Short nonprotein coding RNA molecules, known as microRNAs (miRNAs), are intracellular mediators of adaptive processes, including muscle hypertrophy, contractile force generation, and inflammation. During basal conditions and tissue injury, miRNAs are released into the bloodstream as "circulating" miRNAs (c-miRNAs). To date, the impact of extended-duration, submaximal aerobic exercise on plasma concentrations of c-miRNAs remains incompletely characterized. We hypothesized that specific c-miRNAs are differentially upregulated following prolonged aerobic exercise. To test this hypothesis, we measured concentrations of c-miRNAs enriched in muscle (miR-1, miR-133a, miR-499-5p), cardiac tissue (miR-208a), and the vascular endothelium (miR-126), as well as those important in inflammation (miR-146a) in healthy male marathon runners (N = 21) at rest, immediately after a marathon (42-km foot race), and 24 h after the race. In addition, we compared c-miRNA profiles to those of conventional protein biomarkers reflective of skeletal muscle damage, cardiac stress and necrosis, and systemic inflammation. Candidate c-miRNAs increased immediately after the marathon and declined to prerace levels or lower after 24 h of race completion. However, the magnitude of change for each c-miRNA differed, even when originating from the same tissue type. In contrast, traditional biomarkers increased after exercise but remained elevated 24 h postexercise. Thus c-miRNAs respond differentially to prolonged exercise, suggesting the existence of specific mechanisms of c-miRNA release and clearance not fully explained by generalized cellular injury. Furthermore, c-miRNA expression patterns differ in a temporal fashion from corollary conventional tissue-specific biomarkers, emphasizing the potential of c-miRNAs as unique, real-time markers of exercise-induced tissue adaptation.

Myocardial infarction in patients who have cocaine-associated chest pain is not uncommon. No clinical parameter available to the physician can adequately identify patients at very low risk for myocardial infarction. Therefore, all patients with cocaine-associated chest pain should be evaluated for myocardial infarction.

The early use of tourniquets for extremity hemorrhage in an urban civilian EMS setting appears to be safe, with complications occurring infrequently.

Objective: To determine the one-year mortality and incidence of myocardial infarction (MI) post-hospital discharge or ED release for patients with cocaine-associated chest pain.Methods: A prospective, observational study of an inception cohort of consecutive patients who presented to one of four municipal hospital EDs with cocaine-associated chest pain. Patients were followed for one year from the end of the enrollment period. Main outcome parameters were the one-year actuarial survival and the frequency of nonfatal MI.Results: Mortality data were available for all 203 patients at a mean of 408 days. Additional clinical information was available for 185 patients (91%). There were six deaths (one-year actuarial survival 98%; 95% CI, 95-100%); none from MI. Nonfatal MI occurred in two patients (1%; 95% CI, 0-2%). Continued cocaine use was common (60%; 95% CI, 52-68%) and was associated with recurrent chest pain (75% vs 31%, p < 0.0001). No MI or death was reported for patients who claimed to have ceased cocaine use. Conclusions:Patients who presented with cocaine-associated chest pain commonly continued to use cocaine after discharge. Urgent evaluation of coronary anatomy or cardiac stress tests may not be necessary for patients for whom MI is ruled out and who do not have recurrent potentially ischemic pain. The subsequent risk for MI and death in this group appears to be low. Intervention strategies should emphasize cessation of cocaine use. Acad 180ACADEMIC EMERGENCY MEDICINE MAR 1995 VOL 2/NO 3 1 In the past decade the incidence of cocaine abuse has increased substantially. Twenty-four million Americans have used cocaine at least once,' and 5 million use it regularly.2 As a result, emergency physicians have witnessed an almost 20-fold increase in the number of cocaine-related complaint^.^ By 1986, cocaine had become the most common iIlicit drug of abuse in patients presenting to the ED,4 comprising more than 40% of all such cases.5 Chest pain is the most frequent cocaineassociated complaint6 and myocardial infarction (MI) occurs in approximately 6% of patients with cocaineassociated chest pain.'-" Chronic cocaine use accelerates coronary artery atherosclerosis. l 2 -I 8 Cocaine-using patients with chest pain may therefore represent a high-risk cohort predisposed to ischemic heart disease. Whether these patients should be treated and evaluated like patients with new-onset or unstable angina (unrelated to cocaine) has not been studied. This study was designed to determine the incidence of MI and death over the year following presentation with cocaine-associated chest pain. I METHODS Study Design' This study was a prospective, observational study of an inception cohort of patients who were identified at the time of ED presentation for cocaine-associated chest pain. Patients were followed for one year from the end of the study period to identify the frequency of death and nonfatal MI post-hospital discharge or post-ED release. Population and SettingAll patients with anterior, precordial, or left-sided che...

Objective: To develop new equations for the estimation of basal metabolic rate in children aged 10 ± 15 years, and to evaluate the impact of including pubertal stage into the equations. Design: Mixed longitudinal. Setting: The children were recruited from schools in Oxford, and the measurements were made in the schools. Subjects: 195 school children, aged 10 ± 15 years, were recruited in three cohorts. The gender distribution of the subjects was 40% boys and 60% girls. Methods: Basal metabolic rate (BMR) was measured, by indirect calorimetry, at 6-monthly intervals for 3 years. Anthropometric data, height, weight, body breadths and skinfold measurements (biceps, triceps, subscapular, suprailiac and medial calf) were collected on each occasion. Fat and fat-free mass was calculated from the skinfold measurements. Pubertal development was also assessed on annually by paediatricians. Pubic hair (PH) and gonad (G) development was assessed in boys and breast (B) development in girls. The girls were questioned about menarche. Stepwise multiple regression analysis was used to develop and assess new formulae for BMR that also incorporate pubertal development. 554). Weight was the most important factor in developing the regression equations for the calculation of BMR in both sexes (R 2 0.61 and 0.52 for boys and girls, respectively). Stepwise multiple regression analyses, with independent variables such as gender, weight, height, puberty stage and skinfolds, allowed several BMR regression equations to be developed. The inclusion of the menarche status in the regression equations signi®cantly (P`0.05) improved BMR estimation in the pre-menarche girls. Boys, pubertal stage as assessed by Pubic Hair (PH) and Gonadal Stage (G) did not contribute to a signi®cant improvement in BMR estimation, except for 11-year-olds. Conclusions: The inclusion of pubertal stage afforded only minor improvements in the derivation of regression equations for the estimation of BMR of children aged between 10 and 15 years.