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- Alissa, S., et al.
(författare)
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Low bandwidth network-rtk correction dissemination for high accuracy maritime navigation
- 2021
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Ingår i: TransNav, International Journal on Marine Navigation and Safety of Sea Transportation. - : Faculty of Navigation, Gdynia Maritime University. - 2083-6473 .- 2083-6481. ; 15:1, s. 171-179
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Tidskriftsartikel (refereegranskat)abstract
- More than half of the incidents reported to EMSA relate to nautical events such as collision, groundings and contacts. Knowledge of accurate and high-integrity positioning is therefore not only a need for future automated shipping but a base for today’s safe navigation. Examples on accidents include Ever Given in the Suez Canal and HNoMS Helge Ingstad in Norway. A Network-RTK (NRTK) service can be used as an augmentation technique to improve performance of shipborne GNSS receivers for future positioning of manned and unmanned vessels in restricted areas, such as port areas, fairways, and inland water ways. NRTK service providers generate RTK corrections based on the observations of networks of GNSS reference stations which enables the users to determine their position with centimeter accuracy in real-time using a shipborne GNSS receiver. Selection of appropriate communication channels for dissemination of NRTK corrections data is the key to a secure positioning (localization) service. In PrePare-Ships project, the modern maritime communication system VDES (VHF Data Exchange System) is proposed to distribute SWEPOS (NRTK in Sweden) correction data to shipborne positioning modules. VDES is a very reliable technique and it is compatible with most onboard functionalities. In order to minimize the impact on the overall VDES data capacity in a local area, NRTK correction data shall only occupy a single VDES slot with a net capacity of 650 bytes. Update rates may vary but are preferably at 1Hz. However, NRTK correction data size changes instantly, depending on the number of visible GNSS satellites, and the data rate can therefore sometimes reach in excess of 1000 byte/s. In this study, a smart technique is proposed to reduce size of NRTK correction data to instantly adapt with the VDES requirements by choosing a combination of specific signals, satellites or even constellations such that the data rate is not more than 650 byte/s, and at the same time it achieves optimal positioning performance with the accuracy required by the PrePare-Ships project application.
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- Hensen, P, et al.
(författare)
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Association scan of the novel psoriasis susceptibility region on chromosome 19 : evidence for both susceptible and protective loci
- 2003
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Ingår i: Experimental dermatology. - : John Wiley & Sons. - 0906-6705 .- 1600-0625. ; 12:4, s. 490-496
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Tidskriftsartikel (refereegranskat)abstract
- To follow up the novel psoriasis susceptibility region on chromosome 19 (PSORS6), we performed an association scan for psoriasis vulgaris using 45 evenly spaced DNA microsatellite markers. For this study, a new independent sample of 210 nuclear psoriasis families (trio design) from Northern Germany was recruited. We used the family based association test (FBAT) for an association scan over the chromosome 19 region encompassing 50.8 cM. We obtained a positive association for the markers D19S922 (allele 5, P = 0.008) and D19S916 (allele 13, P = 0.016), which correspond to the peak of the region identified in a previously performed scan. We identified two novel regions by a single marker, each showing negative association at D19S917 on 19p13.1 (allele 8, P = 0.0034) and at D19S425 (allele 9, P = 0.0005), compatible with the hypothesis of protective loci. These two novel regions were explored in more detail using novel microsatellite markers at an average distance of 100 kb. A separate analysis distinguishing between familial (n = 137) and sporadic (n = 73) psoriasis families showed that the familial trios contribute strongly in the region around D19S425 (P = 0.004), while the comparably small subset of 73 sporadic trios has a stronger effect at the locus around D19S917 (P = 0.026). These studies confirm the existence of a psoriasis susceptibility locus on chromosome 19 and give first evidence for the existence of both susceptible and protective loci in this region. Analysis of a dense marker set from these refined regions will eventually allow identification of the underlying susceptibility alleles.
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- Hensen, P, et al.
(författare)
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Interleukin-10 promoter polymorphism IL10.G and familial early onset psoriasis
- 2003
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Ingår i: British Journal of Dermatology. - : John Wiley & Sons. - 0007-0963 .- 1365-2133. ; 149:2, s. 381-385
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The anti-inflammatory cytokine interleukin (IL)-10 is considered to play a major role in the pathophysiology of psoriasis, which is characterized by an IL-10 deficiency. Systemic administration of IL-10 has been shown to be an effective therapy for psoriasis. The IL-10 promoter region contains a highly polymorphic microsatellite (IL10.G) and in a recent case-control study the IL10.G13 (144 bp) allele was found to be associated with familial early onset psoriasis (type 1 psoriasis) having a susceptible effect.OBJECTIVES: As it is essential in multifactorial diseases to replicate findings before definite conclusions can be drawn, we decided to perform a follow-up study and to follow a genetic approach analysing allele transmission in families with a positive family history of psoriasis.METHODS: We studied 137 nuclear families (trio-design) comprising 456 individuals and genotyped the IL10.G marker. For comparison we also genotyped the microsatellite tn62 as a reference marker of the major psoriasis susceptibility locus on chromosome 6p21 (PSORS1). In the present study allele transmission was evaluated using the family-based association test (FBAT) and GENEHUNTER 2.0 based on the transmission/disequilibrium test.RESULTS: The G13 allele (144 bp) had a frequency of 24%, was present in 88 families and clearly showed an even transmission (FBAT, P = 0.753). In contrast, allele 3 (IL10.G9) (136 bp) had a frequency of 39%, was present in 110 families and was transmitted in 43 trios and remained untransmitted in 67 trios (FBAT, P = 0.026), thus showing preferential nontransmission. For the HLA-linked tn62-marker we obtained a P-value of 0.00027 for allele 4 in the same study group.CONCLUSIONS: In conclusion, we failed to confirm the susceptible effect of the G13 allele, but provide the first data for a protective effect of allele 3 (IL10.G9) for familial psoriasis. Our results suggest that the IL10.G polymorphism is not a major locus, but acts as a minor locus.
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