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

Stunning artwork my friend @ballard. The questions is: are they actually planing on funding future studies or are they simply taking credit but are never going to be from again?

 

You dont say. I REALLY hope they have´nt done this just for the credit and then abandon us further.

 

If the NIH funded the earlier nanoneedle work then they still deserve some credit. They aren't doing as much as they should but they're still doing something, which is more than most other funding bodies are doing.

I find it concerning that on Twitter anything the NIH does in relation to ME/CFS gets mostly negative responses. They are one of the few people actually trying to help and doing useful things.

 

Yes, but it is also possibly about what you wish people to infer from the statements. It is easy to draft documents so as not to allow people to mislead themselves.

 

As far as I recall, Rons aim was to develop the technology to, in the long term, save the NIH money (using it to test drugs on particular illnesses); they (the NIH) said that this was not a priority.
It was on one of the early conference videos.

 

Probably the latter

The safe money is abandonment. They are welcome to prove me wrong.

 

One of the things which have been on my mind about this is that initially the "something in the blood" which was effecting cellular energy production in ME was labelled as possibly an autoantibody. I posted that if it were an autoantibody then rituximab would have worked; however, rituximab didn't work therefore it wasn't an autoantibody.

I wonder if it was pretty obvious that there there were other candidates for causing this change in cellular energy production i.e. exosomes.

I think what Prusty brought to the equation was the change in mitochondrial morphology (shape) presumably caused by micro-RNAs in exosomes - after that there was no point in referring to "potentially --- autoantibody". Ron Davis etc. don't choose how the world is (Universities/profit motive); however, they have to work with it.

 

Yes, @Alvin, I am hoping the NIH provides a large grant to continue this work.

 

I don’t think it’s easy to do that at all. Some people will mislead themselves over 2+2=4.

*edit* not talking about anyone in particular on this site.

 

They may not be misleading themselves. Two apples and two pears do not equal four apples. Depending on the definition of "equal".

 

1 apple + 1 apple doesn't necessarily make 2 apples either.

Many factors can prevent it - relative velocity being only 1

 

One suggestion--

If folks still have questions on the methods of this paper, a suggestion would be to see if @JaimeS might be able to send Esfandyarpour an email to see if he would be willing to answer questions on this forum. Suggested Jaime rather than doing it myself because I assume that Jaime likely knows him and he would therefore be more likely to respond positively.

Most academics have some community outreach/service component as part of their work plan and if he participates, we could write a note of acknowledgement.

 

Anthony Komaroff has had a commentary on the study published in the NEJM Journal Watch

Requires a subscription to read it.

https://www.jwatch.org/na49222/2019/06/04/diagnostic-test-chronic-fatigue-syndrome


Diagnostic Test for Chronic Fatigue Syndrome?
Anthony L. Komaroff, MD reviewing Esfandyarpour R et al. Proc Natl Acad Sci U S A 2019 May 21

An electrical impedance assay distinguished CFS patients from healthy controls.

Many biomarkers — objective measurements that distinguish cases from healthy controls — have been identified in people with what is now called myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Collectively, these markers demonstrate an underlying organic pathology in this illness. Yet no identified single biomarker has the high sensitivity and specificity needed for a diagnostic test.

Researchers developed a nanoelectronics assay to measure the impedance of electrical circuit as it was passed through mononuclear white blood cells (incubated in plasma collected from an individual patient) before and after osmotic stress. In all 20 samples from people with ME/CFS, but in no sample from healthy controls (20), impedance rose precipitously following the osmotic stressor. The investigators currently are studying the biological explanations for this clear difference in impedance.

COMMENT
This test achieved perfect sensitivity and specificity for identifying ME/CFS, and the nanoelectronics device used is inexpensive to manufacture and easy to use. However, only a small number of ME/CFS patients and healthy controls were evaluated, and the investigators did not test people with other fatiguing illnesses (such as multiple sclerosis or depression). Larger and more diverse sampling will be needed before this impedance assay can be deemed a diagnostic test. Whether or not this becomes a diagnostic test, studies of impedance might reveal important information about the underlying biology of illness in ME/CFS patients.

 

Does specificity mean something different than I think it does?

As I would have assumed, until reading the second bit, that the first bit means that it's specific to ME/CFS.

 

Maybe the meaning of specificity is being abused somewhat? Just saying it distinguished extremely well between pwME and the other people tested ... i.e. the healthy controls.

 

I don't think it's being abused under the conditions of the test.
It did show specificity between pwme and healthy controls, which is what the test was about.

 

I guess I misunderstand what specificity means. I was thinking it meant unique discrimination of a given disease, full stop.

 

https://en.wikipedia.org/wiki/Sensitivity_and_specificity

Sensitivity: proportion of individuals with the condition being tested for who test positive

Specificity: proportion of individuals without the condition being tested for testing negative