38 research outputs found

    Maximum body temperature decrease within eight hours after administration of dipyrone, acetaminophen or no medication.

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    Patients are grouped according to receiving either dipyrone (blue; n = 341) or acetaminophen (red; n = 71) versus patients receiving no antipyretic treatment (n = 315). P values are uncorrected Kruskal-Wallis p values for each time point. Black lines indicate significant differences (p <0.05, corrected for multiple testing). Two hours after administration, acetaminophen was associated with a higher decrease in body temperature than dipyrone or no medication. Dipyrone led to a higher temperature decrease than no medication starting 4 hours after administration.</p

    Median body temperature trends over time.

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    Patients receiving either dipyrone (blue) or acetaminophen (red) and patients receiving no antipyretic treatment (grey) are shown separately. Median body temperatures with their respective 95% confidence interval are shown. Each four patients in the no medication and dipyrone group were excluded from the eight-hour time point because of missing temperature data. Patients receiving both dipyrone and acetaminophen are not shown. All patient groups presented with a decreasing median body temperature within the eight-hour study interval (Friedman test p<0.001; Friedman test for each of the three subgroups without correction for multiple testing p<0.001).</p

    Comparison of mean differences in temperature decreases.

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    Patients are grouped according to receiving either dipyrone (blue; n = 341) or acetaminophen (red; n = 71) versus patients receiving no antipyretic treatment (n = 315). Graphs display mean differences in temperature decreases between each two comparators (no medication versus dipyrone, no medication versus acetaminophen and dipyrone versus acetaminophen) with their respective 95% confidence intervals. Maximum of temperature decrease in association with dipyrone or acetaminophen was detected four hours after administration. Afterwards, body temperatures converged independent from the treatment group. Acetaminophen was associated with a steeper and more prolonged temperature decrease than dipyrone.</p

    Patient flow chart.

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    Study flowchart showing the number of patients and respective exclusion criteria. Patients receiving both dipyrone and acetaminophen were excluded from primary endpoint analysis for methodical reasons, but remained in the study for further analyses.</p

    Supplemental Material1 - Supplemental material for Etomidate and propylene glycol activate nociceptive TRP ion channels

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    Supplemental material, Supplemental Material1 for Etomidate and propylene glycol activate nociceptive TRP ion channels by Florian Niedermirtl, Mirjam Eberhardt, Barbara Namer, Andreas Leffler, Carla Nau, Peter W Reeh and Katrin Kistner in Molecular Pain</p

    Supplemental Material2 - Supplemental material for Etomidate and propylene glycol activate nociceptive TRP ion channels

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    Supplemental material, Supplemental Material2 for Etomidate and propylene glycol activate nociceptive TRP ion channels by Florian Niedermirtl, Mirjam Eberhardt, Barbara Namer, Andreas Leffler, Carla Nau, Peter W Reeh and Katrin Kistner in Molecular Pain</p

    Pharmacological characterisation of glycine receptors in NPCs differentiated for 3 weeks.

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    <p>A, Whole-cell currents evoked by a glycine EC<sub>70</sub> were all markedly blocked by strychnine and partly inhibited by picrotoxin, pregnenolone sulphate and a high bicuculline concentration. In contrast to the positive modulation by 10 µM ZnCl<sub>2</sub>, a reduction of glycine currents was induced by 100 µM ZnCl<sub>2</sub>. Also, co-application of a glycine EC<sub>70</sub> and tropisetron showed a positive modulatory effect. This pharmacological profile suggests receptor isoforms containing α2β subunits (B, n = 9–10; all data are given as means ± S.E.M.).</p

    Immunocytochemistry of human mesencephalic NPCs after 3 weeks of standard differentiation in vitro.

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    <p>Photomicrographs of NPCs immunoreactive for MAP2 (A) and glycine receptor subunits (B); nuclei were counter-stained with DAPI (C). Merged picture illustrates that neuronal cells express glycine receptor subunits (D). Note, this glycine receptor antibody is specific for all subunits.</p
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