Submarine canyons are the main conduits for sediment transfer from continental shelves to deep abyssal plains. A large number of bathymetric and seismic surveys provide detailed information on their morphology and structure, shedding light on the mechanisms involved in their formation. However, because of the difficulty in deploying instruments in deep marine environments, little is known about the processes by which turbidity currents erode and incise the canyon floors.In this study, we use a micro-scale tank experiment to investigate the incision of a mobile sediment bed by a gravity current. We inject a brine at the top of a ramp covered with low-density plastic sediments. Conditions for channel formation are investigated through systematic exploration of the slope vs. discharge phase space. Measurements of the sediment bed topography and the gravity-current velocity profile allow us to characterize the channel incision dynamics. A channel forms when the bed shear stress exceeds the sediment critical shear stress. In this case, a channel starts forming near the upstream end of the incline and propagates down-slope while slowly deepening. After a transient state of about 1-2 hours, the channel reaches steady state. Experimental results suggest that the slope controls the rate of erosion and the speed of channel incision, while the brine discharge controls the channel geometry. The erosional morphologies created by our experimental gravity currents show strong analogies with the axial incision of canyons, the primary mechanism by which canyons connected to continental shelves or large rivers evolve.
Antibody-mediated rejection (ABMR) is the leading cause of allograft failure in kidney transplantation. Its histological hallmark is represented by lesions of glomerulitis i.e., inflammatory cells within glomeruli. Current therapies for ABMR fail to prevent chronic allograft damage i.e., transplant glomerulopathy, leading to allograft loss. We used laser microdissection of glomeruli from formalin-fixed allograft biopsies combined with mass spectrometry-based proteomics to describe the proteome modification of 11 active and 10 chronic active ABMR cases compared to 8 stable graft controls. Of 1335 detected proteins, 77 were deregulated in glomerulitis compared to stable grafts, particularly involved in cellular stress mediated by interferons type I and II, leukocyte activation and microcirculation remodeling. Three proteins extracted from this protein profile, TYMP, WARS1 and GBP1, showed a consistent overexpression by immunohistochemistry in glomerular endothelial cells that may represent relevant markers of endothelial stress during active ABMR. In transplant glomerulopathy, 137 proteins were deregulated, which favor a complement-mediated mechanism, wound healing processes through coagulation activation and ultimately a remodeling of the glomerular extracellular matrix, as observed by light microscopy. This study brings novel information on glomerular proteomics of ABMR in kidney transplantation, and highlights potential targets of diagnostic and therapeutic interest.
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