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Institution

University of Kiel

EducationKiel, Germany
About: University of Kiel is a education organization based out in Kiel, Germany. It is known for research contribution in the topics: Population & Transplantation. The organization has 27816 authors who have published 57114 publications receiving 2061802 citations. The organization is also known as: Christian Albrechts University & Christian-Albrechts-Universität zu Kiel.


Papers
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Journal ArticleDOI
TL;DR: It is shown how the discovery of susceptibility genes furthers the authors' understanding of the underlying disease mechanisms and how it will, ultimately, give rise to new therapeutic developments.
Abstract: Chronic inflammatory disorders such as Crohn disease, atopic eczema, asthma and psoriasis are triggered by hitherto unknown environmental factors that function on the background of some polygenic susceptibility. Recent technological advances have allowed us to unravel the genetic aetiology of these and other complex diseases. Using Crohn disease as an example, we show how the discovery of susceptibility genes furthers our understanding of the underlying disease mechanisms and how it will, ultimately, give rise to new therapeutic developments. The long-term goal of such endeavours is to develop targeted prophylactic strategies. These will probably target the molecular interaction on the mucosal surface between the products of the genome and the microbial metagenome of a patient.

321 citations

Journal ArticleDOI
24 Nov 2005-Nature
TL;DR: It is surmised that the thermal isolation of Antarctica played a role in providing sustained long-term climatic boundary conditions propitious for ice-sheet formation, and relatively constant, low summer insolation over Antarctica coincident with declining atmospheric carbon dioxide levels at the time of Antarctic ice- sheet expansion and global cooling, suggesting a causal link.
Abstract: The processes causing the middle Miocene global cooling, which marked the Earth's final transition into an 'icehouse' climate about 13.9 million years ago (Myr ago)(1-4), remain enigmatic. Tectonically driven circulation changes(5,6) and variations in atmospheric carbon dioxide levels(7,8) have been suggested as driving mechanisms, but the lack of adequately preserved sedimentary successions has made rigorous testing of these hypotheses difficult. Here we present high-resolution climate proxy records, covering the period from 14.7 to 12.7 million years ago, from two complete sediment cores from the northwest and southeast subtropical Pacific Ocean. Using new chronologies through the correlation to the latest orbital model(9), we find relatively constant, low summer insolation over Antarctica coincident with declining atmospheric carbon dioxide levels at the time of Antarctic ice-sheet expansion and global cooling, suggesting a causal link. We surmise that the thermal isolation of Antarctica played a role in providing sustained long-term climatic boundary conditions propitious for ice-sheet formation. Our data document that Antarctic glaciation was rapid, taking place within two obliquity cycles, and coincided with a striking transition from obliquity to eccentricity as the drivers of climatic change.

320 citations

Journal ArticleDOI
01 Oct 2020-Brain
TL;DR: The existence of brain-first and body-first subtypes of Parkinson's disease is supported by quantifying neuronal dysfunction in structures corresponding to Braak stages I, II and III involvement in three distinct patient groups using multimodal imaging.
Abstract: Parkinson's disease is characterized by the presence of abnormal, intraneuronal α-synuclein aggregates, which may propagate from cell-to-cell in a prion-like manner However, it remains uncertain where the initial α-synuclein aggregates originate We have hypothesized that Parkinson's disease comprises two subtypes A brain-first (top-down) type, where α-synuclein pathology initially arises in the brain with secondary spreading to the peripheral autonomic nervous system; and a body-first (bottom-up) type, where the pathology originates in the enteric or peripheral autonomic nervous system and then spreads to the brain We also hypothesized that isolated REM sleep behaviour disorder (iRBD) is a prodromal phenotype for the body-first type Using multimodal imaging, we tested the hypothesis by quantifying neuronal dysfunction in structures corresponding to Braak stages I, II and III involvement in three distinct patient groups We included 37 consecutive de novo patients with Parkinson's disease into this case-control PET study Patients with Parkinson's disease were divided into 24 RBD-negative (PDRBD-) and 13 RBD-positive cases (PDRBD+) and a comparator group of 22 iRBD patients We used 11C-donepezil PET/CT to assess cholinergic (parasympathetic) innervation, 123I-metaiodobenzylguanidine (MIBG) scintigraphy to measure cardiac sympathetic innervation, neuromelanin-sensitive MRI to measure the integrity of locus coeruleus pigmented neurons, and 18F-dihydroxyphenylalanine (FDOPA) PET to assess putaminal dopamine storage capacity Colon volume and transit times were assessed with CT scans and radiopaque markers Imaging data from the three groups were interrogated with ANOVA and Kruskal-Wallis tests corrected for multiple comparisons The PDRBD- and PDRBD+ groups showed similar marked reductions in putaminal FDOPA-specific uptake, whereas two-thirds of iRBD patients had normal scans (P < 10-13, ANOVA) When compared to the PDRBD- patients, the PDRBD+ and iRBD patients showed reduced mean MIBG heart:mediastinum ratios (P < 10-5, ANOVA) and colon 11C-donepezil standard uptake values (P = 0008, ANOVA) The PDRBD+ group trended towards a reduced mean MRI locus coeruleus: pons ratio compared to PDRBD- (P = 007, t-test) In comparison to the other groups, the PDRBD+ group also had enlarged colon volumes (P < 0001, ANOVA) and delayed colonic transit times (P = 001, Kruskal-Wallis) The combined iRBD and PDRBD+ patient data were compatible with a body-first trajectory, characterized by initial loss of cardiac MIBG signal and 11C-colonic donepezil signal followed by loss of putaminal FDOPA uptake In contrast, the PDRBD- data were compatible with a brain-first trajectory, characterized by primary loss of putaminal FDOPA uptake followed by a secondary loss of cardiac MIBG signal and 11C-donepezil signal These findings support the existence of brain-first and body-first subtypes of Parkinson's disease

320 citations

Journal ArticleDOI
15 Sep 2007-Blood
TL;DR: It is demonstrated that IL6R is shed from apoptotic human neutrophils, which is relevant to the control of acute inflammation, where transition from the initial neutrophil infiltration to a more sustained population of mononuclear cells is essential for the resolution of the inflammatory process.

320 citations

Journal ArticleDOI
14 Mar 2013-PLOS ONE
TL;DR: The results indicate that smoking is an environmental factor modulating the composition of human gut microbiota, suggesting a potential pathogenetic link between weight gain and smoking cessation and giving rise to a potential association of smoking status and the course of IBD.
Abstract: Background The human intestinal microbiota is a crucial factor in the pathogenesis of various diseases, such as metabolic syndrome or inflammatory bowel disease (IBD). Yet, knowledge about the role of environmental factors such as smoking (which is known to influence theses aforementioned disease states) on the complex microbial composition is sparse. We aimed to investigate the role of smoking cessation on intestinal microbial composition in 10 healthy smoking subjects undergoing controlled smoking cessation. Methods During the observational period of 9 weeks repetitive stool samples were collected. Based on abundance of 16S rRNA genes bacterial composition was analysed and compared to 10 control subjects (5 continuing smokers and 5 non-smokers) by means of Terminal Restriction Fragment Length Polymorphism analysis and high-throughput sequencing. Results Profound shifts in the microbial composition after smoking cessation were observed with an increase of Firmicutes and Actinobacteria and a lower proportion of Bacteroidetes and Proteobacteria on the phylum level. In addition, after smoking cessation there was an increase in microbial diversity. Conclusions These results indicate that smoking is an environmental factor modulating the composition of human gut microbiota. The observed changes after smoking cessation revealed to be similar to the previously reported differences in obese compared to lean humans and mice respectively, suggesting a potential pathogenetic link between weight gain and smoking cessation. In addition they give rise to a potential association of smoking status and the course of IBD.

320 citations


Authors

Showing all 28103 results

NameH-indexPapersCitations
Stefan Schreiber1781233138528
Jun Wang1661093141621
William J. Sandborn1621317108564
Jens Nielsen1491752104005
Tak W. Mak14880794871
Annette Peters1381114101640
Severine Vermeire134108676352
Peter M. Rothwell13477967382
Dusan Bruncko132104284709
Gideon Bella129130187905
Dirk Schadendorf1271017105777
Neal L. Benowitz12679260658
Thomas Schwarz12370154560
Meletios A. Dimopoulos122137171871
Christian Weber12277653842
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023197
2022421
20212,760
20202,643
20192,556
20182,247