In cranial skeletal development, the establishment of the ectomesenchymal lineage within the cranial neural crest is of great significance. Fgfs are polypeptide growth factors with diverse functions in development and metabolism. Fgf20b knockdown zebrafish embryos showed dysplastic neurocranial and pharyngeal cartilages. Ectomesenchymal cells from cranial neural crest cells were significantly decreased in Fgf20b knockdown embryos, but cranial neural crest cells with a non-ectomesnchymal fate were increased. However, the proliferation and apoptosis of cranial neural crest cells were essentially unchanged. Fgfr1 knockdown embryos also showed dysplastic neurocranial and pharyngeal cartilages. The present findings indicate that Fgf20b is required for ectomesenchymal fate establishment via the activation of Fgfr1 in zebrafish.
The trigeminal ganglion is a critical structure in the peripheral nervous system, responsible for transmitting sensations of touch, pain, and temperature from craniofacial regions to the brain. Trigeminal ganglion development depends upon intrinsic cellular programming as well as extrinsic signals exchanged by diverse cell populations. With its complex anatomy and dual cellular origin from cranial placodes and neural crest cells, the trigeminal ganglion offers a rich context for examining diverse biological processes, including cell migration, fate determination, adhesion, and axon guidance.
Both the upper and lower jaws develop from cranial neural crest cells (CNCCs) populating the first pharyngeal arch in all gnathostomes. Previous studies showed that the Edn1/Ednra-Dlx5/Dlx6-Hand2 signaling pathway is necessary for lower jaw formation and that ectopic expression of or throughout the CNCCs partly transformed the upper jaw to lower jaw structures, but the molecular mechanisms regulating upper jaw development remain unclear. Here we show that the basic helix-loop-helix transcription factor Twist1 is required for upper jaw development.
We propose a robust framework for quantitatively comparing model-predicted and experimentally measured strain fields in the human brain during harmonic skull motion. Traumatic brain injuries (TBIs) are typically caused by skull impact or acceleration, but how skull motion leads to brain deformation and consequent neural injury remains unclear and comparison of model predictions to experimental data remains limited. Magnetic resonance elastography (MRE) provides high-resolution, full-field measurements of dynamic brain deformation induced by harmonic skull motion.
Background: Medical image segmentation is crucial for clinical diagnostics and treatment planning. Recently, hybrid models often neglect the local modeling capabilities of Transformers for medical image segmentation, despite the complementary nature of local information from both convolutional neural networks (CNNs) and transformers. This limitation is particularly problematic in multi-organ segmentation, where organs are closely adhered, and accurate delineation is essential.
