Wild und Wildäsung im Raum Osnabrück : mit 5 Tabellen

Intensive Nutzung durch den Menschen prägt heute die durch Geologie und Klima geformte Landschaft im Raum Osnabrück. Die dort vorkommenden Wildarten werden in ihrer Lebensweise deutlich durch den Menschen beeinllußt. Insbesondere die Intensivierung der Land- und Forstwirtschaft, der Straßenverkehr und die Erholungsuchenden schränken die Lebensmöglichkeiten des Wildes ein. Die vorkommenden Wild arten werden genannt, wobei Streckenzahlen als Maßstab für ihre Häuligkeit benutzt werden. Unter Berücksichtigung allgemeingültiger und überregionaler Aspekte werden die Ansprüche des Wildes an den Lebensraum verdeutlicht. Lebensraumverbesserungen durch Schaffung von Äsungs- und Deckungsflächen sowie durch Extensivierungsverfahren in der Landwirtschaft werden diskutiert.Geology and climate shaped the countryside of Osnabrück, which is today also characterized by the intensive use by human beings. Human beings have a great inlluence on the way of lile of the game which is lound there. Especially the intensilication of agriculture and forestry, the traffic and the people who go to the countryside in order to recover reduce the living conditions 01 the game. The number of animals shot in a hunt serves as a measure for the Irequency of the different species of game. In view of general and national aspects the demand of the game on its biosphere is shown clearly. Possibilities of improvements concerning the biosphere through creation of grazing- and covering expance and also through extensive methods in agriculture are discussed

Adrenergic Repression of the Epigenetic Reader MeCP2 Facilitates Cardiac Adaptation in Chronic Heart Failure

RATIONALE: In chronic heart failure, increased adrenergic activation contributes to structural remodeling and altered gene expression. Although adrenergic signaling alters histone modifications, it is unknown, whether it also affects other epigenetic processes, including DNA methylation and its recognition. OBJECTIVE: The aim of this study was to identify the mechanism of regulation of the methyl-CpG-binding protein 2 (MeCP2) and its functional significance during cardiac pressure overload and unloading. METHODS AND RESULTS: MeCP2 was identified as a reversibly repressed gene in mouse hearts after transverse aortic constriction and was normalized after removal of the constriction. Similarly, MeCP2 repression in human failing hearts resolved after unloading by a left ventricular assist device. The cluster miR-212/132 was upregulated after transverse aortic constriction or on activation of α1- and β1-adrenoceptors and miR-212/132 led to repression of MeCP2. Prevention of MeCP2 repression by a cardiomyocyte-specific, doxycycline-regulatable transgenic mouse model aggravated cardiac hypertrophy, fibrosis, and contractile dysfunction after transverse aortic constriction. Ablation of MeCP2 in cardiomyocytes facilitated recovery of failing hearts after reversible transverse aortic constriction. Genome-wide expression analysis, chromatin immunoprecipitation experiments, and DNA methylation analysis identified mitochondrial genes and their transcriptional regulators as MeCP2 target genes. Coincident with its repression, MeCP2 was removed from its target genes, whereas DNA methylation of MeCP2 target genes remained stable during pressure overload. CONCLUSIONS: These data connect adrenergic activation with a microRNA-MeCP2 epigenetic pathway that is important for cardiac adaptation during the development and recovery from heart failure