Bioprinting is an emerging technology in the field of tissue engineering and regenerative medicine. The process consists of simultaneous deposition of cells, biomaterial and/or growth factors under pressure through a micro-scale nozzle. Cell viability can be controlled by varying the parameters like pressure and nozzle diameter. The process itself can be a very useful tool for evaluating an in vitro cell injury model. It is essential to understand the cell responses to process-induced mechanical disturbances because they alter cell morphology and function. We carried out analysis and quantification of the degree of cell injury induced by bioprinting process. A parametric study with different process parameters was conducted to analyze and quantify cell injury as well as to optimize the parameters for printing viable cells. A phenomenological model was developed correlating the percentage of live, apoptotic and necrotic cells to the process parameters. This study incorporates an analytical formulation to predict the cell viability through the system as a function of the maximum shear stress in the system. The study shows that dispensing pressure has a more significant effect on cell viability than the nozzle diameter. The percentage of live cells is reduced significantly (by 38.75%) when constructs are printed at 40 psi compared to those printed at 5 psi.

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Composite polymeric scaffolds from alginate and single-walled carbon nanotube (SWCNT) were produced using a freeform fabrication technique. The scaffolds were characterized for their structural, mechanical, and biological properties by scanning electron microscopy, Raman spectroscopy, tensile testing, and cell-scaffold interaction study. Three-dimensional hybrid alginate/SWCNT tissue scaffolds were fabricated in a multinozzle biopolymer deposition system, which makes possible to disperse and align SWCNTs in the alginate matrix. The structure of the resultant scaffolds was significantly altered due to SWCNT reinforcement, which was confirmed by Raman spectroscopy. Microtensile testing presented a reinforcement effect of SWCNT to the mechanical strength of the alginate struts. Ogden constitutive modeling was utilized to predict the stress-strain relationship of the alginate scaffold, which compared well with the experimental data. Cellular study by rat heart endothelial cell showed that the SWCNT incorporated in the alginate structure improved cell adhesion and proliferation. Our study suggests that hybrid alginate/SWCNT scaffolds are a promising biomaterial for tissue engineering applications.

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Ankylosing spondylitis (AS) is not fully explained by inflammatory processes. Clinical, epidemiological, genetic, and course of disease features indicate additional host-related risk processes and predispositions. Collectively, the pattern of predisposition to onset in adolescent and young adult ages, male preponderance, and widely varied severity of AS is unique among rheumatic diseases. However, this pattern could reflect biomechanical and structural differences between the sexes, naturally occurring musculoskeletal changes over life cycles, and a population polymorphism. During juvenile development, the body is more flexible and weaker than during adolescent maturation and young adulthood, when strengthening and stiffening considerably increase. During middle and later ages, the musculoskeletal system again weakens. The novel concept of an innate axial myofascial hypertonicity reflects basic mechanobiological principles in human function, tissue reactivity, and pathology. However, these processes have been little studied and require critical testing. The proposed physical mechanisms likely interact with recognized immunobiological pathways. The structural biomechanical processes and tissue reactions might possibly precede initiation of other AS-related pathways. Research in the combined structural mechanobiology and immunobiology processes promises to improve understanding of the initiation and perpetuation of AS than prevailing concepts. The combined processes might better explain characteristic enthesopathic and inflammatory processes in AS.

Our results suggest that D allele of ACE I/D polymorphism significantly influences the HCM and DCM phenotypes.