Pediatric emergency care capabilities of Indian Health Service emergency medical service agencies serving American Indians/Alaska Natives in rural and frontier areas.

INTRODUCTION: In the USA, the emergency medical services (EMS) system is vital for American Indians and Alaska Natives, who are disproportionately burdened by injuries and diseases and often live in rural areas geographically far from hospitals. In rural areas, where significant health disparities exist, EMS is often a primary source of healthcare providing a safety net for uninsured individuals or families who otherwise lack access to health-related services. EMS is frequently the first entry point for children and their families into the healthcare system. The Indian Health Service (IHS) supports the federally funded, tribally operated EMS agencies to help meet the affiliated American Indian and Alaska Natives' pre-hospital needs. While periodic assessments of state EMS agencies capabilities to care for children occur, it appears a systematic assessment of IHS EMS agencies in regards to children had not been previously conducted. METHODS: A consensus process, involving stakeholders, was used to identify topic areas for a survey for assessing the pediatric capabilities of IHS EMS. The survey was sent to 75 of 88 IHS EMS agency contacts. RESULTS: Sixty-one agencies (81%) responded. Nine agencies (15%) did not have a medical director. Agencies without a medical director were less likely to report the availability of online (p=0.1) or offline (p<0.01) pediatric medical direction. Half (51%) of the agencies had a mass casualties plan; however, 29% reported responding to a mass casualty incident, involving a large number of pediatric patients, that overwhelmed their service. Most agencies were well integrated with their state EMS system with almost all (95%) collecting EMS patient care data and 47% using national standard data elements. CONCLUSIONS: In some areas, IHS EMS agencies did not have the infrastructure to treat pediatric patients during day-to-day operations as well as disasters. Similar to operational challenges faced by rural EMS agencies, the IHS agencies lacked a medical director, were unable to provide pediatric continuing education, and were overwhelmed during mass casualty incidents. Moreover, the overall ratio of IHS EMS to service population is almost double that for other EMS agencies. In other areas, agencies were well integrated with their state EMS system. One possible solution to increase capabilities to care for pediatric patients is combining and sharing of common resources including medical directors with their state EMS systems and authorities.

Risk factors associated with non-fatal adolescent firearm injuries.

STUDY OBJECTIVES: To identify behavioral, environmental, and sociodemographic risk factors associated with non-fatal firearm injuries among inner city adolescents in the United States. DESIGN: A case-control study in which patients with firearm injury serve as cases and those with medical conditions serve as controls. SETTING: A level I trauma center in a metropolitan area serving a predominately lower socioeconomic status population. PARTICIPANTS: Cases were 45 consecutive patients 11-18 years presenting to the emergency department with non-fatal firearm injury; controls were 50 age and gender matched patients presenting with acute medical problems. OUTCOME MEASURE: Odds ratios (OR) and associated 95% confidence interval (CI) as estimates of the magnitude of association between risk factors and non-fatal firearm injury. RESULTS: After adjusting for age, gender and socioeconomic status, multivariate analysis identified four risk factors independently associated with firearm injury: living with less than two parents (OR 3.8, 95% CI 1.2 to 12.2), skipping class (OR 7.1, 95% CI 1.7 to 28.9), previous arrest (OR 6.2, 95% CI 1.9 to 20.7), and being African-American (OR 4.2; 95%CI 1.4 to 14.9). CONCLUSION: Risk factors for adolescents sustaining a non-fatal firearm injury are sociodemographic and environmental, not just behavioral. Thus interventions that foster protective and supportive environments may help prevent firearm injuries.

Effect of gastric mucosal injury on ornithine decarboxylase in young and aged rats.

The present investigation examines the changes in ornithine decarboxylase (ODC) activity, level of the enzyme, and the expression of its gene in gastric mucosa of young (4-month) and aged (24-month) Fischer-344 male rats 6 h after intragastric administration of either 2 M NaCl (1 ml/130 g b.w.) or an equivalent volume of water (controls). In addition, electronmicroscopy was performed to evaluate the ultrastructural changes in the gastric mucosa. Although administration of 2 M NaCl virtually eliminated the surface epithelium in both young and aged rats, the extent to injury in older animals extended beyond the surface epithelium. In aged rats, epithelial cells in the deeper parts of the gastric glands demonstrated severe swelling with vacuolization and disintegration of the cell organelles, with dying and dead cells. Basal gastric mucosal ODC activity (data from the controls) in aged rats was found to be 118% (p less than 0.001) above the young animals. This was also associated with similar increases in the concentration of ODC (as determined by Western-blot analysis) and a steady-state rise in ODC mRNA. Intragastric administration of 2 M NaCl (which caused gastric mucosal injury) resulted in a 625% increase in mucosal ODC activity in young rats, but in aged rats it produced a 112% increase when compared with the corresponding controls. In young rats, the increase in gastric mucosal ODC activity after injury was also associated with about a 2-fold rise in the enzyme protein concentration and a 4-fold increase in steady-state ODC mRNA levels. In contrast, gastric mucosal injury in aged rats, which resulted in a 112% increase in ODC activity, produced about a 30% reduction in the concentration of ODC and a 15-20% reduction in steady-state mRNA levels, when compared with the respective controls. The current data demonstrate that aging is associated with decreased responsiveness of gastric mucosal ODC to injury which may in part be responsible for diminished regenerative capacity of the gastric mucosa in aged animals. Furthermore, in aged rats the injury-induced stimulation of mucosal ODC activity is not associated with increased activation of its gene.

Gastric mucosal tyrosine kinase activity during aging and its relationship to cell proliferation in rats.

The relationship between tyrosine kinase activity and cellular proliferative activity was investigated in the gastric mucosa. For the purpose of comparison, the liver and the pancreas were also included. Groups of 2-, 14- and 22-month-old male Fischer-344 rats were used. Tyrosine kinase activity was determined in the membrane fraction (30,000 x g pellet) utilizing a synthetic polymer, Glu-Tyr (4:1), as substrate. Cellular proliferative activity was assessed by measuring ornithine decarboxylase in the 20,000 x g supernatant. In all age groups, gastric mucosal tyrosine kinase activity was found to be 10-20-fold higher than in the liver or pancreas. In addition, gastric mucosal tyrosine kinase activity in 22-month-old rats was 35-70% higher than in their 2- and 14-month-old counterparts. Gastric mucosal ornithine decarboxylase activity also followed essentially the same pattern as that of tyrosine kinase in that the highest activity was observed in 22-month-old rats. Increased gastric mucosal proliferative activity in 22-month-old rats was also associated with increased tyrosine-phosphorylation of a mucosal membrane protein with an apparent Mr of 53,000. An opposite phenomenon occurred in the pancreas whose proliferative activity was found to be the lowest. It is concluded that the age-associated changes in gastric mucosal proliferative activity are accompanied by parallel alterations in tyrosine kinase activity. Tyrosine-phosphorylation of a 53 kDa membrane protein may play a role in the regulation of cell proliferation.

Gastrin: levels and trophic action during advancing age.

Changes in antral and serum gastrin levels as well as gastrin (G) and somatostatin (D) cell density were examined in 4- to 16-mo-old Fischer-344 rats. In these rats, the responsiveness of the gastric mucosa to the trophic action of gastrin was also examined. It was observed that whereas serum gastrin levels declined steadily between 4 and 16 mo of age, antral gastrin levels rose sharply during this period. In the antrum of 16-mo-old rats, the density of G-cells, but not D-cells, was found to be lower than in their 4-mo-old counterparts. Thus, when D- to G-cell ratios were calculated, 16-mo-old rats revealed a 50% higher D- to G-cell ratio than the 4-mo-old animals. To assess the trophic action of gastrin, groups of 4-, 8-, and 16-mo-old rats were infused subcutaneously (osmotic minipump) with either saline or gastrin (G-17-I; 250 ng.kg-1.h-1) for 14 days. The gastric mucosa was assayed for thymidine kinase (an indicator of proliferative activity) and DNA and protein content. In the saline-infused rats, gastric mucosal thymidine kinase activity increased sharply between 4 and 16 mo of age without significantly affecting DNA or protein content (expressed as milligrams per 100 g of body weight), suggesting that the age-associated rise in proliferative activity is not accompanied by increased mucosal growth.(ABSTRACT TRUNCATED AT 250 WORDS)

Gastric secretion during aging in pyloric-ligated rats and effects of pentagastrin.

Changes in basal- and pentagastrin-stimulated gastric acid, pepsin secretion as well as gastric mucosal histidine decarboxylase activity were examined in 4- to 21-month-old pyloric ligated Fischer-344 rats. In addition, serum gastrin levels, gastric mucosal DNA, and RNA content were determined in these rats. The results revealed that whereas acid secretion decreased progressively with age, pepsin output increased between 4 and 14 months of age and then decreased sharply. Serum gastrin levels decreased progressively with age, and 3 h of pyloric obstruction produced no apparent change in serum gastrin levels in any of the age groups. Gastric mucosal weight, DNA, and RNA content in 4-month-old rats were not significantly different from those of 14-month-old animals. However, in 21-month-old rats, each of these values were found to be significantly lower than in their 4- or 14-month-old counterparts. A single injection of pentagastrin (250 micrograms/kg) significantly stimulated acid and pepsin secretion (45-52%) in 4-month-old rats, but not in 14- and 21-month-old animals, when compared with the corresponding saline-injected controls. Gastric mucosal histidine decarboxylase activity increased steadily between 4 and 21 months of age. Pentagastrin caused a significant 78% stimulation in histidine decarboxylase activity in 4-month-old rats, but had no effect on the enzyme activity in 14-month-old animals, when compared with the corresponding saline-injected controls. However, in 21-month-old rats, pentagastrin inhibited histidine decarboxylase activity by 55% when compared with the saline-injected controls. It is concluded that a) aging decreases capacity of the gastric mucosa to secrete acid and pepsin, b) in aged rats, decreased acid and pepsin output could in part be attributed to mucosal atrophy; c) responsiveness of the gastric mucosa to pentagastrin decreases with age; and d) in aged animals, gastric acid secretion is not regulated by histamine.

Gastrin induction of protein synthesis in isolated gastric mucosal cells.

Exposure of isolated rat gastric mucosal cells to 10(-10) and 10(-9) M gastrin (G-17-I) for 2 hr significantly stimulated [3H]leucine incorporation (15 min pulse) into protein by 100 and 212%, respectively, when compared with the basal levels. Doses beyond 10(-9) M lowered the maximal stimulatory effect of the hormone. Gastrin (10(-9) M) specifically stimulated the synthesis of five proteins in isolated gastric mucosal cells with apparent molecular weights of 105, 76, 71, 63, and 54 kDa. Actinomycin-D (10 micrograms/ml) completely abolished the gastrin-mediated stimulation of protein synthesis in isolated gastric mucosal cells.