Disruption in neural phase synchrony is related to identification of inattentional deafness in real-world setting

Individuals often have reduced ability to hear alarms in real world situations (e.g., anesthesia monitoring, flying airplanes) when attention is focused on another task, sometimes with devastating consequences. This phenomenon is called inattentional deafness and usually occurs under critical high workload conditions. It is difficult to simulate the critical nature of these tasks in the laboratory. In this study, dry electroencephalography is used to investigate inattentional deafness in real flight while piloting an airplane. The pilots participating in the experiment responded to audio alarms while experiencing critical high workload situations. It was found that missed relative to detected alarms were marked by reduced stimulus evoked phase synchrony in theta and alpha frequencies (6–14 Hz) from 120 to 230 ms poststimulus onset. Correlation of alarm detection performance with intertrial coherence measures of neural phase synchrony showed different frequency and time ranges for detected and missed alarms. These results are consistent with selective attentional processes actively disrupting oscillatory coherence in sensory networks not involved with the primary task (piloting in this case) under critical high load conditions. This hypothesis is corroborated by analyses of flight parameters showing greater maneuvering associated with difficult phases of flight occurring during missed alarms. Our results suggest modulation of neural oscillation is a general mechanism of attention utilizing enhancement of phase synchrony to sharpen alarm perception during successful divided attention, and disruption of phase synchrony in brain networks when attentional demands of the primary task are great, such as in the case of inattentional deafness

cAMP/PKA Regulates Osteogenesis, Adipogenesis and Ratio of RANKL/OPG mRNA Expression in Mesenchymal Stem Cells by Suppressing Leptin

BACKGROUND: Mesenchymal stem cells (MSCs) are a pluripotent cell type that can differentiate into adipocytes, osteoblasts and other cells. The reciprocal relationship between adipogenesis and osteogenesis was previously demonstrated; however, the mechanisms remain largely unknown. METHODS AND FINDINGS: We report that activation of PKA by 3-isobutyl-1 methyl xanthine (IBMX) and forskolin enhances adipogenesis, the gene expression of PPARgamma2 and LPL, and downregulates the gene expression of Runx2 and osteopontin, markers of osteogenesis. PKA activation also decreases the ratio of Receptor Activator of the NF-kappaB Ligand to Osteoprotegerin (RANKL/OPG) gene expression - the key factors of osteoclastogenesis. All these effects are mediated by the cAMP/PKA/CREB pathway by suppressing leptin, and may contribute to PKA stimulators-induced in vivo bone loss in developing zebrafish. CONCLUSIONS: Using MSCs, the center of a newly proposed bone metabolic unit, we identified cAMP/PKA signaling, one of the many signaling pathways that regulate bone homeostasis via controlling cyto-differentiation of MSCs and altering RANKL/OPG gene expression