Author Correction: Trade-offs in using European forests to meet climate objectives.

In this Letter, in "About 75% of this reduction is expected to come from emission reductions and the remaining 25% from land use, land-use change and forestry", '25%' should read '1%' and '75%' should read '99%'. In the sentence "The carbon-sink-maximizing portfolio has a small negative effect on annual precipitation (-2 mm) and no effect on air temperature (Table 1)" the word 'precipitation' was omitted. Denmark was accidentally deleted during the conversion of Fig. 1. The original Letter has been corrected online.

Trade-offs in using European forests to meet climate objectives.

The Paris Agreement promotes forest management as a pathway towards halting climate warming through the reduction of carbon dioxide (CO2) emissions1. However, the climate benefits from carbon sequestration through forest management may be reinforced, counteracted or even offset by concurrent management-induced changes in surface albedo, land-surface roughness, emissions of biogenic volatile organic compounds, transpiration and sensible heat flux2-4. Consequently, forest management could offset CO2 emissions without halting global temperature rise. It therefore remains to be confirmed whether commonly proposed sustainable European forest-management portfolios would comply with the Paris Agreement-that is, whether they can reduce the growth rate of atmospheric CO2, reduce the radiative imbalance at the top of the atmosphere, and neither increase the near-surface air temperature nor decrease precipitation by the end of the twenty-first century. Here we show that the portfolio made up of management systems that locally maximize the carbon sink through carbon sequestration, wood use and product and energy substitution reduces the growth rate of atmospheric CO2, but does not meet any of the other criteria. The portfolios that maximize the carbon sink or forest albedo pass only one-different in each case-criterion. Managing the European forests with the objective of reducing near-surface air temperature, on the other hand, will also reduce the atmospheric CO2 growth rate, thus meeting two of the four criteria. Trade-off are thus unavoidable when using European forests to meet climate objectives. Furthermore, our results demonstrate that if present-day forest cover is sustained, the additional climate benefits achieved through forest management would be modest and local, rather than global. On the basis of these findings, we argue that Europe should not rely on forest management to mitigate climate change. The modest climate effects from changes in forest management imply, however, that if adaptation to future climate were to require large-scale changes in species composition and silvicultural systems over Europe5,6, the forests could be adapted to climate change with neither positive nor negative  climate effects.

Europe's forest management did not mitigate climate warming.

Afforestation and forest management are considered to be key instruments in mitigating climate change. Here we show that since 1750, in spite of considerable afforestation, wood extraction has led to Europe's forests accumulating a carbon debt of 3.1 petagrams of carbon. We found that afforestation is responsible for an increase of 0.12 watts per square meter in the radiative imbalance at the top of the atmosphere, whereas an increase of 0.12 kelvin in summertime atmospheric boundary layer temperature was mainly caused by species conversion. Thus, two and a half centuries of forest management in Europe have not cooled the climate. The political imperative to mitigate climate change through afforestation and forest management therefore risks failure, unless it is recognized that not all forestry contributes to climate change mitigation.

Repetitive tests of visual function improved visual acuity in young subjects.

AIMS: To test visual function after repetitive tests of visual acuity (VA) and contrast sensitivity (CS). METHODS: Ten young female subjects performed repetitive tests of visual functions over ten sessions within 5 weeks. Per week they performed two 30 min sessions of repetitive tests of central VA, CS and vernier acuity (VT) using Michael Bach's Freiburg Vision Test FrACT 3.5.5. FrACT presents an optotype in different spatial frequencies or an optotype with decreasing contrast. Using SPSS Statistics we analysed the correlation between the number of repetitive test sessions and the change in visual function of the total group and of the individuals. RESULTS/CONCLUSION: After ten sessions, we found a significant improvement in VA, CS and VT. When compared with the initial session, VA increased by 32%, mean CS improved by 40% and mean VT enhanced by 47%. We also found a significant correlation between the number of test sessions and VA (r=-0.374, p<0.01), CS (r=-0.258, p<0.05) and VT (r=-0.379, p<0.01). Individual changes in vision were variable. In eight subjects, VA and CS improved significantly. VT improved in nine subjects. Our data suggest that repetitive tests of visual function may improve VA significantly.

Streptococcus pyogenes M49 plasminogen/plasmin binding facilitates keratinocyte invasion via integrin-integrin-linked kinase (ILK) pathways and protects from macrophage killing.

The entry into epithelial cells and the prevention of primary immune responses are a prerequisite for a successful colonization and subsequent infection of the human host by Streptococcus pyogenes (group A streptococci, GAS). Here, we demonstrate that interaction of GAS with plasminogen promotes an integrin-mediated internalization of the bacteria into keratinocytes, which is independent from the serine protease activity of potentially generated plasmin. α(1)ß(1)- and α(5)ß(1)-integrins were identified as the major keratinocyte receptors involved in this process. Inhibition of integrin-linked kinase (ILK) expression by siRNA silencing or blocking of PI3K and Akt with specific inhibitors, reduced the GAS M49-plasminogen/plasmin-mediated invasion of keratinocytes. In addition, blocking of actin polymerization significantly reduced GAS internalization into keratinocytes. Altogether, these results provide a first model of plasminogen-mediated GAS invasion into keratinocytes. Furthermore, we demonstrate that plasminogen binding protects the bacteria against macrophage killing.