26 research outputs found

    Organizational change and change readiness : employees’ attitudes during times of proposed merger

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    The objective in this thesis is to investigate the effects of organizational change. This is done through the review of literature and empirical analysis. An important part of this process involves developing measurements of the main constructs of interest; job satisfaction, uncertainty, commitment and change readiness. The relationship between the main constructs and change readiness is then investigated with special emphasis on testing hypotheses introduced under the first of three propositions. Further analysis then investigates two more propositions, one testing the assimilation of attitudes of Executive Managers and employees’ to organizational change, and one testing the relationship between the rate of change and change readiness. The study is based on two types of primary data. One is a questionnaire survey administered among employees of three Icelandic governmental organizations, all considered applicable for a merger. Another type of data was gathered by conducting interviews with Executive Managers of all three organizations. Findings suggest that change readiness increases as measured levels of job satisfaction increases. Findings also suggest that change readiness increases as uncertainty decreases, but the relationship between change readiness and commitment is not determined by the findings. Two of the three organizations surveyed had significantly different levels of change readiness. Findings suggest that employees’ change readiness is reflected in the attitudes of Executive Managers. Findings also suggest that employees and Executive Managers in organizations facing discontinuous or radical change do not report lower levels of change readiness, than those facing incremental organizational change

    Får hjerneinfarktspasienter i Tromsø adekvat utredning for å avdekke karotisstenose og hvordan påvirkes utredningen av alder, kjønn og slagets alvorlighetsgrad?

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    Bakgrunn: Vi vet i dag lite om hva slags utredning som blir gjort blant hjerneslagspasienter i Tromsø. I henhold til nasjonale faglige retningslinjer bør man som hovedregel gjøre utredning med tanke på karotisstenose hos alle pasienter med hjerneinfarkt. I denne studien kartlegges utredningsfrekvensen for karotisstenose blant hjerneinfarktpasienter som deltok i den 5. tromsøundersøkelsen i 2001-02 (Tromsø 5) og hvorvidt alder, kjønn og slagets alvorlighetsgrad påvirker denne. Materiale og metode: I alt 7852 deltakere i Tromsø 5 uten tidligere hjerneinfarkt ble fulgt opp med registrering av førstegangs hjerneinfarkt t.o.m. 2007. Av disse fikk 268 personer førstegangs hjerneinfarkt i oppfølgingsperioden og ble inkludert i studien. Adekvat stenoseutredning ble definert som ultralydsundersøkelse og/eller angiografisk (CT, MR eller konvensjonell angiografi) framstilling av det precerebrale forløp av karotisarteriene. Resultater: Totalt var det 62 % som gjennomgikk adekvat stenoseutredning. Færre ble utredet i de eldste aldersgruppene (p<0,0001), blant dem med registrert demensdiagnose (p=0,06) og de som hadde svekket bevissthet ved innkomst (p=0,01). Det var ingen forskjell i utredning mellom kjønnene. Med 10 års økning i alder ble sjansen for stenoseutredning redusert med 76 % (OR 0,24, KI 0,14 – 0,39). Svekket bevissthet reduserte sjansen for utredning med 72 % (OR 0,27, KI 0,11 – 0,53). Diskusjon: En høy andel av hjerneinfarktpasientene ble ikke utredet for å avdekke eventuell karotisstenose. Selv når man tar hensyn til forhold som bevissthetssvekkelse som uttrykk for slagets alvorlighetsgrad og komorbiditiet i form av demens, synes utredningsfrekvensen å være lavere enn det som er anbefalt i gjeldende nasjonale anbefalinger

    IPA diagrams of the top associated network generated for all the regulated genes in m<i>Cyp27b1</i><sup>−/−</sup> fibroblasts.

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    <p>(A) Genes regulated by 1α,25(OH)<sub>2</sub>D<sub>3</sub> in Cardiovascular System Development and Function, Organismal Development, Cancer. (B) Genes regulated by 25(OH)D<sub>3</sub> in Humoral Immune Response, Inflammatory Response, Cellular Development. (C) Genes regulated by 25(OH)D<sub>3</sub> in Cancer, Cellular Growth and Proliferation, Connective Tissue Disorders. (D) Genes regulated by 24R,25(OH)<sub>2</sub>D<sub>3</sub> in Hematological System Development and Function, Hematopoiesis, Tissue Morphology. Green indicates gene down-regulation and pink to red indicate gene up-regulation (the more intensive the color, the higher the expression level). An asterisk (*) indicates that multiple identifiers in the microarray set map to a single gene.</p

    Gene expression profiles.

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    <p>Hierarchical clustering of the differentially expressed genes in (A) hP29SN stromal cells and (B) m<i>Cyp27b1</i><sup>−/−</sup> fibroblasts after vitamin D<sub>3</sub> treatments. Colored-bands represent the change of the corresponding gene expression, green indicating down-regulation and red up-regulation. The key for deciphering of the color is shown below the clustering image. Venn diagrams of co-expressed and uniquely regulated genes by vitamin D<sub>3</sub> metabolites in (C) hP29SN and (D) m<i>Cyp27b1</i><sup>−/−</sup> fibroblasts.</p

    IPA diagrams of the top associated network generated for genes exclusively regulated by each metabolite in hP29SN stromal cells.

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    <p>(A) Genes regulated by 1α,25(OH)<sub>2</sub>D<sub>3</sub> in Cardiovascular System Development and Function, Tissue Development, Organismal Development. (B) Genes regulated by 25(OH)D<sub>3</sub> in Cell Death and Survival, Gene Expression, Tissue Morphology. (C) Genes regulated by 25(OH)D<sub>3</sub> in Cell Death and Survival, Cellular Growth and Proliferation, Cell Cycle. (D) Genes regulated by 24R,25(OH)<sub>2</sub>D<sub>3</sub> in Cell Morphology, Cellular Function and Maintenance, DNA Replication, Recombination, and Repair. Green indicates gene down-regulation and pink to red indicate gene up-regulation (the more intensive the color, the higher the expression level). An asterisk (*) indicates that multiple identifiers in the microarray set map to a single gene.</p

    Validation of gene expression by qRT-PCR.

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    <p>(A–C) Gene expression in hP29SN stromal cells. <i>CH25H</i>: cholesterol 25-hydroxylase; <i>SSBP2</i>: single-stranded DNA binding protein 2; <i>VHL</i>: von Hippel-Lindau tumor suppressor; <i>IGF1</i>: insulin-like growth factor; <i>EGFR</i>: epidermal growth factor receptor; <i>LAMB1</i>: laminin subunit β1; <i>RAB7</i>: RAB7A, member RAS oncogene family; <i>MED1</i>: mediator complex subunit 1. (D) Fold changes of gene expression in hP29SN detected by either qRT-PCR or microarray are plotted and linear regression is shown by a solid line. (E–F) The expression of endothelial lipase (<i>Lipg</i>) and tumor necrosis factor receptor superfamily, member 11b (<i>Tnfrsf11b</i>) in m<i>Cyp27b1</i><sup>−/−</sup> fibroblasts was measured by qRT-PCR. Randomly selected two sets of experiments were pooled to generate final two sets of RNA samples for both microarray and qRT-PCR. Results are expressed as means ± SD.</p
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