| 1. |
- Clegg, Sue, 1952-, et al.
(författare)
-
The emperor's new clothes : globalisation and e-learning in higher education
- 2003
-
Ingår i: British Journal of Sociology of Education. - Basingstoke : Carfax Publishing. - 0142-5692 .- 1465-3346. ; 24:1, s. 39-53
-
Tidskriftsartikel (refereegranskat)abstract
- Two closely related and over-determining myths have shaped government inspired policy towards Information and Communication Technologies (ICTs) and education: the one is the irresistible power of globalisation, the other is the determining effect of technology. The result of both is to present the acceptance of e-learning throughout the education system as inevitable. The space left for practitioners in Higher Education is either to embrace the new media enthusiastically or to stand aside and watch its inevitable unfolding. In this paper we develop a critical stance towards the dominant discourse and suggest that the shape of new media in education can be, and is being contested. We argue against both technological determinism and the passive acceptance of the neo-liberal globalisation paradigm. No technologies are neutral. They are always the products of real historical social relations as well as the emergent technical capacities they provide. ICTs as artefacts and social processes are already inscribed with gendered assumptions and the accumulation strategies of their purveyors. Moreover, the conditions under which e-learning is being introduced into education are shaped by managerialist agendas. Placing pedagogy at the forefront is therefore to struggle over the terms and shape of the media adopted. We can see this at both the micro and macro level. Our paper exposes the emperor's new clothes while arguing that there is space for critical discourses that can more meaningfully engage with socially available technologies.
|
|
| 2. |
|
|
| 3. |
- McCaddon, Andrew, et al.
(författare)
-
Transcobalamin polymorphism and serum holo-transcobalamin in relation to Alzheimer's disease
- 2004
-
Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 17:3, s. 215-221
-
Tidskriftsartikel (refereegranskat)abstract
- Isoforms of the vitamin B<sub>12</sub> carrier protein transcobalamin (TC) might influence its cellular availability and contribute to the association between disrupted single-carbon metabolism and Alzheimer’s disease (AD). We therefore investigated the relationships between the TC 776C>G (Pro259Arg) genetic polymorphism, total serum cobalamin and holo-TC levels, and disease onset in 70 patients with clinically diagnosed AD and 74 healthy elderly controls. TC 776C>G polymorphism was also determined for 94 histopathologically confirmed AD patients and 107 controls. Serum holo-TC levels were significantly higher in TC 776C homozygotes (p = 0.04). Kaplan-Meier survival functions differed between homozygous genotypes (Cox’s F-Test F(42, 46) = 2.1; p = 0.008) and between 776C homozygotes and heterozygotes (Cox’s F test F(46, 108) = 1.7; p = 0.02). Proportionately fewer TC 776C homozygotes appear to develop AD at any given age, but this will require confirmation in a longitudinal study.
|
|
| 4. |
- Rioux, John D., et al.
(författare)
-
Genetic variation in the 5q31 cytokine gene cluster confers susceptibility to Crohn disease
- 2001
-
Ingår i: Nature Genetics. - : Nature Publishing Group. - 1061-4036 .- 1546-1718. ; 29:2, s. 223-228
-
Tidskriftsartikel (refereegranskat)abstract
- Linkage disequilibrium (LD) mapping provides a powerful method for fine-structure localization of rare disease genes, but has not yet been widely applied to common disease1. We sought to design a systematic approach for LD mapping and apply it to the localization of a gene (IBD5) conferring susceptibility to Crohn disease. The key issues are: (i) to detect a significant LD signal (ii) to rigorously bound the critical region and (iii) to identify the causal genetic variant within this region. We previously mapped the IBD5 locus to a large region spanning 18 cM of chromosome 5q31 (P<10−4). Using dense genetic maps of microsatellite markers and single-nucleotide polymorphisms (SNPs) across the entire region, we found strong evidence of LD. We bound the region to a common haplotype spanning 250 kb that shows strong association with the disease (P<2×10−7) and contains the cytokine gene cluster. This finding provides overwhelming evidence that a specific common haplotype of the cytokine region in 5q31 confers susceptibility to Crohn disease. However, genetic evidence alone is not sufficient to identify the causal mutation within this region, as strong LD across the region results in multiple SNPs having equivalent genetic evidence—each consistent with the expected properties of the IBD5 locus. These results have important implications for Crohn disease in particular and LD mapping in general.
|
|
| 5. |
|
|
| 6. |
- Stoka, Veronika, et al.
(författare)
-
Lysosomal protease pathways to apoptosis - Cleavage of Bid, not pro-caspases, is the most likely route
- 2001
-
Ingår i: Journal of Biological Chemistry. - 1083-351X. ; 276:5, s. 3149-3157
-
Tidskriftsartikel (refereegranskat)abstract
- We investigated the mechanism of lysosome-mediated cell death using purified recombinant pro-apoptotic proteins, and cell-free extracts from the human neuronal progenitor cell line NT2, Potential effectors were either isolated lysosomes or purified lysosomal proteases. Purified lysosomal cathepsins B, H, K, L, S, and X or an extract of mouse lysosomes did not directly activate either recombinant caspase zymogens or caspase zymogens present in an NT2 cytosolic extract to any significant extent. In contrast, a cathepsin L-related protease from the protozoan parasite Trypanosana cruzi, cruzipain, showed a measurable caspase activation rate. This demonstrated that members of the papain family can directly activate caspases but that mammalian lysosomal members of this family may have been negatively selected for caspase activation to prevent inappropriate induction of apoptosis, Given the lack of evidence for a direct role in caspase activation by lysosomal proteases, we hypothesized that an indirect mode of caspase activation may involve the Bcl-2 family member Bid. In support of this, Bid was cleaved in the presence of lysosomal extracts, at a site six residues downstream from that seen for pathways involving capase 8, Incubation of mitochondria with Bid that had been cleaved by lysosomal extracts resulted in cytochrome c release. Thus, cleavage of Bid may represent a mechanism by which proteases that have leaked from the lysosomes can precipitate cytochrome c release and subsequent caspase activation. This is supported by the finding that cytosolic extracts from mice ablated in the bid gene are impaired in the ability to release cytochrome c in response to lysosome extracts, Together these data suggest that Bid represents a sensor that allows cells to initiate apoptosis in response to widespread adventitious proteolysis.
|
|
