Institution
University of Düsseldorf
Education•Düsseldorf, Germany•
About: University of Düsseldorf is a education organization based out in Düsseldorf, Germany. It is known for research contribution in the topics: Population & Transplantation. The organization has 25225 authors who have published 49155 publications receiving 1946434 citations.
Topics: Population, Transplantation, Diabetes mellitus, Gene, Type 2 diabetes
Papers published on a yearly basis
Papers
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TL;DR: This review combines for the first time all aspects of OMS in MOFs, starting from different preparation strategies over theoretical studies on the effects of O MS with host-guest interactions up to distinct OMS-MOF applications.
Abstract: Metal-organic frameworks (MOFs) can contain open metal sites (OMS) or coordinatively unsaturated sites (CUS) or open coordination sites (OCS) when vacant Lewis acid sites on the metal ions or cluster nodes have been generated. This review combines for the first time all aspects of OMS in MOFs, starting from different preparation strategies over theoretical studies on the effects of OMS with host-guest interactions up to distinct OMS-MOF applications. In the experimental part the focus of this review is on MOFs with proven OMS formation which are not only invoked but are clearly verified by analytical methods.
341 citations
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TL;DR: TGR5-immunoreactivity in Kupffer cells was increased in rat livers following bile-duct ligation, suggesting that TGR5 may play a protective role in obstructive cholestasis preventing excessive cytokine production thereby reducing liver injury.
340 citations
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TL;DR: There is now an expanding pool of clinical data on the efficacy of DED therapies that include osmoprotectants such as erythritol, taurine, trehalose and L-carnitine, which may directly protect cells against hyperosmolarity and thereby promote exit from the vicious circle of D ED physiopathology.
Abstract: Dry eye disease (DED), a multifactorial disease of the tears and ocular surface, is common and has a significant impact on quality of life. Reduced aqueous tear flow and/or increased evaporation of the aqueous tear phase leads to tear hyperosmolarity, a key step in the vicious circle of DED pathology. Tear hyperosmolarity gives rise to morphological changes such as apoptosis of cells of the conjunctiva and cornea, and triggers inflammatory cascades that contribute to further cell death, including loss of mucin-producing goblet cells. This exacerbates tear film instability and drives the cycle of events that perpetuate the condition. Traditional approaches to counteracting tear hyperosmolarity in DED include use of hypotonic tear substitutes, which have relatively short persistence in the eye. More recent attempts to counteract tear hyperosmolarity in DED have included osmoprotectants, small organic molecules that are used in many cell types throughout the natural world to restore cell volume and stabilize protein function, allowing adaptation to hyperosmolarity. There is now an expanding pool of clinical data on the efficacy of DED therapies that include osmoprotectants such as erythritol, taurine, trehalose and L-carnitine. Osmoprotectants in DED may directly protect cells against hyperosmolarity and thereby promote exit from the vicious circle of DED physiopathology.
340 citations
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TL;DR: Comparative analysis of different NPQ mutants from Arabidopsis showed that qZ was clearly not related to qE, qT or qI and thus represents a separate, Zx-dependent NPQ component.
340 citations
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TL;DR: There is increasing evidence that the adipose tissue not only produces free fatty acids that contribute to insulin resistance, but also acts as a relevant endocrine organ producing mediators (adipokines) that can modulate insulin signalling.
Abstract: Currently, we observe an epidemic expansion of diabetes mellitus. In subjects with Type 2 diabetes the resistance of fat, muscle and liver to insulin is the central pathophysiological event in the development of this disease. Genetic and environmental factors play a major role in this process, although the precise pathogenesis of insulin resistance and Type 2 diabetes is still largely unknown. However, recent studies have contributed to a deeper understanding of the molecular mechanisms underlying this process. In this review we therefore summarize the current developments in understanding the pathophysiological process of insulin resistance and Type 2 diabetes. Among the many molecules involved in the intracellular processing of the signal provided by insulin, insulin receptor substrate (IRS)-2, the protein kinase B (PKB)-beta isoform and the forkhead transcription factor Foxo1a (FKHR) are of particular interest in this context as recent data have provided strong evidence that dysfunction of these proteins results in insulin resistance in-vivo. Furthermore, we have now increasing evidence that the adipose tissue not only produces free fatty acids that contribute to insulin resistance, but also acts as a relevant endocrine organ producing mediators (adipokines) that can modulate insulin signalling. The identification of the molecular pathophysiological mechanisms of insulin resistance and Type 2 diabetes is essential for the development of novel and more effective therapies to better treat our patients with insulin resistance and Type 2 diabetes.
340 citations
Authors
Showing all 25575 results
Name | H-index | Papers | Citations |
---|---|---|---|
Karl J. Friston | 217 | 1267 | 217169 |
Roderick T. Bronson | 169 | 679 | 107702 |
Stanley B. Prusiner | 168 | 745 | 97528 |
Ralph A. DeFronzo | 160 | 759 | 132993 |
Monique M.B. Breteler | 159 | 546 | 93762 |
Thomas Meitinger | 155 | 716 | 108491 |
Karl Zilles | 138 | 692 | 72733 |
Ruben C. Gur | 136 | 741 | 61312 |
Alexis Brice | 135 | 870 | 83466 |
Michael Schmitt | 134 | 2007 | 114667 |
Michael Weller | 134 | 1105 | 91874 |
Helmut Sies | 133 | 670 | 78319 |
Peter T. Fox | 131 | 622 | 83369 |
Yuri S. Kivshar | 126 | 1845 | 79415 |
Markus M. Nöthen | 125 | 943 | 83156 |