ehhhh iono homie those don’t look enough like oysters to me, normally they have that ‘shelf’-like appearance, with short stipes if they have stipes at all, and dont connect end-to-end to make the cuplike shapes i see here. stipe is a v different color from the cap too, not used to seeing that. there’s variation of course so i could be wrong, but this is making alarm bells go off in my head.
even if they are the translucency makes me think they’re a little too old to eat. in a game where being wrong can cost you your life, best to play it safe imo
These look like unusually light colored jack-o-lantern mushrooms to me, but I’m no expert at all. Do they fluoresce under blacklight, or glow ever so slightly in the dark?
I haven’t heard back from my buddy yet, and the probability that he will offer a definitive ID from those photos is almost zero, however, I am almost certain those are NOT osyters.
I can’t say either one specifically, and honestly I don’t know that even if it did emit a bioluminescence that it would inherently be fluorescent as well. But I know the jackolantern does emit a very faint light, and the thought popped into my head.
In 2004 erythromelalgia became the first human disorder in which it has been possible to associate an ion channel mutation with chronic neuropathic pain,[2] when its link to the SCN9A gene was initially published in the Journal of Medical Genetics .[3] Later that year, in an article in The Journal of Neuroscience , Cummins et al., demonstrated, using voltage clamp recordings, that these mutations enhanced the function of NaV1.7 sodium channels, which are preferentially expressed within peripheral neurons.[4] One year later, in an article in Brain , Dib-Hajj et al., demonstrated that NaV1.7 mutants channels, from families with inherited erythromelalgia (IEM), make dorsal root ganglion (DRG, peripheral and sensory), neurons hyper excitable, thereby demonstrating the mechanistic link between these mutations and pain, thereby firmly establishing NaV1.7 gain-of-function mutations as the molecular basis for IEM.[5]Conversely, in December 2006 a University of Cambridge team reported an SCN9A mutation that resulted in a complete lack of pain sensation in a Pakistani street performer and some of his family members. He felt no pain, walked on hot coals and stabbed himself to entertain crowds.[6]