the estimates. Conclusion. Our results support an association between LTL and fatigue. Further studies are required to confirm this finding and the link of LTL with oxidative stress/inflammation over the life course.
    Journal of aging research 02/2014; 2014:403253. DOI:10.1155/2014/403253
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    ABSTRACT: Telomere length is a marker of cellular aging that varies with the individual, is inherited, and is highly correlated across somatic cell types within persons. Interindividual variability of telomere length may partly explain differences in reproductive aging rates. We examined whether leukocyte telomere length was associated with menopausal age. We evaluated the relationship between leukocyte telomere length and age at natural menopause in 486 white women ≥65 years of age. We fit linear regression models adjusted for age, income, education, body mass index, physical activity, smoking, and alcohol intake. We repeated the analysis in women with surgical menopause. We also performed sensitivity analyses excluding women (1) with unilateral oophorectomy, (2) who were nulliparous, or (3) reporting menopausal age <40 years, among other exclusions. For every 1-kb increase in leukocyte telomere length, average age at natural menopause increased by 10.2 months (95% confidence interval = 1.3 to 19.0). There was no association among 179 women reporting surgical menopause. In all but one sensitivity analysis, the association between leukocyte telomere length and age at menopause became stronger. However, when excluding women with menopausal age <40 years, the association decreased to 7.5 months (-0.4 to 15.5). Women with the longest leukocyte telomere length underwent menopause 3 years later than those with the shortest leukocyte telomere length. If an artifact, an association would likely also have been observed in women with surgical menopause. If these results are replicated, leukocyte telomere length may prove to be a useful predictor of age at menopause.
    Epidemiology (Cambridge, Mass.) 11/2013; 25(1). DOI:10.1097/EDE.0000000000000017 · 6.18 Impact Factor
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    ABSTRACT: Only a few studies, primarily limited to small samples, have examined the relationship between leukocyte telomere length (LTL) data generated by Southern blots, expressed in kilobases, versus quantitative PCR data, expressed in the telomere product/a single gene product (T/S). In the present study, we compared LTL data generated by the two methods in 681 elderly participants (50% African Americans, 50% of European origin, 49.2% women, mean age 73.7±2.9 years) in the Health Aging and Body Composition Study. The correlation between the data generated by the two methods was modest (R(2) = .27). Both methods captured the age effect on LTL and the longer LTL in women than in men. However, only the Southern blot method showed a significantly longer LTL in African Americans than in European decent individuals, which might be attributed to the larger measurement error of the quantitative PCR-based method than the Southern blots.
    The Journals of Gerontology Series A Biological Sciences and Medical Sciences 08/2013; DOI:10.1093/gerona/glt121 · 4.98 Impact Factor
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    ABSTRACT: Allele-specific DNA methylation (ASM) is well studied in imprinted domains, but this type of epigenetic asymmetry is actually found more commonly at non-imprinted loci, where the ASM is dictated not by parent-of-origin but instead by the local haplotype. We identified loci with strong ASM in human tissues from methylation-sensitive SNP array data. Two index regions (bisulfite PCR amplicons), one between the C3orf27 and RPN1 genes in chromosome band 3q21 and the other near the VTRNA2-1 vault RNA in band 5q31, proved to be new examples of imprinted DMRs (maternal alleles methylated) while a third, between STEAP3 and C2orf76 in chromosome band 2q14, showed non-imprinted haplotype-dependent ASM. Using long-read bisulfite sequencing (bis-seq) in 8 human tissues we found that in all 3 domains the ASM is restricted to single differentially methylated regions (DMRs), each less than 2kb. The ASM in the C3orf27-RPN1 intergenic region was placenta-specific and associated with allele-specific expression of a long non-coding RNA. Strikingly, the discrete DMRs in all 3 regions overlap with binding sites for the insulator protein CTCF, which we found selectively bound to the unmethylated allele of the STEAP3-C2orf76 DMR. Methylation mapping in two additional genes with non-imprinted haplotype-dependent ASM, ELK3 and CYP2A7, showed that the CYP2A7 DMR also overlaps a CTCF site. Thus, two features of imprinted domains, highly localized DMRs and allele-specific insulator occupancy by CTCF, can also be found in chromosomal domains with non-imprinted ASM. Arguing for biological importance, our analysis of published whole genome bis-seq data from hES cells revealed multiple genome-wide association study (GWAS) peaks near CTCF binding sites with ASM.
    PLoS Genetics 08/2013; 9(8):e1003622. DOI:10.1371/journal.pgen.1003622 · 8.17 Impact Factor
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    ABSTRACT: Recent longitudinal studies of age-dependent leukocyte telomere length (LTL) attrition have reported that variable proportions of individuals experience LTL lengthening. Often, LTL lengthening has been taken at face value, and authors have speculated about the biological causation of this finding. Based on empirical data and theoretical considerations, we show that regardless of the method used to measure telomere length (Southern blot or quantitative polymerase chain reaction-based methods), measurement error of telomere length and duration of follow-up explain almost entirely the absence of age-dependent LTL attrition in longitudinal studies. We find that LTL lengthening is far less frequent in studies with long follow-up periods and those that used a high-precision Southern blot method (as compared with quantitative polymerase chain reaction determination, which is associated with larger laboratory error). We conclude that the LTL lengthening observed in longitudinal studies is predominantly, if not entirely, an artifact of measurement error, which is exacerbated by short follow-up periods. We offer specific suggestions for design of longitudinal studies of LTL attrition to diminish this artifact.
    Nucleic Acids Research 05/2013; 41(13). DOI:10.1093/nar/gkt370 · 9.11 Impact Factor
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    ABSTRACT: SHORT LEUKOCYTE TELOMERE LENGTH (LTL) IS ASSOCIATED WITH ATHEROSCLEROSIS IN ADULTS AND: diminished survival in the elderly. LTL dynamics are defined by LTL at birth, which is highly variable, and its age dependent attrition thereafter, which is rapid during the first 20 years of life. We examined whether age-dependent LTL attrition during adulthood can substantially affect individuals' LTL ranking (e.g., longer or shorter LTL) in relation to their peers. We measured LTL in samples donated 12 years apart on average by 1156 participants in four longitudinal studies. We observed correlations of 0.91-0.96 between baseline and follow-up LTLs. Ranking individuals by deciles revealed that 94.1% (95%, confidence intervals of 92.6-95.4%) showed no rank change or a 1 decile change over time. We conclude that in adults LTL is virtually anchored to a given rank with the passage of time. Accordingly, the links of LTL with atherosclerosis and longevity appear to be established early in life. It is unlikely that lifestyle and its modification during adulthood exert a major impact on LTL ranking. This article is protected by copyright. All rights reserved.
    Aging cell 04/2013; DOI:10.1111/acel.12086 · 5.94 Impact Factor

Publication Stats

8k Citations
1,332.93 Total Impact Points

Institutions

  • 2014–2015
    • Rutgers, The State University of New Jersey
      Нью-Брансуик, New Jersey, United States
  • 2013–2015
    • New York State Psychiatric Institute
      New York, New York, United States
  • 1985–2015
    • Rutgers New Jersey Medical School
      • • Department of Surgery
      • • Department of Preventive Medicine and Community Health
      • • Division of Neurology
      Newark, New Jersey, United States
  • 2012–2013
    • Columbia University
      • Department of Epidemiology
      New York, New York, United States
  • 2007–2012
    • King's College London
      • Department of Twin Research and Genetic Epidemiology
      Londinium, England, United Kingdom
    • Stanford University
      • Department of Structural Biology
      Palo Alto, California, United States
  • 2011
    • University of Alabama at Birmingham
      Birmingham, Alabama, United States
  • 2010
    • University of Leuven
      Louvain, Flanders, Belgium
  • 2009
    • Second University of Naples
      Caserta, Campania, Italy
    • Albert Einstein College of Medicine
      • Department of Epidemiology & Population Health
      New York City, NY, United States
  • 2008
    • National Heart, Lung, and Blood Institute
      • Division of Cardiovascular Sciences (DCVS)
      Maryland, United States
  • 2006
    • Centre Hospitalier Universitaire de Nancy
      • Department of Geriatrics
      Nancy, Lorraine, France
  • 2005
    • Hochschule für Gesundheit und Medizin
      Berlín, Berlin, Germany
  • 2003–2005
    • Cardiovascular Research Foundation
      New York, New York, United States
  • 2001–2004
    • Centre D'Investigations Préventives Et Cliniques
      Lutetia Parisorum, Île-de-France, France
  • 1998–2004
    • Harvard University
      Cambridge, Massachusetts, United States
  • 1986–1996
    • Newark Academy
      Ливингстон, New Jersey, United States
  • 1992
    • Tel Aviv University
      Tell Afif, Tel Aviv, Israel