Individuals within a single population can vary widely in their phenotype e.g. in their body shape. These differences are an important source of biodiversity and they can precede evolutionary divergence within a population. In this thesis we use the biological invasion of the zebra mussels into Swedish lakes to investigate which processes create or maintain phenotypic diversity within populations of the two native fish species perch and roach and the mussel itself. Both fishes have specially adapted body shapes that depend on whether they feed in the near-shore or open-water habitat of lakes. This habitat-specific divergence was more pronounced in lakes with zebra mussels, probably because resources in both habitats were in higher supply due to the mussels’ effects on the lakes. Divergence in perch body shapes between habitats was also higher in lakes with a higher water clarity, suggesting that visual conditions can affect the resource use and thus also the expression of a habitat-specific body shape. When investigating the diversity of body shapes in the mussel itself we found that mussels from one lake changed their shell shape when exposed to different predators: fish predators induced a more elongated shell shape while crayfish predators induced a rounder shell. These specific shell shapes probably serve as two alternative predator defenses protecting the mussel from predation. We conclude that the availability and use of distinct resources is an important source of diversity within populations. Abiotic conditions can play a previously underappreciated role by promoting or impairing the use of the distinct resources thus affecting the divergence. The diversity of shell shapes we found in the zebra mussels complements our study by demonstrating that not only consumer responses to resources but also resources’ responses to predators can generate phenotypic diversity.

This thesis consists of five self-contained essays. Essay 1. (with Sören Blomquist and Luca Micheletto)  Using a calibrated overlapping-generations model we quantify the welfare gains of an age-dependent labor income tax. Agents face uncertainty regarding future abilities and can transfer consumption across periods through savings. The welfare gain of switching from an age-independent to an age-dependent nonlinear tax varies between 2.4% and 4% of GDP. Part of the welfare gain is due to capital accumulation effects and part descends from relaxing incentive-compatibility constraints. The welfare gain is of about the same magnitude as the welfare gain that can be achieved by moving from a linear- to a nonlinear labor income tax. Finally, the welfare loss from tax-exempting interest income is negligible under an optimal age-dependent labor income tax. Essay 2. (with Sören Blomquist and Luca Micheletto) Previous literature has shown that public provision of private goods can be a welfare-enhancing device in second-best settings where governments pursue redistributive goals. However, three issues have so far been neglected. First, the case for supplementing an optimal nonlinear income tax with public provision of private goods has been made in models where agents differ only in terms of market ability. Second, the magnitude of the welfare gains achievable through public provision schemes has not been assessed. Third, the similarities/differences between public provision schemes and tagging schemes have not been thoroughly analyzed. Our purpose in this paper is therefore threefold: first, to extend previous contributions by incorporating in the theoretical analysis both heterogeneity in market ability and in the need for the publicly provided good; second, to perform numerical simulations to quantify the size of the potential welfare gains achievable by introducing a public provision scheme, and to characterize the conditions under which these welfare gains are sizeable; finally, to compare the welfare gains from public provision with the welfare gains from tagging. Essay 3. (with Sören Blomquist and Luca Micheletto) Subsidized child care is a common phenomenon in both Europe and the United States. In this paper we study the efficiency of some of the most common types of child care subsidies. These are a (refundable) tax credit, tax deductibility and public provision. We evaluate the relative efficiency of these instruments using a quantitative simulation model calibrated to resemble the US economy. In our framework there is a special tax treatment for families with children of child care age, which is based on an assumption that agrees with facts pertaining to actual circumstances in the United States, as well as many other countries. We keep the net tax revenue for this group of tax payers constant, hence the subsidies to child care are paid for by the group itself. It is a commonly held view that in a 'good society' all children should have equal opportunities in life. Many proponents of subsidized childcare argue that one way to move in this direction is to allow all children access to good quality child care. We capture this ideological perspective by using a paternalistic social welfare function which places special emphasis on the quality of child care purchased by households. Using a standard social welfare function we find tax deductibility to be the most efficient instrument to subsidize child care and public provision the least efficient instrument. These results are completely reversed when using the paternalistic welfare function and when  society has the goal of providing all children with access to good quality child care.  Public provision then becomes the best way to subsidize child care.  An important aspect of public provision is that it is an efficient instrument in raising the quality of child care. Essay 4.  In a recent paper Alesina et al. (2011) construct a model in which different labor supply elasticities for men and women emerge endogenously from intra-household bargaining. In this paper I explore the optimal tax implications of their model in an economy with both singles and couples and inequality across as well as within households. In the model, the welfare of married women can be improved by lowering taxes for single women. However, this benefit must be weighed against the welfare cost of taxing single men and women at different rates. Moreover, if single men earn more than single women, the welfare of married women can alternatively be improved by a gender-neutral tax scheme which taxes singles at a higher rate. Because the government is concerned not only with equalizing utilities within families, but also with the redistribution between high income and low income households, gender-based adjustments in the income tax must be weighed against the welfare consequences of changing the progressivity of the tax system. I find that larger lump-sum transfers to women is always optimal. Interestingly, marginal tax rates, on the other hand, should be lower for women only if the exogenous bargaining power of men is moderate. The welfare gains of gender based taxation are sizable and the welfare gains of having tax instruments which depend on household composition are even larger. Essay 5. (with Håkan Selin) Recent microeconometric studies of taxpayers' responsiveness to taxation have shown that intensive margin labor supply and earnings elasticities typically are modest and sometimes equal to zero. However,a common view is that long-run responses might still be large since micro-estimates are downward biased owing to optimization frictions. In this paper we estimate the taxable income elasticity at a very large kink point of the Swedish tax schedule using the bunching method. During the period of study the change in the log net-of-tax rate reached a maximum value of 45.6%. Interestingly, we obtain a precise elasticity estimate of zero for wage earners at this large kink. The size of the kink allows us to derive tighter bounds on the long-run elasticity than previous studies. If wage earners on average tolerate 1% of their disposable income in optimization costs, the upper bound on the long-run taxable income elasticity is 0.39. We also evaluate the performance of the bunching estimator by performing Monte Carlo simulations.

<p>Diss. Stockholm : Handelshögskolan, 2012</p>

<p>The objective of this research was to investigate the relationships between the political change and the access policy changes in Madagascar since independence. In this study qualitative and quantitative data were used. The qualitative research consisted of eleven in-depth interviews and the collection of policy documents from 1960 to 2008. Open-ended questionnaires were utilized to collect data and to achieve the objectives of the research. Policy documents were analyzed to identify government policy changes. The main findings from the research showed that access policy changed with each major change in political leadership. Four major political periods and four respective main access policy changes were identified from 1960 to 2008. Higher education policy in general changed when there was a major change in presidential leadership. The main conclusions of this study were that access policy changes were the result of major changes in presidential leadership and that in spite of rhetoric to the contrary, universities did not have the autonomy to resist changes in access policy because of the top-down state system and the institutional financial dependence on the national government.</p>

One major focus of anxiety research in recent years has been the identification of cognitive factors that promote increased vulnerability to anxiety. Cognitive formulations propose that anxiety is characterised by an increased tendency to attend to negatively valenced emotional information, and that this bias may play a causal role in the development and maintenance of clinical anxiety. Evidence suggests that this anxiety-linked processing bias occurs even in conditions in which the stimuli are masked in order to prevent awareness of the content (i.e., preattentive bias). The present thesis focused principally on the preferential processing of threat-related information that occurs outside awareness. Two different outcome measures were used to index preferential preattentive processing of threat-related information in non-clinical populations: The emotional Stroop task was used to index selective attention to masked presentation of threatening word stimuli, whereas skin conductance responses were used to index selective autonomic responses to masked presentation of threatening pictorial stimuli. The empirical studies in the present thesis showed that elevated levels of trait anxiety promote preferential preattentive processing of negatively valenced information, whereas elevated levels of social desirability (interpreted as defensiveness) generally prevent preferential preattentive processing of negatively valenced information, especially among those at higher levels of trait anxiety, irrespective of outcome measure used. Moreover, previous research has demonstrated that a person’s most common emotional reaction when encountering a stressful event is causally influenced by that person’s habitual tendency to selectively encode the most threatening aspects of all available information. Thus, preattentive bias (as measured with the emotional Stroop task) was used to predict the emotional responses (as seen on self-reported emotional distress and autonomic reactivity) following exposure to a laboratory stressor. This study showed that preattentive bias to negative information had significant effects on both self-reported and physiological measures in response to a laboratory stressor, but in diametrically opposite directions. Specifically, whereas preattentive bias was positively associated with self-reported negative emotional response, it was negatively associated with a physiological indicator of emotional response. The results were discussed in terms of an inability to automatically inhibit the processing of threatening cues, which seems to be a vulnerability marker for anxiety. Whether this bias is ultimately sufficient for the development of clinical anxiety remains to be examined in future research. Additionally, more information is needed before it can be established that the emotional Stroop task can be viewed as a reliable diagnostic tool for determining an individual’s anxiety status.

Background The prevalence of atopic disease among children in the formerly socialist countries in Europe, with a life style similar to that prevailing in Western Europe 30–40 years ago, is low, whereas there has been a pronounced increase in industrialized countries over the last decades. The environment during infancy influences the risk of developing allergy for many years, perhaps even for life. Objective To investigate the development of allergen-specific cytokine responses during the first 2 years of life in two geographically adjacent countries with marked differences in living conditions and incidence of atopic diseases, i.e. Estonia and Sweden. Methods The development of immune responses to food (β-lactoglobulin (BLG) and ovalbumin (OVA)) and inhalant (cat and birch) allergens was studied from birth up to the age of 2 years in 30 Estonian and 76 Swedish infants. Clinical investigation and skin prick tests were performed and blood samples were obtained at birth and at 3, 6, 12 and 24 months. Results The levels of IL-5, IL-10 and IL-13 secreted by peripheral blood mononuclear cells stimulated with BLG, OVA and cat allergen in Estonian and Swedish infants declined during the first 3 months of life. All cytokines then progressively increased in the Swedish infants, indicating the replacement of non-specifically responding immature cord blood T cells with specific T memory cells, which are primed postnatally. The resurgence of allergen-specific responses in the Estonian infants was less marked. These differences were particularly notable for birch-specific T cell responses, which correlated with development of atopic disease in the Swedish children. Conclusions The development of specific T cell memory to food and inhalant allergens during the first 2 years of life differs between infants living in Sweden and Estonia, and mirrors the disparate patterns of expression of allergic disease which subsequently develops in the respective populations.

The objective of this study was to examine symptomatology; stress responses for everyday academic and social stressors; and cognitive coping resources among 11-year-old children adopted from Romanian orphanages. Two groups were established by the amount of time spent within the institutional system. Early adoptees (EAs, n=25) spent less than 6 months while late adoptees (LAs, n=14) endured 6 months or more of institutionalization. A comparison group of non adopted, same-age peers (Canadian Born (CBs), n=25) was included. The first goal was to investigate whether there were differences between EAs and LAs in ratings of symptomatology and stress responses. The second goal was to compare all Romanian adoptees (RAs) to CBs on the same set of factors. The third goal was to identify predictors of symptomatology and predictors of stress responses for RAs only. The main findings were as follows. EAs and LAs did not differ in any symptom ratings or stress responses, showing a lack of evidence for duration of deprivation as a grouping factor. Significant differences were detected by adoption status. Ratings were higher for RAs than CBs in parent-rated symptomatology, including the rate of RAs who exceeded the borderline clinical cut-off. RAs reported less secondary control coping for social stressors than CBs. Models to predict symptoms from stress responses were not supported, with one exception. More disengagement coping for social stress and less involuntary disengagement for academic stress predicted less externalizing and generalized symptoms by teacher report. Models to predict stress responses from cognitive coping resources were significant except for disengagement coping. One of the main findings was that predictors of secondary control coping varied by stressor domain. In conclusion, the findings were important in demonstrating that duration of deprivation does not differentiate between post-institutionalized preadolescents in aspects of psychosocial adjustment. Adoption status is a significant factor. Stress responses do not contribute to models of symptoms. The cognitive coping resources of perceived academic competency and social-support contribute to models of stress responses, yet with room to improve the predictive power of the models. Implications of the findings are discussed along with limitations and directions for future research.

We report herein that IL-10-treated dendritic cells (DC) can be used effectively to reverse established severe asthma-like disease in a mouse model. Our lab had shown previously that allergen-presenting splenic CD8¦Á+ DCs could ¡Ö50% reduce airway hyper responsiveness (AHR), eosinophilia, and Th2 responses in asthma-phenotype mice, but only marginally reduce IgE/IgG1 levels. We now show that bone marrow-derived DCs that have been differentiated in the presence of IL-10 (DCIL-10) are effective in reversing the asthma phenotype. Co-culture of DCIL-10 with T memory (TM) cells from asthma-phenotype mice was associated with lack of Th2 responses, and this was partially reversed by IL-2. Immunostimulatory DC activated these Th2 cells. <i>In vivo</i>, delivery of allergen-pulsed DCIL-10, either into the airway or intraperitoneally abrogated AHR from weeks 3-10 post-treatment, and ameliorated lung eosinophilia and Th2 (IL-4, -5, -9, & -13, IgE) responses, as well as circulating allergen-specific IgE responses for at least 32 weeks following treatment. Repeated OVADCIL-10 treatments kept AHR normalized for 8 weeks as well as Th2 responses significantly low. In vivo, delivery of anti-IL-10R, but not anti-TGF-¦Â from day 12-21 after treatment had moderate effects on DCIL-10-driven tolerance, but 1-methyl tryptophan (inhibitor of indoleamine-2,3-dioxygenase) treatment had significant effects on Th2 responses. The mechanisms mediating tolerance in vivo are likely complex, but we speculate that infectious tolerance sustains this regulatory activity during the 32-week period in which we have observed tolerance to be in place.

Host defense against infection and disease relies on the reciprocal communication between the immune and neuroendocrine systems where sex hormones exert negative and positive feedback actions on immune functions. Indeed, sex hormones have been implicated in gender dimorphic immune response and in the potentiation of immune-related disorders. The female hormone estrogen plays a role as an immunomodulator and may exert immunosuppressive and immunostimulatory effects. Though many studies focus on estrogen’s role in immunity within the female reproductive tract and autoimmunity, the modulatory effects of estrogen on vaccine responses are largely unexplored. The insufficient efficacy of some vaccines in certain target populations, as for example the elderly population, is well recognized. Hormones fluctuate throughout an individual’s life, and females in particular undergo several necessary reproductive (pregnancy and menopause) and lifestyle (oral contraceptive use) changes which involve sex hormones. Vaccine efficacy might be influenced by endogenous estrogen levels or by exogenous estrogen administration. Therefore, in the pursuit of improved vaccine efficacy, it is necessary to consider such hormonal factors and their contribution to immune status. We have studied estrogen’s role in modulation of vaccine responses using a mouse ovariectomy model where exogenous estrogen delivery can be controlled. Our studies included two different types of vaccines, a bacterial toxoid formulation and a bacterial secreted protein formulation. Results from these studies indicate that estrogen enhances vaccine-specific antibody production by likely supporting a general TH2 pathway and also modulates expression of genes encoding molecules critical in innate immune signaling and required for development of proper adaptive immune responses and antigen clearance through antibody-mediated mechanisms. The level at which estrogen modulates antibody responses appears to be dependent on the route of vaccine administration. The enhancement of specific humoral responses may involve mechanisms involving TLR2 and antibody Fc receptor expression on macrophages, cells that link innate and adaptive immune responses. Advances in our understanding of the relationship between sex hormones and the immune system may provide new insights into the mechanisms by which hormones act and thus may be exploited to guide the design of future vaccine strategies.

<i>Salmonella enterica serovar Enteritidis</i> is an important biofilm-forming food-borne pathogen. This study examined the adaptive responses of <i>Salmonella serovar Enteritidis</i> biofilms to different environmental conditions such as flow velocity and benzalkonium chloride (BC) treatment. The influence of a 10-fold difference in nutrient laminar flow velocity on the dynamics of biofilm formation and protein expression profiles was compared. The mode of development and architecture of low-flow and high-flow biofilms were distinct. Exopolymer composition of the two biofilms was also different. However, no major shift in protein expression was seen between the biofilms, nor were there any stress response proteins involved. The biofilms altered their architecture in response to flow, presumably assuming a structure that minimized overall biofilm stress. An empirically-determined shear-inducing flow was applied on high-flow biofilms, fractionating the biofilms into shearable and non-shearable regions. Length:width indices of cells from the two biofilm regions, as well as planktonic cells from biofilm effluent and continuous culture were determined to be 3.2, 2.3, 2.2, and 1.7, respectively. Expression of proteins involved in cold-shock response, adaptation, and broad regulatory functions in the shearable region, and expression of protein involved in heat-shock response and chaperonin function in the non-shearable region indicated that the physiological status of cells in two biofilm regions was also distinct. The development of biofilm adaptive resistance to BC was then examined. Adapted biofilms survived a lethal BC challenge and re-grew, whereas unadapted biofilms did not. Proteins up-regulated following adaptation included those involved in energy metabolism, amino acid and protein biosynthesis, nutrient-transportation, adaptation, detoxification, and 1,2-propanediol degradation. A putative universal stress protein was also up-regulated. Cold-shock response, stress response, and detoxification are suggested to play roles in adaptive resistance to BC. Functional differences in adaptive response and survival of plankonic and biofilm cells adapted to BC were also studied. The proportion of BC-adapted biofilm cells that survived a lethal BC exposure and heat-shock was significantly higher than that of BC-adapted planktonic cells. Enhanced biofilm-specific up-regulation of various proteins, coupled with alterations in cell surface roughness and shift in fatty acid composition are proposed to function in the enhanced survival of BC-adapted biofilm cells, relative to BC-adapted planktonic cells.<p>It is concluded that biofilms adapt to the stress conditions by means of community, cellular, and sub-cellular level responses. These adaptive responses help the biofilms to enhance their ability for survival in the nature, especially those formed in critical environments such as healthcare facilities, the food industry, and households.