HiddenTruth

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So, there are a couple of erratas i found, and some may need some clarification. Feel free to chime in.

1. In the phsyiology of B12 transport from the mouth. From what I understand that B12 exogenously is bound to a protein which is cleaved by pepsin in the stomach and it is there where it binds R-binder protein (which is then taken to the duodenum for cleavage by pancr enz to bind to IF)According to Dr. G, B12 binds to the R protein in the saliva to protect being destoryed by the acid in the stomach. After that, the path he describes is the same. I amnot sure.

2. Also, in B12 deficiency--the folate you give to overcome the anemia exogenously is in THF form? It would have to be, rite? But, then again I thought all folate taken in exogenously is in the N5 THF form?

3. According to BRS, you only get increased levels of HgB F in the MAJOR form of Beta thal. And increased levels of hgBA2 in MINOR Beta thal. Wouldn't you get increased levels of both in both forms, just to a varying degree?

4. Also, I don't understand--in BRS it says, in alpha thal, you have barts HgB in fetal life and HgH in adult life. I thought that those just dependent on the amount of gene deletions u had (3 gene del would produce HgH and 4 would produce Barts). Can anyone explain?

Thanks a lot.
 

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HiddenTruth said:
So, there are a couple of erratas i found, and some may need some clarification. Feel free to chime in.

1. In the phsyiology of B12 transport from the mouth. From what I understand that B12 exogenously is bound to a protein which is cleaved by pepsin in the stomach and it is there where it binds R-binder protein (which is then taken to the duodenum for cleavage by pancr enz to bind to IF)According to Dr. G, B12 binds to the R protein in the saliva to protect being destoryed by the acid in the stomach. After that, the path he describes is the same. I amnot sure.

2. Also, in B12 deficiency--the folate you give to overcome the anemia exogenously is in THF form? It would have to be, rite? But, then again I thought all folate taken in exogenously is in the N5 THF form?

3. According to BRS, you only get increased levels of HgB F in the MAJOR form of Beta thal. And increased levels of hgBA2 in MINOR Beta thal. Wouldn't you get increased levels of both in both forms, just to a varying degree?

4. Also, I don't understand--in BRS it says, in alpha thal, you have barts HgB in fetal life and HgH in adult life. I thought that those just dependent on the amount of gene deletions u had (3 gene del would produce HgH and 4 would produce Barts). Can anyone explain?

Thanks a lot.
1. R-protein is mainly in the mouth.

2. Yes.

3. I think you are right.

4. Every baby born with beta thal has some HgB Bart at birth. If they live, they dont Bart's disease, and they will have HgH as an adult. If they dont, then they had Bart's disease.
 

automaton

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where are the errors from?
 
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HiddenTruth

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automaton said:
where are the errors from?
sorry, i don't know if i would call it an error, but whatever it is, it only applied to q.1 (from the audio).

Idio: I understand that R protein is mainly secreted in the mouth, but according to robbins, it doesn't bind to B12 until protein bound B12 gets into the stomach and is cleaved by pepsin. Realistically speaking, this may be a minutia, and I don't think it is important for the boards, but I thought I would point it out for those of you that are interested. I stated in my OP what Dr G's slightly altered version of this pathway is (according to his audio).
Thanks for your help on the other question--appreciate it.
 

peterson

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HiddenTruth said:
So, there are a couple of erratas i found, and some may need some clarification. Feel free to chime in.

1. In the phsyiology of B12 transport from the mouth. From what I understand that B12 exogenously is bound to a protein which is cleaved by pepsin in the stomach and it is there where it binds R-binder protein (which is then taken to the duodenum for cleavage by pancr enz to bind to IF)According to Dr. G, B12 binds to the R protein in the saliva to protect being destoryed by the acid in the stomach. After that, the path he describes is the same. I amnot sure.

2. Also, in B12 deficiency--the folate you give to overcome the anemia exogenously is in THF form? It would have to be, rite? But, then again I thought all folate taken in exogenously is in the N5 THF form?

3. According to BRS, you only get increased levels of HgB F in the MAJOR form of Beta thal. And increased levels of hgBA2 in MINOR Beta thal. Wouldn't you get increased levels of both in both forms, just to a varying degree?

4. Also, I don't understand--in BRS it says, in alpha thal, you have barts HgB in fetal life and HgH in adult life. I thought that those just dependent on the amount of gene deletions u had (3 gene del would produce HgH and 4 would produce Barts). Can anyone explain?

Thanks a lot.

for 3, in minor Beta thal you have some B chain synthesis, that's why you don't have to treat it. i think you are right, you would get an increase in both hgA2 (with delta) and hgF (with gamma) in both major and minor beta thal. but you would probably have more of both hgA2 and hgF in the major one.