Lawrence @Deep_Chora

@Mattmaximo Wait until you start using spotlight...

You need to take that responsibility seriously. There is a lot of talk about how AI will solve biological problems, advance treatments, and cure disease. As a patient, I want you to know those promises are not going unnoticed, and we will hold the people who make them strictly accountable. If we face economic obsolescence without actual improvements in our quality of life, there will be a serious, justified backlash

Can I please guess how many of the people "having fun" were chronically ill? ✋

Nicholas Fabiano, MD @NTFabiano

a day ago

Life satisfaction is highly consistent with personality traits. The top trait was "Have a lot of fun".

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Covid Institute @Covid_institute

16 hours ago

The same chamber, the same pure oxygen, and two opposite outcomes. Which one you get depends on which mechanism is driving your long COVID. Hyperbaric oxygen therapy, and the question worth asking before you book one.

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quand on sait que tiktok recrute à coup de millions des ingés en neurosciences comportementales et des spécialistes du design persuasif pour hacker nos circuits dopaminergiques, je me félicite chaque jour de n'avoir jamais créé de compte sur cette plateforme mdr regardez ces études scientifiques en IRMF et eeg qui montrent très clairement quele format vidéo court attaque directement le cortex préfrontal et le cortex cingulaire antérieur (pour info ces zones gèrent le contrôle exécutif, la prise de décision et la régulation de l'attention) sachez qu’een bombardant le cerveau de micro stimuli imprévisibles, l'algo altère la densité de matière grise et réduit l'activité du réseau par défaut & cette surstimulation permanente entraîne une incapacité chronique à penser à long terme et détruit la capacité à être focus, 2 facultés qui pour moi sont littéralement indispensables à notre époque pour construire l'avenir  bref je pense que refuser d'entrer dans ce système, c'est simplement préserver son autonomie cognitive et la souveraineté de sa propre attention face à une ingénierie de l'addiction taillée sur mesure

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@G_Commish Already working on that behind the scenes.

Pretty embarrassing list if you consider that LC is also a metabolic disease. There is no systematic assessment of metabolic pathways, cellular respiratory function, or muscle energetics.

Jon Douglas @atranscendedman

3 days ago

FNIH RECOVER-TLC researchers reviewed hundreds of Long COVID biomarker studies and prioritized 82 blood markers spanning immune, vascular, inflammatory, metabolic and neurologic pathways. No single marker can yet diagnose Long COVID. fnih.org/our-programs/r…

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👇👇

Zdenek Vrozina @ZdenekVrozina

a day ago

Sorted by which receptors their antibodies hit, patients split into two clusters, and one of them is defined by antibodies against β1 and β2 adrenergic receptors, endothelin rec A, and muscarinic M4. That's the receptor-targeting axis that runs through the POTS and dysautonomia

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WE NEED MORE B CELL DEPLETION TRIALS AND WE NEED THEM FUCKING NOW

Vipin M. Vashishtha @vipintukur

a day ago

Could some #LongCOVID symptoms be driven by antibodies that turn against the nervous system? ➡️ Researchers found autoantibodies targeting proteins in the central and peripheral nervous systems in a subgroup of people with LongCOVID, particularly those with neurocognitive

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RECOVER-TLC has published a list of 82 blood biomarkers to be measured in its Long COVID treatment trials. It's not a diagnostic test, and it won't change anything in the clinic for now. But it's worth looking at what's on the list, and especially what isn't🧵

Jon Douglas @atranscendedman

3 days ago

FNIH RECOVER-TLC researchers reviewed hundreds of Long COVID biomarker studies and prioritized 82 blood markers spanning immune, vascular, inflammatory, metabolic and neurologic pathways. No single marker can yet diagnose Long COVID. fnih.org/our-programs/r…

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A day in the life of an Effective Altruist.

Introducing Synthetic Hospital: an open, fully synthetic longitudinal EHR benchmark with verifiable ground truth! 1,268 patients, 5,602 encounters, zero PHI. Physicians could not reliably distinguish its charts from real ones. 📄 arxiv.org/abs/2609.30027 💻 github.com/sparkcpark/syn… ✍️ sparkcpark.github.io/posts/finding-…

RECOVER-TLC posted the list of biomarkers it will use for its next round of #LongCovid trials. Thoughts: -This is 81 biomarkers, not 82 (IL-8 = CXCL8 iirc?) -Criteria of >3 months is insufficient; many markers are still abnormal then. Criteria should've been 18 months min. 1/

RECOVER have put out how they chose the biomarkers for their Long COVID trials and it's some of the most uninspired and methodologically questionable work I've seen in this space. They've got over a billion in funding. And what they did was go through other people's studies, look for blood markers that came up abnormal in at least two of them, and use that as their list. So we've got 82 markers, and honestly the reason most of them are in there is because they're cheap to measure, not because they're the right markers. The studies they took them from are mostly small and have most of the limitations Long COVID studies always have. Heterogeneous patient populations, no subgrouping, poor inclusion criteria, no mapping for severity, etc etc. Plus huge batch effects across all the different studies. You can't just pool that together and call it evidence. It gets worse. They only prioritised studies that compared patients to people who'd never had COVID. Researchers from major studies have already pointed out that when you do that, you can't separate Long COVID from leftover inflammation from the infection. So their filter pushed out the better designed studies. And complement, one of the main signals coming out of the larger studies, isn't on their list at all. Not one complement protein in 82 markers. Then there's nothing on their page about how they'll deal with batch effects in their own trials either. This stuff should be centralised, not left to individual sites to run assays. They also removed any markers that weren't "feasible" to measure at trial sites. That's just not true. You can do almost anything nowadays with specialist tubes. RNA tubes, DNA tubes. Process serum and plasma on site and ship it. Isolate PBMCs on site, freeze them and send them on dry ice. All of this exists already. They could have done it for everything they dropped. They had a billion. Long COVID isn't one thing, we all know there are subgroups. Instead they're comparing people with Long COVID to healthy controls on average, which just washes out the differences between us. RECOVER are making ad hoc decisions without thinking them through critically, because they have no skin in the game. It's poor, half baked decisions with zero thought in them, again and again, just to look like they're doing something. They're chasing their tail, and in doing so they're wasting all of our money. They desperately need to take a step back and create a cohesive long term strategy. This is just going to lead to another year, and another press conference saying sorry, our work last year was useless and it failed.

Zdenek Vrozina @ZdenekVrozina

3 days ago

RECOVER-TLC has published a list of 82 blood biomarkers to be measured in its Long COVID treatment trials. It's not a diagnostic test, and it won't change anything in the clinic for now. But it's worth looking at what's on the list, and especially what isn't🧵

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Breaking: Steve and Judy Pagliuca and Governor Maura Healey Accelerate Major Effort to Deliver Treatments for Long COVID

$15 million raised by a coalition of donors to advance diagnostics and clinical trials for Long COVID; with the infrastructure expanding into chronic Lyme disease 1/

There you have it. Don't think in German.

Aleph Alpha @Aleph__Alpha

3 days ago

Reasoning models think in English, even on German prompts. We asked what it costs to make one think in German. Answer: a valley. Small doses of German reasoning data hurt, large doses mostly recover.

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The mouse data are mechanistically useful but limited: young healthy mice were pretreated before stroke, and post-stroke dosing did not work. A33 also appeared to have a narrow effective window, with 0.1 µM outperforming both lower and higher concentrations. More relevantly, in primary human neutrophils stimulated with TNF-α + IL-1β, A33 cut inflammatory ROS by roughly 30–40%. So PDE4B inhibition may be most useful in neutrophil-heavy, oxidative inflammatory states.

PDE4B recently popped up in a secondary genetic analysis of the DecodeME cohort, with PDE4B-associated genetic signatures found across roughly 70% of ME cases. PDE4B breaks down cAMP, an intracellular signal that normally restrains inflammatory programs. Laura Ponsaerts and colleagues therefore selectively inhibited PDE4B in a mouse model of ischemic stroke. Given before the stroke, the PDE4B inhibitor A33 reduced brain lesion size by 57% and more than halved neutrophil infiltration. A pan-PDE4 inhibitor did something similar, while selectively inhibiting PDE4D did essentially nothing. Human neutrophils told the same story. PDE4B inhibition reduced their inflammatory ROS response, suggesting the effect was not simply peculiar to a mouse brain. The catch is timing: giving the inhibitors after stroke did not rescue the mice, so this looks more like prevention of an inflammatory state than reversal once tissue injury is underway. There is another reason PDE4B is attractive. Broad PDE4 inhibitors can cause substantial nausea and vomiting, with PDE4D inhibition implicated in much of that liability. Targeting PDE4B could potentially preserve the anti-inflammatory cAMP effect without paying the full price of pan-PDE4 inhibition. Stroke is obviously not ME/CFS. But when human genetics independently points toward PDE4B, and selective PDE4B inhibition suppresses neutrophil-driven neuroinflammation in vivo, the pathway becomes considerably harder to ignore. doi.org/10.26481/dis.2…

@Taodav UK pays like ass for ML.

@BayouMystere Bingo!

When a healthy cell detects a virus, it has ways to fight back. It can slow down its machinery, call the immune system for help and, if necessary, destroy itself before the virus gets very far. Cancer cells often lose parts of those defenses as they become cancerous.