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- Larsson, Tore J, et al.
(författare)
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New technologies and work : Pulverization of risk - privatization of trauma?
- 2002
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Ingår i: Changing regulation. - Oxford : Emerald Group Publishing Limited. - 978008044 1269 ; , s. 15-30
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Bokkapitel (refereegranskat)abstract
- Synopsis Safety regulation is society's way of keeping the genie of technology in the bottle, whilst still exploiting its power for creating wealth and change. It is a difficult compromise to make. Regulators often have a thankless task. If all seems to go well they are painted as too repressive and anti-technological; if disaster strikes, the searchlight of media attention increasingly focuses on them, looking for lax enforcement, blind eyes being turned and cosy relations with the regulated. This title explores the dilemmas of the regulator through case studies presented by the regulators themselves and through research-based analyses from different disciplines of the workings of the regulators and the regulatory system. More importantly it surveys the tools available to resolve the dilemmas and asks what we know about their successes and shortcomings and what can be learned over the boundaries of industries and technologies about the principles of successful safety regulation. Chapters are written by authors from seven countries, with an international perspective. They examine the role of certification, safety cases, strictly enforced detailed rules, professional regulation and self-regulation. The text covers new risks such as those from medical devices and biotechnology, as well as the well-known fields of nuclear power, chemical plants, mining, oil and gas production, railways and the traditionally difficult area of small companies.
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| 2. |
- Eleme, K., et al.
(författare)
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Cell surface organization of stress-inducible proteins ULBP and MICA that stimulate human NK cells and T cells via NKG2D
- 2004
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Ingår i: Journal of Experimental Medicine. - : Rockefeller University Press. - 0022-1007 .- 1540-9538. ; 199:7, s. 1005-1010
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Tidskriftsartikel (refereegranskat)abstract
- Cell surface proteins major histocompatibility complex (MHC) class I-related chain A (MICA) and UL16-binding proteins (ULBP) 1, 2, and 3 are up-regulated upon infection or tumor transformation and can activate human natural killer (NK) cells. Patches of cross-linked raft resident ganglioside GM1 colocalized with ULBP1, 2, 3, or MICA, but not CD45. Thus, ULBPs and MICA are expressed in lipid rafts at the cell surface. Western blotting revealed that glycosylphosphatidylinositol (GPI)-anchored ULBP3 but not transmembrane MICA, MHC class I protein, or transferrin receptor, accumulated in detergent-resistant membranes containing GM1. Thus, MICA may have a weaker association with lipid rafts than ULBP3, yet both proteins accumulate at an activating human N-K cell immune synapse. Target cell lipid rafts marked by green fluorescent protein-tagged GPI also accumulate with ULBP3 at some synapses. Electron microscopy reveals constitutive clusters of ULBP at the cell surface. Regarding a specific molecular basis for the organization of these proteins, ULBP1, 2, and 3 and MICA are lipid modified. ULBP1, 2, and 3 are GPI anchored, and we demonstrate here that MICA is S-acylated. Finally, expression of a truncated form of MICA that lacks the putative site for S-acylation and the cytoplasmic tall can be expressed at the cell surface, but is unable to activate NK cells.
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| 3. |
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| 4. |
- Robinson, R, et al.
(författare)
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Several interacting genes influence the malignant hyperthermia phenotype
- 2003
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Ingår i: Human Genetics. - : Springer Science and Business Media LLC. - 1432-1203 .- 0340-6717. ; 112:2, s. 217-218
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Tidskriftsartikel (refereegranskat)abstract
- Malignant hyperthermia (MH), a potentially lethal disorder of skeletal muscle calcium homeostasis, manifests only on exposure to certain anaesthetic drugs. The mode of inheritance appears to be autosomal dominant with both locus and allelic heterogeneity having been reported. Association analysis of eight MH candidate loci in UK families has indicated that several genes influence susceptibility in individual families, rather than MH simply being a major gene defect. In support of this hypothesis, we present data on a replica analysis of an independent sample of European MH families.
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