Symptoms/function before and after treatment with Rituximab. Bell went from 10 to 20, so not cured.
The HERV that has previously been associated with MS, ME/CFS, and LC, HERV-W ENV, wasn't high in this patient. They then looked at HERVs across the whole genome and compared to 8 female ME/CFS...
It was too much work for me to understand what it is they're exactly doing, but I got the impression figs 2D-F are the same data as 2A and 2B, just as dots. So LC in fig 2A would be the first column of dots in fig 2D. HC in 2A would be the first column in fig 2E. I might be wrong about this.
For this part, I've thought about this same thing many times, and haven't developed an intuition for why it's done the way it is, and question it for the same reason you say. And apparently so have others:
To adjust, or not to adjust, for multiple comparisons (2025, Journal of Clinical...
I'm not sure if there's an intuitive meaning for the actual value of p values after Bonferroni adjustment.
What Bonferroni does is maintains the same rate of false positives. When you do a single test, there's a 5% chance of a real null result having a p-value of less than 0.05. So in 100...
It's apparently a common email provider in China:
https://www.serviceobjects.com/blog/the-trouble-with-numeric-and-fake-looking-chinese-email-addresses/
Reddit comment
Edit: But yes, I'm not sure if it's weird for a researcher in China to not have a university or hospital email address.
At least one of the three names (Yuwan Gao) and a name from another rapid response you linked (Yulang Fei) seem to be the names of real people that work at the named hospital.
https://www.sciencedirect.com/science/article/abs/pii/S2254887424000638...
I think they may have used non-independent samples which artificially decreased the p-values, though. There were 9 people per group, but they used multiple cells per person, which are expected to be correlated to each other. Technically, you could get a p value as low as you want by using a very...
So I think the p>.9999 (which actually shows up 3 times in the full text) is a result of multiple test adjustment.
Bonferroni adjustment can be done by dividing the p value threshold by the number of tests where you would call it significant, but as described here, you can also keep the p=.05...
Now published:
Low-Dose naltrexone restored TRPM3 ion channel function in natural killer cells from long COVID patients
Etianne Martini Sasso, Natalie Eaton-Fitch, Peter Smith, Katsuhiko Muraki, Sonya Marshall-Gradisnik
Introduction
Long COVID is a multisystemic condition that includes...
Just from a quick Google Scholar search of 'long covid prevalence followup "24 months"'. I didn't read these in detail and they mostly seem to be about long COVID in general, but in case it's helpful:
Determinants of the onset and prognosis of the post-COVID-19 condition: a 2-year prospective...
Treatment of Long Coronavirus Disease in Japan: A Nationwide Study of Symptom-Associated Drug Prescriptions
Yuka Kogure, Wataru Ando , Kyoka Sakamaki, Mitsuhiro Sugawara
[Line breaks added]
Abstract
Long coronavirus disease (COVID) is characterized by symptoms persisting or reappearing at...
Just to be clear, no argument from me. I just meant the specific evidence about sperm cells from using that website. Sounds like an interesting line of thought that I hope someone follows. Ideally the first study done on this takes the initiative to use well-matched, deconditioned controls so...
On the other hand, looking at the random list for neuronal or glial cells, and including the ones I put as "maybe" to be conservative, I get less than half as many compared to the PrecisionLife genes. Whether or not it's statistically significant, I'm not sure.
Randomly selected genes
8/55 or...
I think we can probably forget about the sperm. I took a random sample of 14 genes from the 17,000 genes in the Zhang file, and about the same proportion are high in sperm-related cells:
Edit: 14 more, only 1 definite came up by random this time:
Going to do 28 more.
Edit 2: One had no...
That's a really cool resource, thanks. For reference here is the paper the genes are from: Genetic Risk Factors for ME/CFS Identified using Combinatorial Analysis (Das et al, 2022, J Transl Med)
And here are the 14 genes they found, linked to their Protein Atlas cell type page (GC links to...
The first paragraph you're talking about is the discovery cohort, on which the model was trained. It's made up of the Stanford and CureME cohorts. After training the model, it's tested on the independent dataset, the second paragraph, which is made up of different people, the Cornell cohort. The...
On the independent ME/CFS dataset, though, there is more of a difference (first quote is the simulated independent dataset, +0.358 improvement over HEAL, second quote is the ME/CFS independent dataset +0.124):
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