| Author | Post |
|---|
Prof Trevor Marshall
Foundation Staff
|
Posted: Mon Dec 31st, 2007 23:03 |
|
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 
|
Frans
Member*
|
Posted: Tue Jan 1st, 2008 16:06 |
|
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
____________________
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)
|
Prof Trevor Marshall
Foundation Staff
|
Posted: Tue Jan 1st, 2008 16:30 |
|
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.
|
Jimbbb
inactive guest
|
Posted: Tue Jan 1st, 2008 16:46 |
|
| 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 Tue Jan 1st, 2008 18:35 by Jimbbb
____________________
Interested (healthy) bystander with distant cousin who has Chronic Lyme.
|
Frans
Member*
|
Posted: Sun Jan 6th, 2008 11:05 |
|
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
____________________
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)
|
Frans
Member*
|
Posted: Mon Jan 7th, 2008 12:38 |
|
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
____________________
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)
|
Prof Trevor Marshall
Foundation Staff
|
Posted: Mon Jan 7th, 2008 12:51 |
|
Most human genetic codes and SNPs can be found at:
http://www.ncbi.nlm.nih.gov/genome/guide/human/
|
Frans
Member*
|
Posted: Sun Oct 10th, 2010 04:14 |
|
New Bacterial Foe in Cystic Fibrosis Identified
Exacerbations in cystic fibrosis (CF) may be linked to chronic infection with a bacterium called Stenotrophomonas maltophilia, which was previously thought to simply colonize the CF lung. The finding that chronic infection with S. maltophilia is independently linked with an increased risk of exacerbations gives clinicians and researchers a new potential measure of the health status of CF patients, as well as a new potential target in fighting their disease
- http://tinyurl.com/3xdfoqx
Best, Frans
Last edited on Sun Oct 10th, 2010 04:34 by Frans
____________________
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)
|
Marber144
inactive member
| Joined: | Tue Mar 4th, 2008 |
| Location: | Connecticut USA |
| Posts: | 213 |
| Status: |
Offline
|
|
Posted: Mon Oct 11th, 2010 06:47 |
|
Another article (Oct8) from Science Daily refers to biofilm (as in cystic fibrosis).
"Bacteria exist in two physiological states: the free-swimming, single-celled planktonic state and the surface-mounted biofilm state, a dense, structured, community of cells governed by their own sociology," says Gerald Wong, a professor of bioengineering at the UCLA Henry Samueli School of Engineering and Applied Science and at the California NanoSystems Institute at UCLA.
http://www.sciencedaily.com/releases/2010/10/101007171424.htm
"P. aeruginosa infections are unfortunately the leading cause of death for individuals with cystic fibrosis," Shrout said. "In addition to these lung infections, P. aeruginosa also causes skin, eye and gastrointestinal infections. As we learn how P. aeruginosa colonizes surfaces, perhaps we can develop better methods to treat these infections."
Perhaps the Marshall Protocol? ~Martha
|
Dmitry
Member*
|
Posted: Mon May 7th, 2018 10:45 |
|
Inhalation with Fucose and Galactose for Treatment of Pseudomonas Aeruginosa in Cystic Fibrosis Patients
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2586681/
Background: Colonisation of cystic fibrosis (CF) lungs with Pseudomonas aeruginosa is facilitated by two lectins, which bind to the sugar coat of the surface lining epithelia and stop the cilia beating.
Objectives: We hypothesized that P. aeruginosa lung infection should be cleared by inhalation of fucose and galactose, which compete for the sugar binding site of the two lectins and thus inhibit the binding of P. aeruginosa.
Results: The sugar inhalation was well tolerated and no adverse side effects were observed. Inhalation alone as well as combined therapy (inhalation and antibiotics) significantly decreased P. aeruginosa in sputum (P < 0.05). Both therapies also significantly reduced TNFα expression in sputum and peripheral blood cells (P < 0.05). No change in lung function measurements was observed.
Conclusions: Inhalation of simple sugars is a safe and effective measure to reduce the P. aeruginosa counts in CF patients. This may provide an alternative therapeutical approach to treat infection with P. aeruginosa.
and a followup:
Sugar administration is an effective adjunctive therapy in the treatment of Pseudomonas aeruginosa pneumonia
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3763031/
Treatment of acute and chronic pulmonary infections caused by opportunistic pathogen Pseudomonas aeruginosa is limited by the increasing frequency of multidrug bacterial resistance. Here, we describe a novel adjunctive therapy in which administration of a mix of simple sugars—mannose, fucose, and galactose—inhibits bacterial attachment, limits lung damage, and potentiates conventional antibiotic therapy.
Last edited on Mon May 7th, 2018 10:54 by Dmitry
____________________
MP Sep16 25D17 125D21 | Sep17 25D22 125D27 | May18 25D10 125D29 | brain fog, anxiety, fatigue, depression
|
Current time is 06:25 | |
|
