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This is interesting. But I don't see the preprint talk about the data source for looking for shared intervals with all these other assorted traits like Parkinson's and arthritis. Only depression, pain, and anxiety. @Chris Ponting, is it that all traits in the UK BioBank were checked for similar...

Oh, when you click on that reassigned identifier, it goes to a page on an "Archive" Ensembl website, which I assumed was like an archive for genes that are no longer active. I couldn't find that new identifier on the regular Ensembl.

Oh, snoZ178 actually is/was a gene in humans that looks like it's closer to the DecodeME locus than CA10: LocusZoom But the Ensembl website says it was retired, which I think might mean that it was predicted to be there, but then that turned out not to be the case. So I'm guessing it's not...

So in the pain paper, it looks like it was significant in females, but not males or combined. In DecodeME this locus was genome-wide significant in females and combined, and p=~.01 in males. They also suggest something other than CA10, something called snoZ178, that this locus might be...

Looking at that paper, in table 1, they give the sex-stratified results. Here's the locus that I think is what matches with DecodeME (note the position is based on GRCh37 unlike DecodeME, so needs to be converted): Here's the zoomed in manhattan plot of the chromosome 17 "tower" from...

I think the wrong paper is cited for the matching locus with multisite chronic pain: 41. Harlow CE, Uzochukwu E, Fernando HA, Mordaunt CE, Hughey JM, Eicher JD, et al. GWAS of Extended Prescription Analgesic Use Identifies Novel Genetic Loci in Chronic Pain [Internet]. 2024 [cited 2025 Jul...

As far as I understand, that shouldn't really change anything. h19 and hg38 are just different ways to refer to a SNP and can be converted between each other.

To add to what jnmaciuch explained, I think you might be referring to a common convention. SNVs (single nucleotide variants) are used to describe any places where a single nucleotide/letter is changed in the DNA. SNP (single nucleotide polymorphism) can refer to an SNV that is present in at...

Do they let you know of the edits before they publish? If not, that seems very strange to me to change someone's words in a quote without indicating it and without their approval.

Metabolic brain changes in post-acute COVID-19: systematic review and meta-analysis of [18F]-FDG-PET findings Izabella Fernanda Bastos Siqueira, Lais Almeida Figueiredo, Camila Emanuele Moreira Fernandes, Leandro Pinheiro Cintra, Glauber Fernandes de Oliveira, Maria Angélica Rios, Ricardo...

I'm not sure about the one in your previous post. I would expect it to be in the BioBank. But maybe that website GeneAtlas doesn't show every variant they tested for whatever reason. For the one that Dibble tested in the BioBank that wasn't tested in DecodeME, maybe that's just a variant that...

I checked the summary stats for the variant from the thesis for SLC25A15, rs7337312, which has the ID 13:40779161:G:A. The p-value for this in DecodeME is 0.713705. Dibble found another novel association in males with the gene PDE10A, with the SNP rs76346913, which has the ID 6:165736174:C:T...

I found this blog post about the difficulties and methods of connecting a variant to a gene: https://www.genomicsengland.co.uk/blog/understanding-genetic-links-to-disease-mapping-variants-to-genes Some snippets: Nearest gene So that's why OLFM4 was proposed as the best candidate here. Open...

Oh I agree with all that you said. I meant if the hypothesis is specifically, "if I increase your CRP, that will cause you to be more likely to have ME/CFS". Which admittedly is not accounting for a lot of CRP related hypotheses.

I'm not sure I follow. You've got two identical people, except person A that you know is more likely to have a higher level of CRP than person B on average. If you think that CRP causes ME/CFS, then you'd expect person A to be more likely to have ME/CFS. Person A might also be more likely to...

I'd just say not to put to much stock in such mutations not being genome-wide significant hits because that's quite a high bar to clear. Hopefully, someone who knows how to do it properly digs into the specific mutations. The following is not definitive. I barely know what I'm doing and could...

I think one potential way to find evidence against concepts is a mendelian randomization approach. Not the questionable versions we see pop up here where they just take SNPs associated with eating breakfast or whatever. But the good MR where you take a mutation definitively known to increase or...

That's what makes the natural experiment of the first study above useful. A large portion of the people who didn't take the vaccine didn't take it because they weren't allowed to. I think what they did was more sophisticated, but a crude way to test the effect of vaccine on dementia is just...

A Reddit user's criticism of the study: Link to Reddit Copying the main bulletpoint headings: 1. The reported improvements, while statistically significant, are small and clinically of no significance to patients (MCID not met) 2. The primary endpoint of the study was safety (TEAEs), not...

Isn't it more just indicating that TNF might have nothing to do with ME/CFS? Or is that what you're saying?