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Lausanne, Switzerland

The University of Lausanne in Lausanne, Switzerland was founded in 1537 as a school of theology, before being made a university in 1890. Today about 13,500 students and 2,200 researchers study and work at the university. Approximately 1,500 international students attend the university , which has a wide curriculum including exchange programs with world renowned universities.Since 2005, the University follows the requirements of the Bologna process. The 2011 Times Higher Education World University Rankings ranked the University of Lausanne 116th globally. The CWTS Leiden Ranking 2013 ranks the University of Lausanne 17th in Europe and 68th globally.Together with the École polytechnique fédérale de Lausanne the university forms a vast campus at the shores of Lake Geneva. Wikipedia.

Kaessmann H.,University of Lausanne
Genome Research | Year: 2010

Ever since the pre-molecular era, the birth of new genes with novel functions has been considered to be a major contributor to adaptive evolutionary innovation. Here, I review the origin and evolution of new genes and their functions in eukaryotes, an area of research that has made rapid progress in the past decade thanks to the genomics revolution. Indeed, recent work has provided initial whole-genome views of the different types of new genes for a large number of different organisms. The array of mechanisms underlying the origin of new genes is compelling, extending way beyond the traditionally well-studied source of gene duplication. Thus, it was shown that novel genes also regularly arose from messenger RNAs of ancestral genes, protein-coding genes metamorphosed into new RNA genes, genomic parasites were coopted as new genes, and that both protein and RNA genes were composed from scratch (i.e., from previously nonfunctional sequences). These mechanisms then also contributed to the formation of numerous novel chimeric gene structures. Detailed functional investigations uncovered different evolutionary pathways that led to the emergence of novel functions from these newly minted sequences and, with respect to animals, attributed a potentially important role to one specific tissue - the testis - in the process of gene birth. Remarkably, these studies also demonstrated that novel genes of the various types significantly impacted the evolution of cellular, physiological, morphological, behavioral, and reproductive phenotypic traits. Consequently, it is now firmly established that new genes have indeed been major contributors to the origin of adaptive evolutionary novelties. © 2010 by Cold Spring Harbor Laboratory Press.

Luthi A.,University of Lausanne
Neuroscientist | Year: 2014

Sleep spindles are extensively studied electroencephalographic rhythms that recur periodically during non-rapid eye movement sleep and that are associated with rhythmic discharges of neurons throughout the thalamocortical system. Their occurrence thus constrains many aspects of the communication between thalamus and cortex, ranging from sensory transmission, to cortical plasticity and learning, to development and disease. I review these functional aspects in conjunction with novel findings on the cellular and molecular makeup of spindle-pacemaking circuits. A highlight in the search of roles for sleep spindles is the repeated finding that spindles correlate with memory consolidation in humans and animals. By illustrating that spindles are at the forefront understanding on how the brain might benefit from sleep rhythms, I hope to stimulate further experimentation. © The Author(s) 2013.

Narcolepsy is a rare sleep disorder with the strongest human leukocyte antigen (HLA) association ever reported. Since the associated HLA-DRB1*1501-DQB1*0602 haplotype is common in the general population (15-25%), it has been suggested that it is almost necessary but not sufficient for developing narcolepsy. To further define the genetic basis of narcolepsy risk, we performed a genome-wide association study (GWAS) in 562 European individuals with narcolepsy (cases) and 702 ethnically matched controls, with independent replication in 370 cases and 495 controls, all heterozygous for DRB1*1501-DQB1*0602. We found association with a protective variant near HLA-DQA2 (rs2858884; P < 3 x 10(-8)). Further analysis revealed that rs2858884 is strongly linked to DRB1*03-DQB1*02 (P < 4 x 10(-43)) and DRB1*1301-DQB1*0603 (P < 3 x 10(-7)). Cases almost never carried a trans DRB1*1301-DQB1*0603 haplotype (odds ratio = 0.02; P < 6 x 10(-14)). This unexpected protective HLA haplotype suggests a virtually causal involvement of the HLA region in narcolepsy susceptibility.

Juillerat-Jeanneret L.,University of Lausanne
Journal of Medicinal Chemistry | Year: 2014

The proline-specific dipeptidyl aminopeptidase IV (DPP IV, DPP-4, CD26), widely expressed in mammalians, releases X-Pro/Ala dipeptides from the N-terminus of peptides. DPP IV is responsible of the degradation of the incretin peptide hormones regulating blood glucose levels. Several families of DPP IV inhibitors have been synthesized and evaluated. Their positive effects on the degradation of the incretins and the control of blood glucose levels have been demonstrated in biological models and in clinical trials. Presently, several DPP IV inhibitors, the "gliptins", are approved for type 2 diabetes or are under clinical evaluation. However, the gliptins may also be of therapeutic interest for other diseases beyond the inhibition of incretin degradation. In this Perspective, the biological functions and potential substrates of DPP IV enzymes are reviewed and the characteristics of the DPP IV inhibitors are discussed in view of type 2 diabetes and further therapeutic interest. © 2013 American Chemical Society.

Dion V.,University of Lausanne
Trends in Genetics | Year: 2014

DNA must constantly be repaired to maintain genome stability. Although it is clear that DNA repair reactions depend on cell type and developmental stage, we know surprisingly little about the mechanisms that underlie this tissue specificity. This is due, in part, to the lack of adequate study systems. This review discusses recent progress toward understanding the mechanism leading to varying rates of instability at expanded trinucleotide repeats (TNRs) in different tissues. Although they are not DNA lesions, TNRs are hotspots for genome instability because normal DNA repair activities cause changes in repeat length. The rates of expansions and contractions are readily detectable and depend on cell identity, making TNR instability a particularly convenient model system. A better understanding of this type of genome instability will provide a foundation for studying tissue-specific DNA repair more generally, which has implications in cancer and other diseases caused by mutations in the caretakers of the genome. © 2014 Elsevier Ltd.

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