Terrorist Event Training in US Medical Schools. A Survey of Chemical, Biologic, Radiologic, Nuclear, and High-Yield Explosives Training in US Medical Schools.

UNLABELLED: September 11, 2001 saw the dawn of the US-led global war on terror, a combined diplomatic, military, social, and cultural war on terrorist activities. Chemical, biological, radiological, nuclear, and high-yield explosives (CBRNE), as a group of tactics, are often the preferred weapons of terrorists across the globe. We undertook a survey of US medical schools to determine what their self-reported level of training for terrorist events encompasses during the four years of undergraduate medical education. METHODS: We surveyed 170 medical schools in the US and Puerto Rico using a five-question, internet-based survey, followed by telephone calls to curriculum offices for initial nonresponders. We used simple descriptive statistics to analyze the data. RESULTS: A majority of US medical schools that completed the survey (79 schools or 65.3%) have no required lecture or course on CBRNE or terrorist activities during the first or second year (preclinical years). Ninety-eight out of the 121 respondents (81.0%), however, believed that CBRNE training was either very important or somewhat important, as reflected in survey answers. CONCLUSIONS: Most physician educators believe that training in CBRNE is important; however this belief has not resulted in widespread acceptance of a CBRNE curriculum in US medical schools.

Full-length myosin Va exhibits altered gating during processive movement on actin.

Myosin Va (myoV) is a processive molecular motor that transports intracellular cargo along actin tracks with each head taking multiple 72-nm hand-over-hand steps. This stepping behavior was observed with a constitutively active, truncated myoV, in which the autoinhibitory interactions between the globular tail and motor domains (i.e., heads) that regulate the full-length molecule no longer exist. Without cargo at near physiologic ionic strength (100 mM KCl), full-length myoV adopts a folded (approximately 15 S), enzymatically-inhibited state that unfolds to an extended (approximately 11 S), active conformation at higher salt (250 mM). Under conditions favoring the folded, inhibited state, we show that Quantum-dot-labeled myoV exhibits two types of interaction with actin in the presence of MgATP. Most motors bind to actin and remain stationary, but surprisingly, approximately 20% are processive. The moving motors transition between a strictly gated and hand-over-hand stepping pattern typical of a constitutively active motor, and a new mode with a highly variable stepping pattern suggestive of altered gating. Each head of this partially inhibited motor takes longer-lived, short forward (35 nm) and backward (28 nm) steps, presumably due to globular tail-head interactions that modify the gating of the individual heads. This unique mechanical state may be an intermediate in the pathway between the inhibited and active states of the motor.

Two brief versions of the multidimensional pain readiness to change questionnaire, version 2 (MPRCQ2).

OBJECTIVES: The present study sought to develop 1-item and 2-item versions of subscales from the Multidimensional Pain Readiness to Change Questionnaire, Version 2 (MPRCQ2), a measure of readiness to adopt a variety of pain management and coping strategies commonly taught in multidisciplinary treatment programs. METHODS: One hundred and ninety patients with rheumatic diseases who entered a Rheumatology Day Program completed the MPRCQ2 and an additional criterion measure, the Pain Stages of Change Questionnaire (PSOCQ), before and after treatment. First one and then a second item that best represented each MPRCQ2 scale were selected based on: (1) the correlations between the items and their parent MPRCQ2 scale; (2) responsivity to change following treatment; (3) correlations of the items with the PSOCQ scales; and (4) authors' consensus of face validity and construct representativeness of items. The psychometric properties of the 1-item and 2-item versions of the MPRCQ2 scales were then examined. RESULTS: These brief versions provided good approximations of their parent scales and 9/10 were responsive to change following multidisciplinary treatment. Correlations between the brief scales and the PSOCQ scales showed similar relationships as with the full MPRCQ2 scales. DISCUSSION: The findings support the validity of these brief versions of the MPRCQ2 subscales. We would recommend the use of these versions of the MPRCQ2 when a measure of patient readiness to use a range of pain self-management coping strategies is needed (eg, treatment process research, prediction of success in multidisciplinary treatment), but response burden is a significant issue.

S14 protein in breast cancer cells: direct evidence of regulation by SREBP-1c, superinduction with progestin, and effects on cell growth.

Most breast cancers exhibit brisk lipogenesis, and require it for growth. S14 is a lipogenesis-related nuclear protein that is overexpressed in most breast cancers. Sterol response element-binding protein-1c (SREBP-1c) is required for induction of lipogenesis-related genes, including S14 and fatty acid synthase (FAS), in hepatocytes, and correlation of SREBP-1c and FAS expression suggested that SREBP-1c drives lipogenesis in tumors as well. We directly tested the hypothesis that SREBP-1c drives S14 expression and mediates lipogenic effects of progestin in T47D breast cancer cells. Dominant-negative SREBP-1c inhibited induction of S14 and FAS mRNAs by progestin, while active SREBP-1c induced without hormone and superinduced in its presence. Changes in S14 mRNA were reflected in protein levels. A lag time and lack of progestin response elements indicated that S14 and FAS gene activation by progestin is indirect. Knockdown of S14 reduced, whereas overexpression stimulated, T47D cell growth, while nonlipogenic MCF10a mammary epithelial cells were not growth-inhibited. These data directly demonstrate that SREBP-1c drives S14 gene expression in breast cancer cells, and progestin magnifies that effect via an indirect mechanism. This supports the prediction, based on S14 gene amplification and overexpression in breast tumors, that S14 augments breast cancer cell growth and survival.