Publications by authors named "A Marie-Josee Sasseville"
Article Synopsis
- Circadian adaptation for night workers is often ineffective due to low light exposure at night and morning light on the way home, leading to misalignments that negatively impact sleep and overall health.
- To address this, a study tested the effects of different light conditions (blue, red, and control) on police officers working rotating night shifts, measuring their sleepiness, alertness, and circadian phase.
- Results showed no significant differences in alertness or sleepiness, but officers experienced a phase delay after four night shifts, indicating potential disruptions in their biological clocks.
Introduction: Short-wavelengths can have an acute impact on alertness, which is allegedly due to their action on intrinsically photosensitive retinal ganglion cells. Classical photoreceptors cannot, however, be excluded at this point in time as contributors to the alerting effect of light. The objective of this study was to compare the alerting effect at night of a white LED light source while wearing blue-blockers or not, in order to establish the contribution of short-wavelengths.
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- - Evening chronotypes (E-types) show distinct sleep patterns and behaviors, like lower sleep efficiency and longer wake times after falling asleep, compared to Intermediate-types (I-types) during both night and day shifts among police officers.
- - E-types experience shorter sleep duration, especially when factoring in naps, and are more active during the early hours of their night shifts, reflecting a difference in circadian rhythm adaptation.
- - Overall, while E-types report better sleep on night shifts, they struggle with sleep complaints during day shifts, highlighting the need for more research on day sleep among shift workers.
We previously reported that HSV-2 R1, the R1 subunit (ICP10; UL39) of herpes simplex virus type-2 ribonucleotide reductase, protects cells against apoptosis induced by the death receptor (DR) ligands tumor necrosis factor-alpha- (TNFα) and Fas ligand (FasL) by interrupting DR-mediated signaling at, or upstream of, caspase-8 activation. Further investigation of the molecular mechanism underlying HSV-2 R1 protection showed that extracellular-regulated kinase 1/2 (ERK1/2), phosphatidylinositol 3-kinase (PI3-K)/Akt, NF-κB and JNK survival pathways do not play a major role in this antiapoptotic function. Interaction studies revealed that HSV-2 R1 interacted constitutively with caspase-8.
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