Exploring a Second Level of Parity: Suggestions for Developing an Analytical Framework for Forum Selection in Employment Discrimination Litigation

In April 1990 in Yellow Freight System, Inc. v. Donnelly, the United States Supreme Court resolved a split among the circuit courts and held that state and federal courts have concurrent jurisdiction over Title VII claims. This decision strengthens a presumption that state courts, as a whole, can be equal to their federal counterparts in adjudicating federal employment discrimination claims. It also further complicates the process of forum selection for employment discrimination litigants. Because plaintiffs now may present Title VII claims in state court, the doctrine of res judicata will bar any subsequent presentation of Title VII claims in federal court that the plaintiff could have raised in a prior state court action. Plaintiffs who wish to pursue related state claims in state court without risking removal may have to abandon their Title VII claims to protect their choice of forum.\u27 Consequently, the informed use of the forum selection process in making that choice is increasingly important. Now more than ever, litigants need an analytical framework to guide them in the forum selection process. Scholars and commentators consistently have debated the proper role of the state and federal courts in the adjudication of federal claims. One can trace the origins of this debate to the Framers of the Constitution In recent years this debate often has focused on the issue of parity: whether or not the state courts, as a whole, provide adequate and trustworthy forums for litigants seeking protection of federal rights.\u27 The parity debate raises issues significant to the determination of the proper roles of the federal and state courts in enforcing federal rights. Although no consensus has emerged, the continuing debate is likely to influence the allocation of judicial resources by judges and legislators alike. The Yellow Freight decision forces employment discrimination litigants and their attorneys engaging in the process of forum selection to confront many of the same issues raised by the parity debate. These issues, however, have a different significance for individual litigants confronted with a choice between state and federal forums. For litigants, the important inquiry is not whether state courts as a whole are as capable as their federal counterparts in protecting federal rights, but whether, in a given case, a particular state court or a particular federal court is more amenable to the claims or defenses litigants may raise. Thus, to be of value to individuals in developing a framework for forum selection, the parity debate must move to another level. Although the central question remains whether one forum is better than another, a pragmatic approach to forum selection requires an individualization of the parity debate

Introduction: Caring for the Nation--Current Issues in Health Care Reform

Health care reform is once again on the front burner of American politics. With health care costs in the United States rising at three times the rate of inflation and an increasing portion of the population falling through the cracks of the current health care delivery system,\u27 legislators, health care professionals, and the population at large now have little difficulty agreeing that the system is badly in need of reform. This consensus, however, falls apart when discussion turns to what needs to be fixed and how to fix it. Federal legislators currently have over twenty health bills pending before them, and state governments, tired of waiting for a consistently elusive federal solution, have begun seeking their own solutions to health care problems.\u27 While perhaps the current focus on health care reform is unsurprising in light of election year politics, there is compelling evidence that Americans are rightly concerned about the state of health care in this country. The United States is now one of only two major industrialized nations that have yet to implement some form of universal health care system for their citizens. Despite possession of the most advanced medical technology and the most highly skilled medical personnel in the world, the United States consistently rates well below other countries in life expectancy, infant mortality, and low birth weight.\u27 Rapidly rising costs and the growing number of uninsured and underinsured undoubtedly contribute to these gloomy statistics by limiting the access of many citizens to even basic health care.\u27 Administrative inefficiency, waste, and health care fraud compound the problem by needlessly consuming limited health care funds, both private and public. It is little wonder that the cry for reform has become so universal and so persistent

Trust-mistrust as a design contingency: laboratory experimentation in a counterterrorism context

Trust research assumes organizational managers ought to establish high levels of trust. Research also suggests trust is decreasing and therefor raises an important management dilemma. We study trust from a contingency theory framework and hypothesize that trust levels may vary depending on different organizational designs. Using the ELICIT multiplayer intelligence game we conduct laboratory experiments to examine the effect of trust levels and organizational design on performance. Results are mixed: trust and organizational design have strong interactions, and high levels of trust do not necessarily equate to good performance.recommended for Best Paper Award

Analysis of pore-fluid pressure gradient and effective vertical-stress gradient distribution in layered hydrodynamic systems

A theoretical analysis is carried out to investigate the pore-fluid pressure gradient and effective vertical-stress gradient distribution in fluid saturated porous rock masses in layered hydrodynamic systems. Three important concepts, namely the critical porosity of a porous medium, the intrinsic Fore-fluid pressure and the intrinsic effective vertical stress of the solid matrix, are presented and discussed. Using some basic scientific principles, we derive analytical solutions and explore the conditions under which either the intrinsic pore-fluid pressure gradient or the intrinsic effective vertical-stress gradient can be maintained at the value of the lithostatic pressure gradient. Even though the intrinsic pore-fluid pressure gradient can be maintained at the value of the lithostatic pressure gradient in a single layer, it is impossible to maintain it at this value in all layers in a layered hydrodynamic system, unless all layers have the same permeability and porosity simultaneously. However, the intrinsic effective vertical-stress gradient of the solid matrix can be maintained at a value close to the lithostatic pressure gradient in all layers in any layered hydrodynamic system within the scope of this study

Long-fiber carbon nanotubes replicate asbestos-induced mesothelioma with disruption of the tumor suppressor gene Cdkn2a ( Ink4a/Arf )

Mesothelioma is a fatal tumor of the pleura and is strongly associated with asbestos exposure. The molecular mechanisms underlying the long latency period of mesothelioma and driving carcinogenesis are unknown. Moreover, late diagnosis means that mesothelioma research is commonly focused on end-stage disease. Although disruption of the CDKN2A (INK4A/ARF) locus has been reported in end-stage disease, information is lacking on the status of this key tumor suppressor gene in pleural lesions preceding mesothelioma. Manufactured carbon nanotubes (CNTs) are similar to asbestos in terms of their fibrous shape and biopersistent properties and thus may pose an asbestos-like inhalation hazard. Here we show that instillation of either long CNTs or long asbestos fibers into the pleural cavity of mice induces mesothelioma that exhibits common key pro-oncogenic molecular events throughout the latency period of disease progression. Sustained activation of pro-oncogenic signaling pathways, increased proliferation, and oxidative DNA damage form a common molecular signature of long-CNT- and long-asbestos-fiber-induced pathology. We show that hypermethylation of p16/Ink4a and p19/Arf in CNT- and asbestos-induced inflammatory lesions precedes mesothelioma; this results in silencing of Cdkn2a (Ink4a/Arf) and loss of p16 and p19 protein, consistent with epigenetic alterations playing a gatekeeper role in cancer. In end-stage mesothelioma, silencing of p16/Ink4a is sustained and deletion of p19/Arf is detected, recapitulating human disease. This study addresses the long-standing question of which early molecular changes drive carcinogenesis during the long latency period of mesothelioma development and shows that CNT and asbestos pose a similar health hazard

Rapid game jams with fluidic games: A user study & design methodology

We introduce rapid game jams, a style of game jam that takes only 1–2 h and is focused on design experimentation rather than on programming and technical implementation. To support that kind of rapid game-design experimentation, we have designed a class of games that we call fluidic games. These are mobile games in which the game mechanics and other aspects of the games are editable on the fly, directly on the device, allowing for frequent play/design context shifts. We have conducted four rapid game jams with 105 participants from a local Girlguiding organisation, in order to gain real-world experience with this concept. We analyse results from a survey instrument completed by 69 participants in two of these rapid game jams. In order to guide future work in addressing questions left open by this study, we did a qualitative analysis of the designed games to gain additional insights into participants’ design practice

The HOG Pathway Dictates the Short-Term Translational Response after Hyperosmotic Shock

In the global osmoshock translational response in yeast, some gene products were translationally mobilized without transcriptional up-regulation. Conversely, other transcriptionally up-regulated mRNAs were translationally inhibited. Analogous changes occurred on the protein level. These translational responses were strongly dependent on Hog1 and Rck2

The pathogenic mechanism of the Mycobacterium ulcerans virulence factor, mycolactone, depends on blockade of protein translocation into the ER.

Infection with Mycobacterium ulcerans is characterised by tissue necrosis and immunosuppression due to mycolactone, the necessary and sufficient virulence factor for Buruli ulcer disease pathology. Many of its effects are known to involve down-regulation of specific proteins implicated in important cellular processes, such as immune responses and cell adhesion. We have previously shown mycolactone completely blocks the production of LPS-dependent proinflammatory mediators post-transcriptionally. Using polysome profiling we now demonstrate conclusively that mycolactone does not prevent translation of TNF, IL-6 and Cox-2 mRNAs in macrophages. Instead, it inhibits the production of these, along with nearly all other (induced and constitutive) proteins that transit through the ER. This is due to a blockade of protein translocation and subsequent degradation of aberrantly located protein. Several lines of evidence support this transformative explanation of mycolactone function. First, cellular TNF and Cox-2 can be once more detected if the action of the 26S proteasome is inhibited concurrently. Second, restored protein is found in the cytosol, indicating an inability to translocate. Third, in vitro translation assays show mycolactone prevents the translocation of TNF and other proteins into the ER. This is specific as the insertion of tail-anchored proteins into the ER is unaffected showing that the ER remains structurally intact. Fourth, metabolic labelling reveals a near-complete loss of glycosylated and secreted proteins from treated cells, whereas cytosolic proteins are unaffected. Notably, the profound lack of glycosylated and secreted protein production is apparent in a range of different disease-relevant cell types. These studies provide a new mechanism underlying mycolactone's observed pathological activities both in vitro and in vivo. Mycolactone-dependent inhibition of protein translocation into the ER not only explains the deficit of innate cytokines, but also the loss of membrane receptors, adhesion molecules and T-cell cytokines that drive the aetiology of Buruli ulcer