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| 253. |
- Heymer, Emma J., et al.
(författare)
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Cumulative Absolute Risk of Subsequent Colorectal Cancer After Abdominopelvic Radiotherapy Among Childhood Cancer Survivors : A PanCareSurFup Study
- 2024
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Ingår i: Journal of Clinical Oncology. - 0732-183X. ; 42:3, s. 336-347
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE Childhood cancer survivors are at the risk of developing subsequent colorectal cancers (CRCs), but the absolute risks by treatment modality are uncertain. We quantified the absolute risks by radiotherapy treatment characteristics using clinically accessible data from a Pan-European wide case-control study nested within a large cohort of childhood cancer survivors: the PanCareSurFup Study. METHODS Odds ratios (ORs) from a case-control study comprising 143 CRC cases and 143 controls nested within a cohort of 69,460 survivors were calculated. These, together with standardized incidence ratios for CRC for this cohort and European general population CRC incidence rates and survivors' mortality rates, were used to estimate cumulative absolute risks (CARs) by attained age for different categories of radiation to the abdominopelvic area. RESULTS Overall, survivors treated with abdominopelvic radiotherapy treatment (ART) were three times more likely to develop a subsequent CRC than those who did not receive ART (OR, 3.1 [95% CI, 1.4 to 6.6]). For male survivors treated with ART, the CAR was 0.27% (95% CI, 0.17 to 0.59) by age 40 years, 1.08% (95% CI, 0.69 to 2.34) by age 50 years (0.27% expected in the general population), and 3.7% (95% CI, 2.36 to 7.80) by age 60 years (0.95% expected). For female survivors treated with ART, the CAR was 0.29% (95% CI, 0.18 to 0.62) by age 40 years, 1.03% (95% CI, 0.65 to 2.22) by age 50 years (0.27% expected), and 3.0% (95% CI, 1.91 to 6.37) by age 60 years (0.82% expected). CONCLUSION We demonstrated that by age 40 years survivors of childhood cancer treated with ART already have a similar risk of CRC as those age 50 years in the general population for whom population-based CRC screening begins in many countries. This information should be used in the development of survivorship guidelines for the risk stratification of survivors concerning CRC risk.
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| 256. |
- Holzapfel, Gerhard A., et al.
(författare)
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Layer-specific 3D residual deformations of human aortas with non-atherosclerotic intimal thickening
- 2007
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Ingår i: Annals of Biomedical Engineering. - : Springer Science and Business Media LLC. - 0090-6964 .- 1573-9686. ; 35:4, s. 530-545
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Tidskriftsartikel (refereegranskat)abstract
- Data relating to residual deformations in human arteries are scarce. In this paper we investigate three-dimensional residual deformations for intact strips and for their separate layers from human aortas in their passive state. From 11 abdominal aortas with identified anamnesis, 16 pairs of rings and axial strips were harvested, and the rings cut open. After 16 h images of the resulting geometries were recorded, and the strips were separated into their three layers; after another 6 h images were again recorded. Image processing and analysis was then used to quantify residual stretches and curvatures. For each specimen histological analysis established that the intima, media and adventitia were clearly separated, and the separation was atraumatic. Axial in situ stretches were determined to be 1.196 +/- 0.084. On separation, the strips from the adventitia and media shortened (between 4.03 and 8.76% on average), while the intimal strips elongated on average by 3.84% (circumferential) and 4.28% (axial) relative to the associated intact strips. After separation, the adventitia from the ring sprang open by about 180 degrees on average, becoming flat, the intima opened only slightly, but the media sprang open by more than 180 degrees (as did the intact strip). The adventitia and intima from the axial strips remained flat, while the media (and the intact strip) bent away from the vessel axis. This study has shown that residual deformations are three dimensional and cannot be described by a single parameter such as 'the' opening angle. Their quantification and modeling therefore require consideration of both stretching and bending, which are highly layer-specific and axially dependent.
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| 257. |
- Johansson, Daniel, 1980, et al.
(författare)
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Submillimeter galaxies behind the Bullet cluster (1E 0657-56)
- 2010
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Ingår i: Astronomy and Astrophysics. - : EDP Sciences. - 0004-6361 .- 1432-0746. ; 514:12
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Tidskriftsartikel (refereegranskat)abstract
- Context. Clusters of galaxies are effective gravitational lenses able to magnify background galaxies and making it possible to probe the fainter part of the galaxy population. Submillimeter galaxies, which are believed to be star-forming galaxies at typical redshifts of 2 to 3, are a major contaminant to the extended Sunyaev-Zeldovich (SZ) signal of galaxy clusters. For a proper quantification of the SZ signal the contribution of submillimeter galaxies needs to be quantified. Aims. The aims of this study are to identify submillimeter sources in the field of the Bullet cluster (1E 0657-56), a massive cluster of galaxies at z similar or equal to 0.3, measure their flux densities at 870 mu m, and search for counterparts at other wavelengths to constrain their properties. Methods. We carried out deep observations of the submillimeter continuum emission at 870 mu m using the Large APEX BOlometer CAmera (LABOCA) on the Atacama Pathfinder EXperiment (APEX) telescope. Several numerical techniques were used to quantify the noise properties of the data and extract sources. Results. In total, seventeen sources were found. Thirteen of them lie in the central 10 arcmin of the map, which has a pixel sensitivity of 1.2 mJy per 22 '' beam. After correction for flux boosting and gravitational lensing, the number counts are consistent with published submm measurements. Nine of the sources have infrared counterparts in Spitzer maps. The strongest submm detection coincides with a source previously reported at other wavelengths, at an estimated redshift z similar or equal to 2.7. If the submm flux arises from two images of a galaxy magnified by a total factor of 75, as models have suggested, its intrinsic flux would be around 0.6 mJy, consistent with an intrinsic luminosity below 10(12) L-circle dot.
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| 258. |
- Johnstone, Andrea L., et al.
(författare)
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Dysregulation of the histone demethylase KDM6B in alcohol dependence is associated with epigenetic regulation of inflammatory signaling pathways
- 2021
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Ingår i: Addiction Biology. - : WILEY. - 1355-6215 .- 1369-1600. ; 26:1
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Tidskriftsartikel (refereegranskat)abstract
- Epigenetic enzymes oversee long-term changes in gene expression by integrating genetic and environmental cues. While there are hundreds of enzymes that control histone and DNA modifications, their potential roles in substance abuse and alcohol dependence remain underexplored. A few recent studies have suggested that epigenetic processes could underlie transcriptomic and behavioral hallmarks of alcohol addiction. In the present study, we sought to identify epigenetic enzymes in the brain that are dysregulated during protracted abstinence as a consequence of chronic and intermittent alcohol exposure. Through quantitative mRNA expression analysis of over 100 epigenetic enzymes, we identified 11 that are significantly altered in alcohol-dependent rats compared with controls. Follow-up studies of one of these enzymes, the histone demethylase KDM6B, showed that this enzyme exhibits region-specific dysregulation in the prefrontal cortex and nucleus accumbens of alcohol-dependent rats. KDM6B was also upregulated in the human alcoholic brain. Upregulation of KDM6B protein in alcohol-dependent rats was accompanied by a decrease of trimethylation levels at histone H3, lysine 27 (H3K27me3), consistent with the known demethylase specificity of KDM6B. Subsequent epigenetic (chromatin immunoprecipitation [ChIP]-sequencing) analysis showed that alcohol-induced changes in H3K27me3 were significantly enriched at genes in the IL-6 signaling pathway, consistent with the well-characterized role of KDM6B in modulation of inflammatory responses. Knockdown of KDM6B in cultured microglial cells diminished IL-6 induction in response to an inflammatory stimulus. Our findings implicate a novel KDM6B-mediated epigenetic signaling pathway integrated with inflammatory signaling pathways that are known to underlie the development of alcohol addiction.
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