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11. The Geography of Job Creation and Job Destruction

Author

Kuhn, Moritz, Manovskii, Iourii, and Qiu, Xincheng

Subjects
unemployment, search and matching, ddc:330, local labor markets, economics, J63, E24, J64, vacancies, E32, R13
Abstract

Spatial differences in unemployment rates are large and persistent. Our objective is to develop a quantitative theory of these differences. Considering the local unemployment rate as an (equilibrium) outcome between workers and firms, we document facts on both sides of the labor market. First, we confirm recent findings that differences in separation rates (unemployment inflows) are more important than differences in job-finding rates (unemployment outflows) in accounting for local unemployment differences. Second, we present novel facts on the differences in job-creation and job-filling rates. We document that local labor markets with lower unemployment rates are tighter, have lower vacancy filling rates, and higher average vacancy duration. These facts constitute empirical regularities in the United States, Germany, and the United Kingdom. On the theory side, we demonstrate that a Diamond-Mortensen-Pissarides model with endogenous separations quantitatively accounts for all the documented facts on the geography of job creation and job destruction. Furthermore, we demonstrate that this model not only matches labor market differences across space but also over the business cycle.

Published
2022
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20. Irisin Prevents Cell Death in High Glucose via NLRP3 Inhibition.

Author

Wei H, Zhou J, Qiu X, Niu H, Zhang Z, Liu Y, Bai P, Xin C, Wen W, Lu X, Cao G, and Hu T

Subjects
Animals, Rats, Endothelial Cells drug effects, Endothelial Cells metabolism, Apoptosis drug effects, Cells, Cultured, Humans, Cell Death drug effects, NLR Family, Pyrin Domain-Containing 3 Protein metabolism, Pyroptosis drug effects, Glucose metabolism, Fibronectins metabolism, Fibronectins pharmacology
Abstract

Background: Impaired cardiac microvascular function has been implied in the pathophysiology of diabetic cardiovascular disease. However, the specific mechanism remains to be determined. Pyroptosis is a type of cell death that differs from apoptosis and autophagy. It is caused by the formation of plasma membrane pores through amino-terminal fragments of Gasdermin D (GSDMD), leading to the secretion of IL-1β and IL-18. Recent studies have shown that irisin, a myokine cleaved by the extracellular domain of FNDC5, plays a protective role in cardiovascular diseases. Here, we investigated the potential role of pyroptosis on the cardiac microvascular endothelial cells (CMECs) injury induced by high glucose (HG) and further determined the protective effect of irisin on pyroptosis., Methods: CMECs were cultured with normal glucose (control group, 5.5 mM) and high glucose (25 mM) medium for 12, 24, and 48 h respectively. The pyroptosis of CMECs was measured by immunofluorescence staining, ELISA, and Western blot assays. Moreover, the apoptosis level was determined by flow cytometry and TUNEL staining., Results: Our results showed that HG promoted apoptosis and pyroptosis. However, irisin reversed the increased apoptosis and pyroptosis. To investigate the underlying mechanism, we overexpressed the NLRP3 protein. We found the protective effect of irisin on apoptosis and pyroptosis was abolished by NLRP3 over-expression., Conclusions: Our data suggest that irisin protects CMECs against apoptosis and pyroptosis, at least in part, by inhibiting NLRP3 inflammasome.

Published
2024

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