No abstract

Systematic conservation assessment and conservation planning are two distinct fields of conservation science often confused as one and the same. Systematic conservation assessment is the technical, often computer-based, identification of priority areas for conservation. Conservation planning is composed of a systematic conservation assessment coupled with processes for development of an implementation strategy and stakeholder collaboration. The peer-reviewed conservation biology literature abounds with studies analyzing the performance of assessments (e.g., area-selection techniques). This information alone, however can never deliver effective conservation action; it informs conservation planning. Examples of how to translate systematic assessment outputs into knowledge and then use them for "doing" conservation are rare. South Africa has received generous international and domestic funding for regional conservation planning since the mid-1990s. We reviewed eight South African conservation planning processes and identified key ingredients of best practice for undertaking systematic conservation assessments in a way that facilitates implementing conservation action. These key ingredients include the design of conservation planning processes, skills for conservation assessment teams, collaboration with stakeholders, and interpretation and mainstreaming of products (e.g., maps) for stakeholders. Social learning institutions are critical to the successful operationalization of assessments within broader conservation planning processes and should include not only conservation planners but also diverse interest groups, including rural landowners, politicians, and government employees.

Classical familial adenomatous polyposis (FAP) is a high-penetrance autosomal dominant disease that predisposes to hundreds or thousands of colorectal adenomas and carcinoma and that results from truncating mutations in the APC gene. A variant of FAP is attenuated adenomatous polyposis coli, which results from germ-line mutations in the 5 and 3 regions of the APC gene. Attenuated adenomatous polyposis coli patients have ''multiple'' colorectal adenomas (typically fewer than 100) without the f lorid phenotype of classical FAP. Another group of patients with multiple adenomas has no mutations in the APC gene, and their phenotype probably results from variation at a locus, or loci, elsewhere in the genome. Recently, however, a missense variant of APC (I1307K) was described that confers an increased risk of colorectal tumors, including multiple adenomas, in Ashkenazim. We have studied a set of 164 patients with multiple colorectal adenomas and͞or carcinoma and analyzed codons 1263-1377 (exon 15G) of the APC gene for germ-line variants. Three patients with the I1307K allele were detected, each of Ashkenazi descent. Four patients had a germ-line E1317Q missense variant of APC that was not present in controls; one of these individuals had an unusually large number of metaplastic polyps of the colorectum. There is increasing evidence that there exist germ-line variants of the APC gene that predispose to the development of multiple colorectal adenomas and carcinoma, but without the f lorid phenotype of classical FAP, and possibly with importance for colorectal cancer risk in the general population.