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  • Gilbert, Jonas, 1968- (författare)
  • A Start for Implementing ORCID in the Swedish Research Information Infrastructure
  • 2013
  • Ingår i: ScieCom Info. - 1652-3202. ; 9:2
  • Tidskriftsartikel (populärvet., debatt m.m.)abstract
    • Texten presenterar i korthet det projekt kring författaridentifikatorer och publikationsdatabaser som Kungliga biblioteket finansierade under 2012 under projektledning av Stockholms universitetsbibliotek med deltagande av biblioteken vid Chalmers, Karolinska Institutet samt Malmö högskola.
  • Vincent, Jonathan, 1975-, et al. (författare)
  • Theory of a room-temperature silicon quantum dot device as a sensitive electrometer
  • 2004
  • Ingår i: Journal of Applied Physics. - 0021-8979. ; 95:1, s. 323-326
  • Tidskriftsartikel (refereegranskat)abstract
    • We consider theoretically the use of a room-temperature silicon quantum dot based device for electrometer applications. The low power device includes two split gates that quantize the electronic energy levels in the emitter and collector regions. The base consists of a silicon quantum dot buried in silicon dioxide. The small size of the dot and quantization of the states in the leads combined to allow the device to operate at room temperature. The nonlinear current–voltage characteristics can be significantly altered by small changes to the potential of the split gates. Power dissipation in the device therefore changes with the split gate voltage, and this can be exploited in electrometer applications. A simple model of the power dissipated when the device is part of a microwave resonant inductor-resistor-capacitor tank circuit suggests that large changes in device power can be achieved by changing the gate voltage, thereby forming a measurable signal. We also demonstrate that the power dissipation in the device changes as the base width is varied, and that the current through the device increases exponentially with a decrease in base width.
  • Bergek, Anna, et al. (författare)
  • Analyzing the functional dynamics of technological innovation systems:
  • 2008
  • Ingår i: Research Policy. ; 37:3, s. 407-429
  • Tidskriftsartikel (refereegranskat)abstract
    • Various researchers and policy analysts have made empirical studies of innovation systems in order to understand their current structure and trace their dynamics. However, policy makers often experience difficulties in extracting practical guidelines from studies of this kind. In this paper, we operationalize our previous work on a functional approach to analyzing innovation system dynamics into a practical scheme of analysis for policy makers. The scheme is based on previous literature and our own experience in developing and applying functional thinking. It can be used by policy makers not only to identify the key policy issues but also to set policy goals.
  • Johansson, Helena, 1981-, et al. (författare)
  • High serum adiponectin predicts incident fractures in elderly men: Osteoporotic fractures in men (MrOS) Sweden.
  • 2012
  • Ingår i: Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research. - 1523-4681. ; 27:6, s. 1390-6
  • Tidskriftsartikel (refereegranskat)abstract
    • Adipocytes and osteoblasts share a common progenitor, and there is, therefore, potential for both autocrine and endocrine effects of adiponectin on skeletal metabolism. The aim of the present study was to determine whether high serum adiponectin was associated with an increased risk of fracture in elderly men. We studied the relationship between serum adiponectin and the risk of fracture in 999 elderly men drawn from the general population and recruited to the Osteoporotic Fractures in Men (MrOS) study in Gothenburg, Sweden. Baseline data included general health questionnaires, lifestyle questionnaires, body mass index (BMI), bone mineral density (BMD), serum adiponectin, osteocalcin, and leptin. Men were followed for up to 7.4 years (average, 5.2 years). Poisson regression was used to investigate the relationship between serum adiponectin, other risk variables and the time-to-event hazard function of fracture. Median levels of serum adiponectin at baseline were 10.4 mu g/mL (interquartile range, 7.714.3). During follow-up, 150 men sustained one or more fractures. The risk of fracture increased in parallel with increasing serum adiponectin (hazard ratio HR/SD, 1.46; 95% confidence interval CI, 1.231.72) and persisted after multivariate-adjusted analysis (HR/SD, 1.30; 95% CI, 1.091.55). Serum adiponectin shows graded stepwise association with a significant excess risk of fracture in elderly men that was independent of several other risk factors for fracture. Its measurement holds promise as a risk factor for fracture in men. (C) 2012 American Society for Bone and Mineral Research.
  • Jörnsten, Rebecka, et al. (författare)
  • Network modeling of the transcriptional effects of copy number aberrations in glioblastoma
  • 2011
  • Ingår i: Molecular Systems Biology. - 1744-4292. ; 7
  • Tidskriftsartikel (refereegranskat)abstract
    • DNA copy number aberrations (CNAs) are a hallmark of cancer genomes. However, little is known about how such changes affect global gene expression. We develop a modeling framework, EPoC (Endogenous Perturbation analysis of Cancer), to (1) detect disease-driving CNAs and their effect on target mRNA expression, and to (2) stratify cancer patients into long-and short-term survivors. Our method constructs causal network models of gene expression by combining genome-wide DNA-and RNA-level data. Prognostic scores are obtained from a singular value decomposition of the networks. By applying EPoC to glioblastoma data from The Cancer Genome Atlas consortium, we demonstrate that the resulting network models contain known disease-relevant hub genes, reveal interesting candidate hubs, and uncover predictors of patient survival. Targeted validations in four glioblastoma cell lines support selected predictions, and implicate the p53-interacting protein Necdin in suppressing glioblastoma cell growth. We conclude that large-scale network modeling of the effects of CNAs on gene expression may provide insights into the biology of human cancer. Free software in MATLAB and R is provided.
  • Landgren, Sara, et al. (författare)
  • A novel ARC gene polymorphism is associated with reduced risk of Alzheimer's disease
  • 2012
  • Ingår i: Journal of Neural Transmission. - 0300-9564. ; 119:7, s. 833-842
  • Tidskriftsartikel (refereegranskat)abstract
    • Alzheimers disease (AD) is the most common neurodegenerative disease, and is clinically characterized by cognitive disturbances and the accumulation of the amyloid beta (A beta) peptides in plaques in the brain. Recent studies have shown the links between AD and the immediate-early gene Arc (activity-regulated cytoskeleton-associated protein), involved in synaptic plasticity and memory consolidation. For example, AD mouse models show a decreased expression of Arc mRNA in the brain. In additional, acute A beta application to brain slices leads to a widespread ARC protein diffusion, unlike the normal defined localization to synapses. In this study, we investigated genetic variation in human ARC and the risk of developing AD. To this end, we genotyped 713 subjects diagnosed with AD and 841 controls without dementia. ARC was sequenced in a group of healthy individuals, and seven previously known SNPs and three novel SNPs were identified. Two of the newly found SNPs were intronic and one, +2852(G/A), was located in the 3UTR. Three tag SNPs were selected, including the novel SNP +2852(G/A), to relate to risk of AD, Mini Mental State Examination (MMSE) scores and cerebrospinal fluid (CSF) biomarker levels of total tau (T-tau), hyperphosphorylated tau181 (P-tau(181)) and A beta(1-42). The AA genotype of the newly found 3-UTR SNP +2852(A/G), was associated with a decreased risk of AD (p (c) = 0.005; OR = 0.74; 95 % CI: 0.61-0.89). No associations of single SNPs or haplotypes with MMSE score or CSF biomarkers were found. Here we report a novel ARC SNP associated with a reduced risk of developing AD. To our knowledge, this is the first study associating a gene variant of ARC with any disease. The location of the SNP within the 3UTR indicates that dendritic targeting of ARC mRNA could be involved in the molecular mechanisms underlying this protective function. However, further investigation of the importance of this SNP for ARC function, ARC processing and the pathology of AD is needed.
  • Pecorari, Diane, 1964-, et al. (författare)
  • English for Academic Purposes at Swedish universities
  • 2011
  • Ingår i: Ibérica. - 1139-7241. ; :22, s. 55-78
  • Tidskriftsartikel (refereegranskat)abstract
    • In a parallel-language environment the use of textbooks in English in courses otherwise in the local language is naturalized and not widely discussed or questioned. The aim of this study was to elicit the attitudes and syllabus infrastructure that underlie the practice. A large-scale survey was carried out and answers were obtained from over 20% of teachers at Swedish universities. Results confirmed that a majority regarded English as important during and/or after university studies and showed that they considered the use of Englishlanguage textbooks as providing a useful opportunity for incidental language learning. In strong contrast to the situation in a content and language integrated learning environment, only a small minority of courses were reported to have any specified learning outcome related to English. Open answers showed awareness of the benefits and risks of parallel-language practices, but no interest in making aims explicit. In our view, there is no contradiction between incidental learning and explicit aims, and course aims which remain implicit make rational planning and constructive alignment more difficult. They also inhibit discussion of appropriate methodology.
  • Perman, Jeanna, 1981-, et al. (författare)
  • The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction.
  • 2011
  • Ingår i: The Journal of clinical investigation. - 1558-8238. ; 121:7, s. 2625-40
  • Tidskriftsartikel (refereegranskat)abstract
    • Impaired cardiac function is associated with myocardial triglyceride accumulation, but it is not clear how the lipids accumulate or whether this accumulation is detrimental. Here we show that hypoxia/ischemia-induced accumulation of lipids in HL-1 cardiomyocytes and mouse hearts is dependent on expression of the VLDL receptor (VLDLR). Hypoxia-induced VLDLR expression in HL-1 cells was dependent on HIF-1α through its interaction with a hypoxia-responsive element in the Vldlr promoter, and VLDLR promoted the endocytosis of lipoproteins. Furthermore, VLDLR expression was higher in ischemic compared with nonischemic left ventricles from human hearts and was correlated with the total lipid droplet area in the cardiomyocytes. Importantly, Vldlr-/- mice showed improved survival and decreased infarct area following an induced myocardial infarction. ER stress, which leads to apoptosis, is known to be involved in ischemic heart disease. We found that ischemia-induced ER stress and apoptosis in mouse hearts were reduced in Vldlr-/- mice and in mice treated with antibodies specific for VLDLR. These findings suggest that VLDLR-induced lipid accumulation in the ischemic heart worsens survival by increasing ER stress and apoptosis.
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