User:Ileon2019/Spinal cord injury research
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[edit]Pathophysiology
Secondary injury takes place minutes to weeks after the initial insult and includes a number of cascading processes that further harm tissues already damaged by the primary injury.[1] It results in formation of a glial scar, which impedes axonal growth. Secondary injuries can occur from different forms of stress added to the spinal cord in forms such as additional contusions, compressions, kinking, or stretching of the spinal cord. [1]
Complications from a secondary SCI are a result of a homeostatic imbalance potentially leading to metabolic and hemostatic changes from an inflammatory response. Potential immediate affects of secondary SCI include neuronal injury, neuroinflammation, breakdown of blood-spinal cord barrier (BSCB), ischemic dysfunction, oxidative stress, and daily-life function complications.
Animal models
Animals used as SCI model organisms in research include mice, rats, cats, dogs, pigs, and non-human primates. Typically, rats are used for a majority of the model organism stimulation of SCI based on several factors including their vascular anatomy, adequate cost, and the significant resemblance of their physiology compared to human physiology. The use of animal models raise ethical concerns about primate experimentation.[1] Special devices exist to deliver blows of specific, monitored force to the spinal cord of an experimental animal.[1] There are various mechanical impact classifications of these injuries which include contusion, compression, collagenase and ischemia reperfusion, distraction, dislocation, and transection.
Limitations of these model experiments are common. For instance, ischemia-reperfusion SCI involves the interruption of blood flow to the spinal cord. Complications have been observed to arise from the need to cross clamp the aorta.
Epidural cooling saddles, surgically placed over acutely traumatized spinal cord tissue, have been used to evaluate potentially beneficial effects of localized hypothermia, with and without concomitant glucocorticoids.[2][3]
Embryonic stem cells[edit]
Embryonic stem cells (ESCs) are pluripotent; they can develop into every type of cell in an organism such as oligodendrocytes. Oligodendrocytes and motor neurons have been predicted to be a favorable target for ESCs regarding treating neurological disorders and traumas. [2]After a SCI takes place there is evidence of oligodendrocytes degradation, eventually leading to cell death. This results in a lack of myelination, which enhances signals sent amongst neurons, causing disfunction in signaling. A potential solution could be hESC-derived oligodendrocyte transplantation; however, the success of this process depends off the cell’s ability to differentiate towards neural cell types in vitro. This is where more testing and research is being conducted using animal models.
References
[edit]Mohammad Ronaghi, Slaven Erceg, Victoria Moreno-Manzano, Miodrag Stojkovic, Challenges of Stem Cell Therapy for Spinal Cord Injury: Human Embryonic Stem Cells, Endogenous Neural Stem Cells, or Induced Pluripotent Stem Cells? , Stem Cells, Volume 28, Issue 1, January 2010, Pages 93–99, https://doi.org/10.1002/stem.253
Anwar, M. A., Al Shehabi, T. S., & Eid, A. H. (2016). Inflammogenesis of Secondary Spinal Cord Injury. Frontiers in Cellular Neuroscience, 10. https://doi.org/10.3389/fncel.2016.00098
- ^ Anwar, M. Akhtar; Al Shehabi, Tuqa S.; Eid, Ali H. (2016). "Inflammogenesis of Secondary Spinal Cord Injury". Frontiers in Cellular Neuroscience. 10. doi:10.3389/fncel.2016.00098. ISSN 1662-5102. PMC 4829593. PMID 27147970.
{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link) - ^ academic.oup.com https://academic.oup.com/stmcls/article/28/1/93/6408814. Retrieved 2023-04-25.
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