I got that wrong. Post mortem brain tissue samples were used in his 2018 paper on mood disorders and how HHV-6 affects them.
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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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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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mitoMAN
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Do you happen to have studies indicating the oral intake and its stability in the gastric tract?
Quite interesting!
@mitoMAN well you know there are no human trials, so this is from animal trials.
"40 mg/kg of mdivi-1- treated group). mdivi-1 was administered by oral injection once a day for a month"
https://www.jneurosci.org/content/jneuro/37/20/5099.full.pdf
"40 mg/kg of mdivi-1- treated group). mdivi-1 was administered by oral injection once a day for a month"
https://www.jneurosci.org/content/jneuro/37/20/5099.full.pdf
https://www.mdpi.com/journal/biomolecules/special_issues/Biomarkers_in_CFS
Special Issue "Biomarkers in Chronic Fatigue Syndrome (ME/CFS)"
A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Chemical Biology".
Deadline for manuscript submissions: 30 June 2021.
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Special Issue Editor
Dr. Bhupesh K. Prusty Website
Guest Editor
Julius-Maximilians-Universität Würzburg, Wurzburg, Germany
Interests: Herpesviruses; Small RNAs; Mitochondrial dysfunction; Host-pathogen interaction; microbial pathogenesis
Special Issue Information
Dear Colleagues,
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a systemic disease that affects the central nervous system, the immune system, cell energy metabolism, the autonomic nervous system, etc. The main clinical sign is persistent chronic fatigue that is not relieved by rest and lasts for more than six months. Up to 75% of patients are completely unable to work and remain wheelchair-dependent, and at least 25% are permanently housebound or even bedbound. Accordingly, the socio-economic impact of the disease is huge. At present, no curative treatment options are available. Therefore, patients have practically no prospect of recovery or at least of returning to work. Etiological factors for ME/CFS include genetic predisposition, stress, trauma, exposure to toxins, the ratio of physical activity to rest, and a recent history of infectious disease. ME/CFS can affect individuals from all races, genders, age groups, and social statuses. The pathogenesis of ME/CFS is likely multi-factorial and various microbial and viral infections can serve as possible triggers for ME/CFS. However, to date, no single biomarker has been identified that can be generalized to the entire patient population. Considering the heterogeneity of ME/CFS, it is plausible that a specific set of biomarkers might enable us to define disease subtypes. Identification of biomarkers will allow for prognosis of the disease’s development and promote the development of a specific definition for diagnostics and a treatment plan. Hence, I encourage researchers from diverse backgrounds (clinics, systems medicine, genetics, molecular biology, epidemiology) to contribute original research and review articles on any aspect of biomarker identification, biomarker characterization, or translational approaches of clinical relevance to this Special Issue, which aims to bring ideas from different fields of science to one common platform that may stimulate further research and solve a modern day clinical mystery.
Dr. Bhupesh K. Prusty
Guest Editor
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
Keywords
- Herpesviruses
- Small RNAs
- Mitochondrial dysfunction
- Host-pathogen interaction
- microbial pathogenesis
This special issue is now open for submission.
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Dear raghav,
for me the cause of my ME/CFS has always been gastrointestinal, due to D-Lactic acidosis without short bowel syndrome that took 18 years to diagnose. I most definitely had ME/CFS symptoms and was even diagnosed with Fibromyalgia due to pain.
I have believed for some years that different forms of Organic Acids produced in the Gut may be that universal factor, because D-Lactic acidosis can cause both Mitochondrial and Autonomic dysfunction and I have been diagnosed with both of these and my own belief is that this is caused for at least a Subset of ME.
My other belief is that this is an environmental issue caused through agents such as Fluoride, Antibiotics and Multiple Chemicals, that we have created that pass through the Gut causing dysbiosis, but it is obviously far more complex, because I did have a number of other possible causative factors including Glandular Fever prior to falling ill.
Because so many with ME/CFS have Gut problems including SIBO would it not be possible to verify this through Growing Duodenal Aspirates, Fecal Assay or even Urine Assay for Organic Acids. Would common symptoms not leave traces in Urine.
It would be good to have some mass testing using a simple test to identify those with this condition and find out why they have developed Bacterial Overgrowth and whether it is a primary or secondary cause of symptoms.
for me the cause of my ME/CFS has always been gastrointestinal, due to D-Lactic acidosis without short bowel syndrome that took 18 years to diagnose. I most definitely had ME/CFS symptoms and was even diagnosed with Fibromyalgia due to pain.
I have believed for some years that different forms of Organic Acids produced in the Gut may be that universal factor, because D-Lactic acidosis can cause both Mitochondrial and Autonomic dysfunction and I have been diagnosed with both of these and my own belief is that this is caused for at least a Subset of ME.
My other belief is that this is an environmental issue caused through agents such as Fluoride, Antibiotics and Multiple Chemicals, that we have created that pass through the Gut causing dysbiosis, but it is obviously far more complex, because I did have a number of other possible causative factors including Glandular Fever prior to falling ill.
Because so many with ME/CFS have Gut problems including SIBO would it not be possible to verify this through Growing Duodenal Aspirates, Fecal Assay or even Urine Assay for Organic Acids. Would common symptoms not leave traces in Urine.
It would be good to have some mass testing using a simple test to identify those with this condition and find out why they have developed Bacterial Overgrowth and whether it is a primary or secondary cause of symptoms.
Reading_Steiner
Senior Member
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After looking at that study again, and say we are to run with that theory for now, my question is, what is PEM ? prusty mentions a certain requirement ( TSA (trichostatin-A) ) which draws parallels to the sodium needed so get differential results in the nononeedle test. I find that very interesting in terms of the antiviral behaviour.
Could this mean that PEM is actually the point at which the mitochrondrias fragment ? as according to the study, without a 'stress factor' ( exercise ? )they do not fragment. I feel like references to disease trigger factor must be wrong, because this is an ongoing process of viral reactivation. Alternatively are our mitochrondrias always fragmented and trying to extract energy from them in that state is whats producing toxins which takes a while to clear our of the body ? Is there any technology that could check whether the mitochrondrias are fragmented within our body in real time ?
Could this mean that PEM is actually the point at which the mitochrondrias fragment ? as according to the study, without a 'stress factor' ( exercise ? )they do not fragment. I feel like references to disease trigger factor must be wrong, because this is an ongoing process of viral reactivation. Alternatively are our mitochrondrias always fragmented and trying to extract energy from them in that state is whats producing toxins which takes a while to clear our of the body ? Is there any technology that could check whether the mitochrondrias are fragmented within our body in real time ?
Rufous McKinney
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junkcrap50
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A little disappointing he's not being, nor will be going forward, as candid as he had been in the past. But we'll see what he say these next couple days.
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Rufous McKinney
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Sharing "achievements" but not results.
Ok- I understand- its part of just how the system works. Results require Peer Review, announcing before publication is therefore premature.
I appreciate the hopeful hints, however!
Rufous McKinney
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I'm just recalling some comments Janet Dafoe made regarding similar issues- that if results get presented before publication is harder to get it published, confidentiality agreements which are why every other person is a lawyer, limits to data coming from institutions and universities, grant programs which restrict or limit info when still preliminary. etc etc.
Then of course we see the issue that if anything corrects the signal in a device, its a big secret as we will all rush out and try to obtain the substance.
So we wait.
So, can anyone help me understand why Prusty is looking for the "transferable factor", when we know that it is nucleotides (mainly ATP) given off by cells in CDR what signal other cells into entering into the CDR state?
In one of the autistic murine model studies, Naviaux et al used downregulation of purinergic receptors as a signal for hyperpurinergia, and they found decreased expression of purinergic receptors in autistic mice, and suramin reverted this:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3596371/?report=reader#!po=90.3571
So, can't nucleotides be the transferable factors? Why is Dr. Prusty looking for other substances such as C1q autoantibodies?
Thank you,
Sergio
In one of the autistic murine model studies, Naviaux et al used downregulation of purinergic receptors as a signal for hyperpurinergia, and they found decreased expression of purinergic receptors in autistic mice, and suramin reverted this:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3596371/?report=reader#!po=90.3571
So, can't nucleotides be the transferable factors? Why is Dr. Prusty looking for other substances such as C1q autoantibodies?
Thank you,
Sergio
Rufous McKinney
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I think this is tied to the work at Stanford, that something of a certain size range is in exosomes carried in our plasma, and can be transfered if healthy rbc are introduced to that sick plasma. I don't think its ATP itself...
Thank you Rufous for your reply. Yes, it seems that way, and obviously they must have unpublished info that prompts them to look for this "transferable factor", other than nucleotides.
However, if nucleotides are not the only possible substance that signals the threat and makes the neighboring cells to enter into a CDR state, why does suramin work in autism and could work in ME/CFS? This is what I don't get.
Best!
Sergio
However, if nucleotides are not the only possible substance that signals the threat and makes the neighboring cells to enter into a CDR state, why does suramin work in autism and could work in ME/CFS? This is what I don't get.
Best!
Sergio
Well, I don't remember that they treated the terrain first, this is, lyme, co-infections, heavy metals, mycotoxins, other toxins, EMFs (yes, no ionizing ones, classified as carcinogenic by the WHO) etc. Obviously, we need to get rid of the stressors that induced our cells into the CDR state before trying to get out of it. Yes, autistic children got better from one dose, but they are usually much more responsive than adults.
Learner1
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I had a personal conversation with Nsviaux and he indicated that it would be necessary to remove/repair all of the cell dangers and only then, if the body didn't kick.into normal gear, then one might need suramin.