Institution
University of Basel
Education•Basel, Basel-Stadt, Switzerland•
About: University of Basel is a education organization based out in Basel, Basel-Stadt, Switzerland. It is known for research contribution in the topics: Population & Gene. The organization has 25084 authors who have published 52975 publications receiving 2388002 citations. The organization is also known as: Universität Basel & Basel University.
Topics: Population, Gene, Medicine, Context (language use), Transplantation
Papers published on a yearly basis
Papers
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TL;DR: The Theriak/Domino software as discussed by the authors uses a unique algorithm of scanning and bookkeeping, which allows to compute completely and automatically a great variety of diagrams: phase diagrams, pseudo-binary, pseudoternary, isopleths, modal amounts, molar properties of single phases or bulk-rock properties like total Δ G, volume of solids, etc.
Abstract: In this paper, the term “equilibrium assemblage diagrams” refers to diagrams strictly based on assemblages predicted by Gibbs free energy minimization. The presented Theriak/Domino software uses a unique algorithm of scanning and bookkeeping, which allows to compute completely and automatically a great variety of diagrams: phase diagrams, pseudo-binary, pseudo-ternary, isopleths, modal amounts, molar properties of single phases or bulk-rock properties like total Δ G , volume of solids, etc. The speed and easiness of use makes thermodynamic modeling accessible to any student of Earth sciences and offers a powerful tool to check the consistency of thermodynamic databases, develop new solution models, plan experimental work, and to understand natural systems. The examples described in this paper demonstrate the capacity of the software, but also to show the usefulness and limitations of computed equilibrium assemblage diagrams. For most illustrations, a metapelite (TN205) from the eastern Lepontine Alps is used. The applications include the interpretation of complex diagrams, mineral reactions, the effect of Al content on the equilibrium assemblages, the interpretation of Si per formula unit in white mica, understanding some features of garnet growth, dehydration and isothermal compressibility, a broadening of the concept of AFM diagrams, combining equilibrium assemblage diagram information with thermobarometry, and comparing the results produced with different databases. Equilibrium assemblage diagrams do not always provide straightforward answers, but mostly stimulate further thought.
630 citations
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TL;DR: A bifunctional artificial metalloenzyme is created in which a glutamic acid or aspartic acid residue engineered into streptavidin acts in concert with a docked biotinylated rhodium(III) complex to enable catalytic asymmetric carbon-hydrogen (C–H) activation.
Abstract: Enzymes provide an exquisitely tailored chiral environment to foster high catalytic activities and selectivities, but their native structures are optimized for very specific biochemical transformations. Designing a protein to accommodate a non-native transition metal complex can broaden the scope of enzymatic transformations while raising the activity and selectivity of small-molecule catalysis. Here, we report the creation of a bifunctional artificial metalloenzyme in which a glutamic acid or aspartic acid residue engineered into streptavidin acts in concert with a docked biotinylated rhodium(III) complex to enable catalytic asymmetric carbon-hydrogen (C–H) activation. The coupling of benzamides and alkenes to access dihydroisoquinolones proceeds with up to nearly a 100-fold rate acceleration compared with the activity of the isolated rhodium complex and enantiomeric ratios as high as 93:7.
630 citations
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Vita-Salute San Raffaele University1, UCL Institute of Neurology2, National Institute for Health Research3, University of Siena4, University of Nottingham5, University of Basel6, Autonomous University of Barcelona7, University of Copenhagen8, University of Oxford9, National Institutes of Health10, Children's Hospital of Philadelphia11, VU University Amsterdam12
TL;DR: State-of-the-art MRI findings in patients presenting with a clinically isolated syndrome were discussed in a MAGNIMS workshop, the goal of which was to provide an evidence-based and expert-opinion consensus on diagnostic MRI criteria modifications.
Abstract: In patients presenting with a clinically isolated syndrome, MRI can support and substitute clinical information in the diagnosis of multiple sclerosis by showing disease dissemination in space and time and by helping to exclude disorders that can mimic multiple sclerosis. MRI criteria were first included in the diagnostic work-up for multiple sclerosis in 2001, and since then several modifications to the criteria have been proposed in an attempt to simplify lesion-count models for showing disease dissemination in space, change the timing of MRI scanning to show dissemination in time, and increase the value of spinal cord imaging. Since the last update of these criteria, new data on the use of MRI to establish dissemination in space and time have become available, and MRI technology has improved. State-of-the-art MRI findings in these patients were discussed in a MAGNIMS workshop, the goal of which was to provide an evidence-based and expert-opinion consensus on proposed modifications to MRI criteria for the diagnosis of multiple sclerosis.
627 citations
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TL;DR: Findings with melanoma and colon cancer cells suggest that mTORC2-ribosome association is important in oncogenic PI3K signaling, suggesting that TORC2 is active only in growing cells.
627 citations
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TL;DR: The Parkinson's disease-associated human mutant [A30P]αSYN was found to colocalize with βSYN and synaptophysin in synapses of transgenic mouse brain, however, in addition to their normal presynaptic localization, transgenic wild-type and [A 30P] αSYN abnormally accumulated in neuronal cell bodies and neurites throughout the brain.
Abstract: Mutations in the alpha-synuclein (alphaSYN) gene are associated with rare cases of familial Parkinson's disease, and alphaSYN is a major component of Lewy bodies and Lewy neurites. Here we have investigated the localization of wild-type and mutant [A30P]alphaSYN as well as betaSYN at the cellular and subcellular level. Our direct comparative study demonstrates extensive synaptic colocalization of alphaSYN and betaSYN in human and mouse brain. In a sucrose gradient equilibrium centrifugation assay, a portion of betaSYN floated into lower density fractions, which also contained the synaptic vesicle marker synaptophysin. Likewise, wild-type and [A30P]alphaSYN were found in floating fractions. Subcellular fractionation of mouse brain revealed that both alphaSYN and betaSYN were present in synaptosomes. In contrast to synaptophysin, betaSYN and alphaSYN were recovered from the soluble fraction upon lysis of the synaptosomes. Synaptic colocalization of alphaSYN and betaSYN was directly visualized by confocal microscopy of double-stained human brain sections. The Parkinson's disease-associated human mutant [A30P]alphaSYN was found to colocalize with betaSYN and synaptophysin in synapses of transgenic mouse brain. However, in addition to their normal presynaptic localization, transgenic wild-type and [A30P]alphaSYN abnormally accumulated in neuronal cell bodies and neurites throughout the brain. Thus, mutant [A30P]alphaSYN does not fail to be transported to synapses, but its transgenic overexpression apparently leads to abnormal cellular accumulations.
625 citations
Authors
Showing all 25374 results
Name | H-index | Papers | Citations |
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Yang Yang | 171 | 2644 | 153049 |
Martin Karplus | 163 | 831 | 138492 |
Frank J. Gonzalez | 160 | 1144 | 96971 |
Paul Emery | 158 | 1314 | 121293 |
Matthias Egger | 152 | 901 | 184176 |
Don W. Cleveland | 152 | 444 | 84737 |
Ashok Kumar | 151 | 5654 | 164086 |
Kurt Wüthrich | 143 | 739 | 103253 |
Thomas J. Smith | 140 | 1775 | 113919 |
Robert Huber | 139 | 671 | 73557 |
Peter Robmann | 135 | 1438 | 97569 |
Ernst Detlef Schulze | 133 | 670 | 69504 |
Michael Levine | 129 | 586 | 55963 |
Claudio Santoni | 129 | 1027 | 80598 |
Pablo Garcia-Abia | 126 | 989 | 78690 |