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home:publications:marshall_chlamydia2_2009 [07.18.2011] – [Slide # 18: Summary] cells' posessive apostrophe added jrfoutinhome:publications:marshall_chlamydia2_2009 [09.14.2022] (current) – external edit 127.0.0.1
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 **Location:** Prague, Czech Republic\\ **Location:** Prague, Czech Republic\\
 **Date:**  April 18, 2009\\ **Date:**  April 18, 2009\\
-**See also:** [[http://AutoimmunityResearch.org/prague_2009/science.pdf|Transcript with slides]]+**See also:** [[https://AutoimmunityResearch.org/prague_2009/science.pdf|Transcript with slides]]
  
  
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 ==== Question: What are the methods for measuring the antimicrobial peptides in humans? ==== ==== Question: What are the methods for measuring the antimicrobial peptides in humans? ====
  
-The antimicrobial peptide work that I am relying upon was done by Brahmachary’s group in Singapore. I cite it in all of our papers, actually, I think you’ll find it cited.(({{pubmed>long:17254313}}))  And they used an //in silico// analysis. What they did was look at the DNA and they figured out what activated the DNA. Whether it’s a VDR receptor, whether it was a P300 receptor, and from that they figured out what was responsible for each of the antimicrobial peptides. Cathelicidin, beta-Defensins, and TLR2 have all been confirmed //in vitro// as coming from the VDR. So the 24 families //in silico// and the actual Cathelicidin, the key metabolites have been confirmed //in vitro// by various groups, more than one group.+The antimicrobial peptide work that I am relying upon was done by Brahmachary’s group in Singapore. I cite it in all of our papers, actually, I think you’ll find it cited.(({{pmid>long:17254313}}))  And they used an //in silico// analysis. What they did was look at the DNA and they figured out what activated the DNA. Whether it’s a VDR receptor, whether it was a P300 receptor, and from that they figured out what was responsible for each of the antimicrobial peptides. Cathelicidin, beta-Defensins, and TLR2 have all been confirmed //in vitro// as coming from the VDR. So the 24 families //in silico// and the actual Cathelicidin, the key metabolites have been confirmed //in vitro// by various groups, more than one group.
  
 ==== Slide #32: "Microscopy of of HIV Transfer Across T-cell Virological Synapses" ==== ==== Slide #32: "Microscopy of of HIV Transfer Across T-cell Virological Synapses" ====
  
-This is a slide that just came out last week from a group studying HIV. And what we’ve got here [referring to the animation on the screen] is we’ve got two cells--well a number of cells--but there’s a cell which has been infected with HIV. We have a cell which is brushing up against it. And at the junction of the two cells, the HIV is trying to get through the cell membranes into that [uninfected] cell. And in fact, that’s exactly what’s going to happen. This HIV infection is able to cross the membrane. You can see it frozen there as it’s starting to cross. In a little while you’ll find there will be fluorescent staining inside that cell, or fluorescent artifacts inside that cell to indicate that the tat protein has--there it is, it’s broken off, it’s now inside the other cell. One of the reasons that we don’t find these pathogens in the blood is because they don’t need to be in the blood. They can pass from cell to cell. That’s now been shown in HIV with this very elegant study from March 2009, "Microscopy of of HIV Transfer Across T-cell Virological Synapses"(({{pubmed>long:19325119}})) (which means across the membranes). And of course that cell now also will become infected and will eventually bud into virions. +This is a slide that just came out last week from a group studying HIV. And what we’ve got here [referring to the animation on the screen] is we’ve got two cells--well a number of cells--but there’s a cell which has been infected with HIV. We have a cell which is brushing up against it. And at the junction of the two cells, the HIV is trying to get through the cell membranes into that [uninfected] cell. And in fact, that’s exactly what’s going to happen. This HIV infection is able to cross the membrane. You can see it frozen there as it’s starting to cross. In a little while you’ll find there will be fluorescent staining inside that cell, or fluorescent artifacts inside that cell to indicate that the tat protein has--there it is, it’s broken off, it’s now inside the other cell. One of the reasons that we don’t find these pathogens in the blood is because they don’t need to be in the blood. They can pass from cell to cell. That’s now been shown in HIV with this very elegant study from March 2009, "Microscopy of of HIV Transfer Across T-cell Virological Synapses"(({{pmid>long:19325119}})) (which means across the membranes). And of course that cell now also will become infected and will eventually bud into virions. 
  
 All of this without the bacteria having to have to deal with what’s in the bloodstream. It hasn't had to deal with any antibiotics the patient’s been taking. Because it’s existing totally inside the cytoplasm of the cells. All of this without the bacteria having to have to deal with what’s in the bloodstream. It hasn't had to deal with any antibiotics the patient’s been taking. Because it’s existing totally inside the cytoplasm of the cells.
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 Firstly, **//I//** don’t follow them. But there have been studies done. The two that come to mind, are the study out of Imperial College in London, where they looked at the urine, they looked at the various proteins that were found in the urine that could not be produced by the human body itself, but were being produced by bacteria which were present in the urine--present in the kidneys, one assumes. And what they found was that there were very distinct grouping—the Japanese population, the Chinese population, and the US population—were all different. And when Japanese moved to the US, their microbiota changed to the US population. Because the food changed, their environment changed, everything changes. So we very much are a product of the bacteria that make us. Now, that was not specifically looking at saliva. Firstly, **//I//** don’t follow them. But there have been studies done. The two that come to mind, are the study out of Imperial College in London, where they looked at the urine, they looked at the various proteins that were found in the urine that could not be produced by the human body itself, but were being produced by bacteria which were present in the urine--present in the kidneys, one assumes. And what they found was that there were very distinct grouping—the Japanese population, the Chinese population, and the US population—were all different. And when Japanese moved to the US, their microbiota changed to the US population. Because the food changed, their environment changed, everything changes. So we very much are a product of the bacteria that make us. Now, that was not specifically looking at saliva.
  
-The study from Max Plank that looked at saliva did in fact look at 10 locations throughout the world to make sure that they had good geographic diversity. And if you look up the paper that I cited there you’ll find the detailed data.(({{pubmed>long:19251737}})) +The study from Max Plank that looked at saliva did in fact look at 10 locations throughout the world to make sure that they had good geographic diversity. And if you look up the paper that I cited there you’ll find the detailed data.(({{pmid>long:19251737}})) 
  
 ==== Question: Because there is now a new field of human genomics, then you can track the ‘mother of mother’s’ in Africa, you can see how people moved in Europe, several passages, you can also follow certain tendencies to diseases, such as high blood pressure? ==== ==== Question: Because there is now a new field of human genomics, then you can track the ‘mother of mother’s’ in Africa, you can see how people moved in Europe, several passages, you can also follow certain tendencies to diseases, such as high blood pressure? ====
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