Development of an Early Identification and Response Model of Malpractice Prevention

The dramatic rise in the incidence of malpractice claims over the past thirty years has revealed several problems with the U.S. system of medical dispute resolution. First, the sudden and unexpected increase in claims has created an insurance crisis wherein various medical specialists have had difficulty obtaining affordable insurance coverage. One such crisis occurred in Florida in the mid-1980\u27s, when an inability of many physicians to procure medical malpractice coverage caused some to limit or curtail their practice. This resulted in access problems for the public. This phenomenon has disproportionately befallen physicians practicing obstetric medicine. Second, besides contributing to periodic crises of access, the current medical dispute resolution system is often responsible for long delays in resolving claims and in compensating victims. Third, compensation is sometimes inequitable, encouraging frivolous suits and making the system expensive to operate. Finally, while there is no evidence that the system reduces bad care, it clearly contributes to increased cost by encouraging unjustified defensive medicine

Rethinking Peer Review: Detecting and Addressing Medical Malpractice Claims Risk

A medical center department chair has just been notified that a physician in his department, Dr. G, is being sued for the fifth time in seven years. The CEO of co-defendant hospital wants the chair to solve Dr. G\u27s claims problems. At the chair\u27s request, the hospital peer review committee evaluates Dr. G\u27s malpractice cases. While committee members note some minor concerns in the cases, they conclude that in each circumstance he has met the standard of care. They cannot identify any specific technical or educational need, nor can they supply justification for a disciplinary action. The chair is in a vexing situation. Is Dr. G. the victim of bad luck, or is something more systematic at work? Is there some failure or deficiency other than technical incompetence which is making this physician vulnerable to malpractice suits? If so, is it remediable? In this Article, we analyze the ability of peer review to recognize and reduce physicians\u27 risk of medical malpractice claims. Critics argue that peer review neither consistently identifies substandard physicians, nor ensures their removal, while it unfairly targets colleagues for reasons such as economic competition. They suggest that the solution may be to modify statutes governing privilege and immunity, or to increase penalties for healthcare institutions that violate reporting statutes. Critics\u27 concerns may be misplaced. We will argue that peer review is not deficient in its basic conception, but rather aspects of its design and implementation which often do not directly link it to an institution\u27s risk management activities. We assert that peer review can effectively identify a physician\u27s risk of generating a disproportionate share of medical malpractice claims ex ante, and present a sample methodology which allows peer review to more effectively help physicians address that risk. Part I of this Article discusses the background and authority for peer review. Part II outlines common criticisms of peer review and discusses shortcomings in these analyses. Part III describes background medical malpractice research and introduces the Patient Advocacy Reporting System ( PARSSM ) program for peer review. In Part IV we conclude with a discussion of programmatic elements which, if incorporated into the legal framework for peer review, may allow peer review committees to systematically evaluate, monitor, and, potentially reduce physicians\u27 medical malpractice claims risk

Chronic allograft nephropathy: expression and localization of PAI-1 and PPAR-c

Abstract Background. Chronic allograft nephropathy (CAN) is a major cause of loss of renal allografts. Mechanisms postulated to be involved include sequelae of rejection, warm ischaemia time, drug toxicity, ongoing hypertension and dyslipidaemia. Plasminogen activator inhibitor-1 (PAI-1) is implicated not only in thrombo

Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences

The completion of the human genome sequence has made possible genome-wide studies of retroviral DNA integration. Here we report an analysis of 3,127 integration site sequences from human cells. We compared retroviral vectors derived from human immunodeficiency virus (HIV), avian sarcoma-leukosis virus (ASLV), and murine leukemia virus (MLV). Effects of gene activity on integration targeting were assessed by transcriptional profiling of infected cells. Integration by HIV vectors, analyzed in two primary cell types and several cell lines, strongly favored active genes. An analysis of the effects of tissue-specific transcription showed that it resulted in tissue-specific integration targeting by HIV, though the effect was quantitatively modest. Chromosomal regions rich in expressed genes were favored for HIV integration, but these regions were found to be interleaved with unfavorable regions at CpG islands. MLV vectors showed a strong bias in favor of integration near transcription start sites, as reported previously. ASLV vectors showed only a weak preference for active genes and no preference for transcription start regions. Thus, each of the three retroviruses studied showed unique integration site preferences, suggesting that virus-specific binding of integration complexes to chromatin features likely guides site selection

From Craft to Nature: The Emergence of Natural Teleology

A teleological explanation is an explanation in terms of an end or a purpose. So saying that ‘X came about for the sake of Y’ is a teleological account of X. It is a striking feature of ancient Greek philosophy that many thinkers accepted that the world should be explained in this way. However, before Aristotle, teleological explanations of the cosmos were generally based on the idea that it had been created by a divine intelligence. If an intelligent power made the world, then it makes sense that it did so with a purpose in mind, so grasping this purpose will help us understand the world. This is the pattern of teleological explanation that we find in the Presocratics and in Plato. However, with Aristotle teleology underwent a change: instead of thinking that the ends were explanatory because a mind had sought to bring them about, Aristotle took the ends to operate in natural beings independently of the efforts of any creative intelligence. Indeed, he thought that his predecessors had failed to understand what was distinctive of nature, namely, that its ends work from the inside of natural beings themselves

Aristotle on the Matter for Birth, Life, and the Elements

This essay considers three case studies of Aristotle’s use of matter, drawn from three different scientific contexts: menstrual fluid as the matter of animal generation in the Generation of Animals, the living body as matter of an organism in Aristotle’s On the Soul (De Anima), and the matter of elemental transformation in Generation and Corruption. I argue that Aristotle conceives of matter differently in these treatises (1) because of the different sorts of changes under consideration, and (2) because sometimes he is considering the matter for one specific change, and sometimes the matter for all of a thing’s natural changes. My account allows me to explain some of the strange features that Aristotle ascribes to the matter for elemental transformation in Generation and Corruption II. These features were interpreted by later commentators as general features of all matter. I argue that they are a result of the specific way that Aristotle thinks about the transmutation of the elements

Genome-wide association analyses identify new Brugada syndrome risk loci and highlight a new mechanism of sodium channel regulation in disease susceptibility.

Brugada syndrome (BrS) is a cardiac arrhythmia disorder associated with sudden death in young adults. With the exception of SCN5A, encoding the cardiac sodium channel Na1.5, susceptibility genes remain largely unknown. Here we performed a genome-wide association meta-analysis comprising 2,820 unrelated cases with BrS and 10,001 controls, and identified 21 association signals at 12 loci (10 new). Single nucleotide polymorphism (SNP)-heritability estimates indicate a strong polygenic influence. Polygenic risk score analyses based on the 21 susceptibility variants demonstrate varying cumulative contribution of common risk alleles among different patient subgroups, as well as genetic associations with cardiac electrical traits and disorders in the general population. The predominance of cardiac transcription factor loci indicates that transcriptional regulation is a key feature of BrS pathogenesis. Furthermore, functional studies conducted on MAPRE2, encoding the microtubule plus-end binding protein EB2, point to microtubule-related trafficking effects on Na1.5 expression as a new underlying molecular mechanism. Taken together, these findings broaden our understanding of the genetic architecture of BrS and provide new insights into its molecular underpinnings