Recent advances in bioprinting have granted tissue engineers the ability to assemble biomaterials, cells, and signaling molecules into anatomically relevant functional tissues or organ parts. Scaffold-free fabrication has recently attracted a great deal of interest due to the ability to recapitulate tissue biology by using self-assembly, which mimics the embryonic development process. Despite several attempts, bioprinting of scale-up tissues at clinically-relevant dimensions with closely recapitulated tissue biology and functionality is still a major roadblock. Here, we fabricate and engineer scaffold-free scalable tissue strands as a novel bioink material for robotic-assisted bioprinting technologies. Compare to 400 μm-thick tissue spheroids bioprinted in a liquid delivery medium into confining molds, near 8 cm-long tissue strands with rapid fusion and self-assemble capabilities are bioprinted in solid form for the first time without any need for a scaffold or a mold support or a liquid delivery medium, and facilitated native-like scale-up tissues. The prominent approach has been verified using cartilage strands as building units to bioprint articular cartilage tissue.

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The dependence of aluminum (Al) melting temperature on particle size was studied using a differential scanning calorimeter and thermogravitmetric analyzer for particles encapsulated in an oxide shell. Pressure generation within the Al core leads to an increase in melting temperature in comparison with traditional melting temperature depression calculated using the Gibbs−Thomson equation. On the basis of elasticity theory, the pressure in the Al core at the onset of melting is caused mainly by surface tension at the alumina−air and Al−alumina interfaces. This implies that pressure due to the difference in thermal expansion of aluminum and alumina relaxes. A possible relaxation mechanism is discussed. The static strength of the alumina shell and the maximum static generated pressure in aluminum were evaluated. Mechanically damaging the oxide shell was shown to reduce the melting temperature due to a decrease in generated pressure within the Al core. Thus, reduction in melting temperature can be used as a quantitative measure of damage to the oxide shell. Results from X-ray diffraction studies show that 17-nm diameter Al particles had a 2-nm thick alumina shell in the γ-phase, while for a flat surface Al had an amorphous alumina shell stable to a thickness of 4 nm. Thus, pressure due to surface tension promotes denser γ-phases. Since particles with shells initially in the amorphous or γ-phase show the same flame speed and ignition delay time, fast oxidation observed under high heating rates cannot be explained by a phase transformation in the alumina shell. These findings have important implications for the melt-dispersion mechanism for fast Al oxidation. The dependence of aluminum (Al) melting temperature on particle size was studied using a differential scanning calorimeter and thermogravitmetric analyzer for particles encapsulated in an oxide shell. Pressure generation within the Al core leads to an increase in melting temperature in comparison with traditional melting temperature depression calculated using the Gibbs-Thomson equation. On the basis of elasticity theory, the pressure in the Al core at the onset of melting is caused mainly by surface tension at the alumina-air and Al-alumina interfaces. This implies that pressure due to the difference in thermal expansion of aluminum and alumina relaxes. A possible relaxation mechanism is discussed. The static strength of the alumina shell and the maximum static generated pressure in aluminum were evaluated. Mechanically damaging the oxide shell was shown to reduce the melting temperature due to a decrease in generated pressure within the Al core. Thus, reduction in melting temperature can be used as a quantitative measure of damage to the oxide shell. Results from X-ray diffraction studies show that 17-nm diameter Al particles had a 2-nm thick alumina shell in the γ-phase, while for a flat surface Al had an amorphous alumina shell stable to a thickness of 4 nm. Thus, pressure due to surface tension promotes denser γ-phases. Since particles with shells in...

Bone defects are common and, in many cases, challenging to treat. Tissue engineering is an interdisciplinary approach with promising potential for treating bone defects. Within tissue engineering, three-dimensional (3D) printing strategies have emerged as potent tools for scaffold fabrication. However, reproducibility and quality control are critical aspects limiting the translation of 3D printed scaffolds to clinical use, which remain to be addressed. To elucidate the factors that yield to the generation of defects in bioprinting and to achieve reproducible biomaterial printing, the objective of this article is to frame a systematic approach for optimizing and validating 3D printing of poly(caprolactone) (PCL)-hydroxyapatite (HAp) composite scaffolds. We delineate the effect of PCL-to-HAp ratio, print velocity, print temperature, and extrusion pressure on the architectural and mechanical properties of the 3D printed scaffold. Furthermore, we present an in situ image-based monitoring approach to quantify key quality-related aspects of constructs, such as the ability to deposit material consistently and print elementary shapes with fewer flaws. Our results show that small defects generated during the printing process have a significant role in lowering the mechanical properties of 3D printed polymeric scaffolds. In addition, the in vitro osteoinductivity of the fabricated scaffolds is demonstrated.