Reducing extracellular pH sensitizes the acinar cell
to secretagogue-induced pancreatitis responses in rats.
11) However, s-MRCP may be insensitive for detecting mild exocrine deficiency or small changes in exocrine function, as secretin affects only ductal cell secretion and does not stimulate acinar cell
The radiologic differential diagnosis for these tumors is broad and includes a number of benign and malignant processes, such as mucinous cystic neoplasm, serous microcystic adenoma, ductal adenocarcinoma, pancreatic endocrine neoplasm, acinar cell
carcinoma, solid pseudopapillary tumor, and autoimmune pancreatitis.
1985) reported that the extent to which synthesis of the total pancreatic protein was higher until a maximum of 90% than a control at 6 h and 12 h after secretin injection into the acinar cell
of a rat.
In 1920, however, Banting read a paper by the American pathologist Moses Barron, who reported a rare case of a pancreatic stone (lithiasis) that had obstructed the main pancreatic duct of a human cadaver; all acinar cells
of the pancreas disappeared (atrophied), but most islet cells remained, results similar to those produced by ligation of pancreatic ducts, as reported in the literature by others (Bliss, 1982: p.
This channel is the major pathway for regulating water permeability in acinar cells
, a critical property of the plasma membrane which determines the flow rate and ionic composition of secreted saliva (Krane et al.
Many different cell types can be seen, but the serous acinar cells
are most easily identified.
Suppression of NF-kappaB activation and cytokine production by N-acetyl cysteine in pancreatic acinar cells
In the pancreatic acini, the administration of a-difluoromethylornithine, an irreversible inhibitor of polyamine biosynthesis, blocks tissue regeneration [22, 23] and can cause pancreatitis , while appropriate polyamine synthesis is necessary for growth factors to affect pancreatic acinar cells
The first phase is characterised by the premature activation of trypsin in acinar cells
CFTR is present at higher levels in intralobular and proximal ductular epithelial cells and at lower levels in pancreatic acinar cells
Goth, et al, argue that hemorrhage results from destruction of vascular structures by proteolytic and other enzymes released from dying pancreatic acinar cells