| 1. |
- Arridge, Christopher S., et al.
(författare)
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Uranus Pathfinder : exploring the origins and evolution of Ice Giant planets
- 2012
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Ingår i: Experimental astronomy. - : Springer Science and Business Media LLC. - 0922-6435 .- 1572-9508. ; 33:2-3, s. 753-791
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Tidskriftsartikel (refereegranskat)abstract
- The "Ice Giants" Uranus and Neptune are a different class of planet compared to Jupiter and Saturn. Studying these objects is important for furthering our understanding of the formation and evolution of the planets, and unravelling the fundamental physical and chemical processes in the Solar System. The importance of filling these gaps in our knowledge of the Solar System is particularly acute when trying to apply our understanding to the numerous planetary systems that have been discovered around other stars. The Uranus Pathfinder (UP) mission thus represents the quintessential aspects of the objectives of the European planetary community as expressed in ESA's Cosmic Vision 2015-2025. UP was proposed to the European Space Agency's M3 call for medium-class missions in 2010 and proposed to be the first orbiter of an Ice Giant planet. As the most accessible Ice Giant within the M-class mission envelope Uranus was identified as the mission target. Although not selected for this call the UP mission concept provides a baseline framework for the exploration of Uranus with existing low-cost platforms and underlines the need to develop power sources suitable for the outer Solar System. The UP science case is based around exploring the origins, evolution, and processes at work in Ice Giant planetary systems. Three broad themes were identified: (1) Uranus as an Ice Giant, (2) An Ice Giant planetary system, and (3) An asymmetric magnetosphere. Due to the long interplanetary transfer from Earth to Uranus a significant cruise-phase science theme was also developed. The UP mission concept calls for the use of a Mars Express/Rosetta-type platform to launch on a Soyuz-Fregat in 2021 and entering into an eccentric polar orbit around Uranus in the 2036-2037 timeframe. The science payload has a strong heritage in Europe and beyond and requires no significant technology developments.
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| 2. |
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| 3. |
- Björklund, Andreas, et al.
(författare)
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Listing Triangles
- 2014
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Ingår i: Automata, Languages, and Programming (Lecture notes in computer science). - Berlin, Heidelberg : Springer Berlin Heidelberg. - 1611-3349 .- 0302-9743. - 9783662439487 ; 8572, s. 223-234
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Konferensbidrag (refereegranskat)abstract
- We present new algorithms for listing triangles in dense and sparse graphs. The running time of our algorithm for dense graphs is O~(n^ω+n^3(ω−1)/(5−ω)t^2(3−ω)/(5−ω)), and the running time of the algorithm for sparse graphs is O~(m^2ω/(ω+1)+m^3(ω−1)/(ω+1)t^(3−ω)/(ω+1)), where n is the number of vertices, m is the number of edges, t is the number of triangles to be listed, and ω < 2.373 is the exponent of fast matrix multiplication. With the current bound on ω, the running times of our algorithms are O~(n^2.373+n^1.568t^0.478) and O~(m^1.408+m^1.222t^0.186), respectively. We first obtain randomized algorithms with the desired running times and then derandomize them using sparse recovery techniques. If ω = 2, the running times of the algorithms become O~(n^2+nt^2/3) and O~(m^4/3+mt^1/3), respectively. In particular, if ω = 2, our algorithm lists m triangles in O~(m4/3) time. Pǎtraşcu (STOC 2010) showed that Ω(m^(4/3 − o(1))) time is required for listing m triangles, unless there exist subquadratic algorithms for 3SUM. We show that unless one can solve quadratic equation systems over a finite field significantly faster than the brute force algorithm, our triangle listing runtime bounds are tight assuming ω = 2, also for graphs with more triangles.
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| 4. |
- Björklund, Andreas, et al.
(författare)
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Shortest Two Disjoint Paths in Polynomial Time
- 2014
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Ingår i: Lecture Notes in Computer Science. - Berlin, Heidelberg : Springer Berlin Heidelberg. - 1611-3349 .- 0302-9743. - 9783662439470 ; 8572, s. 211-222
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Konferensbidrag (refereegranskat)abstract
- Given an undirected graph and two pairs of vertices $(s_i,t_i)$ for $i\in\{1,2\}$ we show that there is a polynomial time Monte Carlo algorithm that finds disjoint paths of smallest total length joining $s_i$ and $t_i$ for $i\in\{1,2\}$ respectively, or concludes that there most likely are no such paths at all. Our algorithm applies to both the vertex- and edge-disjoint versions of the problem. Our algorithm is algebraic and uses permanents over the polynomial rings $Z_2[x]$ and $Z_4[x]$ in combination with Mulmuley, Vazirani and Vazirani's isolation lemma to detect a solution. We develop a fast algorithm for permanents over these rings by modifying Valiant's 1979 algorithm for the permanent over $Z_{2^l}$.
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| 5. |
- Ohlsson, Claes, 1965, et al.
(författare)
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Estrogen receptor-α expression in neuronal cells affects bone mass.
- 2012
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 1091-6490. ; 109:3, s. 983-988
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Tidskriftsartikel (refereegranskat)abstract
- It has generally been assumed that bone mass is controlled by endocrine mechanisms and the local bone environment. Recent findings demonstrate that central pathways are involved in the regulation of bone mass. Estrogen is involved in the regulation of bone homeostasis and the CNS is also a target for estrogen actions. The aim of this study was to investigate in vivo the role of central estrogen receptor-α (ERα) expression for bone mass. Nestin-Cre mice were crossed with ERα(flox) mice to generate mice lacking ERα expression specifically in nervous tissue (nestin-ERα(-/-)). Bone mineral density was increased in both the trabecular and cortical bone compartments in nestin-ERα(-/-) mice compared with controls. Femoral bone strength was increased in nestin-ERα(-/-) mice, as demonstrated by increased stiffness and maximal load of failure. The high bone mass phenotype in nestin-ERα(-/-) mice was mainly caused by increased bone formation. Serum leptin levels were elevated as a result of increased leptin expression in white adipose tissue (WAT) and slightly increased amount of WAT in nestin-ERα(-/-) mice. Leptin receptor mRNA levels were reduced in the hypothalamus but not in bone. In conclusion, inactivation of central ERα signaling results in increased bone mass, demonstrating that the balance between peripheral stimulatory and central inhibitory ERα actions is important for the regulation of bone mass. We propose that the increased bone mass in nestin-ERα(-/-) mice is mediated via decreased central leptin sensitivity and thereby increased secretion of leptin from WAT, which, in turn, results in increased peripheral leptin-induced bone formation.
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| 6. |
- Oji, Vinzenz, et al.
(författare)
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Revised nomenclature and classification of inherited ichthyoses : Results of the First Ichthyosis Consensus Conference in Sorèze 2009
- 2010
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Ingår i: The Journal of American Academy of Dermatology. - : Elsevier BV. - 0190-9622 .- 1097-6787. ; 63:4, s. 607-641
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Inherited ichthyoses belong to a large, clinically and etiologically heterogeneous group of mendelian disorders of cornification, typically involving the entire integument. Over the recent years, much progress has been made defining their molecular causes. However, there is no internationally accepted classification and terminology. OBJECTIVE: We sought to establish a consensus for the nomenclature and classification of inherited ichthyoses. METHODS: The classification project started at the First World Conference on Ichthyosis in 2007. A large international network of expert clinicians, skin pathologists, and geneticists entertained an interactive dialogue over 2 years, eventually leading to the First Ichthyosis Consensus Conference held in Sorèze, France, on January 23 and 24, 2009, where subcommittees on different issues proposed terminology that was debated until consensus was reached. RESULTS: It was agreed that currently the nosology should remain clinically based. "Syndromic" versus "nonsyndromic" forms provide a useful major subdivision. Several clinical terms and controversial disease names have been redefined: eg, the group caused by keratin mutations is referred to by the umbrella term, "keratinopathic ichthyosis"-under which are included epidermolytic ichthyosis, superficial epidermolytic ichthyosis, and ichthyosis Curth-Macklin. "Autosomal recessive congenital ichthyosis" is proposed as an umbrella term for the harlequin ichthyosis, lamellar ichthyosis, and the congenital ichthyosiform erythroderma group. LIMITATIONS: As more becomes known about these diseases in the future, modifications will be needed. CONCLUSION: We have achieved an international consensus for the classification of inherited ichthyosis that should be useful for all clinicians and can serve as reference point for future research.
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| 7. |
- Thomsen, Christer, et al.
(författare)
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A conserved N-terminal motif is required for complex formation between FUS, EWSR1, TAF15 and their oncogenic fusion proteins.
- 2013
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Ingår i: FASEB journal : official publication of the Federation of American Societies for Experimental Biology. - : Wiley. - 1530-6860. ; 27:12, s. 4965-74
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Tidskriftsartikel (refereegranskat)abstract
- The three FET (FUS, EWSR1, and TAF15) family RNA binding proteins are expressed in all tissues and almost all cell types. The disordered N-terminal parts are always present in FET fusion oncoproteins of sarcomas and leukemia. Mutations in FUS and TAF15 cause aggregation of FET proteins in neurological disorders. Here we used recombinant proteins in pulldown experiments and mass spectrometry to identify major interaction partners of the FET N-terminal parts. We report that FUS, EWSR1, and TAF15 form homo- and heterocomplexes as major binding partners and identify an evolutionarily conserved N-terminal motif (FETBM1) that is required for this interaction. The binding is RNA and DNA independent and robust up to 1 M of NaCl. The localization of FETBM1 and its target sequences supports a simple model for FET protein aggregation as reported in neurological disorders such as amyotrophic lateral sclerosis, frontotemporal dementia, and essential tremor. The FETBM1 localization also explains the binding of normal full-length FET proteins to their oncogenic fusion proteins.-Thomsen, C., Grundevik, P., Elias, P., Ståhlberg, A., Åman, P. A conserved N-terminal motif is required for complex formation between FUS, EWSR1, TAF15 and their oncogenic fusion proteins.
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