Microfabricated dynamic brain organoid cocultures to assess the effects of surface geometry on assembloid formation.

Organoids have emerged as valuable tools for the study of development and disease. Assembloids are formed by integrating multiple organoid types to create more complex models. However, the process by which organoids integrate to form assembloids remains unclear and may play an important role in the resulting organoid structure.

Compressive molding of engineered tissues thermoresponsive hydrogel devices.

Biofabrication of tissues requires sourcing appropriate combinations of cells, and then arranging those cells into a functionally-useful construct. Recently, organoids with diverse cell populations have shown great promise as building blocks from which to assemble more complex structures. However, organoids typically adopt spherical or uncontrolled morphologies, which intrinsically limit the tissue structures that can be produced using this bioassembly technique.

Hydrogel Mechanics Influence the Growth and Development of Embedded Brain Organoids.

Brain organoids are three-dimensional, tissue-engineered neural models derived from induced pluripotent stem cells that enable studies of neurodevelopmental and disease processes. Mechanical properties of the microenvironment are known to be critical parameters in tissue engineering, but the mechanical consequences of the encapsulating matrix on brain organoid growth and development remain undefined. Here, Matrigel was modified with an interpenetrating network (IPN) of alginate, to tune the mechanical properties of the encapsulating matrix.

Applying hiPSCs and Biomaterials Towards an Understanding and Treatment of Traumatic Brain Injury.

Traumatic brain injury (TBI) is the leading cause of disability and mortality in children and young adults and has a profound impact on the socio-economic wellbeing of patients and their families. Initially, brain damage is caused by mechanical stress-induced axonal injury and vascular dysfunction, which can include hemorrhage, blood-brain barrier disruption, and ischemia. Subsequent neuronal degeneration, chronic inflammation, demyelination, oxidative stress, and the spread of excitotoxicity can further aggravate disease pathology.