Institution
University of Göttingen
Education•Göttingen, Germany•
About: University of Göttingen is a education organization based out in Göttingen, Germany. It is known for research contribution in the topics: Population & Gene. The organization has 43851 authors who have published 86318 publications receiving 3010295 citations. The organization is also known as: Georg-August-Universität Göttingen & Universität Göttingen.
Topics: Population, Gene, Species richness, Context (language use), Catalysis
Papers published on a yearly basis
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TL;DR: In this paper, an algebraic description of the Picard-Lefschetz-monodromy of a singularity is given, and it is shown that the eigenvalues of the monodromy are roots of unity.
Abstract: J. Milnor recently introduced the local Picard-Lefschetz-monodromy of an isolated singularity of a hypersurface. This is an important tool in the investigation of the topology of singularities. The monodromy is an action on a certain cohomology group and is defined in topological terms. In this paper we find an algebraic description of the monodromy. We construct by algebraic methods a regular singular ordinary linear differential operator, such that the monodromy of this singular operator coincides with the Picard-Lefschetz monodromy. As an application we prove that the eigenvalues of the monodromy are roots of unity. Our treatment is close in spirit to Grothendiecks theory of the Gauβ-Manin-connection.
369 citations
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University of Southern California1, Oslo University Hospital2, University of Oslo3, University of California, Irvine4, University of California, San Diego5, University of Göttingen6, University Hospital Heidelberg7, Karolinska Institutet8, Karolinska University Hospital9, University of Gothenburg10, University of California, Los Angeles11, Semel Institute for Neuroscience and Human Behavior12, Yale University13, National University of Ireland, Galway14, Brown University15, University of Pittsburgh16, Cardiff University17, University of Exeter18, King's College London19, Icahn School of Medicine at Mount Sinai20, University of Pennsylvania21, IBM22, French Institute of Health and Medical Research23, University of Paris24, Newcastle University25, University of Oxford26, University of Birmingham27, University Medical Center Utrecht28, Dresden University of Technology29, Dalhousie University30, National Institutes of Health31, University of Edinburgh32
TL;DR: In this paper, the authors quantified case-control differences in intracranial volume (ICV) and each of eight subcortical brain measures: nucleus accumbens, amygdala, caudate, hippocampus, globus pallidus, putamen, thalamus, lateral ventricles.
Abstract: Considerable uncertainty exists about the defining brain changes associated with bipolar disorder (BD). Understanding and quantifying the sources of uncertainty can help generate novel clinical hypotheses about etiology and assist in the development of biomarkers for indexing disease progression and prognosis. Here we were interested in quantifying case–control differences in intracranial volume (ICV) and each of eight subcortical brain measures: nucleus accumbens, amygdala, caudate, hippocampus, globus pallidus, putamen, thalamus, lateral ventricles. In a large study of 1710 BD patients and 2594 healthy controls, we found consistent volumetric reductions in BD patients for mean hippocampus (Cohen’s d=−0.232; P=3.50 × 10−7) and thalamus (d=−0.148; P=4.27 × 10−3) and enlarged lateral ventricles (d=−0.260; P=3.93 × 10−5) in patients. No significant effect of age at illness onset was detected. Stratifying patients based on clinical subtype (BD type I or type II) revealed that BDI patients had significantly larger lateral ventricles and smaller hippocampus and amygdala than controls. However, when comparing BDI and BDII patients directly, we did not detect any significant differences in brain volume. This likely represents similar etiology between BD subtype classifications. Exploratory analyses revealed significantly larger thalamic volumes in patients taking lithium compared with patients not taking lithium. We detected no significant differences between BDII patients and controls in the largest such comparison to date. Findings in this study should be interpreted with caution and with careful consideration of the limitations inherent to meta-analyzed neuroimaging comparisons.
369 citations
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TL;DR: In this article, the authors showed that complement activation in the alternative complement pathway is associated with genetic variants of CFH that were previously linked to AMD susceptibility. But, their results were limited to single nucleotide polymorphisms in factor H (CFH), factor B (BF-C2) and complement C3 (C3) genes.
Abstract: Dysregulation of the alternative pathway (AP) of complement cascade has been implicated in the pathogenesis of age-related macular degeneration (AMD), the leading cause of blindness in the elderly. To further test the hypothesis that defective control of complement activation underlies AMD, parameters of complement activation in blood plasma were determined together with disease-associated genetic markers in AMD patients. Plasma concentrations of activation products C3d, Ba, C3a, C5a, SC5b-9, substrate proteins C3, C4, factor B and regulators factor H and factor D were quantified in patients (n = 112) and controls (n = 67). Subjects were analyzed for single nucleotide polymorphisms in factor H (CFH), factor B-C2 (BF-C2) and complement C3 (C3) genes which were previously found to be associated with AMD. All activation products, especially markers of chronic complement activation Ba and C3d (p<0.001), were significantly elevated in AMD patients compared to controls. Similar alterations were observed in factor D, but not in C3, C4 or factor H. Logistic regression analysis revealed better discriminative accuracy of a model that is based only on complement activation markers Ba, C3d and factor D compared to a model based on genetic markers of the complement system within our study population. In both the controls' and AMD patients' group, the protein markers of complement activation were correlated with CFH haplotypes.This study is the first to show systemic complement activation in AMD patients. This suggests that AMD is a systemic disease with local disease manifestation at the ageing macula. Furthermore, the data provide evidence for an association of systemic activation of the alternative complement pathway with genetic variants of CFH that were previously linked to AMD susceptibility.
368 citations
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Brigham and Women's Hospital1, Radboud University Nijmegen2, Trinity College, Dublin3, King's College London4, Wellcome Trust Centre for Human Genetics5, Heidelberg University6, University of Valencia7, Ghent University8, University of Göttingen9, VU University Amsterdam10, University of Zurich11, Broad Institute12, Harvard University13, State University of New York Upstate Medical University14
TL;DR: Novel genetic associations at viable ADHD candidate genes are identified and confirmatory evidence for associations at previous candidate genes is provided to confirm the proposed genetic variants for ADHD.
Abstract: Attention deficit hyperactivity disorder (ADHD) is a complex condition with environmental and genetic etiologies. Up to this point, research has identified genetic associations with candidate genes from known biological pathways. In order to identify novel ADHD susceptibility genes, 600,000 SNPs were genotyped in 958 ADHD proband-parent trios. After applying data cleaning procedures we examined 429,981 autosomal SNPs in 909 family trios. We generated six quantitative phenotypes from 18 ADHD symptoms to be used in genome-wide association analyses. With the PBAT screening algorithm, we identified 2 SNPs, rs6565113 and rs552655 that met the criteria for significance within a specified phenotype. These SNPs are located in intronic regions of genes CDH13 and GFOD1, respectively. CDH13 has been implicated previously in substance use disorders. We also evaluated the association of SNPs from a list of 37 ADHD candidate genes that was specified a priori. These findings, along with association P-values with a magnitude less than 10(-5), are discussed in this manuscript. Seventeen of these candidate genes had association P-values lower then 0.01: SLC6A1, SLC9A9, HES1, ADRB2, HTR1E, DDC, ADRA1A, DBH, DRD2, BDNF, TPH2, HTR2A, SLC6A2, PER1, CHRNA4, SNAP25, and COMT. Among the candidate genes, SLC9A9 had the strongest overall associations with 58 association test P-values lower than 0.01 and multiple association P-values at a magnitude of 10(-5) in this gene. In sum, these findings identify novel genetic associations at viable ADHD candidate genes and provide confirmatory evidence for associations at previous candidate genes. Replication of these results is necessary in order to confirm the proposed genetic variants for ADHD.
368 citations
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TL;DR: Insect diversity increased across the four treatments in the following order: intensively grazed, extensively grazing, short-term and long-term ungrazed grassland, and intensively and extensively grazed pastures.
368 citations
Authors
Showing all 44172 results
Name | H-index | Papers | Citations |
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Yang Gao | 168 | 2047 | 146301 |
J. S. Lange | 160 | 2083 | 145919 |
Jens J. Holst | 160 | 1536 | 107858 |
Hans Lassmann | 155 | 724 | 79933 |
Walter Paulus | 149 | 809 | 86252 |
Arnulf Quadt | 135 | 1409 | 123441 |
Elizaveta Shabalina | 133 | 1421 | 92273 |
Ernst Detlef Schulze | 133 | 670 | 69504 |
Mark Stitt | 132 | 456 | 60800 |
Meinrat O. Andreae | 131 | 700 | 72714 |
Teja Tscharntke | 130 | 520 | 70554 |
William C. Hahn | 130 | 448 | 72191 |
Vladimir Cindro | 129 | 1157 | 82000 |
Dave Britton | 129 | 1094 | 84187 |
Johannes Haller | 129 | 1178 | 84813 |