Violence in the emergency department: a national survey of emergency medicine residents and attending physicians.

BACKGROUND: Violence in the Emergency Department (ED) is a well-known phenomenon. Few studies have been done to assess the incidence and nature of violence in the ED. STUDY OBJECTIVES: The purpose of this study was to assess the incidence of violence in the ED nationwide. METHODS: This study was a prospective, cross-sectional online survey of Emergency Medicine (EM) residents and attending physicians. Of the 134 accredited United States (US) EM residency programs, 65 programs were randomly selected and invited to participate. RESULTS: Overall, 272 surveys were returned, of which 263 (97%) were completed and further analyzed. At least one workplace violence act in the previous 12 months was reported by 78% (95% confidence interval 73-83%) of respondents, with 21% reporting more than one type of violent act. Workplace violence was experienced similarly between males and females (79% vs. 75%, respectively; p = 0.65), and was more common in EDs with annual volumes over 60,000 patients (82% vs. 67%; p = 0.01). The most common type of workplace violence was verbal threats (75%) followed by physical assaults (21%), confrontations outside the workplace (5%), and stalking (2%). Security was available full time in most settings (98%), but was least likely to be physically present in patient care areas. The majority of respondent EDs did not screen for weapons (40% screened) or have metal detectors (38% had metal detectors). Only 16% of programs provided violence workshops, and less than 10% offered self-defense training. CONCLUSION: Despite the high incidence of workplace violence experienced by the emergency physicians who responded to our survey, less than half of these respondents worked in EDs that screened for weapons or had metal detectors. An even smaller number of physicians worked in settings that provided violence workshops or self-defense training.

Smac is required for cytochrome c-induced apoptosis in prostate cancer LNCaP cells.

Release of cytochrome c from mitochondria to cytosol has been identified as one of the central events of apoptosis. Direct injection of cytochrome c induces apoptosis in some but not in all cell types. We observed that LNCaP prostate cancer cells failed to undergo apoptosis induced by cytochrome c microinjections. Microinjection of cytochrome c with another mitochondrial protein, Smac, was sufficient to activate caspases, however. Smac is believed to function as a neutralizer of caspase inhibitors, and mass spectrometry analysis identified XIAP as a predominant Smac binding protein in LNCaP cells. These findings are consistent with a requirement for a release of Smac from mitochondria to enable caspase activation in prostate cells. Indeed, translocation of Smac from mitochondria to cytosol was observed in LNCaP cells that undergo apoptosis and was inhibited by epidermal growth factor, which is a survival factor for these cells. These results further emphasize the central role of mitochondria in the regulation of apoptosis in prostate cancer cells.