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Sure, I can see that to an extent. But just as often as I see that attitude, I see tons of examples of the opposite. Every time I’m in a meeting with multiple PIs at least half the time is spent on questions of “are we sure X means Y? Have we checked Z? What are we missing here?” Just a few...

Just a random connection that came up in some of my reading: there's a calcium-dependent transcription factor that is known to directly govern the balance of type I/II muscle fibers: https://pmc.ncbi.nlm.nih.gov/articles/PMC317085/

I don’t think it’s necessarily an uncommon skill (it’s certainly the backbone of everything I’m being trained to do every day as a junior scientist), just one that doesn’t really work without theories to give you some place to start in an infinite search space

I think part of it comes from the fact that to answer any question, you need an idea of what type of thing you’re looking for. Even if the question is just “what changes during PEM?”—in order to design an experiment to answer that, you need to have an idea of what changes where (blood or...

Just a quick note—the brain does account for a very large percentage of “energy expenditure” however you measure it. The issue from several months ago mostly comes down to whether a particular demanding task uses much more “energy” than being at rest. It’s a very difficult thing to measure...

Apparently the labeling of pathogenic variants is known to be pretty fraught—even the ones pretty well-established to cause a hereditary disease can be called into question when someone is found with a homozygous mutation and is not sick. Outside of a few projects like Biobank and All of Us...

Those would be the least likely to end up in a study assessing blood analytes, then. Yes, I don’t think there necessarily has to be any relationship to “anerobic threshold”.

Mostly necrotic but apoptotic as well from hypoxia. Both would lead to STING activation, though only the latter would be intracellular from mtDNA ejection through the BAX pore. Cell death isn’t necessary for STING activation, just cytosolic DNA. Cell death would just be the source of STING...

Unless it's transient--I'm inclined to think not every report of abnormal test results here is a fluke because transient lactic acidosis would be entirely consistent with the transient "poisoned" feeling that some pwME describe. And it's been described as the most profoundly uncomfortable state...

So perhaps not “immune perturbation” in general but a specific set of processes that overlap between ischemia, sepsis, and some cases on the more severe end of ME/CFS.

The premise of the paper is basically asking: “Could a group of genetics researchers pull something out of the grab-bag of potentially pathogenic variants that every living human walks around with and come up with an educated guess for why participants X Y and Z might have [insert clinical...

ba dum tsss :D Right, where it’s usually assumed to be a byproduct of insufficient oxygen supply or lactate clearance in a damaged organ. But we don’t fully know what it is about the organ damage that leads to elevated lactate levels—ischemia nearly always co-occurs with macrophage polarization...

Also I thought there wasn’t much evidence for lactate itself causing organ damage in sepsis? In which case it would just be a response to infection or one of the downstream consequences, and could be triggered under other circumstances

If kept at room temperature for long enough, live cells in the sample can artificially increase lactate levels by glycolysis. There’s some additive I’m forgetting the name of that is supposed to suppress this as well. I vaguely remember from discussions a long time ago that processing time...

I should note that when I had a metabolomics lecture in my first year the professor started off the class by asking how many metabolites we thought would detectably change in the blood just 30 mins after eating an apple. Don’t remember the exact number but it certainly wasn’t 0.

What could be plausible is that a bunch of metabolites are induced less in ME/CFS relative to how much they are induced in healthy people (and the converse, metabolites that are downregulated less than they would be in healthy people). Which would also mean that we’d probably see some signs of...

Actually thanks @forestglip for prompting me to go back and check this—looking at some of my old datasets I do see a scenario where I got nothing past the q value threshold in a mouse study with very small n. So I take back my original comment I think what tends to happen in human cohorts of...

Yes, sorry for not clarifying, this was with the assumption that you’re nearly always going to have some low p-value false positives in a screen like this if you include enough features. It’s possible to end up with a situation where absolutely nothing passes the threshold after correction...

Actually, I'm positive it was an error in the code because definitionally for a q-value by BH you should have a number of false positives determined by your false discovery rate above the dotted line. All the plots in that figure seem to have the same issue.

I'll be honest, the chances of this figure reflecting a real biological phenomenon of no change after exercise is so small I would dismiss it outright. What this graph means is that either the intragroup variability for every single metabolite was so wild that there was no way for any data...