112 research outputs found

    modellering og regulering af et stoker system

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    DESERV IT: A Method for Devolving Service Tasks in IT Services

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    Nowadays, IT operations devolve many tasks in IT services to internal customers (i.e., IT self-service). The rationale for this service task devolvement is often to reduce the IT personnel’s workload. However, prior research has shown that IT operations often fail to achieve this goal. Existing methods for modeling and analyzing services fall short of supporting service providers in identifying and specifying service tasks suitable to be devolved to (internal) customers. This paper presents, therefore, the first method for devolving service tasks in IT services (DESERV IT). DESERV IT is a compound of four method components encompassing a joint meta-model, a visual notation for modeling IT services, and procedural recommendations. The DESERV IT meta-model extends the meta-model of service blueprinting by means of concepts required to analyze service task devolvement. DESERV IT is evaluated in four evaluation episodes. The results of the evaluation episodes show that DESERV IT is perceived as effective, useful, complete, and generalizable by experts in the IT service management and enterprise architecture discipline. This paper contributes to enterprise modeling by demonstrating the feasibility of DESERV IT in an example case and describing DESERV IT’s evolution during the evaluation episodes. DESERV IT supports practitioners (e.g., request fulfillment managers) in modeling and analyzing IT services

    Vegetation analysis: A graphical analysis of plant succession in desert communities affected by fire

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    The Mojave Desert is affected by fire every year. With each fire comes the removal of old growth and, in its place, new growth – consisting primarily of those species which thrive in disturbed areas. The focus of my research is to look at plant communities that have been disturbed by fire, and examine the successional pathway of these disturbed environments. The seven environments I analyzed were burned within the last twenty years and are found in the Coleogyne ramosissima ecotone throughout the Spring Mountain range near Las Vegas, Nevada. The data was collected with randomly chosen circle plots in the burned environments, as well as the neighboring unburned environments. There was no correlation found between the length of time since the fire and the level of diversity of the environment. However, the degree of evenness is higher in the burned environments as compared to the unburned environments. It appears that there was not enough time between the fires to see a difference in the composition of the community

    Ca(2+)-mediated mitochondrial ROS metabolism augments Wnt/β-catenin pathway activation to facilitate cell differentiation

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    Emerging evidence suggests that reactive oxygen species (ROS) can stimulate Wnt/{beta}-catenin pathway in a number of cellular processes. However, potential sources of endogenous ROS have not been thoroughly explored. Here, we show that growth factor depletion in human neural progenitor cells induces ROS production in mitochondria. Elevated ROS levels augment activation of Wnt/{beta}-catenin signaling that regulates neural differentiation. We find that growth factor depletion stimulates release of Ca(2+) from the endoplasmic reticulum stores that subsequently accumulates in the mitochondria and triggers ROS production. The inhibition of mitochondrial Ca(2+) uptake with simultaneous growth factor depletion prevents the rise in ROS metabolism. Moreover, low ROS levels block the dissociation of the Wnt effector Dishevelled from Nucleoredoxin. Attenuation of the response amplitudes of pathway effectors delays the onset of Wnt/{beta}-catenin pathway activation and results in markedly impaired neuronal differentiation. Our findings reveal Ca(2+)-mediated ROS metabolic cues that finetune the efficiency of cell differentiation by modulating the extent of the Wnt/{beta}-catenin signaling output

    The granulocyte colony stimulating factor pathway regulates autoantibody production in a murine induced model of systemic lupus erythematosus

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    INTRODUCTION: An NZB-derived genetic locus (Sle2c2) that suppresses autoantibody production in a mouse model of induced systemic lupus erythematosus contains a polymorphism in the gene encoding the G-CSF receptor. This study was designed to test the hypothesis that the Sle2c2 suppression is associated with an impaired G-CSF receptor function that can be overcome by exogenous G-CSF. METHODS: Leukocytes from B6.Sle2c2 and B6 congenic mice, which carry a different allele of the G-CSF receptor, were compared for their responses to G-CSF. Autoantibody production was induced with the chronic graft-versus-host-disease (cGVHD) model by adoptive transfer of B6.bm12 splenocytes. Different treatment regimens varying the amount and frequency of G-CSF (Neulasta(®)) or carrier control were tested on cGVHD outcomes. Autoantibody production, immune cell activation, and reactive oxygen species (ROS) production were compared between the two strains with the various treatments. In addition, the effect of G-CSF treatment was examined on the production autoantibodies in the B6.Sle1.Sle2.Sle3 (B6.TC) spontaneous model of lupus. RESULTS: B6.Sle2c2 and B6 leukocytes responded differently to G-CSF. G-CSF binding by B6.Sle2c2 leukocytes was reduced as compared to B6, which was associated with a reduced expansion in response to in vivo G-CSF treatment. G-CSF in vivo treatment also failed to mobilize bone-marrow B6.Sle2c2 neutrophils as it did for B6 neutrophils. In contrast, the expression of G-CSF responsive genes indicated a higher G-CSF receptor signaling in B6.Sle2c2 cells. G-CSF treatment restored the ability of B6.Sle2c2 mice to produce autoantibodies in a dose-dependent manner upon cGVHD induction, which correlated with restored CD4(+ )T cells activation, as well as dendritic cell and granulocyte expansion. Steady-state ROS production was higher in B6.Sle2c2 than in B6 mice. cGVHD induction resulted in a larger increase in ROS production in B6 than in B6.Sle2c2 mice, and this difference was eliminated with G-CSF treatment. Finally, a low dose G-CSF treatment accelerated the production of anti-dsDNA IgG in young B6.TC mice. CONCLUSION: The different in vivo and in vitro responses of B6.Sle2c2 leukocytes are consistent with the mutation in the G-CSFR having functional consequences. The elimination of Sle2c2 suppression of autoantibody production by exogenous G-CSF indicates that Sle2c2 corresponds to a loss of function of G-CSF receptor. This result was corroborated by the increased anti-dsDNA IgG production in G-CSF-treated B6.TC mice, which also carry the Sle2c2 locus. Overall, these results suggest that the G-CSF pathway regulates the production of autoantibodies in murine models of lupus

    Towards a classification framework for approaches to enterprise architecture analysis

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    Analysis is an important part of the Enterprise Architecture Management Process. Prior to decisions regarding transformation of the Enterprise Architecture, the current situation and the outcomes of alternative action plans have to be analyzed. Many analysis approaches have been proposed by researchers and current Enterprise Architecture Management tools implement Analysis functionalities. However, few work has been done structuring and classifying Enterprise Architecture Analysis approaches. This paper collects and extends existing classification schemes, presenting a framework for Enterprise Architecture Analysis classification. For evaluation, a collection of Enterprise Architecture Analysis approaches has been classified based on this framework. As a result, the description of these approaches has been assessed, a common set of important categories for Enterprise Architecture Analysis classification has been derived and suggestions for further development are drawn

    Investigations on DNA damage and frequency of micronuclei in occupational exposure to electromagnetic fields (EMFs) emitted from video display terminals (VDTs)

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    The potential effect of electromagnetic fields (EMFs) emitted from video display terminals (VDTs) to elicit biological response is a major concern for the public. The software professionals are subjected to cumulative EMFs in their occupational environments. This study was undertaken to evaluate DNA damage and incidences of micronuclei in such professionals. To the best of our knowledge, the present study is the first attempt to carry out cytogenetic investigations on assessing bioeffects in personal computer users. The study subjects (n = 138) included software professionals using VDTs for more than 2 years with age, gender, socioeconomic status matched controls (n = 151). DNA damage and frequency of micronuclei were evaluated using alkaline comet assay and cytochalasin blocked micronucleus assay respectively. Overall DNA damage and incidence of micronuclei showed no significant differences between the exposed and control subjects. With exposure characteristics, such as total duration (years) and frequency of use (minutes/day) sub-groups were assessed for such parameters. Although cumulative frequency of use showed no significant changes in the DNA integrity of the classified sub-groups, the long-term users (> 10 years) showed higher induction of DNA damage and increased frequency of micronuclei and micro nucleated cells

    Biological Effects and Safety in Magnetic Resonance Imaging: A Review

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    Since the introduction of Magnetic Resonance Imaging (MRI) as a diagnostic technique, the number of people exposed to electromagnetic fields (EMF) has increased dramatically. In this review, based on the results of a pioneer study showing in vitro and in vivo genotoxic effects of MRI scans, we report an updated survey about the effects of non-ionizing EMF employed in MRI, relevant for patients’ and workers’ safety. While the whole data does not confirm a risk hypothesis, it suggests a need for further studies and prudent use in order to avoid unnecessary examinations, according to the precautionary principle
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