| 1. |
- Berger, E., et al.
(författare)
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An Intermediate Luminosity Transient in NGC 300 : The Eruption of a Dust-Enshrouded Massive Star
- 2009
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Ingår i: Astrophysical Journal. - 0004-637X .- 1538-4357. ; 699, s. 1850-1865
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Tidskriftsartikel (refereegranskat)abstract
- We present multi-epoch high-resolution optical spectroscopy, UV/radio/X-ray imaging, and archival Hubble and Spitzer observations of an intermediate luminosity optical transient recently discovered in the nearby galaxy NGC 300. We find that the transient (NGC 300 OT2008-1) has a peak absolute magnitude of M bol ≈ -11.8 mag, intermediate between novae and supernovae, and similar to the recent events M85 OT2006-1 and SN 2008S. Our high-resolution spectra, the first for this event, are dominated by intermediate velocity (~200-1000 km s-1) hydrogen Balmer lines and Ca II emission and absorption lines that point to a complex circumstellar environment, reminiscent of the yellow hypergiant IRC+10420. In particular, we detect asymmetric Ca II H&K absorption with a broad red wing extending to ~103 km s-1, indicative of gas inflow at high velocity (possibly the wind of a massive binary companion). The low luminosity, intermediate velocities, and overall similarity to a known eruptive star indicate that the event did not result in a complete disruption of the progenitor. We identify the progenitor in archival Spitzer observations, with deep upper limits from Hubble data. The spectral energy distribution points to a dust-enshrouded star with a luminosity of about 6 × 104 L sun, indicative of a ~10-20 M sun progenitor (or binary system). This conclusion is in good agreement with our interpretation of the outburst and circumstellar properties. The lack of significant extinction in the transient spectrum indicates that the dust surrounding the progenitor was cleared by the outburst. We thus predict that the progenitor should be eventually visible with Hubble if the transient event marks an evolutionary transition to a dust-free state, or with Spitzer if the event marks a cyclical process of dust formation.
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| 2. |
- Beurskens, M. N. A., et al.
(författare)
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Pedestal width and ELM size identity studies in JET and DIII-D; implications for ITER
- 2009
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Ingår i: Plasma Physics and Controlled Fusion. - : IOP Publishing. - 0741-3335 .- 1361-6587. ; 51:12, s. 124051-
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Tidskriftsartikel (refereegranskat)abstract
- The dependence of the H-mode edge transport barrier width on normalized ion gyroradius (rho* = rho/a) in discharges with type I ELMs was examined in experiments combining data for the JET and DIII-D tokamaks. The plasma configuration as well as the local normalized pressure (beta), collisionality (nu*), Mach number and the ratio of ion and electron temperature at the pedestal top were kept constant, while rho* was varied by a factor of four. The width of the steep gradient region of the electron temperature (T-e) and density (n(e)) pedestals normalized to machine size showed no or only a weak trend with rho*. A rho(1/2) or rho(1) dependence of the pedestal width, given by some theoretical predictions, is not supported by the current experiments. This is encouraging for the pedestal scaling towards ITER as it operates at lower rho* than existing devices. Some differences in pedestal structure and ELM behaviour were, however, found between the devices; in the DIII-D discharges, the n(e) and T-e pedestal were aligned at high rho* but the ne pedestal shifted outwards in radius relative to T-e as rho* decreases, while on JET the profiles remained aligned while rho* was scanned by a factor of two. The energy loss at an ELM normalized to the pedestal energy increased from 10% to 40% as rho* increased by a factor of two in the DIII-D discharges but no such variation was observed in the case of JET. The measured pedestal pressures and widths were found to be consistent with the predictions from modelling based on peeling-ballooning stability theory, and are used to make projections towards ITER
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| 3. |
- Sundqvist, A-K, et al.
(författare)
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Unequal contribution of sexes in the origin of dog breeds.
- 2006
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Ingår i: Genetics. - 0016-6731. ; 172:2, s. 1121-8
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Tidskriftsartikel (refereegranskat)abstract
- Department of Evolutionary Biology, Uppsala University, Sweden. anna-karin.sundqvist@ebc.uu.seDogs (Canis familiaris) were domesticated from the gray wolf (Canis lupus) at least 14,000 years ago, and there is evidence of dogs with phenotypes similar to those in modern breeds 4000 years ago. However, recent genetic analyses have suggested that modern dog breeds have a much more recent origin, probably <200 years ago. To study the origin of contemporaneous breeds we combined the analysis of paternally inherited Y chromosome markers with maternally inherited mitochondrial DNA and biparentally inherited autosomal microsatellite markers in both domestic dogs and their wild ancestor, the gray wolf. Our results show a sex bias in the origin of breeds, with fewer males than females contributing genetically, which clearly differs from the breeding patterns in wild gray wolf populations where both sexes have similar contributions. Furthermore, a comparison of mitochondrial DNA and Y chromosome diversity in dog groups recognized by the World Canine Organization, as well as in groups defined by the breeds' genetic composition, shows that paternal lineages are more differentiated among groups than maternal lineages. This demonstrates a lower exchange of males than of females between breeds belonging to different groups, which illustrates how breed founders may have been chosen.
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| 4. |
- van Es, Michael A, et al.
(författare)
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Genome-wide association study identifies 19p13.3 (UNC13A) and 9p21.2 as susceptibility loci for sporadic amyotrophic lateral sclerosis
- 2009
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Ingår i: Nature genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 41:10, s. 1083-1087
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Tidskriftsartikel (refereegranskat)abstract
- We conducted a genome-wide association study among 2,323 individuals with sporadic amyotrophic lateral sclerosis (ALS) and 9,013 control subjects and evaluated all SNPs with P < 1.0 x 10(-4) in a second, independent cohort of 2,532 affected individuals and 5,940 controls. Analysis of the genome-wide data revealed genome-wide significance for one SNP, rs12608932, with P = 1.30 x 10(-9). This SNP showed robust replication in the second cohort (P = 1.86 x 10(-6)), and a combined analysis over the two stages yielded P = 2.53 x 10(-14). The rs12608932 SNP is located at 19p13.3 and maps to a haplotype block within the boundaries of UNC13A, which regulates the release of neurotransmitters such as glutamate at neuromuscular synapses. Follow-up of additional SNPs showed genome-wide significance for two further SNPs (rs2814707, with P = 7.45 x 10(-9), and rs3849942, with P = 1.01 x 10(-8)) in the combined analysis of both stages. These SNPs are located at chromosome 9p21.2, in a linkage region for familial ALS with frontotemporal dementia found previously in several large pedigrees.
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| 5. |
- Anderson, Tovi M., et al.
(författare)
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Molecular and Evolutionary History of Melanism in North American Gray Wolves
- 2009
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Ingår i: Science. - : American Association for the Advancement of Science (AAAS). - 0036-8075 .- 1095-9203. ; 323:5919, s. 1339-1343
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Tidskriftsartikel (refereegranskat)abstract
- Morphological diversity within closely related species is an essential aspect of evolution and adaptation. Mutations in the Melanocortin 1 receptor (Mc1r) gene contribute to pigmentary diversity in natural populations of fish, birds, and many mammals. However, melanism in the gray wolf, Canis lupus, is caused by a different melanocortin pathway component, the K locus, that encodes a beta-defensin protein that acts as an alternative ligand for Mc1r. We show that the melanistic K locus mutation in North American wolves derives from past hybridization with domestic dogs, has risen to high frequency in forested habitats, and exhibits a molecular signature of positive selection. The same mutation also causes melanism in the coyote, Canis latrans, and in Italian gray wolves, and hence our results demonstrate how traits selected in domesticated species can influence the morphological diversity of their wild relatives.
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| 6. |
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| 7. |
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| 8. |
- Van Es, Michael A, et al.
(författare)
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Analysis of FGGY as a risk factor for sporadic amyotrophic lateral sclerosis
- 2009
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Ingår i: Amyotrophic Lateral Sclerosis and other Motor Neuron Disorders. - : Informa UK Limited. - 1466-0822 .- 1743-4483. ; 10:5-6, s. 441-447
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Tidskriftsartikel (refereegranskat)abstract
- A genome-wide association study (GWAS) using pooled DNA samples from 386 sporadic ALS patients and 542 controls from the USA, identified genetic variation in FGGY (FLJ10986) as a risk factor, as well as 66 additional candidate SNPs. Considering the large number of hypotheses that are tested in GWAS, independent replication of associations is crucial for identifying true-positive genetic risk factors for disease. The primary aim of this study was to study the association between FGGY and sporadic ALS in large, homogeneous populations from northern Europe. Genotyping experiments were performed using Illumina Beadchips, Sequenom iPLEX assays and Taqman technology on large case-control series from The Netherlands, Belgium, Sweden and Ireland (total: 1883 sporadic ALS patients and 2063 controls). No significant association between sporadic ALS and the six previously reported associated SNPs in FGGY was observed: rs6700125 (p =0.56), rs6690993 (p =0.30), rs10493256 (p =0.68), rs6587852 (p =0.64), rs1470407 (p =0.28) and rs333662 (p =0.44). Screening of the additional candidate loci did not yield significant associations either, with the lowest p-value in joint analysis for rs7772593 (p =0.14). We concluded that common genetic variation in FGGY is not associated with susceptibility to sporadic ALS in genetically homogeneous populations from northern Europe.
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| 9. |
- van Es, Michael A, et al.
(författare)
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Genetic variation in DPP6 is associated with susceptibility to amyotrophic lateral sclerosis.
- 2008
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Ingår i: Nature genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 40:1, s. 29-31
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Tidskriftsartikel (refereegranskat)abstract
- We identified a SNP in the DPP6 gene that is consistently strongly associated with susceptibility to amyotrophic lateral sclerosis (ALS) in different populations of European ancestry, with an overall P value of 5.04 x 10(-8) in 1,767 cases and 1,916 healthy controls and with an odds ratio of 1.30 (95% confidence interval (CI) of 1.18-1.43). Our finding is the first report of a genome-wide significant association with sporadic ALS and may be a target for future functional studies.
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| 10. |
- van Es, Michael A, et al.
(författare)
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ITPR2 as a susceptibility gene in sporadic amyotrophic lateral sclerosis : a genome-wide association study.
- 2007
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Ingår i: Lancet Neurology. - 1474-4422 .- 1474-4465. ; 6:10, s. 869-77
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Amyotrophic lateral sclerosis (ALS) is a devastating disease characterised by progressive degeneration of motor neurons in the brain and spinal cord. ALS is thought to be multifactorial, with both environmental and genetic causes. Our aim was to identify genetic variants that predispose for sporadic ALS. METHODS: We did a three-stage genome-wide association study in 461 patients with ALS and 450 controls from The Netherlands, using Illumina 300K single-nucleotide polymorphism (SNP) chips. The SNPs that were most strongly associated with ALS were analysed in a further 876 patients and 906 controls in independent sample series from The Netherlands, Belgium, and Sweden. We also investigated the possible pathological functions of associated genes using expression data from whole blood of patients with sporadic ALS and of control individuals who were included in the genome-wide association study. FINDINGS: A genetic variant in the inositol 1,4,5-triphosphate receptor 2 gene (ITPR2) was associated with ALS (p=0.012 after Bonferroni correction). Combined analysis of all samples (1337 patients and 1356 controls) confirmed this association (p=3.28x10(-6), odds ratio 1.58, 95% CI 1.30-1.91). ITPR2 expression was greater in the peripheral blood of 126 ALS patients than in that of 126 healthy controls (p=0.00016). INTERPRETATION: Genetic variation in ITPR2 is a susceptibility factor for ALS. ITPR2 is a strong candidate susceptibility gene for ALS because it is involved in glutamate-mediated neurotransmission, is one of the main regulators of intracellular calcium concentrations, and has an important role in apoptosis.
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