| 11. |
- Anders, Emma, et al.
(författare)
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Globular C1q receptor (p33) binds and stabilizes pro-inflammatory MCP-1 : a novel mechanism for regulation of MCP-1 production and function
- 2018
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Ingår i: Biochemical Journal. - 0264-6021. ; 475:4, s. 775-786
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Tidskriftsartikel (refereegranskat)abstract
- The protein gC1qR (globular C1q receptor), also named p33, was originally identified as a binding partner of the globular heads of C1q in the complement system. gC1qR/p33 is abundantly expressed in many cell types, but the functional importance of this protein is not completely understood. Here, we investigate the impact of gC1qR/p33 on the production and function of the pathophysiologically important chemokine monocyte chemoattractant protein-1 (MCP-1) and the underlying molecular mechanisms. Knockdown of gC1qR/p33 negatively regulated the production of MCP-1, but had no effect on the expression of transcript for MCP-1 in human periodontal ligament cells, suggesting a translational/post-translational mechanism of action. Laser scanning confocal microscopy showed considerable cytosolic co-localization of gC1qR/p33 and MCP-1, and co-immunoprecipitation disclosed direct physical interaction between gC1qR/p33 and MCP-1. Surface plasmon resonance analysis revealed a high-affinity binding (KD = 10.9 nM) between gC1qR/p33 and MCP-1. Using a transwell migration assay, we found that recombinant gC1qR/p33 enhances MCP-1-induced migration of human THP-1 monocytes, pointing to a functional importance of the interaction between gC1qR/p33 and MCP-1. An in vitro assay revealed a rapid turnover of the MCP-1 protein and that gC1qR/ p33 stabilizes MCP-1, hence preventing its degradation. We propose that endogenous gC1qR/p33 physically interacts with MCP-1 causing stabilization of the MCP-1 protein and stimulation of its activity in human periodontal ligament cells, suggesting a novel gC1qR/p33-mediated pro-inflammatory mechanism of action.
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| 12. |
- Barker-Ruchti, Natalie, 1971-, et al.
(författare)
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Don't buy a pig in a poke: Considering challenges of and problems with performance analysis technologies in Swedish men's elite football
- 2021
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Ingår i: Performance Enhancement and Health. - : Elsevier BV. - 2211-2669. ; 9:1
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Tidskriftsartikel (refereegranskat)abstract
- During the last decades, technologies to monitor, test and analyze athletes’ performance and health have rapidly developed. At present, global positioning systems (GPS), stadium camcorders, heart rate monitors and mobile applications are prominent performance analysis technologies (PATs) used in most elite sport environments. While PATs is understood as an aid, there is a growing body of literature that points to negative consequences. These negative consequences are concerning and call for research and measures to develop strategies for effective and productive implementation. To achieve this, this article first outlines key challenges and problems of PATs, using sport sociological research on coaching and athletes, historical knowledge of the scientization of training and the changing role of the coach, as well as scientific and experiential knowledge of performance analysis. Our findings show that key challenges and problems occur in a chain of six steps that concern the implementing of PATs: 1. Investment in PATs; 2. Production of performance data; 3. Interpretation of performance data; 4. Communication of performance data; 5. Decision-making based on performance data; and 6. Influence of PATs on coaches and athletes. The article then answers these challenges and problems by outlining recommendations for how sport managers and administrators can prevent buying “a pig in a poke” by acquiring competence about performance analysis and PATs, investing time, and developing effective communication between those working with PATs. © 2021 The Author(s)
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| 16. |
- Crouse, David F., et al.
(författare)
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The Set MHT
- 2011
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Ingår i: 14th International Conference on Information Fusion, Fusion 2011; Chicago, IL; 5 July 2011 through 8 July 2011. - 9781457702679
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Konferensbidrag (refereegranskat)abstract
- Abstract—We introduce the Set MHT, a tracking algorithmthat maintains multiple hypotheses and produces “smooth”estimates without the track coalescence often associated withMinimum Mean Squared Error (MMSE) estimation or thejitter associated with Maximum Likelihood (ML) estimation.It does this by utilizing Minimum Mean Optimal SubpatternAssignment (MMOSPA) estimation techniques coupled with atheoretically-grounded approach for probabilistically determiningthe identities of the state estimates. Unlike traditional MHTalgorithms, the Set MHT does not “forget” uncertainty in targetidentities, i.e. display an unjustifiably high confidence level inthe target identities, as a result of pruning out competinghypotheses. Rather, it uses merging techniques while avoiding theshortcomings of traditional Gaussian mixture reduction trackers.
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| 20. |
- Estrada, Karol, et al.
(författare)
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Genome-wide meta-analysis identifies 56 bone mineral density loci and reveals 14 loci associated with risk of fracture.
- 2012
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Ingår i: Nature genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 44:5, s. 491-501
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Tidskriftsartikel (refereegranskat)abstract
- Bone mineral density (BMD) is the most widely used predictor of fracture risk. We performed the largest meta-analysis to date on lumbar spine and femoral neck BMD, including 17 genome-wide association studies and 32,961 individuals of European and east Asian ancestry. We tested the top BMD-associated markers for replication in 50,933 independent subjects and for association with risk of low-trauma fracture in 31,016 individuals with a history of fracture (cases) and 102,444 controls. We identified 56 loci (32 new) associated with BMD at genome-wide significance (P < 5 × 10(-8)). Several of these factors cluster within the RANK-RANKL-OPG, mesenchymal stem cell differentiation, endochondral ossification and Wnt signaling pathways. However, we also discovered loci that were localized to genes not known to have a role in bone biology. Fourteen BMD-associated loci were also associated with fracture risk (P < 5 × 10(-4), Bonferroni corrected), of which six reached P < 5 × 10(-8), including at 18p11.21 (FAM210A), 7q21.3 (SLC25A13), 11q13.2 (LRP5), 4q22.1 (MEPE), 2p16.2 (SPTBN1) and 10q21.1 (DKK1). These findings shed light on the genetic architecture and pathophysiological mechanisms underlying BMD variation and fracture susceptibility.
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