Opin vísindi
Opin vísindi er varðveislusafn vísindaefnis og doktorsritgerða í opnum aðgangi á vegum íslenskra háskóla og Landsbókasafns Íslands - Háskólabókasafns.
Opinn aðgangur að rannsóknaniðurstöðum er í samræmi við 10. gr. laga nr. 3/2003 um opinberan stuðning við vísindarannsóknir sem og kröfur innlendra og erlendra rannsóknasjóða. Markmiðið með opnum aðgangi er að niðurstöður rannsókna séu aðgengilegar sem flestum óhindrað og án endurgjalds á rafrænu formi. Vistun í varðveislusafninu er varanleg og ætlað að tryggja aðgang að vísindaefni íslenskra háskóla í opnum aðgangi um ókomna tíð. Varðveislusafnið Opin vísindi er tengt við rannsóknagáttina IRIS og rannsóknaniðurstöður í opnum aðgangi sem eru skráðar í IRIS eru um leið vistaðar og gerðar aðgengilegar til framtíðar í varðveislusafninu. Með því að safna þessu efni saman í eitt safn verður aðgangur að því einfaldur og þægilegur fyrir alla sem vilja kynna sér það og geta þannig notið þess öfluga vísindastarfs sem fram fer í háskólum landsins.
Varðveislusafnið er OpenAIRE / OpenAIREplus samhæft og samrýmist kröfum sem gerðar eru um birtingu rannsóknaniðurstaðna úr verkefnum sem styrkt eru úr evrópsku rannsóknaáætlununum FP7 og H2020.
Varðveislusafnið notar opna hugbúnaðinn DSpace.
Opinn aðgangur að rannsóknaniðurstöðum er í samræmi við 10. gr. laga nr. 3/2003 um opinberan stuðning við vísindarannsóknir sem og kröfur innlendra og erlendra rannsóknasjóða. Markmiðið með opnum aðgangi er að niðurstöður rannsókna séu aðgengilegar sem flestum óhindrað og án endurgjalds á rafrænu formi. Vistun í varðveislusafninu er varanleg og ætlað að tryggja aðgang að vísindaefni íslenskra háskóla í opnum aðgangi um ókomna tíð. Varðveislusafnið Opin vísindi er tengt við rannsóknagáttina IRIS og rannsóknaniðurstöður í opnum aðgangi sem eru skráðar í IRIS eru um leið vistaðar og gerðar aðgengilegar til framtíðar í varðveislusafninu. Með því að safna þessu efni saman í eitt safn verður aðgangur að því einfaldur og þægilegur fyrir alla sem vilja kynna sér það og geta þannig notið þess öfluga vísindastarfs sem fram fer í háskólum landsins.
Varðveislusafnið er OpenAIRE / OpenAIREplus samhæft og samrýmist kröfum sem gerðar eru um birtingu rannsóknaniðurstaðna úr verkefnum sem styrkt eru úr evrópsku rannsóknaáætlununum FP7 og H2020.
Varðveislusafnið notar opna hugbúnaðinn DSpace.
Flokkar í Opnum vísindum
Veldu flokk til að skoða.
- University of Iceland
- University of Akureyri
- Bifröst University
- Hólar University College
- Reykjavík University
- IRIS
- Agricultural University of Iceland
- National and University Library of Iceland
- Iceland University of the Arts
Nýlega bætt við
Passion a key for success : Exploring motivational factors in football players
(2022-04) Sigmundsson, H.; Dybendal, B. H.; Loftesnes, J. M.; Ólafsson, B.; Grassini, S.; Faculty of Education and Diversity; Education
The principal aim of the present study was to investigate whether passion, grit and mindset differ between distinct levels of football competence in two football teams - elite and junior teams. We compared the 30% highest scoring (HFC) and the 30% lowest scoring groups (LFC) of football competence using the trainer's rankings among two teams from west part of Norway. The results showed that the HFC groups scored significant higher on the passion scale than the LFC groups. That was the case for both teams. There was no difference between the groups for grit or mindset total scores. These results may indicate the important role of passion for achievement and for becoming a good football player.
Gene-mapping study of extremes of cerebral small vessel disease reveals TRIM47 as a strong candidate
(2022-06-01) Mishra, Aniket; Duplaà, Cecile; Vojinovic, Dina; Suzuki, Hideaki; Sargurupremraj, Muralidharan; Zilhão, Nuno R.; Li, Shuo; Bartz, Traci M.; Jian, Xueqiu; Zhao, Wei; Hofer, Edith; Wittfeld, Katharina; Harris, Sarah E.; Van Der Auwera-Palitschka, Sandra; Luciano, Michelle; Bis, Joshua C.; Adams, Hieab H.H.; Satizabal, Claudia L.; Gottesman, Rebecca F.; Gampawar, Piyush G.; Bülow, Robin; Weiss, Stefan; Yu, Miao; Bastin, Mark E.; Lopez, Oscar L.; Vernooij, Meike W.; Beiser, Alexa S.; Völker, Uwe; Kacprowski, Tim; Soumare, Aicha; Smith, Jennifer A.; Knopman, David S.; Morris, Zoe; Zhu, Yicheng; Rotter, Jerome I.; Dufouil, Carole; Valdes Hernández, Maria; Muñoz Maniega, Susana; Lathrop, Mark; Boerwinkle, Erik; Schmidt, Reinhold; Ihara, Masafumi; Mazoyer, Bernard; Yang, Qiong; Joutel, Anne; Tournier-Lasserve, Elizabeth; Launer, Lenore J.; Deary, Ian J.; Mosley, Thomas H.; Gudnason, Vilmundur; Faculty of Medicine
Cerebral small vessel disease is a leading cause of stroke and a major contributor to cognitive decline and dementia, but our understanding of specific genes underlying the cause of sporadic cerebral small vessel disease is limited. We report a genome-wide association study and a whole-exome association study on a composite extreme phenotype of cerebral small vessel disease derived from its most common MRI features: white matter hyperintensities and lacunes. Seventeen population-based cohorts of older persons with MRI measurements and genome-wide genotyping (n = 41326), whole-exome sequencing (n = 15965), or exome chip (n = 5249) data contributed 13776 and 7079 extreme small vessel disease samples for the genome-wide association study and whole-exome association study, respectively. The genome-wide association study identified significant association of common variants in 11 loci with extreme small vessel disease, of which the chr12q24.11 locus was not previously reported to be associated with any MRI marker of cerebral small vessel disease. The whole-exome association study identified significant associations of extreme small vessel disease with common variants in the 5′ UTR region of EFEMP1 (chr2p16.1) and one probably damaging common missense variant in TRIM47 (chr17q25.1). Mendelian randomization supports the causal association of extensive small vessel disease severity with increased risk of stroke and Alzheimer's disease. Combined evidence from summary-based Mendelian randomization studies and profiling of human loss-of-function allele carriers showed an inverse relation between TRIM47 expression in the brain and blood vessels and extensive small vessel disease severity. We observed significant enrichment of Trim47 in isolated brain vessel preparations compared to total brain fraction in mice, in line with the literature showing Trim47 enrichment in brain endothelial cells at single cell level. Functional evaluation of TRIM47 by small interfering RNAs-mediated knockdown in human brain endothelial cells showed increased endothelial permeability, an important hallmark of cerebral small vessel disease pathology. Overall, our comprehensive gene-mapping study and preliminary functional evaluation suggests a putative role of TRIM47 in the pathophysiology of cerebral small vessel disease, making it an important candidate for extensive in vivo explorations and future translational work.
Correction : PUFA w-3 and w-6 biomarkers and sleep: a pooled analysis of cohort studies on behalf of the Fatty Acids and Outcomes Research Consortium (FORCE) (The American Journal of Clinical Nutrition (2022) 115:3 (864-876) DOI: 10.1093/ajcn/nqab408)
(2022-07-06) Murphy, Rachel A.; Tintle, Nathan; Harris, William S.; Darvishian, Maryam; Marklund, Matti; Virtanen, Jyrki K.; Hantunen, Sari; De Mello, Vanessa D.; Tuomilehto, Jaakko; Lindstr m, Jaana; Bolt, Matthew A.; Brouwer, Ingeborg A.; Wood, Alexis C.; Senn, MacKenzie; Redline, Susan; Tsai, Michael Y.; Gudnason, Vilmundur; Eiriksdottir, Gudny; Lindberg, Eva; Shadyab, Aladdin H.; Liu, Buyun; Carnethon, Mercedes; Uusitupa, Matti; Djousse, Luc; Ris rus, Ulf; Lind, Lars; Van Dam, Rob M.; Koh, Woon Puay; Shi, Peilin; Siscovick, David; Lemaitre, Rozenn N.; Mozaffarian, Dariush; Faculty of Medicine
In the originally published version of this manuscript, "difficulty falling sleeping" was used instead of "difficulty falling asleep" throughout. The authors apologize for this error. This error has been corrected online.
Genome-wide meta-analyses reveal novel loci for verbal short-term memory and learning
(2022-08-16) Lahti, Jari; Tuominen, Samuli; Yang, Qiong; Pergola, Giulio; Ahmad, Shahzad; Amin, Najaf; Armstrong, Nicola J.; Beiser, Alexa; Bey, Katharina; Bis, Joshua C.; Boerwinkle, Eric; Bressler, Jan; Campbell, Archie; Campbell, Harry; Chen, Qiang; Corley, Janie; Cox, Simon R.; Davies, Gail; De Jager, Philip L.; Derks, Eske M.; Faul, Jessica D.; Fitzpatrick, Annette L.; Fohner, Alison E.; Ford, Ian; Fornage, Myriam; Gerring, Zachary; Grabe, Hans J.; Grodstein, Francine; Gudnason, Vilmundur; Simonsick, Eleanor; Holliday, Elizabeth G.; Joshi, Peter K.; Kajantie, Eero; Kaprio, Jaakko; Karell, Pauliina; Kleineidam, Luca; Knol, Maria J.; Kochan, Nicole A.; Kwok, John B.; Leber, Markus; Lam, Max; Lee, Teresa; Li, Shuo; Loukola, Anu; Luck, Tobias; Marioni, Riccardo E.; Mather, Karen A.; Medland, Sarah; Mirza, Saira S.; Nalls, Mike A.; Faculty of Medicine
Understanding the genomic basis of memory processes may help in combating neurodegenerative disorders. Hence, we examined the associations of common genetic variants with verbal short-term memory and verbal learning in adults without dementia or stroke (N = 53,637). We identified novel loci in the intronic region of CDH18, and at 13q21 and 3p21.1, as well as an expected signal in the APOE/APOC1/TOMM40 region. These results replicated in an independent sample. Functional and bioinformatic analyses supported many of these loci and further implicated POC1. We showed that polygenic score for verbal learning associated with brain activation in right parieto-occipital region during working memory task. Finally, we showed genetic correlations of these memory traits with several neurocognitive and health outcomes. Our findings suggest a role of several genomic loci in verbal memory processes.
Stroke genetics informs drug discovery and risk prediction across ancestries
(2022-09-30) PRECISEQ Consortium; FinnGen Consortium; NINDS Stroke Genetics Network (SiGN); MEGASTROKE Consortium; SIREN Consortium; China Kadoorie Biobank Collaborative Group; VA Million Veteran Program; International Stroke Genetics Consortium (ISGC); Biobank Japan; CHARGE consortium.; GIGASTROKE Consortium; COMPASS Consortium; INVENT Consortium; Dutch Parelsnoer Initiative (PSI) Cerebrovascular Disease Study Group; Estonian Biobank; Faculty of Medicine
Previous genome-wide association studies (GWASs) of stroke - the second leading cause of death worldwide - were conducted predominantly in populations of European ancestry1,2. Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis3, and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach4, we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry5. Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries.