(IMAGE)
Caption
The cover artistically integrates multiple elements central to investigating the developmental origins of Fragile X syndrome. A vibrant DNA double helix structure rendered in rainbow iridescent colors forms the focal point, with two laboratory mice strategically positioned along its length. This visualization is overlaid with molecular structures representing bumetanide and discrete clusters of vocal sequence data displayed through UMAP dimensional reduction. The ethereal background suggests neural networks through subtle branching patterns. This composition reflects the study's comprehensive examination of how prepartum bumetanide treatment affects both early vocal communication and later social behaviors in a mouse model of Fragile X syndrome. The dynamic interplay between genetic, molecular and behavioral elements visualized here connects to two articles in this issue: the research paper “Prepartum bumetanide treatment reverses altered neonatal social communication but non-specifically reduces post-pubertal social behavior in a mouse model of fragile X syndrome” by Y Sakamoto and colleagues and “Noboru Hiroi: Exploring the cellular and developmental origins of neuropsychiatric disorders linked to human copy-number variation,” an interview where senior author Dr. Hiroi discusses his career-long dedication to understanding neuropsychiatric disorders.
Credit
Noboru Hiroi, PhD
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License
CC BY-NC-ND