| 11. |
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| 12. |
- Wagner, W, et al.
(författare)
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Europe ambivalent on biotechnology
- 1997
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Ingår i: Nature. - London : Nature Publishing Group. - 0028-0836 .- 1476-4687. ; 387, s. 845-847
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Tidskriftsartikel (refereegranskat)abstract
- The Eurobarometer on Biotechnology (46.1) was conducted during October and November 1996. The survey conducted in each EU (European Union) country used a multi-stage random sampling procedure and provided a statistically representative sample of national residents aged 15 and over. The total sample within the EU was 16,246 respondents (about 1,000 per EU country). The survey questionnaire was designed by the authors as part of a larger study involving the comparative analysis of public perceptions, media coverage and public policy in relation to biotechnology from 1973 to the present.
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| 13. |
- Nishimoto, G, et al.
(författare)
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Arginine vasopressin stimulates phosphorylation of aquaporin-2 in rat renal tissue.
- 1999
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Ingår i: American Journal of Physiology. - 0002-9513 .- 2163-5773. ; 276:2 Pt 2, s. F254-9
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Tidskriftsartikel (refereegranskat)abstract
- Aquaporin-2 (AQP2), the protein that mediates arginine vasopressin (AVP)-regulated apical water transport in the renal collecting duct, possesses a single consensus phosphorylation site for cAMP-dependent protein kinase A (PKA) at Ser256. The aim of this study was to examine whether AVP, and other agents that increase cAMP levels, could stimulate the phosphorylation of AQP2 in intact rat renal tissue. Rat renal papillae were prelabeled with 32P and incubated with vehicle or drugs, and then AQP2 was immunoprecipitated. Two polypeptides corresponding to nonglycosylated (29 kDa) and glycosylated (35-48 kDa) AQP2 were identified by SDS-PAGE. AVP caused a time- and dose-dependent increase in phosphorylation of both glycosylated and nonglycosylated AQP2. The threshold dose for a significant increase in phosphorylation was 10 pM, which corresponds to a physiological serum concentration of AVP. Maximal phosphorylation was reached within 1 min of AVP incubation. This effect on AQP2 phosphorylation was mimicked by the vasopressin (V2) agonist, 1-desamino-[8-D-arginine]vasopressin (DDAVP), or forskolin. Two-dimensional phosphopeptide mapping indicated that AVP and forskolin stimulated the phosphorylation of the same site in AQP2. Immunoblot analysis using a phosphorylation state-specific antiserum revealed an increase in phosphorylation of Ser256 after incubation of papillae with AVP. The results indicate that AVP stimulates phosphorylation of AQP2 at Ser256 via activation of PKA, supporting the idea that this is one of the first steps leading to increased water permeability in collecting duct cells.
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| 14. |
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| 15. |
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| 16. |
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| 17. |
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| 18. |
- Agren, J, et al.
(författare)
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Aquaporin-1 and -3 in perinatal skin
- 1999
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Ingår i: PEDIATRIC RESEARCH. - : Springer Science and Business Media LLC. - 0031-3998 .- 1530-0447. ; 45:4, s. 47A-47A
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)
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| 19. |
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| 20. |
- 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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