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From the candidate gene list it seems the locus on chromosome 20 is associated with many other interesting looking genes. For instance ZNFX1, where the eQTL data suggests expression of this gene is increased in brain and pancreas. There was an EMBO paper I saw that argues that ZNFX1 inhibits...

RABGAP1L is involved in vesicle trafficking near the cell membrane and is highly expressed in neurons - both also true of ATP9A and USP6NL from precisionLIfe's me/cfs and long covid studies - all three heavily associated with Rabs. I wonder if an alternative possible function to pathogen entry...

CLOCK was one of the genes found in precisionLife's ME/CFS genetics study in the UK biobank, and replicated later in a long covid cohort

Thank you so much @Chris Ponting @Andy and the decode team. There's no words really to properly express the gratitude. Loss of function causes excess culling of mitochondria leading to mitochondrial DNA depletion syndrome or mitochondrial encephalopathy. This reminded me of something from Josh...

The seahorse assay introduces a lot of technical variation in general, but there will be even more in our particular set up because the cells (which are seeded in their wells near confluence) have been incubating in serum for a whole week prior to running the actual assay. We are not looking at...

'in your head' is an idiom meaning 'isn't real / based on worry and overthinking'. It's dismissive to say that about any disease whether psychiatric or of the body. Personally I think it's even a little flippant to say to someone who really is just a bit worried about something.

If you do a statistical test with a significance threshold of p = 0.05, by definition there is a 5% of you getting a positive result by chance. Therefore if you do ~3000 tests as the authors have done in this paper, you expect to see 5% of those tests to be positive completely spuriously = 150...

Very poor response from Alan Carson, he appears to either not understand what multiple testing correction is, or just assume without reading the paper that the authors haven't done it.

@Jonathan Edwards I want to push back on that point about the critic at UCL. I wasn't at the UCL meeting of course but I don't get the impression this person was acting in good faith. The tone was aggressive to the point that people came up to Audrey after her talk to apologise for his...

Yep, so to be clear we did have severe pwME in the study, just relatively few. I believe something like 5 severe out of 67 total. If you just look at the severe people only there is still no difference between them and the healthy controls. To get more would have required at home sampling which...

The points raised about PEM and severity are the biggest limitations I completely agree. All the participants had to have been well enough to physically attend the university, but this doesn't mean they weren't very sick. The complete lack of any even incremental trend towards increased OCR in...

We would have liked to a see a positive result obviously but what we really wanted was to get a clear answer about whether the 'factor in blood' work done previously was real. It's been an unresolved question for quite a while now and we thought we and the community deserved to know. We put a...

See post #76 for peer-reviewed version. Indistinguishable mitochondrial phenotypes after exposure of healthy myoblasts to myalgic encephalomyelitis or control serum Audrey A. Ryback, Charles Hillier, Camila M Loureiro, Chris P Ponting, Caroline F Dalton Myalgic Encephalomyelitis (ME)/Chronic...

haha :D one of my ME symptoms is terrible thermoregulation so both are true!

Thanks Simon :) We submitted the preprint to biorxiv earlier in the week so hopefully it'll be out soon. Maybe monday? EDIT: As if on cue! It came out at the same time I made this comment.

Yep, mean age at time of filling out is very similar but that doesn't mean the underlying distribution has to look the same so we can check. Since we have the age of onset and the age at the time of filling out the form it means we could also check how the age at onset has changed over the...

Perhaps more likely to be temporary, though if there was more permanent damage to types of sensory neurons that don't directly lead to an obvious loss of touch sensation would that really be detectable with neurophysiology techniques? I don't know the extent of what's possible with these...

Fair enough but I'm not suggesting there's retrograde degeneration, but a delay between an event such as damage at the neuron terminals and a phenotype occuring possibly mediated by this retrograde movement. You might be right about sensitisation at the DRG but does it necessarily need to happen...

Yes exactly that's the thinking here. I can't give good answers to these fair questions I'm afraid I can only speculate. I don't know of course whether the smaller PEM events like over a few days and the disastrous huge relapses type PEM are just degrees of the same phenomenon or not. For me...

There appears to be a process called Wallerian(-like) degeneration of nerves which also follows a similar time delay pattern. After nerve damage (eg crush), the neurons can retain electrical activity for (according to wikipedia) 24-36 before the axon degenerates and macrophages infiltrate the...