SwePub
Sök i SwePub databas

  Extended search

Träfflista för sökning "WFRF:(Hallgren Peter) "

Search: WFRF:(Hallgren Peter)

  • Result 1-10 of 24
Sort/group result
   
EnumerationReferenceCoverFind
1.
  • Aartsen, M. G., et al. (author)
  • The Detection Of A Sn Iin In Optical Follow-Up Observations Of Icecube Neutrino Events
  • 2015
  • In: Astrophysical Journal. - 0004-637X .- 1538-4357. ; 811:1
  • Journal article (peer-reviewed)abstract
    • The IceCube neutrino observatory pursues a follow-up program selecting interesting neutrino events in real-time and issuing alerts for electromagnetic follow-up observations. In 2012 March, the most significant neutrino alert during the first three years of operation was issued by IceCube. In the follow-up observations performed by the Palomar Transient Factory (PTF), a Type IIn supernova (SN IIn) PTF12csy was found 0.degrees 2 away from the neutrino alert direction, with an error radius of 0.degrees 54. It has a redshift of z = 0.0684, corresponding to a luminosity distance of about 300 Mpc and the Pan-STARRS1 survey shows that its explosion time was at least 158 days (in host galaxy rest frame) before the neutrino alert, so that a causal connection is unlikely. The a posteriori significance of the chance detection of both the neutrinos and the SN at any epoch is 2.2 sigma within IceCube's 2011/12 data acquisition season. Also, a complementary neutrino analysis reveals no long-term signal over the course of one year. Therefore, we consider the SN detection coincidental and the neutrinos uncorrelated to the SN. However, the SN is unusual and interesting by itself: it is luminous and energetic, bearing strong resemblance to the SN IIn 2010jl, and shows signs of interaction of the SN ejecta with a dense circumstellar medium. High-energy neutrino emission is expected in models of diffusive shock acceleration, but at a low, non-detectable level for this specific SN. In this paper, we describe the SN PTF12csy and present both the neutrino and electromagnetic data, as well as their analysis.
  •  
2.
  •  
3.
  •  
4.
  • Bertheim, Ulf, et al. (author)
  • Loss of hyaluronan in the basement membrane zone of the skin correlates to the degree of stiff hands in diabetes patients
  • 2002
  • In: Acta Dermato-Venereologica. - : Medical Journals Sweden AB. - 0001-5555 .- 1651-2057. ; 82:5, s. 329-334
  • Journal article (peer-reviewed)abstract
    • Glycosaminoglycans are important components of all extracellular matrices. One of the glycosaminoglycans is hyaluronan, which is ubiquitously distributed throughout the connective tissue. Hyaluronan is especially abundant in the skin, in which it is of both structural and functional importance. This study describes the localization and distribution of hyaluronan in the skin of healthy individuals and of 23 patients with insulin-dependent diabetes mellitus and various degrees of limited joint mobility. In normal skin, hyaluronan staining was seen in all layers but most prominently in the papillary dermis and the basement membrane zone. In the skin from diabetic patients with normal or only moderately restricted mobility of the hands (limited joint mobility grades 0 and 1), the distribution of hyaluronan was similar to that of normal skin. In the skin of patients with severe restriction in joint mobility (limited joint mobility grade 2) the staining pattern was significantly different with weak hyaluronan staining in the papillary dermis and the basement membrane zone almost devoid of hyaluronan. Moreover, an increased epidermal thickness in the latter patients was evident as well as a pronounced hyaluronan staining compared with normal epidermis.
  •  
5.
  • Bremer, Hanna, et al. (author)
  • ILF2 and ILF3 are autoantigens in canine systemic autoimmune disease
  • 2018
  • In: Scientific Reports. - : NATURE PUBLISHING GROUP. - 2045-2322. ; 8
  • Journal article (peer-reviewed)abstract
    • Dogs can spontaneously develop complex systemic autoimmune disorders, with similarities to human autoimmune disease. Autoantibodies directed at self-antigens are a key feature of these autoimmune diseases. Here we report the identification of interleukin enhancer-binding factors 2 and 3 (ILF2 and ILF3) as autoantigens in canine immune-mediated rheumatic disease. The ILF2 autoantibodies were discovered in a small, selected canine cohort through the use of human protein arrays; a method not previously described in dogs. Subsequently, ILF3 autoantibodies were also identified in the same cohort. The results were validated with an independent method in a larger cohort of dogs. ILF2 and ILF3 autoantibodies were found exclusively, and at a high frequency, in dogs that showed a speckled pattern of antinuclear antibodies on immunofluorescence. ILF2 and ILF3 autoantibodies were also found at low frequency in human patients with SLE and Sjogren's syndrome. These autoantibodies have the potential to be used as diagnostic biomarkers for canine, and possibly also human, autoimmune disease.
  •  
6.
  • Chester, Alan, et al. (author)
  • Biosynthesis of the blood-group-B-specific trisaccharide in a rhesus monkey
  • 1977
  • In: European Journal of Biochemistry. - 0014-2956. ; 77:1, s. 87-91
  • Journal article (peer-reviewed)abstract
    • A Rhesus monkey, serologically grouped as B, has been shown to excrete low-molecular-weight carbohydrate material in urine closely related to that found in human urine. Galactose feeding resulted in the excretion of a trisaccharide which was shown to be identical to the trisaccharide isolated from the urine of group B humans under the same conditions. Experiments in which [14C]galactose was administered both orally and via an intestinal vein demonstrated that the intestine is the site of biosynthesis.
  •  
7.
  • Chester, Alan, et al. (author)
  • Urinary excretion of oligosaccharides induced by galactose given orally or intravenously
  • 1979
  • In: European Journal of Biochemistry. - 0014-2956. ; 100:2, s. 385-392
  • Journal article (peer-reviewed)abstract
    • The effect of oral administration of galactose, lactose, and sucrose and intravenous injection of galactose on the urinary excretion of blood-group-active oligosaccharides has been studied. Galactose given either as the free sugar, a glycoside (lactose) or a constituent of normal diet was an absolute requirement for the formation and excretion of A-trisaccharide, B-trisaccharide and 2'-fucosylgalactose in blood group A, B and O(H) secretors, respectively. Great individual variation was seen in the amounts of galactose-dependent oligosaccharides excreted. Injection of galactose resulted in excretion of 3-59% of the amount of oligosaccharide formed after oral administration to the same individual. The mean ratio A-trisaccharide/B-trisaccharide was 2.7 in four blood-group-A1B secretors and 0.22 in three A2B secretors and can thus serve as a parameter for chemical differentiation between the two blood groups. The excretion of larger blood-group-active oligosaccharides, including the A-pentasaccharide, the B-pentasaccharide and lactodifucotetraose, that are normal components in urine from, respectively, starved A, B, and H secretors, was about the same after oral administration of galactose or lactose. The B-trisaccharide was the only oligosaccharide detected in plasma after oral galactose administration to a blood-group-B secretor individual. The concentration was 0.38 mg/l of plasma.
  •  
8.
  • Eriksson, Daniel, et al. (author)
  • Common genetic variation in the autoimmune regulator (AIRE) locus is associated with autoimmune Addison’s disease in Sweden
  • 2018
  • In: Scientific Reports. - : Nature Publishing Group. - 2045-2322. ; 8:1
  • Journal article (peer-reviewed)abstract
    • Autoimmune Addison's disease (AAD) is the predominating cause of primary adrenal failure. Despite its high heritability, the rarity of disease has long made candidate-gene studies the only feasible methodology for genetic studies. Here we conducted a comprehensive reinvestigation of suggested AAD risk loci and more than 1800 candidate genes with associated regulatory elements in 479 patients with AAD and 2394 controls. Our analysis enabled us to replicate many risk variants, but several other previously suggested risk variants failed confirmation. By exploring the full set of 1800 candidate genes, we further identified common variation in the autoimmune regulator (AIRE) as a novel risk locus associated to sporadic AAD in our study. Our findings not only confirm that multiple loci are associated with disease risk, but also show to what extent the multiple risk loci jointly associate to AAD. In total, risk loci discovered to date only explain about 7% of variance in liability to AAD in our study population. 
  •  
9.
  • Eriksson, D, et al. (author)
  • Extended exome sequencing identifies BACH2 as a novel major risk locus for Addison's disease
  • 2016
  • In: Journal of Internal Medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 286:6, s. 595-608
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: Autoimmune disease is one of the leading causes of morbidity and mortality worldwide. In Addison's disease, the adrenal glands are targeted by destructive autoimmunity. Despite being the most common cause of primary adrenal failure, little is known about its aetiology.METHODS: To understand the genetic background of Addison's disease, we utilized the extensively characterized patients of the Swedish Addison Registry. We developed an extended exome capture array comprising a selected set of 1853 genes and their potential regulatory elements, for the purpose of sequencing 479 patients with Addison's disease and 1394 controls.RESULTS: We identified BACH2 (rs62408233-A, OR = 2.01 (1.71-2.37), P = 1.66 × 10(-15) , MAF 0.46/0.29 in cases/controls) as a novel gene associated with Addison's disease development. We also confirmed the previously known associations with the HLA complex.CONCLUSION: Whilst BACH2 has been previously reported to associate with organ-specific autoimmune diseases co-inherited with Addison's disease, we have identified BACH2 as a major risk locus in Addison's disease, independent of concomitant autoimmune diseases. Our results may enable future research towards preventive disease treatment.
  •  
10.
  •  
Skapa referenser, mejla, bekava och länka
  • Result 1-10 of 24
Type of publication
journal article (18)
reports (3)
conference paper (3)
Type of content
peer-reviewed (20)
other academic/artistic (4)
Author/Editor
Hallgren, Mats (5)
Andersson, Gunnar (4)
Andersson, Göran (3)
Lindblad-Toh, Kersti ... (3)
Rönnblom, Lars (3)
Sander, H. G. (2)
show more...
Richter, S. (2)
Bai, X. (2)
Kowalski, M. (2)
Barwick, S. W. (2)
Chirkin, D. (2)
Cowen, D. F. (2)
De Clercq, C. (2)
Desiati, P. (2)
DeYoung, T. (2)
Gaisser, T. K. (2)
Gerhardt, L. (2)
Goldschmidt, A. (2)
Gross, A. (2)
Halzen, F. (2)
Hanson, K. (2)
Helbing, K. (2)
Hultqvist, K. (2)
Karle, A. (2)
Madsen, J. (2)
Matis, H. S. (2)
Morse, R. (2)
Nahnhauer, R. (2)
Price, P. B. (2)
Przybylski, G. T. (2)
Rawlins, K. (2)
Resconi, E. (2)
Rhode, W. (2)
Schmidt, T. (2)
Spiczak, G. M. (2)
Stamatikos, M. (2)
Stokstad, R. G. (2)
Tilav, S. (2)
Walck, C. (2)
Wiebusch, C. H. (2)
Wissing, H. (2)
Yodh, G. (2)
Landegren, Nils, 198 ... (2)
Kämpe, Olle (2)
Pielberg, Gerli (2)
Tandre, Karolina (2)
Wennberg, Peter (2)
Dahlqvist, Per (2)
Ekwall, Olov, 1968 (2)
Rantapää-Dahlqvist, ... (2)
show less...
University
Karolinska Institutet (9)
Uppsala University (8)
Royal Institute of Technology (5)
Stockholm University (4)
The Swedish School of Sport and Health Sciences (4)
Umeå University (3)
show more...
Lund University (3)
Swedish University of Agricultural Sciences (3)
University of Gothenburg (2)
Örebro University (2)
Linköping University (2)
Chalmers University of Technology (1)
Linnaeus University (1)
show less...
Language
English (21)
Swedish (3)
Research subject (UKÄ/SCB)
Medical and Health Sciences (11)
Engineering and Technology (4)
Natural sciences (2)
Agricultural Sciences (1)
Social Sciences (1)
Humanities (1)

Year

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Close

Copy and save the link in order to return to this view