| 1. |
|
|
| 2. |
- Dawson, K. S., et al.
(författare)
-
An Intensive Hubble Space Telescope Survey for z>1 Type Ia Supernovae by Targeting Galaxy Clusters
- 2009
-
Ingår i: Astronomical Journal. - : American Astronomical Society. - 0004-6256 .- 1538-3881. ; 138, s. 1271-1283
-
Tidskriftsartikel (refereegranskat)abstract
- We present a new survey strategy to discover and study high-redshift Type Ia supernovae (SNe Ia) using the Hubble Space Telescope (HST). By targeting massive galaxy clusters at 0.9 < z < 1.5, we obtain a twofold improvement in the efficiency of finding SNe compared to an HST field survey and a factor of 3 improvement in the total yield of SN detections in relatively dust-free red-sequence galaxies. In total, sixteen SNe were discovered at z>0.95, nine of which were in galaxy clusters. This strategy provides an SN sample that can be used to decouple the effects of host-galaxy extinction and intrinsic color in high-redshift SNe, thereby reducing one of the largest systematic uncertainties in SN cosmology. Based on observations made with the NASA/ESA Hubble Space Telescope and obtained from the data archive at the Space Telescope Institute. STScI is operated by the Association of Universities for Research in Astronomy, Inc. under the NASA contract NAS 5-26555. The observations are associated with program 10496.
|
|
| 3. |
- Dempsey, M P, et al.
(författare)
-
Genomic deletion marking an emerging subclone of Francisella tularensis subsp. holarctica in France and the Iberian Peninsula.
- 2007
-
Ingår i: Applied and Environmental Microbiology. - 0099-2240 .- 1098-5336. ; 73:22, s. 7465-70
-
Tidskriftsartikel (refereegranskat)abstract
- Francisella tularensis subsp. holarctica is widely disseminated in North America and the boreal and temperate regions of the Eurasian continent. Comparative genomic analyses identified a 1.59-kb genomic deletion specific to F. tularensis subsp. holarctica isolates from Spain and France. Phylogenetic analysis of strains carrying this deletion by multiple-locus variable-number tandem repeat analysis showed that the strains comprise a highly related set of genotypes, implying that these strains were recently introduced or recently emerged by clonal expansion in France and the Iberian Peninsula.
|
|
| 4. |
- Rhodes, J R, et al.
(författare)
-
Optimizing Presence–Absence Surveys For Detecting Population Trends
- 2006
-
Ingår i: Journal of Wildlife Management. - 0022-541X. ; 70:1, s. 8-18
-
Tidskriftsartikel (refereegranskat)abstract
- Presence–absence surveys are a commonly used method for monitoring broad-scale changes in wildlife distributions. However, the lack of power of these surveys for detecting population trends is problematic for their application in wildlife management. Options for improving power include increasing the sampling effort or arbitrarily relaxing the type I error rate. We present an alternative, whereby targeted sampling of particular habitats in the landscape using information from a habitat model increases power. The advantage of this approach is that it does not require a trade-off with either cost or the Pr{type I error} to achieve greater power. We use a demographic model of koala (Phascolarctos cinereus) population dynamics and simulations of the monitoring process to estimate the power to detect a trend in occupancy for a range of strategies, thereby demonstrating that targeting particular habitat qualities can improve power substantially. If the objective is to detect a decline in occupancy, the optimal strategy is to sample high-quality habitats. Alternatively, if the objective is to detect an increase in occupancy, the optimal strategy is to sample intermediate-quality habitats. The strategies with the highest power remained the same under a range of parameter assumptions, although observation error had a strong influence on the optimal strategy. Our approach specifically applies to monitoring for detecting long-term trends in occupancy or abundance. This is a common and important monitoring objective for wildlife managers, and we provide guidelines for more effectively achieving it.
|
|
| 5. |
- Bodger, K., et al.
(författare)
-
Altered colonic glycoprotein expression in unaffected monozygotic twins of inflammatory bowel disease patients
- 2006
-
Ingår i: Gut. - : BMJ. - 0017-5749 .- 1468-3288. ; 55:7, s. 973-977
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND AIMS: Previous chromatographic analysis of colonic mucins from monozygotic twins with inflammatory bowel disease (IBD) suggested a genetic mucin alteration in ulcerative colitis (UC). This study explores this further by assessing mucosal expression of the oncofetal carbohydrate antigen TF (galactose beta1, 3 N-acetylgalactosamine alpha-), among the same IBD twins. MATERIALS AND METHODS: Formalin fixed paraffin embedded rectal biopsies were studied from 22 monozygotic twin pairs with IBD. These included eight UC twin pairs and 14 Crohn's disease (CD) twin pairs, with six pairs concordant for disease and 16 unaffected twin siblings. Closely adjacent sections were assessed by peanut lectin histochemistry for TF expression and immunohistochemically for nuclear factor kappaB (NFkappaB) activation with investigators blinded to the diagnosis. RESULTS: Unaffected twins were almost all TF positive (15/16) compared with 5/29 histologically normal controls (p<0.0001). Unaffected UC (7/8) and CD twins (8/8) were similarly TF positive. TF positivity was confined mainly to the superficial epithelium and absent from the stem cell compartment of the lower crypts, suggesting that glycosylation changes are acquired rather than genetically determined. Activated NFkappaB was present in the surface epithelium of mucosal biopsies from 13/14 unaffected IBD twins but in only 6/22 histologically normal controls (p=0.0004). All 22 affected IBD twins were TF positive and 18 were positive for activated NFkappaB. CONCLUSIONS: Altered mucosal glycosylation in unaffected identical twins of IBD patients was confirmed in this study. This occurred in both UC and CD twins. The changes are probably acquired rather than congenital and may reflect "preinflammatory" NFkappaB activation.
|
|
| 6. |
- Han, Shizhong, et al.
(författare)
-
Evaluation of imputation-based association in and around the integrin-alpha-M (ITGAM) gene and replication of robust association between a non-synonymous functional variant within ITGAM and systemic lupus erythematosus (SLE)
- 2009
-
Ingår i: Human Molecular Genetics. - : Oxford University Press (OUP). - 0964-6906 .- 1460-2083. ; 18:6, s. 1171-1180
-
Tidskriftsartikel (refereegranskat)abstract
- We recently identified a novel non-synonymous variant, rs1143679, at exon 3 of the ITGAM gene associated with systemic lupus erythematosus (SLE) susceptibility in European-Americans (EAs) and African-Americans. Using genome-wide association approach, three other studies also independently reported an association between SLE susceptibility and ITGAM or ITGAM-ITGAX region. The primary objectives of this study are to assess whether single or multiple causal variants from the same gene or any nearby gene(s) are involved in SLE susceptibility and to confirm a robust ITGAM association across nine independent data sets (n = 8211). First, we confirmed our previously reported association of rs1143679 (risk allele 'A') with SLE in EAs (P = 1.0 x 10(-8)) and Hispanic-Americans (P = 2.9 x 10(-5)). Secondly, using a comprehensive imputation-based association test, we found that ITGAM is one of the major non-human leukocyte antigen susceptibility genes for SLE, and the strongest association for EA is the same coding variant rs1143679 (log(10)Bayes factor=20, P = 6.17 x 10(-24)). Thirdly, we determined the robustness of rs1143679 association with SLE across three additional case-control samples, including UK (P = 6.2 x 10(-8)), Colombian (P = 3.6 x 10(-7)), Mexican (P = 0.002), as well as two independent sets of trios from UK (P(TDT) = 1.4 x 10(-5)) and Mexico (P(TDT) = 0.015). A meta-analysis combing all independent data sets greatly reinforces the association (P(meta) = 7.1 x 10(-50), odds ratio = 1.83, 95% confidence interval = 1.69-1.98, n = 10 046). However, this ITGAM association was not observed in the Korean or Japanese samples, in which rs1143679 is monomorphic for the non-risk allele (G). Taken together along with our earlier findings, these results demonstrate that the coding variant, rs1143679, best explains the ITGAM-SLE association, especially in European- and African-derived populations, but not in Asian populations.
|
|
| 7. |
- Jonzén, Niclas, et al.
(författare)
-
Trend detection in source-sink systems: when should sink habitats be monitored?
- 2005
-
Ingår i: Ecological Applications. - : Wiley. - 1051-0761. ; 15:1, s. 326-334
-
Tidskriftsartikel (refereegranskat)abstract
- We determine the power of population monitoring in source or sink habitat to detect declining reproductive success in source habitat using a stochastic population model. The relative power to detect a trend in the source by monitoring either the source or the sink Varies with life history parameters, environmental stochasticity, and observation uncertainty. The power to detect a decline monitoring either source or sink habitat is maximized when the reproductive surplus in the source is low. The power to detect a decline by monitoring the sink increases with increasing reproductive deficit in the sink. If environmental stochasticity in the source increases, the power in the sink goes down due to a lower signal-to-noise ratio. However, the power in the sink increases if environmental stochasticity is increased further, because increasing stochasticity reduces the geometric mean growth rate in the source. Intriguingly, it is often most efficient to monitor the sink even though the actual reproductive decline occurs in the source. If reproductive success is declining in both habitats, censusing the sink will always have higher power. However, the probability of Type 1 error is always higher in the sink. Our results clearly have implications for optimal population monitoring in source-sink landscapes.
|
|
| 8. |
- McGrath, Patrick J., et al.
(författare)
-
Core outcome domains and measures for pediatric acute and chronic/recurrent pain clinical trials : PedIMMPACT recommendations
- 2008
-
Ingår i: Journal of Pain. - : Elsevier BV. - 1526-5900 .- 1528-8447. ; 9:9, s. 771-83
-
Tidskriftsartikel (refereegranskat)abstract
- Under the auspices of the Initiative on Methods, Measurement, and Pain Assessment in Clinical Trials (IMMPACT), 26 professionals from academia, governmental agencies, and the pharmaceutical industry participated in a 2-stage Delphi poll and a consensus meeting that identified core outcome domains and measures that should be considered in clinical trials of treatments for acute and chronic pain in children and adolescents. Consensus was refined by consultation with the international pediatric pain community through announcement of our recommendations on the Pediatric Pain List and inviting and incorporating comments from external sources. There was consensus that investigators conducting pediatric acute pain clinical trials should consider assessing outcomes in pain intensity; global judgment of satisfaction with treatment; symptoms and adverse events; physical recovery; emotional response; and economic factors. There was also agreement that investigators conducting pediatric clinical trials in chronic and recurrent pain should consider assessing outcomes in pain intensity; physical functioning; emotional functioning; role functioning; symptoms and adverse events; global judgment of satisfaction with treatment; sleep; and economic factors. Specific measures or measurement strategies were recommended for different age groups for each domain. PERSPECTIVE: Based on systematic review and consensus of experts, core domains and measures for clinical trials to treat pain in children and adolescents were defined. This will assist in comparison and pooling of data and promote evidence-based treatment, encourage complete reporting of outcomes, simplify the review of proposals and manuscripts, and facilitate clinicians making informed decisions regarding treatment.
|
|
| 9. |
|
|
| 10. |
|
|
