Special Message for you from Ron Davis (video)

[roller]

@Ben H @HTester

those exosomes seem to be analyzed all day long, for years. everywhere in the world.
is it possible to find out, what molecule is causing the mecfs-signaling ?

when can we know?

what is known of it already ?
where does it originate from ?


have other researchers outside the US
a) not yet looked for it
b) looked and not found it
c) looked and found it

 

[Rufous McKinney]

what molecule is causing the mecfs-signalin

So: why don't we all just go get Plasma Transfusions once a month from healthy donors?

It seems like that could be an immediate fix to a major aspect of our problem.

so obviously: I"m missing something because this is too obvious.

 

[Rufous McKinney]

what molecule is causing the mecfs-signaling

So here is a link to Plasma Transfusion risks....so these transfusions do occur quite commonly.

And of course there are risks. Which they say are manageable.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3356109/

so: what am I missing?

 

[roller]

so, thats what i was missing... jeez
does this whole "molecule thing" sound like an infectious disease ?

shouldnt we be clearly excluded from blood donations?
at least, until its clear what it is.

or did they say, the healthy blood recovers ?
if so, does it really do with e.g. "immuno compromised" ppl, too ?

it should be clear, that we are no health risk, as blood donors.

 

[S-VV]

so, thats what i was missing... jeez
i was going to blood donation..

shouldnt we clearly be excluded ?
we are a health risk.
its infectious ?

or did they say, the healthy blood recovers ?
if so, does it really do with e.g. "immuno compromised" ppl, too ?

THIS
No govt will want to admit they poisoned the blood supply for decades because they were too stupid to research correctly.

There is a non zero chance that the exosome research will be forcefully shut down.

 

[Rufous McKinney]

it should be clear, that we are no health risk, as blood donors.

Folks known to have Eppstein Barr exposure I thought were excluded from donating blood.

I would never and have never donated my blood to anyone.....

 

[roller]

vaccines and meds may be derived from human / animal blood, both have been found to be contamined already.

not even today they are able to see, what exactly is in the blood or in feces or in tissue.
they still cant tell if a substance is "clean" or "ok".

 

[Rufous McKinney]

I would never and have never donated my blood to anyone

I really swore we were excluded as Eppstein Barr types....I swore i saw this on a list of exclusions at a blood bank. But: ok, I dreamnt it.

Pretty scary to think they'd willing take any of this and put it into somebody else.

 

[junkcrap50]

I would think many of us are excluded from blood donations because of the medications we take. A lot of medications disqualify you. They like little to no prescription medications for donors. I haven't been able to donate blood for that reason for ~15 years. (Not that I want to or think I should donate blood with ME/CFS.)

 

[junkcrap50]

have other researchers outside the US
a) not yet looked for it
b) looked and not found it
c) looked and found it

Yes. I believe there are 4 ME/CFS researchers that have found "something in the blood": (1) Ron Davis, (2) Bhupesh Prusty, (3) Karl Morten, and (4) Fluge & Mella (each name links to evidence/claim).

I believe only Ron Davis and Bhupesh Prusty believe it's exosomes. Flue & Mella think it's irregular amino acids, and I don't know about Morten. Perhaps Maureen Hanson, who's already been studying exosomes in ME/CFS before Ron Davis's discovery, may also believe it as the cause and is looking for it.

is it possible to find out, what molecule is causing the mecfs-signaling ?

when can we know?

what is known of it already ?
where does it originate from ?

First, they have to isolate the exosome from the serum, remove it and make sure it's the factor "in the serum" causing ME/CFS cells to act ill. Ron Davis doesn't seem totally confident it's an exosome just yet. Second, they have to ID it, figure out what's inside it, what protein labels are on the outside of it. Third, they have to figure out where it's coming from or its source (likely can get clues from what's inside it and what labels it has on it). Fourth, they likely want to be able to separate it, quantify how many these exosomes triggers are in the serum, and if it correlates to illness severity. Fifth, and the next big step, they need to figure what's the cause of these exosomes being released. The exosomes could be a downstream effect of a more original source of ME/CFS pathology. It could be the beginning of a long thread before they get to the origin source.

So: why don't we all just go get Plasma Transfusions once a month from healthy donors?

It seems like that could be an immediate fix to a major aspect of our problem.

so obviously: I"m missing something because this is too obvious.

They could be options similar to this. Filtering the serum seems to work according to Ron Davis's nanochip tests. So, they need to get an exact and consistent size range to filter. There are already techniques in dialysis that make it possible to filter blood targeting a specific molecular size. There also is already a clinical use product on the market that can specifically filter exosomes from blood that is used in cancer treatment. I think would be a great small proof of concept test case. It's called Hemopurifier and made by Aethlon Medical. It's an extra filration cartridge on dialysis machines. It probably wouldn't permanently cure ME/CFS, but could temporarily.

 

[Rufous McKinney]

It probably wouldn't permanently cure ME/CFS, but could temporarily.

Yes: all that sounds much more promising and somehow more feasible, not that a dialysis type experience is something to sign up for.

I just wonder why hasn't somebody who is SEVERE simply gotten a transfusion and found themselves able to get out of bed for instance.

My opinion: (weighted with negative 16 tons) is: where filtering might work is related to the possible notion that maybe we simply have excessive density of exosomes perhaps we have more cell death going on. If the blood has just alot of space occupied by vesicles carrying messages...maybe we can live still with simply fewer of them. Alternatively, perhaps there is some filter, size issue (maybe our exosomes are excessively large?) (again, taking up alot of space). Or perhaps an external tag that can be noted and separated somehow. Maybe CERTAIN exosomes carry bad messages (probably likely)

Keep in mind Ron's comment that: we could have individual cells exhibiting trouble, while some nearby cell is fine. So differing Exosome conditions could arise from differing cell systems, tissues, etc.

The notion that our bodies would survive by removing and filtering out "all exosomes" does not seem logical. Exosomes are necessary communication and removal systems.

Go With the Flow. Enhance the Flow. Something aint flowing right.

 

[ljimbo423]

The notion that our bodies would survive by removing and filtering out "all exosomes" does not seem logical. Exosomes are necessary communication and removal systems.

Go With the Flow. Enhance the Flow. Something aint flowing right.

Even if filtering the blood of exosome would work, I don't think it would get rid of the core issue. My feeling is there's something that's causing the exosomes to be created. That something is what needs to be addressed to put CFS into remission. Just my 2 cents.

 

[roller]

it was quite obvious, that there "is something in the blood" - after the scheibenbogen-plasmapheresis trial.

and (1) is already confirmed (faik): this particle does pitch up the signal in pwmecfs.

to me, its not clear, that this thing is unique to mecfs.
could it be also seen in alz, PD, fibro ...?

its entirely unclear, what symptoms it would fix.
from the scheibenbogen trial, the effect should be quite huge and lasting (up to 12 month).

since its known, the effect wont be lasting, its even less understandable why searching for a med is more important than figuring out what this thing is. (this i understood from the vid)

 

[Rufous McKinney]

to me, its not clear, that this thing is unique to mecfs.
could it be also seen in alz, PD, fibro ...?

It seems the more these issues are teased out, the more inter-related various conditions may be.

On some kinda: continuum.... and so I think we will start to see some momentum and cross over in the research. The cancer folks have exosome interest. Eppstein Barr non-hodgkins exosomes.

I still need to actually read that paper.....sigh

 

[frozenborderline]

So: why don't we all just go get Plasma Transfusions once a month from healthy donors?

It seems like that could be an immediate fix to a major aspect of our problem.

so obviously: I"m missing something because this is too obvious.

David bell spoke of people getting blood transfusions that made them better even for months! He attributed this to blood volume increasing but saline which increases blood volume only improves people for a few hours so I wonder if it is indeed due to getting people plasma that doesn’t have the mysterious factor in it. Would be willing to try this for myself but I would bet that it is expensive and would be hard to find a doctor willing to do it. There are risks to blood transfusions

 

[frozenborderline]

just wonder why hasn't somebody who is SEVERE simply gotten a transfusion and found themselves able to get out of bed for instance

I mean how feasible is it to just “get” a transfusion? I don’t think any cfs doctors are prescribing them routinely. So I don’t know if it’s been thoroughly tested

 

[Rufous McKinney]

I mean how feasible is it to just “get” a transfusion?

Agreed: it likely isn't. If feasible means- capable of being achieved, considering all the various issues..... so its expensive, complicated and can have complications.

So: we just wait, longer.

 

[Rufous McKinney]

Yes. I believe there are 4 ME/CFS researchers that have found "something in the blood"

This article seems quite interesting and somehow related to the swirl of issues we're discussing.

Another: particle, budding off of neurons, containing messages, and conveying mRNA, and possibly hiding viruses and or behaving virus-like.

https://www.theatlantic.com/science...n-using-a-gene-that-came-from-viruses/550403/

 

[percyval577]

@Pyrrhus may I ask you about virus´s and arginine, I found it said that a lot of virus´s would be served by especially arginine. As I understood it then (papers seem to be mostly from the 60´s and 70´s), this would be during replication.

I have found two papers though which say arginine would be hindering. But it would hinder the reactivation (by NO) Agawa et al 2009, or would extend the latend period, Naito et al 2003
Naito et al referate also (in the abstract) that several RNA virus´s would be inhibited by arginine.

Do you have any assessment? What´s your opinion on that?

I rather don´t know anything about virus´s. My EBV may also have targeted IP3, dUTPase, MnSOD2.

 

[Pyrrhus]

@Pyrrhus may I ask you about virus´s and arginine, I found it said that a lot of virus´s would be served by especially arginine. As I understood it then (papers seem to be mostly from the 60´s and 70´s), this would be during replication.

I have found two papers though which say arginine would be hindering. But it would hinder the reactivation (by NO) Agawa et al 2009, or would extend the latend period, Naito et al 2003
Naito et al referate also (in the abstract) that several RNA virus´s would be inhibited by arginine.

Do you have any assessment? What´s your opinion on that?

I rather don´t know anything about virus´s. My EBV may also have targeted IP3, dUTPase, MnSOD2.

Thank you for your question.

Regarding herpesviruses, the general understanding is as described in this 1981 review:

In the studies conducted, arginine deficiency suppressed herpes simplex virus replication in tissue culture. Lysine, an analog of arginine, as an antimetabolite, antagonized the viral growth-promoting action of arginine. The in vitro data may be the basis for the observation that patients prone to herpetic lesions and other related viral infections, particularly during periods of stress, should abstain from arginine excess and may also require supplemental lysine in their diet.

As you mention, work by Naito seems to contradict the general understanding, as described in this 2009 paper:

We investigated the effects of arginine on the multiplication of herpes simplex virus type 1 (HSV-1) and the potential of arginine as an antiherpetic agent. Arginine suppressed the growth of HSV-1 concentration-dependently. Inhibition of HSV-1 by arginine leveled off at 50-60 mM, although the higher concentration was not suitable as an antiviral agent due to cytotoxicity. 'Time of addition' experiments revealed that arginine was particularly effective when added within 6 h post-infection (h p.i.), suggesting that the reagent sensitive step is in the early stages of the infection. A one-step growth curve of HSV-1 in the presence of 30 mM arginine revealed that: i) the latent period was significantly extended, ii) the rate of formation of progeny infectious virus decreased and iii) the final yield of progeny virus decreased to 1%. The addition of arginine at 8 h p.i., after the completion of viral DNA replication in the virus multiplication, allowed the normal formation of progeny virus in the subsequent 4 h, confirming that arginine does not directly interfere with the formation of progeny infectious virus. In addition, arginine also inhibits several RNA viruses.

I don’t know how to reconcile the two general findings. It may be that herpesviruses require an ideal concentration of arginine, and either too much or too little slows down viral replication.

Naito also described experiments on 3 different RNA viruses, which did not show any strong effect of excess arginine:

The antiviral activity of arginine was also examined for RNA viruses of three different families, i.e., influenza virus (Orthomyxoviridae family), poliovirus (Picornaviridae family) and VSV (Rhabdoviridae family).
...
Arginine concentration-dependently inhibited the multiplication of influenza virus and poliovirus, as shown in Fig. 5, although the sensitivities of these two RNA viruses to arginine were much weaker than the response of HSV-1.
...
On the other hand, arginine was ineffective against VSV up to 40 mM (Fig. 5).

I don’t know about any further research that looked into differential amino acid utilization by RNA viruses. I would certainly be interested in any such research.

Hope this helps.