First question is from Chamu WBFF Pro. What is the best way to keep muscle while cutting? Is it possible to still build the body part while in a deficit? Alright, so let's start with the first part. What is the best way to keep muscle while cutting?   That means it's more difficult now to maintain a lean body weight. And the likelihood that you'll gain the weight back later on increases in response to how much muscle you lose. So this should definitely be a number one goal. Now there's two main ways that you prevent this from happening. The first one, lift weights, obviously. Lifting weights sends the right signal to the body. It says we need this muscle. Even though calories are low, we still need to be strong. Now to be more specific, in my experience one of the best ways to keep muscle while dieting is to train for strength. It actually works better to train for strength while you're dieting because strength is such a loud muscle building signal. The second thing is have high protein. High protein, low calorie diets by themselves, even if people don't lift weights, they turn out with less muscle loss. So regardless of how you're working out, if your protein is high with your calories are low, that alone will help you keep muscle. Yeah, which is definitely, like, again, this is counter to a lot of people's thought process when they're trying to lose weight because they're trying to really, you know, put all their attention in that direction. So they'll add on the HIIT training style. They'll add on the circuits and, you know, extra cardio and cut their calories kind of all at once, which, you know, again, inevitably we're going to do this long enough we're going to start losing muscle as a result, you know, as well as the rest of your body mass. So to focus your attention more on strength while you're cutting is such a more effective strategy. I'll add a little bit more to that. I don't think it's as simple as just strength training as far as your training. So if you just came out of a strength cycle and you're going into a cut, you're changing into anything that's novel to the body is ideal. So if I was training a 5x5 routine or I was lifting for strength right before I went into a cut, which was normally very common for me. A lot of times I was in a strength cycle when I was adding calories. When I switch out of that, I want to train what's most novel. So if I'm used to training a 5x5 or a strength routine, going to a more hypertrophy type of routine really kept more muscle on my body than staying in the 5x5 type of training.  So I always like to change my client and my own programming when I transition from either bulking or maintaining whatever you want to call it to a cut for a show. So whatever your programming looks like, heading into the cut, I want to do something a lot different. So that's the first thing. The other thing is I also want to minimize how much cardio I'm doing in order to cut. I like to do it all through calorie and manipulating my training program before I start to add any of the cardio in there. A big mistake that the competitors that I would train would make or assume is, okay, I'm eight weeks or 12 weeks out from a show. It's time to start cutting. They introduce cardio right away. I think that's a mistake when you're trying to hang on to muscle. As much muscle as you have on your body going into a cut, it is not advantageous to keep all that if you're also running on a treadmill or doing the Stairmaster. The body will see that and go or feel that and go, oh, let's get rid of some of this expensive tissue because he or she is making me sit on this Stairmaster for 30 minutes or an hour every single day or in some cases, two hours a day. So minimizing the amount of cardio you're doing during a cut and using your calorie intake and the circulation of your training to create the caloric deficit is a far better strategy than just adding, than cardio. And then I think the obvious one, especially when you're talking to someone who's a WBFF Pro, I'm sure she knows that, you know, keeping up the protein is a must, right? So that's a must. I think that's an obvious one. The common offenders that I see with the competitors is they are following a routine that is similar to the one they were following before the cut and it's not going to send a very loud signal for the body to adapt and change and build muscle. So you want to change the programming and then the other big common offender or mistake I see is the adding cardio right away. I'm saving cardio for that peak week or maybe the week or two before I'm not introducing it until then and that was something that I think was really hard for a lot of people that hired me when I was coaching them to grasp when I would tell them, like, no, we're not doing any cardio. Not yet, not yet. I'm going to save it until the final weeks so I could preserve as much muscle as possible. Now, as far as possible, is it possible to build muscle while in a deficit? Yes. Is it likely? No. It's highly unlikely. On steroids. Yeah, if you're natural. That's when you see it. You can do it, but boy, you need to be at a very small deficit, meaning you're not trying to burn a lot of body fat. You need to have the right amount of training, high protein, good loud muscle building signal and then maybe what will happen is your body will take some of the calories and energy it needs from body fat and you'll have enough that you're intaking to fuel muscle growth, but it's very unlikely. It's very hard to build while in a reduced calorie diet.  When it's a brand new, you're not lifting weights, you're coming to me and you're totally sedentary.  As you become more advanced, it becomes far more difficult to make that happen.


No, I mean, I feel like for everyone, regardless of how long you play, it's going to be an adjustment, but I loved every minute of it, and I feel like the amount I was able to learn was huge, and it kind of felt like it built a foundation that I'm keeping on building on, and I'm definitely grateful for it.


Hey everybody, welcome back to my Star Wars channel and today we're going to look at the 1982 Rebel Transport. We would be honored if you would join us. Hey everybody, welcome back to my Star Wars channel. Thanks for being here. If this is your first time here, this is what I do. I look at Star Wars. Any way that Star Wars touches my life in any capacity, whether it's through books or toys or collecting or the films or new trailers that are dropping, Disney, whatever it is, I love it all. I've been a fan and I've been with the franchise since the very beginning. You won't find any hate here. This is all my love for Star Wars. A little backstory. I did a video a couple of videos back where I went through a G.I. Joe collection. I was able to find homes for all those things and found G.I. Joe guys in my area and abroad that really wanted these toys. I was able to pick it all apart and make sure it got into the right hands. That just created a little bit of nostalgia in me. I was like, I should go back and get a couple more ships and play sets. With no agenda at all, I was not looking for anything. I just went out to eBay and I was like, let's see if there's any ships that are in a state where they're missing a lot of pieces and maybe not too expensive. I'll pick one up and just rebuild it. The Hoth Empire Strikes Back Rebel Transport popped up in my list and it was pretty inexpensive. It wasn't too much and it was missing pretty much everything. It was missing everything and I said this could be a fun little project. It was never on my radar. I never wanted this as a child. Apparently nobody else did either. I never wanted it as an adult. There's still a couple of ships or play sets that are on my dream list as an adult and price has really been what's been keeping me away. I saw this and picked it up and I've had a lot of fun putting it back together and I thought I'd show it to you. Here's our completed ship now and you can see right away there's some color differences between the two end pieces and the center. That's because they came from different sets. When I got this in the mail, it was missing this whole back section and this canopy. In truth, even though it's a spaceship, it's not a fighter. It's not an X-wing, it's not a TIE fighter, it's not a combat ship. It's really a escape ship. The Rebels all get in this and Impression X back and the escape hoth. It's almost a coward's ship because this is what they're always in when they're running away. I don't know that even as a toy it says buy me because it does have guns but the guns are covered in this back section. I can see why as a kid you would take these off and not play with them because these two pieces don't have any playability. You would take these off and probably never put them back on again. The other thing is this ship is a figure carrier really because this holds 40 Star Wars figures. It becomes a little handle and you can carry your ship around and inside the ship is all your figures and we'll look at all of that. Right away, like I said, I had to replace these two pieces. This is the canopy right here. I will say I've never had a ship that had removable parts like this before and aside from the TIE fighter where the wings pop off, but that's a little different. These have little clips where they're supposed to snap into places and I don't know if it's just because these parts didn't all grow up together but they don't fit very well. So again as a child I can see why I would take these off and not put them back on because they're kind of a pain to put on and off. And originally when I got this one of my first thoughts was well I won't replace these pieces because it doesn't look good as a display. As a display piece it just looks like a giant cigar. So as a display piece I think it looks better with your figures here in the canopy flying the ship, that looks cooler. And then in the back section you have some decals for the engine exhaust but again these are just big plastic nothings. But if you look in the back, well now you have a figure and a gun, see that looks cool. So this would be how you would display it, or at least how I would like to display it but then what do you do with these things? So that was one of my first questions but then I decided if I'm going to restore it, restore it, get all the pieces. So there's some movable guns back here. I put a pilot back here and I put two pilots up front. So those didn't come out of my collection. I bought those along with the extra pieces so that I could have a little diorama.  And again it's not easy, it's not easy. So aside from the fact that it's big, aside from the fact that it's not really a fighter and also that it's really more of a like a collector's case really of a ship that nobody liked, I can understand why it probably wasn't every kid's favorite and it wasn't. This came out in 1982, like I said, for Emperor Strikes Back. And by the time Return of the Jedi came out, these were still on the shelf. So they didn't have to make a new one in a new box. The old Emperor Strikes Back ones were still on the shelf. So this did not sell very well. Originally this is a handle right for carrying and it's also a twist.  And if you pulled up then it would take this top part off. See how this just floats off. So that's the entire front or the entire top and you can see all the decals on there. And mine came with all the decals. That was another reason I really wanted to pick this up is because I was like, wow, the decals are on there and it's still vintage looking. So that's pretty dope. So then you have this inside compartment and this is really where you keep all your figures. So all your 40 figures fit inside there. This is the prison or the stocks. This is the jail, right? It's got a little hole there because it drops through to the escape hatch. So the way this would work is you can just take all your figures and place them upright like that and just stack them. I mean, if you've ever seen one of these where all the figures were just in there, I mean, look at that. You can fit a lot of figures in this ship. So that would be cool if you were a kid. You had that many figures, right? The gun section back here, it pops out and you can put it aside and you can have like a little gun section that sits in the ground. And then of course, this is the pilots up here. But once you remove the top, they don't have anything covering their feet. And again, I got both decals there. So that was nice. And the other cool thing is these also become compartments for holding all of your accessories. And this came with accessories. So this actually came with five Hoth backpacks and four gas masks. So there was a mail away set that had those included at one time.  But if you bought this, one of the selling points was that you got five backpacks and four gas masks. So this section right here lifts up. And so you can stick accessories in there. So you can stick all your guns and weapons backpacks and whatnot in there. And then in the back, you can remove the gun. This also lifts up. And so you can stick accessories back there as well. So it really does become a carrier in a lot of ways. You can lift all your men out if you wanted to play with them or put them aside. And then you got a beautiful graphic down there at the bottom as well. And so the other piece that was missing was this black trap door down there. And I was able to pick that up as well. You can see what it looks like on the other side. And it's one of those action points where the character drops through. And I don't want to do it because I don't want to keep putting wear and tear on the hinges on this. And so I was able to get... That was my most recent acquisition was getting the trap door. If you didn't notice, I'm still missing one item. So right here on the end, I am missing one cannon. So one cannon is still not there. And I only need just the cannon itself. I don't need the rest of it. So it's been a little difficult to find just the one item. But I'm sure if I'm patient, I can do it. I can wait, right? So I always do this. I always get figures for my ships. I don't have any ships on display that don't have figures. So I make sure that all my ships have pilots because I'd rather... I just like knowing that every ship up there on my shelf has a pilot. Making sure it all snaps back together. Okay, there we go. And yeah, I'll have to often angle these back on behind the scenes because they don't just snap back. I wish they did. It's a matter of lining them up, kind of squeezing the sides, and then pressing. But yeah, what do you think? How would you display it? Would you display it with these pieces on the front and back? I mean, it kind of works that way. My thought was I was going to take all my figures out of the shoebox that they're in because that's where I store all my figures in the shoebox. I put them all in this and then put this on the shelf where my shoebox is. So this really wouldn't become a display piece because it's not very attractive and it takes up a lot of space. I would actually just use this as storage. And so just make this a fun way to store my characters. When this was first released, it cost $29. And like I said, it wasn't very popular. It's had on the shelf for a long time. What do you think? You like the Rebel Transport? Is this a ship that you've collected? A ship that you've ever wanted in the past? What do you think about its looks? How would you display it? Tell me down below and I'll read every comment and I'll get back to you guys. Thanks for watching. May the Force be with you. I'll see you next time. Bye.


So this bread is called shokupon or Japanese milk bread. And basically it is just a sandwich loaf, but due to the way it's made, it has a pretty unique texture and flavor. It's tender yet chewy, fluffy and almost cloud-like and ever so slightly sweet. And like I said, it's super easy to make, so I think it's a great place to start if you're just getting into the world of bread making. And to make it, we'll start by simply mixing the ingredients. So in a bowl or measuring cup, combine 260 grams or about 250 milliliters of whole milk, which by the way, is just a little over a cup with 10 grams of honey and three grams or about a half packet of instant yeast. So I am using dry commercial yeast, just because that's how this bread is typically made. But it's very easy to convert this recipe to a sourdough version as well. But I'll leave instructions for how to make that one in the full recipe on my website. Now once everything is combined, I'm just gonna let this sit for about 10 to 15 minutes. And by the end of that time, there should be just a bit of foam forming on the surface. Now this resting step isn't 100% necessary, but it basically just allows us to prove that our yeast is alive and active. So if you don't see any sort of foam or activity on the surface, first you may just need to wait longer.  So in the bowl of a stand mixer, combine 350 grams or a little under three cups of bread flour with 20 grams or five teaspoons of granulated sugar and seven grams of salt, which is about two and a half teaspoons if you're using diamond crystal kosher salt as I am. Then just stir everything to combine. I like to use my dough whisk for this. And once the dough has come together, we can start kneading. Now if you have a stand mixer, you'll definitely wanna use it here because this dough requires a lot of kneading in order to develop sufficient gluten to give the final bread its signature soft and chewy texture. So that's not to say that you can't make it by hand, you definitely can, but it's just a bit more work. But assuming you are using a stand mixer, you'll just wanna set it to about a medium speed and using the dough hook attachment, knead the dough for about seven to eight minutes. And by the way, if you're wondering whether you can use all-purpose flour for this recipe rather than bread flour, the short answer is you definitely can. However, I would actually recommend using bread flour if at all possible because again, this dough needs to develop a pretty strong gluten network and higher protein flours like bread flour will allow you to do that much more effectively. Anyways, after about eight minutes of kneading, my dough has come together pretty nicely. So at this point, we can start to add our last ingredient, which is butter. And this is what's really gonna give this bread its soft and luxurious texture. So I've got two tablespoons of unsalted butter warmed up to room temperature and I'll just add it little by little as I run my stand mixer on a low to medium speed. So I added it in about four separate increments, waiting until each was incorporated before adding the next. Then after it's all combined, we can finally crank up the speed and finish kneading. And this is probably the most important step because this is where we're gonna develop that super strong gluten network to give the bread its chewy cloud-like texture. So we'll wanna knead on a high speed for about six to eight more minutes until the dough is extremely smooth and stretches significantly without tearing. And by the way, be careful when you're kneading because this high speed will probably cause your stand mixer to jump around a bit.  Anyways, once you've got your velvety, smooth, voluptuous dough, it's time for the bulk fermentation phase, which is just a fancy way of saying that we're gonna let the dough rest for about an hour or two to let it rise. And we'll be looking for the dough to double or triple in size here. So personally, I like to transfer it to a clear rectangular container just because it's easier to monitor that way. Either way though, it's a good idea to lightly lubricate your container with a neutral oil to make sure the dough doesn't stick to the sides as it rises. So I typically let it rise at room temperature, which again should take about one to two hours. That timeline can vary depending on the temperature of your environment. Anyways, once our dough has more than doubled in size, we're ready to move on to the next step, which is to divide and shape the dough. So place the dough out onto a large work surface and start by dividing it up into three equal sized pieces. I like to use a scale just to make sure they're all exactly the same, but you can just eyeball it if you want to. So once you've got your three pieces of dough, you'll wanna form each of them into a top ball by dragging them along your surface like so. And this is basically just gonna make all of our dough pieces even more uniform so that when we roll them out in the next step, they'll all look exactly the same. But before we get there, we need to let the dough relax for a bit.  Now in the meantime, we can get our baking pan ready. So any standard nine by five loaf pan will work for this recipe. But if you want that perfectly rectangular look, you'll wanna use a Pullman loaf pan. So this has a sliding lid that forces the dough to maintain its shape as it bakes. And this one I have here is the closest that I could find to the traditional Japanese loaf size. And they also come in a smaller size, so of course I'll leave both linked below. Now to prepare the pan for baking, I'll just coat it with a thin layer of butter to prevent the dough from sticking. Then once our resting period is over, we can start shaping the dough. And the first step is to roll each ball out using a rolling pin into flat rectangles with a thickness of about a half inch or exactly 1.27 centimeters. And as you do this, you can dust the dough with a bit more flour if you need to, but you don't wanna use too much because the slight stickiness of the dough actually prevents it from sliding around as we roll it out. So my rectangles here are probably about eight inches by 12 inches or 20 by 30 centimeters, but it really doesn't need to be exact. What's most important if you're concerned with uniformity is that the sizes are consistent between all three loaves. Now once we've got our rectangles, we can roll them up to form the signature Shokupon spirals. And to do that, we'll first fold the rectangle into thirds. I think this is lengthwise, but just look at the video and you'll see what I'm doing. Then roll it one more time using your rolling pin to close off the seams and flatten it out just a bit more. Then roll it up into a spiral starting by folding in the corners as if you're making a paper airplane and then just rolling the rest of the way. Be sure not to roll too tightly here, but you also don't wanna make it too loose. So just a nice light tension here is good. And this folding process is gonna play a big part in creating that flaky texture that these loaves are known for. Then gently place the dough into your greased loaf pan, seam side down, and then repeat that process with the other two dough balls. Now I actually made two loaves this time so that I can make one flat top and one round top. And last minute, I decided to make the round top one a cinnamon sugar swirl loaf. So right before rolling the dough into a spiral, I just brushed it with a bit of butter and then a mixture of granulated sugar, brown sugar and cinnamon. So the loaf turned out okay. You'll see in a minute, but I also know at least one thing I would change for next time, so we'll talk about that when we get there. Anyways, the last step here is to let the dough rise one more time until it fills the pan about 80 to 85% of the way. So this usually takes a bit longer than that initial rise. For me, it took about an hour and a half at room temperature. Now when it comes to baking, you want your oven preheated to 425 degrees Fahrenheit or 218.33 degrees Celsius. If you're making the flat top loaf or if you're making the round top loaf, preheat it to 375 degrees Fahrenheit or 190.556 degrees Celsius. And for the round top loaf, I also like to brush it with an egg wash before I throw it in the oven. Then you'll want to bake the loaf for about 25 to 30 minutes. For me, I found the sweet spot to be about 28 minutes. And if you're making a round top loaf, you may also want to check it after about 20 minutes and cover it with aluminum foil if the top is already brown to your liking to prevent any further browning. Either way, once it's done, just remove it to a wire rack to cool. And you shouldn't have any problem sliding the loaf out of the pan immediately after removing it from the oven. You might need to shake the pan a bit, but it'll come out eventually. Now this is always the hardest part, but you'll need to let it cool for at least 30 minutes and preferably about an hour to allow the interior to finish cooking and to prevent any moisture loss. So here's my cinnamon loaf. And while it does look pretty cool, I realized that I should have used a bit less cinnamon sugar to give it a more subtle flavor. So I actually did that the next day and it turned out a lot better. So I'd highly recommend giving that one a try. Now as far as my square loaf, it made for incredible chicken katsu sandwiches, which is one of the more popular uses for this type of bread in Japan. And if you want to make it, I actually walked through my chicken katsu recipe in a recent video, so I recommend you check that out right here. It's one of my favorite dishes to make and it's delicious with or without shokupan, so I hope you give it a try. Either way, thanks a lot for watching and I'll talk to you in the next one.


So, good morning everyone, and I'll hopefully not put you asleep, so I'll try to keep you awake and keep you innovated by what I think is a pretty interesting target. And it's being looked at in ophthalmology. So you'll see Rokinae's spoken about or referred to her studies in IOVS. You're also going to see clinical studies being reported out in ophthalmology and AJO. And basically the purpose of my talk is to give you a background. I am a retained consultant and serve as the chief medical officer for Altheos, and I do have a lot of familiarity with this class of compounds. This is not specific to Altheos, it is not meant to be, it's meant to be an overview. So I really wanted to give you an unbiased representation of this target and where it's going in ophthalmology. I'm going to cover Rokinae's pathways, I'm going to talk a little bit about the role of Rokinae's in systemic pathology. In particular, how do we inhibit this pathway in ophthalmology and the potential benefit, as well as how they've been inhibiting this pathway in systemic disease. And sort of keep an open mind, because I think again this target is not only useful for glaucoma, but actually could be applicable to a lot of different diseases that we see in the eye. What I want you to walk away with is an understanding of the role. Some of the slides get pretty complicated, but understand what Rok does, both systemically and ophthalmically. Understand the inhibitors currently in development, and then again just see the potential. And you can purchase, for the researchers here, you can purchase these Rok inhibitors through Sigma, and in Japan there is one oral compound approved, and I'll touch upon that. So what is, what's Rok? Well, it's a row A, which is a member of a row class of small GTPases, and these are similar to Rok, you may have seen, or CDC. And they really regulate an amazing amount of cellular responses, and this is what really enamored me into this target. And I thought, wow, this would be a great compound if we could get into the clinic. It affects cell contraction, cell migration, cell proliferation, gene expression, cellular differentiation, adhesions, and also cell apoptosis. It's present on numerous cell tissues throughout the body, and row A is activated by the exchange of GTP and GDP. Once activated, it works intracellularly and acts on two different kinases, two different enzymes, Rok1 and Rok2. Rok and row A are activated by numerous mediators and proteins. And again, if you think about what activates it, you can understand why it's involved in so many processes. So you've got GTPases activating it, endothelan, which is a potent vasoconstrictor. You've got arachidonic acid, which is involved in inflammation, caspases, which are involved in apoptosis. They all activate the row pathway. Busy slide, but the takeaway is row works on the actinomycin cytoskeleton pathways or structure, I guess you can say. And a lot of it is really just phosphorylation. So you're phosphorylating phosphatases or kinases.  And what indeed happens is if the MLC, which is myosin light chain, is phosphorylated, it contracts. So row kinase causes phosphorylation of myosin light chains, which then causes contraction. Cellular contraction, contraction anywhere. This is a little bit easier to understand. We have arachidonic acid and we have endothelan. Again row A, GTP is on the cell surface, activates the kinase. The kinase in the active role takes the myosin light chain phosphatase and phosphorylates it. And what you get is contraction. So phosphorylation contraction. Why rock? I had this question actually come up and I thought, hmm, where did the C come from? Well, it's row-associated, coiled, coiled forming protein. Again, there's two, rock one and rock two. Some people believe there's selectivity and specificity, so if you inhibit rock one more than rock two, you're not going to get as much vasodilation. The data's really sketchy on that. How does it work? Well, it's a serine, theranine kinase. It can work through calcium channels to affect contraction, vascular smooth muscle, but it can also again affect the cytoskeleton within the cell that's independent of calcium. The key here is that row kinase regulates vascular tone and it does it two-fold. It affects smooth muscles again through your actomycin contractions, your smooth muscles surround your blood vessels, vasoconstrict, blood vessels clamp down, but it also can directly affect the endothelial cells. So if you remember back to some of your vascular physiology, nitric oxide vasodilates. How do you inhibit vasodilation? You can also inhibit or lower the amounts of nitric oxide. So there's this counterbalance between row kinase activation, the amount of nitric oxide, and also the amount of vascular contraction. And it's a vascular tone. It's sort of a homeostasis that's achieved. So the pictures are sort of the big takeaways. So contraction, actomycin, smooth muscle. Cell junctions. So if you remember back to your cell biology, what affects the cell-to-cell interactions is these tight junctions, these zonular occludins, the desmosomes, and there are actomycin fibers between those cell-to-cell junctions. This is really cool. So cell migration. And if you remember anything from the talk, I think this is really neat. So the actomycin is involved in the cytostructure of the cell and how does the cell move? Well cells move through protrusions. The push-pull. So you've got the rack and the CDC stimulating the formation of those protrusions anteriorly or forward moving. And then you've got row A in the back pulling those protrusions in, and the cells actually migrate. So rock is very involved in those cells migrating from place to place, whether it's a cancer cell, whether it's a fibroblast, or whether it's a lymphocyte. Because of these sort of three top characteristics, rokinase has been looked at in fibrosis, pulmonary hypertension in particular, cancer, tumor cell metastases again because of the cell being mobile and moving around, cardiovascular atherosclerotic disease because of the endothelial function and also the vasoconstriction, chronic and acute inflammation, and ischemic and reperfusion diseases, as well as CNS injury. I took the picture first. So I found this neat picture and I said, I wonder if every organ named in this picture has been shown to be linked to row? And indeed it was. Down to cochlear outer hair cells. So rock and rokinase apparently have something to do with cochlear outer hair cells. Two, there's one approved compound currently, and that's in Japan, it's called fazadel. It's oral and its indication is for cerebral vascular vasospasm after subarachnoid hemorrhage. So basically this compound has shown a benefit in ischemic reperfusion injury. And again, translate that now to the eye and think about all our ischemic reperfusion injuries. Sigma makes a compound 27632, which is a research grade compound, which when we go through some of the data on the research, this was the compound that was used. In Japan, they've actually worked with fazadel. And fazadel was looked at in the United States for myocardial ischemia and also some other ischemic injuries. So in animal models rock or inhibiting rock has actually been shown beneficial in fibrotic diseases in animals. And this is just sort of a list of possible fibrosis that occur or that are induced in animals. And if you inhibit rock through a rock inhibitor, you have some benefit in these animals. In pulmonary disease, it's sort of twofold. So again, it's working on the fibro, the fibro proliferation and the fibrosis, but it's also working on the vascular aspect. And if you inhibit rokinase, you abolish some of the hyperop, hypoxic vasoconstriction. And again, it's this balance that it's a balance between activation and deactivation of row. And the feeling is that rokinase does play a role in the increased basal pulmonary vascular tone in hypoxic pulmonary hypertension. So there's too much rokinase activated. Vascular disease, very similar type of data. If you inhibit the rock pathway, you can alter ischemic events in the heart. You can also inhibit development of coronary artery lesions perhaps in some of these animal models. They did, again, in Japan, use phasodel clinically, and they showed that if you inhibited the rock pathway with phasodel, you actually improved coronary artery spasm in angina patients. Inflammatory disease, well, if you inhibit rock, you can inhibit T-cell proliferation. You can inhibit proliferation of cytokines and mediators, and again inhibit cell migration, and also alter the epithelial endothelial barrier function. So this is when we start to think about the eye, well, what about in the cornea? You've got your epithelial, you've got your endothelial, and there's some interesting papers coming out with rock inhibitors showing different roles in improving cell migration, inhibiting cell migration, improving corneal epithelial defects, causing epithelial defects, so the data is sort of all over there. Rock does affect the epithelial barriers, we don't really understand why or how, and I put this slide in here because if you think about what we're doing in the clinic with these compounds, we're putting this into the eyes of patients with glaucoma, and I think an interesting finding down the road is going to be what's happening to the cornea. Are we having changes in the chemistry? Are we having changes in the epithelial layer? Are we having breakdown of the tight junctions? Are we having changes in permeability of the compound getting into the eye? And again, this is an open area of research. Some more inflammatory, immune-mediated diseases, again, showing that if you inhibit rock, you can have some benefit. CNS, and this again is sort of where it translates to ophthalmology in glaucoma. So the data in CNS has been very, very interesting and encouraging. And if you think about where the drug is approved, it's approved here in ischemic reperfusion injury. So if you do a clue, the MCA in mice, they have found that rock has actually increased two-fold in that ischemic area. And when those mice were pretreated or treated with phasadel, you decrease the ischemic area. Also spinal cord models, they found that if you gave phasadel, again, this work was done in Japan, you improved the outcome in terms of paralysis and hypoalgesia. And they thought it was because of the involvement of astrocytes and granulocyte colony-stimulating factors, so again, growth factors. So somewhere growth factors are involved, various mediators for cytokines. It's a complicated pathway, but it begs the question, again, what is this role? So in ophthalmology, a little bit more closer to home. So it's an active area of research. Rock is present throughout the eye. It's present in the iris, the cornea, the congenitiva, ciliary muscle, retinal ganglion cells. And most importantly, where the interest is, is it's located in the trapecula pathway. It activates fibronectin and extracellular matrix material. So when you think about glaucoma and some of our thoughts on glaucoma with extracellular matrix being upregulated in the trapecula mesh work, trapecula pathway, again, the question is, what is rock inhibitors doing to this pathology? And there's several companies exploring rock eyes currently. They've also looked at rock in the cornea, as I mentioned. So again, cell-cell adhesions, integrity, differentiation of the epithelium, and also endothelium. So if you read into the literature, it's not quite clear what's happening to the endothelium as well. So this is just to remind everybody that the trapecula pathway has the trapecula mesh work, Schlem's canal, episclerol veins. Trapecula mesh work is composed of collagen beams, extracellular matrix cells, and then your canal, Schlem's canal, has the endothelial cells and a lot of the smooth muscle. The smooth muscle is also present in the trapecula mesh work. So you've got smooth muscle and the endothelial cells, so you've got potential targets for the rock kinase inhibitors. So what happens in IOP when IOP is involved with rokinase? Well, again, trapecula mesh work, you've got these beams, you've got actomycin present, rokinase is going to phosphorylate it, it's going to contract those beams, it's going to decrease outflow, it's going to increase the stiffness of the trapecula mesh work. And Vasanth Rao down in Duke has done a lot of this work with David Epstein. In fact, that's where the aricompound came from, and I'll talk about this. So David Epstein was very involved with the aricompound, which is now in the clinic. Rokinase also alters those tight junctions between those cells. So if you've got cells in the trapecula mesh work that are changing their permeability, that could also affect the outflow of the aqueous through those cells. And then lastly, it's the extracellular matrix. So we think that rokinase in the trapecula mesh work, or the trapecula pathway, is working on three parameters. It's causing constriction, it's causing changes in permeability of the cells themselves, and then it's also involved in laying down more of that extracellular matrix. So if you inhibit it, you should reduce IOP, right? You can vasodilate, you can improve permeability if you believe that the tight junctions are affected. And then perhaps you can even change that extracellular matrix that's being laid down. The problem with these compounds is they vasodilate. So what happens when you put them on the eye? They vasodilate, and they cause a lot of hyperemia. The hypereme is not pro-inflammatory, and it's not detrimental, and it's not toxic to the eye, but it is a cosmetic effect that is undesirable. So in development, preclinically, IOP reduction has been shown with these compounds. From a clinical perspective, well, it's kind of neat. It's a novel pathway. To this date, the only compound that works on conventional trapecula pathway outflow is pylocarpine. So we now have the opportunity to have a new compound that works on conventional outflow. Could also be additive. Could be additive to prostaglandins. Could be additive to your aqueous depressants. And it may offer some of these other interesting attributes for glaucoma. Just want to be mindful of time. So preclinical development. So this is the compound that I'm personally involved with. And we have preclinical data that shows that it does lower IOP. Hopefully we're going to be in the clinic in 2012. Like so many of these compounds, and this is not unique to alpheos, but this is a very sort of common finding with all these compounds, is that it does lower IOP and normal tens of rabbits. And depending upon the compound, you can have variable amounts of hyperemia, which is either bulbar conging tiva. There's also some chemosis in edema, which can be seen. And again, that relates to permeability. Because if you're increasing the permeability through those vessels, you may see some edema. All these compounds have looked at themselves compared to zalatan. Again, this is just an example, not unique to alpheos or ATS907. In the monkeys, now keep in mind, too, that a lot of this is species-specific. And certain species don't respond to certain compounds. Rabbids don't respond well to zalatan. Monkeys respond fairly well to zalatan. And across the board, rokinases and monkeys appear to lower IOP better than a prostaglandin. That's kind of the takeaway. So clinical data. Well, what have these compounds done? What have they shown? Ari, again, is probably the leader in terms of development here in the United States, presented their phase II data. And what they did is they looked at their compound, two different dosing regiments, two different concentrations, versus zalatan. And they show that in the clinic, in humans, in a small number of patients, 217 patients, they were actually slightly inferior to zalatan, 0.9 millimeters of mercury. So that would qualify as Dr. Olson referred to as non-inferior. Senju, which is located in Japan, obviously, they published a phase I in healthy individuals. And what I thought was interesting here, and this is why I put it, was that in normal, intensive, healthy individuals, they got a pretty good drop in IOP. They went from 13 downwards of 10 to episclerol venous pressure. So I thought that was interesting in normal tensives. We don't see that a lot with a lot of our compounds, that amount of a drop. Coa is the leading compound in Japan. And again, if you're looking for this data, it definitely will become available in the next year or so. But they reported at RVO a 24-hour nocturnal study, as well as an eight-week study in glaucoma patients. And they had significant hypoeremia. In fact, they had upwards of like 96% of mild to moderate hypoeremia. And they had an IOP reduction of 15 to 22, which is good. I don't know if I would call it great. I think they were a little disappointed. They also looked to be a TID drug rather than a BID drug. So when we think about what's going to be beneficial to our patients, I mean, would a drug like this that's additive to prostaglandin, if you use it three times a day, be helpful to our patients? Perhaps. It would be much better if it was a once a day drug and got a better IOP lowering. Aries currently in the clinic with a combo study, because the big question that comes up is, are these compounds additive to xalitant? So they're currently conducting this study. I think it may read out or report out at AAO, perhaps. But I'm not sure. And they're also doing a 24-hour efficacy study, which is an open-label study. And they're looking at 24-hour IOP control. And I think this is interesting, because, again, these compounds vasodilate. And they vasodilate all the channels on the eye. Episcleryl venous pressure may play a greater role at night, also contributes to IOP. IOP is higher at night. And again, the questions asked is, what is this compound doing at night? This study's being conducted out of Bob Weinraub's sleep lab. COA has two studies ongoing in Japan, phase three. A little unusual for phase three studies. They're calling them phase three, but they're not traditional phase three, as we know them. And again, just looking at IOP endpoints. So this is sort of just where everything stands in terms of compounds. Senju Novartis had a compound. They just continued it, too much hypoeremia. Santin had a compound, too much hypoeremia. And again, COA, ARRI, and then the alfios compound. There's a compound coming out of Denmark as well, but they're very, very early on. They're not even in preclinical yet, I don't think. So beyond IOP, well, what else could these compounds offer us beyond lowering IOP? Well, they could inhibit fibroblasts and macrophage migration. They can alter ICAM and TGF beta. So maybe they can improve inflammation on the ocular surface. Maybe if we use them in our glaucoma patients with ocular surface disease, we may have less ocular surface disease. Maybe they can improve surgical outcomes if you use them in patients who are having trabeculectomies. Well, they vasodilate as well. So again, maybe we can offer a benefit to these patients in the posterior segment. Maybe we can improve optic nerve perfusion or retinal perfusion. And then neuroprotection, actually. I don't like the term neuroprotection because of all the, I don't know, the controversy around the term. It's of interest, but everyone says you can't achieve it and there's no end points. But this compound does seem to have some role in preserving neurons and perhaps retinal ganglion cells. And it also is anti-apoptotic by inhibiting caspase. Some investigators, again, in Japan, did look at the Sigma compound in glaucoma filtering surgery, and this was in IOVS in 2007. And they looked at human tenon fiberblast gel contraction in vitro at several different concentrations and found that there was a decrease in the fiberblast migration, proliferation, and contraction. And then they put this into a rabbit model where they did a pretty straightforward trabeculectomy, actually a full thickness sclerostomy with a conch flap. And they called it a bleb score. I don't know if this is the best way to characterize your data, but the bleb score consisted of vascularization, scarring, and height. And then they also looked at these blebs, histopathologically, and found that, yes, the ones that had been treated with the rokinase inhibitor had less inflammation and less collagen deposition and fiberblasts. So in terms of vasodilation, that would be the other area. So inflammation, vasodilation, and potentially neuroprotective capabilities. Study done with Fazadel, they induced an ischemic optic nerve model in rabbits, and this was accomplished with endothelin. They gave endothelin intravitrally and caused vasoconstriction. They then treated these animals with Fazadel both topically and systemically. And they did show an improvement in blood flow as well as retinal ganglion cell count and visually evoked potential. So you've got some retention of structure and also retention of function by treating this model with these inhibitors. And then lastly, the neuroprotection. These inhibitors, well, rock is involved in astrocyte neuroinflammation. So again, if you inhibit rock, maybe you can affect astrocytes. And we've been speaking and looking at astrocytes in their involvement in glaucoma now for a while. So perhaps we're working through that pathway. The question came up of, well, if it's neuroprotective, where can it be neuroprotective? Where's the site of injury? So there was an elegant study done where they looked at injuries both to the axon, to the optic nerve, as well as to the retinal ganglion cell bodies. And if you treated, again, with a rokinase inhibitor, you had some preservation of the axons. And increased retinal ganglion cell survival. So again, depending upon where that insult is, whether it's in the cell body or the axons, there may be some role for this compound. Or this class of compounds. So in summary, I hope you can walk away with, just saying, hmm, that's an interesting target. And it's an interesting pathway. It has multifactorial mechanisms of action. And if you inhibit this pathway, there may be some benefits, both systemically and ophthalmologically. I think what I'm trying to push for, and as best I can within Altheos and other companies, is just because it doesn't work for IOP, don't give up on this compound. And it may offer other benefits in ophthalmic diseases. So it may have a role beyond glaucoma, and it also may have a role within glaucoma beyond IOP. There's potential here for research. So you can get the compound through research labs, and now that it's in the clinic, there's open INDs. So you actually can get the compound through the companies and look at other diseases in the clinic. It's a relatively, and I don't wanna use the word safe, but it has a good safety profile. So again, there's open opportunities here. So with that, I'm gonna say thank you. I'm gonna ask you if there's any questions, and the world of drug development. So the mice are doing well. Yes, Randy. So there's a discussion for this for a period of time. I don't know if that's gonna be decided. You're right, and from a preclinical development perspective, to get into the clinic, you can only do so much. This does vasodilate, so at high concentrations, you can imagine that it's gonna drop blood pressure, it's gonna give you reflex tachycardia. I'm talking again, oral prean-animals. Yeah, it affects perfusion. So I think it's really gonna come down to how potent is the compound? Where is it actually penetrating into the eye, and how much exposure there is systemically? They don't really know. They don't, yeah, they don't know, and from what I've gathered and understand, from the, again, the in vitro, so when you look at your inhibitory concentrations, apparently that doesn't translate completely to the clinic because it's a kinase, and there's so many other variables and so many other pathways that are affected. So in the cell culture, you could say, okay, we're inhibiting rock one or rock two, say 60%, but that, when you get into a living species, all bets are off. Well, yes, yes, because it actually affects the phosphorylation, so yes. Yes, Paul?  She actually mentioned ROP, and as I was thinking about this, I'm like, yeah, nobody's looked at that, but it definitely inhibits fibroblasts and fibroblast migration. So it's a good possibility, I would've stopped, sorry about that. Yeah, no, nobody's looked at that. But you're right, I mean, that's a true, it's a great question, Randy, is what is the consequences? And even thinking about patient safety in a first in human study, you try to look at any possible consequence. Yes, Nick? Oh, sorry. Oh, sorry. Phase four. Yep. Yep, exactly. I mean, I think one comfort, but again, every compound's different, is that Fazadel is approved in Japan, and I mean, they're pretty strict, they've got pretty high standards in terms of safety parameters and clinical trials, and their whole development pathway is actually much more complex than ours. They're very in tune to safety, not to say that we're not, but they're even more so. And not too much. You know, it's a relatively well-tolerated drug in an acute setting, that's the other compounding variable. Nick? Mm-hmm. Yep, I saw that paper. So, and maybe a little bit of my personal impressions will come out here, but I'll try to be completely neutral. So what Ari did, if you look at their study and their design, all of these companies are looking at dosing at night, and then looking at the hyperemia scale.  Maybe that'll make it more acceptable to patients. Some people believe it will, but it's, yeah, it's totally related to the mechanism, and it's tied in, and that was my question actually too, is it tied into efficacy? And it may very well be in this case as well. Yes. So from a glaucoma perspective, or from a systemic perspective? I mean, I can only speak to, you know, basically glaucoma in this case, and no, and I think the question is, people have actually looked upstream, so there's some compounds that, I think it was Merck had at, Paul Kaufman was very involved with a few years ago, and there's tons of papers on this, and it's upstream, so it actually hits more kinase pathways, and there he did a lot of work in monkeys, and there was endothelial disruption. Sure, it worked great at lowered IOP, but hyperemia increased corneal thickness because of the permeability, so you're very right. If we can bring it downstream and be more specific, we can probably eliminate a lot of these side effects, but I don't think that, because this pathway is so relatively new in ophthalmology, and you know, I mean, you could see it dying if it's only looked at for glaucoma, and there's too much hyperemia, then I don't see these compounds moving forward unless somebody gets the drive and the money and says, okay, well, let's look at a different indication. You're welcome. Thank you.


Hey friends, today we're hanging out at Epcot. My friend Lily Aldridge is getting her drink added to the menu at Lakava. This was a drink that was during the Festival of the Arts, so she's going to be there today making it and I wanted to come out and be one of the first people to try it. And then we're going to hang out at Epcot, ride some rides, eat some food and have a beautiful Epcot kind of day. But I do warn you, there is a storm brewing, so there might be some rain. Any hoos, let's go do this. Look at how empty the park is right now. I don't think I've ever seen it this empty at 10am, but like I said in the beginning there's a little bit of a storm coming in, so we could be getting a lot of rain any second now. The rain has been intense here in Florida the past couple days. I'm sure some of you guys saw my Hollywood Studios video where they basically just flooded and then Magic Kingdom flooded the following day and now I just found out that there's a tornado warning at Epcot, there's a tornado warning for today. So I mean we're here, might as well proceed with our plans and seek shelter in La Cava. I feel like that's the best place. It says the tornado warning is effective until 11am so an hour to go and it's not like overly like storming out, just a little bit of rain, but look at the way those clouds are moving in the sky. It's like they're almost racing. Well we'll see, we'll see what happens in the next hour. I'm gonna head straight back to the Mexico Pavilion because that's where we're gonna be meeting up with some of our friends and I wanted to point out the Epcot experience is closing down for good so I think we're gonna cut through there. If you have not been able to come out and check out the Epcot experience it is shutting down for good March 14th. So just a couple days away and this is really cool, I actually was really excited when I came here even though it does have a couple of projects that are no longer in the future here at Epcot, but it's still a really amazing thing to actually come and watch. Look at this, it's the metaverse. I am so excited to be here early in the morning to go to La Cava. I feel like it's such like an honor, especially because it doesn't officially open until 11am but we're gonna be able to go in at 10am and I'm so happy for Lily. She's getting her own drink on the menu here at Epcot. That is such an honor, you know what I mean? I feel like if it happened to me I would brag about it and she made this drink. Like she came up with all the ingredients, it's named after her, it's her special little baby so we're definitely gonna want to show it some love. We have officially made it into the Mexico Pavilion and look it's so like empty in here. Like I said I'm really loving the start of the day and if we get stuck in here during the storm, what better place to be stuck? You know what I mean? As I'm sitting here waiting to go in La Cava, it doesn't officially open until 11am but people keep on coming up and asking like what time is it open and I tell them 11am. So they think I'm just sitting here waiting for an hour to get a breakfast margarita and I think it's kind of hysterical. But here we are, just a couple more minutes and the doors will be opening up shortly. I don't think I've ever seen the doors shut here. So that's kind of a kind of a pleasant little surprise there. And here it is, the Lily. This was actually for Festival of the Arts and I ranked it my number one drink at the festival and I'm so happy to be back to actually have it for the first day it being on the menu here at La Cava and Lily's gonna be drinking it with us. And here she is, Lily herself. I'm so excited. I bet it's such a great honor to have your own drink here at La Cava, isn't it? It's such an honor. I love the coffee of Tila. I'm just my favorite bar in the world and that you are here with us. It makes me so happy because I'm such a big fan. Uh-oh. I told Nick this before. See, I just love your videos. They make me so happy and they make me feel like I'm just at Disney when I don't get to be here. So thank you. Oh, no, thank you. Thank you for being here. Alright, so this is Lily more of a makeup. Look at that. Thank you for all your sweet words during Festival of the Arts. It's a little bit different. We changed it for the bar, so it's kind of got like a makeover. So it's something new for La Cava. And then there's this amazing kind of presentation. So I wanted something that'd be fun for like pictures and Instagram videos. Yeah, a fancy drink. Yeah, a fancy drink. So this is our fancy version of the Lily Margarita. So when you order it, you'll get this presentation. This is like floral, so it smells really nice. And then... Voila, look at that. That is it. Oh, wow, it smells amazing. Can it smell good? Wait, I'm gonna have to... Yes! I love it. Alright, here we are. Cheers! So the one at the Festival of the Arts was shaking. Oh! So this one's on ice. I like it. And it's a bigger drink, too. It's a bigger drink.  This is rose petals, which I know a lot. I do? I do like it. I still have the cups from Festival of the Arts. Actually, I have three cups. That's awesome. Yeah, because I bought three different drinks. This one will have a takeaway test that has like a special thing on it to take away as well. So if you wanna think, this is the in-house version, but there's a special thing on it. Oh, I didn't know that. Now I'm excited. Yes! And I have a present for you. Oh, do you? Yes, I do. So, I got you a bottle of Casabucones. That is amazing. The one in the cocktail is Blanco, but this is a Diego. Oh! So it's gonna sign by me a pair of cups. Oh! Look at this! I'm gonna cherish this forever. So you're gonna enjoy it at home. Oh! But I, you know, I love you and I love your channel. Thank you! Please give us a thumbs up. Thank you. Thank you. I'm so excited. Cheers! One more time. Yes! Look at this violent essence right here. That is so majestic looking. Isn't it? It's like very majestic and that's in the drink. Yes. Wow! Oh, yeah. Oh, wow, that smells amazing. Wow! That is so cool. I don't think I've ever seen something like that. The tequila that is actually in the drink is Pasadragonas. And it's one of my favorite tequilas. And the founder and the maker of the tequila is actually here today, so we're gonna be able to try some of that tequila on its own and learn more about it. In Pasadragonas, we're a small batch tequila producer and we're trying to be part of the tequila producers that are pushing the collaboration of tequila production into the future. And we are trying to expand the tequila repertoire through quality and competition. And we really would love to prove that I got the experience in general to keep with our other very well-established categories in the world. So first of all, cheers to la Caba de Tequila. Salud! Salud, cheers! All the support you have always given us throughout the years. Thank you very much. It was really exciting to be here all together again. So, thank you. It is really awesome to be able to be in La Caba before it officially opens up and to be one of the first people to try the lily when it's officially on the menu. But now, it's open. It's open to the public. Instantly, the second the door is open. Look at this. There's already a line going out the door. All the tables are full. La Caba is a very popular spot here at Epcot. Here we go. This is the best part. The reveal of the floral... Here we go. Yes! All right. You ready? Let's do it. Beautiful. Right? Look at everybody buying the lily right now. I love it. Oh, these are the special takeaway cups. I love it. Very fancy. How awesome was that? I love La Caba, but I feel like when you're down there, time goes by so fast. And now, from drinking margaritas at 10 a.m. to coming out to daylight, it kind of messes with your mind because I thought it was going to be dark out. But I love the lily drink and I love Lily Aldridge. She is so awesome. Such a great friend. And I'm so happy that she has her own drink on the menu. Like, what an honor. You know what I mean? I think it's such a cool thing and I love the drink. You know what I mean? And if you do get it to go, you get a special little cup with it too, a little La Caba cup. So I'll definitely be keeping a couple of those. And now I think we're all going to go ride soaring. We're all going to go ride soaring after having margaritas at 10 a.m. It's so strange because it's very breezy out, but the rain like never came. It never got like super stormy out. And there was a lot of hype, you know what I mean, for this storm. So maybe we'll get hit a little bit later. So I'm happy I got my umbrella with me. But we're going to make our way up to Soaring now. B1 is the best way to go because everything is center and you're up the highest. I love it. Oh, here we go. We are ready for take-off. I love riding soaring. It always puts me in such an amazing mood. Now I think we're actually going to head out and grab a little lunch and make our way around World Showcase. You know, it's kind of strange because I thought it was going to be a very rainy day. And all of the forecast said that it was going to be rainy too. We had that severe tornado watch and nothing really happened. Nothing happened. So the one day I come prepared, nothing happens. I think it's just my luck. For lunch today, we're actually heading over to Tepenido. And I love it there. It's one of my all-time favorite restaurants. I've done plenty of dining reviews here. And if you guys watch the videos, you know how much I love it. Today it's going to be just very brief because I'm hanging out with Lily and some friends. So, you know, I don't want to go into a full dining review. But if you do want to see like a full dining review, I'll put a link in the description because it is really amazing. And here we are. Time for lunch at Tepenido. This is going to be so much fun. I love coming to Tepenido. You guys know this is one of my all-time favorite restaurants. And I'm so excited. I can't wait to see all the cool Disney references they do. I feel like it's not always the same thing. They definitely mix it up a little bit. And I'm excited. Very talented. Oh, that's the good stuff. Noodles here. Favorite part. Wow, Tepenido hit so hard. I feel so stuffed. I love that restaurant. And like I said, I really don't want to go into like too much detail, especially when you're with company. So, I was just really light and showed you some of the cool cooking tricks that they do and some of the food. But if you want to see a full review, I will add my video in the description below to check it out. And now I think we're going to make our way back out to future worlds. Maybe Test Track, maybe Club Cool. You know, there's something at Club Cool I really want to show you because it is really interesting and I think it's really fancy. So, definitely Club Cool. As I make my way up to future world, I like to listen to make sure Test Track is running. Instead of opening up the app to see if it's running, I just listen to see if I can hear the cars running in. It is running and it's so strange. Like I said, the weather is very unpredictable here. So, I think we're going to actually head to Club Cool first and then over to Test Track. And now I like pointing with my umbrella. I feel like this is something I can use it for since it's not raining. If you are unaware of what Test... If you don't know what Club Cool is, it's basically where you get to go in and sample all the different sodas from around the world. And it's a really fun, free thing. And I kind of want to do something a little dangerous. The last time I was in Club Cool, I was talking about some of the flavors that I don't like. Like, for instance, the barbecue soda. Like the soda tastes like barbecue. And it's supposed to be like a smart sour plum. So, I thought about mixing it with the Beverly, which is another bad soda.  And I don't even know why I'm doing this. Someone said it would be a good idea. So, we're going to try it. There is no way this is going to be anything but horrible. Look, I don't even know why I'm doing it. Someone said you should mix them together in the comments. And I was like, you know what? That sounds like a good idea. So, here we go. Not the fan. Not... Oh, no. No, David. No, David. I feel like I should try mixing something that might be delicious now. So, like, we'll do the Bon Bon, which is a blend of tropical flavors. And then probably we'll do... Oh, the watermelon from the Philippines. Do a little watermelon mix. A little bit of a mix. That's good. I like that. So, as you can see, some of the flavors when they're mixed together is actually pretty good. But I wouldn't recommend mixing anything with the China soda. I feel like the barbecue just overpowers it. I know you can mix Beverly with other things and it actually makes it a little bit better. But once you add China into the equation, boah. Now that we've done some experiments with soda, I think it's time to head to test track. And I'm also interested because I never really bring an umbrella in, so I'm not too sure what I have to do with my umbrella because I can't bring it in the car with me. It's too big to go in one of those sacs, so I'm going to figure out what I have to do with it. Looks like the wait time for test track is 70 minutes and we're not going to have to wait in line today. But earlier, I know the storm really kept the crowds down. But I think since the sun has come out, everyone's coming back to Epcot. Or they're coming to Epcot because maybe people just stayed at home or in the resorts and they didn't want to come out. But now it's open season. Open season on test track. They just said inclement weather is approaching, so there's a chance that vehicle testing will be suspended. So we're kind of... We're going on a hopin' of prayer here. Well, it looks like we're going to make it on either that or they're going to stop it and then we'll get a lightning lane return time. But we made it. We made it. Oh my Lord, a truck! I was starting to think my hat was not going to make it off that ride. Did you see that? I almost lost it. I went to go hold it because I saw it starting to slip a little bit and then whoop! And I had my hand there just in time. But I was a little sad because I would have lost my new hat because this is one of the newer ones I got. And I mean, Disney's usually really good with like finding them. Like Lost and Found at Disney is expert. Like I've recovered at least two or three different hats. One of them from the bottom of the Tower of Terror. And yeah, I probably would have got it back if I lost it. Now that we got done with test track, I think we're going to head back to the Mexico pavilion and maybe do the Grand Fiesta Tour. You know, I should have done that earlier, but I do have to say having Margaritas and then riding Soren definitely enhances the ride itself. I really, really did enjoy that. I feel like I should make that a tradition now. But now I think we're going to make our way to the Grand Fiesta Tour. I'm getting flashbacks already to this morning at 10 a.m. and look at the line for La Cava now. Holy moly, look at this. It wraps all the way around. A lot of people are excited to get the lily maybe. I mean, it's always a popular spot, but this is like really, really long. It also looks like we got a little lucky. There is no wait for the three Caballeros. That's pretty fun. You know what I mean? It's nice to see some rides where you don't have to wait. You can just walk on. And especially the past couple of weeks it's been so busy here. Like Hollywood Studios, almost impossible. But nice to see a little walk on attraction here at Epcot. The Grand Fiesta Tour starring the three Caballeros.  I don't know when they're going to take down this maze though. Sometimes I really feel claustrophobic coming through here. Oh, luckily we don't have to. We get to just walk around it. We're going to walk around, we're going to walk around the shields. Looks like we're getting front row too. Wait a second, where's my umbrella? I don't know. We're coming in hot. We're coming in hot here. Oh, sorry about that. Sorry about that. Uh-oh, I think I'm going to do it again. Well, this is going to be awkward. Oh no, I'm so sorry. Oh, I'm so sorry. I'm so sorry. Well, this is just getting awkward.  Now that we got off the ride, I have to go find my umbrella. I think I left it near a trash can. So I'm going to retrace my steps. But it's so funny because I went to go get in the ride. And I was just like, where's my umbrella? And then I realized I left it somewhere. And I'm pretty sure I know where it is. So we're going to go check to see if it's still there. Let's go get that umbrella. I hope it's still there. I think it's right on the outside here because I stopped to take a photo. Oh my lord, look at it. Look at it just saying there. Look at that. I can't believe nobody took it yet. But there it is. My umbrella is still here. Excellent. I really thought I was going to lose another umbrella there. I can't believe we're still there because I must have been in there for at least 25 minutes. And look at that. I didn't lose one. I didn't lose it. And since we're over here in World Showcase and we just got done doing the Grand Fiesta Tour, we're not doing another boat ride. Head on into Frozen ever after. I love the boat rides. The post at wait time for Frozen was, I think, 80 minutes when we walked in. But we're going up through the lightning lane. But this queue is not too bad to wait in because at least it's all indoors. I remember having to wait in China to ride Frozen. Even sometimes even far as back as Africa, like the African Outpost. Transitioning from queues that had social distancing to queues now. You always look at them and being like, no that's not a long wait because you're so used to see these gigantic lines. It's so beautiful. Yeah. What I say to say is that I'm selfish. I'm all frozen. I'm all lost. I'm really, really lonely. Now let's just call it a day. What I can't do. What I can't do. What I finally do. What Frozen things do. Frozen, like you might get a little bit, but I literally got splashed in big time. Did you notice the last clip with Olaf? There was water on my lens.  And I'm a soggy bottom boy. Like literally my whole terrace seat is a little pool there and I was sitting in it. Frozen was a lot of fun, but what is going on with the weather here in Florida? Like five hours ago, there was a severe tornado watch and now look at it. It is literally probably such a beautiful day out right now. Wow. Things just changed so quickly. And with that, I think we are done here today. I had such an amazing day today. Seriously, it's been so much fun getting here right at the park opening, thinking I was going to go through a huge storm, but then not going through a storm, having breakfast, margaritas, hanging out with Lily, hanging out with Lily in the La Cava, drinking her drink. Like that is so amazing. And thank you to La Cava for inviting me out and also thank you to Lily for coming up with such a really wonderful drink. And yeah, I hope you enjoyed the video because I enjoyed making it. We'll see you next time. Bye.