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Dr Trevor Marshall
Research Team
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Posted: Mon Jun 9th, 2008 15:03 |
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Nick,
The key words are " If the same technique works in people"
At the conference on aging (in two weeks) I have two slides which point out exactly why mice/rats cannot emulate human chronic disease. We give two different reasons, each a sufficient standard for exclusion.
It's over. The science now explains why mice can never emulate Human Chronic disease, including Cancers. There have been no major breathroughs from murine work, and I now know why there will be none.
Reason 1: The Mouse VDR does not transcribe either the Cathelicidin nor the beta-Defensin anti-microbials. The human VDR does. When a microbe knocks out the mouse VDR it does not knock out these antimicrobial defenses, as it does in man.
Reason 2: The VDR binding pocket homology between mice/rats and humans is poor. Drugs will act differently in the two VDR.
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Markt9452
Member in Phase 3
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Posted: Wed Sep 10th, 2008 01:23 |
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Cryptococcus Yeast Eludes Detection by Using Macrophages to Travel through the Body
"we hypothesise that this process may have significant clinical implications since it allows C. neoformans to remain intracellular, thus avoiding immune recognition. Furthermore, it allows the pathogen to move from weak to healthy phagocytes, thus ensuring intracellular persistence of the pathogen even if the host cell starts to die. Finally, infected macrophage cells may travel widely throughout the host circulatory and lymphatic systems, where they interact intimately with one another and with other cell types through transient contacts"
http://www.biomedcentral.com/1471-2172/8/15 (with videos)
http://www.genengnews.com/news/bnitem.aspx?name=41551063
Yeast fungus cells that commonly attack HIV infected patients escape detection by the immune system by hiding inside the body’s macrophages, according to scientists from the University of Birmingham, U.K. Studying cells of the Cryptococcus yeast, which causes cryptococcal meningitis, the researchers found that they additionally use these white blood cells as vehicles to travel inside the body.
“The yeast cells then escape from inside the macrophages when they arrive at the right destination,” explains Hansong Ma of the University of Birmingham. “Importantly, they do this without killing the macrophage, which would trigger alarm bells.
“This new method of remaining inside the host cells means that the pathogen can spread more efficiently around our bodies and is protected from the natural defenses in our bloodstream that would normally kill the yeast or other invader,” notes Ma.
“Yeast cells avoid killing or damaging the macrophages. They leave by a method that we call vomocytosis.” The investigators used time-lapse microscope photography to identify this new escape mechanism.
They were able to observe the yeast cells escaping into the fluid surrounding cells or directly into other host cells through cell-to-cell transmission, continuing to avoid detection by using this extremely rapid vomocytosis.
“Worryingly, this enables the cryptococci to avoid antifungal drugs and other treatments as well as our normal immune system, and may allow the yeast to become latent, achieving a long-term infectious state, which could then be spread even further to other individuals without anyone realizing,” Ma points out.
This data was presented at the Society for General Microbiology's Autumn meeting being held this week at Trinity College, Dublin.
Last edited on Wed Sep 10th, 2008 01:26 by Markt9452
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Th1 Inflammation Lyme vertigo fatigue brain fog skin lesions tinnitis 125D20 D2510 Ph1Feb08 Ph2Apr08 daily lite exp covered up NoIRs
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Aunt Diana
Advocate
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Posted: Wed Sep 10th, 2008 08:15 |
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| Thank you for that uplifting article. (I couldn't get the first link to work?!) It is music to my ears to hear this.
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Lyme 1987, neuro cardio fatigue achiness brain fog depression, anxiety. Pacemaker, D.1,25 32; D <5; 12/07 <6, Oxycodone, lorazapam, benedryl, zantac, colase, Noirs, cover-up or avoid sun, house <30lux. Feb 08 Phase 3. 6/08 D <4, D1,25 21
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Sunset
Health Professional
| Joined: | Tue Oct 16th, 2007 |
| Location: | USA |
| Posts: | 52 |
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Offline
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Posted: Fri Sep 19th, 2008 21:45 |
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Below is a link to a preprint of an article which I found quite interesting entitled: “Hypothesis: Chronic fatigue syndrome is caused by dysregulation of hydrogen sulfide metabolism”.
The paragraph below peaked my interest because it links hydrogen sulfide (H2S) and bacteria. I’m curious to know if H2S may be responsible for some IP reactions. Could there be an excess accumulation of H2S in the presence of certain bacterial or fungal infections? Would knowing the answer to this question be helpful in managing IP for patient’s using the MP for their Th1 illness? If this is correct, then perhaps a better title for this article would be “Immune response reactions in Th1 illnesses may be caused (in part) by dysregulation of H2S metabolism”
“Finally, H2S plays a pivotal role in both aerobic and non-anaerobic organisms as a signaling molecule. Bacteria in the gut both produce H2S and utilize it as a substrate alternative to oxygen. This is of particular relevance in the gastrointestinal tract, where unusually high levels of gram-negative bacteria, which increase intestinal permeability, have been found in patients with CFS/ME [4]. In addition to bacteria, yeast, mold and other fungi also emit H2S.”
Hypothesis: Chronic fatigue syndrome is caused by dysregulation of hydrogen sulfide metabolism
Journal: Med Hypotheses. 2008 Sep 15. [Epub ahead of print]
Author: Marian Dix Lemle, Washington, DC 20008, United States, Fax: +1 202 775 0045
To see the entire post of this article go to on http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0809C&L=CO-CURE&P=R2505&I=-3
(This is on a listserver, so you may need to register and login to view the article)
Sunset
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FM, CFS, migr HA, low adrenal, 11/07 tests 1,25D70, 25D48, 7/08 tests 25-D 21 ng/mL, olmesartan 40mgQ4H, Nystatin 1 QID, milk thistle, mag suppl, NoIRs, limited lite exp, 22% zinc sunscreen,cover up, wean HC
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Dr Trevor Marshall
Research Team
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Posted: Sat Sep 20th, 2008 03:08 |
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Chronic fatigue syndrome is NOT caused by dysregulation of hydrogen sulfide metabolism
While I understand that 'metagenomic microbiota' might be a bit of a mouthful, the human body does not operate with the simplicity of high-school chemistry (H2S, Acidic/Basic, etc). Please take a look at my UCLA presentation video, and the Porto videos, which should be online in a few days
http://vimeo.com/1268542
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Sunset
Health Professional
| Joined: | Tue Oct 16th, 2007 |
| Location: | USA |
| Posts: | 52 |
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Offline
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Posted: Sat Sep 20th, 2008 05:27 |
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Dr Trevor Marshall wrote:
Chronic fatigue syndrome is NOT caused by dysregulation of hydrogen sulfide metabolism
I agree with your statement.
I'm not trying to contradict your research on the human immune system and the basic underlying cause of Th1 illness. I am suggesting that the author of the article I referenced may have it backwards; that it's not H2S dysregulation that causes Th1 illnesses like CFS, but rather that H2S formation due to bacteria in the human body may be responsible for some of the symptoms in CFS.
My point, which I guess I did not make clear in my first post, is that perhaps part of the HERX reaction symptoms could be attributed to the formation of bacterial byproducts such as H2S.
In this case, basic chemical reactions do apply; combine sulfur with hydrogen and you get H2S.
I for one know that when I take Pepto Bismol (bismuth subsalicylate) my tongue turns black and I feel pretty lousy all the way from my mouth through my gut; HERX symptoms due to the antimicrobial action of this drug. Recall, Pepto-Bismol is used in combination with antibiotics to treat h. pylori infection. This is a basic chemical reaction between Pepto-Bismol and sulfur.
Combining a bismuth(III) salt with hydrogen sulfide can form Bismuth(III) sulfide
citation from Wikapedia:
Pepto-Bismol has been known to cause one's tongue and stool to turn black.[2] This form of "black tongue," however, is a result of the separation of bismuth from salicylate, forming bismuth(III) sulfide (Bi2S3) in combination with the sulfur found in saliva.[3]
I am suggesting that in humans harboring large populations of H2S forming bacteria could result in symptoms associated with H2S toxicity.
Some symptoms of H2S toxicity include: Eye irritation, sore throat and cough, nausea, shortness of breath, fluid on the lungs, fatigue, loss of appetite, headaches, irritability, poor memory, and dizziness.
It is this part of the article that I cited which I found interesting:
Bacteria in the gut both produce H2S and utilize it as a substrate alternative to oxygen. This is of particular relevance in the gastrointestinal tract, where unusually high levels of gram-negative bacteria, which increase intestinal permeability, have been found in patients with CFS/ME
Here is another article that I found interesting:
Distribution of Sulfate-Reducing Bacteria, 02, and H2S in
Photosynthetic Biofilms Determined by Oligonucleotide
Probes and Microelectrodes
NIELS BIRGER RAMSING,t* MICHAEL KUHL,t AND BO BARKER J0RGENSENt
1APPLIED AND ENVIRONMENTAL MICROBIOLOGY, Nov. 1993, p. 3840-3849
http://aem.asm.org/cgi/content/abstract/59/11/3840
Sunset
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FM, CFS, migr HA, low adrenal, 11/07 tests 1,25D70, 25D48, 7/08 tests 25-D 21 ng/mL, olmesartan 40mgQ4H, Nystatin 1 QID, milk thistle, mag suppl, NoIRs, limited lite exp, 22% zinc sunscreen,cover up, wean HC
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Markt9452
Member in Phase 3
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Posted: Sun Sep 21st, 2008 18:26 |
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Unraveling the mystery of Crohn's disease
Could bacteria found in dairy products play a key role in Crohn's disease?
http://www.saturdayeveningpost.com/issues/2004/0304/73701034.shtml
Current treatments focus on the symptoms, but do little to address the root cause of Crohn's, including the potential role of bacteria. Whether infection plays a role remains a hotly contested area among experts. The theory, however, is gaining ground as evidence mounts supporting the connection.
Researchers point to a persuasive body of evidence linking the bacterium, called Mycobacterium avium subspecies paratuberculosis to the disease and underscore the route of transmission into the human population through one of our most popular drinks--milk.
The MAP bug belongs to the group of organisms called mycobacteria. The most notorious mycobacteria are those causing tuberculosis and leprosy.
Apart from some people actually just not doing the procedures properly, the main problem is that the MAP bug is present in Crohn's disease in a very tough "Teflon-coated" invisible form. Standard laboratory reagents that would break open ordinary bugs, even tuberculosis bacilli, and release their DNA don't work for MAP.
Supporters of the theory note that Crohn's is most frequently found in developed countries where milk consumption is high...
The MAP bug was first identified in 1895...
The infection is often subclinical...
"Infected animals secrete the organism in their milk. We showed from 1990 to 1994 that there was a very high risk in Britain, that the MAP bug was being transmitted to the human population in retail pasteurized cow's milk supplies. This has since been confirmed by research carried out for the U.K. government's Food Standards Agency.
But because MAP is so reluctant to grow in culture, the true proportion of retail cartons and bottles of pasteurized cow's milk in Britain contaminated with live MAP is much more likely to be closer to 10 percent than two percent. class="arttext"
19.7 percent of 1,384 bulk tanks of milk from all over Switzerland tested positive for the MAP bug.
11.8 percent of hundreds of bottles and cartons of milk from all over Britain tested positive for the MAP bug.
Last edited on Sun Sep 21st, 2008 18:42 by Markt9452
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Th1 Inflammation Lyme vertigo fatigue brain fog skin lesions tinnitis 125D20 D2510 Ph1Feb08 Ph2Apr08 daily lite exp covered up NoIRs
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kainer
Member
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Posted: Fri Sep 26th, 2008 17:42 |
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Here are two things happening in research...
http://www.temple.edu/newsroom/2008_2009/08/stories/sickfattissue.htm
http://www.temple.edu/newsroom/2008_2009/08/stories/nihgrant.htm
Chipping around the edges...
JGK
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J.G. Kain
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