We provide an in-depth study of applying wireless sensor networks (WSNs) to real-world habitat monitoring. A set of system design requirements were developed that cover the hardware design of the nodes, the sensor network software, protective enclosures, and system architecture to meet the requirements of biologists. In the summer of 2002, 43 nodes were deployed on a small island off the coast of Maine streaming useful live data onto the web. Although researchers anticipate some challenges arising in real-world deployments of WSNs, many problems can only be discovered through experience. We present a set of experiences from a four month long deployment on a remote island. We analyze the environmental and node health data to evaluate system performance. The close integration of WSNs with their environment provides environmental data at densities previously impossible. We show that the sensor data is also useful for predicting system operation and network failures. Based on over one million

No abstract

No abstract

No abstract

Dominantly acting mutations of the fibroblast growth factor (FGF) receptor 2 (FGFR2) gene have been implicated in various craniosynostosis syndromes. Apert syndrome, characterized in addition by syndactyly of the limbs, involves specific mutations at two adjacent residues, Ser252Trp and Pro253Arg, predicted to lie in the linker region between IgII and IgIII of the FGFR2 ligand-binding domain. We have analysed the interaction of FGF ligands with wild-type and Apert-type mutant FGFR2 ectodomains in solution. Wild-type and Apert-type receptors form a complex with FGF ligands with a stoichiometry of 2:2 (ligand:receptor). The kinetics and specificity of ligand binding to wild-type and Apert mutant receptors have been analysed using surface plasmon resonance techniques. This reveals that Apert mutations, compared with wild-type, exhibit a selective decrease in the dissociation kinetics of FGF2, but not of other FGF ligands examined. In contrast, the substitution Ser252Leu in FGFR2, previously observed in several asymptomatic individuals, exhibited wild-type kinetics. These findings indicate that Apert syndrome arises as a result of increased affinity of mutant receptors for specific FGF ligands which leads to activation of signalling under conditions where availability of ligand is limiting.