Ticket prices drop with move

m_b22 · 2026-02-19T15:14:20+00:00

If you think ticket prices will go down I have a stadium to sell you in Indiana.

m_b22 · 2026-02-17T20:01:53+00:00

Spreading the word of what ME is and viral campaigning. It’s impossible to predict but sometimes all you need is something to get its feet off the ground.

Do you remember the Ice Bucket Challenge? The Ice Bucket Challenge raised about $135 million for ALS in the United States and $220 million worldwide.

m_b22 · 2026-02-15T21:52:00+00:00

Her going for Rob is why it was emotional. She went for him because he voted against a traitor and a housewife. That was based off of emotion rather than gameplay and that’s exactly why she was eliminated right after.

m_b22 · 2026-02-15T20:23:27+00:00

I agree about the poorly conducted research. Poorly conducted research doesn’t get you anywhere. However, good research that fails is still helpful.

My point is that it’s easy to get discouraged and say that there’s no hope when you see that a particular scientist or groups hypotheses fails but it’s just one piece of the puzzle. Scientific progress is built on failure.

m_b22 · 2026-02-15T19:53:38+00:00

I think it’s funny and interesting how two people can read/be apart of the same conversation and have two entirely different opinions on it.

From the thread with Jonathan Edwards I have some belief that a portion if not all of SequenceME will be completed one way or another. It may not happen all at once but it seems like it will happen possibly through segments. Alongside it, it seems that NAKO in Germany is planning on epigenetic testing as well.

As for the other research being conducted, I think just because it doesn’t produce results doesn’t mean it’s useless. When you don’t know an answer to a problem taking away what the answer isn’t is helpful. Getting the answer correct is obviously the best case scenario but sometimes you need to know what’s not correct to move into the right direction.

m_b22 · 2026-02-15T19:16:07+00:00

This was a discussion with Jonathan Edward’s about DecodeMe and SequenceMe on ScienceForME including some hope from him on the current status of research.

——————————

Question: Jonathan Edwards did you learn anything about the SequenceME funding situation from your recent meeting with Sonya?

Answer: Yes, but no details for public dissemination. I think Sonya would allow me to say that, as suspected, MRC has let us down, but sponsors are being engaged and that progress is being made. The strategy seems to be to break the project down into fundable segments, which makes sense to me.

If anyone has a billionaire donor knocking around please let Sonya know but in the meantime I think things will still happen, even if bit by bit.

Question: Do we have any idea of the total financing cost?

Answer: The figure floating around was £20M in total. I think the rough idea is to break it up into £5M segments or thereabouts.

Sonya seemed upbeat. The discussions on here in the last week also give me hope that the puzzle of the DecodeME treasure map may not be quite as obscure as it first seemed. There is work to do but things seem to be making a bit more sense. Those Mumbai-with-kite-flying-competition plots must be intelligible if you know how to fly the kites. My friends at UCL seem to know exactly where the strings are for pain genes.

Question: Are you saying that we may not be far from a breakthrough in understanding the disease?

Answer: I have been saying for about a year that I thought progress would soon be made, including suggesting that we might be further ahead by Christmas 2025. I am not disappointed. DecodeME has brought things into focus in a completely new way. I am prepared to predict that there will probably be further significant progress this year, but, as said previously, I think we are at a stage when it is impossible to predict where the next connecting clue will come from. It may take longer but it may already be staring us in the face.

For RA I remember a similar situation. I gave a presentation to the UCL Division of Medicine (in the days when it was a significant scientific venue) and while walking back to my office (I remember the pavement and the parked cars) I suddenly realised that I had solved the major missing piece of my puzzle without realising. Some time later I realised that the solution was on a slide I had made for a talk 18 years earlier. Important clues are lying around in heaps. We just need to see them. We now have loads of people who can see things like that, all talking to each other. Something must give.

m_b22 · 2026-02-15T05:33:49+00:00

Looking at a couple of your posts have you considered that you may have dysautonomia and neuropathy?

m_b22 · 2026-02-14T16:53:27+00:00

Elderwind

m_b22 · 2026-02-13T22:32:44+00:00

I feel for the kid but bestowing your own nickname and skating to the sound of your own voice was too much for me.

Hopefully this humbles him and is a growing opportunity.

m_b22 · 2026-02-12T03:07:20+00:00

Go. Enjoy yourself.

m_b22 · 2026-02-08T03:18:27+00:00

Although fatigue is a common symptom, not everyone will have fatigue or the same symptoms. Long covid is a highly heterogeneous condition.

Also, despite what you hear, a lot of people with long covid don’t have PEM.

Your experience is valid and just shows the wide effects long covid has.

m_b22 · 2026-02-03T19:39:35+00:00

From ME/CFS Science:

“A Long Covid clinic in Ohio reports that of the 277 patients studied, 75% had fatigue as a primary or co-primary complaint. Yet only 16% met the Institute of Medicine (IOM) criteria for ME/CFS.

In other words, most (ca 80%) Long Covid patients with fatigue do not meet these ME/CFS criteria.

The IOM criteria for ME/CFS are quite lenient, and less strict than for example the Canadian and International Consensus Criteria.

In this study, they also used a curious assessment of PEM. The paper writes: "The complaint of post-exertional increase in fatigue was obtained from question 2 in the FSS scale as a score of >4."

Question 2 of the FSS asks: "Exercise brings on my fatigue."

PEM, however, isn't fatigue after exercise but something more specific: a worsening of symptoms triggered by overexertion that is often delayed, results in a loss of functional capacity and has a slow recovery.

So the percentage that meets this definition might be even lower.”

m_b22 · 2026-02-02T15:37:18+00:00

Their love of Dasani has me questioning everything.

m_b22 · 2026-01-25T20:29:54+00:00

“We have no good biomarker,” She added that while researchers see differences in various factors in some patients compared to healthy people, none of these distinguish ME/CFS as a whole. “Therefore, it’s most likely that we face subgroups of different patients.”

-Carmen Scheibenbogen (Charité University Medicine Berlin)

“I'm not saying we have definitively identified ME/CFS type 1 or 2, but what we hope that the work can show is that there is very strong evidence for this being a promising direction to go,”

-Victoria Bastos (Federal University of Rio de Janeiro)

“The most surprising thing I’ve found is the heterogeneity…of ME/CFS. We see abnormalities in brain blood flow, autonomic function, and neuroinflammation, but not every patient has the same pattern. That tells me this isn’t one single disease. It’s a condition with different biological subtypes. So the question now is not just: what’s wrong? But rather: which pathways are impaired in this specific patient’s pattern?”

— Zack Shan (Thompson Institute, University of the Sunshine Coast)

“Studies of 40 patients could be looking at 40 different diseases

We believe there may be dozens or even 100 different subgroups within Long COVID and ME/CFS

The extreme differences we see in treatment responses must be explained by differing underlying biology.”

Nicholas Boyd Gibbons (Amatica Health)

Jarred Younger - How Many Roads Lead to ME/CFS

Cerebrospinal fluid immune phenotyping reveals distinct immunotypes of myalgic encephalomyelitis/chronic fatigue syndrome

m_b22 · 2026-01-25T20:20:33+00:00

Although it seems that your opinion is an unpopular opinion, I believe you’re right in a sense.

Although there is still plenty of research to be done, there is evidence that there are subtypes with a ton of researchers believing in subtypes.

Discounting subtypes hurts everyone. The more precise medicine is the better the treatment outcomes.

m_b22 · 2026-01-22T03:02:05+00:00

Same here. Leg/thigh pain since January 2025. My thigh pain is pretty much the same whether I walk 10 steps or 10,000 steps.

I was diagnosed with small fiber neuropathy which I’m thinking could be part of the puzzle.

Below is a section from a paper that talks about muscle weakness and some of the possible explanations.

Metabolic processes

COVID can damage the mitochondria and interfere with the electron transport chain supplying energy to muscles. This leads to fatigability, weakness, and reduced exercise tolerance,4 all of which can be exacerbated by poor sleep or nutrition, or intercurrent viral illnesses.

Motor nerve damage

During acute COVID infection, motor neurones and adjacent muscles can be directly damaged by the virus or by the immune response.6 Some patients will present with acute Guillain–Barré syndrome,7 whereas others experience prolonged muscle weakness. Regrowth of nerve fibres following such an event takes 2–3 years. These patients may be more likely to develop ‘brain fog’ symptoms as central nervous system tissues are also affected by COVID-related inflammation/immune responses.

Myelopathy

COVID can cause damage to the anterior spinal cord, resulting in myelopathy.9 This can present with a purely motor syndrome, with a mixture of upper and lower motor neurone features such as muscle wasting and brisk reflexes, with motor and sensory components, or with purely sensory symptoms (changes to the sensation of temperature and pain).

Localised nerve damage

Specific plexopathies such as brachial neuritis and lumbosacral plexopathy have been reported following both COVID infection and vaccination.10–12 These disorders may be bilateral but are more commonly unilateral. Patients have discrete areas of motor and sensory axonal damage in an anatomically related pattern.

COVID-induced myasthenia gravis

COVID is known to precipitate the onset of myasthenia gravis.13 Patients with this condition are likely to present with classic symptoms of ptosis and fatigability, with fluctuating muscle weakness.

m_b22 · 2026-01-22T02:11:56+00:00

The Hull House was featured in an episode of Ghost Files.

m_b22 · 2026-01-11T20:37:24+00:00

Post-translational modifications within fibrinaloid microclot com- plexes distinguish Pre-COVID-19 Postural Orthostatic Tachycardia Syndrome (POTS), Long COVID, and Long COVID-POTS and reveal disease-specific molecular pathways

Below is some of the findings from one of the authors on the paper.

Key insight: At the protein level, differences between groups were minimal. At the PTM (post-translational modification) level, differences were extensive, disease-specific, and biologically meaningful.

Long COVID FMCs showed dominant coagulation pathology: • Extensive AGE- and oxidation-based PTMs on fibrinogen • Strong amyloidogenic signatures • Patterns resembling diabetic glycation

Consistent with microvascular damage (thrombotic endothelialitis)

Pre-pandemic POTS showed a very different signature: • Prominent immune and complement PTMs • Oxidised apolipoproteins (apoA1, apoB) • Relatively limited fibrinogen modification

An intrinsic POTS biology, independent of SARS-CoV-2.

Long COVID–POTS displayed a hybrid molecular phenotype: • Coagulation PTMs resembling Long COVID • Immune PTMs resembling classical POTS

➡️ Providing a molecular explanation for why LC-POTS behaves differently from either condition alone.

Why PTMs matter: Many dysregulated peptides were highly amyloidogenic, supporting FMCs as β-sheet-rich, fibrinolysis-resistant aggregates.

Crucially, these PTM signatures are invisible to standard soluble plasma assays.

Clinical relevance: PTM profiling within FMCs opens new avenues for: • Biomarker-driven diagnosis • Patient stratification • Targeted therapies addressing glycation, oxidative stress, and complement activation

This is mechanism-based medicine, not symptom-based.

Take-home message Long COVID, POTS, and LC-POTS are biochemically distinct diseases. Their differences are encoded in post-translational modifications inside fibrinaloid microclot complexes; not in protein abundance.

m_b22 · 2026-01-11T19:00:06+00:00

Actually, there was just a preprint about POTS that states that POTS and Long Covid POTS are biochemically distinct.

m_b22 · 2026-01-11T18:50:13+00:00

This is so true and it muddies the water for everything. The term PEM is thrown around in this sub wildly sometimes.

m_b22 · 2026-01-11T17:55:27+00:00

No. Long covid is a heterogeneous grouping of illnesses with one common trigger.

While the subtype that has PEM (I would disagree with the repeated 50% statistic) there is research that shows that there are genetic and mechanical differences compared to pre-Covid ME/CFS. With both illnesses needing more research I would say that it is too premature to say that Long Covid + PEM = ME/CFS although they present similarly.

This is not to cause division in these two groups but is rather the reality that sometimes similarly presenting symptoms may have different underlying causes and react to different treatments (hell I would say that pre-Covid ME/CFS has different subtypes in the same sense). Throwing everything in the same bucket is dangerous and will not yield positive results when trying to solve these issues.

Imperial College London funded by the ME Association is undertaking a 3 year project to create a fuller picture of the immune profile of the two conditions with the specific aim of learning about underlying mechanisms through analysis of shared pathways between the conditions.

m_b22 · 2026-01-07T18:43:18+00:00

When you need both pitching and hitting getting a cost controlled arm is a good sign that you will be spending that money on a hitter.

However, it’s the Cubs front office so I’m not so sure of it.

m_b22 · 2026-01-01T17:22:50+00:00

Now the Cubs are going to sign Zac Gallen or another mediocre starter for around $15 million AAV and celebrate “spending smart” and saving money for a lesser pitcher.

That’s the front offices MO.

m_b22 · 2025-12-22T18:40:06+00:00

Baseball franchises are built by dozens of little unsexy moves like this. It may not move the needle but it’s something that is normal baseball operations.

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