RESUMO
In this work, we describe a microfluidic three-dimensional (3D) chondrocyte culture mimicking in vivo articular chondrocyte morphology, cell distribution, metabolism, and gene expression. This has been accomplished by establishing a physiologic nutrient diffusion gradient across the simulated matrix, while geometric design constraints of the microchambers drive native-like cellular behavior. Primary equine chondrocytes remained viable for the extended culture time of 3 weeks and maintained the low metabolic activity and high Sox9, aggrecan, and Col2 expression typical of articular chondrocytes. Our microfluidic 3D chondrocyte microtissues were further exposed to inflammatory cytokines to establish an animal-free, in vitro osteoarthritis model. Results of our study indicate that our microtissue model emulates the basic characteristics of native cartilage and responds to biochemical injury, thus providing a new foundation for exploration of osteoarthritis pathophysiology in both human and veterinary patients.
RESUMO
The aim of the study was to show that changes in thoracoabdominal asynchrony (TAA) between quiet breathing and CO2-induced hyperpnoea can be used to differentiate between horses with healthy airways and those suffering from inflammatory airway disease (IAD) or recurrent airway obstruction (RAO). The level of TAA was displayed by the Pearson's correlation coefficient (PCC) of thoracic and abdominal signals, generated by respiratory ultrasonic plethysmography (RUP) during quiet breathing and hyperpnoea. Changes in TAA were expressed as the quotient of the PCCs (PCCQ) during normal breathing and hyperpnoea. Horses with RAO and IAD showed significant higher median PCCQ than healthy horses. Median PCCQ of horses with RAO and IAD was not significantly different. Horses affected by a pulmonary disorder showed lower TAA compared to the control group. This study suggests that TAA provides a useful parameter to differentiate horses with RAO and IAD from healthy horses.
