| 1. |
- Lingois, P., et al.
(författare)
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Chemically induced residual stresses in dental composites
- 2003
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Ingår i: Journal of Materials Science. - 0022-2461 .- 1573-4803. ; 38:6, s. 1321-1331
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Tidskriftsartikel (refereegranskat)abstract
- In several European countries, dental composites are replacing mercury-containing amalgams as the most common restorative materials. One problem with dental composites is residual stresses which may lead to poor performance of the restoration. In the present study, a combined modeling and materials characterization approach is presented and predictions compare well with experimental data on residual stresses. The model takes stress relaxation into account through the complete relaxation time spectrum of the resin. The approach allows for detailed parametric studies where resin and composite composition as well as cure conditions may be tailored with respect to residual stress generation.
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| 2. |
- Lingois, Philippe, et al.
(författare)
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Chemically induced residual stresses in dental composites
- 2001
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Ingår i: Proceedings of the American Society for Composites sixteenth technical conference. - : CRC Press. - 1587160536
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Konferensbidrag (refereegranskat)abstract
- In several European countries, dental composites are replacing mercury-containing amalgams as the most common restorative materials. One problem with dental composites is residual stresses which may lead to poor performance of the restoration. In the present study, a combined modeling and materials characterization approach is presented and predictions are compared with experimental data on residual stresses. The model takes into account vitrification through stress relaxation and non-linear shrinkage models. The predictions show a good agreement with the experimental data, showing that the essential physics of the process is captured in the predictions. The approach allows for detailed parametric studies where resin and composite composition as well as cure conditions may be tailored with respect to residual stress generation.
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| 3. |
- Louka, A S, et al.
(författare)
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The IL12B gene does not confer susceptibility to coeliac disease.
- 2002
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Ingår i: Tissue antigens. - 0001-2815. ; 59:1, s. 70-2
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Tidskriftsartikel (refereegranskat)abstract
- Coeliac disease (CD) is a chronic inflammatory disorder where dietary gluten is not tolerated. In the lesion there are gluten reactive T cells predominantly secreting gamma-interferon. Both HLA and non-HLA genes contribute to CD susceptibility. Interleukin-12 (IL-12) regulates gamma-interferon production. The IL12B gene is located in a region (5q31.1-33.1) where there is evidence for linkage with CD. Allele 1 of an IL12B 3'UTR single-nucleotide polymorphism leads to increased expression of IL-12, and was recently implicated in susceptibility for type 1 diabetes (T1D). We found no evidence for association of allele 1 to CD by the transmission/disequilibrium test or case-control approach. No increased frequency was observed in patients belonging to families where the disease was linked to markers on chromosome 5q. Unlike T1D, allele 1 does not appear to confer susceptibility to CD.
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| 4. |
- Margaritte-Jeannin, P, et al.
(författare)
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HLA-DQ relative risks for coeliac disease in European populations: a study of the European Genetics Cluster on Coeliac Disease.
- 2004
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Ingår i: Tissue antigens. - : Wiley. - 0001-2815 .- 1399-0039. ; 63:6, s. 562-7
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Tidskriftsartikel (refereegranskat)abstract
- Coeliac disease is an enteropathy due to an intolerance to gluten. The association between HLA-DQ genes and CD is well established. The majority of patients carry the HLA-DQ heterodimer encoded by DQA1*05/DQB1*02, either in cis or in trans. The remaining patients carry either part of the DQ heterodimer or DQA1*03-DQB1*0302. The aim of the study was to estimate the risks associated with different DQ genotypes in European populations. HLA information was available for 470 trio families from four countries: France (117), Italy (128), and Norway and Sweden (225). Five DQA1-DQB1 haplotypes were considered and control haplotype frequencies were estimated from the set of parental haplotypes not transmitted to the affected child. The possible genotypes were grouped into five genotype groups, based on the hierarchy of risk reported in the literature. A north-south gradient in the genotype group frequencies is observed in probands: homogeneity is strongly rejected between all country pairs. For each country, the relative risks associated with each genotype group were computed taking into account the control haplotype frequencies. Homogeneity of relative risks between countries was tested pairwise by maximum likelihood ratio statistics. The hypothesis of homogeneity of relative risks is rejected (P is approximately 10(-6)) for all country pairs. In conclusion, the gradient in the genotype group frequencies in probands is not only due to differences in haplotype frequencies but also due to differences in genotype relative risks in the studied populations; the relative risks associated with each DQ genotype group are different between northern and southern European countries; neither are they ordered in the same way.
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