Stephane Bergeron | PubMed Health

PubMed2005

Reconstructive procedure for unstable radial-sided triangular fibrocartilage complex avulsions.

PURPOSE: Radial-sided avulsions of the triangular fibrocartilage complex (TFCC) (Palmer 1D) with distal radioulnar joint (DRUJ) instability remain a challenging pathology to treat. We tested an intra-articular reconstruction that addresses unstable radial-sided TFCC avulsions. METHODS: Ten preserved, dissected, cadaveric forearm specimens with intact TFCC and without ulnar-positive variance had biomechanical testing using a hydraulic testing device. The measurement of total displacement of the ulna relative to the radius was performed with an applied load ranging from 20 N in a volar direction to 20 N in a dorsal direction. Specimens were tested sequentially with intact TFCC, with surgically induced Palmer 1D lesions, and after reconstruction of the TFCC. All tests were performed at neutral, maximal pronation, and maximal supination. RESULTS: The mean total displacements of the DRUJ of the specimens at neutral rotation were as follows: 4.1 +/- 0.4 mm for the intact specimens compared with 11.8 +/- 0.8 mm after creation of the tear and 3.9 +/- 0.7 mm for the reconstructed specimens. In maximal pronation the mean total displacements were as follows: 2.4 +/- 0.3 mm intact versus 4.9 +/- 0.7 mm for torn and 2.1 +/- 0.3 mm after reconstruction. In maximal supination the mean total displacements were as follows: 1.4 +/- 0.2 mm intact versus 5.7 +/- 1.3 mm for torn and 1.0 +/- 0.1 mm after reconstruction. All specimens obtained the preoperative pronation and supination motion after the reconstruction. CONCLUSIONS: Current procedures are unable to restore DRUJ stability without a significant limitation of pronation and supination. This intra-articular reconstruction of radial-sided TFCC avulsions succeeded in restoring baseline stability to the DRUJ without interfering with pronation/supination.

Biomechanical Phenomena↗

PubMed2004

Camptothecin- and etoposide-induced apoptosis in human leukemia cells is independent of cell death receptor-3 and -4 aggregation but accelerates tumor necrosis factor-related apoptosis-inducing ligand-mediated cell death.

During camptothecin- and etoposide (VP-16)-induced apoptosis in HL-60 cells, the expression level of cell death receptor-3 (DR3), cell death receptor-4 (DR4), and FAS remained mostly unchanged, whereas the expression of silencers of death domain (SODD) and FLICE inhibitory proteins, inhibitors of the cell death receptor signaling pathways, decreased substantially. By indirect immunofluorescence and immunoperoxidase imaging and with gel filtration column chromatography, we observed rapid aggregation at the cell surface and the appearance of high molecular weight protein complexes primarily involving DR3, and DR3 and DR4 after camptothecin and VP-16 treatment, respectively. Both drugs failed to rapidly promote FAS aggregation in these cells. The high expression level of SODD or of dominant negative forms of FADD (FADD-DN) and DAP3 (DAP3-DN), or of NH2-terminal deletion mutant of TRADD (TRADD-ND) achieved by transient transfection experiments, did not impair the kinetics of apoptosis after camptothecin and VP-16 treatment in HL-60 and U937 cells. Taken together, these observations suggested that camptothecin and VP-16 induced rapid aggregation of DR4 and DR3, but paradoxically, the importance of these events in signaling apoptosis is uncertain, because the kinetics of apoptosis were unaffected, even in the presence of a high expression level of SODD, FADD-DN, TRADD-ND, and DAP3-DN. However, camptothecin or VP-16 treatment in combination with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) substantially accelerated kinetics of apoptosis than treatment with camptothecin, VP-16, or TRAIL alone. In contrast, cotreatment of camptothecin or VP-16 with TWEAK or TL1A did not facilitate apoptosis in HL60 cells. These findings suggest that DR4 aggregation mediated by camptothecin or VP-16 could represent a mean that accelerates TRAIL-induced apoptosis.

Adaptor Proteins, Signal Transducing↗