Molecular mechanisms of the acute kidney injury to chronic kidney disease transition: An updated view

Increasing evidence has demonstrated the bidirectional link between acute kidney injury (AKI) and chronic kidney disease (CKD) such that, in the clinical setting, the new concept of a unified syndrome has been proposed. The pathophysiological reasons, along with the cellular and molecular mechanisms, behind the ability of a single, acute, apparently self-limiting event to drive chronic kidney disease progression are yet to be explained. This acute injury could promote progression to chronic disease through different pathways involving the endothelium, the inflammatory response and the development of fibrosis. The interplay among endothelial cells, macrophages and other immune cells, pericytes and fibroblasts often converge in the tubular epithelial cells that play a central role. Recent evidence has strengthened this concept by demonstrating that injured tubules respond to acute tubular necrosis through two main mechanisms: The polyploidization of tubular cells and the proliferation of a small population of self-renewing renal progenitors. This alternative pathophysiological interpretation could better characterize functional recovery after AKI

Polarization Dependence of Bulk Ion Acceleration from Ultrathin Foils Irradiated by High-Intensity Ultrashort Laser Pulses

The acceleration of ions from ultrathin (10-100 nm) carbon foils has been investigated using intense (∼ 6 x1020 Wcm-2), ultrashort (45 fs) laser pulses, highlighting a strong dependence of the ion beam parameters on the laser polarization, with circularly polarized (CP) pulses producing the highest energies for both protons and carbons (25-30 MeV/nucleon); carbon ion energies obtained employing CP pulses were signicantly higher (∼2.5 times) than for irradiations employing linearly polarized (LP) pulses. Particle-in-cell simulations indicate that Radiation Pressure Acceleration becomes the dominant mechanism for the thinnest targets and CP pulses