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We present a unified dynamic framework to study the interconnections between international trade and business cycle models. We prove an aggregate equivalence between a competitive, representative firm model that has aggregate production externalities and dynamic trade models that feature monopolistic competition, endogenous entry, and heterogeneous firms. The production externalities in the representative firm model have to be introduced in the intermediate and final good sectors so that the model is isomorphic to dynamic trade models that embody love-of-variety and selection effects. In a quantitative exercise with multiple shocks, we show that to improve the fit of the dynamic trade models with the data, the most important ingredient is negative capital externality in the intermediate good sector. We conclude that this presents a puzzle for the literature as standard dynamic trade models provide micro-foundations for positive capital externality.

We show that the effectiveness of redistribution policy in stimulating the economy and improving welfare is directly tied to how much inflation it generates, which in turn hinges on monetary-fiscal adjustments that ultimately finance the transfers. We compare two distinct types of monetary-fiscal adjustments: In the monetary regime, the government eventually raises taxes to finance transfers while in the fiscal regime, inflation rises, effectively imposing inflation taxes on public debt holders. We show analytically in a simple model how the fiscal regime generates larger and more persistent inflation than the monetary regime. In a quantitative application, we use a two-sector, two-agent New Keynesian model, situate the model economy in a Covid-19 recession, and quantify the effects of the transfer components of the Coronavirus Aid, Relief, and Economic Security (CARES) Act. We find that the transfer multipliers are significantly larger under the fiscal regime—which results in a milder contraction—than under the monetary regime, primarily because inflationary pressures of this regime counteract the deflationary forces during the recession. Moreover, redistribution produces a Pareto improvement under the fiscal regime.

We study aggregate, distributional, and welfare effects of a permanent reduction in the capital tax rate in a dynamic equilibrium model with capital-skill complementarity. Such a tax reform leads to expansionary long-run aggregate effects, but is coupled with an increase in the skill premium. Moreover, the expansionary long-run aggregate effects are smaller when distortionary labor or consumption tax rates have to increase to finance the capital tax rate cut. An extension to a model with heterogeneous households shows that consumption inequality increases in the long-run. We study transition dynamics and show that short-run effects depend critically on the monetary policy response: whether the central bank allows inflation to directly facilitate government debt stabilization and how inertially it raises interest rates. Finally, we contrast the long-term aggregate welfare gains with short-term losses, as well as in the model with heterogeneous households, show that welfare gains for the skilled go together with welfare losses for the unskilled.

We estimate international spillover effects of US Quantitative Easing (QE) on emerging market economies (EMEs). Using a Bayesian VAR on monthly US macroeconomic and financial data, we first identify the US QE shock. The identified US QE shock is then used in a monthly Bayesian panel VAR for EMEs to infer spillover effects on these countries. We find that an expansionary US QE shock has significant effects on financial variables in EMEs. It leads to an exchange rate appreciation, a reduction in long-term bond yields, a stock market boom, and an increase in capital inflows to these countries. These effects on financial variables are stronger for the "Fragile Five" countries compared to other EMEs.

Fil tilgjengelig fra 2019-06-01 Prostate cancer (PCa) is the most commonly diagnosed malignancy and the third leading cause of cancer death among men in western countries. The high incidence of prostate cancer underscores urgent need for clinical indicators (biomarkers) for early detection of the presence and progression of the disease. Emerging evidence suggest that cytokine, chemokine and growth factor are key mediators of prostate inflammation that may play an important role in prostate cancer initiation and progression and may facilitate the exploration of new markers of prostatic neoplasia and inflammation. Cytokine profiling in serum and plasma has become an important biomarker discovery tool in the study of disease mechanism, pathogenesis and treatment. The purpose of this Master thesis was to implement multiplex immunoassay that is capable of measuring multiple cytokines simultaneously within a single sample in order to study the differences of serum cytokine profile between patients with prostate PCa and non-cancer individuals to explore new biomarker of prostatic neoplasia. Concentrations of 27 cytokines (cytokines/chemokine’s and growth factor) were measured in sera of 29 patients with PCa and 21 non-cancer individuals using multiplex ELISA-based immunoassay. Relationships of these cytokine levels to serum PSA, Gleason score and urinePCA3 was also assessed. There was no significant difference in cytokine level between PCa and non-cancer controls. No correlation of cytokine and serum PSA level among non-cancer and whole cohort was observed. However, a significant positive correlation was found between serum levels of twenty different cytokines (IL-1β, IL-1ra, IL-2, IL-4, IL-6, IL-7, IL-9, IL-10, IL-12, IL-13, IL-17, Basic FGF, Eotaxin, G-CSF, GM-CSF, IFN-γ, MCP-1, PDGF-BB, TNF-α, and VEGF) and PSA levels among PCa patients. Interferon gamma-induced Protein 10 (IP-10) was only found to be associated with relationship with age, and no correlation of serum cytokine with Gleason score was found. Negative correlations between the expression levels of IL-2, GM-CSF, MIP1α and urine PCA3 was found before Benjamini and Hochberg multiple corrections. Except IP-10, MCP1, MIP1α, MIP1β, PDGF, the majority of cytokine shows strong correlations between each other. In conclusion, though there was no significant difference in cytokine level between prostate and non-cancer individuals, however the work presented in this thesis shows strong correlation of PSA level with cytokine among PCa and no correlation among non-cancer individuals. This could lead to a better description of disease state and better understanding of the pathophysiology of PCa and may improve clinical management in patients with PCa.