Institution
University of Duisburg-Essen
Education•Essen, Nordrhein-Westfalen, Germany•
About: University of Duisburg-Essen is a education organization based out in Essen, Nordrhein-Westfalen, Germany. It is known for research contribution in the topics: Population & Transplantation. The organization has 16072 authors who have published 39972 publications receiving 1109199 citations.
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TL;DR: In this paper, the magnetic relaxation processes following the dynamical excitation of the spin system of ferromagnets are investigated by ferromagnetic resonance (FMR) between 1 and $70\phantom{\rule{0.3em}{0ex}}\mathrm{GHz}$ using epitaxial Fe 3 films as a prototype system.
Abstract: The magnetic relaxation processes following the dynamical excitation of the spin system of ferromagnets are investigated by ferromagnetic resonance (FMR) between 1 and $70\phantom{\rule{0.3em}{0ex}}\mathrm{GHz}$ using epitaxial ${\mathrm{Fe}}_{3}\mathrm{Si}$ films as a prototype system. Two relaxation channels, i.e., dissipative, isotropic Gilbert damping $G$ as well as anisotropic two-magnon scattering $\ensuremath{\Gamma}$, are simultaneously identified by frequency and angle dependent FMR and quantitatively analyzed. The scattering rates due to two-magnon scattering at crystallographic defects for spin waves propagating in ⟨100⟩ and ⟨110⟩ directions, $\ensuremath{\gamma}{\ensuremath{\Gamma}}_{⟨100⟩}=0.25(2)\phantom{\rule{0.3em}{0ex}}\mathrm{GHz}$ and $\ensuremath{\gamma}{\ensuremath{\Gamma}}_{⟨110⟩}=0.04(2)\phantom{\rule{0.3em}{0ex}}\mathrm{GHz}$, and the Gilbert damping term $G=0.051(1)\phantom{\rule{0.3em}{0ex}}\mathrm{GHz}$ are determined. We show that changing the film thickness from $8\phantom{\rule{0.3em}{0ex}}\text{to}\phantom{\rule{0.3em}{0ex}}40\phantom{\rule{0.3em}{0ex}}\mathrm{nm}$ and slightly modifying the Fe concentration influence the relaxation channels. Our results, which reveal the contributions of longitudinal and transverse relaxation processes may be of general importance for the understanding of spin-wave dynamics in magnetic structures.
224 citations
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TL;DR: Neuropilin 1 mediates anti-tumor control by promoting regulatory T cell infiltration and cell reprograming in mice models of Alzheimer's disease.
Abstract: Infiltration of Foxp3+ regulatory T (T reg) cells is considered to be a critical step during tumor development and progression. T reg cells supposedly suppress locally an effective anti-tumor immune response within tumor tissues, although the precise mechanism by which T reg cells infiltrate the tumor is still unclear. We provide evidence that Neuropilin 1 (Nrp-1), highly expressed by Foxp3+ T reg cells, regulates the immunological anti-tumor control by guiding T reg cells into the tumor in response to tumor-derived vascular endothelial growth factor (VEGF). We demonstrate for the first time that T cell–specific ablation of Nrp-1 expression results in a significant breakdown in tumor immune escape in various transplantation models and in a spontaneous, endogenously driven melanoma model associated with strongly reduced tumor growth and prolonged tumor-free survival. Strikingly, numbers of tumor-infiltrating Foxp3+ T reg cells were significantly reduced accompanied by enhanced activation of CD8+ T cells within tumors of T cell–specific Nrp-1–deficient mice. This phenotype can be reversed by adoptive transfer of Nrp-1+ T reg cells from wild-type mice. Thus, our data strongly suggest that Nrp-1 acts as a key mediator of Foxp3+ T reg cell infiltration into the tumor site resulting in a dampened anti-tumor immune response and enhanced tumor progression.
223 citations
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TL;DR: The identification of inborn deficiency of the mostly adipocyte-derived satiety hormone leptin in extremely obese children from consanguineous families paved the way to the first pharmacological therapy for obesity based on a molecular genetic finding.
Abstract: The heritability of obesity and body weight in general is high. A small number of confirmed monogenic forms of obesity—the respective mutations are sufficient by themselves to cause the condition in food abundant societies—have been identified by molecular genetic studies. The elucidation of these genes, mostly based on animal and family studies, has led to the identification of important pathways to the disorder and thus to a deeper understanding of the regulation of body weight. The identification of inborn deficiency of the mostly adipocyte-derived satiety hormone leptin in extremely obese children from consanguineous families paved the way to the first pharmacological therapy for obesity based on a molecular genetic finding. The genetic predisposition to obesity for most individuals, however, has a polygenic basis. A polygenic variant by itself has a small effect on the phenotype; only in combination with other predisposing variants does a sizeable phenotypic effect arise. Common variants in the first intron of the ‘fat mass and obesity associated’ gene (FTO) result in an elevated body mass index (BMI) equivalent to approximately +0.4 kg/m² per risk allele. The FTO variants were originally detected in a genome wide association study (GWAS) pertaining to type 2 diabetes mellitus. Large meta-analyses of GWAS have subsequently identified additional polygenic variants. Up to December 2009, polygenic variants have been confirmed in a total of 17 independent genomic regions. Further study of genetic effects on human body weight regulation should detect variants that will explain a larger proportion of the heritability. The development of new strategies for diagnosis, treatment and prevention of obesity can be anticipated.
223 citations
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TL;DR: It is argued that both normal and abnormal development in children conceived by ART can be explained by epigenetic mechanisms, which control the establishment and maintenance of gene expression patterns in the placenta and fetus.
Abstract: Developmental pathways in humans and other organisms are buffered against changes in genotype and environment. Therefore, it should not come as a surprise that most of the children conceived by assisted reproduction technology (ART) are healthy, although ART bypasses a lot of biological filters and subjects the gametes and the early embryo to environmental stress. If, however, the buffer breaks down, the development of certain tissues or organs may follow abnormal trajectories. We argue that both normal and abnormal development in children conceived by ART can be explained by epigenetic mechanisms, which control the establishment and maintenance of gene expression patterns in the placenta and fetus. Imprinted genes are of special importance in this respect. There is increasing evidence that genetic factors in infertile couples as well as environmental factors (hormones and culture media) can have adverse effects on epigenetic processes controlling implantation, placentation, organ formation and fetal growth. In addition, loss of epigenetic control may expose hidden genetic variation.
223 citations
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TL;DR: In this article, the authors investigate whether timepersistent cultural borders impede economic exchange across regions of the same country and find that current cross-regional migration is positively affected by historical dialect similarity, suggesting that cultural identities formed in the past still influence economic exchange today.
Abstract: We investigate whether time-persistent cultural borders impede economic exchange across regions of the same country. To measure cultural differences we evaluate, for the first time in economics, linguistic micro-data about phonological and grammatical features of German dialects. These data are taken from a unique linguistic survey conducted between 1879 and 1888 in 45,000 schools. Matching this information to 439 current German regions, we construct a dialect similarity matrix. Using a gravity analysis, we show that current cross-regional migration is positively affected by historical dialect similarity. This suggests that cultural identities formed in the past still influence economic exchange today.
223 citations
Authors
Showing all 16364 results
Name | H-index | Papers | Citations |
---|---|---|---|
Rui Zhang | 151 | 2625 | 107917 |
Olli T. Raitakari | 142 | 1232 | 103487 |
Anders Hamsten | 139 | 611 | 88144 |
Robert Huber | 139 | 671 | 73557 |
Christopher T. Walsh | 139 | 819 | 74314 |
Patrick D. McGorry | 137 | 1097 | 72092 |
Stanley Nattel | 132 | 778 | 65700 |
Luis M. Liz-Marzán | 132 | 616 | 61684 |
Dirk Schadendorf | 127 | 1017 | 105777 |
William Wijns | 127 | 752 | 95517 |
Raimund Erbel | 125 | 1364 | 74179 |
Khalil Amine | 118 | 652 | 50111 |
Hans-Christoph Diener | 118 | 1025 | 91710 |
Bruce A.J. Ponder | 116 | 403 | 54796 |
Andre Franke | 115 | 682 | 55481 |