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dc.creatorMaxwell, Bryan Douglas
dc.date.accessioned2012-06-07T22:45:55Z
dc.date.available2012-06-07T22:45:55Z
dc.date.created1996
dc.date.issued1996
dc.identifier.urihttps://hdl.handle.net/1969.1/ETD-TAMU-1996-THESIS-M395
dc.descriptionDue to the character of the original source materials and the nature of batch digitization, quality control issues may be present in this document. Please report any quality issues you encounter to digital@library.tamu.edu, referencing the URI of the item.en
dc.descriptionIncludes bibliographical references: p. 45-53.en
dc.descriptionIssued also on microfiche from Lange Micrographics.en
dc.description.abstractWound healing in the aged is delayed. A 6 mm punch biopsy wound heals in 13 days in a 3 month old rat, but takes 21 days to heal in a 2 year old rat. It is our belief that this impairment in healing may be due in part to a macrophage defect present in senescence, and that macrophage activation or supplementation may yield an acceleration in wound closure. This thesis focuses on the ability of Acemannan (ACM), a complex plant carbohydrate and macrophage stimulator, to accelerate wound healing in both young and aged rats. Studies were conducted using both ACM injection, and macrophage supplementation to the wound site. Acemannan injection to the wound site was found to accelerate wound healing in young and old rats. Overall time to complete closure decreased and average Cumulative Wound Area (CWA) exposed over the course of healing in both young and old animals was significantly (u.<O.05) reduced. There was no significant difference between young and old ACM-treated wounds, but there was a significant (CC<0.05) difference between the CWA seen in old control versus young control wounds. Likewise, a single injection of peritoneal macrophages to the wound site was found to accelerate wound healing in young and old rats. Again, there was no significant difference between the young and old treated wounds, but there was a significant (cc<0.05) difference between the CWA seen in old control versus young control wounds. Overall time to complete closure decreased and average CWA exposed over the course of healing in both young and old animals was significantly (cc<0.05) reduced. ACM stimulation did not significantly improve the ability of peritoneal macrophages to accelerate wound healing. However, ACM-stimulated killed macrophages were significantly different (cc<0.05) from all other treatments, and exhibited decreased wound closure and CWA over that seen in the control wounds. Killed, untreated macrophages were not effective. Additionally, we observed changes in the cytokine MRNA production for TGF-P, TNF-ot, and IL-6 in young and old macrophages stimulated with ACM. The acceleration seen in these studies strengthens the case of ACM as a wound healing agent, and encourages further studies into the basis of its activity.en
dc.format.mediumelectronicen
dc.format.mimetypeapplication/pdf
dc.language.isoen_US
dc.publisherTexas A&M University
dc.rightsThis thesis was part of a retrospective digitization project authorized by the Texas A&M University Libraries in 2008. Copyright remains vested with the author(s). It is the user's responsibility to secure permission from the copyright holder(s) for re-use of the work beyond the provision of Fair Use.en
dc.subjectveterinary microbiology.en
dc.subjectMajor veterinary microbiology.en
dc.titleAcceleration of wound healing in young and aged ratsen
dc.typeThesisen
thesis.degree.disciplineveterinary microbiologyen
thesis.degree.nameM.S.en
thesis.degree.levelMastersen
dc.type.genrethesisen
dc.type.materialtexten
dc.format.digitalOriginreformatted digitalen


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