Can Rationing through Inconvenience Be Ethical?

In this article, we provide a comprehensive analysis and a normative assessment of rationing through inconvenience as a form of rationing. By "rationing through inconvenience" in the health sphere, we refer to a nonfinancial burden (the inconvenience) that is either intended to cause or has the effect of causing patients or clinicians to choose an option for health-related consumption that is preferred by the health system for its fairness, efficiency, or other distributive desiderata beyond assisting the immediate patient. We argue that under certain conditions, rationing through inconvenience may turn out to serve as a legitimate and, compared to direct rationing, even a preferable tool for rationing; we propose a research agenda to identify more precisely when that might be the case and when, alternatively, rationing through inconvenience remains ethically undesirable.

Conflicts of interest in research: looking out for number one means keeping the primary interest front and center.

Conflicts of interest represent circumstances in which professional judgments or actions regarding a primary interest, such as the responsibilities of a medical researcher, may be at risk of being unduly influenced by a secondary interest, such as financial gain or career advancement. The secondary interest may be financial or non-financial, and the resultant bias may be conscious or unconscious. The presence of conflicts of interest poses a problem for professional, patient, and public trust in research and the research enterprise.

Ethics: Investigators' interests: what should trial participants be told?

Minimizing the potential adverse effects of clinical investigators' financial conflicts of interest involves, in part, determining how much of an investigator's "business" should be disclosed to participants in research studies. What should be disclosed and why? How will we know if disclosure matters?

Regulation of Macrophage-Independent T-Cell Activation by Prostaglandins and Nonsteroidal Anti-Inflammatory Drugs.

We examined the hypothesis that both misoprostol (miso), a prostaglandin E(1) (PGE(1)) analog, and nonsteroidal anti-inflammatory drugs (NSAIDs) have significant and largely inhibitory effects on T-cell activation and, consequently, influence T-cell function. Studies were done using a macrophage-independent system for T-cell activation by mitogenic combinations of immobilized anti-T-cell monoclonal antibodies (mabs), including combinations of anti-CD3 with anti-CD4 or anti-CD6. The results indicate that misoprostol, like other prostaglandins, can inhibit T-cell proliferation and the expression of mRNAs for cytokines critical in T-cell growth and immunoregulation.