Results: 3

1.
Figure 2

Figure 2. From: Activation of the prostaglandin system in response to sleep loss in healthy humans: Potential mediator of increased spontaneous pain.

Intensity ratings of spontaneous measured every 2 hours throughout the protocol. For statistical analysis, ratings were averaged across days and log-transformed (see figure 3)

Monika Haack, et al. Pain. ;145(1-2):136-141.
2.
Figure 1

Figure 1. From: Activation of the prostaglandin system in response to sleep loss in healthy humans: Potential mediator of increased spontaneous pain.

Top left: Urine output in 24h collections at baseline and 3rd day under conditions of TSD (N=15) or control sleep (N=9).
Lower left: Urinary PGE2 metabolite levels/24h urine output at baseline and 3rd day of TSD (N=15) or control sleep (N=9). Lower right: Change of log-transformed urinary PGE2 metabolite levels/24h urine output from baseline to 3rd day of TSD or control sleep. For statistical analysis, data were log-transformed due to skewed distribution. Asterisk indicate p<0.05 between groups.
B=Baseline, Day 1 to 3=Days of TSD or control sleep, R=Recovery.

Monika Haack, et al. Pain. ;145(1-2):136-141.
3.
Figure 3

Figure 3. From: Activation of the prostaglandin system in response to sleep loss in healthy humans: Potential mediator of increased spontaneous pain.

Left panel: Intensity ratings of spontaneous pain (averaged across days), headache, and muscle pain significantly increased throughout three nights of TSD (N=15) compared to 8h control sleep (N=8, p<0.05 for interaction effect).
B=Baseline, Day 1 to 3 = days of TSD or control sleep, R=Recovery. Right panel: Correlation between change in urinary PGE2 metabolite and pain symptoms from baseline to the 3rd day of TSD.
Data are log-transformed due to skewed distribution and presented as differences from baseline. Asterisks indicate p<0.05 between groups. Asterisks in parenthesis indicate trend towards significance (p<0.10) between groups.

Monika Haack, et al. Pain. ;145(1-2):136-141.

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