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- Bonow, Johan M., et al.
(författare)
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A multi-disciplinary study of Phanerozoic landscape development in West Greenland
- 2007
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Ingår i: Geological Survey of Denmark and Greenland Bulletin: Review of Survey activities 2006. - 1604-8156. ; :13, s. 33-36
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Tidskriftsartikel (refereegranskat)abstract
- The western margin of the Greenland craton has been muchless stable in the Phanerozoic than previously thought. Thisnew insight has come from close integration of independentdata sets: geomorphological analysis of large-scale landscapes,apatite fission track analysis (AFTA), onshore and offshorestratigraphy and analysis of onshore fault and fracture sys -tems. Each data set records specific and unique parts of theevent chronology and is equally important to establish a con-sistent model. A key area for understanding the Mesozoic-Cenozoic landscape evolution and into the present is theuplifted part of the Nuussuaq Basin, where remnants of pla-nation surfaces cut across the Cretaceous to Eocene sedimen-tary and volcanic rocks. Our integrated analysis concludedthat the West Greenland mountains were formed by lateNeogene tectonic uplift (Fig. 1) and also provided newinsight into early Phanerozoic development. To understandour model, we present the different methods and the resultsthat can be deduced from them.
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| 2. |
- Sundberg, Erik, et al.
(författare)
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Systemic TNF blockade does not modulate synovial expression of the pro-inflammatory mediator HMGB1 in rheumatoid arthritis patients : a prospective clinical study
- 2008
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Ingår i: Arthritis Research & Therapy. - : Springer Science and Business Media LLC. - 1478-6362 .- 1478-6354. ; 10:2, s. R33-
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Tidskriftsartikel (refereegranskat)abstract
- Introduction High-mobility group box chromosomal protein 1 (HMGB1) has recently been identified as an endogenous mediator of arthritis. TNF and IL-1 beta, pivotal cytokines in arthritis pathogenesis, both have the ability to induce the release of HMGB1 from myeloid and dendritic cells. It was, therefore, decided to investigate whether treatment based on TNF blockade in rheumatoid arthritis (RA) affects the expression of synovial HMGB1. Methods Repeated arthroscopy-guided sampling of synovial tissue was performed in nine patients with RA before and nine weeks after initiation of anti-TNF mAb (infliximab) therapy. Synovial biopsy specimens were analysed for HMGB1 protein by immunohistochemical staining and for HMGB1 mRNA expression by real-time reverse transcriptase PCR (RT-PCR). Statistical evaluations were based on Wilcoxon's signed rank tests or Spearman rank sum tests. Results Aberrant, extranuclear HMGB1 and constitutive nuclear HMGB1 expression, with histological signs of inflammation, were evident in all biopsies obtained before infliximab therapy. Signs of inflammation were still evident in the second biopsies obtained nine weeks after initiation of infliximab therapy. The cytoplasmic and extracellular expression of HMGB1 decreased in five patients, remained unchanged in one patient and increased in three patients, making the overall change in HMGB1 protein expression not significant. No correlation between the clinical response, as measured by disease activity score calculated for 28 joints (DAS28) or the American College of Rheumatology response criteria (ACR 20, 50, and 70), and the direction of change of HMGB1 expression in individual patients could be discerned. In addition, infliximab therapy did not alter HMGB1 mRNA synthesis. Conclusion Pro-inflammatory HMGB1 expression during rheumatoid synovitis was not consistently influenced by TNF-blocking therapy with infliximab. This suggests that TNF is not the main inducer of extranuclear HMGB1 during synovitis and that HMGB1 may represent a TNF-independent molecule that could be considered as a possible target for future therapeutic intervention in RA.
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