How robust is the “nuclear taboo”—the belief that it is wrong to use nuclear weapons—and can it be strengthened? In a series of experimental surveys, we investigate two mechanisms theorized to support the nuclear nonuse norm. First, we examine the moral foundation of the norm by testing whether respondents who receive descriptions of the aftermath of a nuclear blast will be less supportive of nuclear weapons use. Second, we assess the mechanism of self-interest by raising a sense of nuclear risk, and test whether varying the likelihood of nuclear retaliation affects support for a strike. We find that vivid information about the consequences of a nuclear strike, either in moral or self-interested terms, reduces support for nuclear use. These findings indicate that each of the two mechanisms may support the nuclear nonuse tradition, but that the strength of each mechanism is affected by exposure to vivid information.

Ischemic-like insults decrease viability and increase cell death in cultures of human NPCs. Similar conditions have less affect on cell death and promote proliferation in AGS NPCs.

Why do some civil wars end sooner than others? Extant theory focuses on how exogenous factors, such as resources or third parties, exacerbate the commitment problem faced by belligerents. In explaining the duration of civil war, we focus on factors endogenous to the disputing parties. We advance a theory suggesting that the tenure of a state's leader influences war duration. Specifically, we argue that longer-tenured leaders tend to fight longer civil wars. This is because long-tenured leaders have a more predictable policy reputation. Based on this predictable reputation, opposition groups have decided to fight the leader rather than bargain peacefully. Therefore, they will be unlikely to believe any policy concessions the leader might offer. This commitment problem looms larger for leaders who do not have domestic institutions that can credibly commit the leader to policy changes. We find robust statistical support for our conjecture. The findings have important implications for leader-centric studies of conflict, as well as for our understanding of bargaining during war.Why do some civil wars end sooner than others? Owing to the wide variation in civil war durations, this question has become the topic of a large debate in political science. The answers provided to this question have focused on elements ranging from the resources possessed by the state and rebels to whether the conflict experienced intervention by a third party. Each of these elements eventually factors into the commitment problems faced by the state and rebels in negotiating the conclusion of the conflict. If either side does not obtain its

Aging is known to slow the neurogenic capacity of the hippocampus, one of only two mammalian adult neurogenic niches. The reduction of adult-born neurons with age may initiate cognitive decline progression which is exacerbated in chronic neurodegenerative disorders, e.g., Alzheimer’s disease (AD). With physiologic neurogenesis diminished, but still viable in aging, non-invasive therapeutic modulation of this neuron regeneration process remains possible. The discovery of truly novel neuron regenerative therapies could be identified through phenotypic screening of small molecules that promote adult-born neurons from human neural progenitor cells (hNPCs). By identifying neuron-generating therapeutics and potentially novel mechanism of actions, therapeutic benefit could be confirmed through in vivo proof-of-concept studies. The key aging and longevity mTOR/p70S6 kinase axis, a commonly targeted pathway, is substrate for potential selective kinase modulators to promote new hippocampal neurons from NPCs. The highly regulated downstream substrate of mTOR, p70S6 kinase, directly controls pleiotropic cellular activities, including translation and cell growth. Stimulating this kinase, selectively in an adult neurogenic niche, should promote NPC proliferation, and cell growth and survival in the hippocampus. Studies of kinase profiling and immunocytochemistry of human progenitor neurogenesis suggest that the novel small molecule NNI-362 stimulates p70S6 kinase phosphorylation, which, in turn, promotes proliferation and differentiation of NPCs to neurons. NNI-362 promoted the associative reversal of age- and disease-related cognitive deficits in aged mice and Down syndrome-modeled mice. This oral, allosteric modulator may ultimately be beneficial for age-related neurodegenerative disorders involving hippocampal-dependent cognitive impairment, specifically AD, by promoting endogenous hippocampal regeneration.