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Dr Trevor Marshall
Research Team
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Posted: Tue Jan 1st, 2008 08:03 |
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A new paper is out: http://www.ncbi.nlm.nih.gov/pubmed/18077362
"Molecular identification of bacteria in bronchoalveolar lavage fluid from children with cystic fibrosis."
There are a variety of species which were isolated by sequencing their DNA - Strep, Staph, Prevotella, Lysobacter, Pseudomonas aeruginosa, and a variety of unusual Actino and Proteobacteria (the full text has a detailed chart).
In controls there were 121 bacterial species identified, but this had shrunk to 65 in the Cystic Fibrosis patients, as some of the species became dominant. Common to both groups were 33 species.
Oh - and most of the species could not be cultured 
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Frans
Member in Phase 2
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Posted: Wed Jan 2nd, 2008 01:06 |
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Trevor,
I just came across a paper that might provide a link between the most important mutation in CF, the F508del, and the VDR.
They propose that the folding problem responsible for this mutation arises in something called the Hsc70/Hsp70 machinery.
The link I see is that if I search Wang's table 4 with HSP70, I find several genes mentioned there.
Maybe if the VDR doesn't properly transcribe this gene, this folding problem arises ?
I hope you find some time to look this paper over, I feel a little out of my depth here and am not sure I am interpreting things 100% ok.
PMID: 15923638
Sincerely, Frans
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Burn-out/nervous breakdown Jan01 125D 48 25D8.48 Ph1Nov06 ModPh2Jan07 Ph2Apr08 Cipramil Seroquel NoIRs lite exp r/t work cover up 25D3.9(Oct07)
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Dr Trevor Marshall
Research Team
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Posted: Wed Jan 2nd, 2008 01:30 |
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Frans,
Typically 'protein folding' occurs under the influence of an enzyme, or another protein, and is not a transcriptional artifact. The RNA can be truncated, also under the influence of proteins and enzymes.
I doubt that the VDR would improperly transcribe a gene, but then, we really are in unchartered territory where the understanding of mutations in RNA transcription or protein stranlation is involved.
And there is also no guarantee that the proteins being seen in CF as being mutated actually come from the human host, and not from the bacteria. Maybe the VDR has been shut down by the pathogens, so that the host is expressing very little HSP70, with the protein being measured by the geneticists coming from the bacterial species, and not from Homo sapiens. There is no way to know that yet.
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Jimbbb
Member
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Posted: Wed Jan 2nd, 2008 01:46 |
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| What is the explanation for the controls having MORE bacterial species that the CF patients? Ooops nevermind, I see that you mentioned that some species become dominant in CF driving out others. OK! Last edited on Wed Jan 2nd, 2008 03:35 by Jimbbb
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Interested (healthy) bystander with distant cousin who has Chronic Lyme.
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Frans
Member in Phase 2
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Posted: Sun Jan 6th, 2008 20:05 |
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Here is a paper about ulcerative colitis, where they found the same thing, dominance of one bacterial species in the microbiota: E. Coli
- PMID: 16954244
Sincerely, Frans
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Burn-out/nervous breakdown Jan01 125D 48 25D8.48 Ph1Nov06 ModPh2Jan07 Ph2Apr08 Cipramil Seroquel NoIRs lite exp r/t work cover up 25D3.9(Oct07)
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Frans
Member in Phase 2
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Posted: Mon Jan 7th, 2008 21:38 |
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Frans wrote: Trevor,
I just came across a paper that might provide a link between the most important mutation in CF, the F508del, and the VDR.
They propose that the folding problem responsible for this mutation arises in something called the Hsc70/Hsp70 machinery.
Trevor,
If the problem is in the folding, would it be fair to say that the actual genetic code is probably available?
Sincerely, Frans
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Burn-out/nervous breakdown Jan01 125D 48 25D8.48 Ph1Nov06 ModPh2Jan07 Ph2Apr08 Cipramil Seroquel NoIRs lite exp r/t work cover up 25D3.9(Oct07)
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Dr Trevor Marshall
Research Team
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Posted: Mon Jan 7th, 2008 21:51 |
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Most human genetic codes and SNPs can be found at:
http://www.ncbi.nlm.nih.gov/genome/guide/human/
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Current time is 07:17 | |
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