Peculiar Risk in American Tort Law

American tort law includes a significant strand of liability tied to an intriguing concept variously termed “peculiar risk,” “special danger,” and “special risk inherent in the work,” among others. Peculiar risk presents a basis for liability different from other standards or actions that trigger liability in tort law - it is different from intent, recklessness, negligence, nuisance, and abnormally dangerous activity. Both England and the United States endorsed versions of the doctrine in the late nineteenth and early twentieth centuries. Yet, by 1965, American and English tort law had sharply diverged on the doctrine. American courts continued to apply it; meanwhile, the doctrine had been severely limited in England and rejected in several other common law countries. The divide between the American approach and treatment of the doctrine outside the U.S. is a puzzle. In countries that have rejected or severely limited the doctrine, the critiques have included decisional indeterminacy and shaky historical and normative justifications. Yet a doctrine subject to these criticisms elsewhere has remained well accepted in the United States in the last thirty years - a thirty-year period characterized by extensive tort reform across the bandwidth of tort law. This Article explores three points about this divide between American tort law and the tort law of other common law countries: when and how the divide occurred; why this doctrine - whose breadth and indeterminacy spelled its disfavor elsewhere - remained well-accepted in America despite the intensity and duration of American tort reform; and whether the American version of the doctrine offers lessons for tort law outside the United States

What Can We Hope For from Law?

What can a lawyer of faith hope for, and expect from, law? This Essay, based on the 2008 Louis Brandeis Lecture given at Pepperdine University, discusses why and how this question matters not just as a matter of theory but to our real-world lawyering journeys. The Essay discusses two of the frameworks that can shape our answer to the question: a natural law viewpoint and what the Essay calls a “Lutheran” view. After explaining how these two perspectives might lead to different expectations about the effects of law, the Essay discusses whether either of these approaches is more sustaining or explanatory over the long run

Cigarette smoke induces endoplasmic reticulum stress and the unfolded protein response in normal and malignant human lung cells

<p>Abstract</p> <p>Background</p> <p>Although lung cancer is among the few malignancies for which we know the primary etiological agent (i.e., cigarette smoke), a precise understanding of the temporal sequence of events that drive tumor progression remains elusive. In addition to finding that cigarette smoke (CS) impacts the functioning of key pathways with significant roles in redox homeostasis, xenobiotic detoxification, cell cycle control, and endoplasmic reticulum (ER) functioning, our data highlighted a defensive role for the unfolded protein response (UPR) program. The UPR promotes cell survival by reducing the accumulation of aberrantly folded proteins through translation arrest, production of chaperone proteins, and increased degradation. Importance of the UPR in maintaining tissue health is evidenced by the fact that a chronic increase in defective protein structures plays a pathogenic role in diabetes, cardiovascular disease, Alzheimer's and Parkinson's syndromes, and cancer.</p> <p>Methods</p> <p>Gene and protein expression changes in CS exposed human cell cultures were monitored by high-density microarrays and Western blot analysis. Tissue arrays containing samples from 110 lung cancers were probed with antibodies to proteins of interest using immunohistochemistry.</p> <p>Results</p> <p>We show that: 1) CS induces ER stress and activates components of the UPR; 2) reactive species in CS that promote oxidative stress are primarily responsible for UPR activation; 3) CS exposure results in increased expression of several genes with significant roles in attenuating oxidative stress; and 4) several major UPR regulators are increased either in expression (i.e., BiP and eIF2α) or phosphorylation (i.e., phospho-eIF2α) in a majority of human lung cancers.</p> <p>Conclusion</p> <p>These data indicate that chronic ER stress and recruitment of one or more UPR effector arms upon exposure to CS may play a pivotal role in the etiology or progression of lung cancers, and that phospho-eIF2α and BiP may have diagnostic and/or therapeutic potential. Furthermore, we speculate that upregulation of UPR regulators (in particular BiP) may provide a pro-survival advantage by increasing resistance to cytotoxic stresses such as hypoxia and chemotherapeutic drugs, and that UPR induction is a potential mechanism that could be attenuated or reversed resulting in a more efficacious treatment strategy for lung cancer.</p

The Tort Law Debate, Efficiency, and the Kingdom of the Ill: A Critique of the Insurance Theory of Compensation

This article critiques and in large measure rejects the insurance theory of compensation. It contains an argument that the theory has fundamental failings--both normative and practical--that render it untenable as a primary guide to determining the appropriate compensatory sums in any programmatic setting

Flawed Promises: A Critical Evaluation of the American Medical Association's Guides to the Evaluation of Permanent Impairment

This book review describes the system outlined in the American Medical Association's Guides to the Evaluation of Permanent Impairment, criticizes several of the authors' key claims, and discusses aspects of the book that are useful and defensible