While current injury criteria for the automotive industry are based on bone fracture, the majority of knee injuries suffered in collisions each year d o not involve fracture o f bone. Instead, clinical studies of traumatic joint injury often document early pain and development of chronic diseases, such as osteoarthritis. Previous studies suggest chronic disease can be initiated by cell death that occurs in articular cartilage during mechanical trauma to the joint. In the current investigation early necrosis of chondrocytes was investigated after blunt trauma to chondral explants. A non-ionic surfactant (Pl88) was explored as a potential tool for early intervention into the disease process, as this surfactant has been shown to repair damaged membranes in other cell lines. Three groups o f adult bovine chondral explants were equilibrated for 48 h in culture media. Two groups were then loaded to 25 MPa in unconfined compression. Half the specimens in each group were incubated in media supplemented with 8 mg/ml PI88 immediately after loading, while the other half was returned to standard media. At 1 and 24 h the percentages of live and dead cells in compressed and control groups were determined with a cell viability stain. At 1 h post-trauma, P188 incubated specimens had a significantly increased percentage of live cells in the superficial zone versus the no-PI88 group. At 24 h the percentages of live cells in all three zones of the P l 88-treated explants were significantly greater than in the no treatment group. This study showed that P188 surfactant could help restore the integrity of cell membranes in cartilage damaged by blunt mechanical trauma. With the ability of P188 to "save" chondrocytes from early necrotic death using in vitro chondral explants, its role in prevention of a post-traumatic osteoarthritis in a diarthrodial joint should be further explored using in vivo animal models.
We have previously shown that surface lesions and acute necrosis of chondrocytes are produced by severe levels of blunt mechanical load, generating contact pressures greater than 25 MPa, on chondral and osteochondral explants. We have also found surface lesions and chronic degradation of retro-patellar cartilage within 3 years following a 6 J impact intensity with an associated average pressure of 25 MPa in the rabbit patello-femoral joint. We now hypothesized that cellular necrosis is produced acutely in the retropatellar cartilage in this model as a result of a 6 J impact and that an early injection of the non-ionic surfactant, poloxamer 188 (P188), would significantly reduce the percentage of necrotic cells in the traumatized cartilage. Eighteen rabbits were equally divided into a 'time zero' group and two other groups carried out for 4 days. One '4 day' group was administered a 1.5 ml injection ofel88 into the impacted joint immediately after trauma, while the other was injected with a placebo solution. Impact trauma produced surface lesions on retro-patellar cartilage in all groups. Approximately 15% of retro-patellar chondrocytes suffered acute necrosis in the 'time zero' and '4-day no poloxamer' groups. In contrast, significantly fewer cells (7%) suffered necrosis in the poloxamer group, most markedly in the superficial cartilage layer. The use of P188 surfactant early after severe trauma to articular cartilage may allow sufficient time for damaged cells to heal, which may in turn mitigate the potential for post-traumatic osteoarthritis. Additional studies are needed to improve the efficacy of this surfactant and to determine the long-term health ofjoint cartilage after P188 intervention.
A new formulation for obtaining the absolute backscatter coefficient from pulse-echo measurements is presented. Using this formulation, performing the diffraction correction and system calibration is straightforward. The diffraction correction function for the measurement of backscatter coefficient and the acoustic coupling function for a pulse-echo system are defined. Details of these functions for two very useful cases are presented: a flat disk transducer and a spherically focused transducer. Approximations of these functions are also provided. For a flat disk transducer, the final formulation appears as a modification to the established Sigelmann-Reid formulation. For a focused transducer, the final correction is a weak function of frequency when the scattering volume is near the focal area, rather than the frequency squared dependence proposed by earlier investigators.
Pressure wave velocity (PWV) is commonly used as a clinical marker of vascular elasticity. Recent studies have increased clinical interest in also analyzing the impact of heart rate, blood pressure, and left ventricular ejection time on PWV. In this article we focus on the development of a theoretical one-dimensional model and validation via direct measurement of the impact of ejection time and peak pressure on PWV using an in vitro hemodynamic simulator. A simple nonlinear traveling wave model was developed for a compliant thin-walled elastic tube filled with an incompressible fluid. This model accounts for the convective fluid phenomena, elastic vessel deformation, radial motion, and inertia of the wall. An exact analytical solution for PWV is presented which incorporates peak pressure, ejection time, ejection volume, and modulus of elasticity. To assess arterial compliance, the solution is introduced in an alternative form, explicitly determining compliance of the wall as a function of the other variables. The model predicts PWV in good agreement with the measured values with a maximum difference of 3.0%. The results indicate an inverse quadratic relationship ([Formula: see text]) between ejection time and PWV, with ejection time dominating the PWV shifts (12%) over those observed with changes in peak pressure (2%). Our modeling and validation results both explain and support the emerging evidence that, both in clinical practice and clinical research, cardiac systolic function related variables should be regularly taken into account when interpreting arterial function indices, namely PWV.
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