Everybody Hurts Sometimes: How Personal and Collective Insecurities Shape Policy Preferences

Understanding when individuals support government action is central to government responsiveness and democratic policy making. While previous research on political behavior has explored the influence of collective economic conditions, self-interested explanations have heavily swayed work on policy preferences. We bridge these two previously distinct literatures to articulate a theory of public policy preferences that highlights when both common and pocketbook factors influence preferences for social insurance. Using a cross-national sample of developed democracies from 1996 and 2006, we conclude that when personal economic conditions are dire, the pull of self-interest trumps both collective and policy concerns

Replication Data for: Everybody Hurts Sometimes: How Personal and Collective Insecurities Shape Policy Preferences

Replication Data for: Everybody Hurts Sometimes: How Personal and Collective Insecurities Shape Policy Preferences Abstract: Understanding when individuals support government action is central to government responsiveness and democratic policymaking. While previous research on political behavior has explored the influence of collective economic conditions, self-interested explanations have heavily swayed work on policy preferences. We bridge these two previously distinct literatures to articulate a theory of public policy preferences that highlights when both common and pocketbook factors influence preferences for social insurance. Using a cross-national sample of developed democracies from 1996 and 2006, we conclude that when personal economic conditions are dire, the pull of self interest trumps both collective and policy concerns

Everybody Hurts Sometimes: How Personal and Collective Insecurities Shape Policy Preferences

Understanding when individuals support government action is central to government responsiveness and democratic policy making. While previous research on political behavior has explored the influence of collective economic conditions, self-interested explanations have heavily swayed work on policy preferences. We bridge these two previously distinct literatures to articulate a theory of public policy preferences that highlights when both common and pocketbook factors influence preferences for social insurance. Using a cross-national sample of developed democracies from 1996 and 2006, we conclude that when personal economic conditions are dire, the pull of self-interest trumps both collective and policy concerns

Loss of RANKL in osteocytes dramatically increases cancellous bone mass in the osteogenesis imperfecta mouse (oim)

Osteogenesis imperfecta (OI) is characterized by osteopenia and bone fragility, and OI patients during growth often exhibit high bone turnover with the net result of low bone mass. Recent evidence shows that osteocytes significantly affect bone remodeling under physiological and pathological conditions through production of osteoclastogenic cytokines. The receptor activator of nuclear factor kappa-B ligand (RANKL) produced by osteocytes for example, is a critical mediator of bone loss caused by ovariectomy, low-calcium diet, unloading and glucocorticoid treatment. Because OI bone has increased density of osteocytes and these cells are embedded in matrix with abnormal type I collagen, we hypothesized that osteocyte-derived RANKL contributes to the OI bone phenotype. In this study, the conditional loss of RANKL in osteocytes in oim/oim mice (oim-RANKL-cKO) resulted in dramatically increased cancellous bone mass in both the femur and lumbar spine compared to oim/oim mice. Bone cortical thickness increased significantly only in spine but ultimate bone strength in the long bone and spine was minimally improved in oim-RANKL-cKO mice compared to oim/oim mice. Furthermore, unlike previous findings, we report that oim/oim mice do not exhibit high bone turnover suggesting that their low bone mass is likely due to defective bone formation and not increased bone resorption. The loss of osteocyte-derived RANKL further diminished parameters of formation in oim-RANKL-cKO. Our results indicate that osteocytes contribute significantly to the low bone mass observed in OI and the effect of loss of RANKL from these cells is similar to its systemic inhibition. Keywords: Osteocyte, RANKL, Osteogenesis imperfecta, Bone fragilit

Expression characterization and functional implication of the collagen-modifying Leprecan proteins in mouse gonadal tissue and mature sperm

The Leprecan protein family which includes the prolyl 3-hydroxylase enzymes (P3H1, P3H2, and P3H3), the closely related cartilage-associated protein (CRTAP), and SC65 (Synaptonemal complex 65, aka P3H4, LEPREL4), is involved in the post-translational modification of fibrillar collagens. Mutations in CRTAP, P3H1 and P3H2 cause human genetic diseases. We recently showed that SC65 forms a stable complex in the endoplasmic reticulum with P3H3 and lysyl hydroxylase 1 and that loss of this complex leads to defective collagen lysyl hydroxylation and causes low bone mass and skin fragility. Interestingly, SC65 was initially described as a synaptonemal complex-associated protein, suggesting a potential additional role in germline cells. In the present study, we describe the expression of SC65, CRTAP and other Leprecan proteins in postnatal mouse reproductive organs. We detect SC65 expression in peritubular cells of testis up to 4 weeks of age but not in cells within seminiferous tubules, while its expression is maintained in ovarian follicles until adulthood. Similar to bone and skin, SC65 and P3H3 are also tightly co-expressed in testis and ovary. Moreover, we show that CRTAP, a protein normally involved in collagen prolyl 3-hydroxylation, is highly expressed in follicles and stroma of the ovary and in testes interstitial cells at 4 weeks of age, germline cells and mature sperm. Importantly, CrtapKO mice have a mild but significant increase in morphologically abnormal mature sperm (17% increase compared to WT). These data suggest a role for the Leprecans in the post-translational modification of collagens expressed in the stroma of the reproductive organs. While we could not confirm that SC65 is part of the synaptonemal complex, the expression of CRTAP in the seminiferous tubules and in mature sperm suggest a role in the testis germ cell lineage and sperm morphogenesis