Medical illustration, which involves the creation of visual representations of anatomy, has long been an essential tool for medical professionals and educators. The integration of AI and medical illustration has the potential to revolutionize the field of anatomy education, providing highly accurate, customizable images. The authors evaluated three AI‐powered text‐to‐image generators in producing anatomical illustrations of the human skulls, heart, and brain. The generators were assessed for their accurate depiction of foramina, suture lines, coronary arteries, aortic and pulmonary trunk branching, gyri, sulci, and the relationship between the cerebellum and temporal lobes. None of the generators produced illustrations with comprehensive anatomical details. Foramina, such as the mental and supraorbital foramina, were frequently omitted, and suture lines were inaccurately represented. The illustrations of the heart failed to indicate proper coronary artery origins, and the branching of the aorta and pulmonary trunk was often incorrect. Brain illustrations lacked accurate gyri and sulci depiction, and the relationship between the cerebellum and temporal lobes remained unclear. Although AI generators tended toward esoteric imagery, they exhibited significant speed and cost advantages over human illustrators. However, improving their accuracy necessitates augmenting the training databases with anatomically correct images. The study emphasizes the ongoing role of human medical illustrators, especially in ensuring the provision of accurate and accessible illustrations.

Debate remains around the anatomical origins of specific brain cell subtypes and lineage relationships within the human forebrain^{1,2,3,4,5,6,7}. Thus, direct observation in the mature human brain is critical for a complete understanding of its structural organization and cellular origins. Here we utilize brain mosaic variation within specific cell types as distinct indicators for clonal dynamics, denoted as cell-type-specific mosaic variant barcode analysis. From four hemispheres and two different human neurotypical donors, we identified 287 and 780 mosaic variants, respectively, that were used to deconvolve clonal dynamics. Clonal spread and allele fractions within the brain reveal that local hippocampal excitatory neurons are more lineage-restricted than resident neocortical excitatory neurons or resident basal ganglia GABAergic inhibitory neurons. Furthermore, simultaneous genome transcriptome analysis at both a cell-type-specific and a single-cell level suggests a dorsal neocortical origin for a subgroup of DLX1⁺ inhibitory neurons that disperse radially from an origin shared with excitatory neurons. Finally, the distribution of mosaic variants across 17 locations within one parietal lobe reveals that restriction of clonal spread in the anterior–posterior axis precedes restriction in the dorsal–ventral axis for both excitatory and inhibitory neurons. Thus, cell-type-resolved somatic mosaicism can uncover lineage relationships governing the development of the human forebrain.

Astrocyte endfeet surrounding blood vessels are active domains involved in water and potassium ion transport crucial to the maintenance of water and potassium ion homeostasis in brain. A growing body of evidence points to a role for dystroglycan and its interaction with perivascular laminin in the targeting of the dystrophin complex and the water-permeable channel, aquaporin 4 (AQP4), at astrocyte endfeet. However, the mechanisms underlying such compartmentalization remain poorly understood. In the present study we found that AQP4 resided in Triton X-100-insoluble fraction, whereas dystroglycan was recovered in the soluble fraction in astrocytes. Cholesterol depletion resulted in the translocation of a pool of AQP4 to the soluble fraction indicating that its distribution is indeed associated with cholesterol-rich membrane domains. Upon laminin treatment AQP4 and the dystrophin complex, including dystroglycan, reorganized into laminin-associated clusters enriched for the lipid raft markers GM1 and flotillin-1 but not caveolin-1. Reduced diffusion rates of GM1 in the laminin-induced clusters were indicative of the reorganization of raft components in these domains. In addition, both cholesterol depletion and dystroglycan silencing reduced the number and area of laminin-induced clusters of GM1, AQP4, and dystroglycan. These findings demonstrate the interdependence between laminin binding to dystroglycan and GM1-containing lipid raft reorganization and provide novel insight into the dystrophin complex regulation of AQP4 polarization in astrocytes.