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Institution

University of Lausanne

EducationLausanne, Switzerland
About: University of Lausanne is a education organization based out in Lausanne, Switzerland. It is known for research contribution in the topics: Population & Poison control. The organization has 20508 authors who have published 46458 publications receiving 1996655 citations. The organization is also known as: Université de Lausanne & UNIL.


Papers
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01 Jan 2008
TL;DR: In this article, the authors investigate whether systems-level properties of functional networks can be explained by structural properties of the underlying anatomical network, using functional MRI and diffusionspectrum imaging tractography.
Abstract: In the cerebral cortex, the activity levels of neuronal populationsare continuously fluctuating. When neuronal activity, as measuredusing functional MRI (fMRI), is temporally coherent across 2 pop-ulations, those populations are said to be functionally connected.Functional connectivity has previously been shown to correlatewith structural (anatomical) connectivity patterns at an aggregatelevel. In the present study we investigate, with the aid of compu-tational modeling, whether systems-level properties of functionalnetworks—including their spatial statistics and their persistenceacross time—can be accounted for by properties of the underlyinganatomical network. We measured resting state functional con-nectivity (using fMRI) and structural connectivity (using diffusionspectrum imaging tractography) in the same individuals at highresolution. Structural connectivity then provided the couplings fora model of macroscopic cortical dynamics. In both model and data,weobserved(

1,718 citations

Journal ArticleDOI
TL;DR: A perspective on the context and evolutionary significance of hybridization during speciation is offered, highlighting issues of current interest and debate and suggesting that the Dobzhansky–Muller model of hybrid incompatibilities requires a broader interpretation.
Abstract: Hybridization has many and varied impacts on the process of speciation. Hybridization may slow or reverse differentiation by allowing gene flow and recombination. It may accelerate speciation via adaptive introgression or cause near-instantaneous speciation by allopolyploidization. It may have multiple effects at different stages and in different spatial contexts within a single speciation event. We offer a perspective on the context and evolutionary significance of hybridization during speciation, highlighting issues of current interest and debate. In secondary contact zones, it is uncertain if barriers to gene flow will be strengthened or broken down due to recombination and gene flow. Theory and empirical evidence suggest the latter is more likely, except within and around strongly selected genomic regions. Hybridization may contribute to speciation through the formation of new hybrid taxa, whereas introgression of a few loci may promote adaptive divergence and so facilitate speciation. Gene regulatory networks, epigenetic effects and the evolution of selfish genetic material in the genome suggest that the Dobzhansky-Muller model of hybrid incompatibilities requires a broader interpretation. Finally, although the incidence of reinforcement remains uncertain, this and other interactions in areas of sympatry may have knock-on effects on speciation both within and outside regions of hybridization.

1,715 citations

Journal ArticleDOI
TL;DR: Several of the likely causal genes are highly expressed or known to act in the central nervous system (CNS), emphasizing, as in rare monogenic forms of obesity, the role of the CNS in predisposition to obesity.
Abstract: Common variants at only two loci, FTO and MC4R, have been reproducibly associated with body mass index (BMI) in humans. To identify additional loci, we conducted meta-analysis of 15 genome-wide association studies for BMI (n > 32,000) and followed up top signals in 14 additional cohorts (n > 59,000). We strongly confirm FTO and MC4R and identify six additional loci (P < 5 x 10(-8)): TMEM18, KCTD15, GNPDA2, SH2B1, MTCH2 and NEGR1 (where a 45-kb deletion polymorphism is a candidate causal variant). Several of the likely causal genes are highly expressed or known to act in the central nervous system (CNS), emphasizing, as in rare monogenic forms of obesity, the role of the CNS in predisposition to obesity.

1,710 citations

Journal ArticleDOI
TL;DR: The extent of bone-implant interface is positively correlated with an increasing roughness of the implant surface, and hydroxylapatite (HA)-coated implants with 60-70% showed signs of resorption.
Abstract: The purpose of the present study was to evaluate the influence of different surface characteristics on bone integration of titanium implants. Hollow-cylinder implants with six different surfaces were placed in the metaphyses of the tibia and femur in six miniature pigs. After 3 and 6 weeks, the implants with surrounding bone were removed and analyzed in undecalcified transverse sections. The histologic examination revealed direct bone-implant contact for all implants. However, the morphometric analyses demonstrated significant differences in the percentage of bone-implant contact, when measured in cancellous bone. Electropolished as well as the sandblasted and acid pickled (medium grit; HF/HNO3) implant surfaces had the lowest percentage of bone contact with mean values ranging between 20 and 25%. Sandblasted implants with a large grit and titanium plasma-sprayed implants demonstrated 30-40% mean bone contact. The highest extent of bone-implant interface was observed in sandblasted and acid attacked surfaces (large grit; HCl/H2SO4) with mean values of 50-60%, and hydroxylapatite (HA)-coated implants with 60-70%. However, the HA coating consistently revealed signs of resorption. It can be concluded that the extent of bone-implant interface is positively correlated with an increasing roughness of the implant surface.

1,683 citations

Journal ArticleDOI
Qian Zhang1, Paul Bastard2, Paul Bastard3, Zhiyong Liu1  +169 moreInstitutions (34)
23 Oct 2020-Science
TL;DR: The COVID Human Genetic Effort established to test the general hypothesis that life-threatening COVID-19 in some or most patients may be caused by monogenic inborn errors of immunity to SARS-CoV-2 with incomplete or complete penetrance finds an enrichment in variants predicted to be loss-of-function (pLOF), with a minor allele frequency <0.001.
Abstract: Clinical outcome upon infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) ranges from silent infection to lethal coronavirus disease 2019 (COVID-19). We have found an enrichment in rare variants predicted to be loss-of-function (LOF) at the 13 human loci known to govern Toll-like receptor 3 (TLR3)- and interferon regulatory factor 7 (IRF7)-dependent type I interferon (IFN) immunity to influenza virus in 659 patients with life-threatening COVID-19 pneumonia relative to 534 subjects with asymptomatic or benign infection. By testing these and other rare variants at these 13 loci, we experimentally defined LOF variants underlying autosomal-recessive or autosomal-dominant deficiencies in 23 patients (3.5%) 17 to 77 years of age. We show that human fibroblasts with mutations affecting this circuit are vulnerable to SARS-CoV-2. Inborn errors of TLR3- and IRF7-dependent type I IFN immunity can underlie life-threatening COVID-19 pneumonia in patients with no prior severe infection.

1,659 citations


Authors

Showing all 20911 results

NameH-indexPapersCitations
Peer Bork206697245427
Aaron R. Folsom1811118134044
Kari Alitalo174817114231
Ralph A. DeFronzo160759132993
Johan Auwerx15865395779
Silvia Franceschi1551340112504
Matthias Egger152901184176
Bart Staels15282486638
Fernando Rivadeneira14662886582
Christopher George Tully1421843111669
Richard S. J. Frackowiak142309100726
Peter Timothy Cox140126795584
Jürg Tschopp14032886900
Stylianos E. Antonarakis13874693605
Michael Weller134110591874
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023249
2022635
20213,969
20203,508
20193,091
20182,776