Conservation planning in forest landscapes of Fennoscandia and an approach to the challenge of countdown 2010.

Effective management of biodiversity in production landscapes requires a conservation approach that acknowledges the complexity of ecological and cultural systems in time and space. Fennoscandia has experienced major loss of forest biodiversity caused by intensive forestry. Therefore, the Countdown 2010 initiative to halt the loss of biodiversity in Europe is highly relevant to forest management in this part of the continent. As a contribution to meeting the challenge posed by Countdown 2010, we developed a spatially explicit conservation-planning exercise that used regional knowledge on forest biodiversity to provide support for managers attempting to halt further loss of biological diversity in the region. We used current data on the distribution of 169 species (including 68 red-listed species) representing different forest habitats and ecologies along with forest data within the frame of modern conservation software to devise a map of priority areas for conservation. The top 10% of priority areas contained over 75% of red-listed species locations and 41% of existing protected forest areas, but only 58% of these top priorities overlapped with core areas identified previously in a regional strategy that used more qualitative methods. We argue for aggregating present and future habitat value of single management units to landscape and regional scales to identify potential bottlenecks in habitat availability linked to landscape dynamics. To address the challenge of Countdown 2010, a general framework for forest conservation planning in Fennoscandia needs to cover different conservation issues, tools, and data needs.

Failure in post-transcriptional processing is a possible inactivation mechanism of AP-2alpha in cutaneous melanoma.

The loss of transcription factor AP-2alpha expression has been shown to associate with tumourigenicity of melanoma cell lines and poor prognosis in primary cutaneous melanoma. Altogether these findings suggest that the gene encoding AP-2alpha (TFAP2A) acts as a tumour suppressor in melanoma. To learn more of AP-2alpha's down-regulation mechanisms, we compared the immunohistochemical AP-2alpha protein expression patterns with the corresponding mRNA expression detected by in situ hybridization in 52 primary melanomas. Of the 25 samples with AP-2alpha protein negative areas, 16 (64%) expressed mRNA throughout the consecutive section. Nine specimens (36%) contained equally mRNA- and protein-negative areas, suggesting that the loss of AP-2alpha protein associated with lack of the mRNA transcript. The highly AP-2alpha protein-positive tumours (n = 27) were concordantly mRNA positive in 25 (92.6%) cases. Thirteen primary tumours were further analysed using microsatellite markers D6S470 and D6S263 for loss of heterozygosity (LOH) of a locus harbouring TFAP2A. LOHs or chromosome 6 monosomy were found in four out of five (80%) informative AP-2alpha mRNA- and protein-negative tumour areas, but also within five out of 13 (38%) informative AP-2alpha mRNA-positive tumour areas. This chromosome region is thus suggestive of harbouring a putative tumour suppressor gene of cutaneous melanoma, but this referring specifically to TFAP2A could not be completely verified in this analysis. We conclude that a failure in post-transcriptional processing of AP-2alpha is a possible inactivation mechanism of AP-2alpha in cutaneous melanoma.