Climate Change Adaptation for Conservation in Madagascar

Madagascar's imperilled biota are now experiencing the effects of a new threat—climate change (Raxworthy et al. 2008). With more than 90% endemism among plants, mammals, reptiles and amphibians, the stakes are high. The pristine landscapes that allowed this exceptional biodiversity to survive past climate changes are largely gone. Deforestation has claimed approximately 90% of the island's natural forest (Ingram & Dawson 2005; Harper et al. 2007) and what remains is highly fragmented, providing a poor template for large-scale species range shifts. The impacts of current and future climate change may therefore be much different than past impacts, with profound implications for biodiversity.
We review evidence of past response to climate change, models of future change and projected biological response, developing insights to formulate adaptation actions for reducing extinction in Madagascar's biota. We then explore the cost of implementing actions and examine new income opportunities developing through efforts to mitigate climate change.

Real-time error detection but not error correction drives automatic visuomotor adaptation

We investigated the role of visual feedback of task performance in visuomotor adaptation. Participants produced novel two degrees of freedom movements (elbow flexion-extension, forearm pronation-supination) to move a cursor towards visual targets. Following trials with no rotation, participants were exposed to a 60A degrees visuomotor rotation, before returning to the non-rotated condition. A colour cue on each trial permitted identification of the rotated/non-rotated contexts. Participants could not see their arm but received continuous and concurrent visual feedback (CF) of a cursor representing limb position or post-trial visual feedback (PF) representing the movement trajectory. Separate groups of participants who received CF were instructed that online modifications of their movements either were, or were not, permissible as a means of improving performance. Feedforward-mediated performance improvements occurred for both CF and PF groups in the rotated environment. Furthermore, for CF participants this adaptation occurred regardless of whether feedback modifications of motor commands were permissible. Upon re-exposure to the non-rotated environment participants in the CF, but not PF, groups exhibited post-training aftereffects, manifested as greater angular deviations from a straight initial trajectory, with respect to the pre-rotation trials. Accordingly, the nature of the performance improvements that occurred was dependent upon the timing of the visual feedback of task performance. Continuous visual feedback of task performance during task execution appears critical in realising automatic visuomotor adaptation through a recalibration of the visuomotor mapping that transforms visual inputs into appropriate motor commands.

Hyperglycaemia-induced pro-inflammatory responses by retinal Müller glia are regulated by the receptor for advanced glycation end-products (RAGE)

Aims/hypothesis: Up-regulation of the receptor for AGEs (RAGE) and its ligands in diabetes has been observed in various tissues. Here, we sought to determine levels of RAGE and one of its most important ligands, S100B, in diabetic retina, and to investigate the regulatory role of S100B and RAGE in Müller glia.

Methods: Streptozotocin-diabetes was induced in Sprague-Dawley rats. RAGE, S100B and glial fibrillary acidic protein (GFAP) were detected in retinal cryosections. In parallel, the human retinal Müller cell line, MIO-M1, was maintained in normal glucose (5.5 mmol/l) or high glucose (25 mmol/l). RAGE knockdown was achieved using small interfering RNA (siRNA), while soluble RAGE was used as a competitive inhibitor of RAGE ligand binding. RAGE, S100B and cytokines were detected using quantitative RT-PCR, western blotting, cytokine protein arrays or ELISA. Activation of mitogen-activated protein kinase (MAPK) by RAGE was determined by western blotting.

Results: Compared with non-diabetic controls, RAGE and S100B were significantly elevated in the diabetic retina with apparent localisation in the Müller glia, occurring concomitantly with upregulation of GFAP. Exposure of MIO-M1 cells to high glucose induced increased production of RAGE and S100B. RAGE signalling via MAPK pathway was linked to cytokine production. Blockade of RAGE prevented cytokine responses induced by high glucose and S100B in Müller glia.

Conclusions/interpretation: Hyperglycaemia in vivo and in vitro exposure to high glucose induce upregulation of RAGE and its ligands, leading to RAGE signalling, which links to pro-inflammatory responses by retinal Müller glia. These data shed light on the potential clinical application of RAGE blockade to inhibit the progression of diabetic retinopathy.