202 research outputs found

    Organising for sustainability

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    Optimal structures for social systems

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    Enhancing Validity and Reliability Through Feedback-Driven Exploration: A Study in the Context of Conjoint Analysis

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    This study proposes a research design for the enhancement of validity and reliability in conjoint analysis research. For this purpose, we are applying the concept of feedback-driven exploration to conjoint analysis and assess the proposed research design concerning its benefits and limitations in respect of validity and reliability of results. The article is of interest for the field of preference elicitation through stated preference methods, and for model validation in transdisciplinary research. By applying the principle of feedback-driven exploration, we allow for feedback loops between researchers, industry experts and survey participants in order to strengthen both validity and reliability. A multi-case study of the agricultural markets in Switzerland illustrates the functioning of the proposed research design. We find that feedback-driven exploration significantly increases validity and reliability by enhancing methodological rigor and implementing an error-correcting mechanism. Additionally, a better understanding of the underlying decision processes is supported by the design due to increased interaction between researchers, industry experts and market participant

    Enlarged infarct volume and loss of BDNF mRNA induction following brain ischemia in mice lacking FGF-2

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    FGF-2, a potent multifunctional and neurotrophic growth factor, is widely expressed in the brain and upregulated in cerebral ischemia. Previous studies have shown that intraventricularly or systemically administered FGF-2 reduces the size of cerebral infarcts. Whether endogenous FGF-2 is beneficial for the outcome of cerebral ischemia has not been investigated. We have used mice with a null mutation of the fgf2 gene to explore the relevance of endogenous FGF-2 in brain ischemia. Focal cerebral ischemia was produced by occlusion of the middle cerebral artery (MCAO). We found a 75% increase in infarct volume in fgf2 knock-out mice versus wild type littermates (P < 0.05). This difference in the extent of ischemic damage was observed after 24 h, and correlated with decreased viability in fgf2 mutant mice following MCA occlusion. Increased infarct volume in fgf2 null mice was associated with a loss of induction in hippocampal BDNF and trkB mRNA expression. These findings indicate that signaling through trkB may contribute to ameliorating brain damage following ischemia and that bdnf and trkB may be target genes of FGF-2. Together, our data provide the first evidence that endogenous FGF-2 is important in coping with ischemic brain damage suggesting fgf2 as one crucial target gene for new therapeutic strategies in brain ischemia

    The trophoblast clock controls transport across placenta in mice

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    In mammals, 24-h rhythms of physiology and behavior are organized by a body-wide network of clock genes and proteins. Despite the well-known function of the adult circadian system, the roles of maternal, fetal and placental clocks during pregnancy are poorly defined. In the mature mouse placenta, the labyrinth zone (LZ) is of fetal origin and key for selective nutrient and waste exchange. Recently, clock gene expression has been detected in LZ and other fetal tissues; however, there is no evidence of a placental function controlled by the LZ clock. Here, we demonstrate that specifically the trophoblast layer of the LZ harbors an already functional clock by late gestation, able to regulate in a circadian manner the expression and activity of the xenobiotic efflux pump, ATP-binding cassette sub-family B member 1 (ABCB1), likely gating the fetal exposure to drugs from the maternal circulation to certain times of the day. As more than 300 endogenous and exogenous compounds are substrates of ABCB1, our results might have implications in choosing the maternal treatment time when aiming either maximal/minimal drug availability to the fetus/mother.Fil: Demarez, CĂ©cile. UniversitĂ€t Zu LĂŒbeck; AlemaniaFil: de Assis, Leonardo Vinicius Monteiro. UniversitĂ€t Zu LĂŒbeck; AlemaniaFil: Krohn, Markus. UniversitĂ€t Zu LĂŒbeck; AlemaniaFil: Ramella, Nahuel. Consejo Nacional de Investigaciones CientĂ­ficas y TĂ©cnicas. Centro CientĂ­fico TecnolĂłgico Conicet - La Plata. Instituto de Investigaciones BioquĂ­micas de La Plata "Prof. Dr. Rodolfo R. Brenner". Universidad Nacional de la Plata. Facultad de Ciencias MĂ©dicas. Instituto de Investigaciones BioquĂ­micas de La Plata "Prof. Dr. Rodolfo R. Brenner"; ArgentinaFil: Schwaninger, Markus. UniversitĂ€t Zu LĂŒbeck; AlemaniaFil: Oster, Henrik. UniversitĂ€t Zu LĂŒbeck; AlemaniaFil: Astiz, Mariana. UniversitĂ€t Zu LĂŒbeck; Alemania. Consejo Nacional de Investigaciones CientĂ­ficas y TĂ©cnicas; Argentin

    Monetary policy, bank lending and corporate investment

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    The purpose of this study is to shed light on the chain of causality from macroeconomic financial policy to the microeconomic investment function. Concretely, we aim to provide an in-depth analysis of the relationships between the monetary policy of central banks, the loan policy of commercial banks, and the investment behavior of firms. We focus on countries that conduct their monetary policy under the inflation-targeting framework. Our empirical analysis with data from Germany, Switzerland and Thailand provides several new insights. First, after controlling for the US monetary policy, the monetary policy in Germany and Thailand appears to influence the banks’ lending rate in the short run (i.e. within two months), whereas the monetary policy in Switzerland seems to be ineffective at influencing the banks’ lending rate in the short run. Second, our results show that the banks’ lending rate has a negative effect on their loans and that this negative effect is weakened by their growth opportunities. Third, we find that the supply of bank loans plays a more pivotal role in determining firms’ investment than the lending rate. Last but not least, we document that neither the lending rate nor the loan-to-assets ratio moderates the sensitivity of the firms’ investment to growth opportunitie
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