Bhupesh Prusty: "we are on a perfect path for identifying potential transferable factors in ME/CFS blood that can cause mito dysfunction..." GoFundMe

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andyman123

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Treeman said:
I think Prusty demonstrated that HHV 6 is not in that case symbiotic.
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Maybe keep them in a vat in a lab somewhere tucked away (like smallpox), truthfully I think almost any vertebrate (all vertebrates have at least one herpes virus that infects them) would do better (much better) if all herpes viruses were eradicated completely. They've been around for 200+ million years and have sub-speciated out in the last tens of millions into the alpha, beta, and gamma variants.

There has always been a part of the population 2-10% that has had mild to severe disease related to these viruses. The nice thing about people living older is we are going to start seeing just how devastating some of these diseases really are.
 
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raghav

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https://pubmed.ncbi.nlm.nih.gov/20062521/

miR-30 Regulates Mitochondrial Fission Through Targeting p53 and the Dynamin-Related protein-1 Pathway
Abstract
miRNAs participate in the regulation of apoptosis. However, it remains largely unknown as to how miRNAs are integrated into the apoptotic program. Mitochondrial fission is involved in the initiation of apoptosis. It is not yet clear whether miRNAs are able to regulate mitochondrial fission. Here we report that miR-30 family members are able to regulate apoptosis by targeting the mitochondrial fission machinery. Our data show that miR-30 family members can inhibit mitochondrial fission and the consequent apoptosis. In exploring the underlying molecular mechanism, we identified that miR-30 family members can suppress p53 expression. In response to the apoptotic stimulation, the expression levels of miR-30 family members were reduced, whereas p53 was upregulated. p53 transcriptionally activated the mitochondrial fission protein, dynamin-related protein-1 (Drp1). The latter conveyed the apoptotic signal of p53 by initiating the mitochondrial fission program. miR-30 family members inhibited mitochondrial fission through suppressing the expression of p53 and its downstream target Drp1. Our data reveal a novel model in which a miRNA can regulate apoptosis through targeting the mitochondrial fission machinery.



Is there any connection between sncRNA-U14 and miR-30 ? Does the former downregulate miR-30 levels in blood ? How can we increase blood levels of miR-30 ?

Added later - I think the 23 nucleotide molecule could come into play here. Is it the mystery molecule which causes the serum to go antiviral ?
 
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raghav

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Flaming Mitochondria: The Anti-inflammatory Drug Leflunomide Boosts Mitofusins
https://www.cell.com/cell-chemical-biology/fulltext/S2451-9456(18)30078-3?_returnURL=https://linkinghub.elsevier.com/retrieve/pii/S2451945618300783?showall=true

But the side effects scare me !

Added later - The drug also seems to cause hepatotoxicity due to depletion of ATP. The problem with most of the repurposed as well as new drug molecules is they are good in some cell types but cause damage to the mitochondria in some other cell types.
 
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sebaaa

sebaaa

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So, just for the record a few takeaways from the video if the video goes down again...

Note that this only goes for HHV-6 (or a similar virus) infected cells, which go on to produce the "serum factor" that negatively affects healthy cells:
sncRNA-U14 -> ↓ miR-30 -> ↑ p53 -> ↑ Drp1 -> mitochondrial fission
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PrustySlide.png


“We are trying to test several FDA-approved drugs, which are already in the market, which are used for several other mitochondrial diseases.”
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I don't know what these are. I tried to look for them, but there really aren't any FDA-approved drugs for mitochondrial diseases.
 
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wigglethemouse

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sebaaa said:
I don't know what these are. I tried to look for them, but there really aren't any FDA-approved drugs for mitochondrial diseases.
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This is the full quote from the YouTube auto-generated transcript for context.
30:53
this means that if we somehow can
prevent the mitochondrial fragmentation
in mecfs patients we probably have a
chance of recovering completely probably
yeah and
we are trying to test a several
fda-approved drugs which are already in
the market which is used for other
purposes which is used to several other
mitochondrial diseases to prevent
mitochondrial fragmentation if they can
bring the the fragmented mitochondria
into a normal state in mecfs we're not
doing it mecfs patients we still in the
lab but still we're trying to achieve
that we do not know what causes
mitochondrial fragmentation
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raghav

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Prusty also said they have synthesized a drug for which they have applied for patent or are in the process of applying for patent. Wondering what that could be.

Also in one of his tweets he talked about an mRNA molecule which they are testing.
 
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andyguitar

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MonkeyMan said:
@andyguitar Are you saying you doubt Prusty is onto something here? (Not judging you, just curious what you meant by this).
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I dont doubt that there is a connection to something being wrong with the blood and me/cfs. I have posted about it in the past. Little or no interest was shown. When it comes to Prusty I dont think he can have something as great as he makes out. If he did he would not need to do a Go Fund me appeal. How much would a successful drug treatment for me/cfs be worth? £10 million? £100 million? Nobody wants to invest in that?
 
MonkeyMan

MonkeyMan

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andyguitar said:
How much would a successful drug treatment for me/cfs be worth? £10 million? £100 million? Nobody wants to invest in that?
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It is quite baffling, I agree. The pharmaceutical industry could be our biggest ally in coming up with treatment, but so far they have not wanted to touched ME/CFS with a 10-foot pole. Very disappointing, and surprising given the huge goldmine that an effective treatment would be.
 
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Slushiefan

Slushiefan

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raghav said:
Flaming Mitochondria: The Anti-inflammatory Drug Leflunomide Boosts Mitofusins
https://www.cell.com/cell-chemical-biology/fulltext/S2451-9456(18)30078-3?_returnURL=https://linkinghub.elsevier.com/retrieve/pii/S2451945618300783?showall=true
.
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I took leflunomide for some years as an adjunctive treatment for my personal brand of CFS. It didn't do a lot, but it did do a little. You would hardly notice the difference though and I don't bother today.

I had already discovered that methotrexate at full 25mg weekly gave an appreciable amount of improvement (means I can feel it - so like 20%? but that is the second best improvement so far with the first being B12). I wondered what some other DMARD's might do, and I found that Leflunomide was cheap, shippable (meaning mail order), and had a high safety profile.

Overall with Leflunomide the improvement was ~5%. I got so much more out of MTX I decided I would just stay with that.
 
lauluce

lauluce

as long as you manage to stay alive, there's hope
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andyman123 said:
Looks like Bhupesh and whatever other colleagues have finally figured out the molecular mechanics of CFS. This fits in with the metabolic trap and the usual onset caused by a viral infection or an infection that can transactivate latent infections we may already have.

We may be able to take mitochondrial drugs to counteract these effects but until we start completely curing and eradicating viruses from the herpes family and others it's going to keep being a problem.

When they completely eradicate herpes: MS, rheumatoid arthritis, many different vascular diseases, blood carcinomas, bipolar disorder, severe depression, keratitis, bell's palsy, and on and on are simply going to mostly go away if not go away completely.

This video brings molecular proof into what these viruses can do. Unfortunately for crispr to catch up to this is probably still 10-20 years off for complete eradication. Crispr is really progressing still. I hope there is a cure soon as I know the hell many of you on here are in.

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I can't watch the video, it says: "null. If the owner of this video has granted you access, please sign in."
 
lauluce

lauluce

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I really liked this statement:
"the reality is that what we practice in the clinics is the knowledge that we have probably acquired 20 years or 30 years back.
the science has changed dramatically in the last five to ten years, we have learned so much, which immediately should go to the clinic"
 
Rufous McKinney

Rufous McKinney

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lauluce said:
"the reality is that what we practice in the clinics is the knowledge that we have probably acquired 20 years or 30 years back.
the science has changed dramatically in the last five to ten years, we have learned so much, which immediately should go to the clinic"
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This seems like a very significant statement which leaves me feeling a bit outraged, again- at our abandonment by clinicians and actual doctors who treat patients.

We are just getting old shoddy crap and all the latest stuff- is not being integrated into a meaningful treatment strategy - even with what we know at the present time.

So I would really like to know what should be: GOING OUT TO CLINICS (as if there is a clinic, to go out to)
 
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