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| 2. |
- Dunham, I, et al.
(författare)
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The DNA sequence of human chromosome 22
- 1999
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 402:6761, s. 489-495
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Tidskriftsartikel (refereegranskat)
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| 5. |
- Cederwall, Bo, et al.
(författare)
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Collective rotational-vibrational transition in the very neutron-deficient nuclei (171,172)-Pt
- 1998
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Ingår i: Physics Letters B. - AMSTERDAM, NETHERLANDS : ELSEVIER SCIENCE. - 0370-2693 .- 1873-2445. ; 443:1-4, s. 69-76
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Tidskriftsartikel (refereegranskat)abstract
- Excited states have been identified for the first time in very neutron deficient Pt-171.172 nuclei using the recoil-or-decay tagging technique. The ground-state band in Pt-172 has been established up to I-pi = 8+. A similar level sequence, presumably built on the I-pi = 13/2(+) state, is observed for Pt-171. The data are compared with theoretical calculations based on the mean field approach and the random phase approximation and are put into the context of the systematics of platinum isotopes. (C) 1998 Elsevier Science B.V. All rights reserved.
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| 6. |
- King, S L, et al.
(författare)
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First observation of excited states in the neutron deficient nuclei (PT)-P-168 and Pt-170
- 1998
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Ingår i: Physics Letters B. - 0370-2693 .- 1873-2445. ; 443:1-4, s. 82-88
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Tidskriftsartikel (refereegranskat)abstract
- Excited states have been observed for the first time in (XPt)-X-168 and Pt-170 using the alpha-decay recoil-tagging technique. The trend of decreasing deformation moving away from the N = 104 mid-shell continues far Pt-170 but the structure of Pt-168 is significantly different. The low spin level energy systematics in Pt168-184 are presented and discussed within the framework of the interacting boson model. (C) 1998 Elsevier Science B.V. All rights reserved.
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| 7. |
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| 8. |
- Griffiths, PC, et al.
(författare)
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Role of copolymer architecture on adsorption at the solid/liquid interface
- 1998
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Ingår i: Langmuir. - 0743-7463 .- 1520-5827. ; 14, s. 1779-1785
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Tidskriftsartikel (refereegranskat)abstract
- The adsorption of monodisperse block copolymers comprising poly(ethylene oxide)-poly(butylene oxide) onto polystyrene latex from aqueous solution has been investigated by small-angle neutron scattering and photon correlation spectroscopy with particular reference to the role of molecular architecture. It appears that chain architecture is (i) a weak factor in the adsorption behavior when the hydrophobic block is located in the center of the polymer, since the triblock E100B15E100 behaved very similarly to the cyclic c-E200B15, but (ii) a significant factor when the hydrophobic block is located at the end of the copolymer chain, as shown by the more dense and thicker layer formed by E200B15 compared to the triblock E100B15E100. The hydrodynamic thickness of the layer formed by the small diblock E100B15 was approximately half that exhibited by the larger diblock E200B15. Good agreement was observed between depletion and SANS-derived adsorbed amounts. Theoretical predictions and self-consistent mean-field calculations of the adsorption also show excellent qualitative agreement with experiment.
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| 9. |
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| 10. |
- Johannsson, Oscar Thor, et al.
(författare)
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Founding BRCA1 Mutations in Hereditary Breast and Ovarian Cancer in Southern Sweden
- 1996
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Ingår i: American Journal of Human Genetics. - 0002-9297. ; 58:3, s. 441-450
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Tidskriftsartikel (refereegranskat)abstract
- Nine different germ-line mutations in the BRCA1 breast and ovarian cancer susceptibility gene were identified in 15 of 47 kindreds from southern Sweden, by use of SSCP and heteroduplex analysis of all exons and flanking intron region and by a protein-truncation test for exon 11, followed by direct sequencing. All but one of the mutations are predicted to give rise to premature translation termination and include seven frameshift insertions or deletions, a nonsense mutation, and a splice acceptor site mutation. The remaining mutation is a missense mutation (Cys61Gly) in the zinc-binding motif. Four novel Swedish founding mutations were identified: the nucleotide 2595 deletion A was found in five families, the C 1806 T nonsense mutation in three families, the 3166 insertion TGAGA in three families, and the nucleotide 1201 deletion 11 in two families. Analysis of the intragenic polymorphism D17S855 supports common origins of the mutations. Eleven of the 15 kindreds manifesting BRCA1 mutations were breast-ovarian cancer families, several of them with a predominant ovarian cancer phenotype. The set of 32 families in which no BRCA1 alterations were detected included 1 breast-ovarian cancer kindred manifesting clear linkage to the BRCA1 region and loss of the wild-type chromosome in associated tumors. Other tumor types found in BRCA1 mutation/haplotype carriers included prostatic, pancreas, skin, and lung cancer, a malignant melanoma, an oligodendroglioma, and a carcinosarcoma. In all, 12 of 16 kindreds manifesting BRCA1 mutation or linkage contained ovarian cancer, as compared with only 6 of the remaining 31 families (P < .001). The present study confirms the involvement of BRCA1 in disease predisposition for a subset of hereditary breast cancer families often characterized by ovarian cancers.
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