PubMed · 8091927
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
E Berardesca. 1994. Racial differences in skin function.. https://pubmed.ncbi.nlm.nih.gov/8091927/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Elastography is based on the estimation of strain due to tissue compression. Strain is computed from the estimates of time delays between gated precompression and postcompression echo signals. Time delay estimates are obtained from the location of the peak of the crosscorrelation function between gated precompression and postcompression signals. It is of paramount importance to accurately estimate the time delays for good quality elastograms. A main source of time delay estimation (TDE) error in elasticity imaging is the decorrelation of the echo signal as a result of tissue compression (decorrelation noise). The effect of decorrelation on the mean of the crosscorrelation function and the correlation coefficient has been investigated. The expected value of the cross-correlation function between the precompression and postcompression signals was shown to be a filtered version of the autocorrelation function of the precompression signal. In this article, the effect of temporal stretching of the postcompression echo signal on the cross-correlation function will be investigated along the same line. The applied compression is assumed to be uniform; the decorrelations introduced by the lateral and elevational tissue movements are ignored. The theory predicts that if the postcompression echo signals are stretched before the TDE step, then for small strains, the cross-correlation function very closely resembles the autocorrelation function. For larger strains, correlation is improved if temporal stretching is applied. The theory is corroborated by results from simulation and homogeneous phantom experiments. Thus, the decorrelation noise in elastograms can be reduced by temporal stretching of the postcompression signal.
In an accompanying article (Jubran, et al., Am. J. Respir. Crit. Care Med. 155:906-915), we report that patients with chronic obstructive pulmonary disease (COPD) who failed a trial of weaning from mechanical ventilation developed worsening of pulmonary mechanics compared with patients who tolerated the trial and were extubated. We wondered whether the greater derangements in pulmonary mechanics in the weaning failure patients are evident ever before undertaking the weaning trial. We measured mechanics of the respiratory system, lung, and chest wall during passive ventilation at usual ventilator settings in 12 patients who went on to fail a weaning trial and in 12 patients who were successfully weaned. No differences in the resistances of the respiratory system, lung, and chest wall were observed between the two groups or when the resistances were separated into the components derived from ohmic resistance and viscoelastic behavior/time-constant inhomogeneities. Likewise, the groups did not differ in terms of static elastance and dynamic intrinsic positive end-expiratory pressure (PEEPi) of the respiratory system and the respective lung and chest wall components or in terms of dynamic elastances of the respiratory system and chest wall. The failure group had a higher dynamic elastance of the lung than the success group (p < 0.01), but the individual values showed considerable overlap among the patients in the two groups so limiting its usefulness in signaling a patient's ability to sustain spontaneous ventilation. Thus, mechanics of the respiratory system and its lung and chest wall components during passive ventilation did not satisfactorily discriminate between patients who failed a weaning trial and those successfully weaned, and, thus, are unlikely to be useful in signaling a patient's ability to tolerate the discontinuation of mechanical ventilation.
STUDY DESIGN: A finite element model of a lumbar motion segment was constructed. OBJECTIVES: The model was directed toward understanding the effect of compression, bending and twisting, and diurnal fluid changes in the disc on the propensity to disc prolapse. Tensile stresses in the anulus fibers were computed and used to determine the successive steps required to create a fissure in the disc. SUMMARY OF BACKGROUND DATA: Disc prolapse is more likely under combined loading involving compression and bending and twisting. Changes in fluid content in the disc also affect the mechanical behavior of the disc. METHODS: The three-dimensional model accounted for the viscoelastic material properties of the anulus fibers and ligaments. Diurnal fluid exchange was simulated by changing the fluid content in the nucleus of the disc. Combined with bending and twisting, a compressive load was applied at different loading rates. RESULTS: The maximum tensile stress in the anulus fibers always occurred in the fibers at the inner posterior anulus at the junction of the disc and the endplate. Of the three models tested, the "weakest" (or the first to fail) was the saturated disc subjected to compression and bending and twisting. As the loading rate increased, anulus fiber failure was initiated at a lower value of compressive load. An increasing compressive load applied to a flexed, twisted, and saturated disc resulted in progressive failure, or fissure propagation, starting at the posterior inner anulus at the junction of the disc and the endplate. CONCLUSIONS: The results from this study suggest that there are several key factors involved in the initiation and propagation of anulus failure: axial compressive load, bending and twisting, and disc saturation. If one of these is lacking, anulus failure is harder to achieve.