When the Impossible Becomes Possible in Wound Healing

[00:00:09] Hello and welcome back to Health Unlocked, The Power of Salutogenesis with Jasen Petersen. Jasen Petersen, how are you? I'm doing pretty good. We spoke in last episode a lot of things and today we want to do kind of like a next one to that to clarify a few things from that, right? So, and I know that, you know, you came back from SAWC saying they didn't believe the data. I guess, what was that like? Let's start there.

[00:00:35] Well, it wasn't, I mean, I didn't really have people like, you know, outright say, oh, I don't believe you. You're lying. Lots of people were very surprised by the data and then clear that, you know, that they didn't trust all of it entirely. But so to some extent, I guess it was somewhat expected, you know, and I, so let me back up, right? So we didn't really have a whole ton of wound healing experience going into this whole product development in Mexico.

[00:01:05] And our own experience has kind of skewed our understanding of chronic wounds, actually pretty dramatically. So while I was at the SAWC, I learned that 25 to 50% of chronic wounds never heal. And that's, that's even with state of the art care and so on and so forth. We haven't seen a failure yet. So yeah, we didn't understand how good our product really was there.

[00:01:31] We thought that, you know, ah, this is, you know, yeah, we're pretty good, but we didn't understand that our results were going to come off as not really possible. And remember, we didn't start in Mexico trying to sell a product. The, the, the original goal was data collection, right? And the, so the product, the ion gel, DCM 25, it's approved as an antimicrobial and antioxidant for infection control and wound healing. That's all we can really say.

[00:02:00] And so what we were doing was we were just handing out samples to practitioners and asking them to tell us what they thought. Remember, we expected it to be used on surgical site infections. We knew it was an amazing antimicrobial. So that's where we thought that it would actually be used. Had we known that it would be, you know, so much so dramatically better on chronic wounds and DFU specifically, we probably would have mentioned that. And that's why even in Mexico, Mexico, the practitioners were so surprised, right?

[00:02:29] The ion gel looks like it's a generic antimicrobial. And that's also what Mexico normally gets. They don't get these category defining new products before the rest of the world. And so, you know, once we, once we started, even in Mexico, once we started getting the chronic wound results that we were, and we started presenting that to new practitioner contacts in Mexico, we got rebuffed by many.

[00:02:57] Rebuffed might be a strong word, but you know, that, that whole 25 to 50% never heal statistic kind of explains that skepticism, right? So we really just kept handing it out saying, try it. And almost all of them came back with some form of shock. Uh, you know, some even claimed that what they were seeing was impossible. Yeah. But why do you think it is impossible? Why do they think it's impossible?

[00:03:23] Well, um, so I guess that wording really came from a doctor who was using, using it on a skin graft. And so let's see if I can remember everything. The patient had a tumor of some sorts on her forehead. I don't know that it was cancer. I still don't know what it was, but so then they took a bunch of skin off, um, around that removed it and then grafted skin on there. This, the skin graft failed pretty badly in it.

[00:03:52] Everything got infected. Um, and so the patient left the, that facility and went to a free wound clinic instead. You would say that that's maybe not the wisest choice, but luckily that free wound clinic just happened to have the, the ion gel there. And even though the wound from what I can gather the wound, that's, that's not in their wheelhouse, not in this free clinic. And all they could really do was start removing kind of the failed graft tissue.

[00:04:19] Now, I think they were simultaneously using the ion gel to treat the infection or to get rid of the infection. And so that the infection cleared really rapidly, but then the failed graft started to unfail. The viable tissue kind of around the wound started kind of closing in and that, you know, okay. So that, that's surprising. Great.

[00:04:44] But then also the failed skin graft in the middle, some of that tissue became viable and then started spreading out. And that's what they didn't really understand. Right? So practitioners almost think of non-viable tissue in a skin graft is dead. And, and it never goes from, from not taking to take it, but that doesn't happen. You kind of have to start over again. But so this case shows that the tissue obviously isn't dead, right?

[00:05:13] So ion biotechnology is, is good and all, but it's not going to resurrect anything that's dead. This also then explains why at the conference SAWC, the data was hard to believe, right? Again, the, the state of the art still leaves that 25 to 50% of chronic disease or I'm sorry, chronic wounds, um, from completely healing. Right? So it will never heal.

[00:05:39] The, I actually want to back off on that a little bit because there might be some, well, we can get the wound to heal, but then it doesn't stay closed and it just opens back up again. So let's set all that aside for a second because somebody might say, ah, you're not comparing apples to apples. We can get something to close once too. Um, so again, there, there might be some recurrence built into that number that, that, that just confuses what we're talking about. So let's go directly to, to a product comparison.

[00:06:06] Um, if you remember, um, right? So that's the tissue growth factor. Um, that's, you know, a more advanced, uh, wound care. Um, but so even something like that, an advanced product, it doesn't heal non healing wounds. It really is just an accelerator. So healing non healing wounds, that's actually, that's a big deal.

[00:06:35] And even tiny inroads are, are fairly significant. And so, you know, when somebody comes along and presents data saying, well, every non healing wound responded, and we got an average of 80% closure within just a few days over a month. What was it? 33, 34 days. All of the infections cleared, including ones that state of the art antibiotics and antimicrobials can't touch. We didn't find any resistance and, and there were no adverse effects at all. That doesn't sound real.

[00:07:05] And on top of that, this was developed outside of academia by, uh, you know, I'm not a PhD or an MD. So it's really easy to assume that I don't understand the co-founders here. And honestly, right. That would have been my assumption there as well. Yeah. Where would they think that you were wrong? Like, is there a specific area or is just more because of your training and credentials? Yeah.

[00:07:31] So remember that from the cratogenic point of view that this is what they've been trained on. There are four phases for wound healing. There's the, uh, hemiostasis, inflammation, proliferation, and remodeling. And that matches almost directly to the CDR. Each one of those phases has different cellular requirements.

[00:07:54] So if a cratogenic product drives a particular cellular action, a single product works on, or even if a single product works on one phase, it shouldn't work on in another. Much less all three.

[00:08:08] So antimicrobial, which is about all we can say for the ion gel belongs in that inflammatory phase where you're trying to get rid of it, not inflammation, trying to get rid of pathogens and something like growth factors belong in the proliferation phase and some sort of, uh, sort of remodeling support, um, in, in the later phase. And here I presented an antimicrobial used on refractory wounds.

[00:08:34] Now, maybe we've got the best antimicrobial in the world and it eliminated every micro. That's still doesn't explain to them while the other deficiencies in cellular function suddenly appeared and suddenly started, or I guess the deficiencies disappeared, suddenly started working. So from their perspective, something's missing here.

[00:08:56] And it's really easy to see a retrospective study by a non PhD and assume that I just don't understand the bias effects and so on and so forth. So what are those? Most of the cohorts, uh, came from wound clinics in Mexico. That's always difficult. Oftentimes patients don't return if the treatment isn't working. And then most studies will just drop those patients entirely. So you've got this survivor bias.

[00:09:21] When you drop non responders, it over represents your success by a lot and it under represents failures because they don't come back. Then there's also a selection bias, right?

[00:09:33] So maybe practitioners only applied, uh, the, the ion gel to wounds that they thought were healing anyways, or, um, I'll make something up, but maybe there's like, uh, a specific endemic pathogen that was keeping healing from occurring within, uh, you know, a certain area around the, the, the clinic. And then all you had to do is eliminate that one pathogen. And then suddenly all of those people who were coming could heal.

[00:10:02] So maybe something like that was going on or there could also be retrospective artifacts, right? So random data can produce patterns that aren't real or they're real, but not repeatable. But here's a really good example. Have you ever heard of the, uh, the Superbowl market indicator? That was where when a team from the NFC one, the overall market would go up. And if the AFC team one, then the market would go down.

[00:10:29] And that held for like the first 28 years of Superbowls. Obviously there's zero causal mechanism there. It just happened. Yeah. So that's the type of data that you can pull out of a retrospective study. Say, look at, look at what this does. You know, when this team wins the Superbowl, the market gets better. That doesn't make any sense. Okay. Right. I guess, you know, it's also possible that there's a poor followup.

[00:10:57] Maybe the clinics actually, since they were free clinics and let's assume the, the, they understood that the ion gel really was a very good antimicrobial. So it still had value to them. They wanted to tell us what we wanted to hear so that we would continue giving them free samples or something. And then to address it, that, that credentialing gap kind of amplifies all of that, right? Without a PhD or MD or something. The natural assumption is I don't really understand all of these co-founders.

[00:11:25] And that's all of that's kind of reasonable from their position. So I guess then the question is, how do you respond to that? Because it seems like a consistent argument logical from their end. Yes. I know it is. And that's, that's why, uh, yeah, you're right. Okay. So let's talk about the retrospective framing first. So actually a good portion of the data is actually prospective, meaning that we gave the practitioners the gel.

[00:11:53] We told them to apply it to wounds and report back. And they, they tracked patients from the start. They had the patient sign everything that they needed to, so on and so forth. Didn't presented the, the entirety of the cohort as retrospective though, because it wasn't all prospective. And so that's a conservative call, but that also lets critics then assume that the data is significantly worse than it actually was.

[00:12:18] And then I guess for the artifacts, uh, the retrospective artifacts, handing somebody something and letting them tell you what it worked on can actually exacerbate that, that artifact or develop those in the first place. So really normally what retrospective signaling means is, Hey, there might be something here. We're seeing a pattern. Now let's study it directly to see if this is real.

[00:12:42] And once we saw wound healing or that wound healing signal early on, uh, you know, not, not necessarily in this study, but you know, they kept coming back saying, Hey, this stuff works really well on moons. That's when we kind of switched to the, the prospective study of clinical or I'm sorry, chronic, uh, wound healer. And Dr. Cardenas at the IMS system, his subset, I believe is almost completely prospective. Um, and that's 30 some patients.

[00:13:12] Uh, and I'm told that we, it's now made, we were supposed to get another 30 some last month, but you know, again, with a free wound clinic, it's tough to get things done on time. So whenever that's coming, that's coming. Um, and then there's another private hospital group down there that I think is doing a stronger study, probably of about the same number of patients. So that's all going to be prospective as well. So all of these things will be good.

[00:13:41] But again, so some of this is perhaps my experience showing how I, how I presented the data and just assuming that, Oh, well I better call this retrospective because it's not all prospective. Well, yes, but it might've been better for me to actually separate it out and say, this was the retrospective side. This is the prospective side. Because when I did that, the prospective data actually comes out even better for different reasons. Some of it is some of the wounds weren't as large.

[00:14:07] And so if all you're looking at is time to wound closure, well, obviously a smaller wound, assuming both wounds are closing, the smaller one's going to close faster. That just makes sense. But so let's see then on the, the survivor bias or the dropout bias, I think there are only like three patients that dropped out of the entire cohort. And they did that because it stings a little. So those might not have been the diabetic patients because normally diabetic patients can't feel the stinging, but their data was included anyways.

[00:14:36] So, um, I, I mean, it actually, it made it look worse. I didn't drop them out entirely and then just set, you know, not include their data. I assumed that, okay, it didn't do anything because that, that was the only thing I could assume. Cause they didn't come back. So really, I think I had mentioned last time about how up to for, for most wound healing products

[00:14:58] for their clinical trials, they drop like up to 90% of patients that, you know, basically saying, oh, you, you don't have the capacity to heal well enough. We don't want you in our trial. And that's what, that's just the assumption. When I talked to people at that conference, they just assumed that's what we were doing. And that's, you know, we've, we've done just the opposite. Actually almost except for the burn wound.

[00:15:26] I think almost all of the other, if not all of the other cases in the cohort were refractory to whatever care they tried. I listed that as standard of care, but there were a couple that were advanced as well and nothing worked. So we didn't go and select the 10% most likely to heal patients.

[00:15:50] We actually took, I mean, almost a hundred percent of our cohort was patients who for whatever reason are not healing. So dramatically different framing, I suppose. And I guess, you know, so then the other thing is the, as far as the selection bias, I guess, the cohort spans multiple clinics in different locations. So the pathogen, you know, that, that one fictitious pathogen that keeps you from healing that didn't exist.

[00:16:17] And, you know, at least some of them were MRSA. One was Candida. I think all of the others were just something that never got identified. Um, the wound types weren't uniform. We had DFUs, DFIs, venous ulcers, pressure ulcers, a couple of surgical wounds, as I mentioned, the burn and then a skin graft. The biggest commonality across all of the patients or everyone within the cohort was that I think over half of them were diabetic. Yeah.

[00:16:46] But so, and then I guess going forward, um, I should clarify that I'm using a Kaplan-Meier analysis to look at the data. And so what's normal with a KM analysis is that you don't, you know, when somebody drops out at a certain point, you include all of their data up to that point. And it doesn't penalize you for losing them.

[00:17:14] So they, so you don't pull them out of the, out of the data entirely. And so by explicitly stating that people are going to immediately then assume that, oh, well, there's more data in this than pulled out of this. If that makes sense. Yeah, it does. But you know, how is this different from how these testings are done right now? They do the same data collection. There is still the same way they leave out a group. It's not much different from that.

[00:17:43] So I don't understand why the question your data versus what's market data looks like. No, there. So remember retrospective. Nobody does clinical trials with retrospective data. That's, that's not, that's not really how that works. Right. Because again, there are too many holes in retrospect, or there can be too many holes in retrospective data. And that, that was the issue is I was trying to plug all of the holes at the same time, but also call it retrospective data.

[00:18:07] Um, so to do a clinical trial at worst, you would say, this is what we're trying to test. This is what we want to do. And then you look for it. You don't look backwards and say, what was it that we found out? And that's kind of the way that at least that's how it came off with how I presented it. But then on top of that, you know, if you want to have a placebo control and so on and so forth, or at least a comparator. Right.

[00:18:34] Now, in our case, all of that costs money. Right. And you know, we're giving the stuff away at free clinics. Remember, we tried to do this through a nonprofit. Originally, we didn't have the money to do big clinical trials and we didn't really need it at the time because it was an approved product. And all we were really trying to do was gather data. Now that we want to bring this to the US, it does change a little bit and we are going to have to convince people a little bit more. So we're going to have to do some of that.

[00:19:04] Now, one of the things that we'll never be able to do, I don't think we'll ever be able to do a placebo controlled trial because. This sounds weird, but the efficacy is too good, meaning. Well, the efficacy is too good and the visual results from it. Right. You get that kind of dark copper impregnated kind of scabbing. So you immediately see it.

[00:19:31] And I think in almost every case for these wounds that now even at a very small amount, but still within like one application, they've sort of. You saw a change already. Now, you can't have if your placebo doesn't do that. Well, then after one application, both the patients and the doctors immediately know who's in what side of your of your study, whether they're a placebo side or, you know, so it doesn't really make sense to try and do a placebo controlled study here.

[00:20:02] We could do a comparator, perhaps, but, you know, that that gets a lot more expensive. So I guess the then the question is, how do you address the impossible thing is possible part? Okay. Yes. Um, so let's, so this is most of the, the impossible verbiage came from the doctor who saw the effect on the, on the, on the skin graft.

[00:20:27] So remember the four healing phase or the four wound healing phases, each one of those needs kind of a different cellular behavior. And if one product is, you know, forcing a specific cellular output, then one product shouldn't be able to serve all, all of them. Um, that, you know, so that logic is correct.

[00:20:46] If the project product is cratogenic, really it's effectively impossible for a single cratogenic product, whatever it is to do many desired things at once with also without also doing at least some of the things that you don't want. But, but the difference here isn't that, uh, eyeball isn't cratogenic and that's kind of what breaks this frame here. Um, right. So let me run through that again real quick, cause I might've been a little confusing.

[00:21:12] A cratogenic product kind of binds to a target and then forces that particular cellular action. Eyeball doesn't have a target in that sense at all. It simply supplies the ionic cofactors that the cell already uses. And then the cell determines, you know, whatever action it's going to take. That's why so many desired, put that in little finger quotes, desired cellular actions can happen. Yet it's across all the, let's go through the phases.

[00:21:39] So you've got the inflammatory phase, zinc and copper are used for immune signaling. I suppose you've also got the direct antimicrobial action there, oxidative burst regulation, MMM activity, then the proliferation phase. The same ions then start supporting the collagen crosslinking and angiogenesis and fibroblast proliferation.

[00:21:59] Um, and then the last remodeling phase, um, again, same ions, zinc and copper still support scar maturation more kind of now, I guess we're at, uh, MMP, uh, rebalancing and then, you know, full return to homeostasis. And, you know, so that, that from the outside, this looks like a single intervention working across all of those phases from the inside. You know, it's simply the cells are whatever they're, they're running completely different programs.

[00:22:28] They're using the same cofactor pool for each one of those programs, but the doctor didn't understand. And he was thinking about it through a cryogenic mindset. So what he saw happening from his viewpoint was impossible. And really we do have to think of this, something of a, of a nutritional analogy, right?

[00:22:51] So you don't, you don't take vitamin C in the inflammatory phase and then, you know, whatever, take something different in the proliferation phase. You just eat and, and then your cells use whatever raw materials that they've got for whatever it is they need to do. Right. So eyeballs a little bit closer to, well, it actually, absolutely. That's what it is. It is localized nutrition rather than a drug.

[00:23:17] And so for, you know, so really that is terrain support. And, um, I think, I think we discussed this a little bit in the last episode and there might've been some concern that, oh, you know, that's just like regulatory verbiage softening. It's not. That's actually the most scientific description of what eyeball does. The cells are what are doing the healing eyeball simply.

[00:23:45] And in this ion gel as well, simply making sure that the cells have the resources that they need at the local area that they need them. That's it. But I can also completely understand why that looks impossible. When you think that a drug is forcing an action and you think that this is a drug that is forcing actions, how could it force all of these different things? Well, it doesn't. It's not how it works. Yeah.

[00:24:11] I think the key here is the, everything here is that it supplies cofactors the cell already uses, and then its cell decides what to do with them in different phase. Right. Which is why it's like the healing will be different based on whatever is the, you know, the cycle where the wound is. Right. So that's what it is. Exactly. And that's also why it gets discounted because you just described nutrition. Nutrition has been around for a long time.

[00:24:41] People have been supplementing for a long time. There, you know, not too many diabetic footholds have healed from, you know, taking some supplements. It doesn't work that way. But that's because no one's really dug into the local demand versus systemic supply and how there can be a mismatch there. Yeah. So what's the bigger frame here then? Can you go into those details? Yes.

[00:25:05] So I guess the way that I put this is there are really, there are two ways to intervene in a biological system. One is the cratogenic, which is you force a specific action by binding a target or whatever. And then the cellogenic. Um, and maybe I should say enablement for people who don't understand what cellogenic means. That's you supply the cells with the resources they need and then, then let them decide what to do. Most of modern medicine is cratogenic.

[00:25:34] And I don't want to say that that's necessarily wrong. It's just, it's a tool set. Drugs that, you know, block or activate or remodulate different cellular actions. They, they can work when the, whatever the problem is, is, you know, a single dysregulated pathway in an otherwise functional cell. And actually, uh, I know we poo poo cratogenic medicine a lot, especially in this, uh, in this podcast, but it does have its place.

[00:26:02] Um, a really good example is familial hypercholesterolemia. I hope I'm saying that right. Basically that that's when there's a germline mutation of one of the two, uh, LDL receptor, uh, alleles. And so the, what happens is the cholesterol clearing pathway becomes dysfunctional, but the rest of the heptocyte is functional.

[00:26:25] And so statin drugs here in this particular case can block that, the endogenous cholesterol synthesis. And then the cell compensates by upregulating the other receptor. And that whole situation is a single target with a single pathway of an otherwise functional cell. And, but in truth, most disease isn't that kind of problem.

[00:26:50] That's really why we focus on celludogenesis in general and cell eugenesis in particular so much in this podcast. But I also have to admit that cell eugenic medicine isn't perfect either, right? That, that case that, or the, um, the familial hypercholesterolemia that take that as an example and having sufficient metal ions or cofactors wouldn't really do much.

[00:27:18] Cause all of the, I mean, a way to look at it is you can have all the resources in the world to like build any type of house, but if you don't have the blueprints, then all of those resources don't do you much good. Cause you don't know what to do. It's kind of the same thing happening here. And so in that case, yeah, we, we need something to come along and actually send the signal that the body should be sending, but we don't have the DNA program to be able to do that.

[00:27:44] But I guess another thing might be if the cellular damage ever becomes so great that the cell just can't do anything, even if it had the resources, that might be another case where, where, you know, just, just resourcing the cell could fail. But here's what I want to really emphasize and point out. So yes, it's true that having all the resources doesn't necessarily guarantee success, but not having the resources is a pretty sure bet that you're going to fail. Right?

[00:28:12] So from that, I would actually say that there are two kind of big ramifications. One is saluted genus met saluted. Holy cow. Cellogenic medicine should always be first. It actually should resolve most problems. And if it does, then there's no need to, you know, for the, for the more dangerous cratogenic intervention. And remember, cratogenic interventions are dangerous by definition, right? They're forcing a cellular action.

[00:28:41] And that always carries off risk or off target risk kind of every time. Then the second thing. So the first thing was that we should start with cellogenic medicine. The second thing was that even when it's truly indicated, cratogenic medicine can still fail when the cell isn't resourced sufficiently as well. Right? You know, the cratogenic signal is coming through saying cell do this and the cells I'm trying, but I don't have the raw materials to be able to do it.

[00:29:11] So I would say that the second thing here is that cellogenic support should be undertaken even when following the cratogenic model. So those are the two big things that, that I want to say is the bigger frame. Yeah. Okay. And now, of course, the final question. So where does this go from here? Okay. So what I need to continue doing here is a bunch of work.

[00:29:38] First, I do need to start getting into publishing more. So we've talked about that first paper, the Microimmune Dynamics Hypothetical Framework. I've got to get that in somewhere for peer review.

[00:29:51] So, and I'm, I'm actually taking a while there because originally the, that paper was going to talk about mostly kind of general cellular healing and then have a second paper present the chronic wound, the real world experience for the chronic wounds as a quality of validation.

[00:30:12] And I'm shifting that a little bit so that the first paper can now focus a little bit more on the CDR phases themselves. And so with CDR1, we've got chronic wounds and more specifically, I guess, diabetic foot ulcers. That can get presented in another follow on.

[00:30:33] And so the idea here is that the framework paper is going to lay out the framework and then make a bunch of specific predictions based off of what happens in persistent CDR1, 2, and 3. Then that lets us have follow on studies and papers looking at each one of those cases. The first one is that chronic wounds and diabetic foot ulcers and CDR1.

[00:31:00] Then I would probably jump to CDR3 and look at, that's where lots of autoimmune things occur. And I would use the efficacy on psoriasis as psoriasis and eczema, I guess, as the qualitative validator there. And then, then we can go back to CDR2, which would be cancer. It's a reason I'm not doing it second, because that scene is a lot more critical and people are going to.

[00:31:30] Question it a lot more. And so for that one, we're going to go with looking at results on skin cancer. And the reason I'm using, you know, wounds, diabetic foot ulcers, psoriasis and skin cancer for, you know, the CDR1, 3, and 2 or 2 and 3 is because you can also see it really easily.

[00:31:49] You don't have to do really expensive testing to look at, you know, what cofactors, what level cofactors are the, you know, the specifics of where certain cellular functions start to break down or not to happen. And, you know, CDR progression doesn't, we don't have to look at any of that. It's really easy. First of all, also the delivery is very easy. It's topical. You slap it right on there. There's no question about how are these ions getting to where they need to be. You're putting on that. That's straight, really straightforward.

[00:32:18] Then the second is, okay, well, is it doing what you say it should be doing? Well, you can see it. You either see it is or you see it's not. So there's really no way for me to lie with that. So that's all the publication and everything, I suppose. Oh, and actually, I guess I mentioned also with that paper, I do want to tie it all together with aging. And aging really is not one specific CDR persistence.

[00:32:44] It's cells getting stuck across the entire healing cycle somewhere. Then they become senescent. And then everything that follows from that, that maybe at some point, someday we'll have a study to look at that as well. But that's really going to have to, you know, unless we're going to wait, you know, 50 years or decades to see how well this works. That's going to have to be done quantitatively looking at ion levels and so on and so forth. So let's see, what else are we doing?

[00:33:11] We're going to have to, we're going to continue using the ion gel in Mexico, right? So were we a conventional setup company trying to just maximize ROI, we would shut Mexico down now because we got the data we needed. We've identified it. We have identified a high value indication and then we'll develop that indication in the US. And I mean, I don't want to say that we're not doing that. We are also doing that.

[00:33:41] But we've got something in Mexico that's helping people right now. And it's an approved product. It's not the most, it's not going to give us the highest returns. It's not the most profitable thing. We could have done it a much more profitable way. Yeah. But again, it was intended just to collect data. But now that it's helping so many people, remember all of those people that have used it. Well, not all of them.

[00:34:04] Many of them were, you know, at risk of amputation and we've salvaged every single limb. That's, that's a big deal. So we're going to continue doing that even if we don't make a ton of money doing it. Let's see. Oh, the other thing to talk about is the IP. I'm actually still cleaning up a few things with the patents. And then once that's done, then I'm going to really start pushing all of this information out to the world, I guess in as, as many ways as possible. Hopefully I can, I can call on you to help with some of that.

[00:34:32] And then I guess also the business development. So again, the original testing and data collection, all that stuff's been done in Mexico. We are now going to try and start bringing this to the U S for a diabetic foot, um, ulcer and diabetic foot infection. And that means that I'm going to have to start focusing a lot more on fundraising and trying to get the money that, that it will take to bring this to the U S. And we talked a little bit about decentralized science.

[00:35:01] That's still on my radar, but there, there are a bunch of other things that I really need to get better at. And all that's going to be starting here pretty quick. Maybe we can go a little bit more deeper into those in some future episodes as well. Yeah. Okay. Well, it, you know, I know you mentioned about cleaning up the IP. We, do you think we'll have a conversation on this on our next, next episode, more about the patent, go into more details of those. Sure.

[00:35:30] That sounds like a plan. Yeah. Yeah. And, uh, of course, you know, it's a, it was useful conversation today to connect from, I felt like there were some open-ended dots that we left from the previous one as we were covering the whole thing. So this was a good, uh, good to closing the loops on some of the things that probably needed some more explanation. So I, once again, appreciate your thoughtful explanation to everything.

[00:35:58] We'll conclude this, uh, conversation right now today, and we'll be back with next one. Thank you so much. All right. Thank you.