176 research outputs found

    Relationships between phases of business cycles in two large open economies

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    Nonlinear Generalizations of Tucker's Theorem on Inequality Systems

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    This note is to prove Tucker's theorem on linear inequalities based on the proof method of minimax theorems which uses Kakutani's fixed point theorem. One device is necessary to convert the minimax theorems to Tucker's formulation. This is a slight restriction on the image sets when creating a set-valued map. We also present nonlinear generalizations of Tucker's theorem employing the same method. All we need is that the set of variable values for which an objective function attains its maximum is convex. This objective function is a convex combination of functions. We also present a proof of the fact that a local characterization of inequality systems, when a given mapping is differentiable, can be made global provided the mapping is concave

    A Multi-Sector Goodwin Model with n Kinds of Capital Goods

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    In a work concerning stability analysis, Burmeister, Dobell, and Kuga(1968) showed the properties of Solow type growth model with many capital goods. They suggested that the one-sector Solow model is stable not because it has only one capital good, but because it has particularly simple saving function. In the analysis, they proved the global stability of the multi-sector Solow model. The model is, however, unrealistic due to their neoclassical flamework in which full employment is permanetly kept. In this note, we allow for the existence of unemployment in their model. We substitute linear functions for Cobb-Douglas production functions. Also we introduce some elements of Goodwin's model (Goodwin(1965)), thus generalizing Sato's model in Sato(1985). The purpose of this paper is to analyze of the stability of a thus extended Goodwin model. We consider the relationship between the number of capital goods and the stability of the system. This paper is organized as follows. In section 2, we propose an extended Goodwin model and show the existence of a positive equilibrium. In section 3 concerning a neighbourhood of the equilibirium the property of three dimensional case is compared with that of two dimensional case. Section 4 is devoted to a couple of analyses by computer simulations. Some comments are given in the final section

    An Extended Goodwin Model with International Trade

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    Chaos is one of the most interesting topics in resent economic dynamics. Pohjola(1981) cnstructed a simple discrete-time model htat is capable of generating chaotic growth paths by modifying Goodwin's(1967) growth cycle model. His modification is the introduction of a bargaining uquation. Takamasu(1997) indicated by computer simulations that chaotic movements are observed if Skott's output expansion function(See Skott(1989)) replaced the assumtion of fixed capital-output raio. In this paper we demonstrate the emerence of chaos by allowing for international trade to the Goodwin model. Although it involves some 'bold' assumptions, it is meaningful to construct a framwork of Goodwin model with international trade, because it seemed no work has discussed this problem. The plan of this paper is as follows. We set up our model in section 2, then long-run equilibria of the model are considered in section 3. Dynamic properties of the model are analyzed in sections 4 and 5. The final section summarizes the results of the extension

    微小PNH血球陽性骨髄不全症例では多クローン性造血が保たれている

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    取得学位 : 博士(医学), 学位授与番号 : 医博甲第1599号, 学位授与年月日 : 平成15年6月30日, 学位授与大学 : 金沢大

    急性骨髄性白血病に対する造血幹細胞移植

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    初発急性骨髄白血病に対する標準治療は確立され、高い完全寛解率が得られているが、長期予後については未だに満足ができるものではない。その改善には造血幹細胞移植が必要である。しかし、同種移植では高い移植関連死亡率が問題となるため、移植適応の決定に際しては過去のデータに基づいて慎重に判断する必要がある。 The standard treatment for de novo acute myeloid leukemia (AML) has been established. Although patients with AML achieve complete remission at high rates, the long-term prognosis for such patients remains unsatisfactory. It is therefore necessary to perform hematopoietic stem cell transplantation (HSCT) to improve their prognoses, however, a high rate of transplant-related mortality continues to be a problem associated with allogeneic HSCT. We therefore need to carefully determine the indications to safely perform HSCT based on historical data.出版者照会後に全文公

    Programmed cell death 1‐expressing CD56‐negative natural killer (NK) cell expansion is a hallmark of chronic NK cell activation during dasatinib treatment

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    Dasatinib treatment markedly increases the number of large granular lymphocytes including natural killer (NK) cells in a proportion of Ph+ leukemia patients, which associates with a better prognosis. In-depth immune profiling of NK cells can predict therapeutic response in these patients. In the present study, we showed that CD56-negative (CD56neg) NK cells increased exclusively in cytomegalovirus-seropositive (CMV+) patients treated with dasatinib. The increase longitudinally paralleled with progressive differentiation of CD56dim NK cells during dasatinib therapy driven by CMV reactivation as shown by principal component analysis on 19 NK cell markers. The CD56neg NK cells showed downregulation of NK-activating receptors, upregulation of PD-1, and lower cytotoxicity and cytokine production, indicating that these cells are anergic and dysfunctional as seen in chronic infections with HIV-1 or hepatitis C virus. Moreover, cytolytic activity of CD56dim and CD56neg NK cells against leukemia cells was partially restored by nivolumab in proportion to the frequency of PD-1+ NK cells. The proportion of patients who achieved deep molecular responses at 2 years was significantly higher in dasatinib-treated patients with ≥3% CD56neg NK cells than in those with fewer CD56neg NK cells (54.5% vs 15.8%, P = .0419). These findings suggest that CD56neg NK cells may be an exhausted population induced by chronic activation through CMV reactivation during dasatinib therapy. Expansion of CD56neg NK cells is a hallmark of chronic NK cell activation in patients treated with dasatinib and may predict a better clinical outcome. Furthermore, PD-1 blockade may enhance anti-leukemia responses of such NK cells
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