Graft Dysfunction
Graft Dysfunction - Related Videos
07:37
Mouse Models for Graft Arteriosclerosis
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Cited by 17 •
2013
We describe protocols for our mouse graft arteriosclerois (GA) models which involve interposition of a mouse vessel segment into a recipient of the same inbred strain. By backcrossing additional genetic changes into the vessel donor, the model can assess the effect of specific genes on GA.
02:34
Modeling Preservation Injury in Porcine Donor Kidney: A Procedure to Induce Graft Dysfunction by Subjecting Kidney to Prolonged Cold Ischemia
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2025
In this video, we describe a technique to induce preservation injury via the prolonged cold ischemic storage time in porcine donor kidney.
03:35
A Technique for Human Skin Grafting in a Mouse Model
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2025
This video demonstrates a method for grafting human skin onto an immunodeficient mouse with a suppressed neutrophil response. The method involves applying human split-thickness skin to the mouse's graft bed, sealing it, and covering it for recovery. Eventually, the human skin adheres to the mouse's skin, establishing vascularization and circulation, resulting in a successful skin xenograft.
05:47
Isolation and Transplantation of Different Aged Murine Thymic Grafts.
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Cited by 14 •
2015
This report provides a detailed description of transplanting murine thymi from different aged donor mice under the kidney capsule of immunodeficient mouse recipients. The goal of this approach is to model T cell development and thymic selection events in vivo.
13:04
Generation and Grafting of Tissue-engineered Vessels in a Mouse Model
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Cited by 13 •
2015
Here, we present a protocol to generate tissue engineered vessel grafts that are functional for grafting into mice by double seeding partially induced pluripotent stem cell (PiPSC) - derived smooth muscle cells and PiPSC - derived endothelial cells on a decellularized vessel scaffold bioreactor.
FAQs
Immune-mediated rejection, inadequate blood flow, infection, medication toxicity, and other injuries can all disrupt graft cells or tissue structure. Because these mechanisms may lead to impaired performance through different pathways, the same general concern does not identify the cause by itself. Distinguishing among them is essential for selecting treatment that addresses the underlying injury rather than only its consequences.
Rejection occurs when immune activity injures the transplanted tissue, interfering with the cells and structures responsible for its intended function. This mechanism differs from problems caused by poor blood flow, infection, or medication toxicity, even though each can produce graft dysfunction. Recognizing rejection as a possible cause helps clinicians interpret evidence and consider targeted treatment promptly.
Each factor can injure the graft through a different type of stress. Inadequate blood flow limits the conditions needed for graft tissue to function, infection can damage cells and tissue, and medication toxicity can directly impair graft components. These distinctions matter because identifying the source of injury guides the clinical response and helps explain changes in transplant outcomes.
Severity depends on how substantially graft cells and tissue structure have been disrupted and whether the underlying cause is recognized early. Persistent or worsening injury can place the graft at risk of failure, whereas early recognition creates an opportunity for targeted treatment. Monitoring dysfunction therefore supports both immediate clinical decisions and longer-term graft survival.
Evaluation combines several sources of evidence rather than relying on one finding. Clinicians assess symptoms, laboratory tests, and imaging to identify signs of impaired graft performance and possible injury. When these assessments do not sufficiently clarify the cause, a biopsy may be used to examine the graft more directly. Together, these approaches support cause-specific clinical decisions.
A biopsy is useful when symptoms, laboratory findings, and imaging do not adequately identify why the graft is impaired. It provides additional information about changes in graft cells and tissue structure, helping clinicians investigate causes such as immune-mediated injury or other forms of damage. The resulting evidence can support targeted treatment and improve interpretation of transplant outcomes.