Manufacturer Liability for Harms Caused by Consumers to Others

Should the manufacturer of a product be held legally responsible when a consumer, while using the product, harms someone else? We show that if consumers have deep pockets then manufacturer liability is not economically efficient. It is more efficient for the consumers themselves to bear responsibility for the harms that they cause. If homogeneous consumers have limited assets, then the most efficient rule is "residual-manufacturer liability" where the manufacturer pays the shortfall in damages not paid by the consumer. Residual-manufacturer liability distorts the market quantity when consumers' willingness to pay is correlated with their propensity to cause harm. It distorts product safety when consumers differ in their wealth levels. In both cases, consumer-only liability may be more efficient.

Sting Operations, Undercover Agents, and Entrapment

This Article focuses on two distinct functions of sting operations. One is the informational, or investigatory, function of identifying individuals who are engaged in (or likely to engage in) criminal activity. The second is the behavioral function of deterring individuals from engaging in (independent) criminal activity: the threat of being caught in a sting may scare individuals away from genuine criminal opportunities that would otherwise seem appealing. Though complementary in some respects, these functions are also in some tension with each other. A sting operation that does not serve informational purposes may be good for deterrent purposes, and vice versa. Their problematic relation is a main theme of the Article. The Article is organized as follows. Part I is a general overview of the nature of sting operations, their purposes, their potential advantages over other enforcement methods, and the dangers they pose. Parts II and III analyze, respectively, the informational and deterrent effects of sting operations. Part IV considers the relation between the informational and deterrent effects, emphasizing the tensions between them. Part V attempts a model of a socially desirable sting operation, balancing its informational and/or deterrent value against the danger of entrapping otherwise-innocent individuals. 6 The model creates a framework for identifying desirable sting operations, a framework that is necessarily very general in character. To apply it to particular cases would require knowledge of parameters whose value is an empirical question the Article does not attempt to quantify. Part VI briefly discusses some general applications to entrapment doctrine. Part VII concludes

The Drosophila DIAP1 protein is required to prevent accumulation of a continuously generated, processed form of the apical caspase DRONC

Although loss of the inhibitor of apoptosis (LAP) protein DIAP1 has been shown to result in caspase activation and spontaneous cell death in Drosophila cells and embryos, the point at which DIAP1 normally functions to inhibit caspase activation is unknown. Depletion of the DIAP1 protein in Drosophila S2 cells or the Sf-IAP protein in Spodoptera frugiperda Sf21 cells by RNA interference (RNAi) or cycloheximide treatment resulted in rapid and widespread caspase-dependent apoptosis. Co-silencing of dronc or dark largely suppressed this apoptosis, indicating that DIAP1 is normally required to inhibit an activity dependent on these proteins. Silencing of dronc also inhibited DRICE processing following stimulation of apoptosis, demonstrating that DRONC functions as an apical caspase in S2 cells. Silencing of diap1 or treatment with UV light induced DRONC processing, which occurred in two steps. The first step appeared to occur continuously even in the absence of an apoptotic signal and to be dependent on DARK because full-length DRONC accumulated when dark was silenced in non-apoptotic cells. In addition, treatment with the proteasome inhibitor MG132 resulted in accumulation of this initially processed form of DRONC, but not full-length DRONC, in non-apoptotic cells. The second step in DRONC processing was observed only in apoptotic cells. These results indicate that the initial step in DRONC processing occurs continuously via a DARK-dependent mechanism in Drosophila cells and that DIAP1 is required to prevent excess accumulation of this first form of processed DRONC, presumably through its ability to act as a ubiquitin-protein ligase

Compensatory Proliferation Induced by Cell Death in the Drosophila Wing Disc Requires Activity of the Apical Cell Death Caspase Dronc in a Nonapoptotic Role

Achieving proper organ size requires a balance between proliferation and cell death. For example, at least 40%–60% of cells in the Drosophila wing disc can be lost, yet these discs go on to give rise to normal-looking adult wings as a result of compensatory proliferation 1, 2, 3. The signals that drive this proliferation are unknown. One intriguing possibility is that they derive, at least in part, from the dying cells. To explore this hypothesis, we activated cell death signaling in specific populations of cells in the developing wing but prevented these cells from dying through expression of the baculovirus p35 protein, which inhibits the activity of effector caspases that mediate apoptosis [4]. This allowed us to uncouple the activation steps of apoptosis from death itself. Here we report that stimulation of cell death signaling in the wing disc—in the absence of cell death—results in increased proliferation and ectopic expression of Wingless, a known mitogen in the wing. Activation of the apical cell death caspase Dronc is necessary and sufficient to drive both of these processes. Our results demonstrate an unanticipated function, the nonautonomous induction of proliferation, of an apical cell death caspase. This activity is likely to contribute to tissue homeostasis by promoting local compensatory proliferation in response to cell death. We speculate that dying cells may communicate cell fate or behavior instructions to their neighbors in other contexts as well

Expression of baculovirus P35 prevents cell death in Drosophila

The baculovirus P35 protein functions to prevent apoptotic death of infected cells. We have expressed P35 in the developing embryo and eye of the fly Drosophila melanogaster. P35 eliminates most, if not all, normally occurring cell death in these tissues, as well as X-irradiation-induced death. Excess pupal eye cells that are normally eliminated by apoptosis develop into pigment cells when their death is prevented by P35 expression. Our results suggest that one mechanism by which viruses prevent the death of the host cell is to block a cell death pathway that mediates normally occurring cell death. Identification of molecules that interact biochemically or genetically with P35 in Drosophila should provide important insights into how cell death is regulated

The Demoiselles d'Evanston: On the Aesthetics of the Wigmore Chart

Wigmore's ‘The Problem of Proof’, published in 1913, was a path-breaking attempt to systematize the process of drawing inferences from trial evidence. In this paper, written for a conference on visual approaches to evidence, I look at the Wigmore article in relation to cubist art, which coincidentally made its American debut in New York and Chicago the same spring that the article appeared. The point of the paper is to encourage greater attention to the complex meanings embedded in visual diagrams, meanings overlooked by the prevailing cognitive scientific approaches to the Wigmore method