Review: Tsuchi: Earthy Materials in Contemporary Japanese Art

Review of Tsuchi: Earthy Materials in Contemporary Japanese Art by Bert Winther-Tamaki. University of Minnesota Press, June 2022. 312 p. ill. ISBN 978-1-5179-1190-4 $34.95. https://www.upress.umn.edu/book-division/books/tsuchi. Reviewed November 2022 by John Hosford, Art Librarian, Scholes Library, Alfred University, [email protected]

Evolution of the Southwest Indian Ridge from 55°45′E to 62°E : changes in plate-boundary geometry since 26 Ma

Author Posting. © American Geophysical Union, 2007. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Geochemistry Geophysics Geosystems 8 (2007): Q06022, doi:10.1029/2006GC001559.From 55°45′E to 58°45′E and from 60°30′E to 62°00′E, the ultraslow-spreading Southwest Indian Ridge (SWIR) consists of magmatic spreading segments separated by oblique amagmatic spreading segments, transform faults, and nontransform discontinuities. Off-axis magnetic and multibeam bathymetric data permit investigation of the evolution of this part of the SWIR. Individual magmatic segments show varying magnitudes and directions of asymmetric spreading, which requires that the shape of the plate boundary has changed significantly over time. In particular, since 26 Ma the Atlantis II transform fault grew by 90 km to reach 199 km, while a 45-km-long transform fault at 56°30′E shrank to become an 11 km offset nontransform discontinuity. Conversely, an oblique amagmatic segment at the center of a first-order spreading segment shows little change in orientation with time. These changes are consistent with the clockwise rotation of two ~450-km-wide first-order spreading segments between the Gallieni and Melville transform faults (52–60°E) to become more orthogonal to spreading. We suggest that suborthogonal first-order spreading segments reflect a stable configuration for mid-ocean ridges that maximizes upwelling rates in the asthenospheric mantle and results in a hotter and weaker ridge-axis that can more easily accommodate seafloor spreading.Funding for this work came from a JOI-Schlanger Fellowship to Baines and NSF grant 0352054 to Cheadle and John

Absence seizures in C3H/HeJ and knockout mice caused by mutation of the AMPA receptor subunit Gria4

Absence epilepsy, characterized by spike–wave discharges (SWD) in the electroencephalogram, arises from aberrations within the circuitry of the cerebral cortex and thalamus that regulates awareness. The inbred mouse strain C3H/HeJ is prone to absence seizures, with a major susceptibility locus, spkw1, accounting for most of the phenotype. Here we find that spkw1 is associated with a hypomorphic retroviral-like insertion mutation in the Gria4 gene, encoding one of the four amino-3-hydroxy-5-methyl-4isoxazolepropionic acid (AMPA) receptor subunits in the brain. Consistent with this, Gria4 knockout mice also have frequent SWD and do not complement spkw1. In contrast, null mutants for the related gene Gria3 do not have SWD, and Gria3 loss actually lowers SWD of spkw1 homozygotes. Gria3 and Gria4 encode the predominant AMPA receptor subunits in the reticular thalamus, which is thought to play a central role in seizure genesis by inhibiting thalamic relay cells and promoting rebound burst firing responses. In Gria4 mutants, synaptic excitation of inhibitory reticular thalamic neurons is enhanced, with increased duration of synaptic responses—consistent with what might be expected from reduction of the kinetically faster subunit of AMPA receptors encoded by Gria4. These results demonstrate for the first time an essential role for Gria4 in the brain, and suggest that abnormal AMPA receptor-dependent synaptic activity can be involved in the network hypersynchrony that underlies absence seizures

Common genetic variation and susceptibility to partial epilepsies: a genome-wide association study

Partial epilepsies have a substantial heritability. However, the actual genetic causes are largely unknown. In contrast to many other common diseases for which genetic association-studies have successfully revealed common variants associated with disease risk, the role of common variation in partial epilepsies has not yet been explored in a well-powered study. We undertook a genome-wide association-study to identify common variants which influence risk for epilepsy shared amongst partial epilepsy syndromes, in 3445 patients and 6935 controls of European ancestry. We did not identify any genome-wide significant association. A few single nucleotide polymorphisms may warrant further investigation. We exclude common genetic variants with effect sizes above a modest 1.3 odds ratio for a single variant as contributors to genetic susceptibility shared across the partial epilepsies. We show that, at best, common genetic variation can only have a modest role in predisposition to the partial epilepsies when considered across syndromes in Europeans. The genetic architecture of the partial epilepsies is likely to be very complex, reflecting genotypic and phenotypic heterogeneity. Larger meta-analyses are required to identify variants of smaller effect sizes (odds ratio <1.3) or syndrome-specific variants. Further, our results suggest research efforts should also be directed towards identifying the multiple rare variants likely to account for at least part of the heritability of the partial epilepsies. Data emerging from genome-wide association-studies will be valuable during the next serious challenge of interpreting all the genetic variation emerging from whole-genome sequencing studie

Common genetic variation and susceptibility to partial epilepsies: a genome-wide association study

Partial epilepsies have a substantial heritability. However, the actual genetic causes are largely unknown. In contrast to many other common diseases for which genetic association-studies have successfully revealed common variants associated with disease risk, the role of common variation in partial epilepsies has not yet been explored in a well-powered study. We undertook a genome-wide association-study to identify common variants which influence risk for epilepsy shared amongst partial epilepsy syndromes, in 3445 patients and 6935 controls of European ancestry. We did not identify any genome-wide significant association. A few single nucleotide polymorphisms may warrant further investigation. We exclude common genetic variants with effect sizes above a modest 1.3 odds ratio for a single variant as contributors to genetic susceptibility shared across the partial epilepsies. We show that, at best, common genetic variation can only have a modest role in predisposition to the partial epilepsies when considered across syndromes in Europeans. The genetic architecture of the partial epilepsies is likely to be very complex, reflecting genotypic and phenotypic heterogeneity. Larger meta-analyses are required to identify variants of smaller effect sizes (odds ratio <1.3) or syndrome-specific variants. Further, our results suggest research efforts should also be directed towards identifying the multiple rare variants likely to account for at least part of the heritability of the partial epilepsies. Data emerging from genome-wide association-studies will be valuable during the next serious challenge of interpreting all the genetic variation emerging from whole-genome sequencing studies

Review of "Copyright: Best Practices for Academic Libraries"

Copyright: Best Practices for Academic Libraries provides valuable advice for librarians to navigate the complex world of copyright law in their profession. The book consists of twenty chapters, each written by experts, focusing on academic libraries and enhancing copyright literacy. One of the book's aims is to enable readers to become proficient in understanding the intricacies of copyright and take an active part in the ongoing conversations.&nbsp