Biomedical subjects

J S Fine

Publications and source records attributed to J S Fine.

At least 19 recordsLinked to original sources

PubMed2001

Evaluation of signal transduction pathways in chemoattractant-induced human monocyte chemotaxis.

The intracellular signaling pathways involved in human monocyte chemotaxis toward a variety of chemoattractant molecules were evaluated using selected pharmacological agents. Neither phosphatidylinositol-3-kinase (P13K) or extracellular signal-regulated kinase (ERK) activity were required for monocyte migration toward monocyte chemoattractant protein-1 (MCP-1), RANTES (Regulated on Activation, Normal T cell Expressed and Secreted), macrophage inflammatory protein-1alpha (MIP-1alpha) or formyl-Met-Leu-Phe (fMLP), since pretreatment with wortmannin or LY294002, or with PD098059, had no effect on the chemotactic response. Addition of forskolin and IBMX significantly attenuated chemotaxis to each of these chemoattractants and was reversed by co-treatment with Rp-cAMP, a competitive inhibitor of cAMP-dependent protein kinase A. Incubation with the protein kinase C (PKC) inhibitor GF109203X-HCl (GF109) did not affect monocyte migration, but pretreatment of monocytes with PMA significantly impaired the response to each of these chemotactic agents. Inhibition by PMA was reversed by co-treatment with GF109, implying that heterologous PKC activation is capable of desensitizing chemokine and fMLP-induced monocyte chemotaxis. These results help to define the signalling pathways involved in human monocyte chemotaxis and suggest pharmacological approaches to evaluating the cross-desensitization of chemoattractant-induced leukocyte migration.

1-Methyl-3-isobutylxanthine↗

PubMed2000

Evaluation of chemokine- and phlogistin-mediated leukocyte chemotaxis using an in vivo sponge model.

We have directly compared the in vivo activity of a number of chemokines and phlogistins using a modified murine in vivo sponge model in which gelatin sponges are soaked with chemoattractant and implanted in the peritoneal cavity. Sponges soaked with murine JE/MCP-1 (monocyte chemoattractant protein-1) or zymosan promoted the chemotaxis of specific leukocyte populations in a time-dependent manner, as judged by multiparameter flow cytometry, with granulocytes predominating in zymosan-soaked sponges and granulocytes and macrophages present in JE/MCP-1-soaked sponges. Smaller numbers of B, T and dendritic cells were identified as well. Eotaxin selectively chemoattracted eosinophils in this model, while MIG induced significant T cell migration relative to other chemokines. Cell migration was inhibited by administration of methotrexate, piroxicam or dexamethasone, and JE/MCP-1-mediated trafficking was impaired by treatment with anti-JE antibody or with IL-10, suggesting a role for pro-inflammatory factors in amplifying the JE/MCP-1-induced response. This amplification phase involves the production of the chemokine KC, since anti-KC antibody significantly attenuated JE/MCP-1-induced chemotaxis. These results indicate that intraperitoneally implanted chemoattractant-soaked gelatin sponges are capable of inducing a pronounced inflammatory response characterized by the selective migration of leukocyte populations, and suggest that this model may be useful for delineating the activity of novel inhibitors of leukocyte chemotaxis.

Animals↗

PubMed2000

Iron poisoning.

Explore the source record for details and available documents.

Administration, Oral↗

PubMed1999

Macrophage inflammatory protein-3 beta enhances IL-10 production by activated human peripheral blood monocytes and T cells.

We report that the addition of human macrophage inflammatory protein-3 beta (MIP-3 beta) to cultures of human PBMCs that have been activated with LPS or PHA results in a significant enhancement of IL-10 production. This effect was concentration-dependent, with optimal MIP-3 beta concentrations inducing more than a 5-fold induction of IL-10 from LPS-stimulated PBMCs and a 2- to 3-fold induction of IL-10 from PHA-stimulated PBMCs. In contrast, no significant effect on IL-10 production was observed when 6Ckine, the other reported ligand for human CCR7, or other CC chemokines such as monocyte chemoattractant protein-1, RANTES, MIP-1 alpha, and MIP-1 beta were added to LPS- or PHA-stimulated PBMCs. Similar results were observed using activated purified human peripheral blood monocytes or T cells. Addition of MIP-3 beta to nonactivated PBMCs had no effect on cytokine production. Enhancement of IL-10 production by MIP-3beta correlated with the inhibition of IL-12 p40 and TNF-alpha production by monocytes and with the impairment of IFN-gamma production by T cells, which was reversed by addition of anti-IL-10 Abs to the cultures. The ability of MIP-3 beta to augment IL-10 production correlated with CCR7 mRNA expression and stimulation of intracellular calcium mobilization in both monocytes and T cells. These data indicate that MIP-3 beta acts directly on human monocytes and T cells and suggest that this chemokine is unique among ligands binding to CC receptors due to its ability to modulate inflammatory activity via the enhanced production of the anti-inflammatory cytokine IL-10.

Adjuvants, Immunologic↗

PubMed1999

An inhibitor of CD28-CD80 interactions impairs CD28-mediated costimulation of human CD4 T cells.

We have identified and characterized a microbial extract-derived inhibitor of T cell CD28-dependent costimulation, NP1835-2, utilizing an in vitro system in which anti-human CD3 antibody and a human CD80-Ig fusion protein are immobilized on protein A-coated microspheres. This system is CD28-CD80-dependent, as judged by the specific ability of anti-CD80 antibody or cytotoxic T lymphocyte antigen-4-Ig to block human CD4 T cell responses. Activation of CD4 T cells in this system in presence of NP1835-2 resulted in a concentration-dependent inhibition of T cell proliferation (IC50 of 1-4 microg/ml), surface activation marker expression, and the production of many T cell cytokines, with the exception of TGFbeta. Impairment of T cell activation correlated with a blockade of cell cycle progression at G0/G1 and was only partly restored by addition of 100 U/ml IL-2. No inhibition by NP1835-2 of T cell proliferation stimulated by plate-bound anti-CD3 antibody, phorbol 12-myristate 13-acetate + A23187, or P815 cells expressing the costimulatory molecule CD58 was observed. NP1835-2 was unable to modulate anti-IgM-stimulated B cell proliferation or LPS-induced monocyte activation. Suboptimal concentrations of NP1835-2 and cyclosporin together were able to impair T cell activation in an additive fashion. NP1835-2 was also able to inhibit the primary human MLR. These data indicate that NP1835-2 may belong to a class of molecules capable of selectively impairing CD28-mediated T cell costimulation and suggest its potential usefulness in the treatment of a variety of T cell-dependent diseases. Moreover, NP1835-2 may serve as a useful probe for investigating the mechanisms involved in T cell nonresponsiveness.

Abatacept↗

PubMed1999

Cerebrospinal fluid creatine kinase-BB isoenzyme activity and outcome after subarachnoid hemorrhage.

BACKGROUND: The brain is rich in creatine kinase-BB isoenzyme activity (CK-BB), which is not normally present in cerebrospinal fluid (CSF). Results of previous studies have shown that CK-BB can be detected in the CSF of patients with aneurysmal subarachnoid hemorrhage (SAH), but whether CK-BB levels correlate with patients' neurologic outcomes is unknown. OBJECTIVE: To evaluate the relationship between CSF CK-BB level and outcome after SAH. DESIGN: Prospective observational cohort. SETTING: University-affiliated tertiary care center. PATIENTS: Convenience sample of 30 patients seen for cerebral aneurysm clipping. INTERVENTIONS: We sampled and assayed CSF for CK isoenzymes a median of 3 days after SAH in 27 patients, and at the time of unruptured aneurysm clipping in 3 patients. MAIN OUTCOME MEASURES: Without knowledge of CK results, we assigned the Glasgow Outcome Scale score early (approximately 1 week) and late (approximately 2 months) after surgery. RESULTS: Higher CSF CK-BB levels were associated with higher Hunt and Hess grades at hospital admission (Spearman rank correlation, p = 0.69; P<.001), lower Glasgow Coma Scale scores at hospital admission (p = -0.72; P<.001), and worse early outcomes on the Glasgow Outcome Scale (p = -0.64; P<.001). For patients with a favorable early outcome (Glasgow Outcome Scale score, 3-5), all CK-BB levels were less than 40 U/L. With a cutoff value of 40 U/L, CK-BB had a sensitivity of 70% and a specificity of 100% for predicting unfavorable early outcome (Glasgow Outcome Scale score, 1-2). Having a CK-BB level greater than 40 U/L increased the chance of an unfavorable early outcome, from 33% (previous probability) to 100%, whereas a CK-BB level of 40 U/L or less decreased it to 13%. Similar findings were obtained when considering late outcomes. CONCLUSION: The level of CSF CK-BB may help predict neurologic outcome after SAH.

Adult↗

PubMed1999

A two-year study of microscopic urinalysis competency using the urinalysis-review computer program.

BACKGROUND: The microscopic examination of urine sediment is one of the most commonly performed microscope-based laboratory tests, but despite its widespread use, there has been no detailed study of the competency of medical technologists in performing this test. One reason for this is the lack of an effective competency assessment tool that can be applied uniformly across an institution. METHODS: This study describes the development and implementation of a computer program, Urinalysis-ReviewTM, which periodically tests competency in microscopic urinalysis and then summarizes individual and group test results. In this study, eight Urinalysis-Review exams were administered over 2 years to medical technologists (mean, 58 technologists per exam; range, 44-77) at our academic medical center. The eight exams contained 80 test questions, consisting of 72 structure identification questions and 8 quantification questions. The 72 structure questions required the identification of 134 urine sediment structures consisting of 63 examples of cells, 25 of casts, 18 of normal crystals, 8 of abnormal crystals, and 20 of organisms or artifacts. RESULTS: Overall, the medical technologists correctly identified 84% of cells, 72% of casts, 79% of normal crystals, 65% of abnormal crystals, and 81% of organisms and artifacts, and correctly answered 89% of the quantification questions. The results are probably a slight underestimate of competency because the images were analyzed without the knowledge of urine chemistry results. CONCLUSIONS: The study shows the feasibility of using a computer program for competency assessment in the clinical laboratory. In addition, the study establishes baseline measurements of competency that other laboratories can use for comparison, and which we will use in future studies that measure the effect of continuing education efforts in microscopic urinalysis.

Educational Measurement↗

PubMed1998

Regulation of granulocyte colony-stimulating factor gene expression by interleukin-17.

Interleukin-17 (IL-17) has been previously reported to induce stromal cells to produce a number of hematopoietic and proinflammatory cytokines, including granulocyte colony-stimulating factor (G-CSF). Here, we have evaluated the mechanisms responsible for the augmentation of G-CSF gene expression by IL-17, using the murine 3T3 fibroblast cell line. Treatment of 3T3 cells, but not primary bone marrow-derived macrophages or murine monocyte/macrophage cell lines, resulted in increased steady-state G-CSF mRNA levels within 2-4 h and augmented G-CSF protein production. The combination of IL-17 and LPS enhanced G-CSF expression in an additive fashion. Stability studies revealed that IL-17 stabilized G-CSF mRNA levels, with a t1/2 of 4 h, compared to a t1/2 of less than 2 h in medium or LPS-treated cells. Induction of G-CSF expression in 3T3 cells by IL-17 did not appear to require tyrosine kinase activation or de novo protein synthesis. These studies indicate that post-transcriptional mechanisms play an important role in IL-17-induced G-CSF expression in fibroblasts and suggest that IL-17 may be useful for further delineating mechanisms of G-CSF gene regulation.

3T3 Cells↗

PubMed1998

Teaching the microscopic examination of urine sediment to second year medical students using the Urinalysis-Tutor computer program.

The microscopic examination of urine sediment is a common diagnostic tool taught to medical students, medical technologists, and others. The urine microscopic exam is difficult to teach because supervised instruction and textbook-based teaching suffer from numerous drawbacks. Here, we describe Urinalysis-Tutor, a computer program that uses digitized microscope images and computer-based teaching techniques to systematically teach the urine microscopic exam. In addition, we report the results of a 2-year study that evaluated the effectiveness of the program in 314 second year medical students who were required to use the program. The program contained two, 20-question exams. In the first year of the study (1996), one of the exams was chosen as the pretest and the other as the posttest; the pretest had to be completed before the students viewed the contents of the program, and the posttest was taken after finishing the tutorial. In 1997, the order of the two exams was reversed. In 1996, 159 students completed the study. The mean pretest score was 34% (SD, 14%), the mean posttest score was 71% (SD, 13%), and the improvement was significant (P <0.001, paired t-test). In 1997, 155 students participated. The mean pretest score was 41% (SD, 11%), the mean posttest score was 71% (SD, 13%), and the improvement was significant (P <0.001, paired t-test). The study shows that Urinalysis-Tutor helps medical students learn to interpret the microscopic appearance of urine sediment and that it is feasible to implement this tutorial in a medical school class.

Computer-Assisted Instruction↗

PubMed1997

A specific stimulator of granulocyte colony-stimulating factor accelerates recovery from cyclophosphamide-induced neutropenia in the mouse.

We have identified a small molecular weight compound, SCH 14988, which specifically stimulates in vitro granulocyte-colony stimulating factor (G-CSF) production from activated human peripheral blood mononuclear cells and monocytes but not other cytokines or CSFs with hematoregulatory activity. In vivo administration of SCH 14988 to mice rendered neutropenic by cyclophosphamide treatment resulted in the accelerated recovery of the peripheral neutrophil compartment. This activity correlated with increased in vivo G-CSF levels and stimulation of marrow granulopoiesis, and was comparable to that of exogenously administered recombinant human G-CSF. No alterations to other leukocyte populations in peripheral blood, spleen, or the peritoneal cavity were observed. These findings suggest that SCH 14988 may be clinically useful to enhance neutrophil granulopoiesis, as well as to study the mechanisms involved in G-CSF gene regulation.

Animals↗

PubMed1997

Escalator-related injuries in children.

OBJECTIVE: Escalator-related trauma is uncommon but can cause significant injury. This study reviewed escalator-related injuries in children to determine risk factors, types of injuries, medical interventions, and long-term outcomes. DESIGN AND SETTING: Retrospective clinical patient series, Municipal Hospital Pediatric Emergency Service. Participants. All children less than 18 years of age who presented to the Pediatric Emergency Service with an escalator-related injury from August 1990 through February 1995. METHODS: We reviewed the chart and interviewed the parent of each child by telephone. We collected the following information: age, gender, child's supervision and activity while on the escalator, escalator location, direction of motion, presence of escalator defects, nature and extent of injury, medical interventions, and outcome. RESULTS: Twenty-six children had escalator-related injuries. The average age was 6 years (range, 2-16). Thirteen children (50%) were 2 to 4 years old. There were 15 (57%) boys. Eighteen children (69%) were accompanied by an adult. All children 7 years and younger were accompanied by an adult; however, 50% were not holding the hand of their guardian. Eight children (31%) were injured while riding improperly, ie, walking, running, playing, or sitting on the escalator, and among these, all who were standing fell down before the injury. Six (23%) children were injured while stepping off the escalator. Of 9 children less than 4 years old, 7 (78%) were riding the escalator properly. Of 9 children 4 years or older, only 3 (33%) were riding properly. Circumstances of injury included falling down with subsequent blunt trauma, falling down with subsequent entrapment of an extremity, and entrapment of an extremity not related to falling down. Locations of entrapment were between two steps, between a step and the side-rail, and between the last step and the comb plate. Twenty-one (81%) injuries occurred in rail or subway stations. Eight escalators were reported to have functional or structural problems. Seventeen (65%) children sustained lower extremity injuries and 8 (31%) sustained upper extremity injuries. Injuries included lacerations, avulsions and degloving injuries of the extremities, tendon and nerve lacerations, and digit fractures and amputations. Thirteen (50%) children were admitted to the hospital for operative management; the average length of hospitalization was 13 days (range 1-29). Four children (15%) suffered significant functional loss, and 12 (46%) sustained permanent cosmetic deformities. CONCLUSION: Children are at risk for sustaining severe injuries on escalators. Young age, inadequate adult supervision, improper activity while riding on the escalator, and escalator-related mechanical problems all increase the risk of injury. Public and parent education directed toward escalator safety issues may help to reduce escalator-related injuries in children.

Accidents↗

PubMed1995

Interleukin 4 retards dissemination of a human B-cell lymphoma in severe combined immunodeficient mice.

We have examined the antitumor activity of murine interleukin 4 (IL-4) on development of a human B-cell lymphoma (Daudi) in severe combined immunodeficient (SCID) mice. The progression of Daudi cells in SCID mice was followed by histological staining and by flow cytometric analysis of CD20+ cells in spleen, liver, bone marrow, and kidneys. By day 35, CD20+ Daudi cells populate the majority of space in the bone marrow and kidney in vehicle-treated mice. Mice receiving i.p. injections of IL-4, commencing 7 or 14 days after tumor inoculation, exhibit a reduction in tumor burden as well as a decrease in CD20+ cells in both compartments. The antitumor activity of IL-4 does not appear to be due to an antiproliferative effect, since the cytokine does not alter the growth of Daudi cells in vitro, nor does it correlate with any marked cellular infiltrate in tumor-bearing tissues. In 51Cr-release assays, we observed that splenocytes from IL-4-treated mice were capable of lysing YAC-1 but not Daudi cell targets. Our findings demonstrate that: (a) systemic administration of IL-4 retards dissemination of a human B-cell lymphoma in SCID mice; and (b) antitumor activity elicited by IL-4 may not involve a direct effect on proliferation of Daudi cells or on the induction of cytolytic activity.

Animals↗

PubMed1995

D-phenylalanyl-L-prolyl-L-arginine chloromethyl ketone (PPACK): alternative anticoagulant to heparin salts for blood gas and electrolyte specimens.

D-Phenylalanyl-L-prolyl-L-arginine chloromethyl ketone (PPACK), a selective thrombin inhibitor, was evaluated as an alternative anticoagulant to lithium heparin (LiHep) for blood gas and whole-blood electrolyte analyses. Initial studies in serum revealed a negative proportional bias for ionized calcium (iCa) concentration measured in the range of increasing concentrations of LiHep (-0.02 mmol/L iCa per 33 kIU/L), whereas no bias in iCa concentration was detected with increasing concentrations of PPACK. No anticoagulant-dependent changes in serum sodium, potassium, chloride, glucose, lactate, ionized magnesium, or pH were detected with either PPACK or LiHep. Similarly, no bias was observed in the measurement of whole-blood PO2, PCO2, pH, or sodium or potassium concentrations with either anticoagulant. Whole blood anticoagulated with LiHep (33 kIU/L) demonstrated a consistent -0.06 +/- 0.01 mmol/L bias for iCa compared with a nonanticoagulated whole-blood control. In comparison, no iCa bias was observed with PPACK-anticoagulated whole blood. We conclude that PPACK has ideal bias-free properties as an anticoagulant in analyses for blood gases, electrolytes, and iCa.

Amino Acid Chloromethyl Ketones↗

PubMed1995

BibleCard: network-based virtual database for laboratory information.

The clinical laboratory's use of computers has evolved beyond the single minicomputer stand-alone system. Our laboratory information system is now part of an institutional network. The laboratory also uses smaller systems and workstations for a wide variety of functions, often with much data duplication among systems. We have been developing a network-based virtual database for laboratory test information. This system uses World Wide Web standards for hypertext and multimedia displays, which allows for the display of information retrieved from various department computer sources without the necessity of data duplication, modification of existing systems, or centralization of data. The medical technologists can continue to write testing procedures on their word processors. Maintenance of reference values, specimen requirements, etc., can continue as a laboratory information system function. Yet information from all of these disparate sources can be viewed in a consolidated format that has platform independence.

Chemistry, Clinical↗

PubMed1994

Interleukin-10 enhances gamma delta T cell development in the murine fetal thymus.

We have investigated the ability of interleukin-10 (IL-10) to modulate murine intrathymic T cell differentiation using a fetal thymic organ culture (FTOC) model. Addition of as little as 11 ng of recombinant murine IL-10 (mIL-10) per day produced a significant increase in the proportion and number of gamma delta-TCR+ cells in 4-day cultures derived from Gestational Day 14 mice, compared to vehicle-treated cultures. This effect occurred in the absence of any changes in other parameters of intrathymic T cell development. The increase in the gamma delta-TCR population included an enlargement of the V gamma 2+, V gamma 3+, and V delta 4+ populations. The enhancement of gamma delta cell development was not observed in 2- or 7-day cultures, indicating the time dependence of this response. Overall, these results reveal that IL-10 treatment of FTOC can affect murine gamma delta T cell development and suggest that this cytokine may mediate specific events in the generation of the gamma delta T cell repertoire.

Animals↗

PubMed1994

Influence of IL-10 on murine CFU-pre-B formation.

We have examined the ability of interleukin-10 (IL-10) to influence murine B cell development in vitro and in vivo. In vitro treatment of young adult mouse bone marrow cells with 0.5 to 10 ng/ml human IL-10 (hIL-10) produced a significant enhancement of IL-7-mediated colony-forming unit-pre-B (CFU-pre-B) formation, while IL-10 concentrations > 10 ng/ml had no net effect. IL-10 by itself was unable to stimulate pre-B cell colony formation, even at optimal concentrations. The increase in CFU-pre-B produced by IL-10 was specifically blocked by anti-hIL-10 antibody, but not by anti-stem cell factor (SCF) antibody, and was observed with both unfractionated and purified B220+ surface immunoglobulin (sIg-) bone marrow cells. CFU-pre-B from the IL-10 treatment group contained a higher percentage of CD43+B220+ blast-like cells than colonies exposed to IL-7 only. In vivo administration of 0.1 microgram hIL-10 per day to mice treated with a single sublethal dose of cyclophosphamide (CY) resulted in a dramatic and accelerated recovery of CFU-pre-B numbers as compared to vehicle-administered mice. This enhancement was seen as early as day 11 post-CY, and the number of CFU-pre-B was comparable to normal age-matched control mice by day 16. In contrast, the number of CFU-pre-B in vehicle-treated mice remained significantly lower than age-matched and IL-10-treated animals as long as day 22 post-CY. No differences in the number of pre-B and mature B cells in bone marrow or in the number of mature B cells in peripheral lymphoid organs were detected in IL-10-treated mice. Myeloid cell recovery, assessed by the CFU-granulocyte/macrophage (CFU-GM) assay and the number of marrow Mac-1+ cells, was unaffected by IL-10 treatment of CY-dosed animals. These results indicate that IL-10 enhanced IL-7-stimulated murine pre-B cell colony formation and imply a role for IL-10 in normal B lymphopoiesis.

Animals↗

PubMed1993

Effects of media, atmosphere, and incubation time on colonial morphology of Arcanobacterium haemolyticum.

Arcanobacterium haemolyticum causes pharyngitis as well as skin and other wound infections. Although it is a beta-hemolytic organism, the hemolysis is less well defined than that of beta-hemolytic streptococci and may be overlooked in cultures with heavy growth of commensal throat flora. To determine whether routine throat culture conditions are sufficient to produce recognizable colonies of A. haemolyticum, the morphology of six distinct strains was studied after various combinations of incubation time, medium, and atmosphere. The agar media, containing 5% sheep blood, were Trypticase soy agar, Columbia agar, and heart infusion agar. Cultures were incubated in ambient air, 6 to 8% CO2, or an anaerobic atmosphere. Cultures were compared after 24, 48, and 72 h of incubation for colony size, clarity and size of hemolytic zone, and macroscopic evidence of agar pitting. A minimum of 48 h was needed for expression of beta-hemolysis and pitting. Trypticase soy agar was the superior medium and CO2 was the superior atmosphere for beta-hemolysis. Agar pitting was not significantly affected by variations in medium or atmosphere. Strains differed in their expression of hemolysis and production of pits at 48 h. After 72 h of incubation, beta-hemolysis and pitting were visible in over 96% of culture observations.

Atmosphere↗

PubMed1993

The Avianca plane crash: an emergency medical system's response to pediatric survivors of the disaster.

OBJECTIVE: On January 25, 1990, a jetliner crashed on Long Island, New York. Twenty-two children survived the crash. The purpose of this study was to evaluate the emergency medical system's response to these pediatric survivors. METHODS: A questionnaire was sent to all local, acute care hospitals to determine their specific pediatric capabilities and to rank them as level I, II, or III pediatric centers; level I centers are tertiary care facilities. A second questionnaire was sent to all hospitals that received pediatric survivors to collect specific clinical information for each patient. Based on this clinical information a Pediatric Trauma Score (PTS) was assigned to each patient. Children with a PTS < or = 8 are considered to be at increased risk of trauma-related mortality. The assigned PTS was compared to the level of the pediatric center to which each patient was transported. RESULTS: Of 25 children on board the plane, 22 (88%) survived the crash; of 135 adults on board, 70 (52%) survived (chi 2 = 9.9, P = .002). Seven children had a PTs < or = 8; only 1 of these high-risk patients was transported directly to a level I pediatric center, and only 2 of the 5 high-risk children initially transported to level III facilities were transferred to higher level pediatric centers. CONCLUSIONS: Pediatric survivors were neither adequately triaged nor transported to appropriate facilities which could optimize their care. Possible explanations for this include: (1) unique features of the rescue operation, (2) limited pediatric training of prehospital personnel, and (3) deficiencies of the regional disaster plan. Emergency medical services systems and disaster plans can be made more responsive to children's needs by: (1) acknowledging that children have special needs requiring referral, (2) improving the training of prehospital personnel in pediatric emergency care, (3) classifying ill and injured children according to appropriate triage criteria, (4) recognizing existing tertiary care pediatric centers as the optimal location for the treatment of critically ill and injured children, and (5) designating these centers as the appropriate transport destination for critically ill and injured children.

Accidents, Aviation↗