RESUMEN
Printable electronics for neurotechnology is a rapidly emerging field that leverages various printing techniques to fabricate electronic devices, offering advantages in rapid prototyping, scalability, and cost-effectiveness. These devices have promising applications in neurobiology, enabling the recording of neuronal signals and controlled drug delivery. This review provides an overview of printing techniques, materials used in neural device fabrication, and their applications. The printing techniques discussed include inkjet, screen printing, flexographic printing, 3D printing, and more. Each method has its unique advantages and challenges, ranging from precise printing and high resolution to material compatibility and scalability. Selecting the right materials for printable devices is crucial, considering factors like biocompatibility, flexibility, electrical properties, and durability. Conductive materials such as metallic nanoparticles and conducting polymers are commonly used in neurotechnology. Dielectric materials, like polyimide and polycaprolactone, play a vital role in device fabrication. Applications of printable devices in neurotechnology encompass various neuroprobes, electrocorticography arrays, and microelectrode arrays. These devices offer flexibility, biocompatibility, and scalability, making them cost-effective and suitable for preclinical research. However, several challenges need to be addressed, including biocompatibility, precision, electrical performance, long-term stability, and regulatory hurdles. This review highlights the potential of printable electronics in advancing our understanding of the brain and treating neurological disorders while emphasizing the importance of overcoming these challenges.
RESUMEN
Tissue-resident macrophages play important roles in tissue homeostasis and repair. However, how macrophages monitor and maintain tissue integrity is not well understood. The extracellular matrix (ECM) is a key structural and organizational component of all tissues. Here, we find that macrophages sense the mechanical properties of the ECM to regulate a specific tissue repair program. We show that macrophage mechanosensing is mediated by cytoskeletal remodeling and can be performed in three-dimensional environments through a noncanonical, integrin-independent mechanism analogous to amoeboid migration. We find that these cytoskeletal dynamics also integrate biochemical signaling by colony-stimulating factor 1 and ultimately regulate chromatin accessibility to control the mechanosensitive gene expression program. This study identifies an "amoeboid" mode of ECM mechanosensing through which macrophages may regulate tissue repair and fibrosis.