Additional file 4: of Non-technical skills evaluation in the critical care air ambulance environment: introduction of an adapted rating instrument - an observational study

Behavioural descriptor modifications based on content evaluation survey. (PDF 259 kb

Additional file 3: of Non-technical skills evaluation in the critical care air ambulance environment: introduction of an adapted rating instrument - an observational study

Aeromedical non-technical skills assessment form and rating scale. (PDF 266 kb

Does carbon monoxide treatment alter cytokine levels after endotoxin infusion in pigs? A randomized controlled study-2

A dotted (CO group) and solid (controls) line represents means for the two groups (n = 10 except for the CO-group at 270 and 300 min where n = 9 and for controls at 150, 180 and 210 min where n = 9 and at 240, 270 and 300 min where n = 8). Endotoxin was administered (0.05 μg/kg/h) just after time 0, reaching maximum infusion rate (0.25 μg/kg/h) at 30 min. No significant differences were detected between the groups for any of the cytokines (TNF: ANOVA (1, 8) = 1.074, IL-6: ANOVA (1, 8) = 0.892, IL-10: ANOVA (1, 8) = 1.347, IL-1beta: ANOVA (1, 8) = 1.716).<p><b>Copyright information:</b></p><p>Taken from "Does carbon monoxide treatment alter cytokine levels after endotoxin infusion in pigs? A randomized controlled study"</p><p>http://www.journal-inflammation.com/content/5/1/13</p><p>Journal of Inflammation (London, England) 2008;5():13-13.</p><p>Published online 7 Aug 2008</p><p>PMCID:PMC2518540.</p><p></p

Does carbon monoxide treatment alter cytokine levels after endotoxin infusion in pigs? A randomized controlled study-1

N = 9) and controls (closed circles, n = 10 except at 150, 180 and 210 min where n = 9 and at 240, 270 and 300 min where n = 8). Endotoxin was administered (0.05 μg/kg/h) just after time 0, reaching maximum infusion rate (0.25 μg/kg/h) at 30 min. CO was administrated just after time -60 min.<p><b>Copyright information:</b></p><p>Taken from "Does carbon monoxide treatment alter cytokine levels after endotoxin infusion in pigs? A randomized controlled study"</p><p>http://www.journal-inflammation.com/content/5/1/13</p><p>Journal of Inflammation (London, England) 2008;5():13-13.</p><p>Published online 7 Aug 2008</p><p>PMCID:PMC2518540.</p><p></p

Arterial t-PA-concentrations.

<p>Absolute t-PA concentrations in arterial blood are shown for pre-ischemia (baseline), as well as for the period after 10 min of ischemia and 10 min of reperfusion. Both the treated group (filled squares, n = 12) and the control group (open squares, n = 10) are shown. Data are presented as mean ± SEM. No differences were noted within groups over time, or between groups at any of the time intervals (mixed between-within subjects ANOVA). There was no sign here that the valproic acid treatment led to higher systemic blood levels of t-PA in the resting state. These results also showed that the coronary t-PA release did not affect systemic arterial t-PA levels.</p

Hemodynamic results.

<p>HR =  heart rate (bpm); MAP =  mean arterial pressure (mm Hg); CSF  =  coronary sinus blood flow (mL/min). Control group (n = 10), treated group (n = 12). Data are presented as mean ± 95% SEM. * = p<0.05 using repeated measures ANOVA and when significant was followed by paired t test vs. baseline. A between-groups t test was performed, but no differences were found.</p

Coronary t-PA-flux.

<p>Coronary t-PA fluxes are shown in Panel A for pre-ischemia (baseline), after 10 min of ischemia followed by 10 min of reperfusion for treated group (filled squares, n = 12) and for control group (open squares, n = 10). These are point measurements for observed t-PA fluxes at minutes 1, 3, 5, 7, and 10. One can note that there are different baselines for the two groups. The main result is derived from Panel A, and presented as the cumulative t-PA release over time in Panel B, as area under the curve (AUC). There is a clearly higher cumulative t-PA release for the VPA treated group (mixed between-within subjects ANOVA, p = 0.023); treated group (filled diamonds, n = 12) and control group (open diamonds, n = 10) data presented as mean ± SEM. There were also differences between groups (larger cumulative t-PA release in the treatment group) for specific measurements at minutes 10, 7, and 5 (t-test).</p

Absolute values of coronary lactate-fluxes.

<p>These are shown for pre-ischemia (baseline), after 10 min of ischemia followed by 10 min of reperfusion for treated group (filled squares, n = 12) and for control group (open squares, n = 10). Data are presented as mean ± SEM. Sampling of the ischemic area, as confirmed by positive lactate flux (regional myocardial lactate production in response to the local coronary occlusion), was observed in all animals (not shown individually) and is reflected by the immediate high positive lactate flux noted at reperfusion minute 1. This regional lactate flux was quickly ‘washed out’. No difference was found between groups (p = 0.853, mixed between-within subjects ANOVA).</p

Demographic data.

<p>Abbreviations: kg = kilogram, m² = square meter, bpm = beats per minute, mm Hg = millimeters of mercury, g = gram, L = liter, μmol = micromole, mmol = millimole. Results shown as mean ± SD, (n = 16).</p><p>Demographic data.</p