A nanoelectronics-blood-based diagnostic biomarker for ME/CFS (2019) Esfandyarpour, Davis et al

They say the exact mechanisms behind the differences remains unclear and is they have a programme of work to try to narrow things down. They suggested several possibilities, including changes involving the endoplasmic reticulum and plasma membrane, and even increased cytokine production in response to the salt stress.

the first pic with the signal (impedence/resistance) ... it seems that things start after 30-45 minutes only. is this odd ?
and then it basically explodes. its gross steep. then runs out of steam.
could it look like a chemical reaction of some sort ?

also, the healthy controls increase as well.
so, perhaps its not something unusual, just extraordinary intense.

and also, why does the signal "end". does it ?
does it return to baseline ?
why was it cut ? or could they no longer keep cells alive ?



F2.medium.gif
 
Of course Henrik had to have a say...

What exact tools is he referring to? Psychobabble ones?






Vogt is a cult salesman. Opinion not relevant. He can go jump on a STOP mat until he passes his fake tantrum.

The irony is that none of them are actually capable of diagnosing ME patients and constantly misdiagnose people with other conditions, since their own personal fictitious definition is deliberately vague and broad for that purpose.

I guess the "tools" is supposed to be clinical observation, which none of them successfully use so whatever. Vogt and his ilk likely have a 50%+ misdiagnosis rate. The nanoneedle has a 100% rate with no false positives or negatives. It's not perfect, but it's orders of magnitude better than their fake expertise.
 
Does that help? I don't understand the details of the different types of impedance measured.

Not a lot I am afraid. I was aware of it. It is just that as an immunologist familiar with suspensions of peripheral blood mononuclear cells I find it very hard to work out what was actually going on. Why didn't the cells walk off the electrodes from time to time?
 
I completely agree about the need to test all types of controls. However, we must be careful not to make the mistake of thinking or suggesting that people with MDD, or any other types of well-defined psychiatric illnesses, do not have something biologically wrong.

Having this test applied to deconditioned people or depressed people and found to be able to identify the PWME was never going to save us. The Psych lobby will change to whatever newly named group of their choice as being the one that it hasn't been tested against and to top it off regardless GET, GET, Activity, CBT is always going to need a £5 million, 10 year trial to show that it can cure it.

Both very good points.

Thank you for pointing that out @Robert 1973 i would never want to imply that.
 
Cellular sodium pumps seem to be an interesting topic. Anyone know more about them and perhaps relevance to this test?

This is an interesting snippet I read
The Na+-K+-ATPase is a highly-conserved integral membrane protein that is expressed in virtually all cells of higher organisms. As one measure of their importance, it has been estimated that roughly 25% of all cytoplasmic ATP is hydrolyzed by sodium pumps in resting humans. In nerve cells, approximately 70% of the ATP is consumed to fuel sodium pumps.
I wonder if the above has anything to do with the nerve damage many have that results in small fiber neuropathy as measured by skin biopsy (I seem to remember Dr Systrom talking about 40% SFN in his ME/CFS patients at the recent NIH talk)
Depending on cell type, there are between 800,000 and 30 million pumps on the surface of cells.
Wow that's a lot!
Source : http://www.vivo.colostate.edu/hbooks/pathphys/topics/sodium_pump.html

It seems these pumps operate to maintain a resting membrane potential. Here is a brief 2 min video describing sodium and potassium pumps on the cell walls
 
we should ask a wastewater expert for their opinion

"regular" medical profession is not equipped to answer such questions
 
Interesting how the ME/CFS characteristic seems to be a greatly exaggerated version of the controls. From time zero the impedance drops initially, then steadily rises again. For ME/CFS, the drop is much more dramatic and for longer, before then rising far more significantly. Also presumably significant that when not stressed, the impedance is the same for both.

upload_2019-4-30_19-41-28.png
 
It seems I don't have ME, I have cerebrospinal fluid instead (CSF), at least according to the great people at GEN (or should that be GNE?).

Not an odd typo, repeated, repeatedly - does the position of proofreader not exist any more?

Get the damn basics right, the name of the condition your articles on, get it right, FFS!!

(or forget the whole CFS rubbish name completely, but using it, and then getting it wrong....doesn't encourage me to read further)
 
they added a lot of salt as a stressor.
stressor to simulate PEM/exercise/crash.

(i understand)
- there are other stressors, e.g. lipopolysaccarides..
- but no other stressor was tested, only salt
- the stressor caused a non-beneficial event (assuming)

since mecfs cells react that sensitive to a (osmotic) "stressor"
how does this tie in with

- ppl finding benefit in bicarbonate (a salt)
- hyperbaric oxygen therapy / - oxygen therapy

(altitude / diving must be absolutely intolerable for pwmecfs, guessing)

what other things may cause (strong) "osmotic" events ?

perhaps, particular interesting those, that may make one worse and then (later) better.
actually, opposite of "PEM".
 
Last edited:
Not a lot I am afraid. I was aware of it. It is just that as an immunologist familiar with suspensions of peripheral blood mononuclear cells I find it very hard to work out what was actually going on. Why didn't the cells walk off the electrodes from time to time?
Sorry come I had assumed you had seen that’s because of your question about the geometry. As someone without any experience of PBMC is suspended in plasma, I had assumed that there might be some local forces attracting the sounds to be electrode.

But also, I had assumed that some of the cells would wander off but that with 4000 Micro chambers and five samplings a second the device would capture an average-occupancy-based figure.
 
What is the salt doing?

I wonder if this experiment is all about the cellular sodium/potassium pumps and their ability to use ATP to pump. If that is the case there must be other tests that can measure the functioning ability of these pumps, that may not have to rely on the nanoneedle in order to validate and extend the experiment using a different method?

I wonder if you could use fluorescent tags of the mitochondrial membrane and then apply the salt solution while monitoring with a microscope. After 3 hours perhaps there would be a big difference?

This is an excerpt from a talk given by Paul Cheney in 2013
https://paradigmchange.me/wp/cheney...Ieg9aZM2j6goro3ChWzK1LE_52m3nudQFVmmgn_cUnneY
Evidence of Mitochondrial Dysfunction

So what is the evidence for some of this?

This was performed in the cell biology department at UNC Chapel Hill, believe it or not, in 1992, because the chairman of that department’s daughter had this syndrome. He called me up and said, “Is there anything I can do to help you?”

I was in Charlotte at the time. I said, “Yes, do you do any kind of energy measurements?” And he said, “Oh, that’s what we do here.”

And I said, “How do you do it?”

They used fluorescent tags of the mitochondrial membrane, and the intensity of the fluorescence is related to the degree of energy production. The higher the energy being produced, the brighter the intensity, and the lower the energy being produced, the lower the intensity of the fluorescence.

What you see here are the cells plated on a glass plate. And then they stain these lymphocytes on a plate and then they look at them with a confocal microscope that’s focused right on this plate. Then they stain it with these fluorescent dyes, and then they take off the dye in direct proportion to how much energy is being produced.

When he did this, he called me back and said, “It’s really quite shocking. Your patients don’t have any energy in their lymphocytes.”

Unfortunately, they applied for a grant to do this work, and of course, because the grant was labeled “Studying mitochondria in chronic fatigue syndrome,” it was promptly denied by the NIH.
 
Last edited:
When he did this, he called me back and said, “It’s really quite shocking. Your patients don’t have any energy in their lymphocytes.”

it would be interesting to see, what the severe patients had in common.
in terms of meds taken in their lifetime, vaccinations, infectious diseases ...

(things not directly or closely related to falling sick)
 
Looking at the Discussion section, I find it encouraging that Ron and his team have some good insights (albeit not yet proven) into what the biological mechanisms might be for the impedance differences - I don't understand the biology. At this stage there is obviously a lot of ifs and maybes, but it does sound like they are hypothesising that some of the possible biological anomalies with ME, could also be the very things causing the impedance changes. It would be great if they can firm up on that, but there must be an awful lot of work in that, and I imagine those theories will be very tentative at this time. Still a long way to go, but potentially very promising. Certainly way too early to get over confident I would think though.
 
I don't think so. I had an account and started using it right away.

Did your tweets actually appear under the #mecfs hashtag listing though when you used this hashtag in your tweets?

I see other familiar ME/CFS patients' tweets appear in the #mecfs listing, but my tweets never do.

Perhaps I'm some sort of persona non grata on Twitter!
 
Back
Top Bottom