37 research outputs found

    Generation Y : eine Herausforderung für Führungskräfte

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    Im Jahr 2020 wird der größte Teil der Erwerbstätigen der Generation Y angehören. Die Alltagsaufgaben von Führungskräften befinden sich daher in einem kontinuierlichen Umbruch. Herausforderungen in der Führungsarbeit und in der Organisationsentwicklung stellen zukünftig die Fokusarbeit von Führungskräften dar. Generationsbezogene Aspekte werden betrachtet, um eine Führungskultur zu entwickeln, welche der jeweiligen Generation mit ihren Bedürfnissen, Kompetenzen und Wertvorstellungen entspricht. Durch eine generationsübergreifende Kommunikation wird die Zusammenarbeit im Unternehmen stabilisiert und die Teamzusammengehörigkeit gestärkt.Führung bedeutet auch eine Sicherung des Nachwuchses. Orientierung gebend, den Sinn der Arbeit inspirierend und individuell durch Mentoring und Coaching betreuend müssen sich Führungskräfte ihrer zentralen Rolle bewusst werden.Der demographische Wandel prognostiziert einen Fachkräftemangel. Nur ein attraktives Image unterstützt Unternehmen im Ranking um die talentiertesten Jungbewerber und Jungbewerberinnen.Mitunter ist es Ziel, diese jungen MitarbeiterInnen zu gewinnen, und längerfristig an das Unternehmen binden zu können.By 2020 the largest part of the working population will belong to Generation Y. The routine tasks of management staff are therefore in a continuous process of change. The main challenges will lie in establishing an effective management and in focusing on a steady organizational development. Generational aspects will have to be included in developing a management culture, which corresponds to the respective needs, skills and moral concepts.Additional communication strategies, encouraging the inclusion of all generations, will need to be implemented to stabilize teamwork in companies and strengthen team identity. Management will also need to ensure ongoing recruitment. Management staff will have to be aware of their pivotal role in providing orientation, in inspiring and supporting team members by individual mentoring and coaching. Current demographic developments give reason to expect a lack of skilled staff in the future.An attractive company image will help to recruit the most talented job candidates and offer them long term satisfying employment.vorgelegt von DGKP Strommer Sabine-VerenaZusammenfassungen in Deutsch und EnglischAbweichender Titel laut Übersetzung des Verfassers/der VerfasserinKarl-Franzens-Universität Graz, Masterarbeit, 2018(VLID)283250

    Circulating Endothelial Progenitor Cells in Castration Resistant Prostate Cancer: A Randomized, Controlled, Biomarker Study

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    <div><p>Background</p><p>Endothelial progenitor cells (CEPs) and circulating endothelial cells (CECs) are potential biomarkers of response to anti-angiogenic treatment regimens. In the current study, we investigated the effect of docetaxel and sunitinib on CEP/CEC kinetics and clinical response in castration resistant prostate cancer (CRPC) patients.</p><p>Patients and methods</p><p>Chemonaive patients with CRPC were enrolled in this study to receive either sunitinib (37.5 mg/d), in combination with docetaxel (75 mg/m<sup>2</sup>) or docetaxel alone. CEP and CEC kinetics were analyzed for every cycle. The primary objective was to compare CEP/CEC pharmacodynamics between both treatment arms. We also investigated if CEC/CEP spikes, induced by MTD docetaxel, are suppressed by sunitinib in patients treated with docetaxel/sunitinib relative to docetaxel monotherapy.</p><p>Results</p><p>A total of 27 patients were enrolled. We observed a significant increase of CEP/CEC (total/viable) counts over time within each cycle (coefficients 0.29233, 0.22092 and 0.26089, respectively; p<0.001). However, no differences between the treatment groups, in terms of CEP and CEC kinetics, were detected. In the docetaxel monotherapy arm 4 (30%) patients responded to therapy with a 50% PSA decline, while 9 (64%) patients showed a PSA decline in the combination group (n.s.). The median PFS in the docetaxel monotherapy group was 3.1 months (2.6–3.6 months, 95% CI) and 6.2 months (4.9–7.4 months, 95% CI; p = 0.062) in the combination arm. Sunitinib/docetaxel was reasonably well tolerated and toxicity manageable.</p><p>Conclusion</p><p>In summary, no significant differences in CEC and CEP kinetics between the treatment arms were observed, although a highly significant increase of CEPs/CECs within each cycle over time was detected. These results mirror the challenge we have to face when employing anti-angiogenic strategies in CRPC. Additional preclinical research is needed to elucidate the underlying molecular mechanisms. However, docetaxel/sunitinib therapy resulted in a better response in terms of PSA decline and a trend towards improved PFS.</p><p>Trial Registery</p><p>clinicaltrialsregister.eu <a href="https://www.clinicaltrialsregister.eu/ctr-search/search?query=2007-003705-27" target="_blank">EudraCT 2007-003705-27</a></p></div

    PFS between both treatment arms.

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    <p>Kaplan-Meier curves depicting progression free survival between sunitinib/docetaxel arm (orange) and docetaxel monotherapy arm (blue). Black bars represent censored patients.</p

    PSA response.

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    <p>Waterfall plot of PSA response to docetaxel (blue) and sunitinib/docetaxel (yellow) in CRPC patients.</p

    CEP and CEC kinetics.

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    <p>Representative example of flow cytometry dot plots chosen for CEP measurements. The left panel shows CD146 positive endothelial cells of which a small number were CD133 positive accounting for CEPs as indicated by the red arrow (right panel) (a). Regression analysis employing a linear mixed model of total CEC (b), viable CEC (c) and CEP (d) counts on a logarithmic scale of docetaxel (blue) and docetaxel/sunitinib treated patients. Each dot represents a single patient. X-axis represents cycles and time points; Y-axis represents CEP and CEC numbers on a logarithmic scale.</p

    Primary melanoma cells express ErbB3 and ErbB4 as well as the EPO-R.

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    <p><i>A</i>, Freshly isolated primary melanoma cells (patient #3) were stained with fluorochrome-conjugated monoclonal antibodies (mAb) against CD31, CD45, ErbB3, IGF-1-R, and CD146. Melanoma cells were gated as CD31−/CD45− cells and defined as CD146+ cells. Dot plots show expression of ErbB3 (middle panel) and IGF-1-R (right panel) on CD146+ melanoma cells. The isotype control is also shown (left panel). <i>B</i>, Melanoma cells of patient #10 were stained with mAb against CD31, CD45 and CD146 as well as EPO-R and CD24. The dot plot in the right panel shows co-expression of EPO-R and CD24 in a distinct subpopulation of (CD146+) melanoma cells. <i>C</i>, Xenotransplanted EPO-R+ melanoma cells of patient #6 were stained with biotinylated recombinant human EPO, an isotype-matched mouse IgG2b-PE antibody (left panel) and a mAb directed against the EPO-R (right panel). <i>D</i>, Melanoma cells of patient #10 were stained with mAb against CD146, an isotype-matched control antibody (left panel) and an antibody against ErbB4 (right panel). Dot plots show expression of ErbB4 in a distinct subpopulation of melanoma cells.</p
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