33 resultados para Shear connectors


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The Dent Blanche Tectonic System (DBTS) is a composite thrust sheet derived from the previously thinned passive Adriatic continental margin. A kilometric high-strain zone, the Roisan-Cignana Shear Zone (RCSZ) defines the major tectonic boundary within the DBTS and separates it into two subunits, the Dent Blanche s.s. nappe to the northwest and the Mont Mary nappe to the southeast. Within this shear zone, tectonic slices of Mesozoic and pre-Alpine meta-sediments became amalgamated with continental basement rocks of the Adriatic margin. The occurrence of high pressure assemblages along the contact between these tectonic slices indicates that the amalgamation occurred prior to or during the subduction process, at an early stage of the Alpine orogenic cycle. Detailed mapping, petrographic and structural analysis show that the Roisan-Cignana Shear Zone results from several superimposed Alpine structural and metamorphic stages. Subduction of the continental fragments is recorded by blueschist-facies deformation, whereas the Alpine collision is reflected by a greenschist facies overprint associated with the development of large-scale open folds. The postnappe evolution comprises the development of low-angle brittle faults, followed by large-scale folding (Vanzone phase) and finally brittle extensional faults. The RCSZ shows that fragments of continental crust had been torn off the passive continental margin prior to continental collision, thus recording the entire history of the orogenic cycle. The role of preceding Permo-Triassic lithospheric thinning, Jurassic rifting, and ablative subduction processes in controlling the removal of crustal fragments from the reactivated passive continental margin is discussed. Results of this study constrain the temporal sequence of the tectono-metamorphic processes involved in the assembly of the DBTS, but they also show limits on the interpretation. In particular it remains difficult to judge to what extent precollisional rifting at the Adriatic continental margin preconditioned the efficiency of convergent processes, i.e. accretion, subduction, and orogenic exhumation.

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OBJECTIVE: To compare the biomechanical properties of a ventral transarticular lag screw fixation technique, a new dorsal atlantoaxial instability (AAI) clamp, and a new ventral AAI hook plate under sagittal shear loading after transection of the ligaments of the atlantoaxial joint. STUDY DESIGN: Cadaveric biomechanical study. ANIMALS: Canine cadavers (n = 10). MATERIALS AND METHODS: The occipitoatlantoaxial region of Beagles euthanatized for reasons unrelated to the study was prepared leaving only ligamentous structures and the joint capsules between the first 2 cervical vertebrae (C1 and C2). The atlanto-occipital joints were stabilized with 2 transarticular diverging positive threaded K-wires. The occipital bone and the caudal end of C2 were embedded in polymethylmethacrylate and loaded in shear to a force of 50 Newtons. The range of motion (ROM) and neutral zone (NZ) of the atlantoaxial joint were determined after 3 loading cycles with atlantoaxial ligaments intact, after ligament transection, and after fixation with each implant. The testing order of implants was randomly assigned. The implants tested last were subjected to failure testing. RESULTS: All stabilization procedures decreased the ROM and NZ of the atlantoaxial joint compared to transected ligament specimens. Only stabilization with transarticular lag screws and ventral plates produced a significant reduction of ROM compare to intact specimens. CONCLUSION: Fixation with transarticular lag screws and a ventral hook plate was biomechanically similar and provided more rigidity compared to dorsal clamp fixation. Further load cycling to failure tests and clinical studies are required before making clinical recommendations.

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Biomechanical forces, such as fluid shear stress, govern multiple aspects of endothelial cell biology. In blood vessels, disturbed flow is associated with vascular diseases, such as atherosclerosis, and promotes endothelial cell proliferation and apoptosis. Here, we identified an important role for disturbed flow in lymphatic vessels, in which it cooperates with the transcription factor FOXC2 to ensure lifelong stability of the lymphatic vasculature. In cultured lymphatic endothelial cells, FOXC2 inactivation conferred abnormal shear stress sensing, promoting junction disassembly and entry into the cell cycle. Loss of FOXC2-dependent quiescence was mediated by the Hippo pathway transcriptional coactivator TAZ and, ultimately, led to cell death. In murine models, inducible deletion of Foxc2 within the lymphatic vasculature led to cell-cell junction defects, regression of valves, and focal vascular lumen collapse, which triggered generalized lymphatic vascular dysfunction and lethality. Together, our work describes a fundamental mechanism by which FOXC2 and oscillatory shear stress maintain lymphatic endothelial cell quiescence through intercellular junction and cytoskeleton stabilization and provides an essential link between biomechanical forces and endothelial cell identity that is necessary for postnatal vessel homeostasis. As FOXC2 is mutated in lymphedema-distichiasis syndrome, our data also underscore the role of impaired mechanotransduction in the pathology of this hereditary human disease.