Epidemiology of major trauma and trauma deaths in Los Angeles County.

BACKGROUND: Our objective was to study population-based trauma-related injuries and deaths in the county of Los Angeles and to identify trends and progress towards meeting the "Year 2000 National Health Objectives." STUDY DESIGN: We did a retrospective study for the year 1996. Data were obtained from the Trauma Registry of the Emergency Medical Services of the Department of Health Services, and the Coroner's Department of the County of Los Angeles. Traumatic injuries and deaths per 100,000 of the population were calculated according to mechanism, race, age, and gender. RESULTS: During 1996, there were 12,136 major trauma admissions in the 13 trauma centers in Los Angeles County. Another 1,929 victims died at the scene or were certified dead at nontrauma centers and were taken to the Coroner's Department (total 14,065 victims). The overall major injury rate was 151.0 per 100,000 population and the death rate was 30.9 per 100,000. The trauma death rate per 100,000 population was 56.4 for African-Americans, 33.5 for Hispanics, 26.3 for Caucasians, and 11.6 for Asians. Homicides were the leading cause of traumatic deaths (45.3%) followed by traffic accidents (31.9% of deaths). Firearms were responsible for 3,899 major injuries or deaths (41.7 per 100,000 population). The overall homicide rate per 100,000 population was 14.0, with a much higher rate for African-Americans (40.4 per 100,000) and Hispanics (18.7 per 100,000) than Caucasians (4.0 per 100,000) or Asians (3.4 per 100,000). African-American males were at very high risk for homicide (73.3 per 100,000), and in the age group 15 to 34 years, this problem reaches epidemic proportions (164.2 per 100,000). Traffic accidents accounted for 69.0 major injuries and 9.6 deaths per 100,000 people. Males were at significantly higher risk of dying in traffic accidents than females. People over 60 years of age were at significantly higher risk of traffic-accident death than younger people, for both passenger and pedestrian groups (p < 0.01). Firearm-related suicides were responsible for 4.6 deaths per 100,000 population. Caucasian males over 65 years were at much higher risk of suicide by penetrating trauma (29.5 per 100,000) than were Hispanics (6.3 per 100,000), Asians (5.4 per 100,000), or African-Americans (no deaths) in the same gender and age group. CONCLUSIONS: Trauma remains a major health problem in the county of Los Angeles. Despite the significant reduction of intentional trauma in 1996, it still exceeds national figures and is much higher than the targeted "Year 2000 National Health Objectives." Aggressive prevention strategies need to focus on the population groups at excessive risks of injury by assault, traffic accidents, and suicides.

The interaction of amino-deuteromethylated melittin with phospholipid membranes studied by deuterium NMR.

Melittin, deuteromethylated on each of the four amino groups (Gly-1 N alpha and Lys-7, 21, and 23 N epsilon), was prepared by reductive methylation using deuteroformaldehyde and NaBD3CN. Deuterium NMR spectra were obtained for the modified peptide (D-melittin) bound to phospholipid bilayers and erythrocyte ghosts. D-Melittin at 4 mol% (peptide:lipid) induced reversible transitions between extended bilayers and micelles at the phase-transition temperature in dimyristoylphosphatidylcholine (DMPC) bilayers. These changes in lipid morphology did not occur at 1 mol% D-melittin: DMPC and the peptide was highly motionally restricted in gel in gel-phase lipid.

Physiological inhibition and facilitation of adrenocortical response to hemorrhage.

In a search for physiological feedback inhibition, secretion rates of cortisol were measured in intact dogs before and after sequential hemorrhages. The sucond of two sequential hemorrhages of 10 ml/kg separated by 90 min evoked significantly less increase of secretion rate of cortisol than did the first. This result was not explained by differential hemodynamic effects. Exhaustion of pituitary or adrenal capacities was excluded, since dogs responded normally to a second, larger hemorrhage. However, no attenuation response to a second 10 ml/kg hemorrhage was seen after a larger, 20 ml/kg, first hemorrhage. This led in turn to a search for a physiological facilitatory mechanism which might offset the feedback effect. The second of two rapid sequential hemorrhages to isovolemia following preexpansion of plasma volume evoked significantly greater increase of secretion rate of cortisol than did the first. This result also was not explained by differential hemodynamic effects. The results support the hypothesis that hemorrhage elicits both physiological feedback and facilitatory effects which interact and which are (different) functions of the intensity of stimulus.