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  • Result 411-420 of 694
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411.
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412.
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413.
  • Jönsson, Robert, et al. (author)
  • Påverkan på bärighet hos torvjord vid inblandning av gjuterisand samt effekt på koldioxidemission ur marken
  • 2015
  • Reports (other academic/artistic)abstract
    • Odlade organogena jordar står för en betydande del av Sveriges utsläpp av växthusgaser. Att minska dessa utsläpp är mycket intressant och en möjlig åtgärd skulle kunna vara att höja grundvattenytan. När vattenhalten ökar i torvjordar fås dock stora bärighetsproblem vilket innebär att man inte kan använda tunga jordbruksmaskiner på dessa jordar. Sveriges gjuterier lägger varje år 77 000 ton sand på deponi, något som kan bli kostsamt om de i framtiden inte längre skulle vara befriade från att betala deponiskatt. Ett möjligt användningsområde för denna gjuterisand skulle kunna vara inblandning i torvjord då sandinblandning är en beprövad metod för att öka bärigheten i dessa jordar. På så sätt skulle man kunna höja grundvattenytan, vilket skulle minska koldioxidemissionen från dessa jordar, men ändå kunna fortsätta odla. Detta förutsatt att önskad effekt fås på bärigheten och att koldioxidemissionen inte ökar. I detta projekt undersöktes tre olika sandinblandningars effekt på bärighet och koldioxidemission från torv genom försök i labb och i fält. Koldioxidflöde och skjuvmotstånd mättes både i labb- och fältförsök. I fält mättes även spårdjup från cykel. De sandinblandningar som undersöktes var 13 %, 33 % och 46 %. Mätningarna i labb genomfördes på två olika dräneringsdjup, 20 och 40 cm. Cykelspårsmätningarna gav så osäkra resultat att det inte gick att dra några slutsatser utifrån dem. Skjuvtesterna i både labb och i fält visade att skjuvmotståndet ökade vid ökad sandinblandning vilket tyder på att bärigheten förbättrades. Koldioxidmätningarna i labb visade på en minskning av koldioxidemissionen när sand blandades in. Minskningen var ungefär lika stor för samtliga sandinblandningar. I resultaten från fältförsöken syns en kraftig ökning av koldioxidemission när gjuterisand blandats in, vilket berodde på att den sura torven reagerade med kalciumkarbonat i sanden. Den stora emissionen av koldioxid minskade efter ett par dagar och närmade sig efter en tid koldioxidemissionen för torv utan tillsats av gjuterisand. Då försöken i labb och i fält gav olika resultat är det svårt att dra någon riktig slutsats om vad som egentligen hände med koldioxidemissionen när torven blandades med gjuterisand. Inom tidsramen för detta experiment tyder dock inget på att koldioxidemissionen ökar på lång sikt.
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414.
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415.
  • Jönsson, Sverker, et al. (author)
  • Häktning får inte användas som ett universalmedel
  • 2014
  • In: Dagens Nyheter. - 1101-2447. ; , s. 5-5
  • Journal article (pop. science, debate, etc.)abstract
    • Under senare tid har det från olika håll påtalats att det finns allvarliga brister i det svenska häktningssystemet. Debatten har varit livlig och främst gällt det faktum att vi i svensk rätt inte har någon bortre gräns för hur lång tid en misstänkt kan vara häktad. Det har också hävdats att restriktionerna i samband med häktning ofta är alltför hårda och att de tillämpas på ett slentrianmässigt sätt. Man har särskilt uppmärksammat att sådana brister i systemet kan få allvarliga konsekvenser för bland annat personer med psykisk ohälsa och för unga som placeras i häkte. Denna omfattande kritik, som – i vart fall när det gäller de långa häktnings­tiderna – tycks vara samstämmig, har kommit från så vitt skilda håll som FN:s tortyrkommitté, företrädare för kriminalvården, advokatsamfundet och journalister. Häktningen är den mest ingripande tvångsåtgärd som står till buds vid en brottsutredning. Den bör användas med eftertänksamhet och i enlighet med tydligt uttalade syften. Häktning får inte användas som ett universalmedel för allehanda ändamål, låt vara att sådana ändamål i sig kan vara lovvärda. Det är därför viktigt att det avsätts resurser för att såväl forskare som lagstiftare ska kunna beredas tillfälle att finna lösningar på de uppmärksammade problemen.
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416.
  • Jönsson, Ulla-Britt, et al. (author)
  • A (G -> C) transversion in the 3 ' UTR of the human ECP (eosinophil cationic protein) gene correlates to the cellular content of ECP
  • 2006
  • In: Journal of Leukocyte Biology. - : Oxford University Press (OUP). - 0741-5400 .- 1938-3673. ; 79:4, s. 846-851
  • Journal article (peer-reviewed)abstract
    • Eosinophil cationic protein (ECP) is a cytotoxic protein produced by and secreted from human eosinophil granulocytes. ECP may be involved in the injury of epithelial cells in allergic diseases such as asthma. The objectives were to determine the prevalence of the ECP gene polymorphism 562(G > C) in apparently healthy subjects and subjects with allergy and relate the prevalence to clinical disease and to serum and cellular levels of ECP. The 562(G > C) ECP gene polymorphism was determined by gene sequencing of the ECP gene from DNA prepared from 163 apparently healthy subjects and 151 subjects with allergic and nonallergie asthma or other diseases. ECP was measured by a sensitive radioimmunoassay. A polymorphism was detected at position 562, which mapped to the 3' untranslated region (UTR) of the gene encoding the ECP (RNase 3). Sixty-nine percent of the population had the 562GG genotype and 4%, the 562CC genotype. The cellular content of ECP in peripheral blood cosinophid granulocytes was significantly lower in cells from subjects with the 562GC (4.6 +/- 1.5 mu g/10(6) eosinophils) and 562CC (3.2 +/- 0.7 mu g/10(6) eosinophils) genotypes as compared with those with the 562GG genotype (6. 0 +/- 1.9 mu g/10(6) eosinophils; P < 0.001). A close link was found to the 434(G > C) ECP gene polymorphism. Associations between the 562(G > C) polymorphism or haplotypes of the two polymorphisms to allergy were not found. The 562(G > C) polymorphism in the 3'-end of the UTR of the ECP gene may determine the ECP content in human eosinophils, but unlike the 434(G > C) polymorphism, the 562(G > C) polymorphism is not related to allergy.
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417.
  • Jönsson, Ulla-Britt, et al. (author)
  • Associations of ECP (eosinophil cationic protein)-gene polymorphisms to allergy, asthma, smoke habits and lung function in two Estonian and Swedish sub cohorts of the ECRHS II study
  • 2010
  • In: BMC Pulmonary Medicine. - : Springer Science and Business Media LLC. - 1471-2466. ; 10, s. 36-
  • Journal article (peer-reviewed)abstract
    • Background: The Eosinophil Cationic Protein (ECP) is a potent multifunctional protein. Three common polymorphisms are present in the ECP gene, which determine the function and production of the protein. The aim was to study the relationship of these ECP gene polymorphisms to signs and symptoms of allergy and asthma in a community based cohort (The European Community Respiratory Health Survey (ECRHS)).Methods: Swedish and Estonian subjects (n = 757) were selected from the larger cohort of the ECRHS II study cohort. The prevalence of the gene polymorphisms ECP434(G>C) (rs2073342), ECP562(G>C) (rs2233860) and ECP c.-38(A>C) (rs2233859) were analysed by DNA sequencing and/or real-time PCR and related to questionnaire-based information of allergy, asthma, smoking habits and to lung functions.Results: Genotype prevalence showed both ethnic and gender differences. Close associations were found between the ECP434(G>C) and ECP562(G>C) genotypes and smoking habits, lung function and expression of allergic symptoms. Non-allergic asthma was associated with an increased prevalence of the ECP434GG genotype. The ECP c.-38(A>C) genotypes were independently associated to the subject being atopic.Conclusion: Our results show associations of symptoms of allergy and asthma to ECP-genotypes, but also to smoking habits. ECP may be involved in impairment of lung functions in disease. Gender, ethnicity and smoking habits are major confounders in the evaluations of genetic associations to allergy and asthma.
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418.
  • Jönsson, Ulla-Britt, et al. (author)
  • Polymorphism of the eosinophil cationic protein-gene is related to the expression of allergic symptoms
  • 2002
  • In: Clinical and Experimental Allergy. - : Wiley. - 0954-7894 .- 1365-2222. ; 32:7, s. 1092-1095
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: We have found a polymorphism in the ECP (eosinophil cationic protein)-gene at position 434 according to GenBank accession number NM 002935. This polymorphism would cause the change of the amino acid arginine (base at position 434 is G) at position 97 to threonine (base at position 434 is C). OBJECTIVE: To investigate the prevalence of the ECP-polymorphism and to screen for disease associations. METHODS: DNA of 209 medical students and 76 asthmatic subjects was analysed. The 434 genotype in the ECP-gene was detected by cleavage of the amplified DNA sequence with the restriction enzyme PstI and analysis of the cleaved product by agarose gel electrophoresis. RESULTS: The prevalences of the polymorphism in the student population were 53%, 39% and 8% for the 434GG, the 434GC and the 434CC genotype, respectively, with allele frequencies of 72% (434G) and 28% (434C). Subjects reporting allergy had a higher prevalence of the 434G allele than non-allergic subjects (P = 0.0056). Of the students who were Phadiatop-positive and had allergic symptoms, 79% had the 434GG genotype, whereas the 434GC and 434CC genotypes were present in 82% of those who did not express allergic symptoms (P < 0.001). Among the 76 patients with asthma, patients with allergic asthma had a significantly higher proportion of 434GG compared with patients with non-allergic asthma (P = 0.04). None of the 18 subjects of the two groups with the 434CC genotype had allergy. CONCLUSION: The 434(G > C) polymorphism in the ECP-gene is related to the development of allergic symptoms, suggesting a central role for the ECP molecule in the process.
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419.
  • Jönsson, Ulla-Britt, et al. (author)
  • The production of the eosinophil proteins ECP and EPX/EDN are regulated in a reciprocal manner
  • 2014
  • In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS). - : Wiley. - 0903-4641 .- 1600-0463. ; 122:4, s. 283-291
  • Journal article (peer-reviewed)abstract
    • Previous studies showed that the biological activity and the eosinophil content of eosinophil cationic protein (ECP, RNase 3) are determined by single-nucleotide polymorphisms (SNPs) in the ECP (RNase3) gene. In this study, we report the prevalence of a common SNP in the eosinophil protein x/eosinophil-derived neurotoxin (EPX/EDN, RNase2) and the association with the cellular contents of EPX/EDN and ECP. The genes were sequenced and the EPX/EDN405(G>C) rs2013109 SNPs were also determined by TaqMan 5nuclease allelic discrimination assay. ECP and EPX/EDN in purified eosinophils or in whole blood extracts were analysed by sensitive immunoassays. The study included 379 non-allergic and allergic subjects. The genotype prevalence of the EPX/EDN405(G>C) polymorphism was GG 59%, GC 36% and CC 6%. The cellular contents of ECP and EPX/EDN were related in a reciprocal fashion with the sums of the protein contents being constant. The contents were associated with the ECP562(G>C) rs2233860 and EPX/EDN405(G>C) gene polymorphisms. The cellular content of eosinophil peroxidase (EPO) was not associated with the ECP and EPX/EDN genotypes. The prevalence of the EPX/EDN405(G>C) genotypes and the contents of the proteins were similar in non-allergic and allergic subjects. The production and storage of the two ancestral proteins, ECP and EPX/EDN likely share common regulatory mechanisms, which result in opposing productions of the two proteins.
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420.
  • Jönsson, Ulf, et al. (author)
  • MIPMANET-mobile IP for mobile ad hoc networks
  • 2000
  • In: 2000 First Annual Workshop on Mobile and Ad Hoc Networking and Computing (MobiHOC). - Boston, MA, USA. - 0780365348 ; , s. 75-85
  • Conference paper (peer-reviewed)abstract
    • Mobile ad hoc networking allows nodes to form temporary networks and communicate beyond the transmitter range by supporting multihop communication through IP routing. Routing in such networks is often reactive, i.e., performed on-demand, as opposed to Internet routing that is proactive. As ad hoc networks are formed on a temporary basis, any IP address should be allowed to appear in an ad hoc network. This paper presents MIPMANET, a solution for connecting an ad hoc network, in which on-demand routing is used, to the Internet. MIPMANET provides Internet access by using mobile IP with foreign agent care-of addresses and reverse tunneling. This allows nodes to enjoy the mobility services of mobile IP while at the same time the requirements on the ad hoc routing protocol are kept to a minimum. Simulations of MIPMANET have been performed in the Network Simulator 2. The ad hoc on-demand distance vector (AODV) routing protocol has been used for routing within the ad hoc network. These simulations show that the ability to choose the closest access point to the Internet is worth extra work, as less traffic is generated in the network resulting in lower delays and fewer dropped packets.
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  • Result 411-420 of 694
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journal article (463)
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peer-reviewed (483)
other academic/artistic (171)
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Author/Editor
Jönsson, Per (320)
Gaigalas, Gediminas (95)
Godefroid, Michel (64)
Ekman, Jörgen (37)
Froese Fischer, Char ... (36)
Li, Jiguang (32)
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Rynkun, Pavel (32)
Bieron, Jacek (29)
Brage, Tomas (26)
Eklundh, Lars (25)
Jönsson, Per-Anders (25)
Verdebout, Simon (22)
Jönsson, Peter (20)
Stichel, Sebastian (20)
Gaigalas, G. (20)
Wang, Kai (19)
Grumer, Jon (19)
Davidson, Per (19)
Jönsson, Göran B (18)
Planck, Maria (18)
Jönsson, Per-Ebbe (18)
Jirström, Karin (17)
Jönsson, Arne (16)
Staaf, Johan (16)
Hartman, Henrik (16)
Borgehammar, Stephan (15)
Gustafsson, Stefan (15)
Godefroid, M. (15)
Andersson, Martin (14)
Beskow, Per (14)
Johansson, Mikael (14)
Irestedt, Martin (14)
Hutton, Roger (14)
Brunnström, Hans (14)
Ericson, Per G P, 19 ... (13)
Jønsson, Knud A. (13)
Chen, C. Y. (13)
Carlsson, Ingegerd (13)
Li, Wenxian (13)
Borg, Åke (12)
Jönsson, Mats (12)
Zou, Yaming (12)
Fischer, Charlotte F ... (12)
Johansson, Leif (11)
Naze, Cedric (11)
Wang, K. (10)
Jönsson, Karin (10)
Jönsson, Bo A (10)
Jönsson, Birgitta (10)
Indelicato, Paul (10)
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