Effects of a severe storm on seagrass meadows.

Extreme environmental events can strongly affect coastal marine ecosystems but are typically unpredictable. Reliable data on benthic community conditions before such events are rarely available, making it difficult to measure their effects. At the end of October 2018, a severe storm hit the Ligurian coast (NW Mediterranean) producing damages to coastal infrastructures. Thanks to recent data collected just before the event on two Posidonia oceanica seagrass meadows hit by the storm, it has been possible to assess the impact of the event on one of the most valuable habitats of the Mediterranean Sea. By means of seagrass cover and depth data gathered along four depth transects positioned within the two meadows in areas differently exposed to the storm waves, and by using models (WW3® + SWAN + XBeach 1D) to evaluate wave height and bed shear stress, we showed that meadows experienced erosion and burial phenomena according to exposure. Paradoxically, meadows in good conditions suffered more damage as compared to those already suffering from previous local anthropogenic impacts. Besides the direct effect of waves in terms of plant uprooting, a major loss of P. oceanica was due to sediment burial in the deepest parts of the meadows. Overall, the loss of living P. oceanica cover amounted to about 50%. Considering that previous research showed that the loss of the original surface of P. oceanica meadows in 160 years due to anthropogenic pressures was similarly around 50%, the present study documented that an extreme environmental event can generate in a single day a loss of natural capital equal to that produced gradually by more than a century of human impact.

Bone as an ion exchange system: evidence for a pump-leak mechanism devoted to the maintenance of high bone K(+).

To provide evidence of active accumulation of K(+) in bone extracellular fluid (BECF), electric currents driven by damaged living metatarsal bones of weanling mice, immersed in physiological media at different [K(+)], in the presence of blockers of the K(+) channels or of the Na(+)-K(+-)ATPase inhibitor, were measured by means of a voltage-sensitive two-dimensional vibrating probe. At 4 mM extracellular K(+) concentration ([K(+)](o)), an inward steady current density (7.85-38.53 microA/cm(2)) was recorded at the damage site, which was significantly dependent on [K(+)](o). At [K(+)](o) equal to that of BECF (25 mM), current density was reduced by 76%. At [K(+)](o) of 0 mM, the current density showed an increase, which was hindered by tetraethylammonium (TEA). Basal current density was reduced significantly after exposure to TEA or BaCl(2) and was unchanged after long- term exposure to ouabain. By changing control medium with a chloride-free medium, current density was reversed. The results support the view that K(+) excess in bone is maintained by a biologically active cellular system. Because the osteocyte-bone lining cell syncytium was at the origin of the current in bone, it is likely that this system controls the ionic composition of BECF.

Osteocyte-bone lining cell system at the origin of steady ionic current in damaged amphibian bone.

A wound-generated steady electric current was measured by a two-dimensional vibrating probe system in the metatarsal bones of 22 adult frogs (Xenopus laevis) placed in amphibian Ringer. Inward currents were recorded entering a micrometric hole drilled through the cortex at middiaphyseal level. These steady state currents (mean +/- SD 8.50 +/- 2.77 microA/cm2) last approximately 2 hours, were dependent on the presence of sodium in the incubation medium, were no more detectable after fixation, and were reduced to background level when the cell membranes were solubilized. These results agree with previous recordings of metatarsal bones of weanling mice, under identical conditions. Both results suggest that the measured ionic currents have a cellular origin. Metatarsal bones of adult amphibian were purposely selected for this study because, unlike mammalian bones, their shafts are avascular and only contain an osteocyte-bone lining cell system, as documented by scanning and transmission electron observations. Thus, unlike the data from previous investigations on mammals, the results succeeded in giving the first convincing evidence that the osteocyte-bone lining cell system is the origin of damage-generated ionic currents. As damage exposes bone ionic compartment to plasma, damage-generated ionic currents are representative of ion fluxes at bone plasma interface, and cells at the origin of the current generate the driving force of such fluxes. By demonstrating that osteocytes and bone lining cells are at the origin of the current, this study suggests that the osteocyte-bone lining cell system, though operating as a cellular membrane partition, regulates ionic flow between bone and plasma. Since strain-related adaptive remodeling could also depend on ionic characteristics and flow of the bone fluid through the osteocyte lacuno-canalicular network, the results reported here support the view that osteocyte and bone lining cells may constitute a functional syncytium involved in mineral homeostasis as well as in bone adaptation to mechanical loading.