Linked Life Data

7859081

Source:http://linkedlifedata.com/resource/pubmed/id/7859081

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1995-3-22
pubmed:abstractText
Effects of amyloid beta protein fragment 25-35, A beta P(25-35), on membrane permeability and cell viability were examined in the brain neurons dissociated from the rats using a flow cytometer and two fluorescent dyes, fluo-3 to monitor intracellular Ca2+ concentration ([Ca2+]i) of neurons and ethidium which is impermeant to membranes of intact neurons to stain dead and dying neurons. A beta P(25-35) augmented fluo-3 fluorescence of some neurons at concentrations greater than 1 microM, indicating an increase in [Ca2+]i although other neurons (about 80% of total neurons) did not respond to A beta P(25-35) even at 10 microM. A beta P(25-35) at 1 microM or greater increased dose-dependently the number of ethidium-stained neurons, suggesting a dose-dependent increase in number of dead and dying neurons. Results suggest that A beta P(25-35) increases the membrane permeability of brain neurons, resulting in a destabilized intracellular homeostasis that leads to neuonal death.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
31
pubmed:volume
662
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
259-62
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Flow cytometric analysis on cytotoxic action of amyloid beta protein fragment 25-35 on brain neurons dissociated from the rats.
pubmed:affiliation
Laboratory of Cell Signaling [Pharmacology], Faculty of Integrated Arts and Sciences, University of Tokushima, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't