Linked Life Data

12177273

Source:http://linkedlifedata.com/resource/pubmed/id/12177273

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2002-8-14
pubmed:abstractText
Although transplantation of cryopreserved bone allografts has become a routine procedure in orthopaedic surgery, biological and immunological impairment remains an unsolved problem that causes clinical failures. Experimental and clinical evidence has indicated that bone grafts that are revascularized early remain viable and contribute to union at the recipient site. Unprotected cryopreservation, used in most bone banks to reduce graft antigenicity, is associated with complete loss of graft viability, potentially contributing to graft failure. The differences in the survival of various cell types during cryopreservation with use of dimethyl sulfoxide, particularly the increased sensitivity of leukocytes to fast freezing, has resulted in a new approach to modulate immunogenicity. On the basis of this concept, it was proposed that a reduction in the immune response and enhanced revascularization of osteochondral allografts could be achieved by rapid cryopreservation with dimethyl sulfoxide. To test this hypothesis, angiogenesis and immune tolerance were quantified in a murine model with use of intravital microscopy.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0021-9355
pubmed:author
pubmed:issnType
Print
pubmed:volume
84-A
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1420-9
pubmed:dateRevised
2010-10-25
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Cryopreservation of osteochondral allografts: dimethyl sulfoxide promotes angiogenesis and immune tolerance in mice.
pubmed:affiliation
Department of Orthopedic Surgery, University of Berne, Inselspital, Berne, Switzerland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't