Citations

Hip simulators are regularly used by researchers to assess total hip arthroplasty (THA) implants, range of motion, stability, and alignment of acetabular cup and stem. Previous papers have described three types of simulators: three-dimensional protractors, biaxial rocking motion (BRM) protractors, and single-axis prosthetic range-of-motion (PROM) devices. We have developed a new hip simulator in which the ROM device is completely automated in three independent axes (elevation, internal/external rotation, and plane of elevation). Coupled with the simulator, we used a FaroArm Gold Series coordinate measuring machine (CMM) to accurately align the implant components. The results show that the methodology and alignment setup are accurate and repeatable. With this simulator and digitizer, we are able to study the characteristics of numerous THA implants at various orientations of the pelvis, acetabular cup, stem, and femur.

A fracture healing monitoring system with external fixators was analysed using the finite element method. Pin displacement and side bar strain under axial and side loading were evaluated at various stages of simulated fracture healing. In general, a recovery of rigidity at the fracture site of up of 25 percent of intact bone could be sensitively predicted. Effects of cross-sectional distribution and length of callus at the fracture site on pin displacement and side bar strain were studied. Alterations of fixation configuration, such as component failure during the healing process, were found to have relatively little effect on pin displacement but a rather larger effect on side bar strain. In general, the assessment of fracture healing by monitoring the deformation of external fixation devices is a useful idea. However, in practice, great care must be taken to fully understand the implication of the monitoring system before drawing conclusions on such measurements.

In biomechanics, the knowledge of accurate location of a joint center is essential because equilibration of the external loads and muscular forces about the joint is performed about this specific point. This paper focuses on the location of centers of gleno-humeral joint and scapulo-thoracic joint in a subject moving their arm in the scapular plane with a magnitude of 120°. Biplanar radiography with successive exposures has been used locating anatomical axes of bones. Geometric models of bones were defined allowing access to bone morphology by superposing model projections onto X-ray imaged bone contours. Functional models were used so as to represent the behavior in motion of shoulder joints. These techniques allowed us to access to results describing the linear and angular relative displacements of the shoulder bones between two different postures. The gleno-humeral and scapulo-thoracic finite joint centers (F H and F S ) are first defined through the location of the corresponding helical axis of motion (HAM) moving the joint from positions occupied in initial and final postures. The gleno-humeral and scapulo-thoracic mean joint centers (M H and M S ) are then calculated using a new technique, which defines that each joint center has the point having the smallest migrations while moving continuously from initial to final postures. This allows for the analysis of the linear and angular clearances, which affect joint center migration. The whole continuous movement has been parsed into several steps to test the stability of the mean joint center throughout the motion.

The tenosynovium in the human carpal tunnel is connected to the flexor tendons and the median nerve by the subsynovial connective tissue (SSCT). The most common histological finding in carpal tunnel syndrome (CTS), a compression neuropathy of the median nerve, is noninflammatory fibrosis of the SSCT. The relationship, if any, between the fibrosis and nerve pathology is unknown, although some have speculated that a change in the SSCT volume or stiffness might be the source of the compression. Yet, while animal models have been used to study the physiology of nerve compression, so far none have been used to study the relationship of the SSCT pathology to the neurophysiological abnormalities. The purpose of this study was to identify animal models that might be appropriate to study the interaction of SSCT and nerve function in the development of CTS. The front paws of a rat, rabbit, dog, and baboon were dissected. The carpal tunnel anatomy and SSCT of these animals were also examined by light and scanning microscopy and compared to the relevant human anatomy and ultrastructure. The carpal tunnel anatomy and contents of the baboon and rabbit are similar to humans. The canine carpal tunnel lacks the superficial flexor tendons and the rat carpal tunnel is very small. The human, baboon, and rabbit specimens had very similar organization of the SSCT, and content of the carpal canal. We conclude that, while both the baboon and rabbit would be good animal models to study the relationship of the SSCT to CTS, the rabbit is likely to be more practical, in terms of cost and animal care concerns.

Abstract Germ line mutations in several genes (BRCA1, BRCA2, and CHEK2) whose products are involved in the DNA damage–signaling pathway have been implicated in prostate cancer risk. To identify additional genes in this pathway that might confer susceptibility to this cancer, we analyzed a recently identified DNA damage–response gene, p53AIP1 (a gene encoding for p53-regulated apoptosis-inducing protein 1), for genetic variants in prostate cancer. Five novel germ line variants were identified. The two truncating variants (Ser32Stop and Arg21insG) were found in 3% (4 of 132) of unselected prostate tumor samples. Genotyping of the two variants in an additional 393 men with sporadic prostate cancer showed a frequency of 3.1% (12 of 393) in contrast to 0.6% (2 of 327) in 327 unaffected men (Fisher's exact test, P = 0.018), with an odds ratio (OR) of 5.1 [95% confidence interval (95% CI), 1.1-23.0]. In addition, two of six tumors carrying the truncating variants were associated with loss of heterozygosity of the wild-type alleles, suggesting that p53AIP1 may act as a tumor suppressor. We also showed that the truncated p53AIP1 was unable to induce apoptosis and suppress cell growth in HeLa and COS-7 cells. These results suggest that loss-of-function variants in p53AIP1 associated with the risk of sporadic prostate cancer and further support the concept that the genetic defects in the DNA damage–response genes play an important role in the development of prostate cancer. (Cancer Res 2006; 66(21): 10302-7)