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1. Evidence of a causal and modifiable relationship between kidney function and circulating trimethylamine N-oxide

Author: Andrikopoulos, Petros, Aron-Wisnewsky, Judith, Chakaroun, Rima, Myridakis, Antonis, Forslund, Sofia K., Nielsen, Trine, Adriouch, Solia, Holmes, Bridget, Chilloux, Julien, Vieira-Silva, Sara, Falony, Gwen, Salem, Joe Elie, Andreelli, Fabrizio, Belda, Eugeni, Kieswich, Julius, Chechi, Kanta, Puig-Castellvi, Francesc, Chevalier, Mickael, Le Chatelier, Emmanuelle, Olanipekun, Michael T., Hoyles, Lesley, Alves, Renato, Helft, Gerard, Isnard, Richard, Køber, Lars, Coelho, Luis Pedro, Rouault, Christine, Gauguier, Dominique, Gøtze, Jens Peter, Prifti, Edi, Froguel, Philippe, Alili, Rohia, Galijatovic, Ehm Astrid Andersson, Barthelemy, Olivier, Bastard, Jean Philippe, Batisse, Jean Paul, Bel-Lassen, Pierre, Berland, Magalie, Bittar, Randa, Blottière, Hervé, Bosquet, Frederic, Boubrit, Rachid, Bourron, Olivier, Camus, Mickael, Ciangura, Cecile, Collet, Jean Philippe, Dietrich, Arne, Djebbar, Morad, Doré, Angélique, Engelbrechtsen, Line, Fezeu, Leopold, Fromentin, Sebastien, Pons, Nicolas, Graine, Marianne, Grünemann, Caroline, Hartemann, Agnes, Hartmann, Bolette, Hornbak, Malene, Jaqueminet, Sophie, Jørgensen, Niklas Rye, Julienne, Hanna, Justesen, Johanne, Kammer, Judith, Karup, Nikolaj, Kozlowski, Ruby, Kuhn, Michael, Lejard, Véronique, Letunic, Ivica, Levenez, Florence, Marko, Lajos, Martinez-Gili, Laura, Massey, Robin, Maziers, Nicolas, Moitinho-Silva, Lucas, Montalescot, Gilles, Neves, Ana Luisa, Le Pavin, Laetitia Pasero, Pousset, Francoise, Rodriguez-Martinez, Andrea, Schmidt, Sebastien, Schütz, Tatjana, Silva, Lucas, Silvain, Johanne, Svendstrup, Mathilde, Swartz, Timothy D., Vanduyvenboden, Thierry, Verger, Eric O., Walther, Stefanie, Zucker, Jean Daniel, Bäckhed, Fredrik, Vestergaard, Henrik, Hansen, Torben, Oppert, Jean Michel, Blüher, Matthias, Nielsen, Jens, Raes, Jeroen, Bork, Peer, Yaqoob, Muhammad M., Stumvoll, Michael, Pedersen, Oluf, Ehrlich, S. Dusko, Clément, Karine, Dumas, Marc Emmanuel, Andrikopoulos, Petros, Aron-Wisnewsky, Judith, Chakaroun, Rima, Myridakis, Antonis, Forslund, Sofia K., Nielsen, Trine, Adriouch, Solia, Holmes, Bridget, Chilloux, Julien, Vieira-Silva, Sara, Falony, Gwen, Salem, Joe Elie, Andreelli, Fabrizio, Belda, Eugeni, Kieswich, Julius, Chechi, Kanta, Puig-Castellvi, Francesc, Chevalier, Mickael, Le Chatelier, Emmanuelle, Olanipekun, Michael T., Hoyles, Lesley, Alves, Renato, Helft, Gerard, Isnard, Richard, Køber, Lars, Coelho, Luis Pedro, Rouault, Christine, Gauguier, Dominique, Gøtze, Jens Peter, Prifti, Edi, Froguel, Philippe, Alili, Rohia, Galijatovic, Ehm Astrid Andersson, Barthelemy, Olivier, Bastard, Jean Philippe, Batisse, Jean Paul, Bel-Lassen, Pierre, Berland, Magalie, Bittar, Randa, Blottière, Hervé, Bosquet, Frederic, Boubrit, Rachid, Bourron, Olivier, Camus, Mickael, Ciangura, Cecile, Collet, Jean Philippe, Dietrich, Arne, Djebbar, Morad, Doré, Angélique, Engelbrechtsen, Line, Fezeu, Leopold, Fromentin, Sebastien, Pons, Nicolas, Graine, Marianne, Grünemann, Caroline, Hartemann, Agnes, Hartmann, Bolette, Hornbak, Malene, Jaqueminet, Sophie, Jørgensen, Niklas Rye, Julienne, Hanna, Justesen, Johanne, Kammer, Judith, Karup, Nikolaj, Kozlowski, Ruby, Kuhn, Michael, Lejard, Véronique, Letunic, Ivica, Levenez, Florence, Marko, Lajos, Martinez-Gili, Laura, Massey, Robin, Maziers, Nicolas, Moitinho-Silva, Lucas, Montalescot, Gilles, Neves, Ana Luisa, Le Pavin, Laetitia Pasero, Pousset, Francoise, Rodriguez-Martinez, Andrea, Schmidt, Sebastien, Schütz, Tatjana, Silva, Lucas, Silvain, Johanne, Svendstrup, Mathilde, Swartz, Timothy D., Vanduyvenboden, Thierry, Verger, Eric O., Walther, Stefanie, Zucker, Jean Daniel, Bäckhed, Fredrik, Vestergaard, Henrik, Hansen, Torben, Oppert, Jean Michel, Blüher, Matthias, Nielsen, Jens, Raes, Jeroen, Bork, Peer, Yaqoob, Muhammad M., Stumvoll, Michael, Pedersen, Oluf, Ehrlich, S. Dusko, Clément, Karine, and Dumas, Marc Emmanuel
Abstract: The host-microbiota co-metabolite trimethylamine N-oxide (TMAO) is linked to increased cardiovascular risk but how its circulating levels are regulated remains unclear. We applied “explainable” machine learning, univariate, multivariate and mediation analyses of fasting plasma TMAO concentration and a multitude of phenotypes in 1,741 adult Europeans of the MetaCardis study. Here we show that next to age, kidney function is the primary variable predicting circulating TMAO, with microbiota composition and diet playing minor, albeit significant, roles. Mediation analysis suggests a causal relationship between TMAO and kidney function that we corroborate in preclinical models where TMAO exposure increases kidney scarring. Consistent with our findings, patients receiving glucose-lowering drugs with reno-protective properties have significantly lower circulating TMAO when compared to propensity-score matched control individuals. Our analyses uncover a bidirectional relationship between kidney function and TMAO that can potentially be modified by reno-protective anti-diabetic drugs and suggest a clinically actionable intervention for decreasing TMAO-associated excess cardiovascular risk.
Published: 2023

2. Plasma and urine metabolomic analyses in aortic valve stenosis reveal shared and biofluid-specific changes in metabolite levels

Author: Al Hageh, Cynthia, Rahy, Ryan, Khazen, Georges, Brial, Francois, Khnayzer, Rony S., Gauguier, Dominique, Zalloua, Pierre A., Al Hageh, Cynthia, Rahy, Ryan, Khazen, Georges, Brial, Francois, Khnayzer, Rony S., Gauguier, Dominique, and Zalloua, Pierre A.
Abstract: Aortic valve stenosis (AVS) is a prevalent condition among the elderly population that eventually requires aortic valve replacement. The lack of reliable biomarkers for AVS poses a challenge for its early diagnosis and the application of preventive measures. Untargeted gas chromatography mass spectrometry (GC-MS) metabolomics was applied in 46 AVS cases and 46 controls to identify plasma and urine metabolites underlying AVS risk. Multivariate data analyses were performed on pre-processed data (e.g. spectral peak alignment), in order to detect changes in metabolite levels in AVS patients and to evaluate their performance in group separation and sensitivity of AVS prediction, followed by regression analyses to test for their association with AVS. Through untargeted analysis of 190 urine and 130 plasma features that could be detected and quantified in the GC-MS spectra, we identified contrasting levels of 22 urine and 21 plasma features between AVS patients and control subjects. Following metabolite assignment, we observed significant changes in the concentration of known metabolites in urine (n = 14) and plasma (n = 15) that distinguish the metabolomic profiles of AVS patients from healthy controls. Associations with AVS were replicated in both plasma and urine for about half of these metabolites. Among these, 2-Oxovaleric acid, elaidic acid, myristic acid, palmitic acid, estrone, myo-inositol showed contrasting trends of regulation in the two biofluids. Only trans-Aconitic acid and 2,4-Di-tert-butylphenol showed consistent patterns of regulation in both plasma and urine. These results illustrate the power of metabolomics in identifying potential disease-associated biomarkers and provide a foundation for further studies towards early diagnostic applications in severe heart conditions that may prevent surgery in the elderly.
Published: 2023

3. Elevated Lp(a) Levels Correlate with Severe and Multiple Coronary Artery Stenotic Lesions

Author: Al Hageh,Cynthia, Chacar,Stephanie, Ghassibe-Sabbagh,Michella, Platt,Daniel E, Henschel,Andreas, Hamdan,Hamdan, Gauguier,Dominique, El Murr,Yara, Alefishat,Eman, Chammas,Elie, O'Sullivan,SiobhÃ¡n, Abchee,Antoine, Nader,Moni, Zalloua,Pierre A, Al Hageh,Cynthia, Chacar,Stephanie, Ghassibe-Sabbagh,Michella, Platt,Daniel E, Henschel,Andreas, Hamdan,Hamdan, Gauguier,Dominique, El Murr,Yara, Alefishat,Eman, Chammas,Elie, O'Sullivan,SiobhÃ¡n, Abchee,Antoine, Nader,Moni, and Zalloua,Pierre A
Abstract: Cynthia Al Hageh,1,* Stephanie Chacar,2,* Michella Ghassibe-Sabbagh,3 Daniel E Platt,4 Andreas Henschel,5 Hamdan Hamdan,2 Dominique Gauguier,6,7 Yara El Murr,3 Eman Alefishat,8,9 Elie Chammas,10 Siobhán O’Sullivan,1 Antoine Abchee,11 Moni Nader,2,9 Pierre A Zalloua1,9,12 1Department of Molecular Biology and Genetics, College of Medicine and Health Sciences, Khalifa University of Science and Technology, Abu Dhabi, United Arab Emirates; 2Department of Physiology and Immunology, College of Medicine and Health Sciences, Khalifa University of Science and Technology, Abu Dhabi, United Arab Emirates; 3Department of Natural Sciences, School of Arts and Sciences, Lebanese American University, Beirut, Lebanon; 4Computational Biology Center, IBM TJ Watson Research Centre, Yorktown Hgts, NY, USA; 5Department of Electrical Engineering and Computer, Khalifa University of Science and Technology, Abu Dhabi, United Arab Emirates; 6Université Paris Cité, INSERM UMR 1124, Paris, 75006, France; 7McGill University and Genome Quebec Innovation Centre, Montreal, QC, H3A 0G1, Canada; 8Department of Pharmacology, College of Medicine and Health Sciences, Khalifa University of Science and Technology, Abu Dhabi, United Arab Emirates; 9Center for Biotechnology, Khalifa University of Science and Technology, Abu Dhabi, 127788, United Arab Emirates; 10School of Medicine, Lebanese University, Beirut, Lebanon; 11Sheikh Shakhbout Medical City, Abu Dhabi, United Arab Emirates; 12Harvard T.H. Chan School of Public Health, Boston, MA, USA*These authors contributed equally to this workCorrespondence: Pierre A Zalloua; Moni Nader, College of Medicine and Health Sciences, Khalifa University for Science and Technology, PO Box 127788, Abu Dhabi, United Arab Emirates, Email pierre.zalloua@ku.ac.ae; moni.nader@ku.ac.aeBackgrounds and Aims: The role of Lipoprotein(a) (Lp(a)) in increasing the risk of cardiovascular diseases is reported in several populations. The aim o
Published: 2023

4. Genetic Variants in PHACTR1 & LPL Mediate Restenosis Risk in Coronary Artery Patients

Author: Al Hageh,Cynthia, Chacar,Stephanie, Venkatachalam,Thenmozhi, Gauguier,Dominique, Abchee,Antoine, Chammas,Elie, Hamdan,Hamdan, O'Sullivan,Siobhan, Zalloua,Pierre, Nader,Moni, Al Hageh,Cynthia, Chacar,Stephanie, Venkatachalam,Thenmozhi, Gauguier,Dominique, Abchee,Antoine, Chammas,Elie, Hamdan,Hamdan, O'Sullivan,Siobhan, Zalloua,Pierre, and Nader,Moni
Abstract: Cynthia Al Hageh,1,&ast; Stephanie Chacar,2,&ast; Thenmozhi Venkatachalam,2 Dominique Gauguier,3,4 Antoine Abchee,5 Elie Chammas,6 Hamdan Hamdan,2 Siobhan OâSullivan,1 Pierre Zalloua,1,7,8 Moni Nader2,7 1Department of Molecular Biology and Genetics, College of Medicine and Health Sciences, Khalifa University for Science and Technology, Abu Dhabi, United Arab Emirates; 2Department of Physiology and Immunology College of Medicine and Health Sciences, Khalifa University of Science and Technology, Abu Dhabi, UAE; 3McGill University and Genome Quebec Innovation Centre, Montreal, QC, H3A 0G1, Canada; 4UniversitÃ© Paris CitÃ©, INSERM, Paris, France; 5Sheikh Shakhbout Medical City, Abu Dhabi, United Arab Emirates; 6School of Medicine, Lebanese University, Beirut, Lebanon; 7Biotechnology Center, Khalifa University for Science and Technology, Abu Dhabi, United Arab Emirates; 8Harvard T.H. Chan School of Public Health, Boston, MA, USA&ast;These authors contributed equally to this workCorrespondence: Pierre Zalloua; Moni Nader, College of Medicine and Health Sciences, Khalifa University for Science and Technology, PO Box 127788, Abu Dhabi, United Arab Emirates, Email pierre.zalloua@ku.ac.ae; moni.nader@ku.ac.aeBackground and Objective: Coronary artery disease (CAD) is a major cause of death worldwide. Revascularization via stent placement or coronary artery bypass grafting (CABG) are standard treatments for CAD. Despite a high success rate, these approaches are associated with long-term failure due to restenosis. Risk factors associated with restenosis were investigated using a case-control association study design.Methods: Five thousand two hundred and forty-two patients were enrolled in this study and were assigned as follows: Stenosis Group: 3570 patients with CAD > 50% without a prior stent or CABG (1394 genotyped), and Restenosis Group: 1672 patients with CAD > 50% and prior stent deployment or CABG (705 genotyped). Binomial regression models were appli
Published: 2023

5. Microbiome and metabolome features of the cardiometabolic disease spectrum

Author: Fromentin, Sebastien, Forslund, Sofia K., Chechi, Kanta, Aron-Wisnewsky, Judith, Chakaroun, Rima, Nielsen, Trine, Tremaroli, Valentina, Ji, Boyang, Prifti, Edi, Myridakis, Antonis, Chilloux, Julien, Andrikopoulos, Petros, Fan, Yong, Olanipekun, Michael T., Alves, Renato, Adiouch, Solia, Bar, Noam, Talmor-Barkan, Yeela, Belda, Eugeni, Caesar, Robert, Coelho, Luis Pedro, Falony, Gwen, Fellahi, Soraya, Galan, Pilar, Galleron, Nathalie, Helft, Gerard, Hoyles, Lesley, Isnard, Richard, Le Chatelier, Emmanuelle, Julienne, Hanna, Olsson, Lisa, Pedersen, Helle Krogh, Pons, Nicolas, Quinquis, Benoit, Rouault, Christine, Roume, Hugo, Salem, Joe Elie, Schmidt, Thomas S.B., Vieira-Silva, Sara, Li, Peishun, Zimmermann-Kogadeeva, Maria, Lewinter, Christian, Søndertoft, Nadja B., Hansen, Tue H., Gauguier, Dominique, Gøtze, Jens Peter, Køber, Lars, Kornowski, Ran, Vestergaard, Henrik, Hansen, Torben, Zucker, Jean Daniel, Hercberg, Serge, Letunic, Ivica, Bäckhed, Fredrik, Oppert, Jean Michel, Nielsen, Jens, Raes, Jeroen, Bork, Peer, Stumvoll, Michael, Segal, Eran, Clément, Karine, Dumas, Marc Emmanuel, Ehrlich, S. Dusko, Pedersen, Oluf, Fromentin, Sebastien, Forslund, Sofia K., Chechi, Kanta, Aron-Wisnewsky, Judith, Chakaroun, Rima, Nielsen, Trine, Tremaroli, Valentina, Ji, Boyang, Prifti, Edi, Myridakis, Antonis, Chilloux, Julien, Andrikopoulos, Petros, Fan, Yong, Olanipekun, Michael T., Alves, Renato, Adiouch, Solia, Bar, Noam, Talmor-Barkan, Yeela, Belda, Eugeni, Caesar, Robert, Coelho, Luis Pedro, Falony, Gwen, Fellahi, Soraya, Galan, Pilar, Galleron, Nathalie, Helft, Gerard, Hoyles, Lesley, Isnard, Richard, Le Chatelier, Emmanuelle, Julienne, Hanna, Olsson, Lisa, Pedersen, Helle Krogh, Pons, Nicolas, Quinquis, Benoit, Rouault, Christine, Roume, Hugo, Salem, Joe Elie, Schmidt, Thomas S.B., Vieira-Silva, Sara, Li, Peishun, Zimmermann-Kogadeeva, Maria, Lewinter, Christian, Søndertoft, Nadja B., Hansen, Tue H., Gauguier, Dominique, Gøtze, Jens Peter, Køber, Lars, Kornowski, Ran, Vestergaard, Henrik, Hansen, Torben, Zucker, Jean Daniel, Hercberg, Serge, Letunic, Ivica, Bäckhed, Fredrik, Oppert, Jean Michel, Nielsen, Jens, Raes, Jeroen, Bork, Peer, Stumvoll, Michael, Segal, Eran, Clément, Karine, Dumas, Marc Emmanuel, Ehrlich, S. Dusko, and Pedersen, Oluf
Abstract: Previous microbiome and metabolome analyses exploring non-communicable diseases have paid scant attention to major confounders of study outcomes, such as common, pre-morbid and co-morbid conditions, or polypharmacy. Here, in the context of ischemic heart disease (IHD), we used a study design that recapitulates disease initiation, escalation and response to treatment over time, mirroring a longitudinal study that would otherwise be difficult to perform given the protracted nature of IHD pathogenesis. We recruited 1,241 middle-aged Europeans, including healthy individuals, individuals with dysmetabolic morbidities (obesity and type 2 diabetes) but lacking overt IHD diagnosis and individuals with IHD at three distinct clinical stages—acute coronary syndrome, chronic IHD and IHD with heart failure—and characterized their phenome, gut metagenome and serum and urine metabolome. We found that about 75% of microbiome and metabolome features that distinguish individuals with IHD from healthy individuals after adjustment for effects of medication and lifestyle are present in individuals exhibiting dysmetabolism, suggesting that major alterations of the gut microbiome and metabolome might begin long before clinical onset of IHD. We further categorized microbiome and metabolome signatures related to prodromal dysmetabolism, specific to IHD in general or to each of its three subtypes or related to escalation or de-escalation of IHD. Discriminant analysis based on specific IHD microbiome and metabolome features could better differentiate individuals with IHD from healthy individuals or metabolically matched individuals as compared to the conventional risk markers, pointing to a pathophysiological relevance of these features.
Published: 2022

6. Human and preclinical studies of the host-gut microbiome co-metabolite hippurate as a marker and mediator of metabolic health

Author: Brial, Francois, Chilloux, Julien, Nielsen, Trine, Vieira-Silva, Sara, Falony, Gwen, Andrikopoulos, Petros, Olanipekun, Michael, Hoyles, Lesley, Djouadi, Fatima, Neves, Ana L., Rodriguez-Martinez, Andrea, Mouawad, Ghiwa Ishac, Pons, Nicolas, Forslund, Sofia, Le-chatelier, Emmanuelle, Le Lay, Aurelie, Nicholson, Jeremy, Hansen, Torben, Hyotylainen, Tuulia, Clement, Karine, Oresic, Matej, Bork, Peer, Ehrlich, Stanislav Dusko, Raes, Jeroen, Pedersen, Oluf Borbye, Gauguier, Dominique, Dumas, Marc-Emmanuel, Brial, Francois, Chilloux, Julien, Nielsen, Trine, Vieira-Silva, Sara, Falony, Gwen, Andrikopoulos, Petros, Olanipekun, Michael, Hoyles, Lesley, Djouadi, Fatima, Neves, Ana L., Rodriguez-Martinez, Andrea, Mouawad, Ghiwa Ishac, Pons, Nicolas, Forslund, Sofia, Le-chatelier, Emmanuelle, Le Lay, Aurelie, Nicholson, Jeremy, Hansen, Torben, Hyotylainen, Tuulia, Clement, Karine, Oresic, Matej, Bork, Peer, Ehrlich, Stanislav Dusko, Raes, Jeroen, Pedersen, Oluf Borbye, Gauguier, Dominique, and Dumas, Marc-Emmanuel
Abstract: Objective Gut microbial products are involved in regulation of host metabolism. In human and experimental studies, we explored the potential role of hippurate, a hepatic phase 2 conjugation product of microbial benzoate, as a marker and mediator of metabolic health. Design In 271 middle-aged non-diabetic Danish individuals, who were stratified on habitual dietary intake, we applied H-1-nuclear magnetic resonance (NMR) spectroscopy of urine samples and shotgun-sequencing-based metagenomics of the gut microbiome to explore links between the urine level of hippurate, measures of the gut microbiome, dietary fat and markers of metabolic health. In mechanistic experiments with chronic subcutaneous infusion of hippurate to high-fat-diet-fed obese mice, we tested for causality between hippurate and metabolic phenotypes. Results In the human study, we showed that urine hippurate positively associates with microbial gene richness and functional modules for microbial benzoate biosynthetic pathways, one of which is less prevalent in the Bacteroides 2 enterotype compared with Ruminococcaceae or Prevotella enterotypes. Through dietary stratification, we identify a subset of study participants consuming a diet rich in saturated fat in which urine hippurate concentration, independently of gene richness, accounts for links with metabolic health. In the high-fat-fed mice experiments, we demonstrate causality through chronic infusion of hippurate (20 nmol/day) resulting in improved glucose tolerance and enhanced insulin secretion. Conclusion Our human and experimental studies show that a high urine hippurate concentration is a general marker of metabolic health, and in the context of obesity induced by high-fat diets, hippurate contributes to metabolic improvements, highlighting its potential as a mediator of metabolic health.
Published: 2021

7. Molecular genetics of the transcription factor GLIS3 identifies its dual function in beta cells and neurons.

Author: Calderari, Sophie, Ria, Massimiliano, Gérard, Christelle, Nogueira, Tatiane C, Villate, Olatz, Collins, Stephan C, Neil, Helen, Gervasi, Nicolas, Hue, Christophe, Suarez-Zamorano, Nicolas, Prado, Cécilia, Cnop, Miriam, Bihoreau, Marie-Thérèse, Kaisaki, Pamela J, Cazier, Jean-Baptiste, Julier, Cécile, Lathrop, Mark, Werner, Michel, Eizirik, Decio L., Gauguier, Dominique, Calderari, Sophie, Ria, Massimiliano, Gérard, Christelle, Nogueira, Tatiane C, Villate, Olatz, Collins, Stephan C, Neil, Helen, Gervasi, Nicolas, Hue, Christophe, Suarez-Zamorano, Nicolas, Prado, Cécilia, Cnop, Miriam, Bihoreau, Marie-Thérèse, Kaisaki, Pamela J, Cazier, Jean-Baptiste, Julier, Cécile, Lathrop, Mark, Werner, Michel, Eizirik, Decio L., and Gauguier, Dominique
Abstract: The GLIS family zinc finger 3 isoform (GLIS3) is a risk gene for Type 1 and Type 2 diabetes, glaucoma and Alzheimer's disease endophenotype. We identified GLIS3 binding sites in insulin secreting cells (INS1) (FDR q<0.05; enrichment range 1.40-9.11 fold) sharing the motif wrGTTCCCArTAGs, which were enriched in genes involved in neuronal function and autophagy and in risk genes for metabolic and neuro-behavioural diseases. We confirmed experimentally Glis3-mediated regulation of the expression of genes involved in autophagy and neuron function in INS1 and neuronal PC12 cells. Naturally-occurring coding polymorphisms in Glis3 in the Goto-Kakizaki rat model of type 2 diabetes were associated with increased insulin production in vitro and in vivo, suggestive alteration of autophagy in PC12 and INS1 and abnormal neurogenesis in hippocampus neurons. Our results support biological pleiotropy of GLIS3 in pathologies affecting β-cells and neurons and underline the existence of trans‑nosology pathways in diabetes and its co-morbidities., info:eu-repo/semantics/published
Published: 2017

8. Loss of Cardioprotective Effects at the ADAMTS7 Locus as a Result of Gene-Smoking Interactions

Author: Saleheen, Danish, Zhao, Wei, Young, Robin, Nelson, Christopher P., Ho, WeangKee, Ferguson, Jane F., Rasheed, Asif, Ou, Kristy, Nurnberg, Sylvia T., Bauer, Robert C., Goel, Anuj, Do, Ron, Stewart, Alexandre F. R., Hartiala, Jaana, Zhang, Weihua, Thorleifsson, Gudmar, Strawbridge, Rona J., Sinisalo, Juha, Kanoni, Stavroula, Sedaghat, Sanaz, Marouli, Eirini, Kristiansson, Kati, Zhao, Jing Hua, Scott, Robert, Gauguier, Dominique, Shah, Svati H., Smith, Albert Vernon, van Zuydam, Natalie, Cox, Amanda J., Willenborg, Christina, Kessler, Thorsten, Zeng, Lingyao, Province, Michael A., Ganna, Andrea, Lind, Lars, Pedersen, Nancy L., White, Charles C., Joensuu, Anni, Kleber, Marcus Edi, Hall, Alistair S., Maerz, Winfried, Salomaa, Veikko, O'Donnell, Christopher, Ingelsson, Erik, Feitosa, Mary F., Erdmann, Jeanette, Bowden, Donald W., Palmer, Colin N. A., Gudnason, Vilmundur, De Faire, Ulf, Zalloua, Pierre, Wareham, Nicholas, Thompson, John R., Kuulasmaa, Kari, Dedoussis, George, Perola, Markus, Dehghan, Abbas, Chambers, John C., Kooner, Jaspal, Allayee, Hooman, Deloukas, Panos, McPherson, Ruth, Stefansson, Kari, Schunkert, Heribert, Kathiresan, Sekar, Farrall, Martin, Frossard, Philippe Marcel, Rader, Daniel J., Samani, Nilesh J., Reilly, Muredach P., Saleheen, Danish, Zhao, Wei, Young, Robin, Nelson, Christopher P., Ho, WeangKee, Ferguson, Jane F., Rasheed, Asif, Ou, Kristy, Nurnberg, Sylvia T., Bauer, Robert C., Goel, Anuj, Do, Ron, Stewart, Alexandre F. R., Hartiala, Jaana, Zhang, Weihua, Thorleifsson, Gudmar, Strawbridge, Rona J., Sinisalo, Juha, Kanoni, Stavroula, Sedaghat, Sanaz, Marouli, Eirini, Kristiansson, Kati, Zhao, Jing Hua, Scott, Robert, Gauguier, Dominique, Shah, Svati H., Smith, Albert Vernon, van Zuydam, Natalie, Cox, Amanda J., Willenborg, Christina, Kessler, Thorsten, Zeng, Lingyao, Province, Michael A., Ganna, Andrea, Lind, Lars, Pedersen, Nancy L., White, Charles C., Joensuu, Anni, Kleber, Marcus Edi, Hall, Alistair S., Maerz, Winfried, Salomaa, Veikko, O'Donnell, Christopher, Ingelsson, Erik, Feitosa, Mary F., Erdmann, Jeanette, Bowden, Donald W., Palmer, Colin N. A., Gudnason, Vilmundur, De Faire, Ulf, Zalloua, Pierre, Wareham, Nicholas, Thompson, John R., Kuulasmaa, Kari, Dedoussis, George, Perola, Markus, Dehghan, Abbas, Chambers, John C., Kooner, Jaspal, Allayee, Hooman, Deloukas, Panos, McPherson, Ruth, Stefansson, Kari, Schunkert, Heribert, Kathiresan, Sekar, Farrall, Martin, Frossard, Philippe Marcel, Rader, Daniel J., Samani, Nilesh J., and Reilly, Muredach P.
Abstract: BACKGROUND: Common diseases such as coronary heart disease (CHD) are complex in etiology. The interaction of genetic susceptibility with lifestyle factors may play a prominent role. However, gene-lifestyle interactions for CHD have been difficult to identify. Here, we investigate interaction of smoking behavior, a potent lifestyle factor, with genotypes that have been shown to associate with CHD risk. METHODS: We analyzed data on 60 919 CHD cases and 80 243 controls from 29 studies for gene-smoking interactions for genetic variants at 45 loci previously reported to be associated with CHD risk. We also studied 5 loci associated with smoking behavior. Study-specific gene-smoking interaction effects were calculated and pooled using fixed-effects meta-analyses. Interaction analyses were declared to be significant at a P value of < 1.0x10-3 (Bonferroni correction for 50 tests). RESULTS: We identified novel gene-smoking interaction for a variant upstream of the ADAMTS7 gene. Every T allele of rs7178051 was associated with lower CHD risk by 12% in never-smokers (P= 1.3x10(-16)) in comparison with 5% in ever-smokers (P= 2.5x10-4), translating to a 60% loss of CHD protection conferred by this allelic variation in people who smoked tobacco (interaction P value= 8.7x10-5). The protective T allele at rs7178051 was also associated with reduced ADAMTS7 expression in human aortic endothelial cells and lymphoblastoid cell lines. Exposure of human coronary artery smooth muscle cells to cigarette smoke extract led to induction of ADAMTS7. CONCLUSIONS: Allelic variation at rs7178051 that associates with reduced ADAMTS7 expression confers stronger CHD protection in never-smokers than in ever-smokers. Increased vascular ADAMTS7 expression may contribute to the loss of CHD protection in smokers.
Published: 2017
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9. Genomic correlates of glatiramer acetate adverse cardiovascular effects lead to a novel locus mediating coronary risk

Author: Brænne, I, Zeng, L, Willenborg, C, Tragante, V, Kessler, T, Willer, C, Laakso, M, Wallentin, L, Franks, P, Salomaa, V, Dehghan, A, Meitinger, T, Samani, N, Asselbergs, F, Erdmann, J, Schunkert, H, Deloukas, P, Kanoni, S, Farrall, M, Assimes, T, Thompson, J, Ingelsson, E, Saleheen, D, Goldstein, B, Absher, D, König, I, Cazier, J, Johansson, Å, Hall, A, Lee, J, Chambers, J, Esko, T, Folkersen, L, Goel, A, Grundberg, E, Havulinna, A, Ho, W, Hopewell, J, Eriksson, N, Kleber, M, Kristiansson, K, Lundmark, P, Lyytikäinen, L, Rafelt, S, Shun, D, Strawbridge, R, Thorleifsson, G, Tikkanen, E, Van Zuydam, N, Voight, B, Waite, L, Zhang, W, Zieg, A, Altshuler, D, Balmforth, A, Barroso, I, Braund, P, Burgdorf, C, Claudi-Boehm, S, Cox, D, Dimitriou, M, Do, R, Doney, A, El Mokhtari, N, Eriksson, P, Fischer, K, Fontanillas, P, Franco-Cereceda, A, Gigante, B, Groop, L, Gustafsson, S, Hager, J, Hallmans, G, Han, B, Ehunt, S, Kang, H, Illig, T, Knowles, J, Kolovou, G, Kuusisto, J, Langenberg, C, Langford, C, Leander, K, Lokki, M, Lundmark, A, Mccarthy, M, Meisinger, C, Melander, O, Mihailov, E, Maouche, S, Morris, A, Müller-Nurasyid, M, Nikus, K, Peden, J, Rayner, N, Rasheed, A, Rosinger, S, Rubin, D, Rumpf, M, Schäfer, A, Sivananthan, M, Song, C, Stewart, A, Tan, S, Thorgeirsson, G, Van Der Schoot, C, Wagner, P, Wells, G, Wild, P, Yang, T, Amouyel, P, Arveiler, D, Basart, H, Boehnke, M, Boerwinkle, E, Brambilla, P, Cambien, F, Cupples, A, De Faire, U, Diemert, P, Epstein, S, Evans, A, Ferrario, M, Ferrières, J, Gauguier, D, Go, A, Goodall, A, Gudnason, V, Hazen, S, Holm, H, Iribarren, C, Jang, Y, Kähönen, M, Kee, F, Kim, H, Klopp, N, Koenig, W, Kratzer, W, Kuulasmaa, K, Laaksonen, R, Lind, L, Ouwehand, W, Parish, S, Park, J, Pedersen, N, Peters, A, Quertermous, T, Rader, D, Schadt, E, Shah, S, Sinisalo, J, Stark, K, Stefansson, K, Trégouët, D, Virtamo, J, Wareham, N, Zimmermann, M, Nieminen, M, Hengsten, C, Sandhu, M, Pastinen, T, Syvänen, A, Hovingh, G, Dedoussis, G, Lehtimäki, T, Metspalu, A, Zalloua, P, Siegbahn, A, Schreiber, S, Ripatti, S, Blankenberg, S, Perola, M, Clarke, R, Oboehm, B, O’Donnell, C, Reilly, M, März, W, Collins, R, Kathiresan, S, Hamsten, A, Kooner, J, Thorsteinsdottir, U, Danesh, J, Palmer, C, Roberts, R, Watkins, H, Hengstenberg, C, Mcpherson, R, Ziegler, A, Brænne, Ingrid, Zeng, Lingyao, Willenborg, Christina, Tragante, Vinicius, Kessler, Thorsten, Willer, Cristen J., Laakso, Markku, Wallentin, Lars, Franks, Paul W., Salomaa, Veikko, Dehghan, Abbas, Meitinger, Thomas, Samani, Nilesh J., Asselbergs, Folkert W., Erdmann, Jeanette, Schunkert, Heribert, Deloukas, Panos, Kanoni, Stavroula, Farrall, Martin, Assimes, Themistocles L., Thompson, John R., Ingelsson, Erik, Saleheen, Danish, Goldstein, Benjamin A., Absher, Devin, König, Inke R., Cazier, Jean-Baptiste, Johansson, Åsa, Hall, Alistair S., Lee, Jong-Young, Chambers, John C., Esko, Tõnu, Folkersen, Lasse, Goel, Anuj, Grundberg, Elin, Havulinna, Aki S., Ho, Weang K., Hopewell, Jemma C., Eriksson, Niclas, Kleber, Marcus E., Kristiansson, Kati, Lundmark, Per, Lyytikäinen, Leo-Pekka, Rafelt, Suzanne, Shun, Dmitry, Strawbridge, Rona J., Thorleifsson, Gudmar, Tikkanen, Emmi, Van Zuydam, Natalie, Voight, Benjamin F., Waite, Lindsay L., Zhang, Weihua, Zieg, Andreas, Altshuler, David, Balmforth, Anthony J., Barroso, Inês, Braund, Peter S., Burgdorf, Christof, Claudi-Boehm, Simone, Cox, David, Dimitriou, Maria, Do, Ron, Doney, Alex S. F., El Mokhtari, Nour Eddine, Eriksson, Per, Fischer, Krista, Fontanillas, Pierre, Franco-Cereceda, Anders, Gigante, Bruna, Groop, Leif, Gustafsson, Stefan, Hager, Jörg, Hallmans, Göran, Han, Bok-Ghee, Ehunt, Sarah, Kang, Hyun M., Illig, Thomas, Knowles, Joshua W., Kolovou, Genovefa, Kuusisto, Johanna, Langenberg, Claudia, Langford, Cordelia, Leander, Karin, Lokki, Marja-Liisa, Lundmark, Anders, McCarthy, Mark I., Meisinger, Christa, Melander, Olle, Mihailov, Evelin, Maouche, Seraya, Morris, Andrew D., Müller-Nurasyid, Martina, Nikus, Kjell, Peden, John F., Rayner, N. William, Rasheed, Asif, Rosinger, Silke, Rubin, Diana, Rumpf, Moritz P., Schäfer, Arne, Sivananthan, Mohan, Song, Ci, Stewart, Alexandre F. R., Tan, Sian-Tsung, Thorgeirsson, Gudmundur, Van Der Schoot, C. Ellen, Wagner, Peter J., Wells, George A., Wild, Philipp S., Yang, Tsun-Po, Amouyel, Philippe, Arveiler, Dominique, Basart, Hanneke, Boehnke, Michael, Boerwinkle, Eric, Brambilla, Paolo, Cambien, Francois, Cupples, Adrienne L., De Faire, Ulf, Diemert, Patrick, Epstein, Stephen E., Evans, Alun, Ferrario, Marco M., Ferrières, Jean, Gauguier, Dominique, Go, Alan S., Goodall, Alison H., Gudnason, Villi, Hazen, Stanley L., Holm, Hilma, Iribarren, Carlos, Jang, Yangsoo, Kähönen, Mika, Kee, Frank, Kim, Hyo-Soo, Klopp, Norman, Koenig, Wolfgang, Kratzer, Wolfgang, Kuulasmaa, Kari, Laaksonen, Reijo, Lee, Ji-Young, Lind, Lars, Ouwehand, Willem H., Parish, Sarah, Park, Jeong E., Pedersen, Nancy L., Peters, Annette, Quertermous, Thomas, Rader, Daniel J., Schadt, Eric, Shah, Svati H., Sinisalo, Juha, Stark, Klaus, Stefansson, Kari, Trégouët, David-Alexandre, Virtamo, Jarmo, Wareham, Nicholas, Zimmermann, Martina E., Nieminen, Markku S., Hengsten, Christian, Sandhu, Manjinder S., Pastinen, Tomi, Syvänen, Ann-Christine, Hovingh, G. Kees, Dedoussis, George, Lehtimäki, Terho, Metspalu, Andres, Zalloua, Pierre A., Siegbahn, Agneta, Schreiber, Stefan, Ripatti, Samuli, Blankenberg, Stefan S., Perola, Markus, Clarke, Robert, Oboehm, Bernhard, O’Donnell, Christopher, Reilly, Muredach P., März, Winfried, Collins, Rory, Kathiresan, Sekar, Hamsten, Anders, Kooner, Jaspal S., Thorsteinsdottir, Unnur, Danesh, John, Palmer, Colin N. A., Roberts, Robert, Watkins, Hugh, Hall, Alistair, Hengstenberg, Christian, McPherson, Ruth, Ziegler, Andreas, Brænne, I, Zeng, L, Willenborg, C, Tragante, V, Kessler, T, Willer, C, Laakso, M, Wallentin, L, Franks, P, Salomaa, V, Dehghan, A, Meitinger, T, Samani, N, Asselbergs, F, Erdmann, J, Schunkert, H, Deloukas, P, Kanoni, S, Farrall, M, Assimes, T, Thompson, J, Ingelsson, E, Saleheen, D, Goldstein, B, Absher, D, König, I, Cazier, J, Johansson, Å, Hall, A, Lee, J, Chambers, J, Esko, T, Folkersen, L, Goel, A, Grundberg, E, Havulinna, A, Ho, W, Hopewell, J, Eriksson, N, Kleber, M, Kristiansson, K, Lundmark, P, Lyytikäinen, L, Rafelt, S, Shun, D, Strawbridge, R, Thorleifsson, G, Tikkanen, E, Van Zuydam, N, Voight, B, Waite, L, Zhang, W, Zieg, A, Altshuler, D, Balmforth, A, Barroso, I, Braund, P, Burgdorf, C, Claudi-Boehm, S, Cox, D, Dimitriou, M, Do, R, Doney, A, El Mokhtari, N, Eriksson, P, Fischer, K, Fontanillas, P, Franco-Cereceda, A, Gigante, B, Groop, L, Gustafsson, S, Hager, J, Hallmans, G, Han, B, Ehunt, S, Kang, H, Illig, T, Knowles, J, Kolovou, G, Kuusisto, J, Langenberg, C, Langford, C, Leander, K, Lokki, M, Lundmark, A, Mccarthy, M, Meisinger, C, Melander, O, Mihailov, E, Maouche, S, Morris, A, Müller-Nurasyid, M, Nikus, K, Peden, J, Rayner, N, Rasheed, A, Rosinger, S, Rubin, D, Rumpf, M, Schäfer, A, Sivananthan, M, Song, C, Stewart, A, Tan, S, Thorgeirsson, G, Van Der Schoot, C, Wagner, P, Wells, G, Wild, P, Yang, T, Amouyel, P, Arveiler, D, Basart, H, Boehnke, M, Boerwinkle, E, Brambilla, P, Cambien, F, Cupples, A, De Faire, U, Diemert, P, Epstein, S, Evans, A, Ferrario, M, Ferrières, J, Gauguier, D, Go, A, Goodall, A, Gudnason, V, Hazen, S, Holm, H, Iribarren, C, Jang, Y, Kähönen, M, Kee, F, Kim, H, Klopp, N, Koenig, W, Kratzer, W, Kuulasmaa, K, Laaksonen, R, Lind, L, Ouwehand, W, Parish, S, Park, J, Pedersen, N, Peters, A, Quertermous, T, Rader, D, Schadt, E, Shah, S, Sinisalo, J, Stark, K, Stefansson, K, Trégouët, D, Virtamo, J, Wareham, N, Zimmermann, M, Nieminen, M, Hengsten, C, Sandhu, M, Pastinen, T, Syvänen, A, Hovingh, G, Dedoussis, G, Lehtimäki, T, Metspalu, A, Zalloua, P, Siegbahn, A, Schreiber, S, Ripatti, S, Blankenberg, S, Perola, M, Clarke, R, Oboehm, B, O’Donnell, C, Reilly, M, März, W, Collins, R, Kathiresan, S, Hamsten, A, Kooner, J, Thorsteinsdottir, U, Danesh, J, Palmer, C, Roberts, R, Watkins, H, Hengstenberg, C, Mcpherson, R, Ziegler, A, Brænne, Ingrid, Zeng, Lingyao, Willenborg, Christina, Tragante, Vinicius, Kessler, Thorsten, Willer, Cristen J., Laakso, Markku, Wallentin, Lars, Franks, Paul W., Salomaa, Veikko, Dehghan, Abbas, Meitinger, Thomas, Samani, Nilesh J., Asselbergs, Folkert W., Erdmann, Jeanette, Schunkert, Heribert, Deloukas, Panos, Kanoni, Stavroula, Farrall, Martin, Assimes, Themistocles L., Thompson, John R., Ingelsson, Erik, Saleheen, Danish, Goldstein, Benjamin A., Absher, Devin, König, Inke R., Cazier, Jean-Baptiste, Johansson, Åsa, Hall, Alistair S., Lee, Jong-Young, Chambers, John C., Esko, Tõnu, Folkersen, Lasse, Goel, Anuj, Grundberg, Elin, Havulinna, Aki S., Ho, Weang K., Hopewell, Jemma C., Eriksson, Niclas, Kleber, Marcus E., Kristiansson, Kati, Lundmark, Per, Lyytikäinen, Leo-Pekka, Rafelt, Suzanne, Shun, Dmitry, Strawbridge, Rona J., Thorleifsson, Gudmar, Tikkanen, Emmi, Van Zuydam, Natalie, Voight, Benjamin F., Waite, Lindsay L., Zhang, Weihua, Zieg, Andreas, Altshuler, David, Balmforth, Anthony J., Barroso, Inês, Braund, Peter S., Burgdorf, Christof, Claudi-Boehm, Simone, Cox, David, Dimitriou, Maria, Do, Ron, Doney, Alex S. F., El Mokhtari, Nour Eddine, Eriksson, Per, Fischer, Krista, Fontanillas, Pierre, Franco-Cereceda, Anders, Gigante, Bruna, Groop, Leif, Gustafsson, Stefan, Hager, Jörg, Hallmans, Göran, Han, Bok-Ghee, Ehunt, Sarah, Kang, Hyun M., Illig, Thomas, Knowles, Joshua W., Kolovou, Genovefa, Kuusisto, Johanna, Langenberg, Claudia, Langford, Cordelia, Leander, Karin, Lokki, Marja-Liisa, Lundmark, Anders, McCarthy, Mark I., Meisinger, Christa, Melander, Olle, Mihailov, Evelin, Maouche, Seraya, Morris, Andrew D., Müller-Nurasyid, Martina, Nikus, Kjell, Peden, John F., Rayner, N. William, Rasheed, Asif, Rosinger, Silke, Rubin, Diana, Rumpf, Moritz P., Schäfer, Arne, Sivananthan, Mohan, Song, Ci, Stewart, Alexandre F. R., Tan, Sian-Tsung, Thorgeirsson, Gudmundur, Van Der Schoot, C. Ellen, Wagner, Peter J., Wells, George A., Wild, Philipp S., Yang, Tsun-Po, Amouyel, Philippe, Arveiler, Dominique, Basart, Hanneke, Boehnke, Michael, Boerwinkle, Eric, Brambilla, Paolo, Cambien, Francois, Cupples, Adrienne L., De Faire, Ulf, Diemert, Patrick, Epstein, Stephen E., Evans, Alun, Ferrario, Marco M., Ferrières, Jean, Gauguier, Dominique, Go, Alan S., Goodall, Alison H., Gudnason, Villi, Hazen, Stanley L., Holm, Hilma, Iribarren, Carlos, Jang, Yangsoo, Kähönen, Mika, Kee, Frank, Kim, Hyo-Soo, Klopp, Norman, Koenig, Wolfgang, Kratzer, Wolfgang, Kuulasmaa, Kari, Laaksonen, Reijo, Lee, Ji-Young, Lind, Lars, Ouwehand, Willem H., Parish, Sarah, Park, Jeong E., Pedersen, Nancy L., Peters, Annette, Quertermous, Thomas, Rader, Daniel J., Schadt, Eric, Shah, Svati H., Sinisalo, Juha, Stark, Klaus, Stefansson, Kari, Trégouët, David-Alexandre, Virtamo, Jarmo, Wareham, Nicholas, Zimmermann, Martina E., Nieminen, Markku S., Hengsten, Christian, Sandhu, Manjinder S., Pastinen, Tomi, Syvänen, Ann-Christine, Hovingh, G. Kees, Dedoussis, George, Lehtimäki, Terho, Metspalu, Andres, Zalloua, Pierre A., Siegbahn, Agneta, Schreiber, Stefan, Ripatti, Samuli, Blankenberg, Stefan S., Perola, Markus, Clarke, Robert, Oboehm, Bernhard, O’Donnell, Christopher, Reilly, Muredach P., März, Winfried, Collins, Rory, Kathiresan, Sekar, Hamsten, Anders, Kooner, Jaspal S., Thorsteinsdottir, Unnur, Danesh, John, Palmer, Colin N. A., Roberts, Robert, Watkins, Hugh, Hall, Alistair, Hengstenberg, Christian, McPherson, Ruth, and Ziegler, Andreas
Abstract: Glatiramer acetate is used therapeutically in multiple sclerosis but also known for adverse effects including elevated coronary artery disease (CAD) risk. The mechanisms underlying the cardiovascular side effects of the medication are unclear. Here, we made use of the chromosomal variation in the genes that are known to be affected by glatiramer treatment. Focusing on genes and gene products reported by drug-gene interaction database to interact with glatiramer acetate we explored a large meta-analysis on CAD genome-wide association studies aiming firstly, to investigate whether variants in these genes also affect cardiovascular risk and secondly, to identify new CAD risk genes. We traced association signals in a 200-kb region around genomic positions of genes interacting with glatiramer in up to 60 801 CAD cases and 123 504 controls. We validated the identified association in additional 21 934 CAD cases and 76 087 controls. We identified three new CAD risk alleles within the TGFB1 region on chromosome 19 that independently affect CAD risk. The lead SNP rs12459996 was genome-wide significantly associated with CAD in the extended meta-analysis (odds ratio 1.09, p = 1.58×10−12). The other two SNPs at the locus were not in linkage disequilibrium with the lead SNP and by a conditional analysis showed p-values of 4.05 × 10−10 and 2.21 × 10−6. Thus, studying genes reported to interact with glatiramer acetate we identified genetic variants that concordantly with the drug increase the risk of CAD. Of these, TGFB1 displayed signal for association. Indeed, the gene has been associated with CAD previously in both in vivo and in vitro studies. Here we establish genome-wide significant association with CAD in large human samples.
Published: 2017

10. Association of hypertension with coronary artery disease onset in the Lebanese population

Author: Milane, Aline, Abdallah, Jad, Kanbar, Roy, Khazen, Georges, Saad, Aline, Ghassibe-Sabbagh, Michella, Salloum, Angelique K., Youhanna, Sonia, El Bayeh, Hamid, Chammas, Elie, Platt, Daniel E., Hager, Jorg, Gauguier, Dominique, Zalloua, Pierre, Milane, Aline, Abdallah, Jad, Kanbar, Roy, Khazen, Georges, Saad, Aline, Ghassibe-Sabbagh, Michella, Salloum, Angelique K., Youhanna, Sonia, El Bayeh, Hamid, Chammas, Elie, Platt, Daniel E., Hager, Jorg, Gauguier, Dominique, and Zalloua, Pierre
Abstract: The onset of coronary artery disease (CAD) is influenced by cardiovascular risk factors that often occur in clusters and may build on one another. The objective of this study is to examine the relationship between hypertension and CAD age of onset in the Lebanese population. This retrospective analysis was performed on data extracted from Lebanese patients (n = 3,753). Logistic regression examined the association of hypertension with the age at CAD diagnosis after controlling for other traditional risk factors. The effect of antihypertensive drugs and lifestyle changes on the onset of CAD was also investigated. Results showed that hypertension is associated with late onset CAD (OR=0.656, 95% CI=0.504-0.853, p=0.001). Use of antihypertensive drugs showed a similar association with delayed CAD onset. When comparing age of onset in CAD patients with traditional risk factors such as hypertension, diabetes, hyperlipidemia, obesity, smoking and family history of CAD, the age of onset was significantly higher for patients with hypertension compared to those with any of the other risk factors studied (p < 0.001). In conclusion, hypertension and its treatment are associated with late coronary atherosclerotic manifestations in Lebanese population. This observation is currently under investigation to clarify its genetic and/or environmental mechanisms.
Published: 2017

11. No Association of Coronary Artery Disease with X-Chromosomal Variants in Comprehensive International Meta-Analysis

Author: Loley, Christina, Alver, Maris, Assimes, Themistocles L., Bjonnes, Andrew, Goel, Anuj, Gustafsson, Stefan, Hernesniemi, Jussi, Hopewell, Jemma C., Kanoni, Stavroula, Kleber, Marcus E., Lau, King Wai, Lu, Yingchang, Lyytikainen, Leo-Pekka, Nelson, Christopher P., Nikpay, Majid, Qu, Liming, Salfati, Elias, Scholz, Markus, Tukiainen, Taru, Willenborg, Christina, Won, Hong-Hee, Zeng, Lingyao, Zhang, Weihua, Anand, Sonia S., Beutner, Frank, Bottinger, Erwin P., Clarke, Robert, Dedoussis, George, Do, Ron, Esko, Tonu, Eskola, Markku, Farrall, Martin, Gauguier, Dominique, Giedraitis, Vilmantas, Granger, Christopher B., Hall, Alistair S., Hamsten, Anders, Hazen, Stanley L., Huang, Jie, Kahonen, Mika, Kyriakou, Theodosios, Laaksonen, Reijo, Lind, Lars, Lindgren, Cecilia, Magnusson, Patrik K. E., Marouli, Eirini, Mihailov, Evelin, Morris, Andrew P., Nikus, Kjell, Pedersen, Nancy, Rallidis, Loukianos, Salomaa, Veikko, Shah, Svati H., Stewart, Alexandre F. R., Thompson, John R., Zalloua, Pierre A., Chambers, John C., Collins, Rory, Ingelsson, Erik, Iribarren, Carlos, Karhunen, Pekka J., Kooner, Jaspal S., Lehtimaki, Terho, Loos, Ruth J. F., Maerz, Winfried, McPherson, Ruth, Metspalu, Andres, Reilly, Muredach P., Ripatti, Samuli, Sanghera, Dharambir K., Thiery, Joachim, Watkins, Hugh, Deloukas, Panos, Kathiresan, Sekar, Samani, Nilesh J., Schunkert, Heribert, Erdmann, Jeanette, Koenig, Inke R., Loley, Christina, Alver, Maris, Assimes, Themistocles L., Bjonnes, Andrew, Goel, Anuj, Gustafsson, Stefan, Hernesniemi, Jussi, Hopewell, Jemma C., Kanoni, Stavroula, Kleber, Marcus E., Lau, King Wai, Lu, Yingchang, Lyytikainen, Leo-Pekka, Nelson, Christopher P., Nikpay, Majid, Qu, Liming, Salfati, Elias, Scholz, Markus, Tukiainen, Taru, Willenborg, Christina, Won, Hong-Hee, Zeng, Lingyao, Zhang, Weihua, Anand, Sonia S., Beutner, Frank, Bottinger, Erwin P., Clarke, Robert, Dedoussis, George, Do, Ron, Esko, Tonu, Eskola, Markku, Farrall, Martin, Gauguier, Dominique, Giedraitis, Vilmantas, Granger, Christopher B., Hall, Alistair S., Hamsten, Anders, Hazen, Stanley L., Huang, Jie, Kahonen, Mika, Kyriakou, Theodosios, Laaksonen, Reijo, Lind, Lars, Lindgren, Cecilia, Magnusson, Patrik K. E., Marouli, Eirini, Mihailov, Evelin, Morris, Andrew P., Nikus, Kjell, Pedersen, Nancy, Rallidis, Loukianos, Salomaa, Veikko, Shah, Svati H., Stewart, Alexandre F. R., Thompson, John R., Zalloua, Pierre A., Chambers, John C., Collins, Rory, Ingelsson, Erik, Iribarren, Carlos, Karhunen, Pekka J., Kooner, Jaspal S., Lehtimaki, Terho, Loos, Ruth J. F., Maerz, Winfried, McPherson, Ruth, Metspalu, Andres, Reilly, Muredach P., Ripatti, Samuli, Sanghera, Dharambir K., Thiery, Joachim, Watkins, Hugh, Deloukas, Panos, Kathiresan, Sekar, Samani, Nilesh J., Schunkert, Heribert, Erdmann, Jeanette, and Koenig, Inke R.
Abstract: In recent years, genome-wide association studies have identified 58 independent risk loci for coronary artery disease (CAD) on the autosome. However, due to the sex-specific data structure of the X chromosome, it has been excluded from most of these analyses. While females have 2 copies of chromosome X, males have only one. Also, one of the female X chromosomes may be inactivated. Therefore, special test statistics and quality control procedures are required. Thus, little is known about the role of X-chromosomal variants in CAD. To fill this gap, we conducted a comprehensive X-chromosome-wide meta-analysis including more than 43,000 CAD cases and 58,000 controls from 35 international study cohorts. For quality control, sex-specific filters were used to adequately take the special structure of X-chromosomal data into account. For single study analyses, several logistic regression models were calculated allowing for inactivation of one female X-chromosome, adjusting for sex and investigating interactions between sex and genetic variants. Then, meta-analyses including all 35 studies were conducted using random effects models. None of the investigated models revealed genome-wide significant associations for any variant. Although we analyzed the largest-to-date sample, currently available methods were not able to detect any associations of X-chromosomal variants with CAD.
Published: 2016
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12. A comprehensive 1000 Genomes-based genome-wide association meta-analysis of coronary artery disease

Author: Nikpay, Majid, Goel, Anuj, Won, Hong-Hee, Hall, Leanne M., Willenborg, Christina, Kanoni, Stavroula, Saleheen, Danish, Kyriakou, Theodosios, Nelson, Christopher P., Hopewell, Jemma C., Webb, Thomas R., Zeng, Lingyao, Dehghan, Abbas, Alver, Maris, Armasu, Sebastian M., Auro, Kirsi, Bjonnes, Andrew, Chasman, Daniel I., Chen, Shufeng, Ford, Ian, Franceschini, Nora, Gieger, Christian, Grace, Christopher, Gustafsson, Stefan, Huang, Jie, Hwang, Shih-Jen, Kim, Yun Kyoung, Kleber, Marcus E., Lau, King Wai, Lu, Xiangfeng, Lu, Yingchang, Lyytikainen, Leo-Pekka, Mihailov, Evelin, Morrison, Alanna C., Pervjakova, Natalia, Qu, Liming, Rose, Lynda M., Salfati, Elias, Saxena, Richa, Scholz, Markus, Smith, Albert V., Tikkanen, Emmi, Uitterlinden, Andre, Yang, Xueli, Zhang, Weihua, Zhao, Wei, de Andrade, Mariza, de Vries, Paul S., van Zuydam, Natalie R., Anand, Sonia S., Bertram, Lars, Beutner, Frank, Dedoussis, George, Frossard, Philippe, Gauguier, Dominique, Goodall, Alison H., Gottesman, Omri, Haber, Marc, Han, Bok-Ghee, Huang, Jianfeng, Jalilzadeh, Shapour, Kessler, Thorsten, Koenig, Inke R., Lannfelt, Lars, Lieb, Wolfgang, Lind, Lars, Lindgren, Cecilia M., Lokki, Marja-Liisa, Magnusson, Patrik K., Mallick, Nadeem H., Mehra, Narinder, Meitinger, Thomas, Memon, Fazal-ur-Rehman, Morris, Andrew P., Nieminen, Markku S., Pedersen, Nancy L., Peters, Annette, Rallidis, Loukianos S., Rasheed, Asif, Samuel, Maria, Shah, Svati H., Sinisalo, Juha, Stirrups, Kathleen E., Trompet, Stella, Wang, Laiyuan, Zaman, Khan S., Ardissino, Diego, Boerwinkle, Eric, Borecki, Ingrid B., Bottinger, Erwin P., Buring, Julie E., Chambers, John C., Collins, Rory, Cupples, L. Adrienne, Danesh, John, Demuth, Ilja, Elosua, Roberto, Epstein, Stephen E., Esko, Tonu, Feitosa, Mary F., Franco, Oscar H., Franzosi, Maria Grazia, Granger, Christopher B., Gu, Dongfeng, Gudnason, Vilmundur, Hall, Alistair S., Hamsten, Anders, Harris, Tamara B., Hazen, Stanley L., Hengstenberg, Christian, Hofman, Albert, Ingelsson, Erik, Iribarren, Carlos, Jukema, J. Wouter, Karhunen, Pekka J., Kim, Bong-Jo, Kooner, Jaspal S., Kullo, Iftikhar J., Lehtimaki, Terho, Loos, Ruth J. F., Melander, Olle, Metspalu, Andres, Maerz, Winfried, Palmer, Colin N., Perola, Markus, Quertermous, Thomas, Rader, Daniel J., Ridker, Paul M., Ripatti, Samuli, Roberts, Robert, Salomaa, Veikko, Sanghera, Dharambir K., Schwartz, Stephen M., Seedorf, Udo, Stewart, Alexandre F., Stott, David J., Thiery, Joachim, Zalloua, Pierre A., O'Donnell, Christopher J., Reilly, Muredach P., Assimes, Themistocles L., Thompson, John R., Erdmann, Jeanette, Clarke, Robert, Watkins, Hugh, Kathiresan, Sekar, McPherson, Ruth, Deloukas, Panos, Schunkert, Heribert, Samani, Nilesh J., Farrall, Martin, Nikpay, Majid, Goel, Anuj, Won, Hong-Hee, Hall, Leanne M., Willenborg, Christina, Kanoni, Stavroula, Saleheen, Danish, Kyriakou, Theodosios, Nelson, Christopher P., Hopewell, Jemma C., Webb, Thomas R., Zeng, Lingyao, Dehghan, Abbas, Alver, Maris, Armasu, Sebastian M., Auro, Kirsi, Bjonnes, Andrew, Chasman, Daniel I., Chen, Shufeng, Ford, Ian, Franceschini, Nora, Gieger, Christian, Grace, Christopher, Gustafsson, Stefan, Huang, Jie, Hwang, Shih-Jen, Kim, Yun Kyoung, Kleber, Marcus E., Lau, King Wai, Lu, Xiangfeng, Lu, Yingchang, Lyytikainen, Leo-Pekka, Mihailov, Evelin, Morrison, Alanna C., Pervjakova, Natalia, Qu, Liming, Rose, Lynda M., Salfati, Elias, Saxena, Richa, Scholz, Markus, Smith, Albert V., Tikkanen, Emmi, Uitterlinden, Andre, Yang, Xueli, Zhang, Weihua, Zhao, Wei, de Andrade, Mariza, de Vries, Paul S., van Zuydam, Natalie R., Anand, Sonia S., Bertram, Lars, Beutner, Frank, Dedoussis, George, Frossard, Philippe, Gauguier, Dominique, Goodall, Alison H., Gottesman, Omri, Haber, Marc, Han, Bok-Ghee, Huang, Jianfeng, Jalilzadeh, Shapour, Kessler, Thorsten, Koenig, Inke R., Lannfelt, Lars, Lieb, Wolfgang, Lind, Lars, Lindgren, Cecilia M., Lokki, Marja-Liisa, Magnusson, Patrik K., Mallick, Nadeem H., Mehra, Narinder, Meitinger, Thomas, Memon, Fazal-ur-Rehman, Morris, Andrew P., Nieminen, Markku S., Pedersen, Nancy L., Peters, Annette, Rallidis, Loukianos S., Rasheed, Asif, Samuel, Maria, Shah, Svati H., Sinisalo, Juha, Stirrups, Kathleen E., Trompet, Stella, Wang, Laiyuan, Zaman, Khan S., Ardissino, Diego, Boerwinkle, Eric, Borecki, Ingrid B., Bottinger, Erwin P., Buring, Julie E., Chambers, John C., Collins, Rory, Cupples, L. Adrienne, Danesh, John, Demuth, Ilja, Elosua, Roberto, Epstein, Stephen E., Esko, Tonu, Feitosa, Mary F., Franco, Oscar H., Franzosi, Maria Grazia, Granger, Christopher B., Gu, Dongfeng, Gudnason, Vilmundur, Hall, Alistair S., Hamsten, Anders, Harris, Tamara B., Hazen, Stanley L., Hengstenberg, Christian, Hofman, Albert, Ingelsson, Erik, Iribarren, Carlos, Jukema, J. Wouter, Karhunen, Pekka J., Kim, Bong-Jo, Kooner, Jaspal S., Kullo, Iftikhar J., Lehtimaki, Terho, Loos, Ruth J. F., Melander, Olle, Metspalu, Andres, Maerz, Winfried, Palmer, Colin N., Perola, Markus, Quertermous, Thomas, Rader, Daniel J., Ridker, Paul M., Ripatti, Samuli, Roberts, Robert, Salomaa, Veikko, Sanghera, Dharambir K., Schwartz, Stephen M., Seedorf, Udo, Stewart, Alexandre F., Stott, David J., Thiery, Joachim, Zalloua, Pierre A., O'Donnell, Christopher J., Reilly, Muredach P., Assimes, Themistocles L., Thompson, John R., Erdmann, Jeanette, Clarke, Robert, Watkins, Hugh, Kathiresan, Sekar, McPherson, Ruth, Deloukas, Panos, Schunkert, Heribert, Samani, Nilesh J., and Farrall, Martin
Abstract: Existing knowledge of genetic variants affecting risk of coronary artery disease (CAD) is largely based on genome-wide association study (GWAS) analysis of common SNPs. Leveraging phased haplotypes from the 1000 Genomes Project, we report a GWAS meta-analysis of similar to 185,000 CAD cases and controls, interrogating 6.7 million common (minor allele frequency (MAF) > 0.05) and 2.7 million low-frequency (0.005 < MAF < 0.05) variants. In addition to confirming most known CAD-associated loci, we identified ten new loci (eight additive and two recessive) that contain candidate causal genes newly implicating biological processes in vessel walls. We observed intralocus allelic heterogeneity but little evidence of low-frequency variants with larger effects and no evidence of synthetic association. Our analysis provides a comprehensive survey of the fine genetic architecture of CAD, showing that genetic susceptibility to this common disease is largely determined by common SNPs of small effect size.
Published: 2015
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13. Whole-genome sequencing identifies EN1 as a determinant of bone density and fracture

Author: Zheng, Hou-Feng, Forgetta, Vincenzo, Hsu, Yi-Hsiang, Estrada, Karol, Rosello-Diez, Alberto, Leo, Paul J., Dahia, Chitra L., Park-Min, Kyung Hyun, Tobias, Jonathan H., Kooperberg, Charles, Kleinman, Aaron, Styrkarsdottir, Unnur, Liu, Ching-Ti, Uggla, Charlotta, Evans, Daniel S., Nielson, Carrie M., Walter, Klaudia, Pettersson-Kymmer, Ulrika, McCarthy, Shane, Eriksson, Joel, Kwan, Tony, Jhamai, Mila, Trajanoska, Katerina, Memari, Yasin, Min, Josine, Huang, Jie, Danecek, Petr, Wilmot, Beth, Li, Rui, Chou, Wen-Chi, Mokry, Lauren E., Moayyeri, Alireza, Claussnitzer, Melina, Cheng, Chia-Ho, Cheung, Warren, Medina-Gomez, Carolina, Ge, Bing, Chen, Shu-Huang, Choi, Kwangbom, Oei, Ling, Fraser, James, Kraaij, Robert, Hibbs, Matthew A., Gregson, Celia L., Paquette, Denis, Hofman, Albert, Wibom, Carl, Tranah, Gregory J., Marshall, Mhairi, Gardiner, Brooke B., Cremin, Katie, Auer, Paul, Hsu, Li, Ring, Sue, Tung, Joyce Y., Thorleifsson, Gudmar, Enneman, Anke W., van Schoor, Natasja M., de Groot, Lisette C. P. G. M., van der Velde, Nathalie, Melin, Beatrice, Kemp, John P., Christiansen, Claus, Sayers, Adrian, Zhou, Yanhua, Calderari, Sophie, van Rooij, Jeroen, Carlson, Chris, Peters, Ulrike, Berlivet, Soizik, Dostie, Josee, Uitterlinden, Andre G., Williams, Stephen R., Farber, Charles, Grinberg, Daniel, LaCroix, Andrea Z., Haessler, Jeff, Chasman, Daniel I., Giulianini, Franco, Rose, Lynda M., Ridker, Paul M., Eisman, John A., Nguyen, Tuan V., Center, Jacqueline R., Nogues, Xavier, Garcia-Giralt, Natalia, Launer, Lenore L., Gudnason, Vilmunder, Mellstrom, Dan, Vandenput, Liesbeth, Amin, Najaf, van Duijn, Cornelia M., Karlsson, Magnus K., Ljunggren, Osten, Svensson, Olle, Hallmans, Göran, Rousseau, Francois, Giroux, Sylvie, Bussiere, Johanne, Arp, Pascal P., Koromani, Fjorda, Prince, Richard L., Lewis, Joshua R., Langdahl, Bente L., Hermann, A. Pernille, Jensen, Jens-Erik B., Kaptoge, Stephen, Khaw, Kay-Tee, Reeve, Jonathan, Formosa, Melissa M., Xuereb-Anastasi, Angela, Akesson, Kristina, McGuigan, Fiona E., Garg, Gaurav, Olmos, Jose M., Zarrabeitia, Maria T., Riancho, Jose A., Ralston, Stuart H., Alonso, Nerea, Jiang, Xi, Goltzman, David, Pastinen, Tomi, Grundberg, Elin, Gauguier, Dominique, Orwoll, Eric S., Karasik, David, Davey-Smith, George, Smith, Albert V., Siggeirsdottir, Kristin, Harris, Tamara B., Zillikens, M. Carola, van Meurs, Joyce B. J., Thorsteinsdottir, Unnur, Maurano, Matthew T., Timpson, Nicholas J., Soranzo, Nicole, Durbin, Richard, Wilson, ScottG., Ntzani, Evangelia E., Brown, Matthew A., Stefansson, Kari, Hinds, David A., Spector, Tim, Cupples, L. Adrienne, Ohlsson, Claes, Greenwood, Celia M. T., Jackson, Rebecca D., Rowe, David W., Loomis, Cynthia A., Evans, David M., Ackert-Bicknell, Cheryl L., Joyner, Alexandra L., Duncan, Emma L., Kiel, Douglas P., Rivadeneira, Fernando, Richards, J. Brent, Zheng, Hou-Feng, Forgetta, Vincenzo, Hsu, Yi-Hsiang, Estrada, Karol, Rosello-Diez, Alberto, Leo, Paul J., Dahia, Chitra L., Park-Min, Kyung Hyun, Tobias, Jonathan H., Kooperberg, Charles, Kleinman, Aaron, Styrkarsdottir, Unnur, Liu, Ching-Ti, Uggla, Charlotta, Evans, Daniel S., Nielson, Carrie M., Walter, Klaudia, Pettersson-Kymmer, Ulrika, McCarthy, Shane, Eriksson, Joel, Kwan, Tony, Jhamai, Mila, Trajanoska, Katerina, Memari, Yasin, Min, Josine, Huang, Jie, Danecek, Petr, Wilmot, Beth, Li, Rui, Chou, Wen-Chi, Mokry, Lauren E., Moayyeri, Alireza, Claussnitzer, Melina, Cheng, Chia-Ho, Cheung, Warren, Medina-Gomez, Carolina, Ge, Bing, Chen, Shu-Huang, Choi, Kwangbom, Oei, Ling, Fraser, James, Kraaij, Robert, Hibbs, Matthew A., Gregson, Celia L., Paquette, Denis, Hofman, Albert, Wibom, Carl, Tranah, Gregory J., Marshall, Mhairi, Gardiner, Brooke B., Cremin, Katie, Auer, Paul, Hsu, Li, Ring, Sue, Tung, Joyce Y., Thorleifsson, Gudmar, Enneman, Anke W., van Schoor, Natasja M., de Groot, Lisette C. P. G. M., van der Velde, Nathalie, Melin, Beatrice, Kemp, John P., Christiansen, Claus, Sayers, Adrian, Zhou, Yanhua, Calderari, Sophie, van Rooij, Jeroen, Carlson, Chris, Peters, Ulrike, Berlivet, Soizik, Dostie, Josee, Uitterlinden, Andre G., Williams, Stephen R., Farber, Charles, Grinberg, Daniel, LaCroix, Andrea Z., Haessler, Jeff, Chasman, Daniel I., Giulianini, Franco, Rose, Lynda M., Ridker, Paul M., Eisman, John A., Nguyen, Tuan V., Center, Jacqueline R., Nogues, Xavier, Garcia-Giralt, Natalia, Launer, Lenore L., Gudnason, Vilmunder, Mellstrom, Dan, Vandenput, Liesbeth, Amin, Najaf, van Duijn, Cornelia M., Karlsson, Magnus K., Ljunggren, Osten, Svensson, Olle, Hallmans, Göran, Rousseau, Francois, Giroux, Sylvie, Bussiere, Johanne, Arp, Pascal P., Koromani, Fjorda, Prince, Richard L., Lewis, Joshua R., Langdahl, Bente L., Hermann, A. Pernille, Jensen, Jens-Erik B., Kaptoge, Stephen, Khaw, Kay-Tee, Reeve, Jonathan, Formosa, Melissa M., Xuereb-Anastasi, Angela, Akesson, Kristina, McGuigan, Fiona E., Garg, Gaurav, Olmos, Jose M., Zarrabeitia, Maria T., Riancho, Jose A., Ralston, Stuart H., Alonso, Nerea, Jiang, Xi, Goltzman, David, Pastinen, Tomi, Grundberg, Elin, Gauguier, Dominique, Orwoll, Eric S., Karasik, David, Davey-Smith, George, Smith, Albert V., Siggeirsdottir, Kristin, Harris, Tamara B., Zillikens, M. Carola, van Meurs, Joyce B. J., Thorsteinsdottir, Unnur, Maurano, Matthew T., Timpson, Nicholas J., Soranzo, Nicole, Durbin, Richard, Wilson, ScottG., Ntzani, Evangelia E., Brown, Matthew A., Stefansson, Kari, Hinds, David A., Spector, Tim, Cupples, L. Adrienne, Ohlsson, Claes, Greenwood, Celia M. T., Jackson, Rebecca D., Rowe, David W., Loomis, Cynthia A., Evans, David M., Ackert-Bicknell, Cheryl L., Joyner, Alexandra L., Duncan, Emma L., Kiel, Douglas P., Rivadeneira, Fernando, and Richards, J. Brent
Abstract: The extent to which low-frequency (minor allele frequency (MAF) between 1-5%) and rare (MAF <= 1%) variants contribute to complex traits and disease in the general population is mainly unknown. Bone mineral density (BMD) is highly heritable, a major predictor of osteoporotic fractures, and has been previously associated with common genetic variants(1-8), as well as rare, population specific, coding variants(9). Here we identify novel non-coding genetic variants with large effects on BMD (n(total) = 53,236) and fracture (n(total) = 508,253) in individuals of European ancestry from the general population. Associations for BMD were derived from whole-genome sequencing (n = 2,882 from UK10K (ref. 10); a population-based genome sequencing consortium), whole-exome sequencing (n = 3,549), deep imputation of genotyped samples using a combined UK10K/1000 Genomes reference panel (n = 26,534), and de novo replication genotyping (n = 20,271). We identified a low-frequency non-coding variant near a novel locus, EN1, with an effect size fourfold larger than the mean of previously reported common variants for lumbar spine BMD8 (rs11692564(T), MAF51.6%, replication effect size510.20 s.d., P-meta = 2 x 10(-14)), which was also associated with a decreased risk of fracture (odds ratio = 0.85; P = 2 x 10(-11); ncases = 98,742 and ncontrols = 409,511). Using an En1cre/flox mouse model, we observed that conditional loss of En1 results in low bone mass, probably as a consequence of high bone turnover. We also identified a novel low frequency non-coding variant with large effects on BMD near WNT16 (rs148771817(T), MAF = 1.2%, replication effect size +10.41 s.d., P-meta = 1 x 10(-11)). In general, there was an excess of association signals arising from deleterious coding and conserved non-coding variants. These findings provide evidence that low-frequency non-coding variants have large effects on BMD and fracture, thereby providing rationale for whole-genome sequencing and improved imput
Published: 2015
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14. Large-scale association analysis identifies new risk loci for coronary artery disease

Author: Deloukas, Panos, Kanoni, Stavroula, Willenborg, Christina, Farrall, Martin, Assimes, Themistocles L, Thompson, John R, Ingelsson, Erik, Saleheen, Danish, Erdmann, Jeanette, Goldstein, Benjamin A, Stirrups, Kathleen, König, Inke R, Cazier, Jean-Baptiste, Johansson, Åsa, Hall, Alistair S, Lee, Jong-Young, Willer, Cristen J, Chambers, John C, Esko, Tõnu, Folkersen, Lasse, Goel, Anuj, Grundberg, Elin, Havulinna, Aki S, Ho, Weang K, Hopewell, Jemma C, Eriksson, Niclas, Kleber, Marcus E, Kristiansson, Kati, Lundmark, Per, Lyytikäinen, Leo-Pekka, Rafelt, Suzanne, Shungin, Dmitry, Strawbridge, Rona J, Thorleifsson, Gudmar, Tikkanen, Emmi, van Zuydam, Natalie, Voight, Benjamin F, Waite, Lindsay L, Zhang, Weihua, Ziegler, Andreas, Absher, Devin, Altshuler, David, Balmforth, Anthony J, Barroso, Inês, Braund, Peter S, Burgdorf, Christof, Claudi-Boehm, Simone, Cox, David, Dimitriou, Maria, Do, Ron, Doney, Alex S F, Mokhtari, Noureddine El, Eriksson, Per, Fischer, Krista, Fontanillas, Pierre, Franco-Cereceda, Anders, Gigante, Bruna, Groop, Leif, Gustafsson, Stefan, Hager, Jörg, Hallmans, Göran, Han, Bok-Ghee, Hunt, Sarah E, Kang, Hyun M, Illig, Thomas, Kessler, Thorsten, Knowles, Joshua W, Kolovou, Genovefa, Kuusisto, Johanna, Langenberg, Claudia, Langford, Cordelia, Leander, Karin, Lokki, Marja-Liisa, Lundmark, Anders, McCarthy, Mark I, Meisinger, Christa, Melander, Olle, Mihailov, Evelin, Maouche, Seraya, Morris, Andrew D, Müller-Nurasyid, Martina, Nikus, Kjell, Peden, John F, Rayner, N William, Rasheed, Asif, Rosinger, Silke, Rubin, Diana, Rumpf, Moritz P, Schäfer, Arne, Sivananthan, Mohan, Song, Ci, Stewart, Alexandre F R, Tan, Sian-Tsung, Thorgeirsson, Gudmundur, Schoot, C Ellen van der, Wagner, Peter J, Wells, George A, Wild, Philipp S, Yang, Tsun-Po, Amouyel, Philippe, Arveiler, Dominique, Basart, Hanneke, Boehnke, Michael, Boerwinkle, Eric, Brambilla, Paolo, Cambien, Francois, Cupples, Adrienne L, de Faire, Ulf, Dehghan, Abbas, Diemert, Patrick, Epstein, Stephen E, Evans, Alun, Ferrario, Marco M, Ferrières, Jean, Gauguier, Dominique, Go, Alan S, Goodall, Alison H, Gudnason, Villi, Hazen, Stanley L, Holm, Hilma, Iribarren, Carlos, Jang, Yangsoo, Kähönen, Mika, Kee, Frank, Kim, Hyo-Soo, Klopp, Norman, Koenig, Wolfgang, Kratzer, Wolfgang, Kuulasmaa, Kari, Laakso, Markku, Laaksonen, Reijo, Lee, Ji-Young, Lind, Lars, Ouwehand, Willem H, Parish, Sarah, Park, Jeong E, Pedersen, Nancy L, Peters, Annette, Quertermous, Thomas, Rader, Daniel J, Salomaa, Veikko, Schadt, Eric, Shah, Svati H, Sinisalo, Juha, Stark, Klaus, Stefansson, Kari, Trégouët, David-Alexandre, Virtamo, Jarmo, Wallentin, Lars, Wareham, Nicholas, Zimmermann, Martina E, Nieminen, Markku S, Hengstenberg, Christian, Sandhu, Manjinder S, Pastinen, Tomi, Syvänen, Ann-Christine, Hovingh, G Kees, Dedoussis, George, Franks, Paul W, Lehtimäki, Terho, Metspalu, Andres, Zalloua, Pierre A, Siegbahn, Agneta, Schreiber, Stefan, Ripatti, Samuli, Blankenberg, Stefan S, Perola, Markus, Clarke, Robert, Boehm, Bernhard O, O'Donnell, Christopher, Reilly, Muredach P, März, Winfried, Collins, Rory, Kathiresan, Sekar, Hamsten, Anders, Kooner, Jaspal S, Thorsteinsdottir, Unnur, Danesh, John, Palmer, Colin N A, Roberts, Robert, Watkins, Hugh, Schunkert, Heribert, Samani, Nilesh J, Deloukas, Panos, Kanoni, Stavroula, Willenborg, Christina, Farrall, Martin, Assimes, Themistocles L, Thompson, John R, Ingelsson, Erik, Saleheen, Danish, Erdmann, Jeanette, Goldstein, Benjamin A, Stirrups, Kathleen, König, Inke R, Cazier, Jean-Baptiste, Johansson, Åsa, Hall, Alistair S, Lee, Jong-Young, Willer, Cristen J, Chambers, John C, Esko, Tõnu, Folkersen, Lasse, Goel, Anuj, Grundberg, Elin, Havulinna, Aki S, Ho, Weang K, Hopewell, Jemma C, Eriksson, Niclas, Kleber, Marcus E, Kristiansson, Kati, Lundmark, Per, Lyytikäinen, Leo-Pekka, Rafelt, Suzanne, Shungin, Dmitry, Strawbridge, Rona J, Thorleifsson, Gudmar, Tikkanen, Emmi, van Zuydam, Natalie, Voight, Benjamin F, Waite, Lindsay L, Zhang, Weihua, Ziegler, Andreas, Absher, Devin, Altshuler, David, Balmforth, Anthony J, Barroso, Inês, Braund, Peter S, Burgdorf, Christof, Claudi-Boehm, Simone, Cox, David, Dimitriou, Maria, Do, Ron, Doney, Alex S F, Mokhtari, Noureddine El, Eriksson, Per, Fischer, Krista, Fontanillas, Pierre, Franco-Cereceda, Anders, Gigante, Bruna, Groop, Leif, Gustafsson, Stefan, Hager, Jörg, Hallmans, Göran, Han, Bok-Ghee, Hunt, Sarah E, Kang, Hyun M, Illig, Thomas, Kessler, Thorsten, Knowles, Joshua W, Kolovou, Genovefa, Kuusisto, Johanna, Langenberg, Claudia, Langford, Cordelia, Leander, Karin, Lokki, Marja-Liisa, Lundmark, Anders, McCarthy, Mark I, Meisinger, Christa, Melander, Olle, Mihailov, Evelin, Maouche, Seraya, Morris, Andrew D, Müller-Nurasyid, Martina, Nikus, Kjell, Peden, John F, Rayner, N William, Rasheed, Asif, Rosinger, Silke, Rubin, Diana, Rumpf, Moritz P, Schäfer, Arne, Sivananthan, Mohan, Song, Ci, Stewart, Alexandre F R, Tan, Sian-Tsung, Thorgeirsson, Gudmundur, Schoot, C Ellen van der, Wagner, Peter J, Wells, George A, Wild, Philipp S, Yang, Tsun-Po, Amouyel, Philippe, Arveiler, Dominique, Basart, Hanneke, Boehnke, Michael, Boerwinkle, Eric, Brambilla, Paolo, Cambien, Francois, Cupples, Adrienne L, de Faire, Ulf, Dehghan, Abbas, Diemert, Patrick, Epstein, Stephen E, Evans, Alun, Ferrario, Marco M, Ferrières, Jean, Gauguier, Dominique, Go, Alan S, Goodall, Alison H, Gudnason, Villi, Hazen, Stanley L, Holm, Hilma, Iribarren, Carlos, Jang, Yangsoo, Kähönen, Mika, Kee, Frank, Kim, Hyo-Soo, Klopp, Norman, Koenig, Wolfgang, Kratzer, Wolfgang, Kuulasmaa, Kari, Laakso, Markku, Laaksonen, Reijo, Lee, Ji-Young, Lind, Lars, Ouwehand, Willem H, Parish, Sarah, Park, Jeong E, Pedersen, Nancy L, Peters, Annette, Quertermous, Thomas, Rader, Daniel J, Salomaa, Veikko, Schadt, Eric, Shah, Svati H, Sinisalo, Juha, Stark, Klaus, Stefansson, Kari, Trégouët, David-Alexandre, Virtamo, Jarmo, Wallentin, Lars, Wareham, Nicholas, Zimmermann, Martina E, Nieminen, Markku S, Hengstenberg, Christian, Sandhu, Manjinder S, Pastinen, Tomi, Syvänen, Ann-Christine, Hovingh, G Kees, Dedoussis, George, Franks, Paul W, Lehtimäki, Terho, Metspalu, Andres, Zalloua, Pierre A, Siegbahn, Agneta, Schreiber, Stefan, Ripatti, Samuli, Blankenberg, Stefan S, Perola, Markus, Clarke, Robert, Boehm, Bernhard O, O'Donnell, Christopher, Reilly, Muredach P, März, Winfried, Collins, Rory, Kathiresan, Sekar, Hamsten, Anders, Kooner, Jaspal S, Thorsteinsdottir, Unnur, Danesh, John, Palmer, Colin N A, Roberts, Robert, Watkins, Hugh, Schunkert, Heribert, and Samani, Nilesh J
Abstract: Coronary artery disease (CAD) is the commonest cause of death. Here, we report an association analysis in 63,746 CAD cases and 130,681 controls identifying 15 loci reaching genome-wide significance, taking the number of susceptibility loci for CAD to 46, and a further 104 independent variants (r2 < 0.2) strongly associated with CAD at a 5% false discovery rate (FDR). Together, these variants explain approximately 10.6% of CAD heritability. Of the 46 genome-wide significant lead SNPs, 12 show a significant association with a lipid trait, and 5 show a significant association with blood pressure, but none is significantly associated with diabetes. Network analysis with 233 candidate genes (loci at 10% FDR) generated 5 interaction networks comprising 85% of these putative genes involved in CAD. The four most significant pathways mapping to these networks are linked to lipid metabolism and inflammation, underscoring the causal role of these activities in the genetic etiology of CAD. Our study provides insights into the genetic basis of CAD and identifies key biological pathways.
Published: 2013
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15. Genome-wide diversity in the levant reveals recent structuring by culture.

Author: Haber, Marc, Haber, Marc, Gauguier, Dominique, Youhanna, Sonia, Patterson, Nick, Moorjani, Priya, Botigué, Laura, Platt, Daniel, Matisoo-Smith, Elizabeth, Soria-Hernanz, David, Wells, R, Bertranpetit, Jaume, Tyler-Smith, Chris, Comas, David, Zalloua, Pierre, Haber, Marc, Haber, Marc, Gauguier, Dominique, Youhanna, Sonia, Patterson, Nick, Moorjani, Priya, Botigué, Laura, Platt, Daniel, Matisoo-Smith, Elizabeth, Soria-Hernanz, David, Wells, R, Bertranpetit, Jaume, Tyler-Smith, Chris, Comas, David, and Zalloua, Pierre
Abstract: The Levant is a region in the Near East with an impressive record of continuous human existence and major cultural developments since the Paleolithic period. Genetic and archeological studies present solid evidence placing the Middle East and the Arabian Peninsula as the first stepping-stone outside Africa. There is, however, little understanding of demographic changes in the Middle East, particularly the Levant, after the first Out-of-Africa expansion and how the Levantine peoples relate genetically to each other and to their neighbors. In this study we analyze more than 500,000 genome-wide SNPs in 1,341 new samples from the Levant and compare them to samples from 48 populations worldwide. Our results show recent genetic stratifications in the Levant are driven by the religious affiliations of the populations within the region. Cultural changes within the last two millennia appear to have facilitated/maintained admixture between culturally similar populations from the Levant, Arabian Peninsula, and Africa. The same cultural changes seem to have resulted in genetic isolation of other groups by limiting admixture with culturally different neighboring populations. Consequently, Levant populations today fall into two main groups: one sharing more genetic characteristics with modern-day Europeans and Central Asians, and the other with closer genetic affinities to other Middle Easterners and Africans. Finally, we identify a putative Levantine ancestral component that diverged from other Middle Easterners ∼23,700-15,500 years ago during the last glacial period, and diverged from Europeans ∼15,900-9,100 years ago between the last glacial warming and the start of the Neolithic.
Published: 2013

16. Functional annotations of diabetes nephropathy susceptibility loci through analysis of genome-wide renal gene expression in rat models of diabetes mellitus

Author: Hu, Yaomin, Kaisaki, Pamela J, Argoud, Karène, Wilder, Steven P, Wallace, Karin J, Woon, Peng Y, Blancher, Christine, Tarnow, Lise, Groop, Per-Henrik, Hadjadj, Samy, Marre, Michel, Parving, Hans-Henrik, Farrall, Martin, Cox, Roger D, Lathrop, Mark, Vionnet, Nathalie, Bihoreau, Marie-Thérèse, Gauguier, Dominique, Hu, Yaomin, Kaisaki, Pamela J, Argoud, Karène, Wilder, Steven P, Wallace, Karin J, Woon, Peng Y, Blancher, Christine, Tarnow, Lise, Groop, Per-Henrik, Hadjadj, Samy, Marre, Michel, Parving, Hans-Henrik, Farrall, Martin, Cox, Roger D, Lathrop, Mark, Vionnet, Nathalie, Bihoreau, Marie-Thérèse, and Gauguier, Dominique
Abstract: Udgivelsesdato: 2009, BACKGROUND: Hyperglycaemia in diabetes mellitus (DM) alters gene expression regulation in various organs and contributes to long term vascular and renal complications. We aimed to generate novel renal genome-wide gene transcription data in rat models of diabetes in order to test the responsiveness to hyperglycaemia and renal structural changes of positional candidate genes at selected diabetic nephropathy (DN) susceptibility loci. METHODS: Both Affymetrix and Illumina technologies were used to identify significant quantitative changes in the abundance of over 15,000 transcripts in kidney of models of spontaneous (genetically determined) mild hyperglycaemia and insulin resistance (Goto-Kakizaki-GK) and experimentally induced severe hyperglycaemia (Wistar-Kyoto-WKY rats injected with streptozotocin [STZ]). RESULTS: Different patterns of transcription regulation in the two rat models of diabetes likely underlie the roles of genetic variants and hyperglycaemia severity. The impact of prolonged hyperglycaemia on gene expression changes was more profound in STZ-WKY rats than in GK rats and involved largely different sets of genes. These included genes already tested in genetic studies of DN and a large number of protein coding sequences of unknown function which can be considered as functional and, when they map to DN loci, positional candidates for DN. Further expression analysis of rat orthologs of human DN positional candidate genes provided functional annotations of known and novel genes that are responsive to hyperglycaemia and may contribute to renal functional and/or structural alterations. CONCLUSION: Combining transcriptomics in animal models and comparative genomics provides important information to improve functional annotations of disease susceptibility loci in humans and experimental support for testing candidate genes in human genetics.
Published: 2009

17. Progress and prospects in rat genetics: a community view.

Author: Aitman, Timothy J, Critser, John K, Cuppen, Edwin, Dominiczak, Anna, Fernandez-Suarez, Xose M, Flint, Jonathan, Gauguier, Dominique, Geurts, Aron M, Gould, Michael, Harris, Peter C, Holmdahl, Rikard, Hubner, Norbert, Izsvák, Zsuzsanna, Jacob, Howard J, Kuramoto, Takashi, Kwitek, Anne E, Marrone, Anna, Mashimo, Tomoji, Moreno, Carol, Mullins, John, Mullins, Linda, Olsson, Tomas, Pravenec, Michal, Riley, Lela, Saar, Kathrin, Serikawa, Tadao, Shull, James D, Szpirer, Claude, Twigger, Simon N, Voigt, Birger, Worley, Kim, Aitman, Timothy J, Critser, John K, Cuppen, Edwin, Dominiczak, Anna, Fernandez-Suarez, Xose M, Flint, Jonathan, Gauguier, Dominique, Geurts, Aron M, Gould, Michael, Harris, Peter C, Holmdahl, Rikard, Hubner, Norbert, Izsvák, Zsuzsanna, Jacob, Howard J, Kuramoto, Takashi, Kwitek, Anne E, Marrone, Anna, Mashimo, Tomoji, Moreno, Carol, Mullins, John, Mullins, Linda, Olsson, Tomas, Pravenec, Michal, Riley, Lela, Saar, Kathrin, Serikawa, Tadao, Shull, James D, Szpirer, Claude, Twigger, Simon N, Voigt, Birger, and Worley, Kim
Abstract: The rat is an important system for modeling human disease. Four years ago, the rich 150-year history of rat research was transformed by the sequencing of the rat genome, ushering in an era of exceptional opportunity for identifying genes and pathways underlying disease phenotypes. Genome-wide association studies in human populations have recently provided a direct approach for finding robust genetic associations in common diseases, but identifying the precise genes and their mechanisms of action remains problematic. In the context of significant progress in rat genomic resources over the past decade, we outline achievements in rat gene discovery to date, show how these findings have been translated to human disease, and document an increasing pace of discovery of new disease genes, pathways and mechanisms. Finally, we present a set of principles that justify continuing and strengthening genetic studies in the rat model, and further development of genomic infrastructure for rat research., Journal Article, Review, info:eu-repo/semantics/published
Published: 2008

18. Statistical Total Correlation Spectroscopy: An Exploratory Approach for Latent Biomarker Identification from Metabolic 1H NMR Data Sets

Author: Cloarec, Olivier, Dumas, Marc-Emmanuel, Craig, Andrew, Barton, Richard H, Trygg, Johan, Hudson, Jane, Blancher, Christine, Gauguier, Dominique, Lindon, John C, Holmes, Elaine, Nicholson, Jeremy, Cloarec, Olivier, Dumas, Marc-Emmanuel, Craig, Andrew, Barton, Richard H, Trygg, Johan, Hudson, Jane, Blancher, Christine, Gauguier, Dominique, Lindon, John C, Holmes, Elaine, and Nicholson, Jeremy
Abstract: We describe here the implementation of the statistical total correlation spectroscopy (STOCSY) analysis method for aiding the identification of potential biomarker molecules in metabonomic studies based on NMR spectroscopic data. STOCSY takes advantage of the multicollinearity of the intensity variables in a set of spectra (in this case 1H NMR spectra) to generate a pseudo-two-dimensional NMR spectrum that displays the correlation among the intensities of the various peaks across the whole sample. This method is not limited to the usual connectivities that are deducible from more standard two-dimensional NMR spectroscopic methods, such as TOCSY. Moreover, two or more molecules involved in the same pathway can also present high intermolecular correlations because of biological covariance or can even be anticorrelated. This combination of STOCSY with supervised pattern recognition and particularly orthogonal projection on latent structure-discriminant analysis (O-PLS-DA) offers a new powerful framework for analysis of metabonomic data. In a first step O-PLS-DA extracts the part of NMR spectra related to discrimination. This information is then cross-combined with the STOCSY results to help identify the molecules responsible for the metabolic variation. To illustrate the applicability of the method, it has been applied to 1H NMR spectra of urine from a metabonomic study of a model of insulin resistance based on the administration of a carbohydrate diet to three different mice strains (C57BL/6Oxjr, BALB/cOxjr, and 129S6/SvEvOxjr) in which a series of metabolites of biological importance can be conclusively assigned and identified by use of the STOCSY approach.
Published: 2005
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19. A genetic linkage map of the rat derived from recombinant inbred strains.

Author: Pravenec, Michal, Gauguier, Dominique, Schott, J J, Buard, J, Kren, V, Bílá, V, Szpirer, Claude, Szpirer, Josiane, Wang, J M, Huang, Henry, St Lezin, E, Spence, M A, Flodman, P, Printz, M, Lathrop, G M, Vergnaud, G, Kurtz, T W, Pravenec, Michal, Gauguier, Dominique, Schott, J J, Buard, J, Kren, V, Bílá, V, Szpirer, Claude, Szpirer, Josiane, Wang, J M, Huang, Henry, St Lezin, E, Spence, M A, Flodman, P, Printz, M, Lathrop, G M, Vergnaud, G, and Kurtz, T W
Abstract: We have constructed a genetic linkage map in the rat by analyzing the strain distribution patterns of 500 genetic markers in a large set of recombinant inbred strains derived from the spontaneously hypertensive rat and the Brown-Norway rat (HXB and BXH recombinant inbred strains). 454 of the markers could be assigned to specific chromosomes, and the amount of genome covered by the mapped markers was estimated to be 1151 centimorgans. By including a variety of morphologic, biochemical, immunogenetic, and molecular markers, the current map integrates and extends existing linkage data and should facilitate rat gene mapping and genetic studies of hypertension and other complex phenotypes of interest in the HXB and BXH recombinant inbred strains., Journal Article, Research Support, Non-U.S. Gov't, info:eu-repo/semantics/published
Published: 1996

20. Mapping of quantitative trait loci for blood pressure and cardiac mass in the rat by genome scanning of recombinant inbred strains.

Author: Pravenec, Michal, Gauguier, Dominique, Schott, J J, Buard, J, Kren, V, Bílá, V, Szpirer, Claude, Szpirer, Josiane, Wang, J M, Huang, Henry, Pravenec, Michal, Gauguier, Dominique, Schott, J J, Buard, J, Kren, V, Bílá, V, Szpirer, Claude, Szpirer, Josiane, Wang, J M, and Huang, Henry
Abstract: In the HXB and BXH recombinant inbred strains derived from the spontaneously hypertensive rat and the normotensive Brown Norway rat, we determined the strain distribution patterns of 500 genetic markers to scan the rodent genome for quantitative trait loci regulating cardiac mass and blood pressure. The markers spanned approximately 1,139 cM of the genome and were tested for correlations with left ventricular mass adjusted for body weight, and with systolic, diastolic, and mean arterial pressures. The marker for the dopamine 1A receptor (Drd1a) on chromosome 17 showed the strongest correlation with left ventricular heart weight (P = .00038, r = -0.59) and the relationship to heart weight was independent of blood pressure. The markers showing the strongest correlations with systolic, diastolic, and mean arterial pressure were D19Mit7 on chromosome 19 (P = .0012, r = .55), D2N35 on chromosome 2 (P = .0008, r = .56), and Il6 on chromosome 4 (P = .0018, r = .53), respectively. These studies demonstrate that the HXB and BXH strains can be effectively used for genome scanning studies of complex traits and have revealed several chromosome regions that may be involved in the genetic control of blood pressure and cardiac mass in the rat., Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., SCOPUS: ar.j, info:eu-repo/semantics/published
Published: 1995

21. Computational analysis of susceptibility genes for diabetes and cardiovascular diseases in animal models

Author: Wilder, Steven P., Mott, Richard F., and Gauguier, Dominique
Subjects: 616.4, Quantitative genetics, Genomics, Gene expression, Phenotype, Diabetes--Genetic aspects, Cardiovascular system--Diseases--Genetic aspects
Published: 2007

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21 results on '"Gauguier,Dominique"'

1. Evidence of a causal and modifiable relationship between kidney function and circulating trimethylamine N-oxide

2. Plasma and urine metabolomic analyses in aortic valve stenosis reveal shared and biofluid-specific changes in metabolite levels

3. Elevated Lp(a) Levels Correlate with Severe and Multiple Coronary Artery Stenotic Lesions

4. Genetic Variants in PHACTR1 & LPL Mediate Restenosis Risk in Coronary Artery Patients

5. Microbiome and metabolome features of the cardiometabolic disease spectrum

6. Human and preclinical studies of the host-gut microbiome co-metabolite hippurate as a marker and mediator of metabolic health

7. Molecular genetics of the transcription factor GLIS3 identifies its dual function in beta cells and neurons.

8. Loss of Cardioprotective Effects at the ADAMTS7 Locus as a Result of Gene-Smoking Interactions

9. Genomic correlates of glatiramer acetate adverse cardiovascular effects lead to a novel locus mediating coronary risk

10. Association of hypertension with coronary artery disease onset in the Lebanese population

11. No Association of Coronary Artery Disease with X-Chromosomal Variants in Comprehensive International Meta-Analysis

12. A comprehensive 1000 Genomes-based genome-wide association meta-analysis of coronary artery disease

13. Whole-genome sequencing identifies EN1 as a determinant of bone density and fracture

14. Large-scale association analysis identifies new risk loci for coronary artery disease

15. Genome-wide diversity in the levant reveals recent structuring by culture.

16. Functional annotations of diabetes nephropathy susceptibility loci through analysis of genome-wide renal gene expression in rat models of diabetes mellitus

17. Progress and prospects in rat genetics: a community view.

18. Statistical Total Correlation Spectroscopy: An Exploratory Approach for Latent Biomarker Identification from Metabolic 1H NMR Data Sets

19. A genetic linkage map of the rat derived from recombinant inbred strains.

20. Mapping of quantitative trait loci for blood pressure and cardiac mass in the rat by genome scanning of recombinant inbred strains.

21. Computational analysis of susceptibility genes for diabetes and cardiovascular diseases in animal models

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21 results on '"Gauguier,Dominique"'

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