Institution
University of Cologne
Education•Cologne, Germany•
About: University of Cologne is a education organization based out in Cologne, Germany. It is known for research contribution in the topics: Population & Transplantation. The organization has 32050 authors who have published 66350 publications receiving 2210092 citations. The organization is also known as: Universität zu Köln & Universitatis Coloniensis.
Topics: Population, Transplantation, Gene, Star formation, Cancer
Papers published on a yearly basis
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TL;DR: It is shown that Myc expression cooperates with Rb1 and Trp53 loss in the mouse lung to promote aggressive, highly metastatic tumors, that are initially sensitive to chemotherapy followed by relapse, similar to human SCLC.
365 citations
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Bryn Mawr College1, University of Vermont2, University of Helsinki3, University of Southern Denmark4, Columbia University5, National Taiwan University6, Babeș-Bolyai University7, University of Cologne8, Ankara University9, McGill University10, University of Coimbra11, Katholieke Universiteit Leuven12, Chuo University13, University of Missouri14, Norwegian University of Science and Technology15, The Chinese University of Hong Kong16, University of Pittsburgh17, Yonsei University18, University of Adelaide19, Harran University20, University of Zurich21, Harvard University22, Medical University of Warsaw23, Chung Shan Medical University24, Centre national de la recherche scientifique25, Mykolas Romeris University26, Erasmus University Rotterdam27
TL;DR: The authors compared parents' ratings of behavioral and emotional problems on the Child Behavior Checklist (Achenbach, 1991; Achenbach & Rescorla, 2001) for general population samples of children age 5.
Abstract: This study compared parents' ratings of behavioral and emotional problems on the Child Behavior Checklist (Achenbach, 1991;Achenbach & Rescorla, 2001) for general population samples of children age...
364 citations
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TL;DR: There are parallel, somewhat independent neural pain-processing networks for sensory and affective pain elements in patients with fibromyalgia, suggesting that addressing an individual's depression will not necessarily have an impact on the sensory dimension of pain.
Abstract: Objective. Individuals with chronic pain frequently display comorbid depression, but the impact of symptoms of depression on pain processing is not completely understood. This study evaluated the effect of symptoms of depression and/or clinically diagnosed major depressive disorder (MDD) on pain processing in patients with fibromyalgia (FM). Methods. Results of quantitative sensory testing and neural responses to equally painful pressure stimuli (measured by functional magnetic resonance imaging [fMRI]) were compared with the levels of symptoms of depression and comorbid MDD among patients with FM. Results. Neither the level of symptoms of depression nor the presence of comorbid MDD was associated with the results of sensory testing or the magnitude of neuronal activation in brain areas associated with the sensory dimension of pain (primary and secondary somatosensory cortices). However, symptoms of depression and the presence of MDD were associated with the magnitude of pain-evoked neuronal activations in brain regions associated with affective pain processing (the amygdalae and contralateral anterior insula). Clinical pain intensity was associated with measures of both the sensory dimension of pain (results of sensory testing) and the affective dimension of pain (activations in the insula bilaterally, contralateral anterior cingulate cortex, and prefrontal cortex). Conclusion. In patients with FM, neither the extent of depression nor the presence of comorbid major depression modulates the sensory-discriminative aspects of pain processing (i.e., localizing pain and reporting its level of intensity), as measured by sensory testing or fMRI. However, depression is associated with the magnitude of neuronal activation in brain regions that process the affective-motivational dimension of pain. These data suggest that there are parallel, somewhat independent neural pain-processing networks for sensory and affective pain elements. The implication for treatment is that addressing an individual’s depression (e.g., by prescribing an antidepressant medication that has no analgesic properties) will not necessarily have an impact on the sensory dimension of pain.
364 citations
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TL;DR: Not all proteins from hyperthermophiles are thermostable enough to retain their structures and functions at the high physiological temperatures, and it will be shown how this shortcoming can be surpassed by extrinsic factors such as large molecular chaperones and small compatible solutes.
Abstract: Hyperthermophilic organisms optimally grow close to the boiling point of water. As a consequence, their macromolecules must be much more thermostable than those from mesophilic species. Here, proteins from hyperthermophiles and mesophiles are compared with respect to their thermodynamic and kinetic stabilities. The known differences in amino acid sequences and three-dimensional structures between intrinsically thermostable and thermolabile proteins will be summarized, and the crucial role of electrostatic interactions for protein stability at high temperatures will be highlighted. Successful attempts to increase the thermostability of proteins, which were either based on rational design or on directed evolution, are presented. The relationship between high thermo-stability of enzymes from hyperthermophiles and their low catalytic activity at room temperature is discussed. Not all proteins from hyperthermophiles are thermostable enough to retain their structures and functions at the high physiological temperatures. It will be shown how this shortcoming can be surpassed by extrinsic factors such as large molecular chaperones and small compatible solutes. Finally, the potential of thermostable enzymes for biotechnology is discussed.
364 citations
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TL;DR: The role of the mitochondrial QC network for neuronal survival and neurodegeneration is discussed and mitochondrial proteases emerge as central regulators that coordinate different quality control pathways within an interconnected network of mechanisms.
Abstract: Neuronal survival critically depends on the integrity and functionality of mitochondria. A hierarchical system of cellular surveillance mechanisms protects mitochondria against stress, monitors mitochondrial damage and ensures the selective removal of dysfunctional mitochondrial proteins or organelles. Mitochondrial proteases emerge as central regulators that coordinate different quality control (QC) pathways within an interconnected network of mechanisms. A failure of this system causes neuronal loss in a steadily increasing number of neurodegenerative disorders, which include Parkinson's disease, spinocerebellar ataxia, spastic paraplegia and peripheral neuropathies. Here, we will discuss the role of the mitochondrial QC network for neuronal survival and neurodegeneration.
364 citations
Authors
Showing all 32558 results
Name | H-index | Papers | Citations |
---|---|---|---|
Julie E. Buring | 186 | 950 | 132967 |
Stuart H. Orkin | 186 | 715 | 112182 |
Cornelia M. van Duijn | 183 | 1030 | 146009 |
Dorret I. Boomsma | 176 | 1507 | 136353 |
Frederick W. Alt | 171 | 577 | 95573 |
Donald E. Ingber | 164 | 610 | 100682 |
Klaus Müllen | 164 | 2125 | 140748 |
Klaus Rajewsky | 154 | 504 | 88793 |
Frederik Barkhof | 154 | 1449 | 104982 |
Stefanie Dimmeler | 147 | 574 | 81658 |
Detlef Weigel | 142 | 516 | 84670 |
Hidde L. Ploegh | 135 | 674 | 67437 |
Luca Valenziano | 130 | 437 | 94728 |
Peter Walter | 126 | 841 | 71580 |
Peter G. Martin | 125 | 553 | 97257 |