Julius Kieswich
Queen Mary University of London
33 Papers
113 Citations
Julius Kieswich is an academic researcher from Queen Mary University of London. The author has contributed to research in topics: Kidney disease & Kidney. The author has an hindex of 19, co-authored 29 publications. Previous affiliations of Julius Kieswich include Barts Health NHS Trust & Royal London Hospital.
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Papers
Metformin suppresses hepatic gluconeogenesis through induction of SIRT1 and GCN5
Paul W. Caton,Nanda K Nayuni,Julius Kieswich,Noorafza Q. Khan,Muhammed M. Yaqoob,Roger Corder +5 more
TL;DR: Induction of GCN5 and SIRT1 potentially represents a critical mechanism of action of metformin and is identified as a potential therapeutic strategy for treatment of type 2 diabetes mellitus.
Estrogen protects the blood-brain barrier from inflammation-induced disruption and increased lymphocyte trafficking.
Elisa Maggioli,Simon McArthur,Claudio Mauro,Julius Kieswich,D.H.M. Kusters,Chris P. M. Reutelingsperger,Muhammad M. Yaqoob,Egle Solito +7 more
TL;DR: Investigation of the effects of estradiol upon key barrier features, namely paracellular permeability, transendothelial electrical resistance, tight junction integrity and lymphocyte transmigration under basal and inflammatory conditions, modeled by treatment with TNFα and IFNγ enhances understanding of the beneficial role it plays in neurovascular/neuroimmune disease.
Dexamethasone Ameliorates Renal Ischemia-Reperfusion Injury
Sanjeev Kumar,David A. Allen,Julius Kieswich,Nimesh S. A. Patel,Steven Harwood,Emanuela Mazzon,Salvatore Cuzzocrea,Martin Raftery,Christoph Thiemermann,Muhammad M. Yaqoob +9 more
TL;DR: In the setting of renal ischemia-reperfusion injury, dexamethasone directly protects against kidney injury by a receptor-dependent, nongenomic mechanism.
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Nicotinamide mononucleotide protects against pro-inflammatory cytokine-mediated impairment of mouse islet function
TL;DR: Administration of nicotinamide mononucleotide (NMN), a product of the eNAMPT reaction, corrects impaired islet function in Nampt+/− mice and may be an attractive target for amelioration of islet dysfunction associated with inflammation.
Erythropoietin attenuates acute kidney dysfunction in murine experimental sepsis by activation of the β-common receptor
Sina M. Coldewey,Sina M. Coldewey,Areeg I. Khan,Amar Kapoor,Massimo Collino,Mara Rogazzo,Michael Brines,Anthony Cerami,Peter A. Hall,Michael Sheaff,Julius Kieswich,Muhammed M. Yaqoob,Muhammed M. Yaqoob,Nimesh S. A. Patel,Christoph Thiemermann +14 more
TL;DR: In this article, the β-common receptor (βcR) plays a pivotal role in the nonhematopoietic tissue-protective effects of erythropoietin (EPO).
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