A nanoelectronics-blood-based diagnostic biomarker for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)

[Rufous McKinney]

I wonder if trypanosomes

 

[Rufous McKinney]

As unicellular protozoa, Trypanosoma sp. seems likely it could produce exosomes. Magenta above are the critter.

 

[Rufous McKinney]

Magenta above are the critter

With red blood cells. So they look sizable.

It seems possible that a Protozoan could contain or possess virus's themselves. (?)(!!)

 

[Rufous McKinney]

It seems possible that a Protozoan could contain or possess virus's themselves

Uh Oh:

http://www.virology.ws/2012/11/21/viruses-of-protozoan-parasites-may-exacerbate-human-disease/

This is getting interesting....more chances for viruses....the article above says this:

Many protozoan parasites (Trichomonas, Leishmania, Giardia, Plasmodium, Entamoeba, Nagleria, Eimeria, Cryptosporidium) are infected with viruses. These viruses do not infect vertebrates, but their double-stranded RNA genomes are sensed by the innate immune system, leading to inflammatory complications of protozoan infections.

 

[Rufous McKinney]

Protozoans can communicate using exosomes:

https://www.ncbi.nlm.nih.gov/pubmed/23356292

"We discuss how protozoans use this new resource to evade the immune system and establish infection".

 

[Rufous McKinney]

https://pubs.rsc.org/en/content/articlehtml/2018/ra/c7ra12511a

"Nanovesicles, exosomes and other membrane bound particles excreted by cells are currently gaining research attention since they have been shown to play a significant role in many biologically related processes. Vesicles are now thought to mediate cellular communication, transmission of some diseases and pathologically mediated calcification. Matrix vesicles have long been proposed to be central to the controlled mineralisation of bone. They remain relatively poorly studied, however, since they are challenging to extract from biological media. "......


Calcification, including building bone, involves these particular matrix vesicles, which are homologous with exosomes.

I wonder if our non-deforming red blood cells may be the result of a calcification process gone awry.

It seems encouraging that other health research is also looking at the phenomenon, and we may find ourselves with more allies and start to make greater research progress on treatments.

Exosomes clearly are important messengers. Perhaps they are the Hermes messenger. They are clearly very very busy and important mediators and message senders.

 

[roller]

on the powerpoint i think it said "e..g. plasmodium" (malaria like)

 

[Mel9]

on the powerpoint i think it said "e..g. plasmodium" (malaria like)

I found reference to Trypanasoma but the video is quite long.

Whereabouts approximately was the slide for Plasmodium?

 

[roller]

in red blood cell deformability
where are the trypanosomes ?

 

[frozenborderline]

It feels as if our bodies are trying to sabotage any effort to increase our activity levels, and I think this is partly why we've got stuck with the psychosomatic label. If you report this experience to a doctor who's trying to treat your symptoms, it can easily sound as if you've just come up with another excuse for avoiding activity.

I think it's a protective response; what worries me slightly is that we don't really understand whether or not it's an appropriate protective response.

I think it is a protective response. Ibut unlike dauer in which it’s protecting against starvation this one is protective against massive amounts of oxidative stress

 

[mariovitali]

I find the results very interesting. The next most important hurdle is to see whether the test can differentiate between ME/CFS from other conditions such as MS.

Looking further and based on the fact that hyperosmotic stress is induced through the use of NaCl :

a) It appears that Hyperosmotic stress on PBMCs induces inflammatory cytokines :​

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https://www.sciencedirect.com/science/article/pii/S0014482797934765?via=ihub​

​

b) On a paper named "The role of hyperosmotic stress in inflammation and disease" we read :​

​

Link : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3438915/​

Hyperosmotic stress is linked to many maladies, including acute and chronic, as well as local and systemic, inflammatory disorders. Hyperosmolarity triggers cell shrinkage, oxidative stress, protein carbonylation, mitochondrial depolarization, DNA damage, and cell cycle arrest, thus rendering cells susceptible to apoptosis. However, many adaptive mechanisms exist to counter the deleterious effects of hyperosmotic stress, including cytoskeletal rearrangement and up-regulation of antioxidant enzymes, transporters, and heat shock proteins.

I think that this is interesting but it also could be alarming in the sense that many types of disease could lead to the same result we have seen in the paper by Davis et. al ? In the paper linked above (b) we find entries related to eye disease, diabetes, liver disease, inflammatory bowel disease and cardiovascular disease.

​

 

[roller]

important was, that the same healthy cells didnt get into the stress under same conditions.
they may have shown mildest stress.
the mecfs went through the roof, if not further..

the resistance (impedence) in the mecfs substrate increased like an explosion of things, i understand.
but only after 45 minutes or so.
apart from salt + current, nothing else was added.

if mecfs was a cytokine-problem, this should be known by now ?
i dont know, is it ?

it seems unfortunate to me, that we have no wastewater experts in the group ?

 

[percyval577]

if mecfs was a cytokine-problem, this should be known by now ?
i dont know, is it ?

Two recent puplications:
Inflammation correlates with symptoms in cfs Komaroff 2017
Persisitent fatique induced by interferon-alpha: a novel, inflammation-based, proxy model of cfs Russell et al 2018

The 2017 short commentary referres that in mild cases some cytokines would be lower, but in severe cases some would be higher than in controls (though not so significiant). So it would not be directly related to the impedence.

The 2018 article has a nice introduction, and they conclude that an abnormal immuneresponse takes place in the early stage. So this finding would probably also not directly match up with the impedence.


Here an abstract of a meta-analysis https://www.ncbi.nlm.nih.gov/pubmed/26148446 Blundell et al 2015

 

[roller]

it seems there is no infection - at least nothing what we commonly understand as "infection".
the immune system may at times see a "to do", while there never was one. i could imagine.

https://me-pedia.org/wiki/Cytokine

Two large 2015 studies found a general pattern of down regulation in long term patients (Hornig, et al and Landi, et al)
Cytokines are any class of immunoregulatory proteins secreted by cells, especially immune system cells.[1] Cytokines are small proteins important in cell signaling that modulate the immune system

what parasitic infections indeed take influence, davis & co will find out.
with the methods they use.

 

[Rufous McKinney]

in red blood cell deformability
where are the trypanosomes ?

Maybe I am misunderstanding your comment....and I've not watched that video: but the suggestion here seems to be that a variety of illnesses can involve or result in non-deforming red blood cells. I don't find that surprising.

If parasites are involved, they must be releasing something that is resulting in: the reduced deformity. That could be- exosomes with viruses or RNA instructions or some other substance that triggers downstream effects. Or they affect a process which then affects processes that produce these cells. Or maybe: could energy be required to maintain deformability? Could it just be an energy/lack?

So: if one is prediabetic (yes, here); genetically predisposed (likely); also have a Post Viral condition (EBV yes) : gee I feel particularly picked upon! Lets FIX THAT .

 

[roller]

wondered, if he was referencing trypanosomes in the video as well, besides malaria.
havent watched it neither fully.

 

[waiting]

@Cort just interviewed Ron Davis and Rahim Esfandyarpour here: https://www.healthrising.org/blog/2...e-nanoneedle-scores-big-in-first-me-cfs-test/

 

[gbells]

I think that Dr. Davis did some good work here. If the test is just measuring stress then the graph would have had more crossover between the controls and SEIDs patients. Instead what you see is a clear demarcation between them. I think this supports his claim.

I've heard of some dreadful treatment of SEIDs patients in the UK. We had a similar situation in the USA when our government was on a disability insurance company created witch hunt designed to limit claims to two years by falsely stating that the disease was a mental disorder.

Dr. Davis essentially came up with a way to avoid having to do an expensive two-day exercise test and instead can rapidly and more cheaply identify who really has SEIDs vs something else.

 

[Rufous McKinney]

In the paper linked above (b) we find entries related to eye disease, diabetes, liver disease, inflammatory bowel disease and cardiovascular disease

I clearly meet strict ME criteria: but I am also dealing with my versions of everything listed there. Its all hooked together, somehow. Its ALL THAT STUFF.

 

[SNT Gatchaman]

Question on the science.

The nano-needle technique took PBMCs in plasma, stabilised on the sensor array and then added hyperosmotic saline to bring it up to 200 mmol/L. From 60-120 minutes there was a rise in the impedance (in-phase resistance), which was attributed to metabolic stresses / ATP use in the PBMCs of ME patients (highly specific).

Filtering plasma by size reduced the effect significantly, leading to the idea that there was something-in-the-blood.

Does anyone know if they tried that test without the white cells present?

i.e. Were the impedance changes due to the micro-clots in the plasma and not due to the cells?

Could micro-clots in the plasma be degrading enough to expose their anomalous serum amyloid A etc or otherwise amalgamate in the presence of hyperosmotic saline, sufficient to cause impedance changes?