umu.sePublikationer
Ändra sökning
Avgränsa sökresultatet
1 - 9 av 9
RefereraExporteraLänk till träfflistan
Permanent länk
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • 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.
  • 1. Bien, Stephanie A.
    et al.
    Su, Yu-Ru
    Conti, David V.
    Harrison, Tabitha A.
    Qu, Conghui
    Guo, Xingyi
    Lu, Yingchang
    Albanes, Demetrius
    Auer, Paul L.
    Banbury, Barbara L.
    Berndt, Sonja I.
    Bezieau, Stephane
    Brenner, Hermann
    Buchanan, Daniel D.
    Caan, Bette J.
    Campbell, Peter T.
    Carlson, Christopher S.
    Chan, Andrew T.
    Chang-Claude, Jenny
    Chen, Sai
    Connolly, Charles M.
    Easton, Douglas F.
    Feskens, Edith J. M.
    Gallinger, Steven
    Giles, Graham G.
    Gunter, Marc J.
    Hampe, Jochen
    Huyghe, Jeroen R.
    Hoffmeister, Michael
    Hudson, Thomas J.
    Jacobs, Eric J.
    Jenkins, Mark A.
    Kampman, Ellen
    Kang, Hyun Min
    Kuehn, Tilman
    Kury, Sebastien
    Lejbkowicz, Flavio
    Le Marchand, Loic
    Milne, Roger L.
    Li, Li
    Li, Christopher I.
    Lindblom, Annika
    Lindor, Noralane M.
    Martin, Vicente
    McNeil, Caroline E.
    Melas, Marilena
    Moreno, Victor
    Newcomb, Polly A.
    Offit, Kenneth
    Pharaoh, Paul D. P.
    Potter, John D.
    Qu, Chenxu
    Riboli, Elio
    Rennert, Gad
    Sala, Nuria
    Schafmayer, Clemens
    Scacheri, Peter C.
    Schmit, Stephanie L.
    Severi, Gianluca
    Slattery, Martha L.
    Smith, Joshua D.
    Trichopoulou, Antonia
    Tumino, Rosario
    Ulrich, Cornelia M.
    van Duijnhoven, Franzel J. B.
    van Guelpen, Bethany
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi. Department of Public Health Sciences, University of Virginia School of Medicine, Charlottesville, USA.
    Weinstein, Stephanie J.
    White, Emily
    Wolk, Alicja
    Woods, Michael O.
    Wu, Anna H.
    Abecasis, Goncalo R.
    Casey, Graham
    Nickerson, Deborah A.
    Gruber, Stephen B.
    Hsu, Li
    Zheng, Wei
    Peters, Ulrike
    Genetic variant predictors of gene expression provide new insight into risk of colorectal cancer2019Ingår i: Human Genetics, ISSN 0340-6717, E-ISSN 1432-1203, Vol. 138, nr 4, s. 307-326Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Genome-wide association studies have reported 56 independently associated colorectal cancer (CRC) risk variants, most of which are non-coding and believed to exert their effects by modulating gene expression. The computational method PrediXcan uses cis-regulatory variant predictors to impute expression and perform gene-level association tests in GWAS without directly measured transcriptomes. In this study, we used reference datasets from colon (n=169) and whole blood (n=922) transcriptomes to test CRC association with genetically determined expression levels in a genome-wide analysis of 12,186 cases and 14,718 controls. Three novel associations were discovered from colon transverse models at FDR0.2 and further evaluated in an independent replication including 32,825 cases and 39,933 controls. After adjusting for multiple comparisons, we found statistically significant associations using colon transcriptome models with TRIM4 (discovery P=2.2x10(-4), replication P=0.01), and PYGL (discovery P=2.3x10(-4), replication P=6.7x10(-4)). Interestingly, both genes encode proteins that influence redox homeostasis and are related to cellular metabolic reprogramming in tumors, implicating a novel CRC pathway linked to cell growth and proliferation. Defining CRC risk regions as one megabase up- and downstream of one of the 56 independent risk variants, we defined 44 non-overlapping CRC-risk regions. Among these risk regions, we identified genes associated with CRC (P<0.05) in 34/44 CRC-risk regions. Importantly, CRC association was found for two genes in the previously reported 2q25 locus, CXCR1 and CXCR2, which are potential cancer therapeutic targets. These findings provide strong candidate genes to prioritize for subsequent laboratory follow-up of GWAS loci. This study is the first to implement PrediXcan in a large colorectal cancer study and findings highlight the utility of integrating transcriptome data in GWAS for discovery of, and biological insight into, risk loci.

  • 2. Dahl, N
    et al.
    Goonewardena, P
    Chotai, Jayanti
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Anvret, M
    Pettersson, U
    DNA linkage analysis of X-linked retinoschisis.1988Ingår i: Human Genetics, ISSN 0340-6717, E-ISSN 1432-1203, Vol. 78, nr 3, s. 228-32Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Four families with juvenile retionoschisis (RS) have been studied by linkage analysis utilizing eleven polymorphic X-chromosomal markers. The results suggest a close linkage between DXS43, DXS41, and DXS208 and the RS locus at Xp22. The RS locus is distal to the OTC locus, DXS84, and the DMD locus but proximal to DXS85. No recombination events were observed between the RS locus and DXS43 and DXS41. The maximum likelihood estimate of the recombination fraction (theta) was thus zero and the peak lod scores (z) were 4.98 (DXS43) and 4.09 (DXS41). The linkage data suggest that the gene order on Xp is DXS85-(DXS43, RS, DXS41)-DMD-DXS84-OTC.

  • 3. Jin, Guangfu
    et al.
    Lu, Lingyi
    Cooney, Kathleen A
    Ray, Anna M
    Zuhlke, Kimberly A
    Lange, Ethan M
    Cannon-Albright, Lisa A
    Camp, Nicola J
    Teerlink, Craig C
    Fitzgerald, Liesel M
    Stanford, Janet L
    Wiley, Kathleen E
    Isaacs, Sarah D
    Walsh, Patrick C
    Foulkes, William D
    Giles, Graham G
    Hopper, John L
    Severi, Gianluca
    Eeles, Ros
    Easton, Doug
    Kote-Jarai, Zsofia
    Guy, Michelle
    Rinckleb, Antje
    Maier, Christiane
    Vogel, Walther
    Cancel-Tassin, Geraldine
    Egrot, Christophe
    Cussenot, Olivier
    Thibodeau, Stephen N
    McDonnell, Shannon K
    Schaid, Daniel J
    Wiklund, Fredrik
    Grönberg, Henrik
    Emanuelsson, Monica
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Whittemore, Alice S
    Oakley-Girvan, Ingrid
    Hsieh, Chih-Lin
    Wahlfors, Tiina
    Tammela, Teuvo
    Schleutker, Johanna
    Catalona, William J
    Zheng, S Lilly
    Ostrander, Elaine A
    Isaacs, William B
    Xu, Jianfeng
    Validation of prostate cancer risk-related loci identified from genome-wide association studies using family-based association analysis: evidence from the International Consortium for Prostate Cancer Genetics (ICPCG)2012Ingår i: Human Genetics, ISSN 0340-6717, E-ISSN 1432-1203, Vol. 131, nr 7, s. 1095-1103Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Multiple prostate cancer (PCa) risk-related loci have been discovered by genome-wide association studies (GWAS) based on case-control designs. However, GWAS findings may be confounded by population stratification if cases and controls are inadvertently drawn from different genetic backgrounds. In addition, since these loci were identified in cases with predominantly sporadic disease, little is known about their relationships with hereditary prostate cancer (HPC). The association between seventeen reported PCa susceptibility loci was evaluated with a family-based association test using 1,979 hereditary PCa families of European descent collected by members of the International Consortium for Prostate Cancer Genetics, with a total of 5,730 affected men. The risk alleles for 8 of the 17 loci were significantly over-transmitted from parents to affected offspring, including SNPs residing in 8q24 (regions 1, 2 and 3), 10q11, 11q13, 17q12 (region 1), 17q24 and Xp11. In subgroup analyses, three loci, at 8q24 (regions 1 and 2) plus 17q12, were significantly over-transmitted in hereditary PCa families with five or more affected members, while loci at 3p12, 8q24 (region 2), 11q13, 17q12 (region 1), 17q24 and Xp11 were significantly over-transmitted in HPC families with an average age of diagnosis at 65 years or less. Our results indicate that at least a subset of PCa risk-related loci identified by case-control GWAS are also associated with disease risk in HPC families.

  • 4.
    Lindström, Sara
    et al.
    Umeå universitet, Medicinsk fakultet, Strålningsvetenskaper, Onkologi. Onkologi.
    Wiklund, Fredrik
    Umeå universitet, Medicinsk fakultet, Strålningsvetenskaper, Onkologi. Onkologi.
    Jonsson, Björn-Anders
    Umeå universitet, Medicinsk fakultet, Strålningsvetenskaper, Onkologi. Onkologi.
    Adami, Hans-Olov
    Bälter, Katarina
    Brookes, Anthony J
    Xu, Jianfeng
    Zheng, S Lilly
    Isaacs, William B
    Adolfsson, Jan
    Grönberg, Henrik
    Umeå universitet, Medicinsk fakultet, Strålningsvetenskaper, Onkologi. Onkologi.
    Comprehensive genetic evaluation of common E-cadherin sequence variants and prostate cancer risk: strong confirmation of functional promoter SNP2005Ingår i: Human Genetics, ISSN 0340-6717, E-ISSN 1432-1203, Vol. 118, nr 3-4, s. 339-347Artikel i tidskrift (Refereegranskat)
  • 5. Liu, Yanhong
    et al.
    Melin, Beatrice S
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Rajaraman, Preetha
    Wang, Zhaoming
    Linet, Martha
    Shete, Sanjay
    Amos, Christopher I
    Lau, Ching C
    Scheurer, Michael E
    Tsavachidis, Spiridon
    Armstrong, Georgina N
    Houlston, Richard S
    Hosking, Fay J
    Claus, Elizabeth B
    Barnholtz-Sloan, Jill
    Lai, Rose
    Il'yasova, Dora
    Schildkraut, Joellen
    Sadetzki, Siegal
    Johansen, Christoffer
    Bernstein, Jonine L
    Olson, Sara H
    Jenkins, Robert B
    Lachance, Daniel
    Vick, Nicholas A
    Wrensch, Margaret
    Davis, Faith
    McCarthy, Bridget J
    Andersson, Ulrika
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Thompson, Patricia A
    Chanock, Stephen
    Bondy, Melissa L
    Insight in glioma susceptibility through an analysis of 6p22.3, 12p13.33-12.1, 17q22-23.2 and 18q23 SNP genotypes in familial and non-familial glioma2012Ingår i: Human Genetics, ISSN 0340-6717, E-ISSN 1432-1203, Vol. 131, nr 9, s. 1507-1517Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The risk of glioma has consistently been shown to be increased twofold in relatives of patients with primary brain tumors (PBT). A recent genome-wide linkage study of glioma families provided evidence for a disease locus on 17q12-21.32, with the possibility of four additional risk loci at 6p22.3, 12p13.33-12.1, 17q22-23.2, and 18q23. To identify the underlying genetic variants responsible for the linkage signals, we compared the genotype frequencies of 5,122 SNPs mapping to these five regions in 88 glioma cases with and 1,100 cases without a family history of PBT (discovery study). An additional series of 84 familial and 903 non-familial cases were used to replicate associations. In the discovery study, 12 SNPs showed significant associations with family history of PBT (P < 0.001). In the replication study, two of the 12 SNPs were confirmed: 12p13.33-12.1 PRMT8 rs17780102 (P = 0.031) and 17q12-21.32 SPOP rs650461 (P = 0.025). In the combined analysis of discovery and replication studies, the strongest associations were attained at four SNPs: 12p13.33-12.1 PRMT8 rs17780102 (P = 0.0001), SOX5 rs7305773 (P = 0.0001) and STKY1 rs2418087 (P = 0.0003), and 17q12-21.32 SPOP rs6504618 (P = 0.0006). Further, a significant gene-dosage effect was found for increased risk of family history of PBT with these four SNPs in the combined data set (P (trend) <1.0 × 10(-8)). The results support the linkage finding that some loci in the 12p13.33-12.1 and 17q12-q21.32 may contribute to gliomagenesis and suggest potential target genes underscoring linkage signals.

  • 6.
    Nordin, Angelica
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Medicinsk och klinisk genetik.
    Larsson, Elin
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Medicinsk och klinisk genetik.
    Thornell, Lars-Eric
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Anatomi.
    Holmberg, Monica
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Medicinsk och klinisk genetik.
    Tissue-specific splicing of ISCU results in a skeletal muscle phenotype in myopathy with lactic acidosis, while complete loss of ISCU results in early embryonic death in mice2011Ingår i: Human Genetics, ISSN 0340-6717, E-ISSN 1432-1203, Vol. 129, nr 4, s. 371-378Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Hereditary myopathy with lactic acidosis (HML) is caused by an intron mutation in the iron-sulphur cluster assembly gene (ISCU) leading to incorporation of intron sequence into the mRNA. This results in a deficiency of Fe-S cluster proteins, affecting the TCA cycle and the respiratory chain. The proteins involved in the Fe-S machinery are evolutionary conserved and shown to be fundamental in all organisms examined. ISCU is expressed at high levels in numerous tissues in mammals, including high metabolic tissues like the heart, suggesting that a drastic mutation in the ISCU gene would be damaging to all energy-demanding organs. In spite of this, the symptoms in patients with HML are restricted to skeletal muscle, and it has been proposed that splicing events may contribute to the muscle specificity. In this study we confirm that a striking difference in the splicing pattern of mutant ISCU exists between different tissues. The highest level of incorrectly spliced ISCU mRNA was found in skeletal muscle, while the normal splice form predominated in patient heart. The splicing differences were also reflected at a functional level, where loss of Fe-S cluster carrying enzymes and accumulation of iron were present in muscle, but absent in other tissues. We also show that complete loss of ISCU in mice results in early embryonic death. The mice data confirm a fundamental role for ISCU in mammals and further support tissue-specific splicing as the major mechanism limiting the phenotype to skeletal muscle in HML.

  • 7. Rajaraman, Preetha
    et al.
    Melin, Beatrice S
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Wang, Zhaoming
    McKean-Cowdin, Roberta
    Michaud, Dominique S
    Wang, Sophia S
    Bondy, Melissa
    Houlston, Richard
    Jenkins, Robert B
    Wrensch, Margaret
    Yeager, Meredith
    Ahlbom, Anders
    Albanes, Demetrius
    Andersson, Ulrika
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Freeman, Laura E Beane
    Buring, Julie E
    Butler, Mary Ann
    Braganza, Melissa
    Carreon, Tania
    Feychting, Maria
    Fleming, Sarah J
    Gapstur, Susan M
    Gaziano, J Michael
    Giles, Graham G
    Hallmans, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Henriksson, Roger
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Hoffman-Bolton, Judith
    Inskip, Peter D
    Johansen, Christoffer
    Kitahara, Cari M
    Lathrop, Mark
    Liu, Chenwei
    Le Marchand, Loic
    Linet, Martha S
    Lonn, Stefan
    Peters, Ulrike
    Purdue, Mark P
    Rothman, Nathaniel
    Ruder, Avima M
    Sanson, Marc
    Sesso, Howard D
    Severi, Gianluca
    Shu, Xiao-Ou
    Simon, Matthias
    Stampfer, Meir
    Stevens, Victoria L
    Visvanathan, Kala
    White, Emily
    Wolk, Alicja
    Zeleniuch-Jacquotte, Anne
    Zheng, Wei
    Decker, Paul
    Enciso-Mora, Victor
    Fridley, Brooke
    Gao, Yu-Tang
    Kosel, Matthew
    Lachance, Daniel H
    Lau, Ching
    Rice, Terri
    Swerdlow, Anthony
    Wiemels, Joseph L
    Wiencke, John K
    Shete, Sanjay
    Xiang, Yong-Bing
    Xiao, Yuanyuan
    Hoover, Robert N
    Fraumeni, Joseph F
    Chatterjee, Nilanjan
    Hartge, Patricia
    Chanock, Stephen J
    Genome-wide association study of glioma and meta-analysis2012Ingår i: Human Genetics, ISSN 0340-6717, E-ISSN 1432-1203, Vol. 131, nr 12, s. 1877-1888Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Gliomas account for approximately 80 % of all primary malignant brain tumors and, despite improvements in clinical care over the last 20 years, remain among the most lethal tumors, underscoring the need for gaining new insights that could translate into clinical advances. Recent genome-wide association studies (GWAS) have identified seven new susceptibility regions. We conducted a new independent GWAS of glioma using 1,856 cases and 4,955 controls (from 14 cohort studies, 3 case-control studies, and 1 population-based case-only study) and found evidence of strong replication for three of the seven previously reported associations at 20q13.33 (RTEL), 5p15.33 (TERT), and 9p21.3 (CDKN2BAS), and consistent association signals for the remaining four at 7p11.2 (EGFR both loci), 8q24.21 (CCDC26) and 11q23.3 (PHLDB1). The direction and magnitude of the signal were consistent for samples from cohort and case-control studies, but the strength of the association was more pronounced for loci rs6010620 (20q,13.33; RTEL) and rs2736100 (5p15.33, TERT) in cohort studies despite the smaller number of cases in this group, likely due to relatively more higher grade tumors being captured in the cohort studies. We further examined the 85 most promising single nucleotide polymorphism (SNP) markers identified in our study in three replication sets (5,015 cases and 11,601 controls), but no new markers reached genome-wide significance. Our findings suggest that larger studies focusing on novel approaches as well as specific tumor subtypes or subgroups will be required to identify additional common susceptibility loci for glioma risk.

  • 8. Teerlink, Craig C.
    et al.
    Thibodeau, Stephen N.
    McDonnell, Shannon K.
    Schaid, Daniel J.
    Rinckleb, Antje
    Maier, Christiane
    Vogel, Walther
    Cancel-Tassin, Geraldine
    Egrot, Christophe
    Cussenot, Olivier
    Foulkes, William D.
    Giles, Graham G.
    Hopper, John L.
    Severi, Gianluca
    Eeles, Ros
    Easton, Douglas
    Kote-Jarai, Zsofia
    Guy, Michelle
    Cooney, Kathleen A.
    Ray, Anna M.
    Zuhlke, Kimberly A.
    Lange, Ethan M.
    FitzGerald, Liesel M.
    Stanford, Janet L.
    Ostrander, Elaine A.
    Wiley, Kathleen E.
    Isaacs, Sarah D.
    Walsh, Patrick C.
    Isaacs, William B.
    Wahlfors, Tiina
    Tammela, Teuvo
    Schleutker, Johanna
    Wiklund, Fredrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Grönberg, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Emanuelsson, Monica
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Carpten, John
    Bailey-Wilson, Joan
    Whittemore, Alice S.
    Oakley-Girvan, Ingrid
    Hsieh, Chih-Lin
    Catalona, William J.
    Zheng, S. Lilly
    Jin, Guangfu
    Lu, Lingyi
    Xu, Jianfeng
    Camp, Nicola J.
    Cannon-Albright, Lisa A.
    Association analysis of 9,560 prostate cancer cases from the International Consortium of Prostate Cancer Genetics confirms the role of reported prostate cancer associated SNPs for familial disease2014Ingår i: Human Genetics, ISSN 0340-6717, E-ISSN 1432-1203, Vol. 133, nr 3, s. 347-356Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Previous GWAS studies have reported significant associations between various common SNPs and prostate cancer risk using cases unselected for family history. How these variants influence risk in familial prostate cancer is not well studied. Here, we analyzed 25 previously reported SNPs across 14 loci from prior prostate cancer GWAS. The International Consortium for Prostate Cancer Genetics (ICPCG) previously validated some of these using a family-based association method (FBAT). However, this approach suffered reduced power due to the conditional statistics implemented in FBAT. Here, we use a case-control design with an empirical analysis strategy to analyze the ICPCG resource for association between these 25 SNPs and familial prostate cancer risk. Fourteen sites contributed 12,506 samples (9,560 prostate cancer cases, 3,368 with aggressive disease, and 2,946 controls from 2,283 pedigrees). We performed association analysis with Genie software which accounts for relationships. We analyzed all familial prostate cancer cases and the subset of aggressive cases. For the familial prostate cancer phenotype, 20 of the 25 SNPs were at least nominally associated with prostate cancer and 16 remained significant after multiple testing correction (p a parts per thousand currency sign 1E (-3)) occurring on chromosomal bands 6q25, 7p15, 8q24, 10q11, 11q13, 17q12, 17q24, and Xp11. For aggressive disease, 16 of the SNPs had at least nominal evidence and 8 were statistically significant including 2p15. The results indicate that the majority of common, low-risk alleles identified in GWAS studies for all prostate cancer also contribute risk for familial prostate cancer, and that some may contribute risk to aggressive disease.

  • 9.
    Wiklund, Fredrik
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper.
    Jonsson, BA
    Göransson, I
    Bergh, A
    Grönberg, H
    Linkage analysis of prostate cancer susceptibility: confirmation of linkage at 8p22-232003Ingår i: Human Genetics, ISSN 0340-6717, E-ISSN 1432-1203, Vol. 112, nr 4, s. 414-418Artikel i tidskrift (Refereegranskat)
1 - 9 av 9
RefereraExporteraLänk till träfflistan
Permanent länk
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • 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