| 1. |
- Eklöf, Dan, 1964-
(författare)
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Upphovsrätt i konkurrens : särskilt om tvångslicensiering
- 2004
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Although copyright law, on the one hand, establishes far-reaching exclusive rights and institutes legal monopolies while antitrust law, on the other hand, curtails the undue exercise of market power, there is no fundamental incongruity between the two regimes. The general harmony does not, however, preclude the occasional existence of glaring dissonances. Tension does exist on the fringe. The thesis addresses the intersection of copyright and antitrust. More specifically it attempts to ascertain and clarify the circumstances under which a unilateral and unconditional refusal to license violates Article 82 of the EC Treaty, i.e. the provision on abuse of a dominant position, and its Swedish counterpart, Sect. 19 of the National Competition Act, and, consequently, when antitrust based compulsory licensing can be invoked. A general examination of the structure and purpose of copyright, the object of protection and its delimitations in favour of a competitive environment is carried out. The copyright regime’s own system of specific limitations and exceptions is also surveyed, as well as the possible introduction of a “fair use” provision in favour of competition.The methodology used in antitrust to estimate market power in relation to copyright is examined, as well as the prospects of successfully challenging an unconditional, unilateral refusal to license under the abuse of dominance provision. Particular emphasis is placed on the so-called “exceptional circumstances” test. The thesis also addresses the “false dichotomy” between an internal solution (within copyright law) and an external solution (antitrust intervention) to the competition problems caused by copyright. Since the problems vary in character and magnitude an “either… or” approach seems flawed. Instead, the use of both models, simultaneously applied, can be advocated.
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| 2. |
- Grigelioniene, Giedre, et al.
(författare)
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Mutations in short stature homeobox containing gene (SHOX) in dyschondrosteosis but not in hypochondroplasia
- 2000
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Ingår i: Human Genetics. - : Springer Science and Business Media LLC. - 0340-6717 .- 1432-1203. ; 107:2, s. 145-149
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Tidskriftsartikel (refereegranskat)abstract
- Dyschondrosteosis (DCO) and hypochondroplasia (HCH) are common skeletal dysplasias characterized by disproportionate short stature. The diagnosis of these conditions might be difficult to establish especially in early childhood. Point mutations and deletions of the short stature homeobox containing gene (SHOX) are detected in DCO and idiopathic short stature with some rhizomelic body disproportion, whereas mutations in the fibroblast growth factor receptor 3 (FGFR3) gene are found in 40-70% of HCH cases. In this study, we performed mutational analysis of the coding region of the SHOX gene in five DCO and 18 HCH patients, all of whom tested negative for the known HCH-associated FGFR3 mutations. The polymorphic CA-repeat analysis, direct sequencing and Southern blotting were used for detection of deletions and point mutations. The auxological and radiological phenotype of these patients was carefully determined. Three novel mutations in DCO patients were found: (1) a deletion of one base (de1272G) (according to GenBank accession nos. Y11536, Y11535), resulting in a premature stop codon at position 75 of the amino acid sequence; (2) the transversion C485G resulting in the substitution Leu132Val; and (3) the transversion G549T causing an Arg153Leu substitution. These substitutions segregate with the DCO phenotype and affect evolutionarily conserved homeodomain residues, based on a comparison of homeobox containing proteins in 13 species. Moreover, these changes were not found in 80 unrelated, unaffected individuals. This strongly suggests that these mutations are pathogenic. The phenotype of our patients with DCO and HCH varied from mild to severe shortness and body disproportion. These results further support clinical and genetic heterogeneity of dyschondrosteosis and hypochondroplasia.
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| 3. |
- Tentler, Dmitry, et al.
(författare)
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A microdeletion in 19q13.2 associated with mental retardation, skeletal malformations, and Diamond-Blackfan anaemia suggests a novel contiguous gene syndrome
- 2000
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Ingår i: Journal of Medical Genetics. - : BMJ. - 0022-2593 .- 1468-6244. ; 37:2, s. 128-131
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Tidskriftsartikel (refereegranskat)abstract
- Diamond-Blackfan anaemia (DBA) is a constitutional red blood cell hypoplasia which may be associated with a variety of developmental abnormalities. A gene for DBA was recently mapped to chromosome 19q13.2 and subsequently cloned. Analysis of 19q marker alleles in DNA of sporadic DBA cases showed de novo microdeletions in three patients also presenting with mental retardation. We have studied one of these patients and characterised the deletion by fluorescence in situ hybridisation (FISH) to extended DNA fibres. The deletion was shown to be continuous over a 3.2 Mb region and the fibre-FISH analysis showed both chromosomal breakpoints. In combination, the clinical and molecular findings suggest a contiguous gene syndrome with a gene locus for mental retardation and, probably, skeletal malformations included in the deletion.
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