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 & Transplantation. 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, Transplantation, Gene, Poison control, Quantum dot
Papers published on a yearly basis
Papers
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TL;DR: It is reported that selection of highly proliferative stem cells followed by treatment with retinoic acid generated essentially pure precursors that markers identified as Pax-6-positive radial glial cells went on to generate neurons with remarkably uniform biochemical and electrophysiological characteristics.
Abstract: Although it has long been known that cultured embryonic stem cells can generate neurons, the lineage relationships with their immediate precursors remain unclear. We report here that selection of highly proliferative stem cells followed by treatment with retinoic acid generated essentially pure precursors that markers identified as Pax-6-positive radial glial cells. As they do in vivo, these cells went on to generate neurons with remarkably uniform biochemical and electrophysiological characteristics.
502 citations
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TL;DR: The authors of as mentioned in this paper show that the volume of the lithosphere is not necessarily preserved during rifting as advocated by conventional stretching models, and that the structural style of rifts is controlled by the rheological structure of the upper and lower lithosphere, the availability of crustal discontinuities that can be tensionally reactivated, the mode (orthogonal or oblique) and amount of extension, and the lithological composition of pre- and syn-rift sediments.
502 citations
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TL;DR: Transgenic mouse models of cancer have been instrumental in revealing that inflammatory responses within the tumor microenvironment are critically contributing to the onset of tumor angiogenesis, and provided first important concepts to improve anti-angiogenic therapy.
500 citations
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TL;DR: An agenda for the elimination of schistosomiasis would aim to identify the gaps in knowledge, and define the tools, strategies and guidelines that will help national control programmes move towards elimination, including an internationally accepted mechanism that allows verification/confirmation of elimination.
500 citations
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TL;DR: Thy1 transgene expression of wild-type human α-synuclein resulted in similar pathological changes, thus supporting a central role for mutant and wild- type α- Synuclein in familial and idiotypic forms of diseases with neuronal α- synucleinopathy and Lewy pathology.
Abstract: The presynaptic protein α-synuclein is a prime suspect for contributing to Lewy pathology and clinical aspects of diseases, including Parkinson's disease, dementia with Lewy bodies, and a Lewy body variant of Alzheimer's disease. α-Synuclein accumulates in Lewy bodies and Lewy neurites, and two missense mutations (A53T and A30P) in the α-synuclein gene are genetically linked to rare familial forms of Parkinson's disease. Under control of mouse Thy1 regulatory sequences, expression of A53T mutant human α-synuclein in the nervous system of transgenic mice generated animals with neuronal α-synucleinopathy, features strikingly similar to those observed in human brains with Lewy pathology, neuronal degeneration, and motor defects, despite a lack of transgene expression in dopaminergic neurons of the substantia nigra pars compacta. Neurons in brainstem and motor neurons appeared particularly vulnerable. Motor neuron pathology included axonal damage and denervation of neuromuscular junctions in several muscles examined, suggesting that α-synuclein interfered with a universal mechanism of synapse maintenance. Thy1 transgene expression of wild-type human α-synuclein resulted in similar pathological changes, thus supporting a central role for mutant and wild-type α-synuclein in familial and idiotypic forms of diseases with neuronal α-synucleinopathy and Lewy pathology. These mouse models provide a means to address fundamental aspects of α-synucleinopathy and test therapeutic strategies.
498 citations
Authors
Showing all 25374 results
Name | H-index | Papers | Citations |
---|---|---|---|
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 |