A Keratin Biomaterial for Treatment Following Spinal Cord Hemisection Injury and Investigation of Secondary Damage Mechanisms
type: CreativeWork
description: Spinal cord injuries (SCI) are a severely debilitating injury that affects about 200,000 people in the United States alone. The only current treatment options include use of steroids, spinal fixation surgery, and rehabilitation, none of which provide any significant recovery of function. SCIs are particularly difficult to treat because of the inhibitory nature of the lesion site and overcoming it to allow for repair and regeneration. There are many contributing factors to secondary damage, including the inflammatory response that follows SCI. Peripheral immune cells are able to infiltrate to the site of injury through the damaged blood-spinal cord barrier (BSB). It is well-established that macrophages play a major role in this process and, in response to SCI, are known to polarize to a proinflammatory phenotype that promotes secondary degeneration. These M1 macrophages dominate at the lesion site with concurrent downregulation of the M2 anti-inflammatory, growth supporting phenotype.
abstract: Spinal cord injuries (SCI) are a severely debilitating injury that affects about 200,000 people in the United States alone. The only current treatment options include use of steroids, spinal fixation surgery, and rehabilitation, none of which provide any significant recovery of function. SCIs are particularly difficult to treat because of the inhibitory nature of the lesion site and overcoming it to allow for repair and regeneration. There are many contributing factors to secondary damage, including the inflammatory response that follows SCI. Peripheral immune cells are able to infiltrate to the site of injury through the damaged blood-spinal cord barrier (BSB). It is well-established that macrophages play a major role in this process and, in response to SCI, are known to polarize to a proinflammatory phenotype that promotes secondary degeneration. These M1 macrophages dominate at the lesion site with concurrent downregulation of the M2 anti-inflammatory, growth supporting phenotype.
author: Fearing, Bailey
language: en
keywords: biomaterial
date published: 2014
date modified: 2026-07-27T22:01:46Z
provider: Wake Forest University
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: Wake Forest University

PropertyValue
property ID: Handle
value: http://hdl.handle.net/10339/39298