| 1. |
- Dimov, Stefan S., et al.
(författare)
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4M Network of Excellence : Progress Report 2004-2006
- 2007
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Ingår i: 4M 2007. - Dunbeath : Whittles Publishing. - 9781904445531 - 9781420070040 ; , s. xvii-xxxi
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Konferensbidrag (refereegranskat)abstract
- The 4M Network of Excellence started on 1st October 2004. It is a consortium of 30 academic and research organisations that came together to form the network under the European Commission's 6th Framework Research Programme. The Network has developed a knowledge community in Micro- and Nano- Technology (MNT) for the batch-manufacture of microcomponents and devices in a variety of materials for future microsystems products, particularly in non-silicon materials. This paper gives an overview of the structure, operation and activity of the network since its inception, illustrating the network's progress towards its goals.
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| 2. |
- Dimov, Stefan S., et al.
(författare)
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4M Network of Excellence, Progress Report 2006-2008
- 2008
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Ingår i: 4M 2008. - Dunbeath : Whittles Publishing. - 9781904445760 ; , s. xv-xxxi
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Konferensbidrag (refereegranskat)abstract
- This report follows on from last year's "Progress Report 2004-2006" and gives an update on the continuing activities, such as the 4M Network cross-divisional projects and annual conference, as well as a description of the new activities in its third and forth year, such as the first 4M Summer School and Book Series. Finally, as the end of the funded lifetime of the network approaches the steps being taken to set up a 4M Association, which aims to create the organizational infrastructure to support the 4M Knowledge Community established in the last five years, are described.
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| 3. |
- Dimov, Stefan S., et al.
(författare)
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4M Network of Excellence, Progress report 2009
- 2009
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Ingår i: 4M/ICOMM 2009. ; , s. s.1-9
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Konferensbidrag (refereegranskat)abstract
- This paper gives a brief overview of the activities of the 4M Network of Excellence during the last nine months of its funded period. The 4M Divisions summarise their activity and outline their plans to continue to working together in future. Finally a summary of achievements during the whole lifetime of the Network is given
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| 4. |
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| 5. |
- Hoeche, Stefan, et al.
(författare)
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Matching Parton Showers and Matrix Elements
- 2005
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Ingår i: CERN Reports. - 0007-8328. - 9290832657 ; CERN-2005-014, s. 288-299
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- We compare different procedures for combining fixed-order tree-level matrix element generators with parton showers. We use the case of W-production at the Tevatron and the LHC to compare different implementations of the so-called CKKW scheme and one based on the so-called MLM scheme using different matrix element generators and different parton cascades. We find that although similar results are obtained in all cases, there are important differences.
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| 6. |
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| 7. |
- Namjou, Bahram, et al.
(författare)
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High-density genotyping of STAT4 reveals multiple haplotypic associations with systemic lupus erythematosus in different racial groups
- 2009
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Ingår i: Arthritis and Rheumatism. - : Wiley. - 0004-3591 .- 1529-0131. ; 60:4, s. 1085-1095
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: Systemic lupus erythematosus (SLE) is the prototypical systemic autoimmune disorder, with complex etiology and a strong genetic component. Recently, gene products involved in the interferon pathway have been under intense investigation in terms of the pathogenesis of SLE. STAT-1 and STAT-4 are transcription factors that play key roles in the interferon and Th1 signaling pathways, making them attractive candidates for involvement in SLE susceptibility. METHODS: Fifty-six single-nucleotide polymorphisms (SNPs) across STAT1 and STAT4 on chromosome 2 were genotyped using the Illumina platform, as part of an extensive association study in a large collection of 9,923 lupus patients and control subjects from different racial groups. DNA samples were obtained from the peripheral blood of patients with SLE and control subjects. Principal components analyses and population-based case-control association analyses were performed, and the P values, false discovery rate q values, and odds ratios with 95% confidence intervals were calculated. RESULTS: We observed strong genetic associations with SLE and multiple SNPs located within STAT4 in different ethnic groups (Fisher's combined P = 7.02 x 10(-25)). In addition to strongly confirming the previously reported association in the third intronic region of this gene, we identified additional haplotypic association across STAT4 and, in particular, a common risk haplotype that is found in multiple racial groups. In contrast, only a relatively weak suggestive association was observed with STAT1, probably due to its proximity to STAT4. CONCLUSION: Our findings indicate that STAT4 is likely to be a crucial component in SLE pathogenesis in multiple racial groups. Knowledge of the functional effects of this association, when they are revealed, might improve our understanding of the disease and provide new therapeutic targets.
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| 8. |
- Simon-Bouy, Brigitte, et al.
(författare)
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Hypophosphatasia: molecular testing of 19 prenatal cases and discussion about genetic counseling.
- 2008
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Ingår i: Prenatal diagnosis. - : Wiley. - 0197-3851 .- 1097-0223. ; 28:11, s. 993-8
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: We studied hypophosphatasia (HP) mutations in 19 cases prenatally detected by ultrasonography without familial history of HP. We correlated the mutations with the reported ultrasound signs, and discussed genetic counseling with regard to the particular dominantly inherited prenatal benign form of HP. METHOD: The coding sequence of the tissue nonspecific alkaline phosphatase (TNSALP) gene was analyzed by DNA sequencing, and 3D modeling was used to locate the mutated amino acids with regard to the functional domains of TNSALP. RESULTS: Although reported ultrasound signs were heterogeneous, two mutated alleles were found in 18 of the 19 cases studied, indicating recessive transmission of the disease. Functional domains of TNSALP were affected by 74% of missense mutations. In all the cases, including one with only a heterozygous mutation, molecular, biological, and familial data do not corroborate the hypothesis of prenatal benign HP. The mutation c.1133A>T observed in the prenatal benign form of HP and common in USA was not found in this series. CONCLUSION: The results point out the prenatally detectable allelic heterogeneity of HP. The nature of the detected mutations and the evidence of recessive inheritance do not support these cases being affected with prenatal benign HP.
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| 9. |
- Wassermann, Stella, et al.
(författare)
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p16INK4a is a beta-catenin target gene and indicates low survival in human colorectal tumors
- 2009
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Ingår i: Gastroenterology. - : Elsevier BV. - 0016-5085 .- 1528-0012. ; 136:1, s. 196-205.e2
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND & AIMS: Human colorectal carcinomas display an infiltrative front of invasion where tumor cells undergo an epithelomesenchymal transition associated with low survival. Epithelomesenchymal transition is regulated by a nuclear beta-catenin accumulation, and subsequently, activation of beta-catenin/TCF4 target genes similar to CYCLIN D(1). Unexpectedly, these tumor cells are characterized by low proliferation, which correlates with the expression of the cell cycle inhibitor p16(INK4A). Therefore, we investigated the molecular mechanism of the transcriptional regulation of p16(INK4A) in colorectal cancer and its correlation with survival. METHODS: Molecular biological techniques were used for investigating the transcriptional mechanisms of the p16(INK4A) gene regulation. Moreover, p16(INK4A) expression was correlated with the 10-year survival of patients with colorectal carcinomas. RESULTS: In colorectal carcinomas, expression of the p16(INK4A) gene is regulated by beta-catenin/TCF4 and correlates with low survival rates of patients with tumors displaying an infiltrative front of invasion. CONCLUSIONS: beta-catenin/TCF4 regulates cell cycle promoting (c-MYC, CYCLIN D(1)) and inhibiting genes (p16(INK4A)) at the same time in the mesenchymally differentiated tumor cells at the front of invasion. The function of p16(INK4A) seems to supersede in this context thus leading to low proliferation. Moreover, these tumor cells seem to govern the outcome of colorectal cancer independently of their proliferation.
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