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Thread: Miami project trial for Acute injury published

  1. #1
    Senior Member lunasicc42's Avatar
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    Miami project trial for Acute injury published

    forget which phase this is

    http://www.themiamiproject.org/schwa...ial-completed/


    Can't wait to see the chronic trial prelim results
    "That's not smog! It's SMUG!! " - randy marsh, southpark

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    I believe it's Phase I.

  3. #3
    Senior Member lunasicc42's Avatar
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    nice video at the bottom
    "That's not smog! It's SMUG!! " - randy marsh, southpark

    "what???? , you don't 'all' wear a poop sac?.... DAMNIT BONNIE, YOU LIED TO ME ABOUT THE POOP SAC!!!! "


    2010 SCINet Clinical Trial Support Squad Member
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    I just don't understand why for this trail the size of the lesion didn't matter and for chronic it does matter.

  5. #5
    Quote Originally Posted by Sparky831 View Post
    I believe it's Phase I.
    Sub-Acute injury less than 30 days.

  6. #6
    Quote Originally Posted by Sparky831 View Post
    I just don't understand why for this trail the size of the lesion didn't matter and for chronic it does matter.
    Acute and Sub-Acute injury doesn't have a buildup of glia scar. Chronic lesions tend to enlarge over time.

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    Quote Originally Posted by GRAMMY View Post
    Acute and Sub-Acute injury doesn't have a buildup of glia scar. Chronic lesions tend to enlarge over time.
    Hmm I did not know that lesions tend to enlarge over time. Do you know why? Now I want to know what the current size of my lesion is. I'll have to ask my doctor.

  8. #8
    Quote Originally Posted by Sparky831 View Post
    Hmm I did not know that lesions tend to enlarge over time. Do you know why? Now I want to know what the current size of my lesion is. I'll have to ask my doctor.
    I hope this chapter will help explain the situation.

    https://www.nap.edu/read/11253/chapter/4


    Apoptotic Cell Death
    During the acute phase, the mechanical trauma to the spinal cord causes cells to die instantaneously by necrosis, a process of cell swelling and then cell membrane rupture. Within hours, however, another type of cell death assumes center stage: apoptosis. This very active form of death afflicts neurons, oligodendrocytes, astrocytes, and other cells of the spinal cord after injury (Liu et al., 1997; Beattie et al., 2000). Apoptosis has been detected in humans (Emery et al., 1998) and lasts for about one month in animal models (Beattie et al., 2000). With apoptosis, cells do not swell before death; rather, they condense and break apart into small fragments in a very orderly process that requires energy and protein synthesis. These fragments of the apoptotic cell are engulfed by other cells in a process that prevents spillage of the dying cells? contents and avoids elicitation of an inflammatory response. Necrotic cell death, on the other hand, elicits inflammation and spills out neurotransmitters and other contents that build to levels toxic enough to harm or kill nearby cells.
    What triggers apoptosis after spinal cord injury? An answer to this question would immediately open up new targets for treatments that could prevent apoptosis from occurring. A major trigger appears to be the injury-induced rush of calcium into cells (Young, 1992). Calcium influx activates key enzymes inside the cell?the caspases and calpain?that break down proteins in the internal cytoskeleton and membrane of the cell (Ray et al., 2003). With the destruction of its structural integrity, the cell dies. Yet, apoptosis of cortical motor neurons can occur after the axons centimeters away are severed by spinal cord injury, too far for the calcium to diffuse (Hains et al., 2003a). Therefore, besides calcium influx, there are likely other triggers of apoptosis in spinal cord injury.

    Chronic Phase

    The chronic phase of spinal cord injury sets in over a period of months to years. The chronic phase is marked by the emergence of new types of pathology at both the microlevel and the macrolevel (e.g., the formation of a fluid-filled cavity or a glial scar). At the microlevel, the death of oligodendrocytes has an amplifying effect. Because most oligodendrocytes myelinate (i.e., insulate) about 10 to 40 nerve axons, the loss of one oligodendrocyte can leave many healthy nerve axons without conduction capacity. If nerve conduction is stopped entirely, the spinal cord cannot transmit signals to the brain and body, even though axons may be intact. Axons undergo molecular changes, such as alteration of the ion channels that are normally responsible for propagating electrical impulses through nerves (Waxman, 2001; Hains et al., 2003b). The combination of myelin loss and altered ion channel function, among other changes, can lead to molecular changes in the surviving neurons that can produce chronic pain in animals with experimental spinal cord injuries. At the macrolevel, the lesion site becomes increasingly devoid of normal tissue and begins to form a fluid-filled cavity or a glial scar, or both. The cavity forms within a few weeks of injury in animal models and may extend several segments above and below the site of injury. The cavity creates a physical gap that blocks axon regrowth, whereas the glial scar contains substances that inhibit axon regrowth.
    Glial Scar Formation
    Glial scarring (also known as reactive gliosis) creates an environment that inhibits axon regeneration. The glial scar is an extracellular matrix that contains astroyctes, microglia, and oligodendrocytes. It grows in size over time, from weeks to months after the injury, but the groundwork is set within hours of the injury. That is when the remnants of the acute phase?myelin debris and damaged axons?begin to accumulate at the site of the injury. The remnants begin to attract an array of different types of glial cells, from oligodendrocytes and their precursors to activated microglia and astrocytes. Astrocytes are most commonly found in the scar, and they are tightly bound to one another (Fawcett and Asher, 1999). If the spinal cord has been penetrated, meningeal cells, which normally form a protective layer around the spinal cord, also accumulate at the lesion site. Each type of cell expresses and/or releases a host of inhibitory molecules. The collective action of these inhibitory molecules is the prevention of axon regeneration.
    Oligodendrocytes, which are already at the scene because they myelinate axons, express a potent inhibitor of axon growth, Nogo-A, on the exterior surface of the cell membrane (Fournier et al., 2002). The vital importance of Nogo-A was revealed by studies with an animal model that showed that antibodies against this molecule, which block its action, promote some regeneration of severed axons (Schnell and Schwab, 1990). The first glial cells to arrive at the scene, within 3 to 5 days, are thought to be oligodendrocyte precursor cells, although no direct evidence of this has emerged. Oligodendrocyte precursors are immature oligodendrocytes that are destined, with further growth and differentiation, to become mature oligodendrocytes. At the scene they proliferate and release a variety of molecules that block axon growth. Astrocytes also arrive at the injury site and begin to undergo hypertrophy and divide.
    Astrocytes form the bulk of the glial scar. In the scar, they are surrounded by an extracellular matrix made up of several types of proteoglycans, which are proteins on the outside of the cell membrane that have sugar moieties attached to them. Proteoglycans are up-regulated and secreted by astrocytes themselves, and they directly inhibit axon growth (Fawcett and Asher, 1999). The role of astrocytes has perplexed researchers because, in addition to their inhibitory role, they can also play a growth-promoting role under different circumstances (Jones et al., 2003).
    Syringomyelia
    Syringomyelia is a complication that arises as early as 2 months or as late as 30 years after the injury. It results from the formation of a cyst in the center of the spinal cord. This cyst expands and elongates over time, significantly damaging the center of the spinal cord. About 4 percent of individuals with spinal cord injuries develop syringomyelia (Schurch et al., 1996; Terre et al., 2000). Individuals with syringomyelia can present with multiple symptoms, including pain, weakness, headaches, and stiffness of the limbs and the back. The pathogenesis of syringomyelia, however, is not well understood. It may even lie dormant for many years before symptoms arise. Detection was especially difficult because of the wide range of other complications and sensory deficits that result from spinal cord injuries; however, the advent of magnetic resonance imaging (MRI) technologies has greatly enhanced the ability of clinicians to detect syringomyelia.
    Last edited by GRAMMY; 03-10-2017 at 12:50 PM.

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