used_to_race
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According to Davis, the sequence varies from patient to patient, but it is my understanding that there are "subgroups" here.
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(Video) OMF Scientific Advisory Board Member Mark Davis, PhD, Presents An Update on ME/CFS Research
- Thread starter Ben H
- Start date
According to Davis, the sequence varies from patient to patient, but it is my understanding that there are "subgroups" here.
My question above was answered in another thread by @Janet Dafoe (Rose49) ...thought I'd add it here for anyone who hasn't seen it but was following this thread.
jimells
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@Janet Dafoe (Rose49)
Was Dr Theoharides able to convince anyone at the recent Invest in ME Research Conference that mast cells are much more than "an appendix of the immune system"? [1] A patient report from the conference on Dr Theoharides' lecture seemed rather muted.
The ME Association summary of the conference [2] reported:
That is only a tiny fragment of what Professor Theoharides has to say about mast cells in the brain. [4] [7]
I find it fascinating that Naviaux [3] and Theoharides [4] are both working on autism but almost seem to be talking past each other. To me the link between their "competing" work is obvious: extracellular ATP plays a critical role in the Cell Danger Response [5] and also activates mast cells. [6]
What does any of the above have to do with T cell clonal expansion? How about this: [6]
Also, mast cells can act as antigen-presenting cells: [9]
There is much discussion of "leaky gut", LPS (lipopolysaccharide), and how it may be getting into circulation and causing problems, perhaps leading to T cell clonal expansion. Mast cells can do that, too: [8]
Just imagine what might happen if a large dose of extra-cellular ATP stimulated by exceeding our energy envelope is added to the mix. Sure none of these citations "prove" mast cells play a critical role in ME. But when one is choking on smoke, doesn't it make sense to call a fire fighter?
p.s. For reasons I don't understand, immunologists still appear to be dismissive regarding mast cells. I'd like to point out that Geoffrey Burnstock's work on purinergic signalling (extra-cellular ATP and related molecules) was similarly dismissed for *two decades*. He is now recognized as a medical pioneer.
[1] Matsumoto et al; Brain Mast Cells Act as an Immune Gate to the Hypothalamic-Pituitary-Adrenal Axis in Dogs
[2] http://www.meassociation.org.uk/wp-...erd-IiMER-Conference-Report-2018-13.06.18.pdf
[3] Naviaux et al; Low‐dose suramin in autism spectrum disorder: a small, phase I/II, randomized clinical trial
[4] Theoharides et al; Atopic diseases and inflammation of the brain in the pathogenesis of autism spectrum disorders
[5] Naviaux; Metabolic features of the Cell Danger Response
[6] Zhang et al; Stimulated Human Mast Cells Secrete Mitochondrial Components That Have Autocrine and Paracrine Inflammatory Actions
[7] Theoharides et al; Chronic Fatigue Syndrome, Mast Cells, and Tricyclic Antidepressants
[8] Wouters et al; The role of mast cells in functional GI disorders
[9] Zayas et al; Mast Cell Function A New Vision of an Old Cell
Was Dr Theoharides able to convince anyone at the recent Invest in ME Research Conference that mast cells are much more than "an appendix of the immune system"? [1] A patient report from the conference on Dr Theoharides' lecture seemed rather muted.
The ME Association summary of the conference [2] reported:
That is only a tiny fragment of what Professor Theoharides has to say about mast cells in the brain. [4] [7]
I find it fascinating that Naviaux [3] and Theoharides [4] are both working on autism but almost seem to be talking past each other. To me the link between their "competing" work is obvious: extracellular ATP plays a critical role in the Cell Danger Response [5] and also activates mast cells. [6]
What does any of the above have to do with T cell clonal expansion? How about this: [6]
Also, mast cells can act as antigen-presenting cells: [9]
There is much discussion of "leaky gut", LPS (lipopolysaccharide), and how it may be getting into circulation and causing problems, perhaps leading to T cell clonal expansion. Mast cells can do that, too: [8]
To add insult to injury, or maybe injury to injury, mast cells can be activated by LPS [8], and mast cells also increase the brain-blood barrier permeability. [4]
Just imagine what might happen if a large dose of extra-cellular ATP stimulated by exceeding our energy envelope is added to the mix. Sure none of these citations "prove" mast cells play a critical role in ME. But when one is choking on smoke, doesn't it make sense to call a fire fighter?
p.s. For reasons I don't understand, immunologists still appear to be dismissive regarding mast cells. I'd like to point out that Geoffrey Burnstock's work on purinergic signalling (extra-cellular ATP and related molecules) was similarly dismissed for *two decades*. He is now recognized as a medical pioneer.
[1] Matsumoto et al; Brain Mast Cells Act as an Immune Gate to the Hypothalamic-Pituitary-Adrenal Axis in Dogs
[2] http://www.meassociation.org.uk/wp-...erd-IiMER-Conference-Report-2018-13.06.18.pdf
[3] Naviaux et al; Low‐dose suramin in autism spectrum disorder: a small, phase I/II, randomized clinical trial
[4] Theoharides et al; Atopic diseases and inflammation of the brain in the pathogenesis of autism spectrum disorders
[5] Naviaux; Metabolic features of the Cell Danger Response
[6] Zhang et al; Stimulated Human Mast Cells Secrete Mitochondrial Components That Have Autocrine and Paracrine Inflammatory Actions
[7] Theoharides et al; Chronic Fatigue Syndrome, Mast Cells, and Tricyclic Antidepressants
[8] Wouters et al; The role of mast cells in functional GI disorders
[9] Zayas et al; Mast Cell Function A New Vision of an Old Cell
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