Chitin is a structural polysaccharide abundant in the biosphere. Chitin possesses a highly ordered crystalline structure that makes its processing a challenge. In this study, chitin hydrogels and methanogels, prepared by dissolution in calcium chloride/methanol, were subjected to supercritical carbon dioxide (scCO₂) to produce porous materials for use as scaffolds for osteoblasts. The control of the morphology, porosity, and physicochemical properties of the produced materials was performed according to the operational conditions, as well as the co-solvent addition. The dissolution of CO₂ in methanol co-solvent improved the sorption of the compressed fluid into the hydrogel, rendering highly porous chitin scaffolds. The chitin crystallinity index significantly decreased after processing the hydrogel in supercritical conditions, with a significant effect on its swelling capacity. The use of scCO₂ with methanol co-solvent resulted in chitin scaffolds with characteristics adequate to the adhesion and proliferation of osteoblasts.

Enteric stem cells contribute to postnatal intestinal development by generating multiple cell lineages under the influence of distinct signaling pathways. Among these, Hedgehog signaling has been implicated in the development and maintenance of the enteric nervous system. This study evaluated the effects of cyclopamine treatment on intestinal morphology and stem cell marker expression in neonatal mice. Animals received intraperitoneal cyclopamine (10 mg/kg) on postnatal days 0, 2, 4, and 6 and were euthanized on day 7. Cyclopamine treatment resulted in significant changes in villus morphology, decreased expression of several neuronal differentiation markers, and increased expression of SOX2- and Nestin-positive cells. These observations indicate that cyclopamine treatment alters cellular differentiation patterns in the postnatal intestine and may favor the maintenance of a less differentiated cellular phenotype. Further studies are required to determine the specific mechanisms involved and to clarify the contribution of Hedgehog signaling to these effects.