1999), the two PRCs cross the ?0.54 h line at approximately the same phase. According to 95% confidence intervals for both the 1 h and 6.7 h bright white light PRCs (Fig. 5B), the two PRCs were not statistically different (i.e. confidence intervals overlap) except for a small window around the maximal delay and advance region of the 6.7 h PRC. The <3 lux background light PRC was plotted with the <15 lux background light PRC (Fig. 5, right panels). There were significant differences between these two dim light PRCs at most circadian phases according to 95% confidence intervals (Fig. 5D) due to the significant phase delays and advances (relative to the ?0.54 h no net phase shift line) observed in the Dapagliflozin research buy <15 lux background light group. A 1 h bright white light exposure induced Type 1 resetting of the circadian rhythm of melatonin with maximal phase delay and advance shifts of ?2.02 and 1.20 h, respectively. A two-harmonic function fitted to the raw data resulted in a PRC with a fitted peak-to-trough amplitude of 2.20 h. In comparison, a previously published 6.7 h bright white light PRC (Khalsa et al. 2003) had a fitted peak-to-trough amplitude of 5.46 h. The 1 h exposure, which represents only 15% of the duration of the 6.7 h exposure, was therefore able to generate 40% of the response generated in the 6.7 h bright white light PRC, adding to evidence from previous results in human experiments (Rimmer et al. 2000; Gronfier Luminespib et al. 2004) that suggest a non-linear duration?Cresponse function for circadian phase resetting in humans. When the AZD1208 price fitted 1 h bright white light PRC was compared relative to the line of intrinsic circadian drift (?0.54 h over 3 days), we did not observe a dead zone in the PRC, consistent with the previous study with 6.7 h bright white light. The present study therefore suggests that the human circadian pacemaker is sensitive to light at all circadian phases, even for shorter durations of light exposure, and that there is no dead zone when circadian drift is taken into account. This present study includes the first published reports of dim background light PRCs, in which participants were exposed to continuous background dim light using the same procedures that were used to construct PRCs in response to bright white light. The maximal phase delay and advance shifts imposed by the <15 lux background light PRC may have been due to a significant phase-resetting effect of the ?15 lux background (Zeitzer et al. 2000) and/or to non-photic effects due to a shift in the timing of meals, activity and the sleep?Cwake cycle (Duffy et al. 1996; Klerman et al. 1998; Barger et al. 2004; Gronfier et al. 2004; St Hilaire et al. 2007). In the study by Duffy et al. (1996), exposure to a 5 h dark pulse (<0.03 lux) against a ?15 lux background over multiple cycles caused a phase advance shift of 1.74 h over 10 cycles, and phase delay shift of 3.