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AUTHORS: Robert H. Demling, M.D. Leslie DeSanti R.N. Dennis P. Orgill, M.D. Ph.D.

TRANSCYTE

 

The mechanism of action of TransCyte will first be presented by a series of schematic drawings prior to presentation of clinical use. The schemas describe the current view as to how Transcyte closes the wound and optimizes healing.

Mid Dermal (2 degree) Burn

 


Mid-Dermal Burn Injury

(Debrided to viable wound bed)

The area of coagulation or eschar has been completely removed exposing a viable but injured wound surface (zone of injury) which can deepen. The surface itself has an increased content of fibrin produced by activation of the clotting cascade and fibronectin produced by the dermal cells. There is also evidence of the onset of inflammation with vasodilation, increased neutrophils and macrophages. The wound surface also has increased proteolytic activity which if persistent can denature new tissue formation and growth factors.


WOUND CLOSURE USING TRANSCYTE 

The Transcyte is shown ready to be applied to the clean wound surface. The outer synthetic layer (knitted nylon) protects the wound surface from environmental insults. The inner bioactive membrane is composed mainly of human fibronectin and collagen Type I which will produce a contact adherence to the wound surface. These elements and the other components of the inner membrane are produced by human fibroblasts. 


TRANSCYTE IN PLACE


TRANSCYTE REMOVED - HEALED MID-DERMAL BURN

A schematic drawing of a healed wound is shown after removal of Transcyte.

 

 

 

 


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