M
M. Saluja
Researcher at Harvard University
Publications - 19
Citations - 1604
M. Saluja is an academic researcher from Harvard University. The author has contributed to research in topics: Pancreatitis & Acinar cell. The author has an hindex of 12, co-authored 19 publications receiving 1559 citations. Previous affiliations of M. Saluja include Beth Israel Deaconess Medical Center.
Papers
More filters
Journal ArticleDOI
Relationship between severity, necrosis, and apoptosis in five models of experimental acute pancreatitis.
TL;DR: The finding that the severity of acute pancreatitis is inversely related to the degree of apoptosis suggests that apoptosis may be a teleologically beneficial response to acinar cell injury in general and especially in acute Pancreatitis.
Journal ArticleDOI
Pancreatic duct obstruction triggers acute necrotizing pancreatitis in the opossum
Markus M. Lerch,Ashok K. Saluja,Ashok K. Saluja,M. Rünzi,M. Rünzi,Rajinder K. Dawra,Rajinder K. Dawra,M. Saluja,M. Saluja,Michael L. Steer,Michael L. Steer +10 more
TL;DR: Bile reflux into the pancreatic duct, via a common biliopancreatic channel, is not necessary for the development of pancreatitis and does not worsen the severity of pancreatococcal duct obstruction in this model.
Journal ArticleDOI
Subcellular redistribution of lysosomal enzymes during caerulein-induced pancreatitis
TL;DR: Electron microscopic immunolabeling studies revealed localization of cathepsin D in discrete organelles that, in the samples from animals infused with a supramaximally stimulating dose of caerulein, were larger, more abundant, and more concentrated in the pellet centrifuged at 1,300 g for 15 min than in the controls.
Journal ArticleDOI
Acute necrotizing pancreatitis in the opossum: Earliest morphological changes involve acinar cells
TL;DR: Observations indicate that pancreatic and bile duct ligation in the opossum results in the rapid (less than 24 hours) appearance of changes consistent with acute hemorrhagic and necrotizing pancreatitis and that the initial lesion in this model of experimental pancreatitis involves acinar cells.
Journal ArticleDOI
In vivo rat pancreatic acinar cell function during supramaximal stimulation with caerulein
Ashok K. Saluja,I. Saito,M. Saluja,M. J. Houlihan,R. E. Powers,Jacopo Meldolesi,Michael L. Steer +6 more
TL;DR: It is suggested that supramaximal stimulation causes digestive enzymes to become localized in organelles that are fragile and subject to disruption during tissue homogenization.