Paleoenvironmental changes during the late Miocene (Messinian)–Pliocene transition (Bajo Segura Basin, southeastern Spain): sedimentological and ichnological evidence

A detailed sedimentological and paleontological analysis of the uppermost Miocene (Messinian)–Pliocene boundary at the northern border of the Bajo Segura Basin, southeastern Spain, was carried out in order to describe the evolution of the regional paleocoastline during the Pliocene reflooding of the Mediterranean immediately after the sea-level fall related to the Messinian Salinity Crisis. Multiple trace fossils typical of firm- and hardgrounds were recognized, allowing identification of Glossifungites (two different types), Entobia, and Gnathichnus ichnofacies. Trace-fossil analysis showed that lithology and media consistency exerted considerable control on the development of the different ichnocoenoses and that there was a clear decrease in hydrodynamic energy from a coastal to a shallow-water shelf environment related to progressive sea-level rise. Ichnological and sedimentological data provide evidence that the definitive flooding of the Mediterranean was rapid and synchronous throughout the northern margin of the Bajo Segura Basin. The following model for the Pliocene transgression in the study area is therefore proposed: (1) the marine ingression penetrated along the incised paleovalleys carved as a consequence of the fall in sea level, where the first two Pliocene systems were deposited (P0–P1); (2) during the maximum flooding surface of the transgression, the sea overflowed the margins of the paleovalleys and extended throughout the entire northern margin of the basin; and (3) the third Pliocene system was deposited, forming the lower part of a highstand systems tract (P2).

Cellular responses following retinal injuries and therapeutic approaches for neurodegenerative diseases

Retinal neurodegenerative diseases like age-related macular degeneration, glaucoma, diabetic retinopathy and retinitis pigmentosa each have a different etiology and pathogenesis. However, at the cellular and molecular level, the response to retinal injury is similar in all of them, and results in morphological and functional impairment of retinal cells. This retinal degeneration may be triggered by gene defects, increased intraocular pressure, high levels of blood glucose, other types of stress or aging, but they all frequently induce a set of cell signals that lead to well-established and similar morphological and functional changes, including controlled cell death and retinal remodeling. Interestingly, an inflammatory response, oxidative stress and activation of apoptotic pathways are common features in all these diseases. Furthermore, it is important to note the relevant role of glial cells, including astrocytes, Müller cells and microglia, because their response to injury is decisive for maintaining the health of the retina or its degeneration. Several therapeutic approaches have been developed to preserve retinal function or restore eyesight in pathological conditions. In this context, neuroprotective compounds, gene therapy, cell transplantation or artificial devices should be applied at the appropriate stage of retinal degeneration to obtain successful results. This review provides an overview of the common and distinctive features of retinal neurodegenerative diseases, including the molecular, anatomical and functional changes caused by the cellular response to damage, in order to establish appropriate treatments for these pathologies.