 to make a clear-cut assumption, but they may be associated and more experiments are definitely required to obtain condensate inclusions. The possible functions of nestin, nestin may have a pivotal role in the transport and secretory functions, and nestin may also be involved in structural remodeling of tannicytes required to regulate the release of gonadotropanolasing hormone. So where should we go from here? Firstly, we should explore the possibility of other proteins. We shouldn't keep ourselves constrained to simply looking at nestin and proliferation. We should look at g-lasts, which is an immature, reveninous cell marker. We should look at bimentin to see if maybe they are involved in cell proliferation. And we should also study proliferation in cells of the third ventricle for longer durations and by changing the microenvironment, because what happens is these cells are currently in a very quiescent state, and probably we're just not motivating them enough to come out of that state and actually start dividing, which needs to be done. And so I know all that I've told you so far may seem... I mean, so basically there is no clear-cut hypothesis so far, but there's one thing for sure, and that is that nestin is currently being expressed in mature cells, or cells that are not dividing graphically, which means that using it as a universal stem cell marker is slightly out of the way, because we might get misleading results. So it's important that we realize that nestin may not always be present only in stem cells, and it may be present in other radios also. And I'd like to thank the Kareel laboratory, especially Professor Ronald Kareel. I mean, he has been the most brilliant PI ever. He's always, he's literally guided me by hand and shown me how to do everything. I'd like to thank everyone else in the lab, Michael Henrickson, for showing me how to do the editing. Scott for teaching me the entire immunostaining and always being there, whenever I had a problem I'd go to him and he'd always have the answer. I want to thank Maria for the sessions over ice cream that we had. I'd like to thank Professor Raseem Ansari, and I'd like to thank Ms Jenny Darwin and Professor Steve Johnson, they're here, and they took me into their own program and treated me just the same. And I'd like to thank my fellow Karana Scholars and the Karana Scholars Program, IUSSTF and DDT for their family. Thank you. I'd like to take questions. The whole story, what else do you think would be a good marker that I want to use, and where do you think Nestle stands at in that sense? So, that's the problem. Currently, there are many reports that state that Nestle is not a reliable stem cell marker, but simply due to lack of other options, we have been using Nestle. But however, there are more other stem cell markers such as SOX2, which is expressed purely in stem cell. So maybe instead of what I propose instead of simply staying for Nestle and saying that there's maybe a stem cell, we should use other markers also, and maybe if all of them are being expressed at the same time, then we can conclude that it indeed is a stem cell. So point earlier that Vimenta destabilizes Nestle, and Nestle destabilizes Vimenta. Yes. Is this a dynamic process for once you set up the Nestle? So by assembly, I mean that, so we have these monomers of the proteins, and considering the intermediate filament proteins, these monomers have to become dinarized and then they become tetramerized to form the entire cytoskeleton structure. So Vimenta is necessary for Nestle assembly because Nestle is not capable of cell assembly. Usually the IFs are capable of cell assembly, but Nestle has a very short end-terminus sequence, protein sequence, due to which it requires Vimenta. And the converse for Nestle being important for Vimenta in this assembly, it's a very recent paper, in fact. And so this has been observed only in dividing cells, which means it's an ongoing process, not just static one. So at the end there, you had an interesting idea. These rats are like that picture says, they're just basically sitting in a cage doing nothing, eating, sleeping, and so forth. Do you have ideas as to maybe ways to challenge them in either with, I don't know, change environment or toxins or something that might get turned over in the cells in the third ventricle, in the penable cells? I mean, it seems like they might be turning over slowly, but what kind of things would you do to kind of get them to go? There have been reports which state that under injury conditions, the cells begin to divide more rapidly. So some reports have been conducted on specific injury areas to see if the rate of proliferation have increased, but nothing convincing has been discovered so far. So maybe if we could try and make more injury conditions, maybe near the third ventricle or somewhere around the brain stem, which may affect proliferation. And then there are also other factors such as maybe some kind of medications which do, but again, they wouldn't be convincing enough to prove spontaneous proliferation. So that's the thing. That's a totally different area where we would just be proving that they are capable of dividing, but that's not what they're normally doing in the first place.