Coexistence of service- and facility-based competition: The relevance of access prices for "make-or-buy"-decisions

This paper models competition between two firms, which provide broadband Internet access in regional markets with different population densities. The firms, an incumbent and an entrant, differ in two ways. First, consumers bear costs when switching to the entrant. Second, the entrant faces a make-or-buy decision in each region and can choose between service-based and facility-based entry. The usual trade-off between static and dynamic efficiency does not apply in the sense that higher access fees might yield both, lower retail prices and higher total coverage. This holds despite a strategic effect in the entrant's investment decision. While investment lowers marginal costs in regions with facility-based entry, it intensifies competition in all regions. We show that the cost-reducing potential of investments dominates the strategic effect: Higher access fees increase facility-based competition, decrease retail prices and increase total demand. --Broadband access markets,facility- and service-based entry,investments,economies of density,switching costs

On the Use of Formative Measurement Specifications in Structural Equation Modeling: A Monte Carlo Simulation Study to Compare Covariance-Based and Partial Least Squares Model Estimation Methodologies

The broader goal of this paper is to provide social researchers with some analytical guidelines when investigating structural equation models (SEM) with predominantly a formative specification. This research is the first to investigate the robustness and precision of parameter estimates of a formative SEM specification. Two distinctive scenarios (normal and non-normal data scenarios) are compared with the aid of a Monte Carlo simulation study for various covariance-based structural equation modeling (CBSEM) estimators and various partial least squares path modeling (PLS-PM) weighting schemes. Thus, this research is also one of the first to compare CBSEM and PLS-PM within the same simulation study. We establish that the maximum likelihood (ML) covariance-based discrepancy function provides accurate and robust parameter estimates for the formative SEM model under investigation when the methodological assumptions are met (e.g., adequate sample size, distributional assumptions, etc.). Under these conditions, ML-CBSEM outperforms PLS-PM. We also demonstrate that the accuracy and robustness of CBSEM decreases considerably when methodological requirements are violated, whereas PLS-PM results remain comparatively robust, e.g. irrespective of the data distribution. These findings are important for researchers and practitioners when having to choose between CBSEM and PLS-PM methodologies to estimate formative SEM in their particular research situation.PLS, path modeling, covariance structure analysis, structural equation modeling, formative measurement, simulation study

Evidence for the PSL(2∣|2) Wess-Zumino-Novikov-Witten model as a model for the plateau transition in Quantum Hall effect: Evaluation of numerical simulations

In this paper I revise arguments in favour of the PSL(2$|$2) Wess-Zumino-Novikov-Witten (WZNW) model as a theory of the plateau transition in Integer Quantum Hall effect. I show that all available numerical data (including the correlation length exponent $\nu$) are consistent with the predictions of such WZNW model with the level $k=8$.Comment: 11 pages, no figure

Neuronal microRNA eeregulation in response to Alzheimer's disease Amyloid-β

Normal brain development and function depends on microRNA (miRNA) networks to fine tune the balance between the transcriptome and proteome of the cell. These small non-coding RNA regulators are highly enriched in brain where they play key roles in neuronal development, plasticity and disease. In neurodegenerative disorders such as Alzheimer's disease (AD), brain miRNA profiles are altered; thus miRNA dysfunction could be both a cause and a consequence of disease. Our study dissects the complexity of human AD pathology, and addresses the hypothesis that amyloid-beta (Abeta) itself, a known causative factor of AD, causes neuronal miRNA deregulation, which could contribute to the pathomechanisms of AD. We used sensitive TaqMan low density miRNA arrays (TLDA) on murine primary hippocampal cultures to show that about half of all miRNAs tested were down-regulated in response to Abeta peptides. Time-course assays of neuronal Abeta treatments show that Abeta is in fact a powerful regulator of miRNA levels as the response of certain mature miRNAs is extremely rapid. Bioinformatic analysis predicts that the deregulated miRNAs are likely to affect target genes present in prominent neuronal pathways known to be disrupted in AD. Remarkably, we also found that the miRNA deregulation in hippocampal cultures was paralleled in vivo by a deregulation in the hippocampus of Abeta42-depositing APP23 mice, at the onset of Abeta plaque formation. In addition, the miRNA deregulation in hippocampal cultures and APP23 hippocampus overlaps with those obtained in human AD studies. Taken together, our findings suggest that neuronal miRNA deregulation in response to an insult by Abeta may be an important factor contributing to the cascade of events leading to AD.N.S. is supported by the Human Frontier Science Program. L.I. is supported by the National Health and Medical Research Council (NHMRC) and the Australian Research Council (ARC), and J.G. is supported by grants from the University of Sydney, the National Health and Medical Research Council (NHMRC), the Australian Research Council (ARC), and the J.O. & J.R. Wicking Trust. Postgraduate scholarship support has been provided by the Wenkart Foundation, GlaxoSmithKline and Alzheimer’s Australia

Metabolites that confirm induction and release of dormancy phases in sweet cherry buds

Here we report on metabolites found in a targeted profiling of ‘Summit’ flower buds for nine years, which could be indicators for the timing of endodormancy release (t1) and beginning of ontogenetic development (t1*). Investigated metabolites included chrysin, arabonic acid, pentose acid, sucrose, abscisic acid (ABA), and abscisic acid glucose ester (ABA-GE). Chrysin and water content showed an almost parallel course between leaf fall and t1*. After ‘swollen bud’, water content raised from ~60 to ~80% at open cluster, while chrysin content decreased and lost its function as an acetylcholinesterase inhibitor. Both parameters can be suitable indicators for t1*. Arabonic acid showed a clear increase after t1*. Pentose acid would be a suitable metabolite to identify t1 and t1*, but would not allow describing the ecodormancy phase, because of its continuously low value during this time. Sucrose reached a maximum during ecodormancy and showed a significant correlation with air temperature, which confirms its cryoprotective role in this phase. The ABA content showed maximum values during endodormancy and decreased during ecodormancy, reaching 50% of its content t1 at t1*. It appears to be the key metabolite to define the ecodormancy phase. The ABA-GE was present at all stages and phases and was much higher than the ABA content and is a readily available storage pool in cherry buds.Peer Reviewe