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Biomedical subjects

Karin Frank

Publications and source records attributed to Karin Frank.

3 recordsLinked to original sources

A new method for conservation planning for the persistence of multiple species.

Although the aim of conservation planning is the persistence of biodiversity, current methods trade-off ecological realism at a species level in favour of including multiple species and landscape features. For conservation planning to be relevant, the impact of landscape configuration on population processes and the viability of species needs to be considered. We present a novel method for selecting reserve systems that maximize persistence across multiple species, subject to a conservation budget. We use a spatially explicit metapopulation model to estimate extinction risk, a function of the ecology of the species and the amount, quality and configuration of habitat. We compare our new method with more traditional, area-based reserve selection methods, using a ten-species case study, and find that the expected loss of species is reduced 20-fold. Unlike previous methods, we avoid designating arbitrary weightings between reserve size and configuration; rather, our method is based on population processes and is grounded in ecological theory.

Animals↗

Metapopulation persistence in heterogeneous landscapes: lessons about the effect of stochasticity.

This article addresses an important aspect of the analysis of metapopulation persistence. It highlights some consequences of ignoring and including stochasticity in the sequence of extinction and colonization events. The results are based on a comparative analysis of the outcomes of two (one deterministic, one stochastic) spatially realistic metapopulation models and a search for common effects and differences. One key result of the article is that, under certain conditions, there are extra effects of the landscape structure (number and configuration of patches, patch size distribution) on metapopulation persistence if stochasticity is included. In these cases, ignoring or including stochasticity can change conclusions about the persistence status but also ranking orders, relative results, and qualitative trends. A list of conditions is provided under which including stochasticity is vital to prevent counterproductive conclusions about metapopulation persistence. The results of the overall study are condensed in five lessons about the effect of stochasticity. A number of implications for ecological theory and conservation management are discussed. The study demonstrates the potential of three recently published approximation formulas (metapopulation capacity lambdaM, mean lifetime Tm, and effective number of patches N) to serve as tools for ecological analysis and thinking.

Environment↗

Extracellular cysteines define ectopeptidase (APN, CD13) expression and function.

Alanyl aminopeptidase (APN) is a surface-bound metallopeptidase that processes the N-terminals of biologically active peptides such as enkephalins, angiotensins, neurokinins, and cytokines. It exerts profound activity on vital processes such as immune response, cellular growth, and blood pressure control. Inhibition of either APN gene expression or its enzymatic activity severely affects leukocyte growth and function. We show here that oxidoreductase-mediated modulations of the cell surface thiol status affect the enzymatic activity of APN. Additional evidence for the pivotal role of extracellular cysteines in the APN molecule was obtained when substitution of any of these six cysteines caused complete loss of surface expression and enzymatic activity. In contrast, the transmembrane Cys24 appears to have no similar function. Enzymatically inactive cysteine mutants were retained in the endoplasmic reticulum as shown by high-resolution imaging and Endoglycosidase H digestion. In the absence of any crystal-structure data, the demonstration that individual extracellular cysteines contribute to APN expression and function appears to be of particular importance. The data are the first to show thiol-dependent modulation of the activity of a typical surface-bound peptidase at the cell surface, probably reflecting a general regulating mechanism. This may relate to various disease processes such as inflammation or malignant transformation.

Amidohydrolases↗