System and method for determining triage categories

Embodiments disclosed herein provide a system, method, and computer program product for providing a triage clas- sification system. The triage classification system uses a computer model that is developed using historical patient data. The developed computer modelis applied to collected patientattributedatafromapatientinapre-hospitalsetting to generate a triage category. Based on the generated triage category, health care professionals can take desired actions, suchastransportingthepatienttoafacilitymatchingthe generated triage category.Board of Regents, University of Texas Syste

A Review of Blood Substitutes: Examining The History, Clinical Trial Results, and Ethics of Hemoglobin-Based Oxygen Carriers

The complications associated with acquiring and storing whole blood for transfusions have launched substantial efforts to develop a blood substitute. The history of these efforts involves a complicated mixture of science, ethics, and business. This review focuses on clinical trials of the three hemoglobin-based oxygen carriers (HBOC) that have progressed to Phase II or III clinical trials: He-mAssist (Baxter; Deerfield, IL, US), PolyHeme (Northfield; Evanston, IL, US), and Hemopure (Biopure; Cambridge, MA, US). Published animal studies and clinical trials carried out in a perioperative setting have demonstrated that these products successfully transport and deliver oxygen, but all may induce hypertension and lead to unexpectedly low cardiac outputs. Overall, these studies suggest that HBOCs resulted in only modest blood saving during and after surgery, no improvement in mortality and an increased incidence of adverse reactions. To date, the results from these perioperative studies have not led to regulatory approval. All three companies instead chose to focus their efforts on large trials of trauma patients in the pre-hospital setting

PKA and ERK, but not PKC, in the amygdala contribute to pain-related synaptic plasticity and behavior

The laterocapsular division of the central nucleus of the amygdala (CeLC) has emerged as an important site of pain-related plasticity and pain modulation. Glutamate and neuropeptide receptors in the CeLC contribute to synaptic and behavioral changes in the arthritis pain model, but the intracellular signaling pathways remain to be determined. This study addressed the role of PKA, PKC, and ERK in the CeLC. Adult male Sprague-Dawley rats were used in all experiments. Whole-cell patch-clamp recordings of CeLC neurons were made in brain slices from normal rats and from rats with a kaolin/carrageenan-induced monoarthritis in the knee (6 h postinduction). Membrane-permeable inhibitors of PKA (KT5720, 1 μM; cAMPS-Rp, 10 μM) and ERK (U0126, 1 μM) activation inhibited synaptic plasticity in slices from arthritic rats but had no effect on normal transmission in control slices. A PKC inhibitor (GF109203x, 1 μM) and an inactive structural analogue of U0126 (U0124, 1 μM) had no effect. The NMDA receptor-mediated synaptic component was inhibited by KT5720 or U0126; their combined application had additive effects. U0126 did not inhibit synaptic facilitation by forskolin-induced PKA-activation. Administration of KT5720 (100 μM, concentration in microdialysis probe) or U0126 (100 μM) into the CeLC, but not striatum (placement control), inhibited audible and ultrasonic vocalizations and spinal reflexes of arthritic rats but had no effect in normal animals. GF109203x (100 μM) and U0124 (100 μM) did not affect pain behavior. The data suggest that in the amygdala PKA and ERK, but not PKC, contribute to pain-related synaptic facilitation and behavior by increasing NMDA receptor function through independent signaling pathways

PKA and ERK, but not PKC, in the amygdala contribute to pain-related synaptic plasticity and behavior-9

Ent levels posterior to bregma (-1.88 mm and -2.12 mm). Symbols show the positions of the tips of the microdialysis probe (length of exposed membrane = 1 mm) in the CeLC () and striatum (, placement control) in the behavioral experiments. () Application sites of KT5720, n = 11. () U0126, n = 12, filled circles; U0124, n = 3, open circles. () GF109203X, n = 9. () KT5720, n = 4, filled circles; U0126, n = 4, open circles. CeM, CeL, CeLC: medial, lateral and laterocapsular divisions of the central nucleus of the amygdala. Calibration bar (1 mm) applies to each diagram in A-D.<p><b>Copyright information:</b></p><p>Taken from "PKA and ERK, but not PKC, in the amygdala contribute to pain-related synaptic plasticity and behavior"</p><p>http://www.molecularpain.com/content/4/1/26</p><p>Molecular Pain 2008;4():26-26.</p><p>Published online 16 Jul 2008</p><p>PMCID:PMC2490682.</p><p></p

PKA and ERK, but not PKC, in the amygdala contribute to pain-related synaptic plasticity and behavior-3

μM) isolated NMDA receptor-mediated synaptic component in slices from arthritic rats (P < 0.001, repeated-measures ANOVA with Bonferroni post-tests). Co-application of KT5720 and U0126 (1 μM, n = 3) further decreased the synaptic response (P < 0.001, Bonferroni post-tests). U0126 (1 μM, 15 min) applied alone (n = 3) or together with KT5720 (n = 3) inhibited the NMDA component in the arthritis pain model (P < 0.05–0.001, Bonferroni post-tests). Coapplication of KT5720 and U0126 (n = 6) had a significantly greater effect than each compound alone (P < 0.05–0.01, one-way ANOVA with Bonferroni post-tests). A negative structural analogue of U0126 (U0124, 1 μM, n = 3) had no effect. Bar histograms show averaged EPSC amplitudes (mean ± SE) normalized to predrug control values (set to 100%). Monosynaptic EPSCs (average of 8–10 traces) recorded at -60 mV and +20 mV. Time course of drug effects at -60 mV and +20 mV. Each symbol shows averaged EPSC amplitudes (mean ± SE) normalized to predrug control (set to 100%). * P < 0.05, ** P < 0.01, *** P < 0.001 (compared to predrug values); + P < 0.05, ++ P < 0.01 (compared to each drug alone).<p><b>Copyright information:</b></p><p>Taken from "PKA and ERK, but not PKC, in the amygdala contribute to pain-related synaptic plasticity and behavior"</p><p>http://www.molecularpain.com/content/4/1/26</p><p>Molecular Pain 2008;4():26-26.</p><p>Published online 16 Jul 2008</p><p>PMCID:PMC2490682.</p><p></p

PKA and ERK, but not PKC, in the amygdala contribute to pain-related synaptic plasticity and behavior-6

Ficant effect on audible () and ultrasonic () vocalizations and on hindlimb withdrawal reflexes () in normal animals ("normal"; n = 5). In arthritic animals ("arthritis" in ; n = 6) KT5720 significantly inhibited vocalizations and increased mechanical thresholds. In the arthritis group, behaviors were measured before (baseline) and 6 h after arthritis induction and during (15 min) and after (30 min washout) drug application. () Administration of KT5720 (100 μM) into the striatum as placement control had no effect on audible and ultrasonic vocalizations and on spinal reflexes of arthritic rats (n = 4). Vocalizations were evoked by brief (15 s) noxious (2000 g/30 mm) stimulation of the knee with a calibrated forceps. Duration of vocalizations was measured as the arithmetic sum of the duration of each individual vocalization event during a 1 min period beginning with the onset of the stimulus (see Methods for details). Bar histograms and error bars show mean ± SE. * P < 0.05, ** P < 0.01, *** P < 0.001 (repeated-measures ANOVA with Bonferroni post-tests).<p><b>Copyright information:</b></p><p>Taken from "PKA and ERK, but not PKC, in the amygdala contribute to pain-related synaptic plasticity and behavior"</p><p>http://www.molecularpain.com/content/4/1/26</p><p>Molecular Pain 2008;4():26-26.</p><p>Published online 16 Jul 2008</p><p>PMCID:PMC2490682.</p><p></p

Addition of aspirin to venous thromboembolism chemoprophylaxis safely decreases venous thromboembolism rates in trauma patients

Background Trauma patients exhibit a multifactorial hypercoagulable state and have increased risk of venous thromboembolism (VTE). Despite early and aggressive chemoprophylaxis (CP) with various heparin compounds (“standard” CP; sCP), VTE rates remain high. In high-quality studies, aspirin has been shown to decrease VTE in postoperative elective surgical and orthopedic trauma patients. We hypothesized that inhibiting platelet function with aspirin as an adjunct to sCP would reduce the risk of VTE in trauma patients.Methods We performed a retrospective observational study of prospectively collected data from all adult patients admitted to an American College of Surgeons Level I Trauma center from January 2012 to June 2015 to evaluate the addition of aspirin (sCP+A) to sCP regimens for VTE mitigation. Cox proportional hazard models were used to assess the potential benefit of adjunctive aspirin for symptomatic VTE incidence.Results 10,532 patients, median age 44 (IQR 28 to 62), 68% male, 89% blunt mechanism of injury, with a median Injury Severity Score (ISS) of 12 (IQR 9 to 19), were included in the study. 8646 (82%) of patients received only sCP, whereas 1886 (18%) patients received sCP+A. The sCP+A cohort displayed a higher median ISS compared with sCP (13 vs 11; p&lt;0.01). The overall median time of sCP initiation was hospital day 1 (IQR 0.8 to 2) and the median day for aspirin initiation was hospital day 3 (IQR 1 to 6) for the sCP+A cohort. 353 patients (3.4%) developed symptomatic VTE. Aspirin administration was independently associated with a decreased relative hazard of VTE (HR 0.57; 95% CI 0.36 to 0.88; p=0.01). There were no increased bleeding or wound complications associated with sCP+A (point estimate 1.23, 95% CI 0.68 to 2.2, p=0.50).Conclusion In this large trauma cohort, adjunctive aspirin was independently associated with a significant reduction in VTE and may represent a potential strategy to safely mitigate VTE risk in trauma patients. Further prospective studies evaluating the addition of aspirin to heparinoid-based VTE chemoprophylaxis regimens should be sought.Level of evidence Level III/therapeutic

PKA and ERK, but not PKC, in the amygdala contribute to pain-related synaptic plasticity and behavior-0

Itic (6 h postinduction; ) rats. KT5720 (1 μM, 15 min) inhibited synaptic transmission in neurons from arthritic rats 6 h postinduction (, n = 7; P < 0.05, paired t-test) but not in control neurons from normal rats (, n = 7). () Original recordings of EPSCs (average of 8–10 EPSCs) evoked at the two synapses. () Averaged EPSC amplitudes (mean ± SE) in the presence of KT5720 normalized to predrug (ACSF) control values (set to 100%). () Time course of the inhibitory effect of direct intracellular application of KT5720 (1 μM) through the patch pipette. Each symbol shows averaged EPSC amplitudes (mean ± SE; n = 4) at different times after whole-cell configuration was obtained (t = 0). The inhibitory effect was significant (P < 0.001, compared to the first EPSC after patch formation; Dunnett's Multiple Comparison Test). Insets show EPSCs (average of 8–10 trials) evoked at the PB-CeLC synapse at 1 min (predrug) and at 15 min (KT5720) after patch formation. Whole-cell voltage-clamp recordings were made at -60 mV. * P < 0.05, *** P < 0.001.<p><b>Copyright information:</b></p><p>Taken from "PKA and ERK, but not PKC, in the amygdala contribute to pain-related synaptic plasticity and behavior"</p><p>http://www.molecularpain.com/content/4/1/26</p><p>Molecular Pain 2008;4():26-26.</p><p>Published online 16 Jul 2008</p><p>PMCID:PMC2490682.</p><p></p

PKA and ERK, but not PKC, in the amygdala contribute to pain-related synaptic plasticity and behavior-5

Itic (6 h postinduction; ) rats. GF109203X (1 μM, 15 min) had no significant effect (P > 0.05, paired t-test) in neurons from arthritic rats (n = 6) and in control neurons from normal rats (n = 5). () Original recordings of EPSCs evoked at the two synapses (average of 8–10 EPSCs). () Averaged EPSC amplitudes (mean ± SE) in the presence of GF109203X normalized to predrug control values (set to 100%).<p><b>Copyright information:</b></p><p>Taken from "PKA and ERK, but not PKC, in the amygdala contribute to pain-related synaptic plasticity and behavior"</p><p>http://www.molecularpain.com/content/4/1/26</p><p>Molecular Pain 2008;4():26-26.</p><p>Published online 16 Jul 2008</p><p>PMCID:PMC2490682.</p><p></p

PKA and ERK, but not PKC, in the amygdala contribute to pain-related synaptic plasticity and behavior-2

Itic (6 h postinduction; ) rats. U0126 (1 μM, 15 min) inhibited synaptic transmission in neurons from arthritic rats 6 h postinduction (, n = 6; P < 0.05, paired t-test) but not in control neurons (, n = 6). () Original recordings of EPSCs (average of 8–10 trials) evoked at the two synapses. () Averaged EPSC amplitudes (mean ± SE) in the presence of U0126 normalized to predrug control values (set to 100%). Whole-cell voltage-clamp recordings were made at -60 mV. * P < 0.05.<p><b>Copyright information:</b></p><p>Taken from "PKA and ERK, but not PKC, in the amygdala contribute to pain-related synaptic plasticity and behavior"</p><p>http://www.molecularpain.com/content/4/1/26</p><p>Molecular Pain 2008;4():26-26.</p><p>Published online 16 Jul 2008</p><p>PMCID:PMC2490682.</p><p></p