Anomalous acoustic reflection on a sliding interface or a shear band

We study the reflection of an acoustic plane wave from a steadily sliding planar interface with velocity strengthening friction or a shear band in a confined granular medium. The corresponding acoustic impedance is utterly different from that of the static interface. In particular, the system being open, the energy of an in-plane polarized wave is no longer conserved, the work of the external pulling force being partitioned between frictional dissipation and gain (of either sign) of coherent acoustic energy. Large values of the friction coefficient favor energy gain, while velocity strengthening tends to suppress it. An interface with infinite elastic contrast (one rigid medium) and V-independent (Coulomb) friction exhibits spontaneous acoustic emission, as already shown by M. Nosonovsky and G.G. Adams (Int. J. Ing. Sci., {\bf 39}, 1257 (2001)). But this pathology is cured by any finite elastic contrast, or by a moderately large V-strengthening of friction. We show that (i) positive gain should be observable for rough-on-flat multicontact interfaces (ii) a sliding shear band in a granular medium should give rise to sizeable reflection, which opens a promising possibility for the detection of shear localization.Comment: 13 pages, 10 figure

Genome-wide association study of more than 40,000 bipolar disorder cases provides new insights into the underlying biology

Bipolar disorder is a heritable mental illness with complex etiology. We performed a genome-wide association study of 41,917 bipolar disorder cases and 371,549 controls of European ancestry, which identified 64 associated genomic loci. Bipolar disorder risk alleles were enriched in genes in synaptic signaling pathways and brain-expressed genes, particularly those with high specificity of expression in neurons of the prefrontal cortex and hippocampus. Significant signal enrichment was found in genes encoding targets of antipsychotics, calcium channel blockers, antiepileptics and anesthetics. Integrating expression quantitative trait locus data implicated 15 genes robustly linked to bipolar disorder via gene expression, encoding druggable targets such as HTR6, MCHR1, DCLK3 and FURIN. Analyses of bipolar disorder subtypes indicated high but imperfect genetic correlation between bipolar disorder type I and II and identified additional associated loci. Together, these results advance our understanding of the biological etiology of bipolar disorder, identify novel therapeutic leads and prioritize genes for functional follow-up studies. © 2021, The Author(s), under exclusive licence to Springer Nature America, Inc