Restoring brain function after stroke - bridging the gap between animals and humans

Stroke is the leading cause of complex adult disability in the world. Recovery from stroke is often incomplete, which leaves many people dependent on others for their care. The improvement of long-term outcomes should, therefore, be a clinical and research priority. As a result of advances in our understanding of the biological mechanisms involved in recovery and repair after stroke, therapeutic opportunities to promote recovery through manipulation of poststroke plasticity have never been greater. This work has almost exclusively been carried out in preclinical animal models of stroke with little translation into human studies. The challenge ahead is to develop a mechanistic understanding of recovery from stroke in humans. Advances in neuroimaging techniques now enable us to reconcile behavioural accounts of recovery with molecular and cellular changes. Consequently, clinical trials can be designed in a stratified manner that takes into account when an intervention should be delivered and who is most likely to benefit. This approach is expected to lead to a substantial change in how restorative therapeutic strategies are delivered in patients after stroke

The limited impact of acetic acid in archives and libraries

Abstract For over two decades the exposure of paper heritage collections to outdoor and indoor generated gaseous pollutants has been perceived as an important threat to their preservation. Following explicit or implicit advise from conservation science, many archives, libraries and museums have implemented special chemical filtration units to prevent possible pollution induced damage. The most abundant, potentially harmful, indoor generated pollutant found in paper loaded storage rooms is acetic acid. Acids are known to promote the chemical degradation of cellulose, the major constituent of paper. These combined facts make clear why acetic acid has received much attention by conservation science as a prime suspect pollutant causing paper degradation. However, new experimental evidence contradicts the claim that acetic acid in typical storage situations causes significant damage to paper heritage. In this study a mathematical model is presented that expresses our understanding of the causal chain of processes connecting acetic acid exposure to paper damage. The model simply combines existing partial models describing (1) the transfer of acetic acid through air, (2) the pH response of paper and (3) the kinetics of acid-catalyzed hydrolytic depolymerization. The model makes apparent that the impact of acetic acid on archival and library collections is rather limited and poses an insignificant risk and as such requires a re-evaluation of existing data