Piercing the Doctrine of Corporate Hospital Liability

This Comment examines the significance and development of the doctrine of corporate hospital liability, under which hospitals are legally accountable for the negligence of their staff physicians. The author concludes that the courts that have adopted this principle have ignored basic procedural and organizational realities of hospital and medical practice, which make the imposition of corporate liability unsound. The author argues that the more logical defendants are those staff physicians who are aware of the negligent physician\u27s incompetence and fail to take reasonable steps to prevent the plaintiff\u27s injury

Efficacy of BET bromodomain inhibition in Kras-mutant non-small cell lung cancer

PurposeAmplification of MYC is one of the most common genetic alterations in lung cancer, contributing to a myriad of phenotypes associated with growth, invasion and drug resistance. Murine genetics has established both the centrality of somatic alterations of Kras in lung cancer, as well as the dependency of mutant Kras tumors on MYC function. Unfortunately, drug-like small-molecule inhibitors of KRAS and MYC have yet to be realized. The recent discovery, in hematologic malignancies, that BET bromodomain inhibition impairs MYC expression and MYC transcriptional function established the rationale of targeting KRAS-driven NSCLC with BET inhibition.Experimental DesignWe performed functional assays to evaluate the effects of JQ1 in genetically defined NSCLC cells lines harboring KRAS and/or LKB1 mutations. Furthermore, we evaluated JQ1 in transgenic mouse lung cancer models expressing mutant kras or concurrent mutant kras and lkb1. Effects of bromodomain inhibition on transcriptional pathways were explored and validated by expression analysis.ResultsWhile JQ1 is broadly active in NSCLC cells, activity of JQ1 in mutant KRAS NSCLC is abrogated by concurrent alteration or genetic knock-down of LKB1. In sensitive NSCLC models, JQ1 treatment results in the coordinate downregulation of the MYC-dependent transcriptional program. We found that JQ1 treatment produces significant tumor regression in mutant kras mice. As predicted, tumors from mutant kras and lkb1 mice did not respond to JQ1.ConclusionBromodomain inhibition comprises a promising therapeutic strategy for KRAS mutant NSCLC with wild-type LKB1, via inhibition of MYC function. Clinical studies of BET bromodomain inhibitors in aggressive NSCLC will be actively pursued

OPEN COMMUNITY HEALTH: WORKSHOP REPORT

This report summarizes key outcomes from a workshop on open community health conducted at the University of Nebraska at Omaha in April 2018. Workshop members represented research and practice communities across Citizen Science, Open Source, and Wikipedia. The outcomes from the workshop include (1) comparisons among these communities, (2) how a shared understanding and assessment of open community health can be developed, and (3) a taxonomical comparison to begin a conversation between these communities that have developed disparate languages

Biologically-Inspired Computing

A seminar course at the University of Virginia in Spring 2003 considered aspects of biologically-inspired computing. The course homepage has links to journal articles and research papers that range in topic from evolutionary programming to spacecraft designs based on living cells. There is also a page of links that connect users to further information about topics explored on the CS851 page