Buster..I have a question about one of your posts

[peglem]

This one:

Buster

post May 14 2010, 08:20 PM

Post #6

 

 

 

 

Hi Tapiash,

 

I can try to explain the titers, but what they mean isn't quite known yet.

 

Dr. Cunningham is running what is known as Competitive Inhibition ELISAs -- this is a fancy term for seeing who gets there first.

 

 

 

While not perfectly the same, this is sort of similar to what happened when you did titration experiments in high-school chemistry.

 

 

 

What they do is take a substrate of a chemical like a "lysoganglioside". And then have a known quantity of a chemical that changes colors when it binds to the lysoganglioside. They choose the concentration of this chemical to create a pronounced change in the tube. If there was none of your serum added, and only the chemical added, the tube would change colors.

 

Now they take your serum and start diluting it by powers of 2 into each tube. In this way they have very weak concentrations and very strong concentrations. They first add this "diluted serum" and then try to add the "color change chemical". Since the diluted serum is already bonded to the lysogangliosides there's no room for the color changing chemical to attach and so the color doesn't change. They keep diluting the concentration of serum until there's a color change. So the number being reported is the amount of dilution needed before the serum didn't "interfere" with the color change.

 

 

So 640 and 1280 are just one dilution away. So too are 8000 and 16000. Generally they don't look closer.

 

In terms of your numbers, the serum interfered a bit with lysogangliosides (slightly elevated), was within norm for tubulin, was slightly elevated for anti-D1, and normal for D2. Beyond that, we don't know a lot more.

 

 

Probably more than you ever wanted to know and not what you actually wanted to know...

 

Buster

 

Do they know what it is in the serum that is interfering w/ the bonding? I mean, how do they know its from strep and not something else? And wasn't there a correlation between kids on SSRIs having high antiD2? Could the SSRIs be interfering with the dopamine receptor, instead of an antibody? I hope I'm asking that right.

Edited May 17, 2010 by peglem

[Buster]

Hi Peglem,

 

As always, you have great questions. In 2003, Kirvan and Cunningham isolated 3 antibodies in Sydenham Chorea children. These are known as 24.3.1, 31.1.1, and of course 37.2.1. What was unusual about these monoclonal antibodies is that they bonded with lysoganglioside GM1. Kirvan and Cunningham \ showed that these antibodies were absent in convalescent serum, but present during exacerbation. It also turns out that 24.3.1 not only bonded with lysoganglioside GM1 -- but also was sufficient to cause CaM Kinase II activation. Kirvan was sure it was just 24.3.1 because she had gotten rid of all the other material that wasn't 24.3.1.

 

In the current test that Dr. Cunningham is running, I don't believe she isolates the three antibodies but rather is checking the broader category of any antibody (or substance) in the blood serum interacting with the lysoganglioside substrate.

 

An unusual property of 24.3.1 is that it is targeting the GlcNAC epitype (i.e., the carbohydrate on the cell surface of GABHS). However, your point is really valid, do we know that GABHS is the only trigger of 24.3.1? The answer is no. That causality is not shown. So we don't know why 24.3.1 emerges, but there is good evidence it is present in SC and PANDAS children after a strep infection and not in controls. That is not causality, just co-existant.

 

When Dr. Cunningham is running the ELISA, she isn't doing the full antibody isolation, but rather using the serum in the manner of my post. This means there is a potential that something else in the serum is causing the reaction, but I and others have contacted Dr. Cunningham about this and so far none of the things we've mentioned seem to affect the results.

 

I was probably the one starting the question on whether kids on SSRI have higher anti-D2. It made sense to me especially since kid's serum could have elevated serotonin levels. I asked Dr. Cunningham about this and she was checking this and the impact azith might have. I don't know the outcome of that check.

 

Best regards,

 

Buster

 

 

In terms of your numbers, the serum interfered a bit with lysogangliosides (slightly elevated), was within norm for tubulin, was slightly elevated for anti-D1, and normal for D2. Beyond that, we don't know a lot more.

 

Do they know what it is in the serum that is interfering w/ the bonding? I mean, how do they know its from strep and not something else? And wasn't there a correlation between kids on SSRIs having high antiD2? Could the SSRIs be interfering with the dopamine receptor, instead of an antibody? I hope I'm asking that right.

Edited May 17, 2010 by Buster

[peglem]

Thanks for your reply. As always you have great answers!

[kimballot]

Wow! so much to learn... so glad to have folks who can ask the right questions and folks who can explain it!

[fuelforall]

Buster,

It's been two months since my son's second IVIG and no dice. Nothing.

My son's anti-lysogaglioside numbers were thru the roof. 2000.

This should be what the iVIG tries to get at, right?

No abx seem to provide relief either.

My wife needs convincing that doing another IVIG is worth it.

 

Your input as always is welcome.

 

Michael

[Buster]

Reply to Fuelforall moved here: http://www.latitudes.org/forums/index.php?showtopic=8252