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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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Agree @Diwi9 her visuals are great, talk clear and concise! Thanks for posting, worth a watch.She discusses her theories in general with some great visuals and the direction of her research vision of advancing into clinical trials.
and supercomputers analyzing the "Big Data"
If you were to look at the analysis software I bet many AI techniques would be incorporated.instead of super-computing.
@alex3619 your thoughts?
I only know what was in the video.@alex3619 The principle is to inhibit tumour necrosis factor alpha, followed by inhibiting the glucocorticoid response, in a one two fashion.
Do you know how they plan to do this?
For the GWI trial this was the plan as of Aug 2017 - see page 48Do you know how they plan to do this?
For the GWI trial this was the plan as of Aug 2017 - see page 48
https://www.va.gov/RAC-GWVI/meetings/aug2017/KlimasAUG2017.pdf
I think I have heard of it but do not recall details. The issue here is its not a single medication trial. It requires two different meds in sequence according to the hypothesis.Anyone heard of cfsers trying etanercept type meds before?
The principle is to inhibit tumour necrosis factor alpha, followed by inhibiting the glucocorticoid response, in a one two fashion.
This is because the entire energy response is altered, and governed by the brain, possibly from a combination of the hypothalamus and the brain stem. She is trying to shift that set point back to normal, and to do that she has to send the right signals to the brain. The details of why this is so in the model would depend on the specific details of the model, and I do not know what they are.why would you inhibit this furthe
so why would you inhibit this further?
hat is suspected in ME. Nancy Klimas has put forward the hypothesis, which is supported by her animal model, that repeated toxin stress (but presumably other things might work) followed by repeated cortisol surges, trigger the problem
Animal models of CFS have been put forward but mostly are a joke. One study had animals exercised to exhaustion, and that was supposed to represent CFS! Animal models are also expensive to develop if you want to include any genetic predisposition and so get into genetic engineering. Better models based on monkeys are also very expensive, whereas mice are much cheaper.why is there no animal model of CFS?
Animal models of CFS have been put forward but mostly are a joke. One study had animals exercised to exhaustion, and that was supposed to represent CFS! Animal models are also expensive to develop if you want to include any genetic predisposition and so get into genetic engineering. Better models based on monkeys are also very expensive, whereas mice are much cheaper.
We have lacked both funding and sufficient researcher numbers for so very long.
There is also the thorny issue that animal models can show a drug works on the animal, and then it usually fails human testing.
I am a fan of in vitro testbeds, based on samples from real patients, which can then be rapidly tested in many ways without major ethical or health risks. This still does not substitute for real test subjects, but its a way of getting some information and even candidate drugs without risking people.
Nancy uses a range of things, from models of the biochemistry, to in vitro testing, and now an animal model. Human trials are more advanced, and start with a pilot study, which is mainly about finding if the treatment is plausible by using results in human test subjects.