Abstract
This study presents an empirical analysis to detect Minsky's financial fragility and its determinants in non-financial sectors in Japan, with particular attention on the differences between ...sectors and size. While post-Keynesian developed theoretical analyses of financial fragility for economic growth models, its empirical application is limited. Based on the financial fragility indices derived from a cash-flow accounting framework and Minsky's margins of safety, I detect the overall configuration and evolution of financial fragility (hedge, speculative and Ponzi) in Japan. Then, I detect the factors that determine the probability of being Ponzi finance using a panel logistic regression. The results show that although speculative finance dominates many sector and size categories, the evolution of hedge and Ponzi finance is diversified and the determinants of financial fragility differ by category in Japan.
•This study presents a two-sector Kalecki–Kaldor growth model.•It analyses the interactions of income distribution, technical change, and demand.•Short-run steady state is Kaleckian: wage-, ...profit-led, and hybrid demand regimes.•Long-run economic growth mechanism is Kaldorian, featuring technical change.•Wage and productivity growth rates between the two sectors differ in the long run.
This paper presents a two-sector Kalecki–Kaldor model of income distribution, technical change, and economic growth. The model is Kaleckian in the sense that it incorporates mark-up pricing, investment independent of saving, and excess capacity. It is also Kaldorian, in that labour productivity growth is led by Kaldor’s technical progress function. In other words, productivity growth is endogenously realised through the technology embodied in new capital stock, which differentiates our model from previous two-sector models. Our extension drastically changes the standard Kaleckian implications. We find that although the economic activity levels in the short run are led by the demand and income distribution parameters, economic growth in the long run is realised by supply-side (i.e. technical change and the associated productivity and wage growth) parameters. The important implication of our findings is that a two-sector economy faces a trade-off between a high economic growth rate and the local stability of the steady state.
This study examines the sources of labor productivity growth dynamics in Japan (1970–2010) and investigates the extent to which Japanese economic performance has been affected by Baumol's growth ...disease (BGD). We find that BGD silently undermines Japanese economic growth. However, the magnitude is miniscule, and consequently the aggregate labor productivity growth rate has not been decreasing monotonically. We also explore how BGD is arising and why it is small in the Japanese economy. BGD is weak because (1) the positive Baumol growth effect is also working in certain services sectors and (2) BGD is not a durable phenomenon: even if a sector begins to suffer from BGD, it is likely to recover quickly.
Dyslipidemia is a common nutritional and metabolic disorder in patients with chronic kidney disease. Accumulating evidence supports the hypothesis that prolonged metabolic imbalance of lipids leads ...to ectopic fat distribution in the peripheral organs (lipotoxicity), including the kidney, heart, and skeletal muscle, which accelerates peripheral inflammation and afflictions. Thus, lipotoxicity may partly explain progression of renal dysfunction and even extrarenal complications, including renal anemia, heart failure, and sarcopenia. Additionally, endoplasmic reticulum stress activated by the unfolded protein response pathway plays a pivotal role in lipotoxicity by modulating the expression of key enzymes in lipid synthesis and oxidation. Here, we review the molecular mechanisms underlying lipid deposition and resultant tissue damage in the kidney, heart, and skeletal muscle, with the goal of illuminating the nutritional aspects of these pathologies.
This study builds a growth regime model to analyse demand, income distribution, and employment rate. It also examines the causes and effects of the endogenous dynamics of the non-accelerating ...inflation rate of unemployment (NAIRU) from Régulationist and post-Keynesian perspectives. Specifically, this study (1) explores how demand and distribution regimes are established; (2) identifies the stability conditions for the multi-feedback mechanism among demand, distribution, and employment under different regimes; and (3) reveals how different endogenous degrees of NAIRU affect the dynamic behaviour of macroeconomic variables within a growth regime. We identify four types of growth regimes: two types of demand regimes (i.e. wage-led and profit-led) and two types of distribution regimes (i.e. goods market-led and labour market-led). We also demonstrate that the multi-feedback mechanism among demand, distribution, and employment under different growth regimes needs particular institutional coordination to realise stability. Moreover, we show that a certain endogenous degree of NAIRU may induce perpetual cycles in some growth regimes, whereas the stability of other growth regimes is independent of NAIRU’s endogeneity. Thus, our growth regime approach confirms the primary conclusions of the Régulation theory: an economy has business cycles and growth patterns specific to its institutional structures.
Acute kidney injury (AKI) is characterized by mitochondrial dysfunction and activation of the innate immune system. The cyclic GMP-AMP synthase (cGAS) stimulator of interferon genes (STING) pathway ...detects cytosolic DNA and induces innate immunity. Here, we investigate the role of mitochondrial damage and subsequent activation of the cGAS-STING pathway using a genetically engineered animal model of cisplatin-induced AKI and cultured tubular cells. Cisplatin induced mtDNA leakage into the cytosol—probably through BCL-2-like protein 4 (BAX) pores in the mitochondrial outer membrane—in tubules, with subsequent activation of the cGAS-STING pathway, thereby triggering inflammation and AKI progression, which is improved in STING-deficient mice. STING knockdown in cultured tubular cells ameliorates inflammatory responses induced by cisplatin. mtDNA depletion and repletion studies support tubular inflammatory responses via the cGAS-STING signal activation by cytosolic mtDNA. Therefore, we conclude that mitochondrial dysfunction and subsequent activation of the mtDNA-cGAS-STING pathway is a critical regulator of kidney injury.
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•cGAS-STING activation and mitochondrial damage in tubules mediate acute kidney injury•cGAS-STING activation induces tubular inflammation and progression of AKI•Mitochondrial DNA leakage into the cytosol increased in AKI-induced tubular damage•Cytosolic mitochondrial DNA activates cGAS-STING signaling in tubular inflammation
Acute kidney injury (AKI) is associated with tubular inflammation and mitochondrial dysfunction. Maekawa et al. reveal that tubular mitochondrial damage leads to mtDNA leakage into the cytosol, probably via BAX pores on the mitochondria, activating cGAS-STING signaling and subsequent tubular inflammation in cisplatin-induced AKI. Suppression of the STING ameliorates tubular inflammation and progression of AKI.
The complement system is part of the innate immune system. The crucial step in activating the complement system is the generation and regulation of C3 convertase complexes, which are needed to ...generate opsonins that promote phagocytosis, to generate C3a that regulates inflammation, and to initiate the lytic terminal pathway through the generation and activity of C5 convertases. A growing body of evidence has highlighted the interplay between the complement system, coagulation system, platelets, neutrophils, and endothelial cells. The kidneys are highly susceptible to complement-mediated injury in several genetic, infectious, and autoimmune diseases. Atypical hemolytic uremic syndrome (aHUS) and lupus nephritis (LN) are both characterized by thrombosis in the glomerular capillaries of the kidneys. In aHUS, congenital or acquired defects in complement regulators may trigger platelet aggregation and activation, resulting in the formation of platelet-rich thrombi in the kidneys. Because glomerular vasculopathy is usually noted with immunoglobulin and complement accumulation in LN, complement-mediated activation of tissue factors could partly explain the autoimmune mechanism of thrombosis. Thus, kidney glomerular capillary thrombosis is mediated by complement dysregulation and may also be associated with complement overactivation. Further investigation is required to clarify the interaction between these vascular components and develop specific therapeutic approaches.
Background: The cost-effectiveness of sodium-glucose cotransporter 2 (SGLT2) inhibitors for chronic kidney disease (CKD) has not been evaluated in Japan, so we analyzed the cost-effectiveness of ...dapagliflozin, an SGLT2 inhibitor, for CKD stages 3a and 3b.Methods and Results: We used the Markov model for CKD to assess the costs and benefits associated with and without dapagliflozin from a health system perspective. We estimated the incremental cost-effectiveness ratio (ICER), expressed as per quality-adjusted life-years (QALYs). An ICER <5 million Japanese yen (JPY)/QALY was judged to be cost-effective. The effect of dapagliflozin on renal and cardiovascular events was based on published clinical trials. In patients with CKD stage 3a, the ICER of dapagliflozin over standard treatment was 4.03 million JPY/QALY gained. With a cost-effectiveness threshold of 5 million JPY/QALY gained, the cost-effectiveness probability of dapagliflozin over standard treatment was 52.6%. In patients with CKD stage 3b, the ICER of dapagliflozin over standard treatment was 0.12 million JPY/QALY gained. The cost-effectiveness probability of dapagliflozin over standard treatment was 75.2%.Conclusions: The results seemed to show acceptable cost-effectiveness when dapagliflozin was used for CKD stage 3b. On the other hand, cost-effectiveness of dapagliflozin for CKD stage 3a was ambiguous, and further validation is needed.
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