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(2005)
Im nordrhein-westfälischen Teil der Eifel (nördliche Eifel) tritt das Galio odorati-Fagetum Sougnez & Thill 1959 (Waldmeister-Buchenwald) vor allem in Silikat-, seltener auch in Kalkgebieten auf. Seinen Schwerpunkt besitzt es dort, wo unterdevonische Schiefer und Grauwacken von pleistozänen Hochflächenlehmen und Solifluktionsdecken überlagert werden. Die Bestände werden anhand von pflanzensoziologischen Aufnahmen nach BRAUN-BLANQUET dokumentiert und differenziert. Das Galio-Fagetum unterscheidet sich vom Luzulo-Fagetum (Hainsimsen-Buchenwald) durch eine ganze Reihe von Trennarten, größere mittlere Artenzahlen, höhere durchschnittliche Deckungsgrade der Krautschicht und einige feinere floristische Merkmale. Im Untersuchungsgebiet sind zwei Subassoziationen des Galio-Fagetum anzutreffen, das anspruchsvollere Galio-Fagetum typicum und das zum Luzulo-Fagetem überleitende Galio-Fagetum luzuletosum. Diese lassen sich weiter untergliedern in eine leicht verhagerte wechseltrockene Flieracium sylvaticum-Variante, eine frische Typische Variante bzw. Hordelymus europaeus-Variante, eine sickerfeuchte Dryopteris filix-mas-Variante und eine stau- bzw. wechselfeuchte Deschampsia cespitosa-Variante. Anreicherungsstandorte mit dicker Fallaubdecke sind durch Massenbestände von Festuca altissima gekennzeichnet. Ferner läßt sich eine collin-submontane Form mit Rubus fruticosus agg. von einer montanen Form mit Polygonatum verticillatum unterscheiden. Geographisch können die Bestände des Galio-Fagetum innerhalb der subatlantischen Ilexaquifolium-Rasse der nordmitteleuropäischen Melica uniflora-Ausbildung zugeordnet werden.
Bipolar disorder (BD) is a highly heritable neuropsychiatric disease characterized by recurrent episodes of mania and depression. BD shows substantial clinical and genetic overlap with other psychiatric disorders, in particular schizophrenia (SCZ). The genes underlying this etiological overlap remain largely unknown. A recent SCZ genome wide association study (GWAS) by the Psychiatric Genomics Consortium identified 128 independent genome-wide significant single nucleotide polymorphisms (SNPs). The present study investigated whether these SCZ-associated SNPs also contribute to BD development through the performance of association testing in a large BD GWAS dataset (9747 patients, 14278 controls). After re-imputation and correction for sample overlap, 22 of 107 investigated SCZ SNPs showed nominal association with BD. The number of shared SCZ-BD SNPs was significantly higher than expected (p = 1.46x10-8). This provides further evidence that SCZ-associated loci contribute to the development of BD. Two SNPs remained significant after Bonferroni correction. The most strongly associated SNP was located near TRANK1, which is a reported genome-wide significant risk gene for BD. Pathway analyses for all shared SCZ-BD SNPs revealed 25 nominally enriched gene-sets, which showed partial overlap in terms of the underlying genes. The enriched gene-sets included calcium- and glutamate signaling, neuropathic pain signaling in dorsal horn neurons, and calmodulin binding. The present data provide further insights into shared risk loci and disease-associated pathways for BD and SCZ. This may suggest new research directions for the treatment and prevention of these two major psychiatric disorders.
MAPK6/ERK3 is an atypical member of the MAPKs. An essential role has been suggested by the perinatal lethal phenotype of ERK3 knockout mice carrying a lacZ insertion in exon 2 due to pulmonary disfunction and by defects in function, activation and positive selection of T cells. To study the role of ERK3 in vivo, we generated mice carrying a conditional Erk3 allele with exon3 flanked by LoxP sites. Loss of ERK3 protein was validated after deletion of Erk3 in the female germ line using zona pellucida 3 (Zp3)-cre and a clear reduction of the protein kinase MK5 is detected, providing first evidence for the existence of the ERK3/MK5 signaling complex in vivo. In contrast to the previously reported Erk3 knockout phenotype, these mice are viable and fertile, do not display pulmonary hypoplasia, acute respiratory failure, abnormal T cell development, reduction of thymocyte numbers or altered T cells selection. Hence, ERK3 is dispensable for pulmonary and T-cell functions. The perinatal lethality, lung and T-cell defects of the previous ERK3 knockout mice are likely due to ERK3-unrelated effects of the inserted lacZ-neomycin-resistance-cassette. The knockout mouse of the closely related atypical MAPK ERK4/MAPK4 is also normal suggesting redundant functions of both protein kinases.
Bipolar disorder (BD) is a genetically complex mental illness characterized by severe oscillations of mood and behavior. Genome-wide association studies (GWAS) have identified several risk loci that together account for a small portion of the heritability. To identify additional risk loci, we performed a two-stage meta-analysis of >9 million genetic variants in 9,784 bipolar disorder patients and 30,471 controls, the largest GWAS of BD to date. In this study, to increase power we used ~2,000 lithium-treated cases with a long-term diagnosis of BD from the Consortium on Lithium Genetics, excess controls, and analytic methods optimized for markers on the Xchromosome. In addition to four known loci, results revealed genome-wide significant associations at two novel loci: an intergenic region on 9p21.3 (rs12553324, p = 5.87×10-9; odds ratio = 1.12) and markers within ERBB2 (rs2517959, p = 4.53×10-9; odds ratio = 1.13). No significant X-chromosome associations were detected and X-linked markers explained very little BD heritability. The results add to a growing list of common autosomal variants involved in BD and illustrate the power of comparing well-characterized cases to an excess of controls in GWAS.