117 research outputs found

    Morphological Instabilities in a growing Yeast Colony: Experiment and Theory

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    We study the growth of colonies of the yeast Pichia membranaefaciens on agarose film. The growth conditions are controlled in a setup where nutrients are supplied through an agarose film suspended over a solution of nutrients. As the thickness of the agarose film is varied, the morphology of the front of the colony changes. The growth of the front is modeled by coupling it to a diffusive field of inhibitory metabolites. Qualitative agreement with experiments suggests that such a coupling is responsible for the observed instability of the front.Comment: RevTex, 4 pages and 3 figure

    Handling Uncertainty of Strategic Ambitions—The Use of Organizational Identity as a Risk-Reducing Device

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    Organizational identity can be designed to reduce the risks of uncertainty about future states of public organizations and the inherent potential issues related to evaluation and assessment. As such, organizational identity may shape a congruent and credible self-representation of the university, where a consistent narrative articulates compliance to diverse institutional frameworks, commitment to organizational distinctiveness, and a sensible rationale for strategic change. By examining the strategic plans of four European universities over a 10-year period of major organizational change, the paper discusses the subtleties of the specific combinations of the three different functions and the implications for institutional leadership

    The Etiology of Multiple Sclerosis: Genetic Evidence for the Involvement of the Human Endogenous Retrovirus HERV-Fc1

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    We have investigated the role of human endogenous retroviruses in multiple sclerosis by analyzing the DNA of patients and controls in 4 cohorts for associations between multiple sclerosis and polymorphisms near viral restriction genes or near endogenous retroviral loci with one or more intact or almost-intact genes. We found that SNPs in the gene TRIM5 were inversely correlated with disease. Conversely, SNPs around one retroviral locus, HERV-Fc1, showed a highly significant association with disease. The latter association was limited to a narrow region that contains no other known genes. We conclude that HERV-Fc1 and TRIM5 play a role in the etiology of multiple sclerosis. If these results are confirmed, they point to new modes of treatment for multiple sclerosis

    Evaluation of the national surveillance system for point-prevalence of healthcare-associated infections in hospitals and in long-term care facilities for elderly in Norway, 2002-2008

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    <p>Abstract</p> <p>Background</p> <p>Since 2002, the Norwegian Institute of Public Health has invited all hospitals and long-term care facilities for elderly (LTCFs) to participate in two annual point-prevalence surveys covering the most frequent types of healthcare-associated infections (HAIs). In a comprehensive evaluation we assessed how well the system operates to meet its objectives.</p> <p>Methods</p> <p>Surveillance protocols and the national database were reviewed. Data managers at national level, infection control practitioners and ward personnel in hospitals as well as contact persons in LTCFs involved in prevalence data collection were surveyed.</p> <p>Results</p> <p>The evaluation showed that the system was structurally simple, flexible and accepted by the key partners. On average 87% of hospitals and 32% of LTCFs participated in 2004-2008; high level of data completeness was achieved. The data collected described trends in the prevalence of reportable HAIs in Norway and informed policy makers. Local results were used in hospitals to implement targeted infection control measures and to argue for more resources to a greater extent than in LTCFs. Both the use of simplified Centers for Disease Control and Prevention (CDC) definitions and validity of data seemed problematic as compliance with the standard methodology were reportedly low.</p> <p>Conclusions</p> <p>The surveillance system provides important information on selected HAIs in Norway. The system is overall functional and well-established in hospitals, however, requires active promotion in LTCFs. Validity of data needs to be controlled in the participating institutions before reporting to the national level.</p

    Enhancing Biological and Biomechanical Fixation of Osteochondral Scaffold: A Grand Challenge

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    Osteoarthritis (OA) is a degenerative joint disease, typified by degradation of cartilage and changes in the subchondral bone, resulting in pain, stiffness and reduced mobility. Current surgical treatments often fail to regenerate hyaline cartilage and result in the formation of fibrocartilage. Tissue engineering approaches have emerged for the repair of cartilage defects and damages to the subchondral bones in the early stage of OA and have shown potential in restoring the joint's function. In this approach, the use of three-dimensional scaffolds (with or without cells) provides support for tissue growth. Commercially available osteochondral (OC) scaffolds have been studied in OA patients for repair and regeneration of OC defects. However, some controversial results are often reported from both clinical trials and animal studies. The objective of this chapter is to report the scaffolds clinical requirements and performance of the currently available OC scaffolds that have been investigated both in animal studies and in clinical trials. The findings have demonstrated the importance of biological and biomechanical fixation of the OC scaffolds in achieving good cartilage fill and improved hyaline cartilage formation. It is concluded that improving cartilage fill, enhancing its integration with host tissues and achieving a strong and stable subchondral bone support for overlying cartilage are still grand challenges for the early treatment of OA

    Mathematical Modelling as a Proof of Concept for MPNs as a Human Inflammation Model for Cancer Development

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    <p><b>Left:</b> Typical development in stem cells (top panel A) and mature cells (bottom panel B). Healthy hematopoietic cells (full blue curves) dominate in the early phase where the number of malignant cells (stipulated red curves) are few. The total number of cells is also shown (dotted green curves). When a stem cell mutates without repairing mechanisms, a slowly increasing exponential growth starts. At a certain stage, the malignant cells become dominant, and the healthy hematopoietic cells begin to show a visible decline. Finally, the composition between the cell types results in a takeover by the malignant cells, leading to an exponential decline in hematopoietic cells and ultimately their extinction. The development is driven by an approximately exponential increase in the MPN stem cells, and the development is closely followed by the mature MPN cells. <b>Right:</b> B)The corresponding allele burden (7%, 33% and 67% corresponding to ET, PV, and PMF, respectively) defined as the ratio of MPN mature cells to the total number of mature cells.</p

    Within-sibship genome-wide association analyses decrease bias in estimates of direct genetic effects

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    Estimates from genome-wide association studies (GWAS) of unrelated individuals capture effects of inherited variation (direct effects), demography (population stratification, assortative mating) and relatives (indirect genetic effects). Family-based GWAS designs can control for demographic and indirect genetic effects, but large-scale family datasets have been lacking. We combined data from 178,086 siblings from 19 cohorts to generate population (between-family) and within-sibship (within-family) GWAS estimates for 25 phenotypes. Within-sibship GWAS estimates were smaller than population estimates for height, educational attainment, age at first birth, number of children, cognitive ability, depressive symptoms and smoking. Some differences were observed in downstream SNP heritability, genetic correlations and Mendelian randomization analyses. For example, the within-sibship genetic correlation between educational attainment and body mass index attenuated towards zero. In contrast, analyses of most molecular phenotypes (for example, low-density lipoprotein-cholesterol) were generally consistent. We also found within-sibship evidence of polygenic adaptation on taller height. Here, we illustrate the importance of family-based GWAS data for phenotypes influenced by demographic and indirect genetic effects
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