The rise of emergency medicine in the sixties: paving a new entrance to the house of medicine.

Emergency medicine evolved into a medical specialty in the 1960s under the leadership of physicians in small communities across the country. This paper uses three case studies to investigate the political, societal, and local factors that propelled emergency medicine along this path. The case studies-Alexandria Hospital, Hartford Hospital, and Yale-New Haven Hospital-demonstrate that the changes in emergency medicine began at small community hospitals and later spread to urban teaching hospitals. These changes were primarily a response to public demand. The government, the American public, and the medical community brought emergency medical care to the forefront of national attention in the sixties. Simultaneously, patients' relationships with their general practitioners dissolved. As patients started to use the emergency room for non-urgent health problems, emergency visits increased astronomically. In response to rising patient loads and mounting criticism, hospital administrators devised strategies to improve emergency care. Drawing on hospital archives, oral histories, and statistical data, I will argue that small community hospitals' hiring of full-time emergency physicians sparked the development of a new specialty. Urban teaching hospitals, which established triage systems and ambulatory care facilities, resisted the idea of emergency medicine and ultimately delayed its development.

Cytochrome b mutations that modify the ubiquinol-binding pocket of the cytochrome bc1 complex and confer anti-malarial drug resistance in Saccharomyces cerevisiae.

Atovaquone is a new anti-malarial agent that specifically targets the cytochrome bc1 complex and inhibits parasite respiration. A growing number of failures of this drug in the treatment of malaria have been genetically linked to point mutations in the mitochondrial cytochrome b gene. To better understand the molecular basis of atovaquone resistance in malaria, we introduced five of these mutations, including the most prevalent variant found in Plasmodium falciparum (Y268S), into the cytochrome b gene of the budding yeast Saccharomyces cerevisiae and thus obtained cytochrome bc1 complexes resistant to inhibition by atovaquone. By modeling the variations in cytochrome b structure and atovaquone binding with the mutated bc1 complexes, we obtained the first quantitative explanation for the molecular basis of atovaquone resistance in malaria parasites.