Why use control samples from before COVID? Of course they won't have SARS-CoV-2 proteins. We're interested in whether people who have had COVID but didn't get long COVID have those proteins.
Possible long COVID biomarker: identification of SARC-CoV-2 related protein(s) in Serum Extracellular Vesicles
Asghar Abbasi, Ritin Sharma, Nathaniel Hansen, Patrick Pirrotte & William W. Stringer
[Snippets from correspondence with no abstract, bolding added]
Web | PDF | Infection | Open...
Associations between lung and endothelial function in long COVID: Two years after acute infection
Lêda Leonôr Mendonça Carvalho, Cássia da Luz Goulart, Gabriele Da Dalto Pierazzo, Ester Laura Cordeiro-Costa, Audrey Borghi-Silva, Adriana Sanches Garcia-Araújo
Highlights
• This is the first...
I'm imagining if a treatment was widely released and tried with a portion of people recovering and a portion not. There's a good chance there'd be different DNA signals in the two groups that become much clearer when they are looked at separately. And it'd be much cheaper to hold on to existing...
That the finding probably isn't consistent in all people with SSRD (maybe different underlying reasons for getting the diagnosis in the other cohort), if it's a meaningful finding at all.
Edit: Or it's a very tiny effect that the smaller sample size couldn't detect.
Or maybe there is a lot of heterogeneity, but they identified a gene responsible for only a subgroup. With such a large sample size (22k), that might have been enough to get significance for a gene related to only a portion of these people's diagnosis.
But they got a genome wide significant hit. Maybe it's because the gene makes people seek out FND practitioners or participate in studies or some other non-interesting reason. Or maybe the people who get FND/SSRD diagnoses do have some biological causal factor in common, even with the diverse...
What specifically is the concern? You'd agree that the FND group is likely sicker on average than the healthy group, right? If a gene was significantly associated with being in the unhealthy group, then there's a good chance it's causal for being in that group.
GeneCards:
CYP7B1
BHLHE22
CBLN1
CYP7B1 (the main SNP from this study maps to this gene) was previously flagged by @mariovitali:
One person out of twenty from this study had a likely pathogenic variant in the same gene (Supplementary Table 1):
A network medicine approach to investigating...
Genome-wide study of somatic symptom and related disorders identifies novel genomic loci and map genetic architecture
[Line breaks added]
Abstract
Somatic symptom and related disorders (SSRD) are characterized by a mixture of neurological and psychiatric features and include functional...
The AI translations on the non-English songs are probably the best I can get without speaking the language myself, but if any native speakers ever want to correct any parts of the translated lyrics for these songs, I will make the edits.
No need to do everything at once. If there's a study that's central to the hypothesis, you can make a thread for just that one to start. Normally we don't add any color commentary in the first post either, just the abstract, so you don't have to add comments immediately either. Maybe others will...
Nature: 'One potent gene raises risk of Alzheimer’s, Parkinson’s and other brain diseases'
'Massive proteomics database links gene variant APOE4 to chronic inflammation.'
'A gene variant known to increase the risk of Alzheimer’s disease also makes people vulnerable to a host of other...
APOE ε4 carriers share immune-related proteomic changes across neurodegenerative diseases
Artur Shvetcov, Erik C. B. Johnson, Laura M. Winchester, Keenan A. Walker, Heather M. Wilkins, Terri G. Thompson, Jeffrey D. Rothstein, Varsha Krish, Farhad B. Imam, The Global Neurodegeneration Proteomics...
Oh yeah, I'm familiar. I don't think I have an issue with just making the code public immediately.
Thanks for the suggestion! Maybe I'll reach out once I have at least like a couple hundred studies saved.
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