We also report a whole-gene duplication and common noncoding variants in a novel locus, PDZK1, which contribute to FH risk in some patients. This finding replicated in the UK Biobank (UKB), highlighting the value of genetic studies in non-European populations.

We found rare pathogenic variants and structural variants in known FH genes (and APOE, CREB3L3, PLIN1) explaining FH in 67% of families. High LDL ancestry-adjusted PRS (Galatea's StrataRisk PRS) also showed substantial additional risk.

Because FH genetics has been studied mostly in Europeans, we analyzed 300 patients from the Mexican FH registry using exome plus short- and long-read whole-genome sequencing.

Maybe a fitting place for it - next to the historical collection of eugenic journals and books that originated from this building.

You can still find it - inside the Carnegie building back staircase.

And in the meantime China is stating to block for some application purchase of foreign chips to bolster their home brew industry - at some time in the not too far future they will match capabilities and these controls will do more harm than good.

🤣

Very well put. However, how often most coding tasks require truly novel algorithm development outside of the academic arena? Often, the value of having a team member with a CS PhD is their ability to recognize that a problem being tackled has already being solved and applying the proper algorithm?

2. Here's the paper itself: arxiv.org/abs/2510.19894

And there was no abstract search tool this time.