Supreme Emergencies and the protection of non-combatants in war

Is it ever justifiable to target non-combatants deliberately? This article assesses Michael Walzer's claim that the deliberate targeting of non-combatants may be justifiable during 'supreme emergencies', a view that has received some support but that has elicited little debate. It argues that the supreme emergencies exception to the prohibition on targeting non-combatants is problematic for at least four reasons. First, its utilitarianism contradicts Walzer's wider ethics of war based on a conception of human rights. Second, the exception may undermine the principle of non-combatant immunity. Third, it is based on a historical fallacy. Finally, it is predicated on a strategic fallacy-the idea that killing noncombatants can win wars. The case for rejecting the exception, however, has been opposed by those who persuasively argue that it is wrong to tie leaders' hands when they confront supreme emergencies. The final part of the article addresses this question and suggests that the principle of proportionality may give political leaders room for manoeuvre in supreme emergencies without permitting them deliberately to target non-combatants.

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.