Reconciling Regulation with Scientific Autonomy in Dual-Use Research.

In debates over the regulation of communication related to dual-use research, the risks that such communication creates must be weighed against against the value of scientific autonomy. The censorship of such communication seems justifiable in certain cases, given the potentially catastrophic applications of some dual-use research. This conclusion however, gives rise to another kind of danger: that regulators will use overly simplistic cost-benefit analysis to rationalize excessive regulation of scientific research. In response to this, we show how institutional design principles and normative frameworks from free speech theory can be used to help extend the argument for regulating dangerous dual-use research beyond overly simplistic cost-benefit reasoning, but without reverting to an implausibly absolutist view of scientific autonomy.

Dehumanization: its operations and its origins.

Murrow and Murrow offer a novel account of dehumanization, by synthesizing data which suggest that where subject S has a dehumanized view of group G, S's neural mechanisms of empathy show a dampened response to the suffering of members of G, and S's judgments about the humanity of members of G are largely non-conscious. Here I examine Murrow and Murrow's suggestions about how identity-based hate speech bears responsibility for dehumanization in the first place. I identify a distinction between (i) accounts of the nature of the harm effected by identity prejudice, and (ii) accounts of how hate speech contributes to the harms of identity prejudice. I then explain why Murrow and Murrow's proposal is more aptly construed as an account of type (i), and explain why accounts of this type, even if they're plausible and evidentially well-supported, have limited implications in relation to justifications for anti-hate speech law.

Climate change, cooperation and moral bioenhancement.

The human faculty of moral judgement is not well suited to address problems, like climate change, that are global in scope and remote in time. Advocates of 'moral bioenhancement' have proposed that we should investigate the use of medical technologies to make human beings more trusting and altruistic and hence more willing to cooperate in efforts to mitigate the impacts of climate change. We survey recent accounts of the proximate and ultimate causes of human cooperation in order to assess the prospects for bioenhancement. We identify a number of issues that are likely to be significant obstacles to effective bioenhancement, as well as areas for future research.

EGFR-targeted therapy results in dramatic early lung tumor regression accompanied by imaging response and immune infiltration in EGFR mutant transgenic mouse models.

Lung adenocarcinoma patients harboring kinase domain mutations in Epidermal growth factor receptor (EGFR) have significant clinical benefit from EGFR-targeted tyrosine kinase inhibitors (TKIs). Although a majority of patients experience clinical symptomatic benefit immediately, an objective response can only be demonstrated after 6-8 weeks of treatment. Evaluation of patient response by imaging shows that 30-40% of patients do not respond due to intrinsic resistance to these TKIs. We investigated immediate-early effects of EGFR-TKI treatment in mutant EGFR-driven transgenic mouse models by FDG-PET and MRI and correlated the effects on the tumor and the tumor microenvironment. Within 24 hours of erlotinib treatment we saw approximately 65% tumor regression in mice with TKI-sensitive EGFRL858R lung adenocarcinoma. However, mice with EGFRL858R/T790M-driven tumors did not respond to either erlotinib or afatinib monotherapy, but did show a significant tumor response to afatinib-cetuximab combination treatment. The imaging responses correlated with the inhibition of downstream EGFR signaling, increased apoptosis, and decreased proliferation in the tumor tissues. In EGFRL858R-driven tumors, we saw a significant increase in CD45+ leukocytes, NK cells, dendritic cells, macrophages and lymphocytes, particularly CD8+ T cells. In response to erlotinib, these dendritic cells and macrophages had significantly higher MHC class II expression, indicating increased antigen-presenting capabilities. Together, results of our study provide novel insight into the immediate-early therapeutic response to EGFR TKIs in vivo.