Visual stress (VS) affects reading in 5-12% of the general population and 31-36% of children with reading disorders. Symptoms include print distortions and visual discomfort when reading, and are exacerbated by fluorescent lighting. Prior research has indicated that VS can also affect proficient readers. We therefore examined levels of visual discomfort in a group of expert readers (n = 24) under both standard and spectrally-filtered fluorescent lighting. Participants rated their awareness of six symptoms of VS under each lighting condition. Under the standard condition, 4(16.7%) of the group recorded moderate to high levels of VS. Differences in symptom levels and reading speed between conditions were analysed using the Wilcoxon Signed Rank Test. Under the filter condition, the group reported less discomfort regarding all six symptoms of VS surveyed. The differences were significant with respect to three of the symptoms (p = .029 - p < .001), with a medium effect size in all of them (r = .31 - r = .46) and total score (p = .007; r = .39). Variations in reading proficiency included significantly fewer self-corrections (p = .019) and total errors (p = .004). Here we present evidence that VS-type symptoms of reading discomfort are not confined to populations with reading difficulties and may also occur in proficient readers, and that simple adaptations to fluorescent lighting may alleviate such symptoms.
Platelet-associated complications including thrombosis, thrombocytopenia, and hemorrhage are commonly observed during various inflammatory diseases such as sepsis, inflammatory bowel disease, and psoriasis. Despite the reported evidence on numerous mechanisms/molecules that may contribute to the dysfunction of platelets, the primary mechanisms that underpin platelet-associated complications during inflammatory diseases are not fully established. Here, we report the discovery of formyl peptide receptor 2, FPR2/ALX, in platelets and its primary role in the development of platelet-associated complications via ligation with its ligand, LL37. LL37 acts as a powerful endogenous antimicrobial peptide, but it also regulates innate immune responses. We demonstrate the impact of LL37 in the modulation of platelet reactivity, hemostasis, and thrombosis. LL37 activates a range of platelet functions, enhances thrombus formation, and shortens the tail bleeding time in mice. By utilizing a pharmacological inhibitor and Fpr2/3 (an ortholog of human FPR2/ALX)-deficient mice, the functional dependence of LL37 on FPR2/ALX was determined. Because the level of LL37 is increased in numerous inflammatory diseases, these results point toward a critical role for LL37 and FPR2/ALX in the development of platelet-related complications in such diseases. Hence, a better understanding of the clinical relevance of LL37 and FPR2/ALX in diverse pathophysiological settings will pave the way for the development of improved therapeutic strategies for a range of thromboinflammatory diseases.