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Anne Jörns

Researcher at Hannover Medical School

Publications -  98
Citations -  4026

Anne Jörns is an academic researcher from Hannover Medical School. The author has contributed to research in topics: Insulin & Beta cell. The author has an hindex of 29, co-authored 95 publications receiving 3598 citations.

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Mechanisms of pancreatic beta-cell death in type 1 and type 2 diabetes: many differences, few similarities.

TL;DR: Cytokines and nutrients trigger beta-cell death by fundamentally different mechanisms, namely an NF-kappaB-dependent mechanism that culminates in caspase-3 activation for cytokines and anNF-kappB-independent mechanism for nutrients.
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Mitochondrial Catalase Overexpression Protects Insulin-Producing Cells Against Toxicity of Reactive Oxygen Species and Proinflammatory Cytokines

TL;DR: It can be concluded that targeted overexpression of catalase in the mitochondria provides particularly effective protection against cell death in all situations in which ROS are generated intramitochondrially.
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Systems biology of the IMIDIA biobank from organ donors and pancreatectomised patients defines a novel transcriptomic signature of islets from individuals with type 2 diabetes

TL;DR: These studies enabled the stringent definition of a novel transcriptomic signature of type 2 diabetic islets, regardless of islet source and isolation procedure, which indicates differences possibly due to peculiarities of these hyperglycaemic conditions.
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Norovirus Triggered Microbiota-driven Mucosal Inflammation in Interleukin 10-deficient Mice

TL;DR: Despite its subclinical course in wild-type animals, MNV causes epithelial barrier disruption in Il10−/− animals representing a potent colitogenic stimulus that largely depends on the presence of the enteric microbiota.
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Immune Cell Infiltration, Cytokine Expression, and β-Cell Apoptosis During the Development of Type 1 Diabetes in the Spontaneously Diabetic LEW.1AR1/Ztm-iddm Rat

TL;DR: A sequence of pathological changes leading to apoptotic beta-cell death in the IDDM rat provides a mechanistic explanation for the development of the diabetic syndrome in this animal model of human type 1 diabetes.