How to make different injury degree animal model of spinal cord injury?

[frank.hsu]

How to make different degree of injury animal model of spinal cord inury?
The aim to produce the different injury degree animal model of spinal cord injury is to copy the injured status with humanbeing. The mechanism of humanbeing suffered SCI is complex. There are so many influence factors should be consider well how to shield them.

[Lindox]

Originally Posted by frank.hsu

How to make different degree of injury animal model of spinal cord inury?
The aim to produce the different injury degree animal model of spinal cord injury is to copy the injured status with humanbeing. The mechanism of humanbeing suffered SCI is complex. There are so many influence factors should be consider well how to shield them.

I guess just drop the weights at different heights.
Still though will that be exactly like a natural injury?

Like with dogs that naturally have a SCI. Each case is different. Even dogs that are hit by cars or whichever way they become injured.

It's amazing though how the level of injury in dogs recovery and non-recovery almost mimics that of humans. They experience the spasticity..the loss of bladder control and every secondary problem associated with that. Atrophy. Pressure wounds. Pain/no pain.

Some recover to walk again some don't ever recover much of any function. If injured severely in the cervical level..they stop breathing.

It's a very difficult injury in both species.
And they also are not having any post cure parties YET.

I think though when they do put on their party hats..humans too will be wearing theirs.

[frank.hsu]

Thank you Lindox for your message.
Let us review the details:
As for the nosogenesis of SCI, the popular theories had:

1).Blood vessel theory: after the spinal cord is injury, blood vessel will be directly injured of spasmodic, which can reduce the motor ability of blood, thus result ischemia and degenerative necrosis of local tissue.

2).Catecholamine theory: After the sci, a great number of neurohumors such as histamine, catecholamine, accumulate in the tissue, this kind of medium can act on vascular smooth muscle receptor of the spinal cord and cause angiospasm, which will result in ischemia, anoxia and necrosis of the tissue;

3).Free radical theory: the content of unsaturated fatty acid on the spinal nerve cytomembrane is quite high, prone to the attack of FR, the resistance to FR will drop after the sci. Under the attack of FR, matrix will generate overoxidation, which can cause tissue injury;

4). Spinal cord neurocyte edema (Calcium ion storage) theory :the tissue edema after sci can reduce the motor ability of blood, hence, result in severer edema, in such a vicious cycle, cause the degeneratio and necrosis of neruocyte.

The detail discussion is going on!

[Wise Young]

frank,

You are talking about 30-50 year old theories, some of which have been debunked. For example, the catecholamine theory is no longer talked about very much, if at all. I don't know where you got the blood vessel theory but you may be referring nitric oxide and early endothelial damage that some scientists have reported in injured spinal cords. The neuronal edema theory was never well accepted.

The theories that are currently still being discussed include:
• Free radical theory. Several species of free radicals have been implicated in spinal cord injury, including superoxide, hydroxyl radical, and nitric oxide. These can interact with membranes to produce lipid peroxides. A number of antioxidants have been taken to clinical trial, including tirilazad mesylate. Inititally, the mechanism of methylprednisolone was thought to be mediated through the antioxidant effects of that drug.
• Inflammation theory. Injury causes a very rapid and large rise of pro-inflammatory cytokines, including interleukin (IL)-1, IL-6, tumor necrosis factor (TNF), and others. In 12-24 hours, many inflammatory cells accumulate in the injury site. Methylprednisolone is of course a powerful anti-inflammatory drug that shuts down the expresssion of inflammatory cytokines.
• Calcium theory. This is probably the initiation of the injury and calcium entry into cells is what is responsible for the free radicals and the inflammatory process.

I will write later about the actual mechanical injury of the spinal cord.

Wise.

[Wise Young]

frank,

You are talking about 30-50 year old theories, some of which have been debunked. For example, the catecholamine theory is no longer talked about very much, if at all. I don't know where you got the blood vessel theory but you may be referring nitric oxide and early endothelial damage that some scientists have reported in injured spinal cords. The neuronal edema theory was never well accepted.

The theories that are currently still being discussed include:
• Free radical theory. Several species of free radicals have been implicated in spinal cord injury, including superoxide, hydroxyl radical, and nitric oxide. These can interact with membranes to produce lipid peroxides. A number of antioxidants have been taken to clinical trial, including tirilazad mesylate. Inititally, the mechanism of methylprednisolone was thought to be mediated through the antioxidant effects of that drug.
• Inflammation theory. Injury causes a very rapid and large rise of pro-inflammatory cytokines, including interleukin (IL)-1, IL-6, tumor necrosis factor (TNF), and others. In 12-24 hours, many inflammatory cells accumulate in the injury site. Methylprednisolone is of course a powerful anti-inflammatory drug that shuts down the expresssion of inflammatory cytokines.
• Calcium theory. This is probably the initiation of the injury and calcium entry into cells is what is responsible for the free radicals and the inflammatory process. Axons and cells, when they are injured, allow calcium into the cells. At 1 micromolar concentrations, the calcium activates many enzymes, including phospokinases, phosphatases, calcineurin, and receptors.

I will write later about the actual mechanical injury of the spinal cord.

Wise.

[frank.hsu]

Thank you wise for your answers!

I want to know more details about how to make the animal model of spinal cord injury. And now, I am try my best to look for more details around injury .
Overview the current methods, it does not imitate the status of humanbeings which suffer. And one more thing is worthing to point out about the NYU IMPACTOR.

There are four important parameters about the movement of the rod, These are Imp_V, Ct, Cd, and Cr, all of which could describe the movement of the rod and the spine. All of the data are recorded by one rotate disk which generate one stream of +_5V pulses reflecting the each details about the rod and spine.
Yes , what a wonderful idea!

[Lindox]

frank,
How is your brother doing?
Are you studying medicine? Is your brother also going to school?

Surely he really appreciates your efforts on his behalf.

Is he a member here?
The best to you frank.

[frank.hsu]

hello Lindox
yes, I am a medical student in chengdu medical college , Sichuan province of PRC. Since he suffered the spinal cord injury in Denver in 2004, I followed my advisor to do the research on cell transplantation to care the spinal cord injury.

And now, he has received a prefect therapy in USA, but he still could not stand and live indenpently.

I found one lovely girl who suffered SCI in our school, I could never forget the lovely face,even the micro brow which caused me to miss my brother! He is abroad, I could not take good care of him. So now, I could take care of her to deliver my heart.

More story of me , please visit on :
http://281547389.photo.163.com