Annals of biomedical engineering
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In recent years, development of rheumatoid arthritis (RA) drug therapy has been more directly targeted to counteract specific mechanisms of inflammation, and it is now believed that early aggressive treatment with disease modifying drugs is important to inhibit future structural joint damage. The development of these new treatments has increased the need for methodologies to assess disease activity in RA and monitor the effectiveness of drug therapy. Unlike X-ray, which shows only structural bone damage, magnetic resonance imaging (MRI) can depict soft tissue damage and synovitis, the primary pathology of RA. ⋯ Preliminary results show good correlation to early enhancement rate, which has previously been shown to be a useful clinical marker of RA activity. However, the use of tracer kinetic modeling methods potentially provides more specific information regarding underlying RA physiology. This approach could provide a useful new tool in RA patient management and could substantially improve RA therapeutic studies by calculating objective biomarkers of the disease state.
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In vitro models of brain injury that use thick 3-D cultures and control extracellular matrix constituents allow evaluation of cell-matrix interactions in a more physiologically relevant configuration than traditional 2-D cultures. We have developed a 3-D cell culture system consisting of primary rat cortical neurons distributed throughout thick (>500 microm) gels consisting of type IV collagen (Col) conjugated to agarose. Neuronal viability and neurite outgrowth were examined for a range of agarose (AG) percentages (1.0-3.0%) and initial collagen concentrations ([Col](i); 0-600 microg/mL). ⋯ Following high rate deformation, neuronal viability significantly decreased with increasing [Col](i), implicating cell-matrix adhesions in acute mechanotransduction events associated with traumatic loading. These results suggest interrelated roles for matrix mechanical properties and receptor-mediated cell-matrix interactions in neuronal viability, neurite outgrowth, and transduction of high rate deformation. This model system may be further exploited for the elucidation of mechanotransduction mechanisms and cellular pathology following mechanical insult.
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A novel approach for detection of polynomial nonlinearity in the neuro-cardiovascular system based on cyclostationary analysis is presented. Metronome breathing is employed to provide a sinusoidal input to the neuro-cardiovascular system in which Heart Rate Variability (HRV) and Blood Pressure Variation (BPV) are considered as its outputs. ⋯ It is shown that a second order polynomial nonlinear system is actually involved in producing the HRV and BPV. The strength of this nonlinearity decreases with increasing the breathing rate.