My Publications

Here is the list of publications to which I have contributed during my PhD at INSERM, as a member of the Cardiogenics European Consortium, or during my research position at the University of Luebeck (Germany).

Search PubMed for an updated list of publications.

My ORCID ID: orcid.org/0000-0001-8186-1635#sthash.A8PtrnQT.dpuf

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AI-enhanced coding in bioinformatics: legal and ethical considerations.

Maouche S

Journal Paper International Review of Information Ethics; 34Vol. 34 No. 1 (2024). : Journal Link

Abstract

In this article, we describe a case study that explores the ethical and legal issues relating to the introduction of Artificial Intelligence (AI)-enhanced coding in bioinformatics and related life science research. Using this case study, we highlight the potential dangers posed by the introduction of AI-assisted coding in programming and analysis of health data. The aim is to understand and consider the potential harms it poses and to help students and young researchers on how to use AI responsibly in their work. Recent developments in generative artificial intelligence (Gen AI) and the emergence of Large Language Models (LLMs)-based chatbots such as Chat Generative Pre-Trained Transformer (ChatGPT) launched by OpenAI on November 30, 2022 are currently matter of many debates mainly about AI-generated scientific research and publications. Several scientists, editors, and publishers disapproved that ChatGPT made its way into scientific production by being listed as a co-author. Programming is another domain where LLMs-based chatbots have proven immense potential. These AI systems have the ability to assist human programmers at different stages, including writing and debugging code. The rapid development of AI and related emerging technologies and its wide deployment in different domains, including life-science research gives rise to multiple ethical, legal and technical considerations. We designed the present case study to describe a plausible situation in biomedical research, and to elucidate some legal and ethical issues resulting from the introduction of AI in life-science research.

Google AI: Opportunities, risks, and ethical challenges.

Maouche S

Journal PaperContemporary French and Francophone Studies; 23(4): 447-455. : Journal Link

Abstract

Emerging technologies (ET) are novel and relatively fast-growing technologies that can have massive socio-economic impact and bring new ethical and regulatory challenges. Although they cannot be considered as new technologies, artificial intelligence (AI) and related data driven technologies are examples of ET. AI is advancing at a rapid pace, in both public and private sectors, and being more widely deployed in different domains, including healthcare and education. In today's digital age, our societies are facing rapid and massive technological transformations. It is important to ensure that the behavior of AI systems is beneficial to humanity. Policymakers and the research community need to identify the greatest barriers to AI adoption and related risks. In recent years, Google's plans and visions to use ET gained serious and intense criticism. This situation pushed Google in March 2019 to announce an AI ethics panel which is supposed to offer guidance on ethical issues relating to AI, machine learning, and related technologies. This AI ethics panel was shut down just days after it was launched. The episode illustrates how ethical debates relating to ET are often characterized by ambiguity, dishonesty, and demagoguery. In this paper, I discuss the ethics of ET, focusing on Google and its AI platform.

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

The CARDIoGRAMplusC4D Consortium, Deloukas P, Kanoni S, Willenborg C, Farrall M, Assimes TL,Thompson JR, Ingelsson E, Saleheen D, Erdmann J, Goldstein BA, Stirrups K, König IR, Cazier JB, Johansson A, Hall AS, Lee JY, Willer CJ, Chambers JC, Esko T, Folkersen L, Goel A, Grundberg E, Havulinna AS, Ho WK, Hopewell JC, Eriksson N, Kleber ME, Kristiansson K, Lundmark P, Lyytikäinen LP, Rafelt S, Shungin D, Strawbridge RJ, Thorleifsson G, Tikkanen E, Van Zuydam N, Voight BF, Waite LL,Zhang W, Ziegler A, Absher D, Altshuler D, Balmforth AJ, Barroso I, Braund PS, Burgdorf C, Claudi-Boehm S, Cox D, Dimitriou M, Do R; DIAGRAM Consortium; CARDIOGENICS Consortium, Doney AS, Mokhtari NE, Eriksson P, Fischer K, Fontanillas P, Franco-Cereceda A, Gigante B, Groop L, Gustafsson S, Hager J, Hallmans G, Han BG, Hunt SE, Kang HM, Illig T, Kessler T, Knowles JW, Kolovou G, Kuusisto J, Langenberg C, Langford C, Leander K, Lokki ML, Lundmark A, McCarthy MI, Meisinger C, Melander O, Mihailov E, Maouche S, Morris AD, Mueller-Nurasyid M; MuTHER Consortium, Nikus K, Peden JF, Rayner NW, Rasheed A, Rosinger S, Rubin D, Rumpf MP, Schäfer A, Sivananthan M, Song C, Stewart AF, Tan ST, Thorgeirsson G, Schoot CE, Wagner PJ; Wellcome Trust Case Control Consortium, Wells GA Wild PS, Yang TP, Amouyel P, Arveiler D, Basart H, Boehnke M, Boerwinkle E, Brambilla P, Cambien F, Cupples AL, de Faire U, Dehghan A, Diemert P, Epstein SE, Evans A, Ferrario MM, Ferrières J, Gauguier D, Go AS, Goodall AH, Gudnason V, Hazen SL, Holm H, Iribarren C, Jang Y, Kähönen M, Kee F, Kim HS, Klopp N, Koenig W, Kratzer W, Kuulasmaa K, Laakso M, Laaksonen R, Lee JY, Lind L, Ouwehand WH, Parish S, Park JE, Pedersen NL, Peters A, Quertermous T, Rader DJ, Salomaa V, Schadt E, Shah SH, Sinisalo J, Stark K, Stefansson K, Tregouet DA, Virtamo J, Wallentin L, Wareham N, Zimmermann ME, Nieminen MS, Hengstenberg C, Sandhu MS, Pastinen T, Syvänen AC, Hovingh GK, Dedoussis G, Franks PW, Lehtimäki T, Metspalu A, Zalloua PA, Siegbahn A, Schreiber S, Ripatti S, Blankenberg SS, Perola M, Clarke R, Boehm BO, O’Donnell C, Reilly MP, März W, Collins R, Kathiresan S, Hamsten A, Kooner JS, Thorsteinsdottir U, Danesh J, Palmer CN, Roberts R, Watkins H, Schunkert H, Samani NJ.

Journal Paper Nature Genetics. 2013;45(1): 25-33. PubMed ID : 23202125

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 (r(2) < 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.

Strategies beyond genome-wide association studies for atherosclerosis.

Maouche S and Schunkert H

Journal Paper Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB). 2012; 32(2):170-81. PubMed ID : 22258900

Abstract

Atherosclerotic diseases, including coronary artery disease (CAD) and myocardial infarction (MI), are the leading causes of death in the world. The genetic basis of CAD and MI, which are caused by multiple interacting endogenous and exogenous factors, has gained considerable interest in the last years as genome-wide association studies (GWASs) have identified many new susceptibility loci for CAD and MI, and the underlying genes provide new insights into the genetic architecture of these diseases. Here we summarize the recent findings from GWASs of atherosclerosis and discuss their functional and biological implications. We also discuss the different post-GWAS strategies that are currently used for refining the location of causal variants, understanding their role, and shedding light on molecular mechanisms explaining their association to CAD. We finally discuss potential clinical translations of GWAS findings for individual risk prediction, advanced clinical strategies, and personalized treatments..

Powerful Identification of Cis-regulatory SNPs in Human Primary Monocytes Using Allele-Specific Gene Expression.

Carlsson-Almloef J, Lundmark P, Lundmark L, Ge B, Maouche S, Goering HH, Liljedahl U, Enstroem C, Brocheton J, Proust P, Godefroy T, Sambrook JG, Jolley J, Crisp-Hihn A, Foad N, Lloyd-Jones H, Stephens J, Gwilliam R, Rice CM, Hengstenberg C, Samani NJ, Erdmann J, Schunkert H, Pastinen T, Deloukas P, Goodall AH, Ouwehand WH, Cambien F, Syvenen AC, Cardiogenics Consortium.

Journal Paper PLOS One. 2012;7(12):e52260. PubMed ID : 23300628

Abstract

A large number of genome-wide association studies have been performed during the past five years to identify associations between SNPs and human complex diseases and traits. The assignment of a functional role for the identified disease-associated SNP is not straight-forward. Genome-wide expression quantitative trait locus (eQTL) analysis is frequently used as the initial step to define a function while allele-specific gene expression (ASE) analysis has not yet gained a wide-spread use in disease mapping studies. We compared the power to identify cis-acting regulatory SNPs (cis-rSNPs) by genome-wide allele-specific gene expression (ASE) analysis with that of traditional expression quantitative trait locus (eQTL) mapping. Our study included 395 healthy blood donors for whom global gene expression profiles in circulating monocytes were determined by Illumina BeadArrays. ASE was assessed in a subset of these monocytes from 188 donors by quantitative genotyping of mRNA using a genome-wide panel of SNP markers. The performance of the two methods for detecting cis-rSNPs was evaluated by comparing associations between SNP genotypes and gene expression levels in sample sets of varying size. We found that up to 8-fold more samples are required for eQTL mapping to reach the same statistical power as that obtained by ASE analysis for the same rSNPs. The performance of ASE is insensitive to SNPs with low minor allele frequencies and detects a larger number of significantly associated rSNPs using the same sample size as eQTL mapping. An unequivocal conclusion from our comparison is that ASE analysis is more sensitive for detecting cis-rSNPs than standard eQTL mapping. Our study shows the potential of ASE mapping in tissue samples and primary cells which are difficult to obtain in large numbers..

Temporal transcriptional changes in human monocytes after acute myocardial infarction: The GerMIFs monocyte study.

Maouche S, Sager HB, Aherrahrou Z, Belz S, Brocheton J, Krishnan U, Proust C, Tennstedt S, Ammerlahn H, Riedel C, Stritzke J, Jensen H , Kurowski V, The Cardiogenics consortium, Rice CM, Rengstenberg C, Ouwehand WH, Samani NJ, Goodall AH , Erdmann E, Schunkert S, and Diemert P.

[Manuscript in revision]

Abstract

Maouche S, Sager HB, Aherrahrou Z, Belz S, Brocheton J, Krishnan U, Proust C, Tennstedt S, Ammerlahn H, Riedel C, Stritzke J, Jensen H , Kurowski V, The Cardiogenics consortium, Rice CM, Rengstenberg C, Ouwehand WH, Samani NJ, Goodall AH , Erdmann E, Schunkert S, and Diemert P.
[Manuscript in revision]

Integrating genome-wide genetic variations and monocyte expression data reveals trans-regulated gene modules in humans.

Rotival M, Zeller T, Wild PS, Maouche S, Szymczak S, Schillert A, Castagne R, Deiseroth A, Proust C, Brocheton J, Godefroy T, Perret C, Germain M,Eleftheriadis M, Sinning CR, Schnabel RB, Lubos E, Lackner KJ, Rossmann H, Munzel T, Rendon A; Cardiogenics Consortium, Erdmann J, Deloukas P, Hengstenberg C, Diemert P, Montalescot G, Ouwehand WH, Samani NJ, Schunkert H, Tregouet DA, Ziegler A, Goodall AH, Cambien F, Tiret L, Blankenberg S.

Journal Paper PLOS Genetics 2011; 7(12):e1002367. PubMed ID : 22144904

Abstract

One major expectation from the transcriptome in humans is to characterize the biological basis of associations identified by genome-wide association studies. So far, few cis expression quantitative trait loci (eQTLs) have been reliably related to disease susceptibility. Trans-regulating mechanisms may play a more prominent role in disease susceptibility. We analyzed 12,808 genes detected in at least 5% of circulating monocyte samples from a population-based sample of 1,490 European unrelated subjects. We applied a method of extraction of expression patterns-independent component analysis-to identify sets of co-regulated genes. These patterns were then related to 675,350 SNPs to identify major trans-acting regulators. We detected three genomic regions significantly associated with co-regulated gene modules. Association of these loci with multiple expression traits was replicated in Cardiogenics, an independent study in which expression profiles of monocytes were available in 758 subjects. The locus 12q13 (lead SNP rs11171739), previously identified as a type 1 diabetes locus, was associated with a pattern including two cis eQTLs, RPS26 and SUOX, and 5 trans eQTLs, one of which (MADCAM1) is a potential candidate for mediating T1D susceptibility. The locus 12q24 (lead SNP rs653178), which has demonstrated extensive disease pleiotropy, including type 1 diabetes, hypertension, and celiac disease, was associated to a pattern strongly correlating to blood pressure level. The strongest trans eQTL in this pattern was CRIP1, a known marker of cellular proliferation in cancer. The locus 12q15 (lead SNP rs11177644) was associated with a pattern driven by two cis eQTLs, LYZ and YEATS4, and including 34 trans eQTLs, several of them tumor-related genes. This study shows that a method exploiting the structure of co-expressions among genes can help identify genomic regions involved in trans regulation of sets of genes and can provide clues for understanding the mechanisms linking genome-wide association loci to disease.

Large-scale association analysis identifies 13 new susceptibility loci for coronary artery disease.

Schunkert H, Konig IR, Kathiresan S, Reilly MP, Assimes TL, Holm H, Preuss M, Stewart AF, Barbalic M, Gieger C, Absher D, Aherrahrou Z, Allayee H, Altshuler D, Anand SS, Andersen K, Anderson JL, Ardissino D, Ball SG, Balmforth AJ, Barnes TA,Becker DM, Becker LC, Berger K, Bis JC, Boekholdt SM, Boerwinkle E, Braund PS,Brown MJ, Burnett MS, Buysschaert I; Cardiogenics, Carlquist JF, Chen L, Cichon S, Codd V, Davies RW, Dedoussis G, Dehghan A, Demissie S, Devaney JM, Diemert P, Do R, Doering A, Eifert S, Mokhtari NE, Ellis SG, Elosua R, Engert JC, Epstein SE, de Faire U, Fischer M, Folsom AR, Freyer J, Gigante B, Girelli D, Gretarsdottir S, Gudnason V, Gulcher JR, Halperin E, Hammond N, Hazen SL, Hofman A, Horne BD, Illig T, Iribarren C, Jones GT, Jukema JW, Kaiser MA, Kaplan LM, Kastelein JJ, Khaw KT, Knowles JW, Kolovou G, Kong A, Laaksonen R, Lambrechts D, Leander K, Lettre G, Li M, Lieb W, Loley C, Lotery AJ, Mannucci PM, Maouche S, Martinelli N, McKeown PP, Meisinger C, Meitinger T, Melander O, Merlini PA, Mooser V, Morgan T, Muhleisen TW, Muhlestein JB, Munzel T, Musunuru K, Nahrstaedt J, Nelson CP, Nothen MM, Olivieri O, Patel RS, Patterson CC, Peters A, Peyvandi F, Qu L, Quyyumi AA, Rader DJ, Rallidis LS, Rice C, Rosendaal FR, Rubin D, Salomaa V, Sampietro ML, Sandhu MS, Schadt E, Schafer A, Schillert A, Schreiber S, Schrezenmeir J, Schwartz SM, Siscovick DS, Sivananthan M, Sivapalaratnam S, Smith A, Smith TB, Snoep JD, Soranzo N, Spertus JA, Stark K, Stirrups K, Stoll M, Tang WH, Tennstedt S, Thorgeirsson G, Thorleifsson G, Tomaszewski M, Uitterlinden AG, van Rij AM, Voight BF, Wareham NJ, Wells GA, Wichmann HE, Wild PS, Willenborg C, Witteman JC, Wright BJ, Ye S, Zeller T, Ziegler A, Cambien F, Goodall AH, Cupples LA, Quertermous T, Marz W, Hengstenberg C, Blankenberg S, Ouwehand WH, Hall AS, Deloukas P, Thompson JR, Stefansson K, Roberts R, Thorsteinsdottir U, O'Donnell CJ, McPherson R, Erdmann J; CARDIoGRAM Consortium, Samani NJ.

Journal Paper Nature Genetics 2011; 6;43(4):333-8. PubMed ID : 21378990

Abstract

We performed a meta-analysis of 14 genome-wide association studies of coronary artery disease (CAD) comprising 22,233 individuals with CAD (cases) and 64,762 controls of European descent followed by genotyping of top association signals in 56,682 additional individuals. This analysis identified 13 loci newly associated with CAD at P < 5 x 10-8 and confirmed the association of 10 of 12 previously reported CAD loci. The 13 new loci showed risk allele frequencies ranging from 0.13 to 0.91 and were associated with a 6% to 17% increase in the risk of CAD per allele. Notably, only three of the new loci showed significant association with traditional CAD risk factors and the majority lie in gene regions not previously implicated in the pathogenesis of CAD. Finally, five of the new CAD risk loci appear to have pleiotropic effects, showing strong association with various other human diseases or traits.

Antagonistic regulation of macrophage phenotype by M-CSF and GM-CSF: implication in atherosclerosis.

Brocheriou I, Maouche S, Durand H, Braunersreuther V, Le Naour G, Gratchev A, Koskas F, Mach F, Kzhyshkowska J, Ninio E.

Journal Paper Atherosclerosis 2011; 214(2):316-24. PubMed ID : 21159337

Abstract

OBJECTIVES: We characterized the transcriptional profiles of GM-CSF- (GM-MØ) and M-CSF-induced macrophages (M-MØ) and investigated in situ a subset of differentially expressed genes in human and mouse atherosclerotic lesions.
METHODS AND RESULTS:Using microarrays we identified a number of genes and biological processes differentially regulated in M-MØ vs GM-MØ. By varying in culture the M-CSF/GM-CSF ratio (0-10), a spectrum of macrophage phenotypes was explored by RT-QPCR. M-CSF (10 ng/ml) stimulated expression of several genes, including selenoprotein-1 (SEPP1), stabilin-1 (STAB1) and CD163 molecule-like-1 (CD163L1) which was inhibited by a low dose of GM-CSF (1 ng/ml); M-CSF inhibited the expression of pro-platelet basic protein (PPBP) induced by GM-CSF. Combining tissue microarrays/quantitative immunohistochemistry of human aortic lesions with RT-QPCR expression data either from human carotids vs mammary non-atherosclerotic arteries or from the apoE null mice normal and atherosclerotic aortas showed that, STAB1, SEPP1 and CD163L1 (M-CSF-sensitive genes) and PPBP (GM-CSF-sensitive gene) were expressed in both human arterial and apoE null mice atherosclerotic tissues.
CONCLUSION: A balance between M-CSF vs GM-CSF defines macrophage functional polarisation and may contribute to the progression of atherosclerosis.

A trans-acting locus regulates an anti-viral expression network and type 1 diabetes risk.

Heinig M, Petretto E, Wallace C, Bottolo L, Rotival M, Lu H, Li Y, Sarwar R, Langley SR, Bauerfeind A, Hummel O, Lee YA, Paskas S, Rintisch C, Saar K, Cooper J, Buchan R, Gray EE, Cyster JG; Cardiogenics Consortium, Erdmann J, Hengstenberg C, Maouche S, Ouwehand WH, Rice CM, Samani NJ, Schunkert H, Goodall AH, Schulz H, Roider HG, Vingron M, Blankenberg S, Munzel T, Zeller T, Szymczak S, Ziegler A, Tiret L, Smyth DJ, Pravenec M, Aitman TJ, Cambien F, Clayton D, Todd JA, Hubner N, Cook SA.

Journal Paper Nature 2010; 23;467(7314):460-4. PubMed ID : 20827270

Abstract

Background: Variability of gene expression in human may link gene sequence variability and phenotypes; however, non-genetic variations, alone or in combination with genetics, may also influence expression traits and have a critical role in physiological and disease processes.
Methodology/Principal Findings : To get better insight into the overall variability of gene expression, we assessed the transcriptome of circulating monocytes, a key cell involved in immunity-related diseases and atherosclerosis, in 1,490 unrelated individuals and investigated its association with >675,000 SNPs and 10 common cardiovascular risk factors. Out of 12,808 expressed genes, 2,745 expression quantitative trait loci were detected (P<5.78x10-12), most of them (90%) being cis-modulated. Extensive analyses showed that associations identified by genome-wide association studies of lipids, body mass index or blood pressure were rarely compatible with a mediation by monocyte expression level at the locus. At a study-wide level (P<3.9x10-7), 1,662 expression traits (13.0%) were significantly associated with at least one risk factor. Genome-wide interaction analyses suggested that genetic variability and risk factors mostly acted additively on gene expression. Because of the structure of correlation among expression traits, the variability of risk factors could be characterized by a limited set of independent gene expressions which may have biological and clinical relevance. For example expression traits associated with cigarette smoking were more strongly associated with carotid atherosclerosis than smoking itself.
Conclusions/Significance : This study demonstrates that the monocyte transcriptome is a potent integrator of genetic and non-genetic influences of relevance for disease pathophysiology and risk assessment.

Genetics and beyond -the transcriptome of human monocytes and disease susceptibility.

Zeller T, Wild P, Szymczak S, Rotival M, Schillert A, Castagne R, Maouche S, Germain M, Lackner K, Rossmann H, Eleftheriadis M, Sinning CR, Schnabel RB, Lubos E, Mennerich D, Rust W, Perret C, Proust C, Nicaud V, Loscalzo J, Hubner N, Tregouet D, Munzel T, Ziegler A, Tiret L, Blankenberg S, Cambien F.

Journal Paper PLOS One 2010; 18;5(5):e10693. PubMed ID : 20502693

Abstract

BACKGROUND: Variability of gene expression in human may link gene sequence variability and phenotypes; however, non-genetic variations, alone or in combination with genetics, may also influence expression traits and have a critical role in physiological and disease processes.
METHODOLOGY/PRINCIPAL FINDINGS: To get better insight into the overall variability of gene expression, we assessed the transcriptome of circulating monocytes, a key cell involved in immunity-related diseases and atherosclerosis, in 1,490 unrelated individuals and investigated its association with >675,000 SNPs and 10 common cardiovascular risk factors. Out of 12,808 expressed genes, 2,745 expression quantitative trait loci were detected (P<5.78x10(-12)), most of them (90%) being cis-modulated. Extensive analyses showed that associations identified by genome-wide association studies of lipids, body mass index or blood pressure were rarely compatible with a mediation by monocyte expression level at the locus. At a study-wide level (P<3.9x10(-7)), 1,662 expression traits (13.0%) were significantly associated with at least one risk factor. Genome-wide interaction analyses suggested that genetic variability and risk factors mostly acted additively on gene expression. Because of the structure of correlation among expression traits, the variability of risk factors could be characterized by a limited set of independent gene expressions which may have biological and clinical relevance. For example expression traits associated with cigarette smoking were more strongly associated with carotid atherosclerosis than smoking itself.
CONCLUSIONS/SIGNIFICANCE: This study demonstrates that the monocyte transcriptome is a potent integrator of genetic and non-genetic influences of relevance for disease pathophysiology and risk assessment.

Phospholipolyzed LDL induces an inflammatory response in endothelial cells through endoplasmic reticulum stress signaling.

Gora S, Maouche S, Atout R, Wanherdrick K, Lambeau G, Cambien F, Ninio E, Karabina SA.

Journal Paper FASEB Journal 2010; 24(9):3284-97. PubMed ID : 20430794

Abstract

Secreted phospholipases A2 (sPLA2s) are present in atherosclerotic plaques and are now considered novel attractive therapeutic targets and potential biomarkers as they contribute to the development of atherosclerosis through lipoprotein-dependent and independent mechanisms. We have previously shown that hGX-sPLA2-phospholipolyzed LDL (LDL-X) induces proinflammatory responses in human umbilical endothelial cells (HUVECs); here we explore the molecular mechanisms involved. Global transcriptional gene expression profiling of the response of endothelial cells exposed to either LDL or LDL-X revealed that LDL-X activates multiple distinct cellular pathways including the unfolded protein response (UPR). Mechanistic insight showed that LDL-X activates UPR through calcium depletion of intracellular stores, which in turn disturbs cytoskeleton organization. Treatment of HUVECs and aortic endothelial cells (HAECs) with LDL-X led to activation of all 3 proximal initiators of UPR: eIF-2alpha, IRE1alpha, and ATF6. In parallel, we observed a sustained phosphorylation of the p38 pathway resulting in the phosphorylation of AP-1 downstream targets. This was accompanied by significant production of the proinflammatory cytokines IL-6 and IL-8. Our study demonstrates that phospholipolyzed LDL uses a range of molecular pathways including UPR to initiate endothelial cell perturbation and thus provides an LDL oxidation-independent mechanism for the initiation of vascular inflammation in atherosclerosis.

Performance comparison of two microarray platforms to assess differential gene expression in human monocyte and macrophage cells.

Maouche S, Poirier O, Godefroy T, Olaso R, Gut I, Collet JP, Montalescot G, Cambien F.

Journal Paper BMC Genomics 2008; 9:302. PubMed ID : 18578872

Abstract

Background : In this study we assessed the respective ability of Affymetrix and Illumina microarray methodologies to answer a relevant biological question, namely the change in gene expression between resting monocytes and macrophages derived from these monocytes. Five RNA samples for each type of cell were hybridized to the two platforms in parallel. In addition, a reference list of differentially expressed genes (DEG) was generated from a larger number of hybridizations (mRNA from 86 individuals) using the RNG/MRC two-color platform.
Results : Our results show an important overlap of the Illumina and Affymetrix DEG lists. In addition, more than 70% of the genes in these lists were also present in the reference list. Overall the two platforms had very similar performance in terms of biological significance, evaluated by the presence in the DEG lists of an excess of genes belonging to Gene Ontology (GO) categories relevant for the biology of monocytes and macrophages. Our results support the conclusion of the MicroArray Quality Control (MAQC) project that the criteria used to constitute the DEG lists strongly influence the degree of concordance among platforms. However the importance of prioritizing genes by magnitude of effect (fold change) rather than statistical significance (p-value) to enhance cross-platform reproducibility recommended by the MAQC authors was not supported by our data.
Conclusion : Functional analysis based on GO enrichment demonstrates that the 2 compared technologies delivered very similar results and identified most of the relevant GO categories enriched in the reference list.

OMICtools: a community-driven search engine for biological data analysis.

Maouche S.
Submitted Manuscript.

Abstract

With high-throughput biotechnologies generating unprecedented quantities of data, researchers are faced with the challenge of locating and comparing an exponentially growing number of programs and websites dedicated to computational biology, in order to maximize the potential of their data. OMICtools is designed to meet this need with its open-access search engine offering an easy means of locating the right tools corresponding to each researcher and their specific biological data analyses. The OMICtools website (this https URL) centralizes more than 18,500 software tools and databases, manually classified, by a team of biocurators including many scientific experts. Key information, a direct link, and access to discussions and evaluations by the biomedical community are provided for each tool. Anyone can join the OMICtools community and create a profile page, to share their expertise and comment on tools. In addition, developers can directly upload their code versions which are registered for identification and citation in scientific publications, improving research traceability. The OMICtools community links thousands of life scientists and developers worldwide, who use this bioinformatics platform to accelerate their projects and biological data analyses.

Manuscript submitted.

The Replicability Crisis in Cardiovascular Omics Research.

Maouche S.
Submitted Manuscript.

Maouche S.

Manuscript submitted.

Whole-exome sequencing by numbers.

Maouche S.
Submitted Manuscript.

Maouche S.

Manuscript submitted.

Global transcriptional profile of monocytes and M-CSF-driven macrophages and association with coronary heart disease risk factors in a large multi-center collaborative study: The Cardiogenics Transcriptomic Study.

Maouche S, Diemert P, Rendon R, Sambrooke J, Moore JS, Belz S, Attwood T, Brocheton J, Crisp-Hihn A, Erdmann J, Foad N, Godfroy T, Gracey J, Heimerl S, Jolley J, Krishnan U, , Lloyd-Jones H, Lugauer I, Muir D, Murray E, Neudert J, Niblett D, O'Leary K, Poirier O, Pollard H, Proust C, Rankin A, Sager HB, Schmitz G, Scholz M, Schroeder L, Montalescot M, Hengstenberg C, Samani NJ, Ouwehand WH, Rice CM, Schunkert H, Cambien F, Goodall AH.
Submitted Manuscript.

Maouche S, Diemert P, Rendon R, Sambrooke J, Moore JS, Belz S, Attwood T, Brocheton J, Crisp-Hihn A, Erdmann J, Foad N, Godfroy T, Gracey J, Heimerl S, Jolley J, Krishnan U, , Lloyd-Jones H, Lugauer I, Muir D, Murray E, Neudert J, Niblett D, O'Leary K, Poirier O, Pollard H, Proust C, Rankin A, Sager HB, Schmitz G, Scholz M, Schroeder L, Montalescot M, Hengstenberg C, Samani NJ, Ouwehand WH, Rice CM, Schunkert H, Cambien F, Goodall AH.

From single marker analysis to SNP-set enrichment approaches for genome-wide association studies : recent advances, applications, and methodological challenges..

Maouche S, Yang X, Quertermous T, Schunkert H, Assimes T. L.
Submitted Manuscript.

From single marker analysis to SNP-set enrichment approaches for genome-wide association studies : recent advances, applications, and methodological challenges.

Maouche S, Yang X, Quertermous T, Schunkert H, Assimes T. L.

A common nonsynonymous polymorphism in X-linked GPR101 is associated with susceptibility to coronary artery disease in European men..

Blankenberg S, Zeller S, Maouche S, Wenzel J, Perret C, Germain G, Collet JP, Proust C, Arveiler D, Nicaud V, Schnabel R, Ferrieres J, Brocheton J, Lubos E, Amouyel P, de Suremain M, Bingham A, Wild P, Stegmayr B, Hulot JS, Muenzel T, Lackner KJ, Kuulasmaa K, Morrison C, Tregouet DA, Montalescot G, Saloma V, Evans A, Ducimetiere P, Cambien F, and Tiret T.
Submitted Manuscript.

Blankenberg S, Zeller S, Maouche S, Wenzel J, Perret C, Germain G, Collet JP, Proust C, Arveiler D, Nicaud V, Schnabel R, Ferrieres J, Brocheton J, Lubos E, Amouyel P, de Suremain M, Bingham A, Wild P, Stegmayr B, Hulot JS, Muenzel T, Lackner KJ, Kuulasmaa K, Morrison C, Tregouet DA, Montalescot G, Saloma V, Evans A, Ducimetiere P, Cambien F, and Tiret T.

Manuscript submitted.

Gene expression at the 9p21 locus and CAD risk.

Nelson CP, Lundmark P, Codd V, Kaiser M, Maouche S, Koekemoer A, Cambien F, Goodall AH, Brocheton J, Deloukas P, Erdmann J, Gwillians R, Hengstenberg C, Moore J, Linsel-Nitschke P, Ouwehand WH, Rice CM, Sambrook J, Schunkert H, Syvanen AC, Samani NJ on behalf of Cardiogenics.
Submitted Manuscript.

Nelson CP, Lundmark P, Codd V, Kaiser M, Maouche S, Koekemoer A, Cambien F, Goodall AH, Brocheton J, Deloukas P, Erdmann J, Gwillians R, Hengstenberg C, Moore J, Linsel-Nitschke P, Ouwehand WH, Rice CM, Sambrook J, Schunkert H, Syvanen AC, Samani NJ on behalf of Cardiogenics.

Manuscript submitted.

e-Health and digital technologies in cardiovascular healthcare and research

Seraya Maouche
Book (Book Submitted).

The « Matilda » effect in sciences

Seraya Maouche
Book (Book Submitted).

e-Health and digital technologies in cardiovascular healthcare and research

The International Digital Health Congress (Doctors 2.0 & You).
1-2 June 2017, Paris - France.

Seraya Maouche
Conference Abstract

Abstract

Maouche S.
e-Health and digital technologies in cardiovascular healthcare and research

The digital revolution is rapidly transforming the delivery of health services and biomedical research around the world. Although e-health is a relatively recent field of healthcare practice, 58% of WHO´s Member States have already an eHealth strategy. The European Commission adopted its second Action Plan 2012-2020 that defines the Commission´s vision on eHealth. This widely used umbrella term encompasses a range of applications and innovative digital technologies, including mobile health (mHealth), electronic health record, remote patient monitoring, and Internet of Medical Things (IoMT). In cardiology, eHealth offers many opportunities to transform healthcare systems and research. The first European Congress on e-Cardiology & e-Health that was held in 2014 has shown a broad range of applications in prevention, treatment, monitoring, rehabilitation using new sensors and technologies, and improved ways to access medical data for patients, researchers and medical professionals. The present research explores the role of digital technologies in cardiovascular disease management and research. We discuss our application of Big Data for digital pharmacovigilance and the advantage of leveraging Omics data with real-time adverse drug events to study drug-drug and drug-gene interactions.

Keywords : e-Cardiology, eHealth, Digital Health, mHealth, Digital Pharmacovigilance, Big Data, Omics, Cardiovascular Research

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Big Data and BioNLP approaches for pharmacovigilance and pharmacogenomics in oncology.

Seraya Maouche
The 15th European Conference on Computational Biology (ECCB 2016).

3-7 September 2016, the Hague, the Netherlands.

Conference Abstract
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resExomeDB: An Online Catalog for Whole-Exome Sequencing (WES) Results

Seraya Maouche

The European Conference on Computational Biology (ECCB12).

September 9-12th, 2012, Congress Center Basel, Switzerland.

Conference Abstract

Abstract

Chami ME, Benatchba K, Koudil M, Tazir M, and Maouche S

resExomeDB: An Online Catalog for Whole-Exome Sequencing (WES) Results

Whole-Exome Sequencing (WES) has emerged as powerful sequencing strategy to identify novel mutations and genes associated with Mendelian disorders and complex traits. Managing sequence data and results from WES studies is computationally challenging task. We present resExomeDB, an online catalog we developed for WES results and related publications. resExomeDB provides access to mutations and genes underling human disease that have been identified recently by WES. In addition, our catalog relates WES results to 1) external gene-centered resources, 2) disease oriented databases such as OMIM and the International Classification of Diseases (ICD), 3) genome-wide association studies catalogs, and 4) external pathways and functional annotation databases. resExomeDB centralize all publications, software, platforms related to exome/whole genome sequencing and provides functionalities that allow browsing and searching the catalog by mutation, gene, study, or publication. The current release of resExomeDB database contains more than 300 mutations in 259 genes associated to 175 diseases/traits manually curated from more than 600 publications. resExomeDB is freely available for academic, non-commercial use at: http://www.exomedb.org

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Network-driven integrative genomics analysis of the CARDIoGRAM GWAS reveals key drivers and subnetworks of coronary artery disease.

Assimes TL, Huan T, Maouche S., Zhu J, Zhang B, Erdmann J, Nelson C, Snell KIE, Quertermous T, Samani N, Schunkert H, Yang X, Coronary ARtery DIsease Genome wide Replication and Meta-analysis (CARDIoGRAM).

The 12th International Congress of Human Genetics and the American Society of Human Genetics 61st Annual Meeting October 11-15, 2011 Montreal, Canada..

Conference Abstract

Abstract

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Integrating network co-expression analysis and gene expression in the analysis of coronary artery disease GWAS: application to CARDIoGRAM data.

Maouche et al.

The 19th Annual International conference on Intelligent Systems for molecular Biology and 10th European Conference on Computational Biology (ISMB/ECCB 2011)

15 - 19 July , 2011, Vienna, Austria.

Conference Abstract

Abstract

Maouche S, Yang Y, CARDIoGRAM consortium, Quertermous T, Samani NJ, Assimes TL, Erdmann J, Diemert P, and Schunkert H.

Genome-wide association studies have been very successful in identifying risk variant loci for complex diseases, including coronary artery disease (CAD) and myocardial infarction (MI). Recently, to increase power and identifying additional CAD/MI risk loci, we founded the CARDIoGRAM (Coronary ARtery DIsease Genome-Wide Replication and Meta-Analysis) consortium and meta-analyzed 14 GWAS datasets including > 22,000 cases and > 64,000 controls. We identified 13 new susceptibility loci. However, the mechanisms by which these loci lead to CAD/MI remain elusive. To provide insights into the mechanisms driving the disease, we propose a system genetics approach integrating biological knowledge, network co-expression analysis of gene expression profiles of monocyte from patients following myocardial infarction, into the analysis of CARDIoGRAM CAD/MI GWAS data..

Time-series and gene co-expression analyses of transcriptional changes in human monocyte RNAs after acute myocardial infarction. The GerMIFS study.

Maouche et al.

The 17th Annual International conference on Intelligent Systems for molecular Biology and 8th European Conference on Computational Biology (ISMB/ECCB 2009)

June 27 - July 2, 2009, Stockholm, Sweden.

Conference Abstract

Abstract

Maouche S, Belz S, Brocheton J, Proust C, Erdmann J, Schunkert H, Cambien F, and Linsel-Nitschke P.

Myocardial Infarction is associated with an-inflammatory reaction and peripheral recruitment of monocytes to the injured-area. We investigated the temporal-transcriptional changes in monocytes post-MI. Co-expression modules identification combined to gene-set enrichment analysis identified genes of putative interest and revealed enrichment in major pathways pertaining to chemokine-receptor-activity, and regulation of heart contraction.

Establishing bioinformatics infrastructures in Algeria for health research, toxicogenomics and military medical applications.

Maouche et al.

The 2nd Meeting with Algerian Researchers Resident Abroad.

Algerian Ministry of Research, December, 6-8th , 2011, Algiers, Algeria.

Conference Abstract

Maouche S, Bennecer A, Chami MK, Koudil M, and Benatchba K.

[Invited Oral Presentation]

The role of bioinformatics in biotechnology.

Maouche et al.

The 1st International Forum of Biopharmacy, Research and Medical Biotechnology.

Institut Pasteur d´Algérie (IPA), December, 11th , 2011, Algiers, Algeria.

Conference Abstract

Maouche S

[Invited Oral Presentation]

Global Transcriptional Profiling of Monocytes and Macrophages and Association with Coronary Artery Disease Risk Factors in a Large Multi-Center Collaborative Study: The Cardiogenics Transcriptomic Study.

Maouche et al.

The American Heart Association (AHA) Scientific Sessions. Session: developmental regulation and gene expression.

November 12-16th, 2011, Orlando, Florida.

Conference Abstract

Maouche S, Cardiogenics consortium, Hengstenberg C, Samani NJ, Ouwehand W, Cambien F, Goodall AH, Schunkert H.

Abstract

Objective: Global transcriptional profile of cells involved in the pathogenesis of coronary artery disease (CAD) is poorly characterized. We thus aimed to identify biological processes and transcription factors (TFs) accompanying the transition of monocytes to macrophages as well as expression patterns associated to CAD risk factors.

Methods: Within Cardiogenics Consortium, we recruited 459 CAD patients and 458 healthy subjects. Most CAD patients had a validated MI within the previous 3-36 months and were aged between 40 and 65 years. Healthy subjects were all blood donors (42% male), without history of CAD. 1,533 RNA samples (849 monocytes and 684 macrophages) from the 917 subjects were analyzed on the Illumina Ref-8 v3.0 arrays.

Results: Monocyte to macrophages differentiation process involves massive changes in gene expression with 4.181 genes being significantly (P<10-3) modulated. Overall, this process is characterized by repression of large numbers of genes involved in the immune response and over-expression of genes of the lipid metabolism. Specifically, multiple genes expressed only in macrophages are involved in cholesterol metabolism such as APOE, PLAU, A2M, and SPP1. We found 155 TFs being significantly modulated between monocytes and macrophages. Among which 84.5% were down-regulated in macrophages. We found 28 and 14 genes being associated with gender in monocyte and macrophages, respectively. In monocytes, the expression of 21 genes was associated with BMI, including genes involved in cholesterol, steroid and lipid metabolic processes such as ABCG1, YWHAH, SARD5A1, and SORT1, and genes involved in obesity such as ADRB2 and GPX3. Only two genes, NEFH and AGPAT4 were found to be associated with age in monocytes.

Conclusions: We provide the first comprehensive large-scale analyses of monocyte and macrophage transcriptomes. The finding that multiple genes of the lipid system were over-expressed in macrophages is not only concordant with the fact that these cells are essential modulators of lipid metabolism but shows that macrophages express lipid handling genes even in the absence of exposure to exogenous lipids. Our results might be used to interpret GWAS finding and shed light on the role of monocyte and macrophage cells in CAD.

Analysis and integration of genomics data in cardiovascular research.

Maouche et al.

The European Molecular Biology Laboratory (EMBL) Seminars.

EMBL Heidelberg, September, 27th, 2011, Heidelberg, Germany.

Conference Abstract

Maouche S.

Invited Oral Presentation

Network-Driven Integrative Genomics Analysis of the Cardiogram GWAS Reveals Key Drivers and Sub networks of Coronary Artery Disease.

Yang X, Huan T, Maouche S, Zhu J, Zhang B, Preuss M, Erdmann J, Nelson CP, Snell KI, Segre AV, McPherson R, Quertermous T, Samani NJ, Schunkert H, and Assimes AT.

The American Heart Association (AHA) Scientific Sessions. Session: novel approaches to defining risk of coronary artery and valvular disease.

Nov 12-16th, 2011, Orlando, Florida.

Conference Abstract

Yang X, Huan T, Maouche S, Zhu J, Zhang B, Preuss M, Erdmann J, Nelson CP, Snell KI, Segre AV, McPherson R, Quertermous T, Samani NJ, Schunkert H, and Assimes AT.

Abstract

Objective: The molecular mechanisms underlying most CAD susceptibility loci remain unclear and a large proportion of the heritability of CAD remains unexplained. We hypothesize that genetic variation with both strong and subtle effects drives gene subnetworks that affect risk of CAD.

Methods: We surveyed CAD related molecular interactions by integrating CARDIoGRAM GWAS associations, expression SNPs (eSNPs), and gene networks constructed from 6 tissues of orthogonal mouse and human studies. We first mapped eSNPs to 12 established CAD gene sets or expression signatures from the literature (positive controls) and 2652 coexpression network modules to derive corresponding eSNP sets. We assessed the degree of enrichment for low p value associations with CAD within each eSNP set using Fisher's exact and Kolmogorov-Smirnov (KS) tests. We screened coexpression modules in the Wellcome Trust case control cohort and took 18 forward for testing in all of CARDIoGRAM. Enriched eSNP sets were in turn integrated with tissue-specific Bayesian networks and a protein-protein interaction (PPI) network to identify central network nodes driving these CAD-related gene sets (key drivers or KDs). Top KDs were then used as seeds to derive subnetworks linking KDs.

Results: We found 11 of 12 positive control gene sets and 12 of 18 coexpression network modules to be significantly enriched for eSNPs with low p values (Bonferroni-corrected p<0.05 for both tests). We identified both tissue-specific KDs and KDs common to multiple tissues and found them to be enriched for CAD-related biological processes such as circulation, inflammatory response, and coagulation. The top KDs across tissues are IL1RN, EGR2, NCF2, and LDLR, and the tissue-specific KDs include LPL and APOE from liver, ALOX5AP and ACE from kidney, F7 and ANAX2 from adipose, BACH1 and FER1L3 from blood, and CD36 and PPARG from the PPI network. We found KDs to be highly connected in the networks. We derived representative subnetworks of the top KDs (21 known and 27 novel).

Conclusions: Our network-driven integrative analysis not only identified known and novel CAD risk genes but also defined a network structure that sheds light on the molecular interactions of CAD risk genes within, between and across tissues.

[Contributed Oral Presentation]

Transcriptional profiling of monocytes and MCSFdriven macrophages in a large multi-centre collaborative study.

Maouche S.

The 3rd Annual Meeting of NGFN-Plus and NGFN-Transfer in the Program of Medical Genome Research, IG Genomics of Atherosclerosis.

25-27 Nov. 2010; the Freie Universitaet (FU) - Campus in Berlin-Dahlem Berlin, Germany

Conference Abstract
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Counter-regulation of macrophage phenotype by M-CSF and GM-CSF. Possible implication in atherosclerosis.

Maouche S.

The 3rd Annual Meeting of NGFN-Plus and NGFN-Transfer in the Program of Medical Genome Research, IG Genomics of Atherosclerosis.

25-27 Nov. 2010; the Freie Universitaet (FU) - Campus in Berlin-Dahlem Berlin, Germany

Conference Abstract
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Temporal transcriptional changes in human monocyte RNAs following myocardial infarction: The GerMIFs monocyte expression study.

Maouche S.

The 3rd Annual Meeting of NGFN-Plus and NGFN-Transfer in the Program of Medical Genome Research, IG Genomics of Atherosclerosis.

25-27 Nov. 2010; the Freie Universitaet (FU) - Campus in Berlin-Dahlem Berlin, Germany

Conference Abstract
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Counter-regulation of macrophage phenotype by M-CSF and GM-CSF. Possible implication in atherosclerosis. Keystone Symposia on Molecular and Cellular Biology.

Brocheriou I, Maouche S, Durand H, Braunersreuther V, Le Naour G, Kzhyshkowska J, Mach F, Cambien F, and Ninio E.

The Advances in Molecular Mechanisms of Atherosclerosis 2010.

February 12-17, Banff, Alberta.

Conference Abstract

Brocheriou I, Maouche S, Durand H, Braunersreuther V, Le Naour G, Kzhyshkowska J, Mach F, Cambien F, and Ninio E.

[Contributed Oral Presentation]

HumanGeneSetsGUI: a Bioconductor package for gene sets construction and knowledge extraction from biological and literature databases.

Maouche S.

The Advances in Molecular Mechanisms of Atherosclerosis 2010.

The Bioinformatics Workshop (BW-09)

24th April 2009, Fez, Morocco.

Conference Abstract

[Invited Oral Presentation]

Dissecting the signaling pathways that are implicated in the proinflammatory effects of PLA2GX modified LDL on endothelial cells..

Maouche S.

The 5th annual congress of the French Atherosclerosis Society

June 12- 14th 2008, Biarritz, France.

Conference Abstract

Gora S, Maouche S, Gautam N, Wanherdrick K, Lambeau G, Cambien F, Ninio E, Karabina A.S.

[Contributed Oral Presentation]

A GSEA-like approach to integrate biological knowledge in the analysis of association between gene expression profiles and SNPs variation..

Maouche S.

Genome to Systems conference

March 17-19th, 2008, Manchester, UK.

Conference Abstract

Maouche S, Tiphaine G, Poirier O, Montalescot G and Cambien F.

Explaining the Sources of Discrepancies in Gene Expression Profiles Generated on three Whole-Genome Gene Expression Microarray Platforms.

Maouche S.

The EMERALD (Empowering the Microarray-Based European Research Area to Take a Lead in Development and Exploitation) Workshop

December13-14th 2007; Valencia, Spain

Conference Abstract

Maouche S, Poirier O, Godefroy T, Olaso R, Gut I, Montalescot G and Cambien F.

[Iniviated Oral Presentation]

Sources of Discrepancies in Gene Expression Profiles Generated on three Whole-Genome Gene Expression Microarray Platforms.

Maouche S.

The 7th international conference for the Critical Assessment of Microarray Data Analysis (CAMDA)

December13-14th 2007; Valencia, Spain

Conference Abstract

Maouche S, Poirier O, Godefroy T, Olaso R, Gut I, Montalescot G and Cambien F.

Profiling of macrophage gene expression in response to LDL particles modified by human group X secreted phospholipase.

Gora S, Karabina S-A, Maouche S, Lambeau G, Cambien F and Ninio E.

The 4th annual congress of the French Atherosclerosis Society, Biarritz, France, June 14- 16th, 2007

Conference Abstract

Gora S, Karabina S-A, Maouche S, Lambeau G, Cambien F and Ninio E.

Profiling of macrophage gene expression in response to LDL particles modified by human group X secreted phospholipase A2.

Maouche S.

The 76th congress of the European Atherosclerosis Society

June 10 - 13, 2007; Helsinki, Finland.

Conference Abstract

Karabina S-A, Maouche S, Gora S, Lambeau G, Cambien F, Ninio E.

[Contributed Oral Presentation]

PhD Thesis in Bioinformatics

Seraya Maouche
Theses.

Title: Bioinformatics approaches for analyzing genomics and microarray data in cardiovascular research.


Supervisor(s):
Dr F. Cambien

Master´s of Research of History of Sciences and Techniques

Seraya Maouche
Theses.

Title: History of reverse engineering in biology: a new systems biology approach or a new interface between engineering and life-sciences?

University Paris 1 - Pantheon-Sorbonne
Supervisor(s):
Prof. Belhoste B (Sorbonne, Paris, France) &
Prof. Fox Keller E (Massachusetts Institute of Technology, USA)

University Diploma of Bioengineering, Valorization of Applied Research and Biomedical Innovation

Seraya Maouche
Theses.

Title: Protection of persons in biomedical research: risks related to the introduction of new communication technologies such as wireless and mobile communication

University Pierre & Marie Curie (Paris VI), Paris, France
Supervisor: Prof. Sezeur A (University Paris VI)
Dissertation defended on October 2005

Master´s of Research of Medical Informatics and Communication Technologies

Seraya Maouche
Theses.

Title: Quantitative and visual assessment of a medical image compression algorithm based on wavelet transformation. Elaboration of optimized compression approach.

University Pierre et Marie Curie (Paris VI)
Supervisors:
Dr. Heudes D. (European Hospital George Pompidou (HEGP) and SPIM laboratory) &
Dr. Topin S (CIRA, a high technology company)
Dissertation defended on July 2004

Engineering in Computer Science

Seraya Maouche
Theses.

Title: Integrating new information and communication technologies in healthcare. Deployment of an intranet and shared medical record in the University Hospital of Constantine.

University of Constantine (Algeria)
Faculty of Engineering Sciences
University Hospital of Constantine
Supervisors:
Prof Ouchtati M (University Hospital of Constantine) &
Dr Boussouf M (Faculty of Engineering Sciences, Constantine)
Dissertation defended on July 2001

University Diploma of Computer Science Studies

Seraya Maouche
Theses.

Title: Development of an automated commercial management system.

University of Batna (Algeria)
NAFTAL (the principal company of petroleum-based fuels in Algeria), Batna, Algeria
Dissertation defended on July 1997

[French] Séquencage de l´ADN dans l´espace : une première expérience réalisée par Kathleen Rubins cet été.

Maouche S.

Les Echos - Le Cercle

September 8th, 2016 .

Press Article

[French] Séquencage de l´ADN dans l´espace : une première expérience réalisée par Kathleen Rubins cet été.

[French] Big data : l´oiseau bleu a fait son nid en santé et en recherche biomédicale sur le cancer.

Maouche S.

Les Echos - Le Cercle

March 3rd, 2016.

Press Article

[French] Big data : l´oiseau bleu a fait son nid en santé et en recherche biomédicale sur le cancer.