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.
Nýlega bætt við
Fault-tolerant algorithms for tick-generation in asynchronous logic : Robust pulse generation
(2014-09-08) Dolev, Danny; Függer, Matthias; Schmid, Ulrich; Lenzen, Christoph; Department of Computer Science
Today's hardware technology presents a new challenge in designing robust systems. Deep submicron VLSI technology introduces transient and permanent faults that were never considered in low-level system designs in the past. Still, robustness of that part of the system is crucial and needs to be guaranteed for any successful product. Distributed systems, on the other hand, have been dealing with similar issues for decades. However, neither the basic abstractions nor the complexity of contemporary fault-tolerant distributed algorithms match the peculiarities of hardware implementations. This article is intended to be part of an attempt striving to bridge over this gap between theory and practice for the clock synchronization problem. Solving this task sufficiently well will allow to build an ultrarobust high-precision clocking system for hardware designs like systems-on-chips in critical applications. As our first building block, we describe and prove correct a novel distributed, Byzantine fault-tolerant, probabilistically self-stabilizing pulse synchronization protocol, called FATAL, that can be implemented using standard asynchronous digital logic: Correct FATAL nodes are guaranteed to generate pulses (i.e., unnumbered clock ticks) in a synchronized way, despite a certain fraction of nodes being faulty. FATAL uses randomization only during stabilization and, despite the strict limitations introduced by hardware designs, offers optimal resilience and smaller complexity than all existing protocols. Finally, we show how to leverage FATAL to efficiently generate synchronized, self-stabilizing, high-frequency clocks. 2014 Copyright held by the Owner/Author.
Rigorously modeling self-stabilizing fault-tolerant circuits : An ultra-robust clocking scheme for systems-on-chip
(2014-06) Dolev, Danny; Függer, Matthias; Posch, Markus; Schmid, Ulrich; Steininger, Andreas; Lenzen, Christoph; Department of Computer Science
We present the first implementation of a distributed clock generation scheme for Systems-on-Chip that recovers from an unbounded number of arbitrary transient faults despite a large number of arbitrary permanent faults. We devise self-stabilizing hardware building blocks and a hybrid synchronous/asynchronous state machine enabling metastability-free transitions of the algorithm's states. We provide a comprehensive modeling approach that permits to prove, given correctness of the constructed low-level building blocks, the high-level properties of the synchronization algorithm (which have been established in a more abstract model). We believe this approach to be of interest in its own right, since this is the first technique permitting to mathematically verify, at manageable complexity, high-level properties of a fault-prone system in terms of its very basic components. We evaluate a prototype implementation, which has been designed in VHDL, using the Petrify tool in conjunction with some extensions, and synthesized for an Altera Cyclone FPGA.
Molecular signatures of obstructive sleep apnea in adults : A review and perspective
(2009-04-01) Arnardottir, Erna S.; Mackiewicz, Miroslaw; Gislason, Thorarinn; Teff, Karen L.; Pack, Allan I.; Department of Engineering
The consequences of obstructive sleep apnea (OSA) are largely mediated by chronic intermittent hypoxia and sleep fragmentation. The primary molecular domains affected are sympathetic activity, oxidative stress and infammation. Other affected domains include adipokines, adhesion molecules and molecules that respond to endoplasmic reticulum stress. Changes in molecular domains affected by OSA, assessed in blood and/or urine, can provide a molecular signature for OSA that could potentially be used diagnostically and to predict who is likely to develop different OSA-related comorbidities. High-throughput discovery strategies such as microarrays, assessing changes in gene expression in circulating blood cells, have the potential to fnd new candidates and pathways thereby expanding the molecular signatures for OSA. More research is needed to fully understand the pathophysiological signifcance of these molecular signatures and their relationship with OSA comorbidities. Many OSA subjects are obese, and obesity is an independent risk factor for many comorbidities associated with OSA. Moreover, obesity affects the same molecular pathways as OSA. Thus, a challenge to establishing a molecular signature for OSA is to separate the effects of OSA from obesity. We propose that the optimal strategy is to evaluate the temporal changes in relevant molecular pathways during sleep and, in particular, the alterations from before to after sleep when assessed in blood and/or urine. Such changes will be at least partly a consequence of chronic intermittent hypoxia and sleep fragmentation that occurs during sleep.
Bayesian testing of many hypotheses × many genes : A study of sleep apnea
(2009-03) Jensen, Shane T.; Erkan, Ibrahim; Arnardottir, Erna S.; Small, Dylan S.; Department of Engineering
Substantial statistical research has recently been devoted to the analysis of large-scale microarray experiments which provide a measure of the simultaneous expression of thousands of genes in a particular condition. A typical goal is the comparison of gene expression between two conditions (e.g., diseased vs. nondiseased) to detect genes which show differential expression. Classical hypothesis testing procedures have been applied to this problem and more recent work has employed sophisticated models that allow for the sharing of information across genes. However, many recent gene expression studies have an experimental design with several conditions that requires an even more involved hypothesis testing approach. In this paper, we use a hierarchical Bayesian model to address the situation where there are many hypotheses that must be simultaneously tested for each gene. In addition to having many hypotheses within each gene, our analysis also addresses the more typical multiple comparison issue of testing many genes simultaneously. We illustrate our approach with an application to a study of genes involved in obstructive sleep apnea in humans.
Kæfisvefn veldur hjarta- og æðasjúkdómum - segir doktorsnemi í líffræöi
(2009) Arnardóttir, Erna Sif; Verkfræðideild
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- University of Iceland
- University of Akureyri
- Bifröst University
- Hólar University College
- IRIS
- Agricultural University of Iceland
- National and University Library of Iceland
- Iceland University of the Arts