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- Formicola, A, et al.
(författare)
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Astrophysical S-factor of 14N(p,γ)15O
- 2004
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Ingår i: Physics Letters B. - : Elsevier BV. - 0370-2693 .- 1873-2445. ; 591:1-2, s. 61-68
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Tidskriftsartikel (refereegranskat)abstract
- We report on a new measurement of the 14N(p,γ) 15O capture cross section at Ep=140 to 400 keV using the 400 kV LUNA accelerator facility at the Laboratori Nazionali del Gran Sasso (LNGS). The uncertainties have been reduced with respect to previous measurements and their analysis. We have analyzed the data using the R-matrix method and we find that the ground state transition accounts for about 15% of the total S-factor. The main contribution to the S-factor is given by the transition to the 6.79 MeV state. We find a total S(0)=1.7±0.2 keVb, in agreement with recent extrapolations. The result has important consequences for the solar neutrino spectrum as well as for the age of globular clusters. © 2004 Elsevier B.V. All rights reserved.
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| 2. |
- Imbriani, G., et al.
(författare)
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The bottleneck of CNO burning and the age of Globular Clusters
- 2004
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Ingår i: Astronomy and Astrophysics. - : EDP Sciences. - 0004-6361 .- 1432-0746. ; 420:2, s. 625-629
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Tidskriftsartikel (refereegranskat)abstract
- The transition between the Main Sequence and the Red Giant Branch in low mass stars is powered by the onset of CNO burning, whose bottleneck is 14N(p, γ) 15O. The LUNA collaboration has recently improved the low energy measurements of the cross section of this key reaction. We analyse the impact of the revised reaction rate on the estimate of the Globular Cluster ages, as derived from the turnoff luminosity. We found that the age of the oldest Globular Clusters should be increased by about 0.7-1 Gyr with respect to the current estimates.
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| 6. |
- Ropero, Santiago, et al.
(författare)
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Epigenetic loss of the familial tumor-suppressor gene exostosin-1 (EXT1) disrupts heparan sulfate synthesis in cancer cells.
- 2004
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Ingår i: Human molecular genetics. - : Oxford University Press (OUP). - 0964-6906 .- 1460-2083. ; 13:22, s. 2753-65
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Tidskriftsartikel (refereegranskat)abstract
- Germline mutations in the Exostoses-1 gene (EXT1) are found in hereditary multiple exostoses syndrome, which is characterized by the formation of osteochondromas and an increased risk of chondrosarcomas and osteosarcomas. However, despite its putative tumor-suppressor function, little is known of the contribution of EXT1 to human sporadic malignancies. Here, we report that EXT1 function is abrogated in human cancer cells by transcriptional silencing associated with CpG island promoter hypermethylation. We also show that, at the biochemical and cellular levels, the epigenetic inactivation of EXT1, a glycosyltransferase, leads to the loss of heparan sulfate (HS) synthesis. Reduced HS production can be reversed by the use of a DNA demethylating agent. Furthermore, the re-introduction of EXT1 into cancer cell lines displaying methylation-dependent silencing of EXT1 induces tumor-suppressor-like features, e.g. reduced colony formation density and tumor growth in nude mouse xenograft models. Screening a large collection of human cancer cell lines (n=79) and primary tumors (n=454) from different cell types, we found that EXT1 CpG island hypermethylation was common in leukemia, especially acute promyelocytic leukemia and acute lymphoblastic leukemia, and non-melanoma skin cancer. These findings highlight the importance of EXT1 epigenetic inactivation, leading to an abrogation of HS biosynthesis, in the processes of tumor onset and progression.
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