Linked Life Data

10576337

Source:http://linkedlifedata.com/resource/pubmed/id/10576337

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
29
pubmed:dateCreated
2000-1-4
pubmed:abstractText
A large, sustained increase in acinar [Ca2+]i may play a key role in the pathogenesis of acute pancreatitis. Many mechanisms which lead to cell damage in vitro and pancreatitis in vivo, such as free radicals or supraphysiological cerulein concentrations, cause a rapid increase in [Ca2+]i in pancreatic acinar cells. Little is known about why [Ca2+]i increases in some instances stimulate secretion and in other instances initiate cell death. So far, [Ca2+]i increases were thought to represent physiological signals when they occurred as oscillations at the single cell level.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0172-6390
pubmed:author
pubmed:issnType
Print
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2723-30
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
The role of calcium in pancreatitis.
pubmed:affiliation
Department of Internal Medicine, St. Josef Hospital Oberhausen, Germany. claus.niederau@uni-duesseldorf.de
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't