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Pius Hildebrand

Researcher at University Hospital of Basel

Publications -  47
Citations -  3008

Pius Hildebrand is an academic researcher from University Hospital of Basel. The author has contributed to research in topics: Cholecystokinin & Gastrin-releasing peptide. The author has an hindex of 25, co-authored 47 publications receiving 2874 citations.

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Cardiovascular safety of non-steroidal anti-inflammatory drugs: network meta-analysis.

TL;DR: Although uncertainty remains, little evidence exists to suggest that any of the investigated drugs are safe in cardiovascular terms, and Naproxen seemed least harmful.
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Role of cholecystokinin in regulation of gastrointestinal motor functions.

TL;DR: It is concluded that CCK is an important mediator of meal-induced gallbladder contraction and is involved in the regulation of gastrointestinal motility in man.
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Transforming growth factor-beta1 induces interleukin-6 expression via activating protein-1 consisting of JunD homodimers in primary human lung fibroblasts.

TL;DR: It is demonstrated by reverse transcriptase polymerase chain reaction and enzyme-linked immunoassay that TGF-β1 is a potent inducer of IL-6 mRNA and protein in primary human lung fibroblasts and this complex was found to be a JunD homodimer, which may be essential for a majority of the biological effects induced by TGF -β1 in this cell type.
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Effects of a cholecystokinin receptor antagonist on intestinal phase of pancreatic and biliary responses in man.

TL;DR: Intravenous loxiglumide was highly potent in antagonizing CCK8-induced pancreatic enzyme and bile acid secretion as well as pancreatic polypeptide release, suggesting that CCK is a physiological mediator of the intestinal phase of meal-stimulated pancreatic and biliary responses.
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Molecular mechanisms of TGF-β antagonism by interferon γ and cyclosporine A in lung fibroblasts

TL;DR: The JunD homodimer of the transcription factor AP‐1 is identified as an essential mediator of TGF‐β‐induced effects in lung fibroblasts and offers novel targets for future therapy of fibrotic lung disease.