Although many studies have attempted to examine the consequences of Mexico-U.S. migration for Mexican immigrants' health, few have had adequate data to generate the appropriate comparisons. In this article, we use data from two waves of the Mexican Family Life Survey (MxFLS) to compare the health of current migrants from Mexico with those of earlier migrants and nonmigrants. Because the longitudinal data permit us to examine short-term changes in health status subsequent to the baseline survey for current migrants and for Mexican residents, as well as to control for the potential health selectivity of migrants, the results provide a clearer picture of the consequences of immigration for Mexican migrant health than have previous studies. Our findings demonstrate that current migrants are more likely to experience recent changes in health status-both improvements and declines-than either earlier migrants or nonmigrants. The net effect, however, is a decline in health for current migrants: compared with never migrants, the health of current migrants is much more likely to have declined in the year or two since migration and not significantly more likely to have improved. Thus, it appears that the migration process itself and/or the experiences of the immediate post-migration period detrimentally affect Mexican immigrants' health. © 2014 Population Association of America.

Glaucoma, a blinding neurodegenerative disease, whose risk factors include elevated intraocular pressure (IOP), age, and genetics, is characterized by accelerated and progressive retinal ganglion cell (RGC) death. Despite decades of research, the mechanism of RGC death in glaucoma is still unknown. Here, we demonstrate that the genetic effect of the SIX6 risk variant (rs33912345, His141Asn) is enhanced by another major POAG risk gene, p16INK4a (cyclin-dependent kinase inhibitor 2A, isoform INK4a). We further show that the upregulation of homozygous SIX6 risk alleles (CC) leads to an increase in p16INK4a expression, with subsequent cellular senescence, as evidenced in a mouse model of elevated IOP and in human POAG eyes. Our data indicate that SIX6 and/or IOP promotes POAG by directly increasing p16INK4a expression, leading to RGC senescence in adult human retinas. Our study provides important insights linking genetic susceptibility to the underlying mechanism of RGC death and provides a unified theory of glaucoma pathogenesis. Zhang et al. report p16INK4a as a downstream integrator of diverse signals, such as inherited genetic risk, age, and intraocular pressure, in the pathogenesis of glaucoma. They demonstrate that upregulation of SIX6 upon stress directly increases p16INK4a, leading to retinal ganglion cell senescence and death.