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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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  1. necessary8

    Deep phenotyping of post-infectious myalgic encephalomyelitis/chronic fatigue syndrome

    Except we can? And we get worse from it? That's completely different from some brain dysfunction making it so you always have a preference to not push through. What you're saying is literally contrary to the clinical picture of the disease and all the experimental data, including the ones from...
  2. necessary8

    Deep phenotyping of post-infectious myalgic encephalomyelitis/chronic fatigue syndrome

    Broooo... Who wrote this paper? There is some really good data hidden deep in it but the conclusions completely ignore it and contradict it! They found energy metabolism impairments in the muscle! This is the first study ever that finally checked gene expression in skeletal muscle. I was saying...
  3. necessary8

    Heterogenous circulating miRNA changes in ME/CFS converge on a unified cluster of target genes: A computational analysis (Kaczmarek 2023)

    Btw I should mention, hypoxia in ME/CFS is more complicated than just VEGF suppression. I do think VEGF is important but the whole picture is way more complex. I will have a full paper on that somewhere in the next few years probably (taking me a long time cause the paper is huge and there are a...
  4. necessary8

    Heterogenous circulating miRNA changes in ME/CFS converge on a unified cluster of target genes: A computational analysis (Kaczmarek 2023)

    Well it's a good thing I mapped out every single known, high-confidence direct interaction between all of them then ;) Fig 3: As you can see, for the most part VEGF is the one being induced by the rest of them, not the other way around. This is why it scores so highly as the most inhibited...
  5. necessary8

    Heterogenous circulating miRNA changes in ME/CFS converge on a unified cluster of target genes: A computational analysis (Kaczmarek 2023)

    Their methodology is interesting, tho mine will probably be completely different.
  6. necessary8

    Heterogenous circulating miRNA changes in ME/CFS converge on a unified cluster of target genes: A computational analysis (Kaczmarek 2023)

    No, definitely not. Bear in mind drugs mainly work by binding to receptors and eliciting intercellular actions indirectly. Transnational suppression by miRNA doesn't care about receptors. It cannot be directly overcome by any drugs or phytochemicals. The only two ways would be to either have...
  7. necessary8

    Heterogenous circulating miRNA changes in ME/CFS converge on a unified cluster of target genes: A computational analysis (Kaczmarek 2023)

    miRNA interaction with double-stranded DNA has been proposed computationally, but I've never seen a paper that would show this actually happening in any living organism at all, let alone mammals, let alone ME/CFS patients. I wouldn't categorically exclude it as a possibility, but no, I don't...
  8. necessary8

    Heterogenous circulating miRNA changes in ME/CFS converge on a unified cluster of target genes: A computational analysis (Kaczmarek 2023)

    @datadragon Sure, it's easy to find something that changes miRNA expression in some way. That's not the difficulty. The difficulty is trying to elicit a very specific change, in a very specific set of cells, which I remind you, we don't know what they are yet. The space of all possible changes...
  9. necessary8

    Heterogenous circulating miRNA changes in ME/CFS converge on a unified cluster of target genes: A computational analysis (Kaczmarek 2023)

    If you're talking about epigenetically upregulating the target genes of the miRNAs, then no, definitely not. Translational suppression doesn't care about epigenetics, it will persist no matter what you do on transcription level. This might be a different case. If you can find stuff upstream of...
  10. necessary8

    Heterogenous circulating miRNA changes in ME/CFS converge on a unified cluster of target genes: A computational analysis (Kaczmarek 2023)

    Lol, my next study is about metabolomics actually. XD Also, @Murph, could you please edit your initial post to include the link to the actual paper of mine? There was quite a hefty fee to publish open-access, so I want everyone to be able to find the link without scouring the thread or googling...
  11. necessary8

    Heterogenous circulating miRNA changes in ME/CFS converge on a unified cluster of target genes: A computational analysis (Kaczmarek 2023)

    I don't think that's likely. I think for the patients who seem to have a lot of neuro symptoms but not much in the other organs like muscle, a separate mechanism is likey at play. I think the recent OMF study showing demyelinating antibodies is a good candidate for it. Hardly, tho thanks for...
  12. necessary8

    Heterogenous circulating miRNA changes in ME/CFS converge on a unified cluster of target genes: A computational analysis (Kaczmarek 2023)

    I think zinc is good to take anyways, but it won't do anything about the VEGF suppression. None of these dysfunctions can be treated directly, actually. Because this is miRNA, suppression on the translational level is nearly impossible to overcome with a drug. For treatment, we'd need to do more...
  13. necessary8

    Heterogenous circulating miRNA changes in ME/CFS converge on a unified cluster of target genes: A computational analysis (Kaczmarek 2023)

    Lmao you posted it before I could. Hi, that's my paper. I'm the author. Ask me anything, (Yes, this is where I've been the past few years. Learning bioinf and doing projects like these behind the scenes. This is the first one that turned out good enough to publish. More to come in the next few...
  14. necessary8

    The RBC-NOX hypothesis

    Yes. We talk via email and have a very loose and informal collaboration. I'm doing some bioinformatics for him right now, we'll see if it goes anywhere, not sure at the moment yet.
  15. necessary8

    The RBC-NOX hypothesis

    Yeah, but I'm not the one who found it, dr Prusty is. The suppression of SOD2 due to mitochondrial fission can explain the oxidative damage. We joined our hypotheses.
  16. necessary8

    The Adenosine - Phosphatidic Acid Hypothesis

    I feel like this discussion is kinda pointless until we see a study examining SFN in CFS because for now I'm skeptical of notions standing on shaky grounds and we're just arguing how shaky the grounds are because you think that they're less shaky than I do. Which ultimately doesn't matter. In...
  17. necessary8

    The Adenosine - Phosphatidic Acid Hypothesis

    Then he should publish, I would love to see actual numbers. Also, do you happen to know how he tests it?
  18. necessary8

    The Adenosine - Phosphatidic Acid Hypothesis

    "Autonomic dysfunction" can be a lot of things so I can't address that because it's too unspecific. SFN is not at the top of the list because we have no evidence of it happening in ME/CFS, where as for other mechanisms, like say decreased erythrocyte deformability, or dysfunctional adrenergic...
  19. necessary8

    IgG stimulated β2 adrenergic receptor activation is attenuated in patients with ME/CFS

    Good point about the whole IgG fraction, but I can't find any part that would contradict my third point. They outright say: Now, I agree that we don't specifically know why its attenuated, there might be multiple mechanisms for it. But it is attenuated. Maybe that's what you meant as well, and...
  20. necessary8

    Assessing diagnostic value of microRNAs from peripheral blood mononuclear cells and extracellular vesicles in ME/CFS (Almenar-Perez et al. 2020)

    This is actually an extremely important study, even if it doesn't look like much at first glance. In december dr Eguchi had a paper which examined all proteins in EVs from CFS plasma, and this study examines all miRNAs. Together, those two studies are a giant step forward in ascertaining how the...
  21. necessary8

    The Adenosine - Phosphatidic Acid Hypothesis

    I think I've seen them all, but the thing is, hypoperfusion can be mediated by many, many possible mechanisms. And I don't think SFN is anywhere near the top of that list. Like, for example, oxidative damage to erythrocytes can explain all of this sufficiently (yes, even in light of the study...
  22. necessary8

    The Adenosine - Phosphatidic Acid Hypothesis

    Idk man, I've seen very few hypotheses that can actually explain this. And most of them are mine. People always gloss over it, because it actually doesn't fit with many things. I can't comment on this because this statement is too vaugue and non-specific. Hm, yeah, upon googling, the support...
  23. necessary8

    The Adenosine - Phosphatidic Acid Hypothesis

    Okay but then I don't think we can say preload failure explains PEM. Not by itself. I can perhaps see it being part of a larger mechanism, but until I see how it explain the delay, this is just one of dozens upon dozens of mechanisms that can cause exercise intolerance. So I don't really see...
  24. necessary8

    The Adenosine - Phosphatidic Acid Hypothesis

    Okay but then how does the delay work? In most cases PEM is delayed, usually by something like a day, sometimes even two. How would preload failure cause someone to get worse not immediately during the exertion but the next day instead?
  25. necessary8

    The Adenosine - Phosphatidic Acid Hypothesis

    How?
  26. necessary8

    IgG stimulated β2 adrenergic receptor activation is attenuated in patients with ME/CFS

    I'll ELI5 it for people I guess: 1. There is a subgroup of CFS patients who have autoantibodies to beta2 adrenergic receptors and muscarinic receptors, which are two types of GPCRs. It's about 30% of patients. This is not new, we knew this for a long time. 2. There is new research showing that...
  27. necessary8

    The Adenosine - Phosphatidic Acid Hypothesis

    This is an interesting idea. You could probably explain fatigue with it. But I don't think you could explain PEM. Right? Also, do we have any data showing SFN in CFS already? I know studies on it are underway but do we have results yet? This is really interesting as well. When I talked with...
  28. necessary8

    The RBC-NOX hypothesis

    Okay, so, before we get ahead of ourselves, I will clarify. I am aware of dr Eguchi's paper. I've talked to him directly about it. It nullifies half of this hypothesis - he found no NOX in the exosomes from ME/CFS plasma, and his methodology looks solid. So everything here that hinged on there...
  29. necessary8

    Identification of actin network proteins, talin-1 and filamin-A, in circulating extracellular vesicles as blood biomarkers for human CFS/ME

    Yeah, I know about this study (and I bet Davis knows too). It is a extremely important one, in my opinion. Perhaps the most important paper of this year. I have some thoughts about it but I will reserve them for now, until after I speak with dr Eguchi directly, and possibly after I can make some...
  30. necessary8

    Endothelin, Multiple Sclerosis, Systemic Sclerosis, Anti-ETAR AAb, Exosomes and CFS/ME

    This text is from this study: http://www.remedypublications.com/annals-of-arthritis-and-clinical-rheumatology/articles/pdfs_folder/aacr-v2-id1014.pdf which also does not show the presence of anti ETAR antibodies in POTS. I'm sorry but "this one lab added that test to their POTS panel" is not...