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Masaki Ohmuraya

Researcher at Hyogo College of Medicine

Publications -  98
Citations -  9196

Masaki Ohmuraya is an academic researcher from Hyogo College of Medicine. The author has contributed to research in topics: Pancreatitis & Pancreas. The author has an hindex of 29, co-authored 91 publications receiving 7377 citations. Previous affiliations of Masaki Ohmuraya include Kumamoto University.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
Journal ArticleDOI

Involvement of autophagy in trypsinogen activation within the pancreatic acinar cells.

TL;DR: It is found that cytoplasmic vacuoles induced in pancreatic acinar cells by experimental pancreatitis were autophagic in origin, as demonstrated by microtubule-associated protein 1 light chain 3 expression and electron microscopy experiments, and trypsinogen activation was greatly reduced in the absence of autophagy.
Journal ArticleDOI

The role of trypsin, trypsin inhibitor, and trypsin receptor in the onset and aggravation of pancreatitis.

TL;DR: If trypsin activation (due to excessive stimulation of pancreatic acinar cells) exceeds the capacity of PSTI, a subsequent cascade of events leads to the activation of various proteases that damage cells, and this can be interpreted as the main causative event of pancreatitis onset.