Eradicating feral cats to protect Galapagos Land Iguanas: methods and strategies

A three-year programme to eradicate Feral Cats Felis catus from the island of Baltra in the Galapagos archipelago achieved good results by Initially poisoning with sodium monofluoroacetate (compound 1080) then trapping or shooting the remaining cats. The poisoning campaign removed 90% of the cats, its success being attributable to pre-baiting with unpolsoned baits to accustom cats to eating baits and placing enough baits to ensure that all cats encountered several baits within their home range. This, together with the use of metaclopromide (Pileran) as an anti-emetic, overcame a problem associated with poor retention of 1080 in thawed fish baits that limited the dose available to 1 mg 1080lbait, a quality Insufficient to kill large cats. Removal of the remaining cats was delayed by a weather-Induced irruption of Black Rats Rattus rattus and House Mice Mus musculus that enabled recruitment of kittens in 2002, but made cats more susceptible to trapping and shooting in 2003 when rodent populations collapsed. Since July 2003 no sign of a cat has been detected on Baltra despite extensive searching and monitoring throughout 2004. As cat abundance has decreased there have been more locally-bred Juvenile iguanas (Conolophus subcristatus) seen during annual censuses. However, such recruitment may reflect the increasing maturity and higher fecundity of iguanas repatriated from 1991 onwards rather than being a direct result of reduced cat predation alone. More time is necessary to determine the benefits of reduced cat predation on the Iguana population.

Suppressor of cytokine signaling 3 limits protection of leukemia inhibitory factor receptor signaling against central demyelination

Enhancement of oligodendrocyte survival through activation of leukemia inhibitory factor receptor (LIFR) signaling is a candidate therapeutic strategy for demyelinating disease. However, in other cell types, LIFR signaling is under tight negative regulation by the intracellular protein suppressor of cytokine signaling 3 (SOCS3). We, therefore, postulated that deletion of the SOCS3 gene in oligodendrocytes would promote the beneficial effects of LIFR signaling in limiting demyelination. By studying wild-type and LIF-knockout mice, we established that SOCS3 expression by oligodendrocytes was induced by the demyelinative insult, that this induction depended on LIF, and that enclogenously produced LIF was likely to be a key determinant of the CNS response to oligodendrocyte loss. Compared with wild-type controls, oligo-dendrocyte-specific SOCS3 conditional-knockout mice displayed enhanced c-fos activation and exogenous LIF-induced phosphorylation of signal transducer and activator of transcription 3. Moreover, these SOCS3-deficient mice were protected against cupri-zone-induced oligodendrocyte loss relative to wild-type animals. These results indicate that modulation of SOCS3 expression could facilitate the endogenous response to CNS injury.