The 12th Invest in ME Conference, Part 1
OverTheHills presents the first article in a series of three about the recent 12th Invest In ME international Conference (IIMEC12) in London.
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Abstract: "Assessment of Cellular Bioenergetics in CFS" (Newton team, Newcastle, UK)

Discussion in 'Latest ME/CFS Research' started by Tom Kindlon, Nov 11, 2016.

  1. Tom Kindlon

    Tom Kindlon Senior Member

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    Poster presentation, IACFS/ME 2016 conference

     
  2. Valentijn

    Valentijn Senior Member

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    It's great to see Newton on a more productive track again :love:
     
  3. Mary

    Mary Senior Member

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    Southern California
    I wonder if this has any correlation to the theory that people with ME/CFS are very often in a state of anaerobic metabolism, while doing very minimal effort, as opposed to the much more efficient aerobic metabolism. I think anaerobic metabolism is typically only used under stressful or strenuous circumstances, by ordinary healthy people.
     
    Luther Blissett likes this.
  4. Jonathan Edwards

    Jonathan Edwards "Gibberish"

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    This is an interesting finding. I wonder, however, why PBMC are studied. PBMC are a mixture of T and B lymphocytes, NK cells and monocytes. In general in the blood they are not expected to do anything at all. They are just 'in the post' to some tissue where they might function. Lymphocytes in blood have hardly any cytoplasm - just a thin ring you can hardly see - because they have no work to do. Monocytes have a bit more but increase their cytoplasm about tenfold when they get into tissue.

    If you put B cells into tissue culture they almost all die rapidly. They are programmed to die anywhere where there are no VCAM-1 expressing 'nurse cells'. T cells hang around but do not do much unless you feed them an antigen. Monocytes turn into macrophages and start trying to eat the plastic with the result they spread out flat. I am not quite sure what this odd mix of cells is going to tell us.

    In tissue culture more or less all the signals present in an acquired (i.e. not genetically programmed) disease are likely to be washed away. So any difference found in culture seems likely to be due either to genetics, or due to some sort of sampling bias due to the cells circulating being skewed in type or age before you start. A genetic difference would be interesting but I cannot see how it can be related to fatigue directly since people with ME are not born fatigued.

    So I am not sure quite how one would interpret these findings. It seems worthwhile trying to study mitochondrial function but I am unsure this sort of approach will show anything up that we can make sense of.
     

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