Accurately quantifying evapotranspiration (ET) is essential for modelling regional-scale ecosystem water balances. This study assembled an ET data set estimated from eddy flux and sapflow measurements for 13 ecosystems across a large climatic and management gradient from the United States, China, and Australia. Our objectives were to determine the relationships among monthly measured actual ET (ET), calculated FAO-56 grass reference ET (ET o ), measured precipitation (P), and leaf area index (LAI)-one associated key parameter of ecosystem structure. Results showed that the growing season ET from wet forests was generally higher than ET o while those from grasslands or woodlands in the arid and semi-arid regions were lower than ET o . Second, growing season ET was found to be converged to within š10% of P for most of the ecosystems examined. Therefore, our study suggested that soil water storage in the nongrowing season was important in influencing ET and water yield during the growing season. Lastly, monthly LAI, P, and ET o together explained about 85% of the variability of monthly ET. We concluded that the three variables LAI, P, and ET o , which were increasingly available from remote sensing products and weather station networks, could be used for estimating monthly regional ET dynamics with a reasonable accuracy. Such an empirical model has the potential to project the effects of climate and land management on water resources and carbon sequestration when integrated with ecosystem models.

The acute lung injury (ALI) that occurs after the highly pathogenic avian influenza H5N1 virus infection is associated with an abnormal host innate immune response. Because the complement system plays a central role in innate immunity and because aberrant complement activation is associated with a variety of autoimmune and inflammatory diseases, we investigated the complement involvement in the pathogenesis of ALI induced by H5N1 virus infection. We showed that ALI in H5N1-infected mice was caused by excessive complement activation, as demonstrated by deposition of C3, C5b-9, and mannose-binding lectin (MBL)-C in lung tissue, and by up-regulation of MBL-associated serine protease-2 and the complement receptors C3aR and C5aR. Treatment of H5N1-infected mice with a C3aR antagonist led to significantly reduced inflammation in lungs, alleviating ALI. Furthermore, complement inhibition with an anti-C5a antibody or complement depletion with cobra venom factor after H5N1 challenge resulted in a similar level of protection to that seen in C3aR antagonist-treated mice. These results indicate that excessive complement activation plays an important role in mediating H5N1-induced ALI and that inhibition of complement may be an effective clinical intervention and adjunctive treatment for H5N1-induced ALI.

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