A Historical Evaluation of Financial Accelerator Effects in Japan's Economy

In this paper, we carry out a historical evaluation of the financial accelerator effects, which were mainly generated by the changes in asset prices, operating on Japan's economy since the 1980s. For this purpose, we estimate a Japanese financial accelerator model, which is a modified version of Bernanke, Gertler and Gilchrist [1999]'s model, and identify the historical exogenous shocks affecting the evolution of firms' net worth. As a result, we confirm that the estimated parameter on the corporate balance sheet channel is statistically significant. We also find that the identified net worth shocks, which change the amount of firms' debt holdings relative to their total values, produced a large and persistent impact on Japan's output and prices. This result strongly suggests that the negative financial accelerator effects were indispensable to explain the mechanism behind Japan's long stagnation during the 1990s and early 2000s, as well as indicating that the deflation of general prices since the late 1990s has been at least partly attributed to the same cause.

A Historical Evaluation of Financial Accelerator Effects in Japan's Economy

In this paper, we carry out a historical evaluation of the financial accelerator effects, which were mainly generated by the changes in asset prices, operating on Japan's economy since the 1980s. For this purpose, we estimate a Japanese financial accelerator model, which is a modified version of Bernanke, Gertler and Gilchrist [1999]'s model, and identify the historical exogenous shocks affecting the evolution of firms' net worth. As a result, we confirm that the estimated parameter on the corporate balance sheet channel is statistically significant. We also find that the identified net worth shocks, which change the amount of firms' debt holdings relative to their total values, produced a large and persistent impact on Japan's output and prices. This result strongly suggests that the negative financial accelerator effects were indispensable to explain the mechanism behind Japan's long stagnation during the 1990s and early 2000s, as well as indicating that the deflation of general prices since the late 1990s has been at least partly attributed to the same cause

Promotion of IL-4- and IL-5-dependent differentiation of anti-μ-primed B cells by ascorbic acid 2-glucoside

The stable ascorbic acid derivative 2-O-alpha-D-glucopyranosyl-L-ascorbic acid (AA-2G) was used to investigate the role of ascorbic acid (AA) in B cell differentiation in vitro. AA-2G is stable in a solution unlike AA but is hydrolyzed by cellular alpha-glucosidase to release AA. Mouse spleen B cells were primed for 2 days with an anti-mu antibody in the presence of interleukin (IL)-4 and IL-5 and then washed and recultured with AA-2G in the presence of IL-4 and IL-5. AA-2G, but not AA, dose-dependently increased IgM production, the greatest enhancement being 150% at concentrations of more than 0.5 mM. In the absence of IL-4 and IL-5, primed B cells produced a negligible amount of IgM, and AA-2G had no effect. AA-2G-induced IgM production in the presence of IL-4 and IL-5 was inhibited by the alpha-glucosidase inhibitor castanospermine. Intracellular AA content, depleted during the priming period, increased by adding AA-2G at the start of reculture. Treatment of B cells with AA-2G resulted in an increase in the number of IgM-secreting cells, CD138-positive cells and CD45R/B220-negative cells. The number of viable cells in untreated cultures decreased gradually, but the decrease was significantly attenuated by AA-2G, resulting in about 70% more viable cells in AA-2G-treated cultures. AA-2G caused a slight but reproducible enhancement of DNA synthesis and a slight decrease in the number of cells with a sub-G1 DNA content. These results demonstrated that AA released from AA-2G enhanced cytokine-dependent IgM production in anti-mu-primed B cells and suggest that its effect is caused through promoting the differentiation of B cells to plasma cells and attenuating the gradual decrease in the number of viable cells

Microscopic description of nuclei in the middle of the pf-shell by a shell model calculation with G-matrix interaction

Energy levels and electromagnetic properties of with $N=28\sim 30$ nuclides are studied in terms of a large-scale shell model calculation, which contains no newly adjusted parameters. The Kuo-Brown $G$-matrix interaction is shown to reproduce energy levels of 205 low-lying states of these nuclei. We evaluate effective charges by incorporating the core-polarization effects caused by the coupling to GQR's. We then compute E2 moments and transition probabilities. The M1 moments and transition rates are calculated by quoting the effective $g$-factors of Towner, which are obtained by taking into account the meson-exchange and the core-polarization mechanisms. By this microscopic calculation most of the E2 properties and the magnetic moments are reproduced. Although there are agreements and disagreements in the M1 transition rates, the general tendency is reproduced. The $(e,e')$ and $(p,p')$ excitation from the ground state to some low-lying $2^+$ states is also discussed.Comment: 63 pages (LaTeX, to be published in Nucl. Phys. A

DOCK2 is involved in the host genetics and biology of severe COVID-19

「コロナ制圧タスクフォース」COVID-19疾患感受性遺伝子DOCK2の重症化機序を解明 --アジア最大のバイオレポジトリーでCOVID-19の治療標的を発見--. 京都大学プレスリリース. 2022-08-10.Identifying the host genetic factors underlying severe COVID-19 is an emerging challenge. Here we conducted a genome-wide association study (GWAS) involving 2, 393 cases of COVID-19 in a cohort of Japanese individuals collected during the initial waves of the pandemic, with 3, 289 unaffected controls. We identified a variant on chromosome 5 at 5q35 (rs60200309-A), close to the dedicator of cytokinesis 2 gene (DOCK2), which was associated with severe COVID-19 in patients less than 65 years of age. This risk allele was prevalent in East Asian individuals but rare in Europeans, highlighting the value of genome-wide association studies in non-European populations. RNA-sequencing analysis of 473 bulk peripheral blood samples identified decreased expression of DOCK2 associated with the risk allele in these younger patients. DOCK2 expression was suppressed in patients with severe cases of COVID-19. Single-cell RNA-sequencing analysis (n = 61 individuals) identified cell-type-specific downregulation of DOCK2 and a COVID-19-specific decreasing effect of the risk allele on DOCK2 expression in non-classical monocytes. Immunohistochemistry of lung specimens from patients with severe COVID-19 pneumonia showed suppressed DOCK2 expression. Moreover, inhibition of DOCK2 function with CPYPP increased the severity of pneumonia in a Syrian hamster model of SARS-CoV-2 infection, characterized by weight loss, lung oedema, enhanced viral loads, impaired macrophage recruitment and dysregulated type I interferon responses. We conclude that DOCK2 has an important role in the host immune response to SARS-CoV-2 infection and the development of severe COVID-19, and could be further explored as a potential biomarker and/or therapeutic target