We exploit between-cohort variation in the probability of military service to investigate how World War II and the G.I. Bill altered the structure of marriage, and find that they had important spillover effects beyond their direct effect on men's educational attainment. Our analyses further motivate instruments to help identify the effect of men's education on spousal "quality." We find that the additional education received by returning veterans allowed them to "sort" into wives with comparably higher levels of education. This suggests an important mechanism by which socioeconomic status may be passed on to the next generation.

Prior research suggests that families prefer schools with higher test scores, shorter distances from home, and certain student demographics. We build on this using data from New Orleans, a context well suited to identification of parent preferences because of its deferred acceptance algorithm and extensive, standardized, and broadly accessible school information. This allows us to study revealed preferences for a richer set of characteristics. We find that families prefer schools with higher school value-added, more extracurricular activities, and after-school childcare. We also find heterogeneity by family income that is more consistent with income constraints than preference heterogeneity. Finally, we show how methodology and data shape the results.

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We investigated effects of paramyotonia congenita mutations F1473S and F1705I on gating of skeletal muscle Na + channels. We used on-cell recordings from Xenopus oocytes to compare fast inactivation and deactivation in wild-type and mutant channels. Then, we used gating current recordings to determine how these actions of PC mutants might be reflected in their effects on charge movement and its immobilization. F1473S, but not F1705I, accelerated deactivation from the inactivated state and enhanced the remobilization of gating charge. F1473S and F1705I decreased the completion of closed-state fast inactivation, and decreased charge movement over the voltage range at which channels did not activate. An unexpected result was that F1705I increased the extent of charge immobilization in response to strong depolarization. Our results suggest that the DIV S4-S5 linker mutation F1473S promotes the hyperpolarized position of DIVS4 to accelerate recovery. Inhibition of charge movement by F1473S and F1705I in the absence of channel opening is discussed with respect to their effects on closed-state fast inactivation.