Just a little update.
The data collection is complete, the A2 seems to be out of the test subjects systems (all readings on vision have returned to normal).
We will now begin the process of writing up the project and then will be sending it to associates for editing.
I’m late to the NIR vision party, but I just found out about your work through the ce6 sensationalist reports.
Please consider in your writeup the fact that 11-cis retinal, the typical chromophore used by both rods and cones, has a peak absorptance of ~380 nm in a spec. It is the tertiary structure of the opsin molecules that defines their absorption peaks, not the chromophore itself. Vit A2 or 2-dehydro-retinal, much like the photo-inactive counterpart all-trans retinal, shouldn’t function in normal opsins at any wavelength.
The reactions that occur in the retinoid cycle between photoreceptors and the RPE involve numerous intermediates as vitamin A1 is converted to the chromophore 11-cis form. Have you considered how VitA2 is being isomerized to an 11-cis form (if at all)? Have you thought about how vit A2 is sterically different from A1, and how will those differences change the interaction of the chromophore with the lysine 296 residue on the opsin molecule? How might a similar, but not perfect match, for the natural retinal destabilize the opsin that it binds to?
The secondary point that most of these discussions/comments have missed is that once an opsin molecule is active, it doesn’t matter what set that activation off. It doesnt need to have been a photon of any particular wavelength. Color vision or opsin peaks simply represent the most efficiently absobed wavelengths. Cone opsins in particular are inherently unstable, and spontaneously activate multiple times each minute. Rhodopsin is much more stable, but it still occurs (~0.01 events/minute IIRC). Ever been in a photon-free environment like a cave for a few minutes? Those spontaneous random little flashes you see are aberrant rod signals. Spontaneous isomerization is also sometimes called thermal isomerization. See where I’m going with this? When interpretting and presenting your results, I think your group should carefully consider (1) the potentially destabilizing effects that vit A2 may have on opsin molecules and (2) the potential increase in thermal isomerization rates that would occur due to heating of the retina by exposure to infrared light. Possibly begin by asking the test subjects what kind of form (if any) could they perceive with IR stimulation, because if stimulation were predominantly thermal, acuity would likey be limited. You would probably still record higher amplitude a- and b- waves, although the recovery times might be delayed if the opsin-chromophore complex is actually destabilized.
Now, having just read the (somewhat petty) argument between your group and Dr Jones, I wonder what kinds of issues your group has since resolved, and what a peer reviewed publication might constitute at this point. I’m currently on my phone, but would be happy to provide references to my statements and open a dialogue on this topic.