Institution
University of Geneva
Education•Geneva, Switzerland•
About: University of Geneva is a education organization based out in Geneva, Switzerland. It is known for research contribution in the topics: Population & Planet. The organization has 26887 authors who have published 65265 publications receiving 2931373 citations. The organization is also known as: Geneva University & Universite de Geneve.
Topics: Population, Planet, Galaxy, Exoplanet, Stars
Papers published on a yearly basis
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TL;DR: In this paper, the components of nucleus-independent chemical shift tensors for Dnhn-annulenes are discussed as indexes of the aromatic character of electronic π systems and the component corresponding to the principal axis perpendicular to the ring plane is found to be a good measure for the characterisation of the π system of the ring.
Abstract: The components of nucleus-independent chemical shift (NICS) tensors for Dnhn-annulenes are discussed as indexes of the aromatic character of electronic π systems. The component corresponding to the principal axis perpendicular to the ring plane, NICSzz, is found to be a good measure for the characterisation of the π system of the ring. Isotropic NICS values at ring centres contain large influences from the σ system and from all three principal components of the NICS tensor. At large distances away from the ring center, NICSzz, which is dominated by contributions from the π system, characterizes NICS well.
406 citations
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University of Nevada, Reno1, Purdue University2, Monsanto3, Old Dominion University4, North Carolina State University5, University College London6, Spanish National Research Council7, Oklahoma State University–Stillwater8, National Institutes of Health9, Wellcome Trust10, University of Cambridge11, J. Craig Venter Institute12, Leidos13, Broad Institute14, University of Notre Dame15, University of Nevada, Las Vegas16, University of Barcelona17, Carlos III Health Institute18, University of Massachusetts Medical School19, University of Connecticut20, University of Lausanne21, University of Oxford22, Virginia Tech23, West Virginia University24, Indiana University25, University of Maryland, Baltimore26, Kansas State University27, Texas A&M University28, University of Minnesota29, University of Manchester30, National University of Singapore31, University of California, San Francisco32, Iowa State University33, Colorado State University34, Pennsylvania State University35, Max Planck Society36, University of California, Riverside37, ANSES38, University of Santiago de Compostela39, Pompeu Fabra University40, California State Polytechnic University, Pomona41, University of Queensland42, University of the Sunshine Coast43, University of Geneva44, Swiss Institute of Bioinformatics45, University of Copenhagen46, University of Tennessee Health Science Center47, Wellcome Trust Sanger Institute48, University of Vigo49, University of Illinois at Urbana–Champaign50, Quinnipiac University51, International Livestock Research Institute52
TL;DR: Insights from genome analyses into parasitic processes unique to ticks, including host ‘questing', prolonged feeding, cuticle synthesis, blood meal concentration, novel methods of haemoglobin digestion, haem detoxification, vitellogenesis and prolonged off-host survival are reported.
Abstract: Ticks transmit more pathogens to humans and animals than any other arthropod. We describe the 2.1 Gbp nuclear genome of the tick, Ixodes scapularis (Say), which vectors pathogens that cause Lyme disease, human granulocytic anaplasmosis, babesiosis and other diseases. The large genome reflects accumulation of repetitive DNA, new lineages of retro-transposons, and gene architecture patterns resembling ancient metazoans rather than pancrustaceans. Annotation of scaffolds representing ∼57% of the genome, reveals 20,486 protein-coding genes and expansions of gene families associated with tick-host interactions. We report insights from genome analyses into parasitic processes unique to ticks, including host 'questing', prolonged feeding, cuticle synthesis, blood meal concentration, novel methods of haemoglobin digestion, haem detoxification, vitellogenesis and prolonged off-host survival. We identify proteins associated with the agent of human granulocytic anaplasmosis, an emerging disease, and the encephalitis-causing Langat virus, and a population structure correlated to life-history traits and transmission of the Lyme disease agent.
406 citations
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TL;DR: It is concluded that anion-pi interactions on monomeric surfaces are ideal for chloride recognition, whereas their supramolecular enhancement by pi,pi-interactions appears perfect to target nitrate.
Abstract: Attractive in theory and confirmed to exist, anion–π interactions have never really been seen at work. To catch them in action, we prepared a collection of monomeric, cyclic and rod-shaped naphthalenediimide transporters. Their ability to exert anion–π interactions was demonstrated by electrospray tandem mass spectrometry in combination with theoretical calculations. To relate this structural evidence to transport activity in bilayer membranes, affinity and selectivity sequences were recorded. π-acidification and active-site decrowding increased binding, transport and chloride > bromide > iodide selectivity, and supramolecular organization inverted acetate > nitrate to nitrate > acetate selectivity. We conclude that anion–π interactions on monomeric surfaces are ideal for chloride recognition, whereas their supramolecular enhancement by π,π-interactions appears perfect to target nitrate. Chloride transporters are relevant to treat channelopathies, and nitrate sensors to monitor cellular signaling and cardiovascular diseases. A big impact on organocatalysis can be expected from the stabilization of anionic transition states on chiral π-acidic surfaces.
406 citations
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TL;DR: It is proposed that mitochondria represent a selective target for HS-mediated protection against oxidative injury and is correlated best with the expression of the 70-kDa HSP, hsp70.
Abstract: Heat shock (HS) proteins (HSPs) induce protection against a number of stresses distinct from HS, including reactive oxygen species. In the human premonocytic line U937, we investigated in whole cells the effects of preexposure to HS and exposure to hydrogen peroxide (H2O2) on mitochondrial membrane potential, mass, and ultrastructure. HS prevented H2O2-induced alterations in mitochondrial membrane potential and cristae formation while increasing expression of HSPs and the protein product of bcl-2. Protection correlated best with the expression of the 70-kDa HSP, hsp70. We propose that mitochondria represent a selective target for HS-mediated protection against oxidative injury.
406 citations
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TL;DR: It is proposed that VEGF is actively responsible for hypertrophic cartilage neovascularization through a paracrine release by chondrocytes, with invading endothelial cells as a target.
Abstract: Vascular endothelial growth factor/vascular permeability factor (VEGF/VPF) induces endothelial cell migration and proliferation in culture and is strongly angiogenic in vivo. VEGF synthesis has been shown to occur in both normal and transformed cells. The receptors for the factor have been shown to be localized mainly in endothelial cells, however, the presence of VEGF synthesis and the VEGF receptor in cells other than endothelial cells has been demonstrated. Neoangiogenesis in cartilage growth plate plays a fundamental role in endochondral ossification. We have shown that, in an avian in vitro system for chondrocyte differentiation, VEGF was produced and localized in cell clusters totally resembling in vivo cartilage. The factor was synthesized by hypertrophic chondrocytes and was released into their conditioned medium, which is highly chemotactic for endothelial cells. Antibodies against VEGF inhibited endothelial cell migration induced by chondrocyte conditioned media. Similarly, endothelial cell migration was inhibited also by antibodies directed against the VEGF receptor 2/Flk1 (VEGFR2). In avian and mammalian embryo long bones, immediately before vascular invasion, VEGF was distinctly localized in growth plate hypertrophic chondrocytes. In contrast, VEGF was not observed in quiescent and proliferating chondrocytes earlier in development. VEGF receptor 2 colocalized with the factor both in hypertrophic cartilage in vivo and hypertrophic cartilage engineered in vitro, suggesting an autocrine loop in chondrocytes at the time of their maturation to hypertrophic cells and of cartilage erosion. Regardless of cell exposure to exogenous VEGF, VEGFR-2 phosphorylation was recognized in cultured hypertrophic chondrocytes, supporting the idea of an autocrine functional activation of signal transduction in this non-endothelial cell type as a consequence of the endogenous VEGF production. In summary we propose that VEGF is actively responsible for hypertrophic cartilage neovascularization through a paracrine release by chondrocytes, with invading endothelial cells as a target. Furthermore, VEGF receptor localization and signal transduction in chondrocytes strongly support the hypothesis of a VEGF autocrine activity also in morphogenesis and differentiation of a mesoderm derived cell.
406 citations
Authors
Showing all 27203 results
Name | H-index | Papers | Citations |
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JoAnn E. Manson | 270 | 1819 | 258509 |
Joseph L. Goldstein | 207 | 556 | 149527 |
Kari Stefansson | 206 | 794 | 174819 |
David Baltimore | 203 | 876 | 162955 |
Mark I. McCarthy | 200 | 1028 | 187898 |
Michael S. Brown | 185 | 422 | 123723 |
Yang Gao | 168 | 2047 | 146301 |
Napoleone Ferrara | 167 | 494 | 140647 |
Marc Weber | 167 | 2716 | 153502 |
Alessandro Melchiorri | 151 | 674 | 116384 |
Andrew D. Hamilton | 151 | 1334 | 105439 |
David P. Strachan | 143 | 472 | 105256 |
Andrew Beretvas | 141 | 1985 | 110059 |
Rainer Wallny | 141 | 1661 | 105387 |
Josh Moss | 139 | 1019 | 89255 |