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
Role of MITF in olfactory bulb neurons. Putative MITF target genes in neurons and the effects of its loss in the aging olfactory bulb.
(University of Iceland, School of Health Sciences, Faculty of Medicine, 2025) Mechmet, Fatich; Pétur Henry Petersen, Eiríkur Steingrímsson; Læknadeild (HÍ); Faculty of Medicine (UI); Heilbrigðisvísindasvið (HÍ); School of Health Sciences (UI)
Microphthalmia-associated transcription factor (MITF) is a master regulator in melanocytes and plays and important role in mast cells. Mitf is also expressed in the mitral and tufted (M/T) cells which are projection neurons (PNs), in the olfactory bulb (OB). Lack of MITF leads to neuronal hyperactivity in primary M/T cells but the general function of MITF in neurons is currently unknown. In this study, putative MITF target genes in M/T cells of mice were identified. They differ from target genes in other cell types including melanocytes and can be grouped into two categories: those likely to be involved in inhibiting neuronal activity and those specific to a subgroup of tufted cells called middle tufted cells (mTCs). This work also shows that the mTCs are reduced in number in the absence of Mitf, suggesting a role for Mitf in the generation or survival of the mTCs and/or their function. Altered response to odors is also observed in Mitfmi-vag9/mi-vga9 mice, indicating a role of MITF in olfactory adaptation. Aging affects various brain structures and sensory systems, including the OB, resulting in a decline in olfactory ability. Decline in the OB is associated with early signs of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. However, the underlying reasons remain unclear. Primary PNs from OBs of young Mitfmi-vga9/mi-vga9 mice show hyperactivity, potentially linked to reduced expression of the potassium channel subunit Kcnd3/Kv4.3, which impacts intrinsic plasticity. In aged Mitfmi-vag9/mi-vag9 mice, reduced olfactory ability was observed without any signs of neuroinflammation or reduction in neuronal number. An increase in the expression of genes coding for potassium channel subunits was found in the OBs of aged Mitfmi-vga9/mi-vga9 mice. This suggests that increased expression of potassium channel subunits in aging Mitfmi-vga9/mi-vga9 mice may compensate for or stabilize neuronal hyperactivity observed in the OB of young Mitfmi-vga9/mi-vga9 mice.
The Impact of Smoothened Cholesterol-Binding Pocket Mutations on Hedgehog Signaling and Osteoarthritis
(University of Iceland, School of Health Sciences, Faculty of Medicine, 2025-10) Smith, Abbi Elise; Sara Sigurbjörnsdóttir and Eiríkur Steingrímsson; Læknadeild (HÍ); Faculty of Medicine (UI); Heilbrigðisvísindasvið (HÍ); School of Health Sciences (UI)
A genome wide association study identified a risk variant of Smoothened (p.Arg173Cys;
SMOR173C) associated with hip osteoarthritis. Smoothened (SMO), a 7-transmembrane G
protein coupled receptor-like protein, is a key component of the hedgehog signal
transduction mechanism. The hedgehog signaling pathway is known to be activated in
osteoarthritic chondrocytes, but this was the first identified osteoarthritis risk variant in a
hedgehog pathway gene. Interestingly, even though hedgehog signaling is elevated in
osteoarthritis tissues, structural analysis predicted the SMOR173C variant to reduce the
binding capability of SMO to cholesterol. The binding of cholesterol to the extracellular
domain of SMO was recently discovered to be a critical step in SMO activation. As such,
the predicted effect of this variant on SMO conflicts with the current known relationship
between hedgehog signaling and osteoarthritis. Thus, the aim of the studies described
in this thesis was to elucidate the role of the SMOR173C variant in the development of
osteoarthritis.
To determine whether the SMOR173C variant alters downstream hedgehog signaling
activity, we introduced the mutation to the prechondrogenic cell line, ATDC5 in two ways:
by overexpressing the human SMO protein containing the SMOR173C mutation, and by
generating an endogenously expressing mutation by restoring a null allele in the ATDC5
Smo-null cell line. We showed in both models that the SMOR173C did not abolish
downstream hedgehog signaling activity, disproving the structural predictions for the
variant. Additionally, we microinjected hSMOR173C mRNA into smo-/- zebrafish embryos
and showed that the hSMOR173C mRNA more efficiently recovered a normal morphological
phenotype than the hSMOWT mRNA or mRNAs with mutations known to abolish
cholesterol binding and downstream hedgehog signaling.
To determine the effect of the SMOR173C mutation on osteoarthritis development, we
developed a three-dimensional hydrogel cell culture system to better recapitulate the
native environment of chondrocytes and found that in the hydrogel system the ATDC5
cells showed indications of precocious differentiation when compared to ATDC5 cell
cultured in differentiation medium in a monolayer. Next, we used a cytokine cocktail to
stimulate the ATDC5 cells and drive them toward an osteoarthritis-like phenotype. Then
we employed both methods using the endogenous mutant ATDC5 cell lines. Cells
expressing the R173C variant expressed more than three-fold elevated levels of Mmp13
mRNA at baseline. The effect increased to over four-fold elevation in response to cytokine
treatment. As MMP13 is a key catabolic enzyme responsible for cartilage degradation in
osteoarthritis, we concluded that chronically increased MMP13 mRNA expression could
be responsible for the increased risk of hip osteoarthritis associated with the SMOR173C
variant.
Finally, we used evolutionary and phylogenetic analyses of smo mutations in teleost fish
to identify sites predicted to cause species diversification. We paired this information
with clinical reports of disease and cancer driven by SMO mutations to gain a better
understanding of the genetic plasticity of SMO. We also found a gene-dose response in
the transgenic smo+/- zebrafish with evidence of a heterochronic shift in hedgehog
signaling-driven developmental processes: somitogenesis and chondrogenesis. From this
we concluded that smo is permissive of mutations largely located outside of the
transmembrane domain and likely contributed to species diversification related to jaw
structure and body plan morphologies throughout evolutionary history in teleost fishes.
The human clinical data follow the same trend: SMO variants associated with skeletal
changes lie outside the transmembrane domain, while oncogenic SMO mutations largely
occur within the transmembrane domain.
This project used in vitro and in vivo models to investigate the role of the SMOR173C variant
in downstream hedgehog signaling as well as an osteoarthritis-like phenotype and
identified a potentially pathological increase in Mmp13 mRNA expression associated with
the SMOR173C variant that likely contributes to osteoarthritis initiation and progression.
Refining marine polysaccharides and their immunomodulatory effects
(University of Iceland, School of Health Sciences, Faculty of Food Science and Nutrition, 2025-10-02) Daugbjerg Christensen, Monica; Guðmundur Óli Hreggviðsson; Matvæla- og næringarfræðideild (HÍ); Faculty of Food Science and Nutrition (UI); Heilbrigðisvísindasvið (HÍ); School of Health Sciences (UI)
Brown seaweed is a rich source of structurally diverse polysaccharides with promising bioactive properties. This study investigated in four ways how enzymatic refining can modify marine polysaccharides and influence their immunomodulatory effects. 1) A novel sulfatase, SulA1, cloned from a marine Arthrobacter strain, was characterized, and shown to selectively act on the chondroitin sulfate monosaccharide N-Acetyl-D-galactosamine-4-sulfate. This introduced the possibilities for the use of SulA1 in targeted desulfation strategies to alter bioactivity of targeted molecules. 2) Laminarin from three brown seaweed species (Laminaria digitata, L. hyperborea, and Saccharina latissima) was extracted and enzymatically modified. The laminarin derivatives were structurally analysed and found to distinctly regulate dendritic cell activity depending on their molecular size and branching pattern. These data suggest that different laminarin derivatives may have different therapeutic applications within the immune system. 3) Fucoidan from S. latissima was enzymatically refined into defined molecular weight fractions. The low molecular weight fucoidan fraction significantly suppressed the secretion of the pro-inflammatory cytokine by dendritic cells, indicating potential therapeutic applications against inflammatory diseases. 4) Two enzymatically generated alginate oligosaccharide fractions, enhanced cytokines secretion by dendritic cells and promoted Th1 responses in co-cultures with T cells. These findings highlight distinct immunomodulatory properties of alginate oligosaccharides with potential therapeutic relevance in inducing inflammatory responses, e.g. as adjuvants or in cancer treatment. Collectively, these results demonstrate that targeted enzymatic modifications can reshape the immunomodulatory activity of marine-derived polysaccharides, positioning them as promising candidates for therapeutic development. At the same time, this strategy enhances the efficient use of seaweed biomass and supports the creation of sustainable, high-value products with potential applications in pharmaceuticals and nutraceuticals.
Impact of anticoagulation and immunosuppressive drugs on the prognosis of patients with colorectal cancer: a population-based study
(University of Iceland, School of Health Sciences, Faculty of Medicine, 2025-10-01) Agustsson, Arnar; Einar Stefán Björnsson; Læknadeild (HÍ); Faculty of Medicine (UI); Heilbrigðisvísindasvið (HÍ); School of Health Sciences (UI)
Nýgengi ristil- og endaþarmskrabbameina fer vaxandi og eru þau ein algengasta orsök andláta vegna krabbameina. Oftast greinast þau vegna blæðingartengdra einkenna frá meltingarvegi og blóðþynningarlyf hafa verið tengd við auknar líkur á blæðingum frá þessum krabbameinum. Hins vegar er það ekki rannsakað hvaða áhrif blóðþynningarlyf geti haft á orsakir meltingavegsblæðinga, hvort þau auki greiningar þessara krabbameina og geti leitt til snemmgreiningar. Engar rannsóknir hafa kannað hvort stigun ristilkrabbameinsins eða lifun einstaklinga á blóðþynningu sé frábrugðin við almennt þýði. Þá hafa rannsóknir á áhrifum hjartamagnýl á lifun einstaklinga ekki borið saman um hvort hjartanagnýl sé verndandi og þá ekki með hvaða hætti það væri verndandi. Hvorki sterar né bólgueyðandi gigtarlyf (e. DMARDs) hafa verið rannsökuð hvort þau geti haft áhrif á lifun einstaklinga með ristil- og endaþarmskrabbamein, en þau hafa bæði sýnt bæta lifun í há áhættu sjúklingahópum.
Efni og aðferðir: Allar fjórar rannsóknirnar voru lýðgrundaðar afturskyggnar rannsóknir sem byggðu á gagnagrunnum. Fyrsta rannsóknin nýtti blóðþynningargagnagrunn til að kanna orsakir meltingarvegsblæðinga frá 2014-2019. Hinar þrjár rannsóknirnar byggðu á gagnagrunni yfir alla sjúklinga sem greindust með ristil- og endaþarmskrabbamein frá 2000- 2019 á Íslandi og báru saman lyfjanotkun fyrir greiningu og útkomur vegna krabbameins. Lyfjaupplýsingum var safnað beint úr uppflettingum sjúkraskráa fyrir blóðþynningarlyf og hjartamagnýl, og svo fengust upplýsingar um stera og bólgueyðandi gigtarlyf frá Lyfjagagnagrunni Landlæknis. Niðurstöður: Í fyrsta hluta verkefnisins reyndust 12.005 einstaklingar vera á blóðþynningu og af þeim greindust 752 með meltingarvegsblæðingar, þar af 273 (36%) sem höfðu bráða efri meltingarvegsblæðingu og 391 (52%) bráða neðri. Bæði ristil- og endaþarmskrabbamein (OR 3.7, 95% CI: 2.0 – 7.0, p< 0.001). Sjúklingar á hjartamagnýli höfðu svipaða heildarlifun en betri krabbameinssértæka lifun (HR: 0.79, 95% CI (0.65 – 0.95), p= 0.01). Í fjórða hluta voru 2388 sjúklingar og þar af 816 (34%) sem tóku stera og 91 (3.8%) sem tóku bólgueyðandi gigtarlyf. Sjúklingar sem tóku stera voru að jafnaði eldri og oftar kvenkyns. Sterahópurinn hafði svipaða heildarlifun, klára en ómarktæka fylgni við verri krabbameinssértæka lifun (HR: 1.15, 95% CI (0.96 – 1.38), p= 0.12) og verri sjúkdómsfría lifun (HR: 1.14, 95% CI (1.03 – 1.27), p= 0.02) miðað við samanburðarhópinn. Sjúklingar sem notuðu bólgueyðandi gigtarlyf voru af svipuðum aldri, kyni og með svipaða fylgisjúkdómabyrði og samanburðarhópurinn en voru oftar með krabbamein á stigi I (32% vs 21%, p= 0.02). Hópurinn á bólgueyðandi gigtarlyfjum hafði sambærilega heildarlifun og samanburðarhópurinn og krabbameinssértæka lifun. Ályktun: Niðurstöður þessara rannsókna renna frekari stoðum undir þá kenningu að blóðþynningarlyf geti leitt til snemmgreiningar einstaklinga með ristil- og endaþarmskrabbamein. Blóðþynningarlyf tengdust oftar blæðingartengdum einkennum sem orsökuðust af ristil- og endaþarmskrabbameini og blóðþynningarhópurinn hafði betri krabbameinssértæka lifun. Þetta undirstrikar mikilvægi þess að einstaklingar á blóðþynningu séu undir vökulu eftirliti. Hjartamagnýl tengdist betri krabbameinssértækri lifun, mögulega með því að draga úr eða hindra meinvörp. Steranotkun tengdist verri sjúkdómsfrírri lifun og með fylgi við verri krabbameinssértæka lifun. Bólgueyðandi gigtarlyf tengdust hærra hlutfalli sjúklinga á stigi I, en virtust ekki hafa nein teljandi áhrif á lifun. Niðurstöður rannsóknarinnar á sterum og bólgueyðandi gigtarlyfjum gefa tilefni til frekari rannsókna á þessu sviði til að kanna til hlýtar áhrif þeirra á útkomur einstaklinga með ristil- og endaþarmskrabbamein.
Papierforschung im Dienste der Buchgeschichte: Einbände des 18. Jahrhunderts in der Handschriftensammlung Árni Magnússons
(International Association of Paper Historians, 2025-03-01) Stegmann, Beeke
Many different bindings are preserved in the manuscript collection once owned by the Icelander Árni Magnússon
(1663-1730). Especially with regard to the eighteenth-century bindings, only a few types have hitherto been
described and dated. The present contribution shows that watermark research – in particular the analysis of the
paper used in the bindings’ endleaves – can help distinguish more styles and provide descriptions and at least rough
datings for four additional ones. A single bookbinder could produce several different types of bindings, but it is
clear that the book binder Bertel Wolck used various old paper for his bindings, possibly leftover sheets that still
circulated in Copenhagen in the 1720s.