There seems to be a very common ‘it won’t happen to me’ bias in humans. We can’t stop that and there are probably reasons why risky behaviour has had evolutionary benefits, but we probably should be aware of it.
Would it be worth checking the statistical significance of say, all cytokine related genes? To get an understanding of if they were just below the threshold or nowhere near? Would that be useful info or even feasible?
What about rare genes, how do they fit i to this picture? What do we need...
Thinking about this more widely now we have some genes, is it correct to say we’re not looking for a mechanism which requires all of these genetic differences to be present but a mechanism which each of these genetic differences makes more likely to occur? Or is it even broader than that?
I was just about to mention the readme :) That’s as far I got into the data though, so seem to have come from the opposite side of it as you.
Great that you reproduced the manhattan plot. Are you using straight python or r for this?
That’s good. Another possible positive opener could be something like: What has surprised you most about these results?
How has patient involvement improved the project/made it different and/or more successful than it would have been without?
Is there anything you’d do differently now after...
From another thread and perhaps too forward looking for this webinar, but some questions on SequenceME and exactly what the plans are as there seems to be some discrepancies which some of us are unclesr on
Is this because of analysis time or the need to get more samples...
Going through the candidate genes pdf and SLC9C2 is mentioned which I don’t think we’ve had much discussion of
Which reminded me of discussion in the Zhang paper starting with his from @chillier
There was a fair bit of speculation about shared ion channels, results in PrecisionLife and if...
I think you’re right, the numbers and emphasis seem different from this announcement
https://www.actionforme.org.uk/sequenceme-first-of-a-kind-genetic-study/
https://nanoporetech.com/news/oxford-nanopore-action-for-me-and-university-of-edinburgh-launch-groundbreaking-study-into-the-genetics-of-me
Is this because of analysis time or the need to get more samples?
https://megenetics.org.uk/our-projects/sequence-me-long-covid/
What are the pros/cons from a scientific or funding perspective of including a new cohort of LC patients?
Would it be possible to do analysis of existing ME/CFS...
Agree. It’s a point I’ve repeatedly made. I had a good job, now I can’t do it. If there is a moral duty to get people back into work there’s a moral duty to invest in treatments so they can and in adequate care and support until those treatments are available.
Will you be looking at stratified analysis by severity to see if this changes the genetic signals found or the strength of them? The Data Analysis plan seemed to indicate 2k was enough to do this for co-morbidities.
I suppose you could say they’re a bit like seagulls. Good at regurgitation but you wouldn’t depend on them for reliable deduction.
Well crafted promote definitely help, out of the box their system prompts can give a tendency to be sycophantic, although there are some recent examples of Gemini...
Absolutely this. These tools can create plausible sounding results from anything.
They’re great when used responsibly, for anything which is verifiable, as they can be trained and trained to ensure they behave. That’s why they often make good information retrieval, summarising, code...
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