uu.seUppsala universitets publikationer
Ändra sökning
Avgränsa sökresultatet
1234567 151 - 200 av 66176
RefereraExporteraLänk till träfflistan
Permanent länk
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Annat format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annat språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf
Träffar per sida
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sortering
  • Standard (Relevans)
  • Författare A-Ö
  • Författare Ö-A
  • Titel A-Ö
  • Titel Ö-A
  • Publikationstyp A-Ö
  • Publikationstyp Ö-A
  • Äldst först
  • Nyast först
  • Skapad (Äldst först)
  • Skapad (Nyast först)
  • Senast uppdaterad (Äldst först)
  • Senast uppdaterad (Nyast först)
  • Disputationsdatum (tidigaste först)
  • Disputationsdatum (senaste först)
  • Standard (Relevans)
  • Författare A-Ö
  • Författare Ö-A
  • Titel A-Ö
  • Titel Ö-A
  • Publikationstyp A-Ö
  • Publikationstyp Ö-A
  • Äldst först
  • Nyast först
  • Skapad (Äldst först)
  • Skapad (Nyast först)
  • Senast uppdaterad (Äldst först)
  • Senast uppdaterad (Nyast först)
  • Disputationsdatum (tidigaste först)
  • Disputationsdatum (senaste först)
Markera
Maxantalet träffar du kan exportera från sökgränssnittet är 250. Vid större uttag använd dig av utsökningar.
  • 151.
    Abelo, A
    et al.
    Uppsala universitet, Medicinska vetenskapsområdet, Farmaceutiska fakulteten, Institutionen för farmaceutisk biovetenskap.
    Holstein, B
    Eriksson, UG
    Gabrielsson, J
    Uppsala universitet, Medicinska vetenskapsområdet, Farmaceutiska fakulteten, Institutionen för farmaceutisk biovetenskap.
    Karlsson, MO
    Uppsala universitet, Medicinska vetenskapsområdet, Farmaceutiska fakulteten, Institutionen för farmaceutisk biovetenskap.
    Gastric acid secretion in the dog: a mechanism-based pharmacodynamic modelfor histamine stimulation and irreversible inhibition by omeprazole.2002Ingår i: J Pharmacokinet Pharmacodyn, Vol. 29, s. 365-Artikel i tidskrift (Refereegranskat)
  • 152.
    Abels, M.
    et al.
    Lund Univ, Ctr Diabet, Malmo, Sweden..
    Riva, M.
    Lund Univ, Ctr Diabet, Malmo, Sweden..
    Poon, W.
    Lund Univ, Ctr Diabet, Malmo, Sweden..
    Bennet, H.
    Lund Univ, Ctr Diabet, Malmo, Sweden..
    Nagaraj, V.
    Lund Univ, Ctr Diabet, Malmo, Sweden..
    Dyachok, Oleg
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk cellbiologi.
    Isomaa, B.
    Folkhalsan Res Ctr, Helsinki, Finland.;Dept Social Serv & Hlth Care, Jacobstad, Finland..
    Tuomi, T.
    Folkhalsan Res Ctr, Helsinki, Finland.;Dept Med, Helsinki, Finland..
    Ahren, B.
    Lund Univ, Ctr Diabet, Lund, Sweden..
    Tengholm, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk cellbiologi.
    Fex, M.
    Lund Univ, Ctr Diabet, Malmo, Sweden..
    Renstrom, E.
    Lund Univ, Ctr Diabet, Malmo, Sweden..
    Groop, L.
    Lund Univ, Ctr Diabet, Malmo, Sweden..
    Lyssenko, V.
    Lund Univ, Ctr Diabet, Malmo, Sweden..
    Wierup, N.
    Lund Univ, Ctr Diabet, Malmo, Sweden..
    CART is a novel glucose-dependent peptide with antidiabetic actions in humans2015Ingår i: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 58, nr Suppl. 1, s. S279-S280Artikel i tidskrift (Övrigt vetenskapligt)
  • 153.
    Abels, Mia
    et al.
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden..
    Riva, Matteo
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden..
    Bennet, Hedvig
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden..
    Ahlqvist, Emma
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden..
    Dyachok, Oleg
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk cellbiologi.
    Nagaraj, Vini
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden..
    Shcherbina, Liliya
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden..
    Fred, Rikard G.
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden..
    Poon, Wenny
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden..
    Sorhede-Winzell, Maria
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden..
    Fadista, Joao
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden..
    Lindqvist, Andreas
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden..
    Kask, Lena
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden..
    Sathanoori, Ramasri
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden..
    Dekker-Nitert, Marloes
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden..
    Kuhar, Michael J.
    Emory Univ, Yerkes Res Ctr, Atlanta, GA 30322 USA..
    Ahren, Bo
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden..
    Wollheim, Claes B.
    Univ Med Ctr, Dept Cell Physiol & Metab, Geneva, Switzerland..
    Hansson, Ola
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden..
    Tengholm, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk cellbiologi.
    Fex, Malin
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden..
    Renström, Erik
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden..
    Groop, Leif
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden..
    Lyssenko, Valeriya
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden.;Steno Diabet Ctr AS, Gentofte, Denmark..
    Wierup, Nils
    Lund Univ, Ctr Diabet, Skane Univ Hosp, Lund, Sweden.;Lund Univ, Ctr Diabet, Skane Univ Hosp, Malmo, Sweden.;Lund Univ, Clin Res Ctr 91 12, Ctr Diabet, Skane Univ Hosp,Dept Clin Sci Malmo,Unit Neuroend, Jan Waldenstroms Gata 35, S-20502 Malmo, Sweden..
    CART is overexpressed in human type 2 diabetic islets and inhibits glucagon secretion and increases insulin secretion2016Ingår i: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 59, nr 9, s. 1928-1937Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Aims/hypothesis Insufficient insulin release and hyperglucagonaemia are culprits in type 2 diabetes. Cocaine- and amphetamine-regulated transcript (CART, encoded by Cartpt) affects islet hormone secretion and beta cell survival in vitro in rats, and Cart(-/-) mice have diminished insulin secretion. We aimed to test if CART is differentially regulated in human type 2 diabetic islets and if CART affects insulin and glucagon secretion in vitro in humans and in vivo in mice. Methods CART expression was assessed in human type 2 diabetic and non-diabetic control pancreases and rodent models of diabetes. Insulin and glucagon secretion was examined in isolated islets and in vivo in mice. Ca2+ oscillation patterns and exocytosis were studied in mouse islets. Results We report an important role of CART in human islet function and glucose homeostasis in mice. CART was found to be expressed in human alpha and beta cells and in a subpopulation of mouse beta cells. Notably, CART expression was several fold higher in islets of type 2 diabetic humans and rodents. CART increased insulin secretion in vivo in mice and in human and mouse islets. Furthermore, CART increased beta cell exocytosis, altered the glucose-induced Ca2+ signalling pattern in mouse islets from fast to slow oscillations and improved synchronisation of the oscillations between different islet regions. Finally, CART reduced glucagon secretion in human and mouse islets, as well as in vivo in mice via diminished alpha cell exocytosis. Conclusions/interpretation We conclude that CART is a regulator of glucose homeostasis and could play an important role in the pathophysiology of type 2 diabetes. Based on the ability of CART to increase insulin secretion and reduce glucagon secretion, CART-based agents could be a therapeutic modality in type 2 diabetes.

  • 154.
    Abelson, Anna-Karin
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Genetic Risk Factors for Systemic Lupus Erythematosus: From Candidate Genes to Functional Variants2008Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
    Abstract [en]

    The aim of this thesis has been to identify genetic variants that increase the susceptibility for Systemic Lupus Erythematosus (SLE), an autoimmune disease caused by a complex interplay between various genetic and environmental factors.

    Five different candidate genes were selected through different strategies, and were analysed for association with SLE in an attempt to distinguish some of the underlying mechanisms of this disease. Two of these genes, PD-L1 and PD-L2, appeared not to contain any major risk factors for SLE in the analysed European and Latin American populations. In two other genes, CD24 and STAT4, there appeared to be population-specific effects. The A57V amino acid substitution in the CD24 gene, previously implicated with multiple sclerosis, was associated in a Spanish cohort, with a weak trend in German samples, and no association in Swedish. The previously reported and highly convincing association of the STAT4 transcription factor gene was confirmed in all our cohorts. Interestingly, the results indicate the presence of at least two independent risk variants: the first, represented by a previously reported SNP, was the strongest in individuals of Northern European ancestry, and the second was more pronounced in individuals from Southern Europe and Latin America. We also report the identification of a novel susceptibility gene. The BANK1 gene, encoding a scaffold protein involved in B-cell activation, contains functional variants affecting important domains, which are associated in all investigated cohorts from Europe and Latin America.

    These results confirm the existence of replicable associations between genetic variants and SLE, which are common and present in many populations. The results also illustrate a certain degree of heterogeneity, where some risk factors could have variable effect in different populations.

    Delarbeten
    1. No evidence of association between genetic variants of the PDCD1 ligands and SLE
    Öppna denna publikation i ny flik eller fönster >>No evidence of association between genetic variants of the PDCD1 ligands and SLE
    Visa övriga...
    2007 (Engelska)Ingår i: Genes and Immunity, ISSN 1466-4879, E-ISSN 1476-5470, Vol. 8, nr 1, s. 69-74Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    PDCD1, an immunoreceptor involved in peripheral tolerance has previously been shown to be genetically associated with systemic lupus erythematosus (SLE). PDCD1 has two ligands whose genes are located in close proximity on chromosome 9p24. Our attention was drawn to these ligands after finding suggestive linkage to a marker (gata62f03, Z=2.27) located close to their genes in a genome scan of Icelandic families multiplex for SLE. Here, we analyse Swedish trios (N=149) for 23 single nucleotide polymorphisms (SNPs) within the genes of the PDCD1 ligands. Initially, indication of association to eight SNPs was observed, and these SNPs were therefore also analysed in Mexican trios (N=90), as well as independent sets of patients and controls from Sweden (152 patients, 448 controls) and Argentina (288 patients, 288 controls). We do not find support for genetic association to SLE. This is the first genetic study of SLE and the PDCD1 ligands and the lack of association in several cohorts implies that these genes are not major risk factors for SLE.

    Nyckelord
    systemic lupus erythematosus, genetic association, linkage disequilibrium, autoimmunity, PD-L1, PD-L2
    Nationell ämneskategori
    Medicin och hälsovetenskap
    Identifikatorer
    urn:nbn:se:uu:diva-97760 (URN)10.1038/sj.gene.6364360 (DOI)000243783500009 ()17136123 (PubMedID)
    Tillgänglig från: 2008-11-14 Skapad: 2008-11-14 Senast uppdaterad: 2017-12-14Bibliografiskt granskad
    2. Association of a CD24 Gene Polymorphism with Susceptibility to Systemic Lupus Erythematosus
    Öppna denna publikation i ny flik eller fönster >>Association of a CD24 Gene Polymorphism with Susceptibility to Systemic Lupus Erythematosus
    Visa övriga...
    2007 (Engelska)Ingår i: Arthritis and Rheumatism, ISSN 0004-3591, E-ISSN 1529-0131, Vol. 56, nr 9, s. 3080-3086Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    Objective. To determine the potential role of the CD24 A57V gene polymorphism in systemic lupus erythematosus (SLE).

    Methods. We studied 3 cohorts of Caucasian patients and controls. The Spanish cohort included 696 SLE patients and 539 controls, the German cohort included 257 SLE patients and 317 controls, and the Swedish cohort included 310 SLE patients and 247 controls. The CD24 A57V polymorphism was genotyped by polymerase chain reaction, using a predeveloped TaqMan allele discrimination assay. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated.

    Results. In the Spanish cohort there was a statistically significant difference in the distribution of the CD24 V allele between SLE patients and controls (OR 3.6 [95% CI 2.13-6.16], P < 0.0001). In addition, frequency of the CD24 V/V genotype was increased in SLE patients compared with controls (OR 3.7 [95% CI 2.16-6.34], P < 0.00001). We sought to replicate this association with SLE in a German population and a Swedish population. A similar trend was found in the German group. The CD24 V/V genotype and the CD24 V allele were more frequent in SLE patients than in controls, although this difference was not statistically significant. No differences were observed in the Swedish group. A meta-analysis of the Spanish and German cohorts demonstrated that the CD24 V allele has a risk effect in SLE patients (pooled OR 1.25 [95% Cl 1.08-1.46], P = 0.003). In addition, homozygosity for the CD24 V risk allele significantly increased the effect (pooled OR 2.1,9 [95% Cl 1.50-3.22], P = 0.00007).

    Conclusion. These findings suggest that the CD24 A57V polymorphism plays a role in susceptibility to SLE in a Spanish population.

    Nyckelord
    Antigens; CD24/*genetics, Cohort Studies, Female, Genetic Predisposition to Disease, Humans, Lupus Erythematosus; Systemic/*genetics, Male, Polymorphism; Genetic
    Nationell ämneskategori
    Medicin och hälsovetenskap
    Identifikatorer
    urn:nbn:se:uu:diva-97761 (URN)10.1002/art.22871 (DOI)000249832600030 ()17763438 (PubMedID)
    Tillgänglig från: 2008-11-14 Skapad: 2008-11-14 Senast uppdaterad: 2017-12-14Bibliografiskt granskad
    3. Functional Variants in the B-Cell Gene BANK1 are Associated with Systemic Lupus Erythematosus
    Öppna denna publikation i ny flik eller fönster >>Functional Variants in the B-Cell Gene BANK1 are Associated with Systemic Lupus Erythematosus
    Visa övriga...
    2008 (Engelska)Ingår i: Nature Genetics, ISSN 1061-4036, E-ISSN 1546-1718, Vol. 40, nr 2, s. 211-216Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    Systemic lupus erythematosus (SLE) is a prototypical autoimmune disease characterized by production of autoantibodies and complex genetic inheritance(1-3). In a genome-wide scan using 85,042 SNPs, we identified an association between SLE and a nonsynonymous substitution (rs10516487, R61H) in the B-cell scaffold protein with ankyrin repeats gene, BANK1. We replicated the association in four independent case-control sets (combined P = 3.7 x 10(-10); OR = 1.38). We analyzed BANK1 cDNA and found two isoforms, one full-length and the other alternatively spliced and lacking exon 2 (Delta 2), encoding a protein without a putative IP3R-binding domain. The transcripts were differentially expressed depending on a branch point-site SNP, rs17266594, in strong linkage disequilibrium (LD) with rs10516487. A third associated variant was found in the ankyrin domain (rs3733197, A383T). Our findings implicate BANK1 as a susceptibility gene for SLE, with variants affecting regulatory sites and key functional domains. The disease-associated variants could contribute to sustained B cell-receptor signaling and B-cell hyperactivity characteristic of this disease.

    Nationell ämneskategori
    Medicin och hälsovetenskap
    Identifikatorer
    urn:nbn:se:uu:diva-97762 (URN)10.1038/ng.79 (DOI)000252732900020 ()
    Tillgänglig från: 2008-11-14 Skapad: 2008-11-14 Senast uppdaterad: 2017-12-14Bibliografiskt granskad
    4. STAT4 Associates with SLE through two independent effects that correlate with gene expression and act additively with IRF5 to increase risk
    Öppna denna publikation i ny flik eller fönster >>STAT4 Associates with SLE through two independent effects that correlate with gene expression and act additively with IRF5 to increase risk
    Visa övriga...
    2009 (Engelska)Ingår i: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 68, nr 11, s. 1746-1753Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    OBJECTIVES: To confirm and define the genetic association of STAT4 and systemic lupus erythematosus, investigate the possibility of correlations with differential splicing and/or expression levels, and genetic interaction with IRF5. METHODS: 30 tag SNPs were genotyped in an independent set of Spanish cases and controls. SNPs surviving correction for multiple tests were genotyped in 5 new sets of cases and controls for replication. STAT4 cDNA was analyzed by 5'-RACE PCR and sequencing. Expression levels were measured by quantitative PCR. RESULTS: In the fine-mapping, four SNPs were significant after correction for multiple testing, with rs3821236 and rs3024866 as the strongest signals, followed by the previously associated rs7574865, and by rs1467199. Association was replicated in all cohorts. After conditional regression analyses, two major independent signals represented by SNPs rs3821236 and rs7574865, remained significant across the sets. These SNPs belong to separate haplotype blocks. High levels of STAT4 expression correlated with SNPs rs3821236, rs3024866 (both in the same haplotype block) and rs7574865 but not with other SNPs. We also detected transcription of alternative tissue-specific exons 1, indicating presence of tissue-specific promoters of potential importance in the expression of STAT4. No interaction with associated SNPs of IRF5 was observed using regression analysis. CONCLUSIONS: These data confirm STAT4 as a susceptibility gene for SLE and suggest the presence of at least two functional variants affecting levels of STAT4. Our results also indicate that both genes STAT4 and IRF5 act additively to increase risk for SLE.

    Nationell ämneskategori
    Medicin och hälsovetenskap
    Identifikatorer
    urn:nbn:se:uu:diva-102290 (URN)10.1136/ard.2008.097642 (DOI)000270700900016 ()19019891 (PubMedID)
    Tillgänglig från: 2009-05-06 Skapad: 2009-05-06 Senast uppdaterad: 2017-12-13Bibliografiskt granskad
  • 155.
    Abelson, Anna-Karin
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Delgado-Vega, Angélica Maria
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Kozyrev, Sergey V.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Sánchez, Elena
    Velázquez-Cruz, Rafael
    Eriksson, Niclas
    Wojcik, Jerome
    Linga Reddy, Prasad
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Lima, Guadalupe
    D'Alfonso, Sandra
    Migliaresi, Sergio
    Baca, Vicente
    Orozco, Lorena
    Witte, Torsten
    Ortego-Centeno, Norberto
    Abderrahim, Hadi
    Pons-Estel, Bernardo A.
    Gutiérrez, Carmen
    Suárez, Ana
    González-Escribano, Maria Francisca
    Martin, Javier
    Alarcón-Riquelme, Marta E.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    STAT4 Associates with SLE through two independent effects that correlate with gene expression and act additively with IRF5 to increase risk2009Ingår i: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 68, nr 11, s. 1746-1753Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    OBJECTIVES: To confirm and define the genetic association of STAT4 and systemic lupus erythematosus, investigate the possibility of correlations with differential splicing and/or expression levels, and genetic interaction with IRF5. METHODS: 30 tag SNPs were genotyped in an independent set of Spanish cases and controls. SNPs surviving correction for multiple tests were genotyped in 5 new sets of cases and controls for replication. STAT4 cDNA was analyzed by 5'-RACE PCR and sequencing. Expression levels were measured by quantitative PCR. RESULTS: In the fine-mapping, four SNPs were significant after correction for multiple testing, with rs3821236 and rs3024866 as the strongest signals, followed by the previously associated rs7574865, and by rs1467199. Association was replicated in all cohorts. After conditional regression analyses, two major independent signals represented by SNPs rs3821236 and rs7574865, remained significant across the sets. These SNPs belong to separate haplotype blocks. High levels of STAT4 expression correlated with SNPs rs3821236, rs3024866 (both in the same haplotype block) and rs7574865 but not with other SNPs. We also detected transcription of alternative tissue-specific exons 1, indicating presence of tissue-specific promoters of potential importance in the expression of STAT4. No interaction with associated SNPs of IRF5 was observed using regression analysis. CONCLUSIONS: These data confirm STAT4 as a susceptibility gene for SLE and suggest the presence of at least two functional variants affecting levels of STAT4. Our results also indicate that both genes STAT4 and IRF5 act additively to increase risk for SLE.

  • 156. Abelson, Anna-Karin
    et al.
    Johansson, Cecilia
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Kozyrev, Sergey
    Alarcón-Riquelme, Marta
    The PD-1 Pathway in Systemic Lupus Erythematosus: The Ligands of PD-1, PD-L1 and PD-L2, are also Susceptibility FactorsManuskript (Övrigt vetenskapligt)
  • 157.
    Abelson, Anna-Karin
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Johansson, Cecilia M.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Kozyrev, Sergey V.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Kristjansdottir, Helga
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Gunnarsson, Iva
    Svenungsson, Elisabet
    Jönsen, Andreas
    Lima, Guadalupe
    Scherbarth, Hugo R
    Gamron, Susana
    Allievi, Alejandro
    Palatnik, Sergio A
    Alvarellos, Antonio
    Paira, Sergio
    Graf, Cesar
    Guillerón, Carlos
    Catoggio, Luis J
    Prigione, Carlos
    Battagliotti, Cesar G
    Berbotto, Guillermo A
    García, Mercedes A
    Perandones, Carlos E
    Truedsson, Lennart
    Steinsson, Kristjan
    Sturfelt, Gunnar
    Pons-Estel, Bernardo
    Alarcón-Riquelme, Marta E.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    No evidence of association between genetic variants of the PDCD1 ligands and SLE2007Ingår i: Genes and Immunity, ISSN 1466-4879, E-ISSN 1476-5470, Vol. 8, nr 1, s. 69-74Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    PDCD1, an immunoreceptor involved in peripheral tolerance has previously been shown to be genetically associated with systemic lupus erythematosus (SLE). PDCD1 has two ligands whose genes are located in close proximity on chromosome 9p24. Our attention was drawn to these ligands after finding suggestive linkage to a marker (gata62f03, Z=2.27) located close to their genes in a genome scan of Icelandic families multiplex for SLE. Here, we analyse Swedish trios (N=149) for 23 single nucleotide polymorphisms (SNPs) within the genes of the PDCD1 ligands. Initially, indication of association to eight SNPs was observed, and these SNPs were therefore also analysed in Mexican trios (N=90), as well as independent sets of patients and controls from Sweden (152 patients, 448 controls) and Argentina (288 patients, 288 controls). We do not find support for genetic association to SLE. This is the first genetic study of SLE and the PDCD1 ligands and the lack of association in several cohorts implies that these genes are not major risk factors for SLE.

  • 158. Abelson, K.
    et al.
    Jacobsen, K. R.
    Kalliokoski, O.
    Teilmann, C.
    Sundbom, Renée
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Försöksdjursvetenskap.
    Hau, J.
    Limitations of the Usefulness of Fecal Corticosterone as Biomarker for Stress in Mice2012Ingår i: Journal of the American Association for Laboratory Animal Science, ISSN 1559-6109, Vol. 51, nr 5, s. 639-639Artikel i tidskrift (Refereegranskat)
  • 159.
    Abelson, Klas
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap.
    Acetylcholine in Spinal Pain Modulation: An in vivo Study in the Rat2005Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
    Abstract [en]

    The spinal cord is an important component in the processing and modulation of painful stimuli. Nerve signals from the periphery are relayed and further conducted to the brain (nociception) in the spinal cord, and the most essential modulation of painful information (antinociception) occurs here. Several neurotransmitters are involved in spinal pain modulation, among them acetylcholine. However, the role of acetylcholine has previously been little investigated.

    In the present thesis, the acetylcholine release in the spinal cord was studied in vivo. By using spinal microdialysis on anaesthetised rats, the effects on the intraspinal acetylcholine release of various receptor ligands and analgesic agents were examined. This, together with pain behavioural tests and in vitro pharmacological assays, was used to evaluate the role of acetylcholine in spinal pain modulation. The four studies in this thesis resulted in the following conclusions:

    An increased release of spinal acetylcholine is associated with an elevated pain threshold, while a decreased acetylcholine release is associated with hyperalgesia, as seen after systemic treatment with a muscarinic agonist and an antagonist.

    Lidocaine is a potent analgesic when given systemically. It was found to produce an increase of intraspinal acetylcholine after intravenous injection of analgesic doses. This effect was attenuated after muscarinic, and abolished after nicotinic, receptor blockade.

    Various a2-adrenergic ligands, associated with nociceptive or antinociceptive effects, were found to affect intraspinal acetylcholine release via action on nicotinic receptors.

    Finally, the involvement of spinal acetylcholine in the analgesic effects of aspirin and paracetamol was examined. It was found that spinal acetylcholine could participate in the analgesic effects of aspirin, but not of paracetamol.

    The present thesis provides data that clearly demonstrate a relationship between intraspinal acetylcholine and antinociception, and elucidate interactions between acetylcholine and other mechanisms that mediate antinociception in the spinal cord.

    Delarbeten
    1. Intravenously administered oxotremorine and atropine, in doses known to affect pain threshold, affect the intraspinal release of acetylcholine in rats
    Öppna denna publikation i ny flik eller fönster >>Intravenously administered oxotremorine and atropine, in doses known to affect pain threshold, affect the intraspinal release of acetylcholine in rats
    2002 (Engelska)Ingår i: Pharmacology and Toxicology, ISSN 0901-9928, E-ISSN 1600-0773, Vol. 90, nr 4, s. 187-192Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    Abstract:Both systemically and intrathecally administered cholinergic agonists produce antinociception while cholinergic antagonists decrease pain threshold. The mechanism and the site of action of these substances are not known. In the present study it was hypothesized that systemically administered muscarinic agonists and antagonists modify nociceptive threshold by affecting intraspinal release of acetylcholine (ACh). Catheters were inserted into the femoral vein in rats maintained on isoflurane anaesthesia for administration of oxotremorine (10–300 μg/kg) and atropine (0.1, 10, 5000 μg/kg). Spinal microdialysis probes were placed intraspinally at approximately the C2–C5 spinal level for sampling of acetylcholine and dialysis delivery of atropine (0.1, 1, 10 nM). Additionally, the tail-flick behaviour was tested on conscious rats injected intraperitoneally with saline, atropine (10, 100 and 5000 μg/kg), or subcutaneously with oxotremorine (30, 100, 300 μg/kg). Subcutaneous administration of oxotremorine (30, 100, 300 μg/kg) significantly increased the tail-flick latency. These doses of oxotremorine dose-dependently increased the intraspinal release of acetylcholine. Intravenously administered atropine, in a dose that produced hyperalgesia (5000 μg/kg) in the tail-flick test, significantly decreased the intraspinal release of acetylcholine. Our results suggest an association between pain threshold and acetylcholine release in spinal cord. It is also suggested that an approximately 30% increase in basal ACh release produces antinociception and that a 30% decrease in basal release produces hyperalgesia.

    Ort, förlag, år, upplaga, sidor
    Blackwell, 2002
    Nationell ämneskategori
    Biomedicinsk laboratorievetenskap/teknologi
    Identifikatorer
    urn:nbn:se:uu:diva-7215 (URN)10.1034/j.1600-0773.2002.900403.x (DOI)
    Tillgänglig från: 2006-10-18 Skapad: 2006-10-18 Senast uppdaterad: 2017-12-14Bibliografiskt granskad
    2. Intravenously administered lidocaine in therapeutic doses increases the intraspinal release of acetylcholine in rats
    Öppna denna publikation i ny flik eller fönster >>Intravenously administered lidocaine in therapeutic doses increases the intraspinal release of acetylcholine in rats
    2002 (Engelska)Ingår i: Neuroscience Letters, ISSN 0304-3940, E-ISSN 1872-7972, Vol. 317, nr 2, s. 93-6Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    The local anesthetic lidocaine suppresses different pain conditions when administered systemically. Part of the antinociceptive effect appears to be mediated via receptor mechanisms. We have previously shown that muscarinic and nicotinic agonists that produce antinociception increase the intraspinal release of acetylcholine. In the present study it was hypothesized that systemically administered lidocaine is acting through the same mechanisms as cholinergic agonists and affects the intraspinal release of acetylcholine. Microdialysis probes were placed in anesthetized rats for sampling of acetylcholine. Ten and 30 mg/kg lidocaine injected intravenously significantly increased the intraspinal release of acetylcholine. The effect of lidocaine could be reduced by pretreatment with intraspinally administered atropine or mecamylamine. Our results suggest that the antinociceptive effect produced by systemically administered lidocaine is mediated through an action on muscarinic and nicotinic receptors.

    Ort, förlag, år, upplaga, sidor
    Elsevier, 2002
    Nyckelord
    Lidocaine; Spinal cord; Pain; Microdialysis; Acetylcholine; Muscarinic; Nicotinic
    Nationell ämneskategori
    Biomedicinsk laboratorievetenskap/teknologi
    Identifikatorer
    urn:nbn:se:uu:diva-7227 (URN)10.1016/S0304-3940(01)02440-5 (DOI)
    Tillgänglig från: 2006-10-24 Skapad: 2006-10-24 Senast uppdaterad: 2017-12-14Bibliografiskt granskad
    3. The effects of the alpha2-adrenergic receptor agonists clonidine and rilmenidine, and antagonists yohimbine and efaroxan, on the spinal cholinergic receptor system in the rat
    Öppna denna publikation i ny flik eller fönster >>The effects of the alpha2-adrenergic receptor agonists clonidine and rilmenidine, and antagonists yohimbine and efaroxan, on the spinal cholinergic receptor system in the rat
    2004 (Engelska)Ingår i: Basic & Clinical Pharmacology & Toxicology, ISSN 1742-7835, E-ISSN 1742-7843, Vol. 94, nr 4, s. 153-60Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    Cholinergic agonists produce spinal antinociception via mechanisms involving an increased release of intraspinalacetylcholine. The cholinergic receptor system interacts with several other receptor types, such as a2-adrenergic receptors.To fully understand these interactions, the effects of various receptor ligands on the cholinergic system must be investigatedin detail. This study was initiated to investigate the effects of the a2-adrenergic receptor agonists clonidine and rilmenidineand the a2-adrenergic receptor antagonists yohimbine and efaroxan on spinal cholinergic receptors in the rat. Spinalmicrodialysis was used to measure in vivo changes of acetylcholine after administration of the ligands, with or withoutnicotinic receptor blockade. In addition, in vitro binding properties of the ligands on muscarinic and nicotinic receptorswere investigated. It was found that clonidine and rilmenidine increased, while yohimbine decreased spinal acetylcholinerelease. Efaroxan affected acetylcholine release differently depending on concentration. Nicotinic receptor blockade atten-uated the effect of all ligands. All ligands showed poor binding affinity for muscarinic receptors. On the other hand, allligands possessed affinity for nicotinic receptors. Clonidine and yohimbine binding was best fit to a one site binding curveand rilmenidine and efaroxan to a two site binding curve. The present study demonstrates that the tested a2-adrenergicreceptor ligands affect intraspinal acetylcholine release in the rat evoked by nicotinic receptor mechanisms in vivo, andthat they possess binding affinity to nicotinic receptors in vitro. The binding of a2-adrenergic receptor ligands to nicotinicreceptors might affect the intraspinal release of acetylcholine.

    Ort, förlag, år, upplaga, sidor
    Blackwell, 2004
    Nationell ämneskategori
    Biomedicinsk laboratorievetenskap/teknologi
    Identifikatorer
    urn:nbn:se:uu:diva-92739 (URN)10.1111/j.1742-7843.2004.pto940401.x (DOI)15078339 (PubMedID)
    Tillgänglig från: 2005-03-30 Skapad: 2005-03-30 Senast uppdaterad: 2017-12-14Bibliografiskt granskad
    4. Spinal cholinergic involvement after treatment with aspirin and paracetamol in rats
    Öppna denna publikation i ny flik eller fönster >>Spinal cholinergic involvement after treatment with aspirin and paracetamol in rats
    2004 Ingår i: Neurosci. Lett., ISSN 0304-3940, Vol. 368, nr 1, s. 116-120Artikel i tidskrift (Refereegranskat) Published
    Identifikatorer
    urn:nbn:se:uu:diva-92740 (URN)
    Tillgänglig från: 2005-03-30 Skapad: 2005-03-30Bibliografiskt granskad
  • 160.
    Abelson, Klas
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Försöksdjursvetenskap.
    Adem, Bashir
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Försöksdjursvetenskap.
    Royo, Felix
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Försöksdjursvetenskap.
    Carlsson, Hans-Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Försöksdjursvetenskap.
    Hau, Jann
    High plasma corticosterone levels persist during frequent automatic blood sampling in rats2005Ingår i: In Vivo, ISSN 0258-851X, E-ISSN 1791-7549, Vol. 19, nr 5, s. 815-19Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Corticosterone levels in blood may be used as a marker of stress in rodents, provided that the blood sampling procedure itself is non-stressful. Automated blood sampling equipment (Accusampler®) allows blood sampling without any interference with the animal and might be useful as a tool for an on-line measurement of stress markers in blood. However, the impact of the blood sampling itself on the corticosterone levels in blood is unknown. The present study was designed to evaluate whether the frequency of blood sampling influences the plasma corticosterone levels in male and female rats. During anaesthesia, a catheter was placed in the jugular vein and attached to an Accusampler®. Blood samples (200 μl) were withdrawn with a high (24 samples) or low frequency (3 samples) during a six-hour period immediately after the catheter insertion. The corticosterone levels in the plasma were quantified with ELISA. The corticosterone levels persisted at high post-operation concentrations when blood was collected frequently, while the levels steadily declined significantly during low-frequency sampling. The corticosterone levels were higher in female than in male rats, but the curves were similar. The present study elucidates the importance of considering the frequency of blood withdrawal during automated blood sampling. This parameter may have an impact on the experimental results when using blood corticosterone levels as a stress marker, but also during any in vivo study where blood is collected, since high corticosterone levels may affect the normal physiology of the animals.

  • 161.
    Abelson, Klas
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Försöksdjursvetenskap.
    Hau, Jann
    Carlsson, Hans-Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Försöksdjursvetenskap.
    Undergraduate and postgraduate students' responses to mandatory courses (FELASA category C) in laboratory animal science 1997-20032005Ingår i: Internationalisation and Harmonisation of Laboratory Animal Care and Use Issues: Proceedings of the Ninth FELASA Symposium 14-17 June 2004, Nantes, France / [ed] M. R. Gamble, 2005Konferensbidrag (Övrigt vetenskapligt)
  • 162.
    Abelson, Klas
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Försöksdjursvetenskap.
    Höglund, Urban
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Försöksdjursvetenskap.
    Intravenously administered lidocaine in therapeutic doses increases the intraspinal release of acetylcholine in rats2002Ingår i: Neuroscience Letters, ISSN 0304-3940, E-ISSN 1872-7972, Vol. 317, nr 2, s. 93-6Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The local anesthetic lidocaine suppresses different pain conditions when administered systemically. Part of the antinociceptive effect appears to be mediated via receptor mechanisms. We have previously shown that muscarinic and nicotinic agonists that produce antinociception increase the intraspinal release of acetylcholine. In the present study it was hypothesized that systemically administered lidocaine is acting through the same mechanisms as cholinergic agonists and affects the intraspinal release of acetylcholine. Microdialysis probes were placed in anesthetized rats for sampling of acetylcholine. Ten and 30 mg/kg lidocaine injected intravenously significantly increased the intraspinal release of acetylcholine. The effect of lidocaine could be reduced by pretreatment with intraspinally administered atropine or mecamylamine. Our results suggest that the antinociceptive effect produced by systemically administered lidocaine is mediated through an action on muscarinic and nicotinic receptors.

  • 163.
    Abelson, Klas
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Försöksdjursvetenskap.
    Höglund, Urban
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Försöksdjursvetenskap.
    Intravenously administered oxotremorine and atropine, in doses known to affect pain threshold, affect the intraspinal release of acetylcholine in rats2002Ingår i: Pharmacology and Toxicology, ISSN 0901-9928, E-ISSN 1600-0773, Vol. 90, nr 4, s. 187-192Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Abstract:Both systemically and intrathecally administered cholinergic agonists produce antinociception while cholinergic antagonists decrease pain threshold. The mechanism and the site of action of these substances are not known. In the present study it was hypothesized that systemically administered muscarinic agonists and antagonists modify nociceptive threshold by affecting intraspinal release of acetylcholine (ACh). Catheters were inserted into the femoral vein in rats maintained on isoflurane anaesthesia for administration of oxotremorine (10–300 μg/kg) and atropine (0.1, 10, 5000 μg/kg). Spinal microdialysis probes were placed intraspinally at approximately the C2–C5 spinal level for sampling of acetylcholine and dialysis delivery of atropine (0.1, 1, 10 nM). Additionally, the tail-flick behaviour was tested on conscious rats injected intraperitoneally with saline, atropine (10, 100 and 5000 μg/kg), or subcutaneously with oxotremorine (30, 100, 300 μg/kg). Subcutaneous administration of oxotremorine (30, 100, 300 μg/kg) significantly increased the tail-flick latency. These doses of oxotremorine dose-dependently increased the intraspinal release of acetylcholine. Intravenously administered atropine, in a dose that produced hyperalgesia (5000 μg/kg) in the tail-flick test, significantly decreased the intraspinal release of acetylcholine. Our results suggest an association between pain threshold and acetylcholine release in spinal cord. It is also suggested that an approximately 30% increase in basal ACh release produces antinociception and that a 30% decrease in basal release produces hyperalgesia.

  • 164.
    Abelson, Klas
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Försöksdjursvetenskap.
    Höglund, Urban
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Försöksdjursvetenskap.
    The effects of the alpha2-adrenergic receptor agonists clonidine and rilmenidine, and antagonists yohimbine and efaroxan, on the spinal cholinergic receptor system in the rat2004Ingår i: Basic & Clinical Pharmacology & Toxicology, ISSN 1742-7835, E-ISSN 1742-7843, Vol. 94, nr 4, s. 153-60Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Cholinergic agonists produce spinal antinociception via mechanisms involving an increased release of intraspinalacetylcholine. The cholinergic receptor system interacts with several other receptor types, such as a2-adrenergic receptors.To fully understand these interactions, the effects of various receptor ligands on the cholinergic system must be investigatedin detail. This study was initiated to investigate the effects of the a2-adrenergic receptor agonists clonidine and rilmenidineand the a2-adrenergic receptor antagonists yohimbine and efaroxan on spinal cholinergic receptors in the rat. Spinalmicrodialysis was used to measure in vivo changes of acetylcholine after administration of the ligands, with or withoutnicotinic receptor blockade. In addition, in vitro binding properties of the ligands on muscarinic and nicotinic receptorswere investigated. It was found that clonidine and rilmenidine increased, while yohimbine decreased spinal acetylcholinerelease. Efaroxan affected acetylcholine release differently depending on concentration. Nicotinic receptor blockade atten-uated the effect of all ligands. All ligands showed poor binding affinity for muscarinic receptors. On the other hand, allligands possessed affinity for nicotinic receptors. Clonidine and yohimbine binding was best fit to a one site binding curveand rilmenidine and efaroxan to a two site binding curve. The present study demonstrates that the tested a2-adrenergicreceptor ligands affect intraspinal acetylcholine release in the rat evoked by nicotinic receptor mechanisms in vivo, andthat they possess binding affinity to nicotinic receptors in vitro. The binding of a2-adrenergic receptor ligands to nicotinicreceptors might affect the intraspinal release of acetylcholine.

  • 165.
    Abelson, Klas
    et al.
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap.
    Kommalage, Mahinda
    Höglund, Urban
    Spinal cholinergic involvement after treatment with aspirin and paracetamol in rats2004Ingår i: Neurosci. Lett., ISSN 0304-3940, Vol. 368, nr 1, s. 116-120Artikel i tidskrift (Refereegranskat)
  • 166.
    Abelson, Klas
    et al.
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Försöksdjursvetenskap.
    Kommalage, Mahinda
    Höglund, Urban
    Spinal cholinergic involvement after treatment with aspirin and paracetamol in rats2004Ingår i: Neuroscience Letters, ISSN 0304-3940, Vol. 368, nr 1, s. 116-120Artikel i tidskrift (Refereegranskat)
  • 167.
    Abelson, Klas
    et al.
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap. Försöksdjursvetenskap.
    Röstlinger Goldkuhl, Renée
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap. Försöksdjursvetenskap.
    Nylund, Anders
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap. Försöksdjursvetenskap.
    Höglund, Urban
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap. Försöksdjursvetenskap.
    The effect of ketamine on intraspinal acetylcholine release: Involvement of spinal nicotinic receptors2006Ingår i: Eur J Pharmacol, Vol. 534, s. 122-128Artikel i tidskrift (Refereegranskat)
  • 168.
    Abelson, Klas S. P.
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Försöksdjursvetenskap.
    Fard, Shahrzad Shirazi
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Försöksdjursvetenskap.
    Nyman, Julia
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Försöksdjursvetenskap.
    Goldkuhl, Renée
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Försöksdjursvetenskap.
    Hau, Jann
    Distribution of [3H]-corticosterone in urine, feces and blood of male Sprague-Dawley rats after tail vein and jugular vein injections2009Ingår i: In Vivo, ISSN 0258-851X, E-ISSN 1791-7549, Vol. 23, nr 3, s. 381-386Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The present study aimed to investigate the time-course and distribution of [(3)H]-corticosterone in urine, feces and blood of male Sprague-Dawley rats after intravenous administration of a low dose (1 microCi), and to investigate whether different intravenous routes of administration may affect the dynamics of excreted [(3)H]-corticosterone in the feces. One microCi [(3)H]-corticosterone was injected intravenously either through the tail vein in manually restrained rats or through a jugular vein catheter three days after surgical implantation. Urine and feces were collected at different time points over 78 h from the rats injected in the tail vein, and blood and feces were collected over 48 h from rats injected in the jugular vein. In the blood, radioactivity peaked immediately and decreased rapidly within 90 minutes. The radioactivity was excreted in urine within six h and in feces after at least 12 h. Sixty percent of the radioactivity was detected in the urine and 40% in feces during the study period of 78 h. The detected amount of radioactivity in feces was higher and displayed a more pronounced peak 12 h after injection when the substance was administered through a jugular vein catheter compared to tail vein injection. The data obtained in the present study may serve as an important benchmark when choosing time points for fecal collection for quantification of corticosterone or corticosterone metabolites as a non-invasive measure of preceding HPA-axis activation.

  • 169. Abelson, Klas S. P.
    et al.
    Jacobsen, Kirsten R.
    Sundbom, Renée
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Försöksdjursvetenskap.
    Kalliokoski, Otto
    Hau, Jann
    Voluntary ingestion of nut paste for administration of buprenorphine in rats and mice2012Ingår i: Laboratory Animals. Journal of the Laboratory Animal Science Association, ISSN 0023-6772, E-ISSN 1758-1117, Vol. 46, nr 4, s. 349-351Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    An adequate analgesic strategy is important to improve the postoperative recovery and welfare of laboratory rats and mice. It is desirable that the method for administering the drug is non-invasive and stress-free. We have previously validated a method for administering buprenorphine in a nut paste for voluntary ingestion. This method has many advantages over parenteral administration. To use the method in a successful way, however, it is important to prepare and administer the mix correctly. The present paper describes in detail how to implement the method, by means of habituation, presentation, adequate concentrations and amounts of buprenorphine/nut paste, and dosage of buprenorphine to rats and mice.

  • 170. Abelsson, J
    et al.
    Merup, M
    Birgegård, Gunnar
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Hematologi.
    WeisBjerrum, O
    Brinch, L
    Brune, M
    Johansson, P
    Kauppila, M
    Lenhoff, S
    Liljeholm, M
    Malm, C
    Remes, K
    Vindelöv, L
    Andréasson, B
    The outcome of allo-HSCT for 92 patients with myelofibrosis in the Nordic countries2012Ingår i: Bone Marrow Transplantation, ISSN 0268-3369, E-ISSN 1476-5365, Vol. 47, nr 3, s. 380-386Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Between 1982 and 2009 a total of 92 patients with myelofibrosis (MF) in chronic phase underwent allo-SCT in nine Nordic transplant centers. Myeloablative conditioning (MAC) was given to 40 patients, and reduced intensity conditioning (RIC) was used in 52 patients. The mean age in the two groups at transplantation was 46±12 and 55±8 years, respectively (P<0.001). When adjustment for age differences was made, the survival of the patients treated with RIC was significantly better (P=0.003). Among the RIC patients, the survival was significantly (P=0.003) better for the patients with age <60 years (a 10-year survival close to 80%) than for the older patients. The type of stem cell donor did not significantly affect the survival. No significant difference was found in TRM at 100 days between the MAC- and the RIC-treated patients. The probability of survival at 5 years was 49% for the MAC-treated patients and 59% in the RIC group (P=0.125). Patients treated with RIC experienced significantly less aGVHD compared with patients treated with MAC (P<0.001). The OS at 5 years was 70, 59 and 41% for patients with Lille score 0, 1 and 2, respectively (P=0.038, when age adjustment was made). Twenty-one percent of the patients in the RIC group were given donor lymphocyte infusion because of incomplete donor chimerism, compared with none of the MAC-treated patients (P<0.002). Nine percent of the patients needed a second transplant because of graft failure, progressive disease or transformation to AML, with no significant difference between the groups. Our conclusions are (1) allo-SCT performed with RIC gives a better survival compared with MAC. (2) age over 60 years is strongly related to a worse outcome and (3) patients with higher Lille score had a shorter survival.

  • 171. Abelsson, Johanna
    et al.
    Andreasson, Bjorn
    Samuelsson, Jan
    Hultcrantz, Malin
    Ejerblad, Elisabeth
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Hematologi.
    Johansson, Berit
    Emanuel, Robyn
    Mesa, Ruben
    Johansson, Peter
    Patients with polycythemia vera have worst impairment of quality of life among patients with newly diagnosed myeloproliferative neoplasms2013Ingår i: Leukemia and Lymphoma, ISSN 1042-8194, E-ISSN 1029-2403, Vol. 54, nr 10, s. 2226-2230Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The quality of life (QoL) at the time of diagnosis of myeloproliferative neoplasm (MPN) has, to date, not been studied. One hundred and seventy-nine patients with MPN: 80 with essential thrombocythemia (ET), 73 with polycythemia vera (PV), 22 with primary myelofibrosis (PMF) and four with MPN undifferentiated, were included in this study. European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire Core 30 (EORTC-QLQC30) and the MPN-Symptom Assessment Form (MPN-SAF) were used to evaluate QoL. Fatigue was the most reported symptom in these patients. Patients with PV reported significantly higher mean scores for inactivity, dizziness, cough, itching, depression and lower total QoL compared to patients with ET. Patients with PV had significantly more headache and itching compared to patients with PMF. When the newly diagnosed patients with MPN were compared with a cohort of patients with MPN with mean disease duration of 7.8 years, the differences were most striking for patients with PMF, with significantly more fatigue, abdominal discomfort, concentration problems, insomnia, fever, weight loss and lower overall QoL developed over time.

  • 172.
    Aberg, AC
    et al.
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    Lindmark, B
    Institutionen för neurovetenskap.
    Lithell, H
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    Development and reliability of the General Motor Function Assessment Scale(GMF)-A performance-based measure of function-related dependence, pain andinsecurity.2003Ingår i: Disabil Rehabil, Vol. 25, s. 11-Artikel i tidskrift (Refereegranskat)
  • 173.
    Aberg, AC
    et al.
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    Lindmark, B
    Institutionen för neurovetenskap.
    Lithell, H
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    Evaluation and application of the General Motor Function assessment scalein geriatric rehabilitation.2003Ingår i: Disabil Rehabil, Vol. 25, s. 9-Artikel i tidskrift (Refereegranskat)
  • 174.
    Aberg, AC
    et al.
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    Sidenvall, B
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    Hepworth, M
    O'Reilly, K
    Lithell, H
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    Continuity of the self in later life: perceptions of informal caregivers.2004Ingår i: Qual Health Res, ISSN 1049-7323, Vol. 14, nr 6, s. 24-Artikel i tidskrift (Refereegranskat)
  • 175.
    Aberg, AC
    et al.
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    Sidenvall, B
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    Hepworth, M
    O'Reilly, K
    Lithell, H
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    On loss of activity and independence, adaptation improves lifa satisfaction in old age: - a qualitative study of patients' perceptions2005Ingår i: Quality of Life Research, Vol. 14, nr 4, s. 1111-25Artikel i tidskrift (Refereegranskat)
  • 176.
    Aberg, Fredrik
    et al.
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap.
    Kozlova, Elena N
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap.
    Metastasis-associated Mts1 (S100A4) protein in the developing and adult central nervous system2000Ingår i: J Comp Neurology, Vol. 424, s. 269-Artikel i tidskrift (Refereegranskat)
  • 177. Aberg, H
    et al.
    Morlin, C
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Lithell, Hans
    Institutionen för folkhälso- och vårdvetenskap.
    Different long-term metabolic effects of enalapril and atenolol in patients with mild hypertension. EGTA Group1995Ingår i: J Hum Hypertens, Vol. 9, s. 149-Artikel i tidskrift (Refereegranskat)
  • 178.
    Aberg, Mikael
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Koagulation och inflammationsvetenskap.
    Eriksson, Oskar
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Koagulation och inflammationsvetenskap.
    Siegbahn, Agneta
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Koagulation och inflammationsvetenskap.
    Tissue Factor Noncoagulant Signaling: Mechanisms and Implications for Cell Migration and Apoptosis2015Ingår i: Seminars in Thrombosis and Hemostasis, ISSN 0094-6176, E-ISSN 1098-9064, Vol. 41, nr 7, s. 691-699Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Tissue factor (TF) is a 47-kDa transmembrane glycoprotein and the main initiator of the blood coagulation cascade. Binding to its ligand factor VIIa (FVIIa) also initiates noncoagulant signaling with broad biological implications. In this review, we discuss how TF interacts with other cell-surface proteins, which affect biological functions such as cell migration and cell survival. A vast number of publications have demonstrated the importance of TF-induced activation of protease-activated receptors, but recently published research has indicated a more complicated picture. As it has been discovered that TF interacts with integrins and receptor tyrosine kinases, novel signaling mechanisms for the TF/FVIIa complex have been presented. The knowledge of these new aspects of TF signaling may, for instance, facilitate the development of new treatment strategies for cancer and acute coronary syndromes, two examples of diseases characterized by aberrant TF expression and signaling.

  • 179. Aberg-Wistedt, A
    et al.
    Agren, H
    Ekselius, Lisa
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap.
    Bengtsson, F
    Akerblad, AC
    Sertraline vs Paroxetine in major depression: Clinical outcome after6 months of continuation therapy.2000Ingår i: J Clin Psychopharmacol. , Vol. 20, s. 645-Artikel i tidskrift (Refereegranskat)
  • 180.
    Abiri, Pojan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Farmaceutiska fakulteten, Institutionen för farmaceutisk biovetenskap.
    Användandet av webbsajten Sil Online – Svenska informationstjänster för läkemedel: En enkät- och intervjustudie2015Självständigt arbete på avancerad nivå (masterexamen), 20 poäng / 30 hpStudentuppsats (Examensarbete)
    Abstract [sv]

    Introduktion: Sil, Svenska informationstjänster för läkemedel, tillhandahåller kvalitetssäkrad läkemedelsinformation till aktörer inom hälso- och sjukvård. Sil Online (www.silonline.se) möjliggör åtkomsten till informationen i Sil databasen.

    Syfte: Att utvärdera vilka som är användare av Sil Online, i vilket ändamål användningen sker samt vilken information som söks på Sil Online för att skapa underlag för framtidsutveckling av webbsajten.

    Material och metoder: En deskriptiv tvärsnittsstudie bestående av en kvantitativ webbenkätundersökning (tidsperiod: 2015-03-05 till 2015-04-02) och en kvalitativ intervjuerundersökning bland frivilliga respondenter på webbenkäten.

    Resultat: Den största användargruppen bland respondenterna av webbenkäten var farmacevter (67 %), följt av systemutvecklare (16 %) varav majoriteten (43 %) jobbade inom hälso- och sjukvård eller förvaltning och administration inom landsting och kommuner (24 %). Aktuell läkemedelsinformation söktes av majoriteten av användarna (78 %) och mer än hälften (77 %) tyckte att det var lätt att hitta på webbsajten. Intervjurespondenterna saknade information om syftet med Sil Online men tyckte att det var en informativ sajt med unik information om licensläkemedel och listor med landstingens rekommenderade läkemedel. Tydligare instruktioner skulle förbättra användarvänlighet och marknadsföring skulle vidga användarkretsen.

    Konklusion: Sil Online upplevs vara en användarvänlig och informativ webbsajt. Studien visar att det finns potential för utveckling inom presentation och marknadsföring av webbsajten.

  • 181.
    Ablikim, M.
    et al.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Achasov, M. N.
    GI Budker Inst Nucl Phys SB RAS BINP, Novosibirsk 630090, Russia..
    Ahmed, S.
    Helmholtz Inst Mainz, D-55099 Mainz, Germany..
    Ai, X. C.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Albayrak, O.
    Carnegie Mellon Univ, Pittsburgh, PA 15213 USA..
    Albrecht, M.
    Ruhr Univ Bochum, D-44780 Bochum, Germany..
    Ambrose, D. J.
    Univ Rochester, Rochester, NY 14627 USA..
    Amoroso, A.
    GI Budker Inst Nucl Phys SB RAS BINP, Novosibirsk 630090, Russia.;Helmholtz Inst Mainz, D-55099 Mainz, Germany.;Johannes Gutenberg Univ Mainz, D-55099 Mainz, Germany.;Chinese Acad Sci, Beijing 100049, Peoples R China.;Univ Hawaii, Honolulu, HI 96822 USA.;Univ Punjab, Lahore 54590, Pakistan.;Univ Turin, I-10125 Turin, Italy.;INFN, I-10125 Turin, Italy..
    An, F. F.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    An, Q.
    Univ Sci & Technol China, Hefei 230026, Peoples R China..
    Bai, J. Z.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Ferroli, R. Baldini
    INFN Lab Nazl Frascati, I-00044 I- Frascati, Italy..
    Ban, Y.
    Peking Univ, Beijing 100871, Peoples R China..
    Bennett, D. W.
    Indiana Univ, Bloomington, IN 47405 USA..
    Bennett, J. V.
    Carnegie Mellon Univ, Pittsburgh, PA 15213 USA..
    Berger, N. B.
    Johannes Gutenberg Univ Mainz, D-55099 Mainz, Germany..
    Bertani, M.
    INFN Lab Nazl Frascati, I-00044 I- Frascati, Italy..
    Bettoni, D.
    INFN, Sez Ferrara, I-44122 Ferrara, Italy..
    Bian, J. M.
    Univ Minnesota, Minneapolis, MN 55455 USA..
    Bianchi, F.
    Univ Turin, I-10125 Turin, Italy.;INFN, I-10125 Turin, Italy..
    Boger, E.
    Joint Inst Nucl Res, Dubna 141980, Moscow Region, Russia..
    Boyko, I.
    Joint Inst Nucl Res, Dubna 141980, Moscow Region, Russia..
    Briere, R. A.
    Carnegie Mellon Univ, Pittsburgh, PA 15213 USA..
    Cai, H.
    Wuhan Univ, Wuhan 430072, Peoples R China..
    Cai, X.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Cakir, O.
    Ankara Univ, TR-06100 Ankara, Turkey..
    Calcaterra, A.
    INFN Lab Nazl Frascati, I-00044 I- Frascati, Italy.;Johannes Gutenberg Univ Mainz, D-55099 Mainz, Germany.;Chinese Acad Sci, Beijing 100049, Peoples R China.;Univ Turin, I-10125 Turin, Italy.;INFN, I-10125 Turin, Italy..
    Cao, G. F.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Cetin, S. A.
    Istanbul Bilgi Univ, TR-34060 Istanbul, Turkey..
    Chang, J. F.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Chelkov, G.
    Joint Inst Nucl Res, Dubna 141980, Moscow Region, Russia..
    Chen, G.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Chen, H. S.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Chen, H. Y.
    Beihang Univ, Beijing 100191, Peoples R China..
    Chen, J. C.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Chen, M. L.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Chen, S.
    Chinese Acad Sci, Beijing 100049, Peoples R China..
    Chen, S. J.
    Nanjing Univ, Nanjing 210093, Peoples R China..
    Chen, X.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Chen, X. R.
    Lanzhou Univ, Lanzhou 730000, Peoples R China..
    Chen, Y. B.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Cheng, H. P.
    Huangshan Coll, Huangshan 245000, Peoples R China..
    Chu, X. K.
    Peking Univ, Beijing 100871, Peoples R China..
    Cibinetto, G.
    INFN, Sez Ferrara, I-44122 Ferrara, Italy..
    Dai, H. L.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Dai, J. P.
    Shanghai Jiao Tong Univ, Shanghai 200240, Peoples R China..
    Dbeyssi, A.
    Helmholtz Inst Mainz, D-55099 Mainz, Germany..
    Dedovich, D.
    Joint Inst Nucl Res, Dubna 141980, Moscow Region, Russia..
    Deng, Z. Y.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Denig, A.
    Johannes Gutenberg Univ Mainz, D-55099 Mainz, Germany..
    Denysenko, I.
    Joint Inst Nucl Res, Dubna 141980, Moscow Region, Russia..
    Destefanis, M.
    Univ Turin, I-10125 Turin, Italy.;INFN, I-10125 Turin, Italy..
    De Mori, F.
    Liaoning Univ, Shenyang 110036, Peoples R China..
    Ding, Y.
    Liaoning Univ, Shenyang 110036, Peoples R China..
    Dong, C.
    Nankai Univ, Tianjin 300071, Peoples R China..
    Dong, J.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Dong, L. Y.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Dong, M. Y.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Dou, Z. L.
    Nanjing Univ, Nanjing 210093, Peoples R China..
    Du, S. X.
    Zhengzhou Univ, Zhengzhou 450001, Peoples R China..
    Duan, P. F.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Fan, J. Z.
    Tsinghua Univ, Beijing 100084, Peoples R China..
    Fang, J.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Fang, S. S.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Fang, X.
    Univ Sci & Technol China, Hefei 230026, Peoples R China..
    Fang, Y.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Farinelli, R.
    INFN, Sez Ferrara, I-44122 Ferrara, Italy.;Univ Ferrara, I-44122 Ferrara, Italy..
    Fava, L.
    Univ Piemonte Orientale, I-15121 Alessandria, Italy.;INFN, I-10125 Turin, Italy..
    Fedorov, O.
    Joint Inst Nucl Res, Dubna 141980, Moscow Region, Russia..
    Feldbauer, F.
    Johannes Gutenberg Univ Mainz, D-55099 Mainz, Germany..
    Felici, G.
    INFN Lab Nazl Frascati, I-00044 I- Frascati, Italy..
    Feng, C. Q.
    Univ Sci & Technol China, Hefei 230026, Peoples R China..
    Fioravanti, E.
    INFN, Sez Ferrara, I-44122 Ferrara, Italy..
    Fritsch, M.
    Helmholtz Inst Mainz, D-55099 Mainz, Germany.;Johannes Gutenberg Univ Mainz, D-55099 Mainz, Germany..
    Fu, C. D.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Gao, Q.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Gao, X. L.
    Univ Sci & Technol China, Hefei 230026, Peoples R China..
    Gao, X. Y.
    Beihang Univ, Beijing 100191, Peoples R China..
    Gao, Y.
    Tsinghua Univ, Beijing 100084, Peoples R China..
    Gao, Z.
    Univ Sci & Technol China, Hefei 230026, Peoples R China..
    Garzia, I.
    INFN, Sez Ferrara, I-44122 Ferrara, Italy..
    Goetzen, K.
    GSI Helmholtzcentre Heavy Ion Res GmbH, D-64291 Darmstadt, Germany..
    Gong, L.
    Nankai Univ, Tianjin 300071, Peoples R China..
    Gong, W. X.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Gradl, W.
    Johannes Gutenberg Univ Mainz, D-55099 Mainz, Germany..
    Greco, M.
    Univ Turin, I-10125 Turin, Italy.;INFN, I-10125 Turin, Italy..
    Gu, M. H.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Gu, Y. T.
    Guangxi Univ, Nanning 530004, Peoples R China..
    Guan, Y. H.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Guo, A. Q.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Guo, L. B.
    Nanjing Normal Univ, Nanjing 210023, Peoples R China..
    Guo, R. P.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Guo, Y.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Guo, Y. P.
    Johannes Gutenberg Univ Mainz, D-55099 Mainz, Germany..
    Haddadi, Z.
    Univ Groningen, KVI CART, NL-9747 AA Groningen, Netherlands..
    Hafner, A.
    Johannes Gutenberg Univ Mainz, D-55099 Mainz, Germany..
    Han, S.
    Wuhan Univ, Wuhan 430072, Peoples R China..
    Hao, X. Q.
    Henan Normal Univ, Xinxiang 453007, Peoples R China..
    Harris, F. A.
    Univ Hawaii, Honolulu, HI 96822 USA..
    He, K. L.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Heinsius, F. H.
    Ruhr Univ Bochum, D-44780 Bochum, Germany..
    Held, T.
    Ruhr Univ Bochum, D-44780 Bochum, Germany..
    Heng, Y. K.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Holtmann, T.
    Ruhr Univ Bochum, D-44780 Bochum, Germany..
    Hou, Z. L.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Hu, C.
    Nanjing Normal Univ, Nanjing 210023, Peoples R China..
    Hu, H. M.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Hu, J. F.
    Univ Turin, I-10125 Turin, Italy.;INFN, I-10125 Turin, Italy..
    Hu, T.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Hu, Y.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Huang, G. S.
    Univ Sci & Technol China, Hefei 230026, Peoples R China..
    Huang, J. S.
    Henan Normal Univ, Xinxiang 453007, Peoples R China..
    Huang, X. T.
    Shandong Univ, Jinan 250100, Peoples R China..
    Huang, X. Z.
    Nanjing Univ, Nanjing 210093, Peoples R China..
    Huang, Y.
    Nanjing Univ, Nanjing 210093, Peoples R China..
    Huang, Z. L.
    Liaoning Univ, Shenyang 110036, Peoples R China..
    Hussain, T.
    Univ Punjab, Lahore 54590, Pakistan..
    Ji, Q.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Ji, Q. P.
    Nankai Univ, Tianjin 300071, Peoples R China..
    Ji, X. B.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Ji, X. L.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Jiang, L. W.
    Wuhan Univ, Wuhan 430072, Peoples R China..
    Jiang, X. S.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Jiang, X. Y.
    Nankai Univ, Tianjin 300071, Peoples R China..
    Jiao, J. B.
    Shandong Univ, Jinan 250100, Peoples R China..
    Jiao, Z.
    Huangshan Coll, Huangshan 245000, Peoples R China..
    Jin, D. P.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Jin, S.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Johansson, T
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Julin, A.
    Univ Minnesota, Minneapolis, MN 55455 USA..
    Kalantar-Nayestanaki, N.
    Univ Groningen, KVI CART, NL-9747 AA Groningen, Netherlands..
    Kang, X. L.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Kang, X. S.
    Nankai Univ, Tianjin 300071, Peoples R China..
    Kavatsyuk, M.
    Univ Groningen, KVI CART, NL-9747 AA Groningen, Netherlands..
    Ke, B. C.
    Carnegie Mellon Univ, Pittsburgh, PA 15213 USA..
    Kiese, P.
    Johannes Gutenberg Univ Mainz, D-55099 Mainz, Germany..
    Kliemt, R.
    Helmholtz Inst Mainz, D-55099 Mainz, Germany..
    Kloss, B.
    Johannes Gutenberg Univ Mainz, D-55099 Mainz, Germany..
    Kolcu, O. B.
    Istanbul Bilgi Univ, TR-34060 Istanbul, Turkey..
    Kopf, B.
    Ruhr Univ Bochum, D-44780 Bochum, Germany..
    Kornicer, M.
    Univ Hawaii, Honolulu, HI 96822 USA..
    Kupsc, Andrzej
    Uppsala universitet, The Svedberg-laboratoriet. Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Fysiska sektionen, Institutionen för fysik och astronomi, Kärnfysik.
    Khn, W.
    Justus Liebig Univ Giessen, Phys Inst 2, D-35392 Giessen, Germany..
    Lange, J. S.
    Justus Liebig Univ Giessen, Phys Inst 2, D-35392 Giessen, Germany..
    Lara, M.
    Indiana Univ, Bloomington, IN 47405 USA..
    Larin, P.
    Helmholtz Inst Mainz, D-55099 Mainz, Germany..
    Leithoff, H.
    Johannes Gutenberg Univ Mainz, D-55099 Mainz, Germany..
    Leng, C.
    INFN, I-10125 Turin, Italy..
    Li, Cui
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Fysiska sektionen, Institutionen för fysik och astronomi, Kärnfysik.
    Li, Cheng
    Univ Sci & Technol China, Hefei 230026, Peoples R China..
    Li, D. M.
    Zhengzhou Univ, Zhengzhou 450001, Peoples R China..
    Li, F.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Li, F. Y.
    Peking Univ, Beijing 100871, Peoples R China..
    Li, G.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Li, H. B.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Li, H. J.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Li, J. C.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Li, Jin
    Seoul Natl Univ, Seoul 151747, South Korea..
    Li, K.
    Hangzhou Normal Univ, Hangzhou 310036, Peoples R China.;Shandong Univ, Jinan 250100, Peoples R China..
    Li, Lei
    Beijing Inst Petrochem Technol, Beijing 102617, Peoples R China..
    Li, P. R.
    Chinese Acad Sci, Beijing 100049, Peoples R China..
    Li, Q. Y.
    Shandong Univ, Jinan 250100, Peoples R China..
    Li, T.
    Shandong Univ, Jinan 250100, Peoples R China..
    Li, W. D.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Li, W. G.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Li, X. L.
    Shandong Univ, Jinan 250100, Peoples R China..
    Li, X. M.
    Guangxi Univ, Nanning 530004, Peoples R China..
    Li, X. N.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Li, X. Q.
    Nankai Univ, Tianjin 300071, Peoples R China..
    Li, Y. B.
    Beihang Univ, Beijing 100191, Peoples R China..
    Li, Z. B.
    Sun Yat Sen Univ, Guangzhou 510275, Guangdong, Peoples R China..
    Liang, H.
    Univ Sci & Technol China, Hefei 230026, Peoples R China..
    Liang, J. J.
    Guangxi Univ, Nanning 530004, Peoples R China..
    Liang, Y. F.
    Sichuan Univ, Chengdu 610064, Peoples R China..
    Liang, Y. T.
    Justus Liebig Univ Giessen, Phys Inst 2, D-35392 Giessen, Germany..
    Liao, G. R.
    Guangxi Normal Univ, Guilin 541004, Peoples R China..
    Lin, D. X.
    Helmholtz Inst Mainz, D-55099 Mainz, Germany..
    Liu, B.
    Shanghai Jiao Tong Univ, Shanghai 200240, Peoples R China..
    Liu, B. J.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Liu, C. X.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Liu, D.
    Univ Sci & Technol China, Hefei 230026, Peoples R China..
    Liu, F. H.
    Shanxi Univ, Taiyuan 030006, Peoples R China..
    Liu, Fang
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Liu, Feng
    Cent China Normal Univ, Wuhan 430079, Peoples R China..
    Liu, H. B.
    Guangxi Univ, Nanning 530004, Peoples R China..
    Liu, H. H.
    Inst High Energy Phys, Beijing 100049, Peoples R China.;Henan Univ Sci & Technol, Luoyang 471003, Peoples R China..
    Liu, H. M.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Liu, J.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Liu, J. B.
    Univ Sci & Technol China, Hefei 230026, Peoples R China..
    Liu, J. P.
    Wuhan Univ, Wuhan 430072, Peoples R China..
    Liu, J. Y.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Liu, K.
    Tsinghua Univ, Beijing 100084, Peoples R China..
    Liu, K. Y.
    Liaoning Univ, Shenyang 110036, Peoples R China..
    Liu, L. D.
    Peking Univ, Beijing 100871, Peoples R China..
    Liu, P. L.
    Inst High Energy Phys, Beijing 100049, Peoples R China..
    Liu, Q.
    Chinese Acad Sci, Beijing 100049, Peoples R China..
    Liu, S. B.
    Univ Sci & Technol China, Hefei 230026, Peoples R China..
    Liu, X.
    Lanzhou Univ, Lanzhou 730000, Peoples R China..