Inventory-Theoretic Model of Money Demand, Multiple Goods, and Price Dynamics

Despite the theoretical prediction based on sticky-price models, it is empirically suggested that the tie between the frequencies of price adjustment across goods and the relative price responses of goods (price index of specific goods over non-durable aggregate price index) to a monetary policy change is limited.We offer an alternative view of the price dynamics of goods. We develop a multi-sector extension of an inventory-theoretic model of money demand (segmented market model). In our model, the diversity in the characteristics of goods, that is, durability, luxuriousness and cash intensity (the portion of the payment that is paid by cash in the purchase of goods), yields the dispersion of relative prices responses to a monetary policy shock, across goods. The model implies that the relative prices of durables, luxuries and less cash-intensive goods tend to decline in a monetary contraction. We test the empirical plausibility of our model, using two approaches: a measure of monetary policy shock developed by Romer and Romer (2004), and a factor-augmented VAR used in Bernanke et al. (2005). In both econometric methodologies, we find that the data are consistent with our model, in terms of durability and luxuriousness.Baumol-Tobin model, Durable; Luxury, Credit goods, Monetary policy

"Aggregate Returns to Social Capital: Estimates Based on the Augmented Augmented-Solow Model"

This paper estimates the aggregate output elasticity of social capital that characterizes the aggregate returns to social capital. With this aim, we apply Nonneman and Vanhoudt's (1996) augmented version of the augmented Solow model of Mankiw et al. (1992) by including social capital as an additional production input. The estimated output elasticity of social capital is approximately 0.1. While our results largely indicate that social capital positively affects economic growth, the magnitude of the effects is smaller than that of physical and human capital as well as labor inputs. Moreover, the median value of the implied aggregate return of social capital is approximately 9.77% at the global level and, in OECD countries, it is likely to be considerably smaller than the individual returns, suggesting the fallacy of composition. As a by product, the depreciation rate of social capital is estimated to be approximately 10% per annum which is significantly higher than that of physical capital.

末梢神経自家移植によるラット脳神経の再生

金沢大学医学部附属病院末梢神経の自家移植を末梢神経および中枢神経に行ない,graft内の神経線維の再生過程を形熊学的に調ベた。雌Wistar ratを用い,座骨神経を顔面神経(末梢神経)に,腓骨神経を脊髄(中枢神経)に端々吻合して移植し,1〜24週後に電顕にて観察した。通常の超薄切片のほか,陽イオン染色と凍結割断法を施行し軸索およびこれを包むSchwann細胞とミエリン鞘を調べた。超薄切片では,全ての時期でWaller変性が認められた。4週以内のものでは,graft内にリンパ球やマクロファージの浸潤が強く認められた。末梢神経への移植では,10匹全例で4週以後次第にSchwann細胞と無髄線維が増生し,薄いミエリン鞘と短にinternodeが観察された。中枢神経への移植では,9匹中4匹でgraftが生着したが,ミエリン鞘と内髄線維が認められたのは2匹のみであった。そのミエリンは末梢型で,周囲にコラーゲンの増生を伴っていた。陽イオン染色では(末梢神経へのgraftで施行),電子密度の濃い部分が無髄線維の軸索の一部や有髄線維のミエリン鞘の間隙(おそらく後のRanvier絞輪)に,4週以後に観察された。凍結割断レプリカでは(末梢神経へのgraftで施行),有髄線維の軸索の一部に粒子が200/μm^2程度の密度で集積し,その約半分は直径10nm以上の粒子でナトリウムチャンネルと考えられた。無髄線維に接する細胞膜表面のpinocytosisの密度を計算し,血管の内皮細胞とも比較して同定した結果,ミエリン形成の有無を問わず,4週以後のgraft内の軸索に接するものはSchwann細胞が主体をなしていた。結論:末梢神経の自家移植片は,末梢神経のみならず中枢神経においても生着し,軸索とミエリン鞘が再生する。ミエリン形成の初期の段階で,ナトリウムチャンネルのinternode間への集積がおこる。再生した軸索周囲には,Schwann細胞がミエリン鞘の形成の有無に拘らず,間質を介さずに接している。Peripheral nerve autografts were transplanted either to a peripheral nerve or to the spinal cord to study axonal regeneration and remyelination in rats. The sciatic nerve graft was transplanted to the cut ends of the facial nerve in ten rats and the peroneal nerve graft was to the spinal cord in nine rats. The nerve grafts were examined by electron microscopy after one to 24 weeks. Cation staining and freeze-fracture methods were performed as well to know the further information of sodium channels in axon membrane. In thin sections, a lot of lymphocytes and macrophages were seen with Wallerian degeneration in grafts within four weeks. After four weeks, Schwann cells and unmyelinated fibers were increased in number and thin myelin sheaths and short internodes were observed in sciatic grafts. In peroneal grafts, myelinated and unmyelinated fibers were seen only in two rats although four out of nine showed tight adhesion to the spinal cord in gross inspection. These myelin sheaths were of peripheral type surrounded by collagen fibers. In cation staining, performed only in sciatic nerves, electron-dense patches were seen on the unmyelinated axons and at the node-like areas between short internodes after four weeks. In freeze-fracture replicas, also performed in sciatic nerves, Axolemmal E-face particles were distributed in a concentration of 200/mum^2, half of which were large (>10nm) and were supposed to be sodium channels. In conclusion, an electron microscopic examination of the peripheral nerve graft both into the peripheral and central nervous system showed a number of regenerated unmyelinated and myelinated fibers of peripheral type. Sodium channels were concentrated at the area between the internodes at the early stage of remyelination. Schwann cells directly surrounded the regenerated axons with or without myelin sheaths.研究課題/領域番号:02807131, 研究期間(年度):1990 – 1992出典：研究課題「末梢神経自家移植によるラット脳神経の再生」課題番号02807131（KAKEN：科学研究費助成事業データベース（国立情報学研究所）） （https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-02807131/028071311992kenkyu_seika_hokoku_gaiyo/）を加工して作

左肺動脈欠損症における肺血流の評価： RIアンギオグラフイの有用性

金沢大学大学院医学系研究

Neuro-cardiac interaction in malignant ventricular arrhythmia and sudden cardiac death

Sudden cardiac death as a result of lethal ventricular arrhythmias is a major cause of death in cardiac diseases such as heart failure and prior myocardial infarct. Activity of the autonomic nervous system is often abnormal where sympathetic activity is upregulated and vagal activity reduced in these conditions. The abnormal autonomic state has been shown to be a strong prognostic marker of increased mortality and propensity to lethal arrhythmias, for which there is no effective prevention. Research effort over the years has established good evidence for a causal link between autonomic disturbance and ventricular arrhythmias. However, the detailed electrophysiological mechanisms by which ventricular fibrillation occurs are still not clear and molecular processes which are modulated by autonomic nerve influences that either predispose the heart to or protect it from these arrhythmias are not fully understood. This review presents data from studies investigating the link between activity of the autonomic nervous system and ventricular arrhythmias, from seminal findings in classical studies to ongoing investigations, in the quest for a better understanding of the arrhythmogenic mechanisms underlying neurocardiac interactions with a view to the development of effective preventative and therapeutic strategies which are very much needed