Instability, investment, disasters, and demography: natural disasters and fertility in Italy (1820–1962) and Japan (1671–1965)

This article examines whether natural disasters affect fertility—a topic little explored but of policy importance given relevance to policies regarding disaster insurance, foreign aid, and the environment. The identification strategy uses historic regional data to exploit natural variation within each of two countries: one European country—Italy (1820–1962), and one Asian country—Japan (1671–1965). The choice of study settings allows consideration of Jones’ (The European miracle, Cambridge University Press, Cambridge, 1981) theory that preindustrial differences in income and population between Asia and Europe resulted from the fertility response to different environmental risk profiles. According to the results, short-run instability, particularly that arising from the natural environment, appears to be associated with a decrease in fertility—thereby suggesting that environmental shocks and economic volatility are associated with a decrease in investment in the population size of future generations. The results also show that, contrary to Jones’ (The European miracle, Cambridge University Press, Cambridge, 1981) theory, differences in fertility between Italy and Japan cannot be explained away by disaster proneness alone. Research on the effects of natural disasters may enable social scientists and environmentalists alike to better predict the potential effects of the increase in natural disasters that may result from global climate change

Vimentin and PSF Act in Concert to Regulate IbeA+ E. coli K1 Induced Activation and Nuclear Translocation of NF-κB in Human Brain Endothelial Cells

IbeA-induced NF-κB signaling through its primary receptor vimentin as well as its co-receptor PSF is required for meningitic E. coli K1 penetration and leukocyte transmigration across the blood-brain barrier (BBB), which are the hallmarks of bacterial meningitis. However, it is unknown how vimentin and PSF cooperatively contribute to IbeA-induced cytoplasmic activation and nuclear translocation of NF-κB, which are required for bacteria-mediated pathogenicities.IbeA-induced E. coli K1 invasion, polymorphonuclear leukocyte (PMN) transmigration and IKK/NF-κB activation are blocked by Caffeic acid phenethyl ester (CAPE), an inhibitor of NF-κB. IKKα/β phosphorylation is blocked by ERK inhibitors. Co-immunoprecipitation analysis shows that vimentin forms a complex with IκB, NF-κB and tubulins in the resting cells. A dissociation of this complex and a simultaneous association of PSF with NF-κB could be induced by IbeA in a time-dependent manner. The head domain of vimentin is required for the complex formation. Two cytoskeletal components, vimentin filaments and microtubules, contribute to the regulation of NF-κB. SiRNA-mediated knockdown studies demonstrate that IKKα/β phosphorylation is completely abolished in HBMECs lacking vimentin and PSF. Phosphorylation of ERK and nuclear translocation of NF-κB are entirely dependent on PSF. These findings suggest that vimentin and PSF cooperatively contribute to IbeA-induced cytoplasmic activation and nuclear translocation of NF-κB activation. PSF is essential for translocation of NF-κB and ERK to the nucleus.These findings reveal previously unappreciated facets of the IbeA-binding proteins. Cooperative contributions of vimentin and PSF to IbeA-induced cytoplasmic activation and nuclear translocation of NF-κB may represent a new paradigm in pathogen-induced signal transduction and lead to the development of novel strategies for the prevention and treatment of bacterial meningitis