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On this episode of the sports physical therapy----podcast, I'm joined by Dave Sherman. After graduating PT school from Boston university, Dave received a PhD from the university of Toledo. And is now doing postdoctoral research work in the area of arthrogenic muscle inhibition. In this podcast, we're going to talk about AMI and his recent research publication on neural drive and motor unit characteristics after ACL reconstruction. But don't worry we're going to discuss what the clinician can do with this information as well Hey, Dave, welcome to the podcast. Really excited to have you. Thanks, Mike. I'm glad to be here. Not everybody knows this. Some people do know this about podcasts, but Dave and I've been talking for months and he's had a lot of exciting things going on in his life that's been keeping him all busy. But we've been really excited to try to get together and have this podcast episode. So it's, it's, it's great to finally have you on. Um, I, I've been following a little bit of your research lately and you've been producing some really good stuff. Um, why don't we start by, you know, maybe filling the listeners in a little bit if they're unfamiliar with. Somebody to work, but when you give them a brief information, just like on your background, what you're currently up to, where you're at. Um, I think that'd be a great start. Yeah, definitely. So I'm a physical therapist and athletic trainer. I trained at Boston University, uh, graduated now with my DPT almost 10 years ago and then, uh, moved down to Fort Worth, Texas. We worked, uh, we worked, my wife and I, she is also a sports PT. She did a residency at Texas Health Sports Medicine, Ben Hogan at the time. I was fortunate enough to convince them to give me a job so they could keep her around. Uh, we stayed there for about five years. Um, you know, five years later, 2018, we're looking around and, um, I kind of had this, this research bug. I was frustrated with some of my, uh, clinical outcomes at the time. I thought, you know, we were doing well applying the science and, um, and still I was falling short of my patient's expectations and decided, okay, there's something more to this that I should go back and look into. Did kind of a nationwide search and ended up in Toledo with a PhD program that was well aligned with a mentor, um, and like the questions, uh, looking at the questions that I wanted to answer. So I just wrapped up that PhD after five years, um, or five, sorry, four years in Toledo and I've been in Boston, back in Boston ever since. So currently a postdoc at Boston University in the division of rheumatology that's in the school of medicine and I study, um, essentially arthrogenic muscle inhibition in knee osteoarthritis, which is amazing, which obviously has tons of carry over to other pathologies and stuff. But I think that's, that's such a great way to do it. Um, you know. There's a ton I want to talk about, obviously, to your expertise, um, but I do know that sometimes people have this question, so I thought you'd be a great person to ask this too, but like, what, what made you go back to get your PhD after you were treating PT? I know you kind of alluded to it a little bit there, but like, like, I know a lot of PTs are, Maybe considering that, or maybe they don't completely understand that process, but that's like in their, their thought process. But why don't you tell us a little bit about that and like what went into trying to go, go back to school? You know, did you really love school that much? Like what was it that you wanted to go get your PhD? Yeah, uh, well, that's funny. So in PT school, I think I was the only one in my class that actually liked the evidence based practice course, you know, just thought it was like more interesting than everyone else. That's awesome. So that was something. And, uh, and so it was always seemed like a possibility. Oh, maybe there's something to this research thing. And then at Texas Health. Um, you know, it's a it was kind of a clinical scientist full time that worked there. Craig Garrison, he was running the research lab at multiple different clinics. We had force plates in the floor, motion capture cameras in the clinic. Um, so I was being a research assistant, recording data, range of motion strength, um, on participants that were also my patients. And so that kept kind of the research bug alive and then as, as I mentioned, um, in that environment, we're applying what seems like the best evidence that the stuff that's currently coming out and I'm still falling short with my outcomes with what I think my patient should be able to get back to. So that's really the motivation is I have these lingering questions surrounding, you know, what's going on in the nervous system. You have this, um, 50 percent of your census is patients with ACL injury. Um, they have this quad knockdown that you just can't seem to address. And, um, it's, it's not my, my strength program, at least I don't think it is. Uh, and they're still falling short with that persistent muscle inhibition. So, um, that's the motivation to go back. I love it. And you know, you're helping all of us at such a higher level with that, which I think is really, really great, but. Um, Arthrogenic muscle inhibition, you know, what you've essentially said you're, you're focusing your career on, at least at this point, until you figure it out and move on to the next thing, I'm sure. But, you know, this isn't, excuse me, this is an enormous thing that we face in rehab, right? You, like you said, even yourself as a clinician, you're, I don't know what the, you know, were you disappointed what it was, but like, you know, you're doing your best. You're applying all the principles of basic science, strength and conditioning stuff. We're trying to get these people stronger and they're just not getting stronger. And we feel like we're failing them, right? Um, so, you know, it's tough. And, you know, on a, on a past podcast episode with Terry Grindstaff, we talked a little about some of these neuromuscular consequences, but, you know, I'd be kind of curious from, from your perspective, like, you know, why do you think this is so prevalent? Why do you think like, I know you've Put your head down and try to figure this out. Like, you know, why do you think this, this muscle inhibition after surgery is so common? Um, the reason is it's a, it's a reflex. I mean, on the neurological level, you have pain and swelling in a joint. Um, there's a change in sensation in the periphery. Uh, your nervous system is going to integrate that change and, and respond. Um, I try to explain this as it's really no different than touching a hot stove. You have your agonist that's reaching, uh, now inhibited and your antagonist pulling back facilitated. Uh, similar phenomenon is what's going on in the quadriceps. That's why it shuts down. I mean, you have, you can have a patient the day before a knee surgery, they have a meniscus tear in their knee, they can get a nice quad activation. It's the actual going in and having the meniscectomy that creates inhibition. Um, Entering into the joint, little pain, little swelling, and the quad is now inhibited for the next few hours, days, months, depends on the pathology. Um, so, the thing to me is that a clinician cannot treat this unless they can assess it. And, um, it's really hard to see the nervous system in clinical practice. I mean, there are some... Some techniques like you could use EMG. Uh, whether or not that's valid for measuring, uh, reduction in activation is, is a, a broader discussion. Um, but that's, that's the reason why focus on, on AMI and the, and the scientific lab as opposed to in the clinic is, is hard to assess and know who has it and who doesn't, and to what extent. Um, when you're out in the wild in the clinic, so. Yeah, for sure, and you know, you recently just published a really great paper, um, kind of that, that, you know, tried to dig into this a little bit. You're looking at neural drive, motor unit characteristics after ACL reconstruction in particular, which again, hopefully we can extrapolate to other types of injuries and stuff here, but. None of us want to struggle with regaining strength, right? None of us want to deal with the long term issues that may come from that, like maybe even, you know, failure of the procedure or, you know, not returning to their activities or sport that they want to get to or worse, like. away down the road, right? I, I'm starting to have friends now at my demographic that, hey, ACL is 20 years ago that are now getting total knee replacements. And I, I think we're young, right? We're PTs. We treat total knee patients. I don't see a lot of people, you know, 45, 50 years old getting total knee replacements. So, um, so let, so let's talk a little bit about that article and let's kind of shift gears there and, and, and kind of explain that. I, I think it was a really great article. It was. It was in depth, dude. I'll give you that. It was, um, that was a detail. That was a thick paper. I loved it. I read it. I took notes. I'm highlighting it. Um, I love that stuff. You did an amazing job kind of like expanding on that. So, um, I'm going to put a link to that in the show notes for the listeners that want to read it. Like I didn't in detail. It was awesome. But tell us a little bit about why you wanted to conduct, conduct that study and really what you looked at in, in, in that actual study. Yeah. So Thanks. And, um, it's a very exciting study for me. That was over three years of work now, now finally published and out of the world to see it. So appreciate you highlighting it here. Um, the history and like the motivation behind the study is. Arthrogenic muscle inhibition first described, as far as I can tell, almost a hundred years ago called arthritic muscle inhibition described in cats with osteoarthritis. 25 years ago, Chris Ingersoll and Ty Hopkins are talking about this as it relates to sports pathologies like ACL injury and meniscus injury. Um, and they're starting to do some of the first neurophys studies, uh, quantifying the amount of like quadriceps knockdown and really hypothesizing like why that happens on a neurological motor output level, like what's happening to the motor neuron pool or the actual motor unit firing behaviors, um, et cetera, right? Our muscles are, are neurological effectors, right? They only respond to the input that they get from the nervous system. We sought out in this study to do a kind, kind of a comprehensive assessment of neurophysiology in the face of new technologies, um, in, in the laboratory. And so the, the primary one in this study is what's called decomposition, EMG. So electromyography. It records electrical activity of a muscle, uh, during a contraction and by using like a higher density array, multiple different electrodes in a small space. you can break down that signal into individual motor units, uh, and get a sense of how fast they're firing, when they turned on, when they turned off, and how large their firing amplitude was. So that's kind of the outcomes that we present in this study. We also collect some of the more traditional, um, neurophysiological outcomes being Hoffman reflex, which is a degree of Um, basically your tendon tap reflex, how excitable your muscle is in that, uh, rudimentary spinal level loop. And then, uh, central activation ratio, which is how much of your muscle capacity as a percentage of your, of your capacity, can you activate during a maximum voluntary contraction? And so, uh, we took, uh, the sample here is, uh, patients with ACL reconstruction. I think there are 14 in this study, uh, and controls. And, um, we we've put them through this array of tests. We had them trace some force. We decompose their their muscle activity. Um, and and then we can characterize in the sense of a normal or abnormal spinal reflexive loop and with respect to the amount of muscle capacity that they can activate. What are their motor unit behaviors? And how are they actually going about conducting a muscle contraction on the neural level? So that's the motivation for the study. Yeah, and, and again, amazing clinicians like myself, and I like to consider myself like with a past, you know, history of some clinical research and stuff. Uh, it's this level of in depth research that really makes such huge significant impacts on our profession and then eventually our patients. Right. Um, so, you know, again, like, you know, people, you know, obviously if Dave hasn't, hasn't convinced you yet that this, this was a lot of hard work. three years putting together such an amazing project. You should be ridiculously proud of getting this thing out there so we can all learn from it. So, you know, again, thank you. Um, but you know, my next question is going to be like, okay, so what did you find? Yeah. So what, so, um, the, uh, the big findings are that. The individuals with ACL reconstruction in their involved limb, the motor units fired more slowly at any given recruitment threshold. So overall in the muscle contraction, their motor units are firing, um, more slowly, which means that they're using more of that like type one endurant, um, muscle fiber, right? The less fatigable, uh, slower firing, um, fiber type. This was in the context of normal activation, so they could activate the same proportion of their muscle capacity, normal, what's called central activation ratio, and normal spinal reflex excitability. So we, um, we recorded those and all the participants and those were no different between group or limb. And they also had muscle weakness. So, um, that reduction in firing rate tends to explain the, the weakness in, um, in the quadriceps because we also quantified the compact muscle capacity, the percentage of motor neuron pool. Um, we also kind of hypothesized, although it's difficult to prove with the limitations in technology, that there are individuals with ACL reconstruction are also activating fewer motor units, so they're just not turning on as much motor units, and therefore we would conclude that there's less available. So, um, whether it's the inhibition process or the time since injury, um, or muscle weakness, they've actually like reduced or catabolized some of their, their muscle capacity over the years. Uh, which would not be a good thing. Correct. I agree with that. So, you know, when I was reading the study, one of the questions I had for you about this too, is that I think you noted in your subject pool that had ACL reconstruction, that they had asymmetries, they had weakness, correct? They did, yeah, so the involved limb was, um, was quite a bit weaker than the contralateral limb, uh, as well as the healthy control limb. I don't know the exact numbers, but the way I like to think of this is... I think it's easy clinicians to record strength and normalize the body mass. Three, everyone throws out the 2. 99 or three newton meters per kilogram. The ACLR group was below that threshold in this study. So I, what I wondered, right, was. If we looked at people, because you had a wide range of, you know, how far out from surgery they were, um, I wonder if we looked at people that didn't have that asymmetry and that restored their strength to, you know, would, would you assume that these findings would be essentially reversed, right? The fewer and slower motor units, like, would, would be different? Is that, you know, and, and, you know, I guess the million dollar question is going to be, you know, why are some people like that and some people aren't, right? But is, am I thinking about that correctly? Yeah, so, um, we did not, like, have the numbers, uh, quite frankly, to look at, like, who was driving that, that effect, um, and we have a follow up study that I'm working on now with similar methods, um, actually more neurophysiological methods, uh, looking at similar outcomes, and we do see a, a, a, we will replicate these findings, fortunately, um, But you're right to say that these, this sample was far away from surgery, so these, uh, the recovery of the spinal reflex has, has happened, as we know happens after about three months, um, and their, their kind of recovery of muscle capacity has, has maybe plateaued and that they're not going to get any stronger, they're out of rehab, they're playing sports, um, and we see this effect. So I think the question is, like, yeah. If somebody has recovered full strength, do they show the kind of detriments in their motor neuron pool? I can't answer that question, but to me, what's more applicable to the clinician is when you still have the patient in in your hands, and you can actually potentially impact these. Longer term consequences as we recorded in this study, um, with interventions, that's kind of what I would like to take away from the study, at least in the short term is something you need to investigate for sure. For sure. Um, all right. So help the clinician then. So how do we take this research? How do we apply it in practice? Right? And maybe we maybe we use Sure. Two scenarios, right? And I know this is a little bit beyond the scope of your paper too, but conceptually, like, how do we deal with this? Like, how do you work with somebody, you know, acutely following an ACL reconstruction? We say that they have pain in their swelling, they have muscle inhibition. What do you think's going on? What's your goal here? What would your suggestions for clinicians to do for interventions for somebody like that? Yeah. So I think, uh, about the natural history of. Of, um, arthrogenic muscle inhibition in this case. So natural history being, um, why is it happening and how does that change over time? Um, early on pain and swelling are the catalyst for muscle inhibition. And so a clinician that's seeing somebody immediately after surgery or even before surgery, after their injury, getting ready for surgery should look to reduce, uh, the catalyst. So that's pain and swelling. So, um, Interventions that do that, uh, are, are, uh, focal joint cooling or cryotherapy that's icing down the joint, the, on the joint before exercise. It's a little counterintuitive, but we know that that can restore, uh, that spinal reflex excitability and restore access to muscle capacity. Um, that's what we would call it are in open and exploit strategy. So you're basically. allowing them this therapeutic window of access to their muscle by numbing the pain or reducing the swelling. And then you can, you can exploit that in, in rehab. So for the next 45 minutes, their joint is cold. Um, do your quadriceps exercises, uh, work on, on open, open chain, the extension, uh, use NMES use biofeedback. Uh, throw everything you have at them during that, uh, during that therapeutic window. Uh, so that's, that's one intervention that kind of masks the unmask the inhibition, allows them access. And then I think of, uh, others like NMDS and biofeedback is having different mechanisms, right? You want to send all you can, all your neural power to the motor neuron pool to prevent atrophy and retrain the quad. Um, so cryotherapy affects one thing, and then NMES is forced use, right? You're, you're forcing the muscle to contract. You're throwing an electrical stimulus, uh, through it. Uh, it's non volitional, but you can still, uh, use those motor units. And then biofeedback, uh, is more of a top down approach. That would be giving them a signal, uh, that they can, they can try to amplify, by trying to increase either EMG activity. Um, or increased torque if you're, if you're using like a 10 deck or something more clinically like dynamometer. Um, that's a cognitive, like throw more resources, try to make the muscle contract harder. So all three of those things, like take those three approaches are really going to optimize your, your, uh, immediate post op phase. And then like more emerging study, which I, I, I do think, uh, has a lot of evidence at this point is, is the metabolic cascade. And Lindsay Lefley is doing really exciting work here, and whether eccentrics, early eccentrics, or, or tools like blood flow restriction can address the metabolic cascade of, um, of post operative muscle atrophy. Which, which is great. And, um, you know, the, the internet, social media has, uh, shamed anyone that has said the word ICE in the last eight years. So, um, you know, so it's, it's good to see, you know, and we try to tell everybody, it's like, this is a very simplistic viewpoint that we're having here. There's pros and cons to everything, right? So it's good to hear that there is, uh, you know, some beneficial use of ICE because, you know, we, we still use it for some of its pros and, and, and, you know, I've taken it away at other points as well, but I love that. Um, you know, one, one thing I've always kind of educated and I'm, I'm curious from your perspective, you know, maybe if you can tell me if I'm barking up the right tree, if I'm doing this right. But, um, we've kind of shifted to the same thing, some cryotherapy beforehand for the same reasons. And then, um, um, we use NMES when a person is having a very difficult time with volitional control. But as soon as they tend to have volitional control, we then almost switch to biofeedback to try to get them to have better control. Um, am I doing that well? Should I do anything different or, or better? What, what do you think about that thought process? If you're using EMG biofeedback, then you can't use them at the same time, right? The NMES would saturate the signal. So you don't have to discontinue NMES. And some people would say that you shouldn't for, for many months after surgery. But you do want to apply both interventions. So, um, NMES units at this point are pretty affordable. Send them home with a patient. At our clinic, we send NMES units home with people who are post op. We have them do it twice a day, uh, during their, during their Therax home exercise program. Um, and then bring it back for for clinical sessions. Um, and and biofeedback is harder to recreate in many cases at home. So, um, you can you can use your time in the clinic with the patient to focus on that. You really, I think, want to throw everything you you can at them. So Makes sense. I like, you know, in the sports world, I like that approach, right? Like, there's, you know, why not, right? We want, we want to get these, these people better as fast as possible. So, awesome. Well, throw everything you can that's evidence based, I should say. Yeah. I like that. Good answer. I like that. Alright, so tell me now, how would your perspective change here? Now we have somebody, let's say it's a few months out, or more than a few months out I should say, chronic persistent weakness. Maybe they don't have pain and swelling at this point, right? Because I think if they do have pain and swelling, we'd probably still use the same thought process to an extent. But now this is the person that comes to your clinic. Right there a few months out, maybe they did rehab elsewhere. Maybe, maybe something happened, whatever, but they're still super weak, have terrible volitional control. What do you think is going on here now in this chronic setting and how would your interventions change for that person? Yep. So from, again, the natural history. You're now getting months out, the kind of catalyst of inhibition being pain and effusion are resolving. Um, the nervous system is integrating this change and, uh, what we see in now systematic reviews is that people farther out have cortical driven inhibitions. So the muscle activation failure, the muscle weakness. is more associated with what's going on in the brain than what's going on in the spinal cord. Um, and for that reason, you can probably discontinue interventions that target the spinal cord being cryotherapy or TENS if you're using that and focus more on interventions that would address the cortex, um, or the, or the top down control. So for that, you're going to apply biofeedback, you're going to apply NMES still if it's appropriate. Um, and you can do things like, like eccentrics, eccentric overload, because that, uh, is like a throw everything you have at this from a neural standpoint to try to control that eccentric, um, contraction. Uh, so that's, that's really the, the big changes there, um, when, when you're looking at, uh, longer, longer out is you just say that the spinal level control or the spinal level interventions are probably less indicated now. Um, that being said, we don't know when you look at a patient in the clinic, what's going on in their nervous system. That's one of the limitations of. of applying any of these interventions in the first place. You're kind of just looking at them and where they're at in the recovery and, and, and assuming kind of what their neurological activation might be. Um, and I've seen anecdotes and videos on, on Twitter and LinkedIn and stuff of people saying, Hey Dave, this person's, you know, six months out of surgery. I iced them and their strength went up 20%. So. whether that single individual still had spinal level inhibition, it's, it's hard to say. We can't know. So look at the patient in front of you. Um, a lot of times if you do this like pre post intervention, like just film their muscle contraction or get a, get a MVIC before and after an intervention, you'll know whether or not it's having an effect. Um, just that, that simple like AB test pre post. And if it doesn't, then you don't have to do the intervention. If it does, then you should use it. And to me, that's actually amazing advice for so much we do in our profession right there. That's the, you know, the assess reassess model that sometimes a lot of people just forget about, right? You know, they're so tied up with, you know, what they want to do and what's next that they don't, they don't, they don't look at basics like that. So I think that's fantastic. So, um, Dave, awesome stuff. This is going to be super helpful for clinicians that I know that this has helped me, right? You've, you've taught me some stuff on this and obviously reading your, your article and your past. Stuff that you've published has been great. So I'm going to put some links in the show notes to some of Dave's work, especially this, this current article that we're talking about, because I think it's a, it's a really important one that hopefully will have an impact on our professions for some time and hopefully stimulate people like Dave to do more and more research in this area so we can get to the bottom of this. Right. Um, but Dave, before I let you go. Quick high five at the end, five quick questions, five quick answers. Just kind of want to hear a little bit more about you teach everybody a little bit about your thoughts here. But first question, what are you currently doing? And like this question is never fair, basically to the PhDs, by the way, because you guys have very finite topics you're working on, but what are you currently working on for your own professional development right now? Um, yeah, that's a good question. So I, you know. And changing in the midst of changing populations of interest. I worked my PhD at ACL reconstruction. Now I study neo osteoarthritis. I did a postdoc in between about technology development for, for, uh, patients with, with, uh, neurologically driven muscle inhibition after stroke. Um, so I'm just kind of learning and trying to, to find consilience in the literature and in the nervous system about what's going on. Um, one of the multiple different avenues for driving muscle inhibition and what applies to which interventions when, um, I'm also trying to like, enjoy the postdoctoral period and that I'm not a faculty member and just relax a bit, which is, which is new for me. So, um, you know, read, read a few books here and there and, uh, and just enjoy time with family. So. I love it. Yeah, you put your work in the last 15 plus years. Uh, it's, it's, it's time to spend a little, little time for yourself. I love it. Thanks for recognizing that. Yeah, absolutely. You got my support. But, um, what, what, what's one thing you've recently changed your mind about? I think that, that no one is coming to help me translate my, my research, um, and that's like runs counter to being on this podcast. So thanks for inviting me. But what I mean is like in the academic world and in physical therapy research specifically, um, we call it like we have researchers and we have clinicians. And what the way they would treat this in industry is they would have a research and development department, right? Right, and there's no development in academic research. So when I publish something it's up to me to market it and disseminate it Um to teach and engage with clinicians, uh and to innovate and like develop the technology that's going to make the difference Or else we're stuck with that same like 17 year gap between us publishing a study and clinicians Um, you know, picking it up and applying it, right? I'm not, I'm not placing the blame on anyone. I think it's just like this huge disconnect between our worlds. In industry, when you look at technology and like, especially artificial intelligence right now is a hot topic. They have the development side of things, like they're paying people. They have people. And, uh, and I think that that job, as far as I can tell, falls on me, if I'm, I'm in academia, so. That's right. That's, that's why research and academia go so well together. You do the research, then you, you put it into everybody's mind. So, you know, no pressure, but like you've got to make sure you have good methodology and, and you're doing a good job. You're not giving false misinformation out there to the students. Yeah, well, that's, and that's true. So the development part of things is if you have to, if I have to take my research and put it into a technology that people will adapt, adopt. They need to actually see that it works, right? So if my research is flawed, the technology will never work. It's a nice kind of litmus test to see, you know, is it, is it worth it? For sure. Can, can my research interests be actually marketed and translated to, um, to the industry? Yeah. Awesome. So that's one thing I'm realizing. Yeah. What's your favorite piece of advice you love to give, uh, students? Um, I just talk to people, people want to talk to you, if you have a question, read an article, reach out to them, um, say hello, introduce yourself, uh, talk about a problem you're working on, um, and yeah, and this is a great profession, it's, it's done a lot of great things for me, and, um, yeah, network, connect, don't be afraid. I love it. I think Dave just gave you all a, uh, open invite to email him, by the way, but I didn't, I didn't want to say it, but yeah, you can go on our website. You can, you can, anyone can just click a link and schedule a video call with me to talk about any AMI interventions. That's, that's, that's amazing. That's pretty much what I did for this podcast episode. So yeah, it pretty much worked. That's how Dave and I met, but, uh, awesome. Uh, what's coming up next for you, Dave, I know you've alluded to some new research, but what else you got brewing? Um, just focusing on family time. I think, like, I just had a son, uh, about four months ago. So I have some, some job applications out for faculty appointments. Uh, it's kind of the season for that. So we'll see if anything, anything hits. And in the meantime, just, uh, continue the postdoc grind. That's amazing. Uh, I'll put some info in the show notes, but where can people find out more about you and your work? I'm on X and LinkedIn, and then people can go to live4pt. com to check out some of the blogs I have on these topics, or as I said, find a link to schedule on my calendar to meet up and just problem solve clinical cases or whatever. That's great. I think you're the first person I know to embrace calling it x by the way. So, um, yeah, you know, I figured I'd go for it. It's been a few months now. I mean, it's, it's accurate. So everybody else is wrong still. So yeah, I love it. That's, that's, that's what, that's what makes you, you Dave. I like that. Awesome. But But Dave, thank you so much. This was awesome. Love sharing your stuff. Love learning from, from some of your research. So please check out Dave and some of these, um, these great topics that he's working on and take them up on that offer. He, he wants to talk to you and, and, and, and help. So anything you can do. So, um, thanks again, Dave. Thanks for coming on the podcast today. Cool. Yeah. Thanks Mike. Thanks for having me.