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Ulla Vogel  - - - 
Top co-authors See all
Anne Tjønneland

962 shared publications

Danish Cancer Society Research Center; Copenhagen Denmark

Håkan Wallin

641 shared publications

National Research Centre for the Working Environment, Lersø Parkallé, DK Copenhagen, Denmark

V. Stone

162 shared publications

Institute of Biological Chemistry, Biophysics and Bioengineering School of Engineering and Physical Sciences, Heriot-Watt University, Edinburgh, UK

Vibeke Andersen

111 shared publications

Medical Department; Regional Hospital of Viborg; Viborg Denmark

Janeck J. Scott-Fordsmand

108 shared publications

Department of Bioscience, Aarhus University, Vejlsovej 25, PO BOX 314, DK-8600 Silkeborg, Denmark

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Distribution of Articles published per year 
(1992 - 2018)
Total number of journals
published in
 
34
 
Publications See all
Article 0 Reads 0 Citations Genetic polymorphisms in genes of class switch recombination and multiple myeloma risk and survival: an IMMEnSE study Daniele Campa, Alessandro Martino, Angelica Macauda, Marek D... Published: 11 January 2019
Leukemia & Lymphoma, doi: 10.1080/10428194.2018.1551536
DOI See at publisher website
PREPRINT-CONTENT 0 Reads 0 Citations Intake of red and processed meat, use of non-steroid anti-inflammatory drugs, genetic variants and risk of colorectal ca... Vibeke Andersen, Ulrich Halekoh, Anne Tjønneland, Ulla Vogel... Published: 14 December 2018
bioRxiv, doi: 10.1101/496968
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Red and processed meat have been associated with increased risk of colorectal cancer (CRC), whereas long-term use of non-steroid anti-inflammatory drugs (NSAIDs) may reduce the risk. The aim was to investigate potential interactions between meat intake, NSAID use, and gene variants in fatty acid metabolism and NSAID pathways in relation to the risk of CRC. A nested case-cohort study of 1038 CRC cases and 1857 randomly selected participants from the Danish prospective “Diet, Cancer and Health” study encompassing 57,053 persons was performed using the Cox proportional hazard models. Gene variants in SLC25A20, PRKAB1, LPCAT1, PLA2G4A, ALOX5, PTGER3, TP53, CCAT2, TCF7L2, BCL2 were investigated. CCAT2 rs6983267 was associated with risk of CRC per se (p
Article 0 Reads 1 Citation Safety Assessment of Graphene-Based Materials: Focus on Human Health and the Environment Bengt Fadeel, Cyrill Bussy, Sonia Merino, Ester Vázquez, Emm... Published: 02 November 2018
ACS Nano, doi: 10.1021/acsnano.8b04758
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Article 0 Reads 0 Citations Physicochemical predictors of Multi-Walled Carbon Nanotube-induced pulmonary histopathology and toxicity one year after ... Kristina Bram Knudsen, Trine Berthing, Petra Jackson, Sarah ... Published: 18 October 2018
Basic & Clinical Pharmacology & Toxicology, doi: 10.1111/bcpt.13119
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Multi‐walled carbon nanotubes (MWCNT) are widely used nanomaterials that cause pulmonary toxicity upon inhalation. The physicochemical properties of MWCNT vary greatly, which makes general safety evaluation challenging to conduct. Identification of the toxicity‐inducing physicochemical properties of MWCNT is therefore of great importance. We have evaluated histological changes in lung tissue 1year after a single intratracheal instillation of 11 well‐characterized MWCNT in female C57BL/6N BomTac mice. Genotoxicity of liver and spleen was evaluated by the Comet assay. The dose of 54 μg MWCNT corresponds to three times the estimated dose accumulated during a work life at a NIOSH recommended exposure limit (0.001 mg/m3). Short and thin MWCNT were observed as agglomerates in lung tissue 1 year after exposure, whereas thicker and longer MWCNT were detected as single fibres, suggesting biopersistence of both types of MWCNT. The thin and entangled MWCNT induced varying degree of pulmonary inflammation, in terms of lymphocytic aggregates, granulomas and macrophage infiltration, whereas two thick and straight MWCNT did not. By multiple regression analysis, larger diameter and higher content of iron predicted less histopathological changes, whereas higher cobalt content significantly predicted more histopathological changes. No MWCNT‐related fibrosis or tumours in the lungs or pleura was found. One thin and entangled MWCNT induced increased levels of DNA strand breaks in liver; however, no physicochemical properties could be related to genotoxicity. This study reveals physicochemical‐dependent difference in MWCNT‐induced long‐term, pulmonary histopathological changes. Identification of diameter size and cobalt content as important for MWCNT toxicity provides clues for designing MWCNT, which cause reduced human health effects following pulmonary exposure. This article is protected by copyright. All rights reserved.
Article 0 Reads 0 Citations Genetically determined high activities of the TNF-alpha, IL23/IL17, and NFkB pathways were associated with increased ris... Jacob Sode, Steffen Bank, Ulla Vogel, Paal Skytt Andersen, S... Published: 12 September 2018
BMC Medical Genetics, doi: 10.1186/s12881-018-0680-z
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Ankylosing spondylitis (AS) results from the combined effects of susceptibility genes and environmental factors. Polymorphisms in genes regulating inflammation may explain part of the heritability of AS. Using a candidate gene approach in this case-control study, 51 mainly functional single nucleotide polymorphisms (SNPs) in genes regulating inflammation were assessed in 709 patients with AS and 795 controls. Data on the patients with AS were obtained from the DANBIO registry where patients from all of Denmark are monitored in routine care during treatment with conventional and biologic disease modifying anti-rheumatic drugs (bDMARDs). The results were analyzed using logistic regression (adjusted for age and sex). Nine polymorphisms were associated with risk of AS (p < 0.05). The polymorphisms were in genes regulating a: the TNF-α pathway (TNF -308 G > A (rs1800629), and − 238 G > A (rs361525); TNFRSF1A -609 G > T (rs4149570), and PTPN22 1858 G > A (rs2476601)), b: the IL23/IL17 pathway (IL23R G > A (rs11209026), and IL18–137 G > C (rs187238)), or c: the NFkB pathway (TLR1 743 T > C (rs4833095), TLR4 T > C (rs1554973), and LY96–1625 C > G (rs11465996)). After Bonferroni correction the homozygous variant genotype of TLR1 743 T > C (rs4833095) (odds ratios (OR): 2.59, 95% confidence interval (CI): 1.48–4.51, p = 0.04), and TNFRSF1A -609 G > T (rs4149570) (OR: 1.79, 95% CI: 1.31–2.41, p = 0.01) were associated with increased risk of AS and the combined homozygous and heterozygous variant genotypes of TNF -308 G > A (rs1800629) (OR: 0.56, 95% CI: 0.44–0.72, p = 0.0002) were associated with reduced risk of AS. We replicated associations between AS and the polymorphisms in TNF (rs1800629), TNFRSF1A (rs4149570), and IL23R (rs11209026). Furthermore, we identified novel risk loci in TNF (rs361525), IL18 (rs187238), TLR1 (rs4833095), TLR4 (rs1554973), and LY96 (rs11465996) that need validation in independent cohorts. The results suggest that genetically determined high activity of the TNF-α, IL23/IL17, and NFkB pathways increase risk of AS.
Article 0 Reads 0 Citations Maternal inhalation of carbon black nanoparticles induces neurodevelopmental changes in mouse offspring Masakazu Umezawa, Atsuto Onoda, Irina Korshunova, Alexander ... Published: 10 September 2018
Particle and Fibre Toxicology, doi: 10.1186/s12989-018-0272-2
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Engineered nanoparticles are smaller than 100 nm and designed to improve or creating even new physico-chemical properties. Consequently, toxicological properties of materials may change as size reaches the nm size-range. We examined outcomes related to the central nervous system in the offspring following maternal inhalation exposure to nanosized carbon black particles (Printex 90). Time-mated mice (NMRI) were exposed by inhalation, for 45 min/day to 0, 4.6 or 37 mg/m3 aerosolized carbon black on gestation days 4–18, i.e. for a total of 15 days. Outcomes included maternal lung inflammation (differential cell count in bronchoalveolar lavage fluid and Saa3 mRNA expression in lung tissue), offspring neurohistopathology and behaviour in the open field test. Carbon black exposure did not cause lung inflammation in the exposed females, measured 11 or 28–29 days post-exposure. Glial fibrillary acidic protein (GFAP) expression levels were dose-dependently increased in astrocytes around blood vessels in the cerebral cortex and hippocampus in six weeks old offspring, indicative of reactive astrogliosis. Also enlarged lysosomal granules were observed in brain perivascular macrophages (PVMs) in the prenatally exposed offspring. The number of parvalbumin-positive interneurons and the expression levels of parvalbumin were decreased in the motor and prefrontal cortices at weaning and 120 days of age in the prenatally exposed offspring. In the open field test, behaviour was dose-dependently altered following maternal exposure to Printex 90, at 90 days of age. Prenatally exposed female offspring moved a longer total distance, and especially males spent significantly longer time in the central zone of the maze. In the offspring, the described effects were long-lasting as they were present at all time points investigated. The present study reports for the first time that maternal inhalation exposure to Printex 90 carbon black induced dose-dependent denaturation of PVM and reactive astrocytes, similarly to the findings observed following maternal exposure to Printex 90 by airway instillation. Of note, some of the observed effects have striking similarities with those observed in mouse models of neurodevelopmental disorders.
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