The goal of the present investigation was to explore the effects of automatic emotion regulation on the desirability bias. The desirability bias is the tendency to believe that one will experience desirable outcomes and not experience undesirable outcomes. Previous research has demonstrated that the desirability bias is due to affective reactions to potential events. Further, deliberate emotion regulation has been shown to reduce the desirability bias. The present investigation explored whether the desirability bias can be reduced by priming a nonconscious goal to regulate emotion before experience of affective reactions to an event. Participants were primed to either express or regulate their emotions before playing a game of chance where cards could result in positive, negative or neutral outcomes. Results showed that the method of priming emotion regulation or expression did not effectively elicit nonconscious goals. Because the manipulation was not effective, the effect of automatic emotion regulation on the desirability bias could not be examined and there was no effect of the prime on bias. Despite the failed manipulation, the findings are still beneficial to the desirability bias literature in that they demonstrate a clear desirability bias in participants' predictions with the use of a within-subjects design. A follow up study using a stronger prime of regulation to test the influence of automatic emotion regulation in reducing the desirability bias is discussed.

<p> Body temperature regulation at high ambient temperatures was compared in pregnant and non-pregnant female albino rats. At an ambient temperature of 40°C, pregnant rats maintained lower body temperatures than non-pregnant rats without added expenditure of moisture for evaporative cooling. This was surprising because of the increased heat load on the pregnant animal resulting from a large weight gain and increased food intake. The maintenance of lower body temperatures in the heat by pregnant rats was possible because (1) pregnant rats produce less heat; i.e. consume less oxygen during exposure to 40°C than do non-pregnant rats and thus need to dissipate less heat; and (2) pregnant rats have a lower body temperature threshold for increased submaxillary salivary gland output in the heat, which makes more water for evaporative cooling available to them at lower body temperatures.</p> <p> The maintenance of lower body temperatures in the heat by pregnant rats suggests that pregnant rats have a need or a preference for lower body temperatures in the heat. The change in body temperature regulation during pregnancy is likely related to physiological and anatomical changes in the body which accompany pregnancy. Alterations in body temperature regulation to meet the changed physiological state of pregnancy provide another example of the body's remarkable ability to maintain homeostasis.</p> / Thesis / Doctor of Philosophy (PhD)

This thesis is a collection of essays on the problem of overfishing in multifirm fisheries with a common property fish stock. We focus on the case of marine industrial fisheries, where the costs of preventing free riding tend to preclude cooperative harvesting. We study the overfishing problem by analysing harvesting incentives that stem from variations in (i) technological (cost, production and biological growth) functions, (ii) institutional factors (access schemes, regulatory agencies' instruments and their monitoring and enforcement powers, harvesting competition), and (iii) objective functions (private firms' planning horizons, welfare functions). Chapter 2 discusses conditions under which a fishing collapse can occur and examines the commonly held argument that fishing collapse is a public bad. Chapter 3 studies Chilean fishing regulations over the last five decades. The regulator's persistent inability to enforce annual quotas is analysed. Distributive disputes and triggered lobbying powers are examined. The late 1980s controversies over a new Chilean fishing law are analysed in-depth from this perspective. Chapter 4 explains the main motivations and key assumptions leading us to the oligopoly harvesting models of chapters 5 (static setting) and 6 (dynamic setting). These models focus on a deterministic single fish species and a single sector harvesting fishery composed of profit maximizing and price taking private firms that compete with each other by following non-cooperative harvesting strategies. These models examine the overfishing rankings that result from comparing Cournot-Nash and Stackelberg equilibria. First best and second best welfare benchmarks are considered. The Cournot-Nash setting is intended to illustrate a large number oligopolistic fishery, while the Stackelberg equilibrium is meant to be a first approximation to analyse the implications of harvesting fisheries subject to industrial concentration. Empirical evidence suggesting the presence of industrial concentration in a series of important marine industrial fisheries is described in chapters 3 and 4.

Cell signaling pathways are frequently used in multiple tissue and stage-specific contexts during multicellular development. The integration of these signaling pathways by transcriptional enhancers controls the tissue specific gene expression necessary for proper development. Enhancers are segments of DNA that interpret developmental signals to produce patterns of gene expression. A set of operational rules defines how different enhancers targeted by the same signals interpret and act on these signals. Using the Drosophila model system, my thesis work focuses on determining the operational rules used by developmental enhancers that integrate the Notch signaling pathway with other pathways. During development, the Notch signaling pathway in used to pattern cell territories involved in cell fate determination, and plays a role in differentiation. I first used a computational approach to identify a set of candidate Notch-target enhancers. From this set I carefully studied one specific enhancer from the nab gene that integrates the Notch and Bone Morphogenetic Protein (BMP) signaling pathways in the developing wing. This nab enhancer is a part of a cluster of enhancers that work together to drive the global nab expression pattern during development. Each of these enhancers drives the expected expression patterns as well as atypical expression patterns, which are silenced by adjacent enhancers. These results suggest that Notch targeted enhancers are involved in both tissue specific gene activation and gene silencing.

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No description available.

Bacteria have the ability to sense different environmental signals. When an environmental stress is detected, bacteria rapidly adjust their gene expression profile to be able to survive and thrive. The transduction of such environmental signals often requires the coordinated involvement of several factors that constitute complex regulatory networks. Hence, depending on the combination of signals, a unique gene expression profile required to adapt to the specific stress conditions is generated. Proteins are the best-known regulatory factors. However, non-proteinaceous molecules are also important in signal-responsive control of bacterial gene expression. Alarmones are low molecular weight non-proteinaceous regulatory factors which can characteristically be rapidly turned-over to mediate instant changes in gene expression. One such alarmone is the modified nucleotide ppGpp, which directly binds to RNA polymerase to alter its activity. The levels of this alarmone are expected to rapidly increase in response to any environmental stress that result in slow proliferation. DksA, a putative ppGpp co-regulator that likewise directly targets RNA polymerase, has been suggested to be required for both the positive and negative regulation mediated by ppGpp in Escherichia coli. This thesis describes dissection of the role of ppGpp and DksA on transcriptional regulation, primarily using the fim genetic determinant that encodes for the type 1 fimbriae. Type 1 fimbriae are involved in adhesion to abiotic surface and initial adhesion/invasion of bladder cells, as well as in biofilm formation. We found that ppGpp regulates phase variation by increasing the sub-population of cells that express the fimbriae. The effect of ppGpp was ultimately traced to its role in transcription of the fimB gene that encodes a recombinase involved in the phase variation process (paper 1). In contrast, we unexpectedly found that lack of DksA causes an increase, rather than a decrease, in transcription from the fimB P2 promoter in vivo. However, in vitro transcription studies demonstrated that ppGpp and DksA, both independently and co-dependently, stimulate transcription from the fimB P2 promoter. These seemingly contradictory results from the in vivo and in vitro transcriptional studies were shown to be, at least in part, a consequence of the increased association of Gre-factors with RNA polymerase that can occur in the absence of DksA in vivo (paper 2). The results outlined above have implications for the role of ppGpp and/or DksA in global gene expression. Using gene expression profile (microarray analysis) during the transition from logarithmic to stationary phase of E. coli, we found that while most of the genes regulated by ppGpp and DksA are regulated in the same direction by the two factors, many were not. In addition to the fim genes, genes involved in flagella functioning, taxis responses, and a few genes encoding different transport systems are also differentially regulated in ppGpp- and DksA-deficient strains in vivo. Our results clearly indicate that the effect of deficiencies in ppGpp and DksA is far more complex than phenotypic similarity of the corresponding mutants anticipated by the proposed concerted action of ppGpp and DksA on gene expression (paper 2 &amp; 3).

Tuberkulose ist auch heute noch eine der bedrohlichsten Infektionskrankheiten weltweit, verantwortlich für über 1.5 Millionen Todesfälle jährlich. Diese „Erfolgsgeschichte“ ihres Erregers Mycobacterium tuberculosis ist dabei wesentlich durch einen extrem flexiblen Stoffwechsel bestimmt, der dem Bakterium das Wachstum unter den restriktiven Bedingungen der menschlichen Wirtszelle erlaubt. Diese Arbeit erkundet die Flexibilität des zentralen Kohlenstoffmetabolismus in Mykobakterien mit Hilfe mathematischer Modellierungsansätze, ergänzt durch die Integration von qualitativ hochwertigen experimentellen Daten. Ausgehend von einem Überblick über die metabolische Landschaft des zentralen Kohlenstoffmetabolismus, erhöht sich Schritt für Schritt die Detailtiefe bis hin zur genauen Analyse spezieller infektionsrelevanter metabolischer Wege. Die Verknüpfung des zentralen Kohlenstoffmetabolismus zu umgebenden Stoffwechsel- und Biosynthesewegen wird systematisch offen gelegt, als Voraussetzung für eine thermodynamische Charakterisierung des Systems, welche die Glykolyse als limitierenden Stoffwechselweg unter verschiedenen Wachstumsbedingungen charakterisiert. Basierend auf Protein- und Metabolitdaten im Fleißgleichgewicht, erlaubt eine neu vorgestellte Methode die Vorhersage regulatorischer Punkte für den metabolischen Übergang zwischen verschiedenen Kohlenstoffquellen. Abschließend wird mit Hilfe thermodynamisch-kinetischer Modellierung das Zusammenspiel zweier Stoffwechselwege mechanistisch erklärt, welche den robusten Abbau einer intrazellulären Kohlenstoffquelle ermöglichen. Durch die Entwicklung neuer Modellierungstechniken in Kombination mit hochauflösenden experimentellen Daten, trägt diese Arbeit zum besseren Verständnis der kontextabhängigen Flexibilität des mycobakteriellen Stoffwechsels bei, einem vielversprechenden Angriffspunkt für die Entwicklung neuer Medikamente gegen Tuberkulose. / Tuberculosis remains one of the major global health threats responsible for over 1.5 million deaths each year. This ’success story’ of the causative agent Mycobacterium tuberculosis is thereby closely linked to a flexible metabolism, allowing growth despite the restrictive conditions within the human host. In this thesis, the flexibility of the mycobacterial central carbon metabolism is explored by modeling approaches integrating high-quality experimental data. The analyses zoom in from a network based view to the detailed functionalities of individual, virulence relevant pathways. The interconnection of the central carbon metabolism to the remaining metabolic network is charted as a prerequisite to characterize its thermodynamic landscape, debunking glycolysis as bottleneck in different nutritional conditions. Based on steady state metabolomics and proteomics data, regulatory sites for the metabolic transition between different carbon sources are predicted by a novel method. Finally, the flexible interplay between two seemingly redundant pathways for the catabolism of an in vivo-like carbon source is explained mechanistically by means of thermodynamic-kinetic modeling. By employing novel modeling methods in combination with high-resolution experimental data, this work adds to the mechanistic understanding of the context dependent flexibility of mycobacterial metabolism, an important target for the development of novel drugs in the battle against tuberculosis.