Institution
Humboldt University of Berlin
Education•Berlin, Germany•
About: Humboldt University of Berlin is a education organization based out in Berlin, Germany. It is known for research contribution in the topics: Population & Transplantation. The organization has 33671 authors who have published 61781 publications receiving 1908102 citations. The organization is also known as: Humboldt-Universität zu Berlin & Universitas Humboldtiana Berolinensis.
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TL;DR: Supporting the singular hypothesis for plant diversity, the results suggest that plant species are unique, each contributing to the functioning of the belowground system and reinforce the need for long-term biodiversity experiments to fully appreciate consequences of current biodiversity loss for ecosystem functioning.
Abstract: The global decline in biodiversity has generated concern over the consequences for ecosystem functioning and services. Although ecosystem functions driven by soil microorganisms such as plant productivity, decomposition, and nutrient cycling are of particular importance, interrelationships between plant diversity and soil microorganisms are poorly understood. We analyzed the response of soil microorganisms to variations in plant species richness (1-60) and plant functional group richness (1-4) in an experimental grassland system over a period of six years. Major abiotic and biotic factors were considered for exploring the mechanisms responsible for diversity effects. Further, microbial growth characteristics were assessed following the addition of macronutrients. Effects of plant diversity on soil microorganisms were most pronounced in the most diverse plant communities though differences only became established after a time lag of four years. Differences in microbial growth characteristics indicate successional changes from a disturbed (zymogeneous) to an established (autochthonous) microbial community four years after establishment of the experiment. Supporting the singular hypothesis for plant diversity, the results suggest that plant species are unique, each contributing to the functioning of the belowground system. The results reinforce the need for long-term biodiversity experiments to fully appreciate consequences of current biodiversity loss for ecosystem functioning.
427 citations
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University of Bonn1, University of Göttingen2, University of Ferrara3, The Feinstein Institute for Medical Research4, Humboldt University of Berlin5, University of Cologne6, Radboud University Nijmegen7, Leipzig University8, Otto-von-Guericke University Magdeburg9, University of Duisburg-Essen10, University of Dundee11
TL;DR: A 640-kb region at chromosome 8q24.21 was found to contain multiple markers with highly significant evidence for association with the cleft phenotype, including three markers that reached genome-wide significance.
Abstract: We conducted a genome-wide association study involving 224 cases and 383 controls of Central European origin to identify susceptibility loci for nonsyndromic cleft lip with or without cleft palate (NSCL/P). A 640-kb region at chromosome 8q24.21 was found to contain multiple markers with highly significant evidence for association with the cleft phenotype, including three markers that reached genome-wide significance. The 640-kb cleft-associated region was saturated with 146 SNP markers and then analyzed in our entire NSCL/P sample of 462 unrelated cases and 954 controls. In the entire sample, the most significant SNP (rs987525) had a P value of 3.34 x 10(-24). The odds ratio was 2.57 (95% CI = 2.02-3.26) for the heterozygous genotype and 6.05 (95% CI = 3.88-9.43) for the homozygous genotype. The calculated population attributable risk for this marker is 0.41, suggesting that this study has identified a major susceptibility locus for NSCL/P.
426 citations
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TL;DR: The presented approach is considered as a useful means to determine valid conditions for the analysis of prosthesis loading, bone modeling or remodeling processes around implants and fracture stability following internal fixation.
425 citations
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TL;DR: It is shown that stimulation of single neurons in somatosensory cortex affects behavioural responses in a detection task, and single neuron activity can cause a change in the animal’s detection behaviour, suggesting a much sparser cortical code for sensations than previously anticipated.
Abstract: Understanding how neural activity in sensory cortices relates to perception is a central theme of neuroscience. Action potentials of sensory cortical neurons can be strongly correlated to properties of sensory stimuli and reflect the subjective judgements of an individual about stimuli. Microstimulation experiments have established a direct link from sensory activity to behaviour, suggesting that small neuronal populations can influence sensory decisions. However, microstimulation does not allow identification and quantification of the stimulated cellular elements. The sensory impact of individual cortical neurons therefore remains unknown. Here we show that stimulation of single neurons in somatosensory cortex affects behavioural responses in a detection task. We trained rats to respond to microstimulation of barrel cortex at low current intensities. We then initiated short trains of action potentials in single neurons by juxtacellular stimulation. Animals responded significantly more often in single-cell stimulation trials than in catch trials without stimulation. Stimulation effects varied greatly between cells, and on average in 5% of trials a response was induced. Whereas stimulation of putative excitatory neurons led to weak biases towards responding, stimulation of putative inhibitory neurons led to more variable and stronger sensory effects. Reaction times for single-cell stimulation were long and variable. Our results demonstrate that single neuron activity can cause a change in the animal's detection behaviour, suggesting a much sparser cortical code for sensations than previously anticipated.
424 citations
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Utrecht University1, University of Cologne2, University of Kiel3, University of Washington4, University of Bonn5, Humboldt University of Berlin6, University of Marburg7, University of Ulm8, Innsbruck Medical University9, Medical University of Vienna10, University of Copenhagen11, University of Antwerp12, Ludwig Maximilian University of Munich13
TL;DR: The present results indicate an involvement of micro deletions at 15q11.2 and 16p13.11 in epileptogenesis and strengthen the evidence that recurrent microdeletions in this cohort confer a pleiotropic susceptibility effect to a broad range of neuropsychiatric disorders.
Abstract: Idiopathic generalized epilepsies account for 30% of all epilepsies. Despite a predominant genetic aetiology, the genetic factors predisposing to idiopathic generalized epilepsies remain elusive. Studies of structural genomic variations have revealed a significant excess of recurrent microdeletions at 1q21.1, 15q11.2, 15q13.3, 16p11.2, 16p13.11 and 22q11.2 in various neuropsychiatric disorders including autism, intellectual disability and schizophrenia. Microdeletions at 15q13.3 have recently been shown to constitute a strong genetic risk factor for common idiopathic generalized epilepsy syndromes, implicating that other recurrent microdeletions may also be involved in epileptogenesis. This study aimed to investigate the impact of five microdeletions at the genomic hotspot regions 1q21.1, 15q11.2, 16p11.2, 16p13.11 and 22q11.2 on the genetic risk to common idiopathic generalized epilepsy syndromes. The candidate microdeletions were assessed by high-density single nucleotide polymorphism arrays in 1234 patients with idiopathic generalized epilepsy from North-western Europe and 3022 controls from the German population. Microdeletions were validated by quantitative polymerase chain reaction and their breakpoints refined by array comparative genomic hybridization. In total, 22 patients with idiopathic generalized epilepsy (1.8%) carried one of the five novel microdeletions compared with nine controls (0.3%) (odds ratio = 6.1; 95% confidence interval 2.8–13.2; χ2 = 26.7; 1 degree of freedom; P = 2.4 × 10−7). Microdeletions were observed at 1q21.1 [Idiopathic generalized epilepsy (IGE)/control: 1/1], 15q11.2 (IGE/control: 12/6), 16p11.2 IGE/control: 1/0, 16p13.11 (IGE/control: 6/2) and 22q11.2 (IGE/control: 2/0). Significant associations with IGEs were found for the microdeletions at 15q11.2 (odds ratio = 4.9; 95% confidence interval 1.8–13.2; P = 4.2 × 10−4) and 16p13.11 (odds ratio = 7.4; 95% confidence interval 1.3–74.7; P = 0.009). Including nine patients with idiopathic generalized epilepsy in this cohort with known 15q13.3 microdeletions (IGE/control: 9/0), parental transmission could be examined in 14 families. While 10 microdeletions were inherited (seven maternal and three paternal transmissions), four microdeletions occurred de novo at 15q13.3 (n = 1), 16p13.11 (n = 2) and 22q11.2 (n = 1). Eight of the transmitting parents were clinically unaffected, suggesting that the microdeletion itself is not sufficient to cause the epilepsy phenotype. Although the microdeletions investigated are individually rare (<1%) in patients with idiopathic generalized epilepsy, they collectively seem to account for a significant fraction of the genetic variance in common idiopathic generalized epilepsy syndromes. The present results indicate an involvement of microdeletions at 15q11.2 and 16p13.11 in epileptogenesis and strengthen the evidence that recurrent microdeletions at 15q11.2, 15q13.3 and 16p13.11 confer a pleiotropic susceptibility effect to a broad range of neuropsychiatric disorders.
424 citations
Authors
Showing all 34115 results
Name | H-index | Papers | Citations |
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Karl J. Friston | 217 | 1267 | 217169 |
Peer Bork | 206 | 697 | 245427 |
Raymond J. Dolan | 196 | 919 | 138540 |
Stefan Schreiber | 178 | 1233 | 138528 |
Andreas Pfeiffer | 149 | 1756 | 131080 |
Thomas Hebbeker | 148 | 1984 | 114004 |
Thomas Lohse | 148 | 1237 | 101631 |
Jean Bousquet | 145 | 1288 | 96769 |
Hermann Kolanoski | 145 | 1279 | 96152 |
Josh Moss | 139 | 1019 | 89255 |
R. D. Kass | 138 | 1920 | 107907 |
W. Kozanecki | 138 | 1498 | 99758 |
U. Mallik | 137 | 1625 | 97439 |
C. Haber | 135 | 1507 | 98014 |
Christophe Royon | 134 | 1453 | 90249 |