Abstract. In this manuscript, we summarize prior research on the agent-based modeling of financial markets. While extensive research related to agent-based modeling has been done in various economic disciplines, we focus mainly on the evolution of the models and their applications to financial markets. A large number of studies have adopted agent-based modeling methodologies to explain various empirical findings in financial markets. Our summary shows the benefits of using such modeling to account for various financial market phenomena. We confirm that small changes in initial parameter values can lead to relatively large fluctuations through the financial markets that can be viewed as complex or chaotic systems. This also means that financial markets become volatile due to small unexpected changes in the parameters of the models that describe the market.
Alloy oxidation has significant technological importance because of the possibility of dramatically improving corrosion resistance through compositional control. The possible effects of alloying elements on behavior also motivate fundamental study of oxidation mechanisms. Surprisingly, the previous lack of tools capable of probing atomic-level and mesoscale behavior have resulted in the initial stages of oxidation being the least well-understood regime of oxidation. Improvements in vacuum technology and nano-characterization have, however, recently led to many novel experiments providing new insights into the details of how oxygen reacts with surfaces. Our focus is on the nucleation and growth of oxides on metal and alloy surfaces, where in situ ultra-high vacuum transmission electron microscopy (UHV-TEM) is ideal for providing information of structural changes at this scale where surface conditions are very well controlled. Using primarily in situ UHV-TEM experiments of Cu oxidation, we have previously shown that heteroepitaxial concepts describe surprisingly well the nucleation, and growth to coalescence of Cu 2 O islands on Cu(001) [1,2], where oxygen surface diffusion is the dominant mechanism controlling nucleation and growth. We now focus on Cu-Au oxidation as a model binary alloy system, which is a natural extension of our extensive previous work on Cu [4,5]. Au is a noble element and does not form a stable oxide, and Cu and Au are miscible at the elevated temperatures where oxidation behavior is of interest.These experiments were carried out in a modified JEOL 200CX TEM [6]. This microscope is equipped with an ultra-high vacuum (UHV) chamber with base pressure ~ 10 -8 Torr. The microscope was operated at 100KeV to minimize the possibility of radiation-induced effects. A controlled leak valve attached to the column permits the introduction of oxygen gas directly into the microscope at a partial pressure (pO 2 ) between 5×10 -5 and ~5×10 -4 Torr. CuAu(100) single crystal films with 1000Å thickness were grown on irradiated NaCl(100) by sputter deposition. The alloy films were removed from the substrate by flotation in deionized water, washed and mounted on a specially prepared sample holder that allows for resistive heating to a maximum temperature of 1000°C.For temperatures ranging from 550 °C to 750 °C and constant oxygen partial pressure of 5x10 -4 Torr, Cu 2 O islands formed initially with cube-on-cube crystallographic orientation relative to the Cu-Au film. In comparison to Cu(100), the incubation time for Cu 2 O nucleation is longer on the alloy surface. However, once the oxide islands start to appear, the nucleation rate is faster in Cu 0.5 Au 0.5 (001) alloy, i.e. the time from the appearance of the first oxide island to when the island saturation density is reached is significantly shorter for the Cu-Au alloy as compared to Cu. Figure 1 is a bright field TEM image showing how the morphology of a typical Cu 2 O island changes due to composition and temperature. We speculate how the secondary element...
Aims: Reconstitution of lethally irradiated B10.AKM (H-2K k ) mice with syngeneic bone marrow cells infected with retroviruses carrying the allogeneic MHC class I gene H-2K b resulted in stable and lifelong expression of K b on bone marrow-derived cells. More importantly, these mice were specifically tolerant to H-2K b skin grafts while still retaining the ability to reject third party skin grafts. Using CD8 transgenic mice, we discovered that alloreactive CD8 T cells underwent negative selection in the thymus, leading to the absence of these potentially alloreactive T cells in the periphery. In this study, we utilize Tg361 CD4 transgenic mice (CBA/Ca (H-2 k )) expressing a TCR specific for the MHC class I gene H-2K b to determine the fate of potentially alloreactive CD4 T cells using our gene therapy protocol. Methods: Tg361 CD4 TCR transgenic mice which express an alloreactive TCR on CD4 T cells specific for K b were utilized to determine the mechanism by which genetic engineering of bone marrow induces donor specific CD4 T cell tolerance after bone marrow transplantation. Lethally irradiated B10.AKM mice were reconstituted with a 6:1 ratio of mock or K b -transduced B10.AKM bone marrow to Tg361 bone marrow. Starting at four weeks after bone marrow transplantation, mice were analyzed for H-2K b expression as well as for the development of Tg361 CD4 T cells. Results: Lethally irradiated recipients that received CD4 transgenic bone marrow in combination with autologous bone marrow transduced with virus encoding H-2K b displayed stable and long-term expression of K b on bone marrow-derived cells. Alloreactive CD4 transgenic T cells were readily detectable in the peripheral blood, spleen and thymus of chimeric recipients; although their levels were 2-fold lower than mock-transduced bone marrow recipients. Despite the presence of potentially alloreactive CD4 T cells in the periphery, chimeric recipients were specifically tolerant to H-2K b expressing skin grafts. Interestingly, chimeric mice which received K b -transduced and CD4 transgenic bone marrow expressed CD25 on 20-30% of Tg361-derived CD4 T cells, compared to only 6% of Tg361-derived CD4 T cells in mock transduced controls. Conclusions: We conclude that genetic engineering of bone marrow induces donor specific CD4 T cell tolerance through deletional and non-deletional mechanisms. We further hypothesize that expression of K b on bone marrow derived cells induces CD4 T cells capable of inhibiting alloreactive T cells.Aims: A substantial level of donor lymphocyte chimerism is required to protect donor-specific islet allografts in the mouse model with autoimmune diabetes. Donor islet allografts can be rejected in diabetic NOD mice with a low level of donor lymphocyte chimerism. In this study, we investigated whether posttransplant donor lymphocyte infusion increases donor chimerism and induces donor-specific tolerance to islet allografts in diabetic NOD mice. Methods: Donor BALB/c (H-2 d ) splenocytes were injected into prediabetic NOD/Lt mice (H-2 g7 ) and dia...
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