Causes and Consequences of a Father’s Child Leave: Evidence from a Reform of Leave Schemes

Many OECD countries have implemented policies to induce couples to share parental leave. This paper investigates how responsive intra-household leave-sharing is to changes in economic incentives. To investigate this fundamental question, we are forced to look at one of the Nordic countries which are the most progressive when it comes to family-friendly policies. An extensive reform of child leave schemes in Denmark affected couples differently depending on whether the parents where employed in the same or in different parts of the public sector. Based on a difference-in-differences strategy, I find that economic incentives are very important for intra-household leave-sharing. Increasing the couples' after tax income by $9 per day of leave which is transferred from the mother to the father is found to lead to a one day transfer. This corresponds to a supply elasticity close to unity

Bioluminescence imaging of Smad signaling in living mice shows correlation with excitotoxic neurodegeneration

The TGF-β signaling pathway is a key organizer of injury and immune responses, and recent studies suggest it fulfills critical roles in CNS function and maintenance. TGF-β receptor activation results in phosphorylation of Smad proteins, which subsequently translocate to the nucleus to regulate gene transcription by binding to Smad binding elements (SBE). Using SBE-luciferase reporter mice, we recently discovered that the brain has the highest Smad baseline activity of any major organ in the mouse, and we now demonstrate that this signal is primarily localized to pyramidal neurons of the hippocampus. In vivo excitatory stimulation with kainic acid (KA) resulted in an increase in luciferase activity and phosphorylated Smad2 (Smad2P), and nuclear translocation of Smad2P in hippocampal CA3 neurons correlated significantly with luciferase activity. Although this activation was most prominent at 24 h after KA administration in neurons, Smad2P immunoreactivity gradually increased in astrocytes and microglial cells at 3 and 5 days, consistent with reactive gliosis. Bioluminescence measured over the skull in living mice peaked at 12–72 h and correlated with the extent of microglial activation and pathological markers of neurodegeneration 5 days after injury. Treatment with the glutamate receptor antagonist MK-801 strongly reduced bioluminescence and pathology. These results show that Smad2 signaling is a sensitive marker of neuronal activation and CNS injury that can be used to monitor KA-induced neuronal degeneration. This and related mouse models may provide valuable tools to study mechanisms and treatments for neurodegeneration