"The great tragedy of science - the slaying of a beautiful hypothesis by an ugly fact."
My background includes both experience as a wet lab biologist, as well as several years of training in bioinformatics and computational biology. I started as a biology major, however, during my Master's studies I developed a great interest in bioinformatics and engaged in a database development project, involving the prediction of protein-protein interactions based on correlated mutations in their respective domains, currently part of the DIMA database.
Later during my PhD thesis, I worked at the cutting edge between in silico analysis and wet lab experiments, investigating the regulatory networks of hematopoietic stem cells and their niche.
Here, my task was to generate a high-throughput transcriptomics data set, followed by computational analysis involving candidate gene prioritization and biological hypothesis generation, which I then validated experimentally both in vitro and in vivo.
Finally, for the last 4-5 years as a PostDoc in bioinformatics, mainly focusing on integrative systems-level investigations linking genetic and transcriptomic data, both in mice and man, in the context of coronary artery disease, I have greatly expanded my computational skills regarding the analysis of diverse high-throughput data sets.
Postdoctoral Research Fellow
The German Heart Centre Munich, Department of Cardiovascular Diseases in Adults, Technical University Munich
Aug. 2013 - PRESENT
Computational and systems biology-based integrative mutli-omics analysis of high-throughput data, mainly genomics and transcriptomics, related to atherosclerosis and coronary artery disease (CAD), with a particular focus on the roles of mitochondria in disease patho-physiology.
Towards the goal of precision medicine, I am currently generating a bio-bank of clinically well-characterized CAD patients, involving molecular profiling of genome, multi-tissue transcriptome, metabolome and gut microbiome.
PhD Student in Computational Systems Biology
Technical University Munich, Laboratory of Stem Cell Physiology, 3rd Department of Internal Medicine, Klinikum rechts der Isar | Institute for Bioinformatics and Systems Biology, Helmholtz Zentrum Munich
Graduate School of Bioengineering (GSB) Scholarship
Mar. 2009 - Aug. 2013
Thesis: "Regulatory networks of hematopoietic stem cells and their microenvironment"
Generation and system-level bioinformatics analysis of time-resolved gene expression data in co-cultured UG26-1B6 stromal cells and Lineage-Sca-1+ Kit+ (LSKs) stem cells, followed by computational analysis and candidate gene prioritization, which were then validated experimentally, both in vitro an in vivo.
MSc Student in Molecular Biotechnology with Bioinformatics as a Major
Technical University Munich, Department of Genome Oriented Bioinformatics
The German Academic Exchange Service (DAAD) Scholarship
Oct. 2006 - Mar. 2009
Thesis: "Reconstruction of Domain Interactions based on Correlated Mutation Analysis"
The aim here was inferring putative domain-domain interactions (DDIs) from protein interaction data. For this, we made use of the concept of co-evolution, which assumes that interacting partners should co-evolve to maintain structural and functional complementarity and that co-evolution of interacting domains can be detected by the presence of compensatory substitutions in the corresponding domain sequences of distinct organisms. This method is integrated within the Domain Interaction MAp (DIMA) database.
BSc Student in Biology with Microbiology as a Major
University of Latvia, Faculty of Biology, Department of Microbiology and Biotechnology
Sep. 2003 - Oct. 2006
Thesis: "The influence of statically curved DNA regions and the deletion of rafA promoter on the replication stability of plasmid pRU984 and its derivatives"
Here, we investigated whether and how statically curved DNA regions and the presence or absence of the rafA promoter influence replication stability of plasmids, using pRU984 and its derivatives, and E.coli strains HB101 and XL-1 Blue as a model system. The rafA promoter is a strong promoter that is required for the catabolism of raffinose, however, it also counteracts the RNS II plasmid replication promoter. Therefore, we hypothesized that it might have an additional effect on the replication stability of pRU984 and its derivatives.