Is Inequality Among Universities Increasing? Gini Coefficients and the Elusive Rise of Elite Universities

One of the unintended consequences of the New Public Management (NPM) in universities is often feared to be a division between elite institutions focused on research and large institutions with teaching missions. However, institutional isomorphisms provide counter-incentives. For example, university rankings focus on certain output parameters such as publications, but not on others (e.g., patents). In this study, we apply Gini coefficients to university rankings in order to assess whether universities are becoming more unequal, at the level of both the world and individual nations. Our results do not support the thesis that universities are becoming more unequal. If anything, we predominantly find homogenization, both at the level of the global comparisons and nationally. In a more restricted dataset (using only publications in the natural and life sciences), we find increasing inequality for those countries, which used NPM during the 1990s, but not during the 2000s. Our findings suggest that increased output steering from the policy side leads to a global conformation to performance standards

Vitamin K supplementation increases vitamin K tissue levels but fails to counteract ectopic calcification in a mouse model for pseudoxanthoma elasticum

Pseudoxanthoma elasticum (PXE) is an autosomal recessive disorder in which calcification of connective tissue leads to pathology in skin, eye and blood vessels. PXE is caused by mutations in ABCC6. High expression of this transporter in the basolateral hepatocyte membrane suggests that it secretes an as-yet elusive factor into the circulation which prevents ectopic calcification. Utilizing our Abcc6−/− mouse model for PXE, we tested the hypothesis that this factor is vitamin K (precursor) (Borst et al. 2008, Cell Cycle). For 3 months, Abcc6−/− and wild-type mice were put on diets containing either the minimum dose of vitamin K required for normal blood coagulation or a dose that was 100 times higher. Vitamin K was supplied as menaquinone-7 (MK-7). Ectopic calcification was monitored in vivo by monthly micro-CT scans of the snout, as the PXE mouse model develops a characteristic connective tissue mineralization at the base of the whiskers. In addition, calcification of kidney arteries was measured by histology. Results show that supplemental MK-7 had no effect on ectopic calcification in Abcc6−/− mice. MK-7 supplementation increased vitamin K levels (in skin, heart and brain) in wild-type and in Abcc6−/− mice. Vitamin K tissue levels did not depend on Abcc6 genotype. In conclusion, dietary MK-7 supplementation increased vitamin K tissue levels in the PXE mouse model but failed to counteract ectopic calcification. Hence, we obtained no support for the hypothesis that Abcc6 transports vitamin K and that PXE can be cured by increasing tissue levels of vitamin K