A pig kidney was vitrified, stored at -150 °C for 366 days, rewarmed in under six minutes, and made urine again (albeit in reduced amounts). The Bischof and Finger groups at the University of Minnesota, just posted a preprint on vitrification and nanowarming of ~100 g pig kidneys. The interesting thing is that's roughly human kidney size and about 100-fold larger than the rat kidneys from a few years ago. The key factors that make this work are: - A new CPA named “PEZ42” which allowed them to scale up to the 100 g kidney, which was not possible with M22 - Loading at temperatures below -15 °C to suppress toxicity. - Annealing at -114 °C to avoid cracking. - Their nanowarming technology (Iron oxide nanoparticles,RF coil, rewarming at ~32 °C per min). How PEZ42 differs from M22: both include DMSO, ethylene glycol and the ice blockers X-1000 and Z-1000. But PEZ42 doesn’t include formamide, N-methylformamide, 3-methoxy-1,2-propanediol and PVP, and adds propylene glycol and a bit more Z-1000, and is less concentrated overall. PEZ42 is also less stable: M22 vitrifies at ~0.1 °C/min and needs only ~0.4 °C/min on rewarming. PEZ42 needs 2.3 °C/min on rewarming at the expected concentration. But that is not an issue in this case, since nanowarming achieves a warming rate ≈14x faster than that. Short summary of the results: 8 kidneys on machine perfusion showed immediate blood flow and urine. Function was worse than after 24 h of cold storage. But it was similar to kidneys that only had CPA loaded and unloaded, but not cooled. 3 transplants into pigs made urine immediately over a 2 h observation. The CPA-only comparison is the key result. If vitrification and rewarming add little measurable damage on top of the chemicals, the physics at this scale is largely handled. There are a couple of caveats to keep in mind: it's a preprint, so no peer review yet, it was only one kidney at 366 days, no survival data, and the transplanted grafts showed more endothelial injury on histology than cold-stored ones. So what does that mean for Human Biostasis (my take): 1) Humans, even brains, are still much bigger. And viability is not yet the primary endpoint for human Biostasis but rather complete perfusion and structural preservation. 2) Progress is always great. The Biostasis field is still small and every win makes it bigger. 3) The technologies developed can be translated to large(r) scale use in humans. At least fundamentally. Case in point: CPA toxicity during long perfusions is also our biggest unsolved problem. 4) There is still a lot to do. Remember that a brain is ≈1.4 kg and a body ≈70 kg, those kidneys were 100g. They also had under 10 minutes of warm ischemia and ideal perfusion under lab conditions. So does biostasis “work” now? No. But every step that turns reversible organ cryopreservation into an engineering problem raises the odds that it will. Paper: doi.org/10.64898/2026.10.07.…

Total Recall is upon us. 🧊🧠 View the full proposal and vote: snapshot.org/#/s:vote.cryoda…

officially announcing the next @cryodao research project: $259,000 for "TOTAL RECALL" 🧊🧠 setting out to prove that complex mammalian memory can survive cryopreservation with legendary cryobiologist greg fahy and principal investigator regina monaco two complementary approaches will be pursued: testing whether learned responses survive cryopreservation in neural cultures and/or hippocampal slices, and whether the molecular changes associated with training are preserved together, these approaches target one of the central questions for cryopreservation: can the information underlying memory survive?

Cryopreservation is hard. Not least because perfusion under adverse conditions is difficult to do right. Ischemia is clearly the most common and most complex to handle. We just published our thoughts here: "Overcoming Perfusion Impairment in the Ischemic Brain: A Review" mdpi.com/2673-4087/7/4/89 Thanks to all co-authors: Andrew T. McKenzie, Aschwin de Wolf, Alexander Grotemeyer, and Alexander German