Three Essays in International Macroeconomics.

This thesis deals with a number of different topics in the field of international macroeconomics. It proposes theoretical models of the open economy to think about and analyze questions such as the effects of financial globalization, countries' external adjustment mechanism, international relative prices, or the world's state of global imbalances.Macroeconomics;

Histone deacetylase 2-mediated deacetylation of the Ribonuclease 1 promoter in inflamed human endothelial cells

Endothelial cells (ECs) function as protective barrier to separate the blood from the surrounding tissue by conducting crucial roles in regulation and maintenance of vascular homeostasis, such as control of vessel permeability or coagulation. Therefore, dysfunction of the EC barrier due to inflammation, infection or injury can cause a variety of vascular pathologies, such as thrombosis or atherosclerosis. In this context, the circulating extracellular endonuclease Ribonuclease 1 (RNase1) was identified as a vessel- and tissue-protective enzyme and a potent regulator of vascular homeostasis. Upon acute inflammation, RNase1 functions as a natural counterpart to extracellular RNA (eRNA), a damage-associated molecular pattern, via degradation to protect the EC cell layer from excessive inflammation. However, long-term inflammation disrupts the RNase1-eRNA system. Thereby, eRNA accumulates in the extracellular space to induce massive proinflammatory cytokine release from circulating inflammatory cells, such as tumor necrosis factor alpha (TNF-α) or interleukin 1 beta (IL-1β). These cytokines negatively affect the EC layer by downregulation of RNase1 presumably through activation of histone deacetylases (HDACs). In this regard, this study investigated whether inflammation-mediated deacetylase function of HDACs suppresses RNase1 expression in human ECs through modulation of chromatin modifications. Proinflammatory stimulation with TNF-α or IL-1β of human umbilical vein endothelial cells significantly reduced RNase1 expression. Thus, identification of the RNASE1 promoter region and analysis of its chromatin state revealed the association of RNASE1 repression with deacetylation of histone 3 at lysine 27 and histone 4. The important role of HDACs in this process was further confirmed by administration of the specific class I HDAC1-3 inhibitor MS275 that successfully restored RNASE1 promoter acetylation and mRNA abundance upon TNF-α or IL-1β treatment. These results indicate an essential impact of HDAC1-3 in RNase1 regulation. Additionally, identification of specific HDACs involved in RNase1 regulation was obtained by chromatin immunoprecipitation kinetics confirming significant accumulation of HDAC2 at the RNASE1 promoter upon TNF-α stimulation. These findings were further validated by siRNA double knockdown of HDAC2 and its redundant enzyme HDAC1, which also recovered RNase1 mRNA abundance upon proinflammatory stimulation. In conclusion, our data identified HDAC2 as a crucial factor in RNase1 regulation in human ECs. HDAC2 is recruited to the RNASE1 promoter site to attenuate histone acetylation and suppress subsequent gene repression. This effect can be blocked by the specific HDAC inhibitor MS275 implicating the potential of HDAC inhibitors as novel therapeutic strategy to promote vascular integrity by preventing RNase1 downregulation in EC inflammation

A note on compactifications on spin(7)-holonomy manifolds

In this note we consider compactifications of Script M-theory on Spin(7)-holonomy manifolds to three-dimensional Minkowski space. In these compactifications a warp factor is included. The conditions for unbroken N = 1 supersymmetry give rise to determining equations for the 4-form field strength in terms of the warp factor and the self-dual 4-form of the internal manifold

Effects of Mold Exposure on Immune Cells

The relationship between exposure to mold spores and human disease is only beginning to be understood. While evidence exists of strong correlations between moldy environments and allergic and infectious diseases, the relationship between exposure to specific species and human immune responses to them is not fully understood. This paper seeks to clarify this relationship by analyzing the effects of exposing murine immune cells to volatile organic compounds (VOCs) produced by different mold species. Mold species studied include Stachybotrys alternans; tests performed include cell viability studies and immunoassays. Results have implications for further research and treatment of mold-related diseases