Revisiting Productivity Differences and Firm Turnover: Evidence from product-based TFP measures in the Japanese manufacturing industries

Following Foster, Haltiwanger, and Syverson (2008), we construct physical output based TFP (TFPQ) measures using data from the Census of Manufactures. We find that productivity differences among business establishments using TFPQ are larger than those using the traditional revenue-based TFP measures (TFPR). The negative correlation between physical output and output prices implies that establishments are facing a downward demand curve and the traditional measures of TFP are affected by idiosyncratic demand shocks. Probit estimations regarding exit behavior show that the combined effects of physical productivity improvement and higher prices through the increase in demand result in a lower probability of exit. Breaking down aggregate productivity growth using TFPQ, we find that the contribution of the net entry effects the largest factor to productivity improvement, in contrast to previous Japanese studies. Our results provide a more positive foundation for "creative destruction" policies than previous studies suggest.

Product Dynamics and Aggregate Shocks: Evidence from Japanese Product and Firm Level Data

Conceptually linking product adding and dropping to business cycles goes back to at least Shumpeter. We examine the effects of shocks to aggregate productivity, foreign demand, government expenditures, and demand for foreign liquidity on the dynamics of products of heterogeneous firms. Our structural empirical specifications connecting macroeconomic shocks to product dynamics are based on a neoclassical dynamic general equilibrium model (Dekle, Kiyotaki, and Jeong, 2014). We first construct unique firm level data on products and exports from the Japanese Census of Manufactures. The data are more disaggregated than comparable U.S. data and available at the annual frequency (while U.S. product level data are only available at five year intervals), which makes our data more suitable for examining the interaction between the business cycle and firm-product dynamics. We find that positive macroeconomic shocks in total factor productivity, government demand, and real exchange rates strongly increase the number of products

Productivity and Financing of Startups (Japanese)

Economists have pointed out that the Japanese slow productivity growth in the 90s was caused by the lack of creative destruction. To investigate the topic, we focus on the behavior of newly founded firms. First, we study how long they keep high productivity by examining the effect of firm age on productivity. The results indicate that firms reach their highest productivity approximately eight years after they are established. Second, we investigate whether the establishment of firms is constrained by financing. A multinomial logit model is then used for analyses of each type of financial institution to see if loans are approved for firms with high productivity. The estimation results indicate that while major commercial banks do provide loans to high-productivity firms, government-affiliated financial institutions conversely provide loans to low-productivity firms. The findings for the 90s also indicate that the tendency of major commercial banks to provide loans to high-productivity firms intensified from the 90s.

Induction of cyclooxygenase-2 in human synovial cells by β2-microglobulin

Induction of cyclooxygenase-2 in human synovial cells by β2-microglobulin.BackgroundProstaglandins (PGs) are important mediators of inflammation in arthritis. We evaluated the role of the cyclooxygenase-2 (COX-2) enzyme, which regulates PG biosynthesis, in osteoarthropathy associated with hemodialysis-associated amyloidosis (HAA) by characterizing COX-2 expression in β2-microglobulin–treated human synovial cells.MethodsWe examined the effects of β2-microglobulin (β2m), a major constituent protein of amyloid fibrils in HAA, on the COX-2 protein and mRNA expression in human synovial cells using Western blot and reverse transcriptase-polymerase chain reaction.Resultsβ2m selectively increased the biosynthesis of COX-2 protein and induction of COX-2 mRNA in a dose-dependent manner. Immunoabsorption of β2m–containing media by anti-β2m–specific antibody abrogated β2m–mediated COX-2 expression on synovial cells. On the other hand, dexamethasone markedly suppressed the induction of COX-2 protein and mRNA in β2m–stimulated synovial cells.ConclusionsOur results suggest that induction of COX-2 expression by β2m may be an important component of the inflammatory process in hemodialysis-associated osteoarthropathy

A fatal case of acute exacerbation of interstitial lung disease in a patient with rheumatoid arthritis during treatment with tocilizumab.

A 68-year-old man, who was a patient with established rheumatoid arthritis (RA) with RA-associated interstitial lung disease (RA-ILD) and pulmonary emphysema, began taking tocilizumab. Subsequently, he developed dyspnea parallel to improvement of RA. At 10 months after the administration of tocilizumab, he was urgently admitted because of exacerbation of ILD. He died despite receiving steroid pulse therapy and antibiotic therapy on a respirator. This is the first case report to describe the exacerbation of ILD during treatment with tocilizumab in the postmarketing surveillance (PMS) period

Tyrphostin AG 1478 Accelerates Hydrogen Peroxide-Induced Apoptosis in A431 Cells

Oxidative stress is a potent inducer of apoptosis and activates protein tyrosine kinases and cytokine receptors, such as the epidermal growth factor receptor (EGFR). Previous studies suggest that cytokine receptors are potential effectors for anti-apoptotic signals, but it has not previously been determined whether cytokine receptors regulate down-stream protein kinases. To investigate the role of EGFR on oxidative stress-induced apoptosis and its downstream protein kinases, we blocked EGFR activation with Tyrphostin AG1478, a highly selective EGFR inhibitor. We determined that Tyrphostin AG1478 accelerated hydrogen peroxide-induced apoptosis in A431 cells, with activation of caspases 3 and 9, and decreased mitochondrial membrane potential. Hydrogen peroxide induced-activation of EGFR, Akt/PKB, MAPK, and Bad (both Ser-112 and Ser-136 residues) were inhibited by Tyrphostin AG1478. These results suggest that early upstream signaling events, such as EGFR activation, exert anti-apoptotic effects by regulating MAPK, Akt/PKB, and phosphorylation of Bad