M
Matthias Banasch
Researcher at Ruhr University Bochum
Publications - 26
Citations - 687
Matthias Banasch is an academic researcher from Ruhr University Bochum. The author has contributed to research in topics: Breath test & Mitochondrial toxicity. The author has an hindex of 15, co-authored 26 publications receiving 644 citations.
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Journal ArticleDOI
Predictors of gastric emptying in Parkinson's disease
Oliver Goetze,Alice B. Nikodem,J Wiezcorek,Matthias Banasch,Horst Przuntek,Thomas Mueller,Wolfgang E. Schmidt,Dirk Woitalla +7 more
TL;DR: Multiple regression analysis showed that motor handicaps such as rigour and action tremor are independent predictors of solid GE and the severity of motor impairment, but not any other neurological symptom, as assessed by UPDRS is associated with gastroparesis in PD and solid emptying is more likely to be delayed.
Journal ArticleDOI
Glucagon-like Peptide 1 (GLP-1) Suppresses Ghrelin Levels in Humans via Increased Insulin Secretion
D. Hagemann,Jens J. Holst,Arnica Gethmann,Matthias Banasch,Wolfgang E. Schmidt,Juris J. Meier +5 more
TL;DR: GLP-1 reduces the rise in ghrelin levels in the late postprandial period at supraphysiological plasma levels and most likely is indirectly mediated through its insulinotropic action.
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Hepatic mitochondrial dysfunction in manifest and premanifest Huntington disease
Sven H. Stüwe,Oliver Goetze,Carsten Lukas,Peter Klotz,Rainer Hoffmann,Matthias Banasch,Michael Orth,Wolfgang Schmidt,Ralf Gold,Carsten Saft +9 more
TL;DR: This study demonstrates for the first time in vivo a subclinical, hepatic involvement in manifest and premanifest Huntington disease (HD) by using the 13C-methionine breath test.
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The non-invasive 13C-methionine breath test detects hepatic mitochondrial dysfunction as a marker of disease activity in non-alcoholic steatohepatitis
TL;DR: The 13C-methionine breath test indicates mitochondrial dysfunction in non-alcoholic fatty liver disease and predicts higher stages of disease activity and may, therefore, be a valuable diagnostic addition for longitudinal monitoring of hepatic (mitochondrial) function inNon- alcoholic fatty Liver disease.
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Glucagon like peptide-2 induces intestinal restitution through VEGF release from subepithelial myofibroblasts
Kerem Bulut,C Pennartz,P. Felderbauer,Juris J. Meier,Matthias Banasch,Daniel Bulut,Frank Schmitz,Wolfgang E. Schmidt,Peter R. Hoffmann +8 more
TL;DR: The mechanisms underlying GLP-2 induced intestinal wound repair seem to involve the secretion of VEGF and, subsequently, TGF-beta from subepithelial fibroblasts, whereas KGF appeared to be less important.