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Background: Burn injury, it was hypothesized, may induce changes in resistin expression that contribute to postburn metabolic derangements. This study examined resistin gene expression, serum levels of resistin protein, and glucose levels in burned mice. Methods: Ten male Balb-c mice were anesthetized and then given a 30% total burn surface area using heated probes. Burned and sham-burned mice were killed at 2, 4, 24, and 48 hours. The total ribonucleic acid from gonadal fat tissues was isolated for the measurement of resistin gene expression using real-time reverse transcriptase-polymerase chain reaction. Serum levels of resistin, insulin, and glucose were measured. Statistical analysis was performed by two-way analysis of variance using Bonferroni's test to find differences between groups. All p values less than 0.05 were considered significant. Results: Increases in resistin gene expression and serum resistin levels were detected in the burned animals, and these correlated with relative insulin resistance. Conclusion: The findings suggest a potential role for resistin in the pathophysiology of the metabolic response to injury.

Background: A randomized, prospective, multicenter, double-blind, placebo-controlled, phase II clinical trial was performed to determine whether inhibition of leukocyte adherence by administration of monoclonal antibody directed against intercellular adhesion molecule-1 would improve burn wound healing. Methods: One hundred ten patients with burn injury ranging from 10% to 30% total body surface area were enrolled. Fifty-six patients received placebo (saline) and 54 patients received murine monoclonal antibody to the human intercellular adhesion molecule-1 (enlimomab). Treatment was initiated within 6 hours of injury. Patients had three distinct partial-thickness wound sites assessed. Laser Doppler flowmetry was used to stratify wounds on the day of injury. Wounds were assessed for healing status on day 21 postburn and categorized as healed, non-healed, or grafted. Results: Patients treated with enlimomab had a significantly increased percentage of wounds that healed spontaneously in less than 21 days overall and when stratified by burn wound laser Doppler blood flow readings for those wounds at greatest risk for nonhealing. Conclusion: These results support the concept that leukocyte adherence is involved in the pathogenesis of burn wound necrosis and suggest a therapeutic mechanism for modulating the inflammatory response after the burn injury that may improve wound healing.

The clinical benefit of aeromedical transportation of injured patients in the civilian population has been debated. The purpose of this study was to examine the effects of discontinuing a hospital-based helicopter transport program on trauma patient outcomes, with the hypothesis that the loss of an air ambulance would result in increased transport time and increased mortality among severely injured patients.Data on injury severity and patient outcomes were collected prospectively for the 12 months immediately preceding and 24 months following discontinuation of the helicopter ambulance service. Transport time, mortality rate, and hospital length of stay was compared.The number of trauma patient admissions decreased 12%, with a 17% decrease in admissions of severely injured patients. Transport time decreased, with no change in mortality.Discontinuation of a hospital-based air ambulance service did not increase transport time or increase mortality for trauma patients.

Objective : To determine if the shock-induced alterations in whole blood monocyte tumor necrosis factor (TNF) response are mediated by the CD14 receptor. Design : Prospective controlled animal experiments. Materials and Methods : New Zealand White rabbits (n = 15) were subjected to hemorrhage and resuscitation. Blood samples obtained before shock and 24, 72, and 120 hours after shock were stimulated with lipopolysaccharide in the presence or absence of the anti-CD14 monoclonal antibody, 63D3. Tumor necrosis factor was assayed using L929 cells. Measurements and Main Results : There was no detectable TNF activity in unstimulated blood. The CD14 inhibition resulted in a 55% reduction in baseline TNF activity. After shock, there was a marked increase in TNF activity with lipopolysaccharide stimulation. Addition of 63D3 resulted in a dose-dependent 95% reduction in TNF activity at 24 and 72 hours after shock, (p < 0.05). Conclusion : The enhanced whole blood monocyte TNF response after hemorrhage is CD14 dependent.

Objective : To determine if thermal injury alters the expression of leukocyte adhesion molecules. Design : This is a controlled experimental animal study. Materials and Methods : Partial thickness burns were created on the backs of New Zealand White rabbits. At 30 minutes, 2 hours, 4 hours, and 24 hours after burn, skin was harvested for immunohistochemistry. Monoclonal antibodies were used to study changes in intercellular adhesion molecule 1 (ICAM-1), E-selectin, and leukocyte CDlla. Staining was graded on a scale of 0 to 4. Measurements and Main Results : ICAM-1 was significantly decreased at 24 hours after burn (p < 0.007, Wilcoxon signed rank test). CDlla was increased at 30 minutes (p < 0.02), 2 hours (p < 0.02), and 24 hours (p < 0.006). E-selectin was increased at 2 hours (p < 0.03). Conclusion : Thermal injury alters the expression of leukocyte adhesion molecules.

Leukocyte (WBC) adherence to endothelial cells has been implicated in the pathogenesis of microvascular injury. The process of leukocyte adherence is mediated by both the integrin and selectin families of molecules, and their interaction with specific endothelial ligands. Antibodies directed against the leukocyte integrin CD18 and L-selectin have been developed and functionally inhibit leukocyte adherence in models of inflammatory injury. We asked the question: Does inhibition of leukocyte adherence by administration of monoclonal antibody directed against either CD18, integrins (R15.7, R7.1) or against L-selectin (DREG 200) increase susceptibility to infection? New Zealand white rabbits were shaved and injected subcutaneously on their dorsum with Pseudomonas aeruginosa (ATCC#27853) at two sites each of 10(8) and 10(7) colony forming units. Animals were monitored with daily determination of weight, temperature, WBC counts, hematocrit, and killed at 1 week for determination of abscess formation. There were four blinded experimental groups: (1) Saline (2 mL/kg); (2) DREG 200 (2 mg/kg); (3) R7.1 (2 mg/kg); or (4) R15.7 (2 mg/kg). At the 10(7) and 10(8) injection sites the R15.7 group had an increased rate and size of abscess formation compared with controls. The R7.1 group had an increased rate at the 10(8) injection site. There was no significant difference in the percentage of the abscess formation or mean area between the controls and DREG 200-treated groups. We conclude that giving antibody to CD18 increased susceptibility to infection while giving antibody to L-selectin does not.