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Lars Eide
University of Oslo
63Publications
20H-index
3,423Citations
Publications 63
Newest
#1Marie Rodinova (First Faculty of Medicine, Charles University in Prague)H-Index: 2
#2Jana Krizova (First Faculty of Medicine, Charles University in Prague)H-Index: 1
Last.Hana Hansikova (First Faculty of Medicine, Charles University in Prague)H-Index: 14
view all 13 authors...
ABSTRACT Skeletal muscle wasting and atrophy is one of the more severe clinical impairments resulting from the progression of Huntington9s disease (HD). Mitochondrial dysfunction may play a significant role in the etiology of HD, but the specific condition of mitochondria in muscle has not been widely studied during the development of HD. To determine the role of mitochondria in skeletal muscle during the early stages of HD, we analyzed quadriceps femoris muscle from 24-, 36-, 48- and 66-month-o...
#1Paula A. Bousquet (Ahus: Akershus University Hospital)H-Index: 1
#2Sebastian Meltzer (University of Oslo)H-Index: 3
Last.Anne Hansen Ree (University of Oslo)H-Index: 24
view all 12 authors...
Abstract Tumor hypoxia contributes to therapy resistance and metastatic progression of locally advanced rectal cancer (LARC). We postulated that the tumor mitochondrial metabolism, manifested by reactive oxygen species (ROS) and mitochondrial DNA (mtDNA) damage, reflects how hypoxic conditions connect to cancer-induced systemic inflammation and poor outcome. Levels of ROS and mtDNA damage were analyzed in three colorectal cancer (CRC) cell lines cultured for 24 hours under normoxia (21% O2) or h...
#1Georgina Askeland (University of Oslo)H-Index: 2
#2Zaneta Dosoudilova (Charles University in Prague)H-Index: 2
Last.Lars Eide (University of Oslo)H-Index: 20
view all 11 authors...
Huntington’s disease (HD) is a progressive neurodegenerative disorder primarily affecting the basal ganglia and is caused by expanded CAG repeats in the huntingtin gene. Except for CAG sizing, mitochondrial and nuclear DNA (mtDNA and nDNA) parameters have not yet proven to be representative biomarkers for disease and future therapy. Here, we identified a general suppression of genes associated with aerobic metabolism in peripheral blood mononuclear cells (PBMCs) from HD patients compared to cont...
#1Georgina Askeland (University of Oslo)H-Index: 2
#2Marie Rodinova (Charles University in Prague)H-Index: 2
Last.Lars Eide (University of Oslo)H-Index: 20
view all 14 authors...
ABSTRACT Huntington9s disease (HD) is a monogenic, progressive, neurodegenerative disorder with currently no available treatment. The Libechov transgenic minipig model for HD (TgHD) displays neuroanatomical similarities to humans and exhibits slow disease progression, and is therefore more powerful than available mouse models for the development of therapy. The phenotypic characterization of this model is still ongoing, and it is essential to validate biomarkers to monitor disease progression an...
#1Marie Rodinova (First Faculty of Medicine, Charles University in Prague)H-Index: 2
#2Jana Krizova (First Faculty of Medicine, Charles University in Prague)H-Index: 1
Last.Hana Hansikova (First Faculty of Medicine, Charles University in Prague)H-Index: 14
view all 12 authors...
Background Skeletal muscle wasting and atrophy is one of the severe clinical impairment connected with progression of Huntington’s disease (HD). Mitochondrial dysfunction may play significant role in aetiology of the HD but exact condition of mitochondria as the major energy-producing organelles during development of the HD in muscle has not yet been carefully investigated. The aim of the study was the longitudinal monitoring of mitochondrial function in skeletal muscle of transgenic minipigs ex...
Background Huntington´s disease (HD) is devastating neurodegenerative disorder caused by the mutation in huntingtin gene. One of the largest contributors to HD pathology represents oxidative stress, though the exact mechanism of its cause remains unclear. Molecular characterization of a unique porcine model of HD could serve for better understanding of the disease pathogenesis as well as for better evaluation of the therapeutic efficiency of preclinical studies on this large animal model. Aims I...
#1Katja Scheffler (Oslo University Hospital)H-Index: 10
#2Lyudmila I. Rachek (USA: University of South Alabama)H-Index: 16
Last.Lars Eide (Oslo University Hospital)H-Index: 20
view all 9 authors...
Abstract Mitochondrial DNA (mtDNA) resides in close proximity to metabolic reactions, and is maintained by the 8-oxoguanine DNA glycosylase (Ogg1) and other members of the base excision repair pathway. Here, we tested the hypothesis that changes in liver metabolism as under fasting/feeding conditions would be sensed by liver mtDNA, and that Ogg1 deficient mice might unravel a metabolic phenotype. Wild type (WT) and ogg1 −/− mice were either fed ad libitum or subjected to fasting for 24 h, and th...
#1Henok Kassahun (Ahus: Akershus University Hospital)H-Index: 10
#2Tanima SenGupta (Ahus: Akershus University Hospital)H-Index: 5
Last.Hilde Nilsen (Ahus: Akershus University Hospital)H-Index: 27
view all 11 authors...
Abstract Oxidation of DNA bases, an inevitable consequence of oxidative stress, requires the base excision repair (BER) pathway for repair. Caenorhabditis elegans is a well-established model to study phenotypic consequences and cellular responses to oxidative stress. To better understand how BER affects phenotypes associated with oxidative stress, we characterised the C. elegans nth-1 mutant, which lack the only DNA glycosylase dedicated to repair of oxidative DNA base damage, the NTH-1 DNA glyc...
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