3 research outputs found

    Policy Solutions to Address Mass Shootings

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    In the past decade, mass shootings, particularly those that take place in public areas, have increasingly become part of the national conversation in the United States. Mass public shootings instill widespread fear, in part because of their seeming randomness and unpredictability. Yet when these incidents occur, which has been with somewhat greater frequency and lethality as of late, public calls for policy responses are immediate. In this policy brief, we review efforts to evaluate the effect of gun control measures on mass public shootings, including a discussion of our recently published study on the relationship between state gun laws and the incidence and severity of these shootings. The findings of this work point to gun permits and bans on large-capacity magazines as having promise in reducing (a) mass public shooting rates and (b) mass public shooting victimization, respectively. Interestingly, however, most gun laws that we examined, including assault weapon bans, do not appear to be causally related to the rate of mass public shootings

    Spatially organized multicellular immune hubs in human colorectal cancer.

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    Immune responses to cancer are highly variable, with mismatch repair-deficient (MMRd) tumors exhibiting more anti-tumor immunity than mismatch repair-proficient (MMRp) tumors. To understand the rules governing these varied responses, we transcriptionally profiled 371,223 cells from colorectal tumors and adjacent normal tissues of 28 MMRp and 34 MMRd individuals. Analysis of 88 cell subsets and their 204 associated gene expression programs revealed extensive transcriptional and spatial remodeling across tumors. To discover hubs of interacting malignant and immune cells, we identified expression programs in different cell types that co-varied across tumors from affected individuals and used spatial profiling to localize coordinated programs. We discovered a myeloid cell-attracting hub at the tumor-luminal interface associated with tissue damage and an MMRd-enriched immune hub within the tumor, with activated T cells together with malignant and myeloid cells expressing T cell-attracting chemokines. By identifying interacting cellular programs, we reveal the logic underlying spatially organized immune-malignant cell networks
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