Sustainability and Quality of Life: A Study on the Religious Worldviews, Values and Environmental Impact of Amish, Hutterite, Franciscan and Benedictine Communities

Boersema, J.J. [Promotor]Ester, P. [Copromotor

Taxes, Trading or Both?: An Experimental Investigation of Abatement Investment under Alternative Emissions Regulation

Emissions taxes and emissions permit trading schemes are designed to reduce greenhouse gas (GHG) emissions by providing incentives for large emitters to invest in less emissions-intensive production technologies. Whereas taxes place a fixed price on emissions, tradable permit schemes include a secondary permit market, from which allowance prices emerge after the regulation enters into force. Under a newly imposed regulation, the delay in price information contributes to uncertainty about the future cost of compliance that liable emitters will face, thereby challenging liable entities’ ability to make optimal abatement investment decisions. Using laboratory experiments, this thesis examines the effects of a policy regime that is similar to the one implemented in Australia in 2012. The regime includes a staged transition over time from a regulation-free environment, to an emissions tax and then to emissions trading. The thesis examines the effects of such a staged transition on investment decisions, the level of emissions, permit prices and trading behavior, comparing it to standard policy regimes of only an emissions tax and only emissions permit trading. The findings suggest that a regime based on a staged transition from a tax to permit trading results in lower compliance costs and higher overall allocative efficiency compared to a regime based solely on emissions trading in a market of heterogeneous producing firms

Convergent evolution of toxin resistance in animals

Convergence is the phenomenon whereby similar phenotypes evolve independently in different lineages. One example is resistance to toxins in animals. Toxins have evolved many times throughout the tree of life. They disrupt molecular and physiological pathways in target species, thereby incapacitating prey or deterring a predator. In response, molecular resistance has evolved in many species exposed to toxins to counteract their harmful effects. Here, we review current knowledge on the convergence of toxin resistance using examples from a wide range of toxin families. We explore the evolutionary processes and molecular adaptations driving toxin resistance. However, resistance adaptations may carry a fitness cost if they disrupt the normal physiology of the resistant animal. Therefore, there is a trade-off between maintaining a functional molecular target and reducing toxin susceptibility. There are relatively few solutions that satisfy this trade-off. As a result, we see a small set of molecular adaptations appearing repeatedly in diverse animal lineages, a phenomenon that is consistent with models of deterministic evolution. Convergence may also explain what has been called 'autoresistance'. This is often thought to have evolved for self-protection, but we argue instead that it may be a consequence of poisonous animals feeding on toxic prey. Toxin resistance provides a unique and compelling model system for studying the interplay between trophic interactions, selection pressures and the molecular mechanisms underlying evolutionary novelties.Naturali

Topological A-Type Models with Flux

We study deformations of the A-model in the presence of fluxes, by which we mean rank-three tensors with antisymmetrized upper/lower indices, using the AKSZ construction. Generically these are topological membrane models, and we show that the fluxes are related to deformations of the Courant bracket which generalize the twist by a closed 3-from $H$, in the sense that satisfying the AKSZ master equation implies the integrability conditions for an almost generalized complex structure with respect to the deformed Courant bracket. In addition, the master equation imposes conditions on the fluxes that generalize $dH=0$. The membrane model can be defined on a large class of $U(m)$- and $U(m) \times U(m)$-structure manifolds, including geometries inspired by $(1,1)$ supersymmetric $\sigma$-models with additional supersymmetries due to almost complex (but not necessarily complex) structures in the target space. Furthermore, we show that the model can be defined on three particular half-flat manifolds related to the Iwasawa manifold. When only $H$-flux is turned on it is possible to obtain a topological string model, which we do for the case of a Calabi-Yau with a closed 3-form turned on. The simplest deformation from the A-model is due to the $(2,0)+ (0,2)$ component of a non-trivial $b$-field. The model is generically no longer evaluated on holomorphic maps and defines new topological invariants. Deformations due to $H$-flux can be more radical, completely preventing auxiliary fields from being integrated out.Comment: 30 pages. v2: Improved Version. References added. v3: Minor changes, published in JHE

Serum peptide signatures for pancreatic cancer based on mass spectrometry: a comparison to CA19-9 levels and routine imaging techniques

Cellular mechanisms in basic and clinical gastroenterology and hepatolog

Is It Rational to Assume that Infants Imitate Rationally? A Theoretical Analysis and Critique

It has been suggested that preverbal infants evaluate the efficiency of others' actions (by applying a principle of rational action) and that they imitate others' actions rationally. The present contribution presents a conceptual analysis of the claim that preverbal infants imitate rationally. It shows that this ability rests on at least three assumptions: that infants are able to perceive others' action capabilities, that infants reason about and conceptually represent their own bodies, and that infants are able to think counterfactually. It is argued that none of these three abilities is in place during infancy. Furthermore, it is shown that the idea of a principle of rational action suffers from two fallacies. As a consequence, is it suggested that it is not rational to assume that infants imitate rationally. Copyright (C) 2012 S. Karger AG, Base

KCNA5 gene is not confirmed as a systemic sclerosis-related pulmonary arterial hypertension genetic susceptibility factor

<p>Introduction: Potassium voltage-gated channel shaker-related subfamily member 5 (KCNA5) is implicated in vascular tone regulation, and its inhibition during hypoxia produces pulmonary vasoconstriction. Recently, a protective association of the KCNA5 locus with systemic sclerosis (SSc) patients with pulmonary arterial hypertension (PAH) was reported. Hence, the aim of this study was to replicate these findings in an independent multicenter Caucasian SSc cohort.</p> <p>Methods: The 2,343 SSc cases (179 PAH positive, confirmed by right-heart catheterization) and 2,690 matched healthy controls from five European countries were included in this study. Rs10744676 single-nucleotide polymorphism (SNP) was genotyped by using a TaqMan SNP genotyping assay.</p> <p>Results: Individual population analyses of the selected KCNA5 genetic variant did not show significant association with SSc or any of the defined subsets (for example, limited cutaneous SSc, diffuse cutaneous SSc, anti-centromere autoantibody positive and anti-topoisomerase autoantibody positive). Furthermore, pooled analyses revealed no significant evidence of association with the disease or any of the subsets, not even the PAH-positive group. The comparison of PAH-positive patients with PAH-negative patients showed no significant differences among patients.</p> <p>Conclusions: Our data do not support an important role of KCNA5 as an SSc-susceptibility factor or as a PAH-development genetic marker for SSc patients.</p&gt

The role of MORC3 in silencing transposable elements in mouse embryonic stem cells

Background Microrchidia proteins (MORCs) are involved in epigenetic gene silencing in a variety of eukaryotic organisms. Deletion of MORCs result in several developmental abnormalities and their dysregulation has been implicated in developmental disease and multiple cancers. Specifically, mammalian MORC3 mutations are associated with immune system defects and human cancers such as bladder, uterine, stomach, lung, and diffuse large B cell lymphomas. While previous studies have shown that MORC3 binds to H3K4me3 in vitro and overlaps with H3K4me3 ChIP-seq peaks in mouse embryonic stem cells, the mechanism by which MORC3 regulates gene expression is unknown. Results In this study, we identified that mutation in Morc3 results in a suppressor of variegation phenotype in a Modifiers of murine metastable epialleles Dominant (MommeD) screen. We also find that MORC3 functions as an epigenetic silencer of transposable elements (TEs) in mouse embryonic stem cells (mESCs). Loss of Morc3 results in upregulation of TEs, specifically those belonging to the LTR class of retrotransposons also referred to as endogenous retroviruses (ERVs). Using ChIP-seq we found that MORC3, in addition to its known localization at H3K4me3 sites, also binds to ERVs, suggesting a direct role in regulating their expression. Previous studies have shown that these ERVs are marked by the repressive histone mark H3K9me3 which plays a key role in their silencing. However, we found that levels of H3K9me3 showed only minor losses in Morc3 mutant mES cells. Instead, we found that loss of Morc3 resulted in increased chromatin accessibility at ERVs as measured by ATAC-seq. Conclusions Our results reveal MORC3 as a novel regulator of ERV silencing in mouse embryonic stem cells. The relatively minor changes of H3K9me3 in the Morc3 mutant suggests that MORC3 acts mainly downstream of, or in a parallel pathway with, the TRIM28/SETDB1 complex that deposits H3K9me3 at these loci. The increased chromatin accessibility of ERVs in the Morc3 mutant suggests that MORC3 may act at the level of chromatin compaction to effect TE silencing.Molecular Technology and Informatics for Personalised Medicine and Healt