Dynamische modellering van streeflasten voor bossen in Vlaanderen

For forest and nature policy it is important to know the highest level of atmospheric nitrogen (N) and sulphur (S) deposition below which harmful acidifying effects on forest soils do not occur. Therefore, target loads for acidification were determined for Flemish forests according to the harmonized methodology of the Coordination Center of Effects. Target loads are calculated in a similar way as critical loads, but account for soil buffer mechanims. Critical loads are based on a steady-state mass balance and equal the highest long-term deposition that still respects a pre-defined soil-chemical status. A target load is the deposition for which the chosen status is respected from the target year on. This requires taking into account the buffering capacity of soil processes such as cation exchange and N immobilisation, as these create a time lag in soil recovery when the potentially acidifying deposition declines. Critical loads were calculated for 1438 Flemish forest locations; on the one hand for the protection of roots against acidification using a maximum ratio of aluminum vs. base cation concentration in soil water, on the other hand for eutrophication using a maximum nitrate leaching. For non-calcareous forest soils in Flanders, the median critical load of S (criterion Al:Bc = 1) amounted to 1754 eq ha-1 year-1. The median critical load of acidifying N was 3010 eq ha-1 year-1 including denitrification and 2227 eq ha-1 year-1 assuming no denitrifi-cation. The median critical load for nutrient N with respect to eutrophication (criterion NO3le,acc = 100 eq ha-1 year-1) was 935 eq ha-1 year-1. Target loads for acifidication were determined for 83 non-calcareous Flemish forest stands of the forest soil and forest vitality network (Level I and II plots). The Very Simple Dynamic (VSD) model was used for simulating the chemical composition of soil and soil water throughout time based on soil characteristics and rainfall, deposition and growth data. Target loads were calculated for the target years 2030, 2050 and 2100. To respect the Al:Bc criterion from 2050 on, for example, a N and S deposition reduction was needed in 84% of the plots according to the VSD model. In 12% of the plots no additional deposition reduction was needed compared to the Gothenburg agreements, while for 4% the Al:Bc criterion could not be reached in 2050 even when N and S deposition would be reduced to zero from 2010 on. The median target load of S for target year 2030 amounted to 58% of the median critical load of S; for the years 2050 and 2100 this ratio was 65% and 86%, respectively. For N the difference between target loads and critical loads was smaller than for S due to the time dependent N immobilisation. The critical and target loads of S were lower for deciduous stands than for coniferous stands because of the higher nutrient uptake by deciduous trees. The acceptable acidifying deposition was lower for forests on sandy sails than on loamy or clayey soils due to the lower mineral weathering rate in sandy soils. According to the sensitivity analysis, the calculated target loads depended mostly on the base cation fluxes mineral weathering, deposition, and net growth uptake. Furthermore, the chosen cation exchange model and the assumed relationship between the soil solution pH and aluminium concentration clearly affected the results. Despite the inherent uncertainty in modelling soil acidification at a regional level, the present research implies that important N and S deposition reductions are needed to allow recovery of Flemish forest soils to a minimal chemical quality

Crown ethers: novel permeability enhancers for ocular drug delivery?

Crown ethers are cyclic molecules consisting of a ring containing several ether groups. The most common and important members of this series are 12-crown-4 (12C4), 15-crown-5 (15C5), and 18-crown-6 (18C6). These container molecules have the ability to sequester metal ions and their complexes with drugs are able to traverse cell membranes. This study investigated 12C4, 15C5 and 18C6 for their ability to increase solubility of ocular drugs and enhance their penetration into the cornea. Phase solubility analysis determined crown ethers’ ability to enhance the solubility of riboflavin, a drug used for the therapy of keratoconus, and these solutions were investigated for ocular drug permeation enhancing properties. Atomic absorption spectroscopy demonstrated crown ether solutions ability to sequester Ca2+ from corneal epithelia and crown ether mediated adsorption of riboflavin into the stroma was investigated. Induced corneal opacity studies assessed potential toxicity of crown ethers. Crown ethers enhanced riboflavin’s aqueous solubility and its penetration into in vitro bovine corneas; the smaller sized crown ethers gave greatest enhancement. They were shown to sequester Ca2+ ions from corneal epithelia, doing so loosens cellular membrane tight junctions thus enhancing riboflavin penetration. Induced corneal opacity was similar to that afforded by benzalkonium chloride and less than is produced using polyaminocarboxylic acids. However, in vivo experiments performed in rats with 12C4 did not show any statistically significant permeability enhancement compared to enhancer-free formulation

Exceedance of critical loads and of critical limits impacts tree nutrition across Europe

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The bashful and the boastful : prestigious leaders and social change in Mesolithic Societies

The creation and maintenance of influential leaders and authorities is one of the key themes of archaeological and historical enquiry. However the social dynamics of authorities and leaders in the Mesolithic remains a largely unexplored area of study. The role and influence of authorities can be remarkably different in different situations yet they exist in all societies and in almost all social contexts from playgrounds to parliaments. Here we explore the literature on the dynamics of authority creation, maintenance and contestation in egalitarian societies, and discuss the implications for our interpretation and understanding of the formation of authorities and leaders and changing social relationships within the Mesolithic

Surgical resection and radiofrequency ablation initiate cancer in cytokeratin-19(+)- liver cells deficient for p53 and Rb

The long term prognosis of liver cancer patients remains unsatisfactory because of cancer recurrence after surgical interventions, particularly in patients with viral infections. Since hepatitis B and C viral proteins lead to inactivation of the tumor suppressors p53 and Retinoblastoma (Rb), we hypothesize that surgery in the context of p53/Rb inactivation initiate de novo tumorigenesis. We, therefore, generated transgenic mice with hepatocyte and cholangiocyte/liver progenitor cell (LPC)-specific deletion of p53 and Rb, by interbreeding conditional p53/Rb knockout mice with either Albumin-cre or Cytokeratin-19-cre transgenic mice. We show that liver cancer develops at the necrotic injury site after surgical resection or radiofrequency ablation in p53/Rb deficient livers. Cancer initiation occurs as a result of specific migration, expansion and transformation of cytokeratin-19+-liver (CK-19+) cells. At the injury site migrating CK-19+ cells formed small bile ducts and adjacent cells strongly expressed the transforming growth factor β (TGFβ). Isolated cytokeratin-19+ cells deficient for p53/Rb were resistant against hypoxia and TGFβ-mediated growth inhibition. CK-19+ specific deletion of p53/Rb verified that carcinomas at the injury site originates from cholangiocytes or liver progenitor cells. These findings suggest that human liver patients with hepatitis B and C viral infection or with mutations for p53 and Rb are at high risk to develop tumors at the surgical intervention site

Inherited liver shunts in dogs elucidate pathways regulating embryonic development and clinical disorders of the portal vein

Congenital disorders of the hepatic portal vasculature are rare in man but occur frequently in certain dog breeds. In dogs, there are two main subtypes: intrahepatic portosystemic shunts, which are considered to stem from defective closure of the embryonic ductus venosus, and extrahepatic shunts, which connect the splanchnic vascular system with the vena cava or vena azygos. Both subtypes result in nearly complete bypass of the liver by the portal blood flow. In both subtypes the development of the smaller branches of the portal vein tree in the liver is impaired and terminal branches delivering portal blood to the liver lobules are often lacking. The clinical signs are due to poor liver growth, development, and function. Patency of the ductus venosus seems to be a digenic trait in Irish wolfhounds, whereas Cairn terriers with extrahepatic portosystemic shunts display a more complex inheritance. The genes involved in these disorders cannot be identified with the sporadic human cases, but in dogs, the genome-wide study of the extrahepatic form is at an advanced stage. The canine disease may lead to the identification of novel genes and pathways cooperating in growth and development of the hepatic portal vein tree. The same pathways likely regulate the development of the vascular system of regenerating livers during liver diseases such as hepatitis and cirrhosis. Therefore, the identification of these molecular pathways may provide a basis for future proregenerative intervention

TGF-β in progression of liver disease

Transforming growth factor-β (TGF-β) is a central regulator in chronic liver disease contributing to all stages of disease progression from initial liver injury through inflammation and fibrosis to cirrhosis and hepatocellular carcinoma. Liver-damage-induced levels of active TGF-β enhance hepatocyte destruction and mediate hepatic stellate cell and fibroblast activation resulting in a wound-healing response, including myofibroblast generation and extracellular matrix deposition. Being recognised as a major profibrogenic cytokine, the targeting of the TGF-β signalling pathway has been explored with respect to the inhibition of liver disease progression. Whereas interference with TGF-β signalling in various short-term animal models has provided promising results, liver disease progression in humans is a process of decades with different phases in which TGF-β or its targeting might have both beneficial and adverse outcomes. Based on recent literature, we summarise the cell-type-directed double-edged role of TGF-β in various liver disease stages. We emphasise that, in order to achieve therapeutic effects, we need to target TGF-β signalling in the right cell type at the right time