Vegetation and longitudinal coarse sediment connectivity affect the ability of ecosystem restoration to reduce riverbank erosion and turbidity in drinking water.

It is a substantial challenge to quantify the benefits which ecosystems provide to water supply at scales large enough to support policy making. This study tested the hypothesis that vegetation could reduce riverbank erosion, and therefore contribute to reducing turbidity and the cost of water supply, during a large magnitude flood along a 62 km riparian corridor where land cover differed substantially from natural conditions. Several lines of evidence were used to establish the benefits that vegetation provided to reducing eleven riverbank erosion processes over 1688 observations. The data and analyses confirmed that vegetation significantly reduced the magnitude of the riverbank erosion process which was the largest contributor to total erosion volume. For this process, a 1% increase in canopy cover of trees higher than five metres reduced erosion magnitude by between 2 and 3%. Results also indicate that riverbank erosion was likely to be affected by direct changes to the riparian corridor which influenced longitudinal coarse sediment connectivity. When comparing the impact of these direct changes on a relative basis, sand and gravel extraction was likely to be the dominant contributor to changed erosion rates. The locations where erosion rates had substantially increased were of limited spatial extent and in general substantial change in river form had not occurred. This suggests that the trajectory of river condition and increasing turbidity are potentially reversible if the drivers of river degradation are addressed through an ecosystem restoration policy.

Cyclosporin A pretreatment in a rat model of warm ischaemia/reperfusion injury.

BACKGROUND/AIMS: These studies investigated the role of apoptosis following ischaemia/reperfusion (I/R) injury to the liver and the effect of pretreatment with Cyclosporin A. METHODS: Male Sprague-Dawley rats received 30 min of warm ischaemia followed by a period of reperfusion of 6 h. Rats were given olive oil or Cyclosporin A (30 mg/kg p.o.) the day before surgery. Neutrophil numbers were assessed in haematoxylin-eosin-stained sections of liver. In situ staining of sections using TdT-mediated dUTP-fluorescein nick-end labelling was carried out to determine the extent of apoptosis, followed by electron microscopy. Semi-quantitative polymerase chain reaction (PCR) analysis of the transcript for Fas antigen was performed. RESULTS AND CONCLUSIONS: High levels of apoptosis were observed in I/R injury, which were greatly ameliorated in Cyclosporin A-pretreated groups. PCR analysis indicated a reduction in the level of expression of Fas transcript in Cyclosporin A-treated rats. Histological analysis showed a significant increase in the number of neutrophils infiltrating I/R-injured tissue (62 +/- 10.69, n=16), which was markedly reduced by Cyclosporin A pretreatment (16 +/- 7, n=6, P<0.05). These results indicate a role of parenchymal apoptosis in the pathogenesis of I/R injury, which occurs in association with neutrophil infiltration, both of which can be significantly reduced by Cyclosporin A pretreatment.