Comparing built-up area datasets to assess urban exposure to coastal hazards in Europe.

Information on urban land use, beyond the urban-rural dichotomy, can improve the assessment of potential impacts of coastal hazards by refining estimates of damages and supporting adaptation planning. However, the lack of a consistent definition of "urban" in previous studies has led to exposure estimates that vary considerably. Here, we explore the sensitivity of exposed population and built-up area in four settlement types, defined by four different built-up area datasets.

Setback zones can effectively reduce exposure to sea-level rise in Europe.

Coastal space is one of the most valuable assets of the EU coastal member states, as the coast is highly urbanized. Hard engineering has traditionally been employed to protect communities in coastal lowlands, but as this alternative becomes less sustainable and more costly, coastal managers are increasingly turning to landuse planning strategies, such as setback zones or managed retreat. To explore the efficiency of these planning tools in reducing future urban exposure to sea-level rise and associated hazards, we developed spatially explicit projections of urban extent that account for different socio-economic futures and various types of setback zones.

Endogenous brain-derived neurotrophic factor and neurotrophin-3 antagonistically regulate survival of axotomized corticospinal neurons in vivo.

Neuronal growth factors regulate the survival of neurons by their survival and death-promoting activity on distinct populations of neurons. The neurotrophins nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) promote neuronal survival via tyrosine kinase (Trk) receptors, whereas NGF and BDNF can also induce apoptosis in developing neurons through p75(NTR) receptors in the absence of their respective Trk receptors. Using mutant mice and inactivation of neurotrophins and their receptors with antibodies in rats, we show that endogenous NT-3 induces death of adult BDNF-dependent, axotomized corticospinal neurons (CSNs).

An axotomy model for the induction of death of rat and mouse corticospinal neurons in vivo.

To study trophic dependencies of rat and mouse corticospinal neurons (CSN), we established a lesion model for the induction of death of analogous populations of CSN in these rodent species. Before lesion, CSN were retrogradely labeled with Fast Blue (FB). A stereotaxic cut lesion through the entire internal capsule (ICL) was used to axotomize CSN.