At least we still got to hit those combos even when it don't matter. How's he going everybody? Dato Doi here back with another round of Dragon Ball Fighters Rank Matches. This time we're playing a team of Cell, Super Saiyan Goku and Yamcha. Cell is obviously the forefront of our team here and mostly because I just, I really like this character. He's always been one of the, the more smoother, like right there. Oh, didn't mean to do that. Oh, damn it, that's right. Forgot Cell is one of those guys with Audi standard 2H. Okay, sliding, I'll take it. Ah, I pushed my luck there. I saw the sparking, I just got a little too aggressive anyway. Oh, 2M, something about that 2M animation looked a little aggressive. Ah, I couldn't 2H that, I'm going to get out of here though. Save a little bit of health, I don't want Cell dying out here too early. Oh, I thought my beam would be fast. Switch, there we go. And maybe this will kill? I don't think so.  How about I jump and drag it rough? Okay, okay, I'm liking what I'm seeing.  I got hit with a 2L. Oh, he just shot me into the air, jeering. I don't have any, level one, why? Oh, damn, that kind of, that level one is kind of nice. I forgot it brings you back down. I thought I was still going to be in the air, so I just kind of up decked. All right, well, we set the stage for him without Sparky. So I'm not too worried about the game. Well, maybe I am now. Okay, raw 2H, the damage potential is here. Let me go ahead and, oh my goodness, he just flipped me. All right, all right, comment down with the reflex and the counters and the whatnot. We got a game to win, boys. Now we got to go through his cell. Oh man, that was why the wake up counter, that was sick. That is, is the last time I'll go for a reset there. No super dash? I'm going to do it then. Okay. Yup, Yonchus is always waiting in the wings. I would like to get Goku out of here though, save the Sparky. You know what, I'll just do it. I'll just do it right now, because I'm going to miss my chance. Save it. Oh, damn it. I thought if I cut it early, he would get confused, the one for the reset. I was looking for an empty place to vanish and it looks like I just got my wish. Two, three, four, Goku assist. That might not have worked. It would have worked. All right, good. At least we still got to hit those combos even when it don't matter. And he's out of there. And he's gone, baby. He's gone.  All right, not going to lie. I feel a little tricked by the cell icon, all things considered, but I mean, it's a Vegeta blue player and his team is actually kind of unique. So I'll let it slide, I'll let it slide. That being said, I am expecting him to know how to guard against Cell, especially my young cell. Got him. Okay, but it was all a trick anyway. Nice, get him in the corner. I'm liking this, dude. Oh, that was a lot of lag there. I feel like I may have gotten the lucky end of that. Is it, there was a lot of, this wasn't this green? Hopefully it calms down. All right, it's getting there, it's getting there. This was a green bar match from what I remembered. Dragon rush is in my snap. Okay, I don't even think he knew what side. That was unlucky. Overhead. Oh, goodness. The overheads are here. All right, we're just gonna go back out to Cell. Why not? Why not let Cell take the reins? Faked it out, dude. Ooh, that should be a kill. Yeah, that is. All right, nice. Nicely done. I'm getting reflected a lot on Wake Up, but I honestly don't mind that too, too much. Cause we can play around that pretty easily. One, two. Damn, that was bad. Oh, Vegeta. You can't reflect the Cell, baby. You can't reflect Cell, dude. My man is too nice. Ah, let's go. Cell is too nice with it. And admittedly the frames might not help with the threat of a dragon rush around every corner, so every bit of pressure is even more important. Man, I feel dumb, I feel mad, dumb for that. Okay, let's block it, I'll block it out. Nice. Nice again, that should be a kill. All right, well, didn't have too much to say there. I was kind of just focused on trying to get through it. I don't know if he's gonna rematch. I think I'd be down. I think I'd be down for a rematch. He got a little better, it got better at the end. Way better compared to the beginning, but I would not blame him if he did. All right, we found another match. It's another Super Saiyan Rose, so there is quite a lot of points on the line. Playing an interesting team, another base Vegeta player. Whether or not he's, oh, right away calling me out with a little jab. All right, all right. So we're gonna have to play a little more defensively.  Okay, this guy clearly, this guy's been taking IQ pills. Snappy up back in the cell, okay, I can respect it. Two overheads didn't get that reflect or the blocks, for that matter. How do I down attack here? All right, car cancel, we out. That's good, that's good. That's gonna get us the corner as well. Ooh, all right, this is where we gotta take back a little bit of that momentum. Okay, momentum has been successfully taken back. I didn't mean for it to absolutely whiff, but I did think the reflect was coming. You know what, looking back, I think I, it's fine, I'll keep the beam assist out. We'll keep the beam assist out so we can get done.  Sometimes that happens. Oh God, poor, poor cell, I'm so sorry, man.  Welcome back, welcome back to Goku and he's still putting on a show, dude. But I think it is time for a little yamcha to get some time. Now, is he gonna spark here? That would be interesting, I'm not gonna predict it. Oh my God, we actually landed. That's a death, that is a one big pickup of a knockout, baby. That's a huge pickup for us and now we're moving into the final character. Beam assist starter, pretty strong here. Yep, super strong. You just gotta kind of take that block and then decide from there what you wanna do.  Okay, now the question here, it's gonna get pretty like, dude, does he spark? I mean, he kind of has to, right? Didn't do it enough. Okay, I'm not afraid to level two spark here, honestly. I think that might be brighter to do. There we go, that down heavy's gonna be massive. The healing factor just isn't there for him right now. That being said, I don't know if we got the burst damage we do on deck. Okay, I was worried about the odds of us actually bursting him there, but it seemed like the sparking would be sparking. I kind of got rid of a huge part of that heal factor. It just kind of made for a nice pickup of a win. I'll definitely, I'll definitely go again. I mean, I don't know how long this video is with how much we're cutting around. Hello, how's it going, man? How's it going, fellow Yancis sticker user? Oh, that cut me up a new one, dude. Okay, Super Dash, any, none of that, huh? Okay, okay, not the worst. You know what? I think we're not gonna go snap meta, but I am going to get the knockdown. Shouldn't the EX, I mean, I have to, good. Here we go, we're gonna get just enough. Am I, I might be done. I might be done to have held it for that long, but gotta live with our mistakes now. I can't believe I held it so long. Dantek worked out for us. Now give me back, give me back. Damn it. I am finding new and innovative ways to suck. New and innovative ways. These aren't your granddaddy solutions on how to get an old rousing round of Dragon Ball Fighters in. Again, I'm staggering too much. I gotta remember this was the guy that immediately punched me in the face for trying that. Level one into somebody's level three. Or, yeah, okay, get the power up while you get it, I guess. Makes sense to me, but it is looking like this is gonna be a big spark. Big spark hours. No, I gotta hit, I gotta hit right away. Hey, not the best. Where am I, oh my goodness. Yeah, that was us, that was a bit confusing. I probably would have masked there if I was him as well. I did not know whose turn that was. Come on down to sell, Tom, baby. That's all there is to it, come on down now. Let's see what the mix is. The mix was just an old-fashioned low. I wanted to test them, wanted to test them there. Damn it. Damn, I wonder if he's off, he's liking that. Coming down.  I love this team. Yeah, that might be the death of him. All right, good pick up on that one. Great win there, great team win, boys. Woo, all right, do we go another one? Because if we do go another one, that means we're going first to three and this might be a long video, but I do. I do go another one, I'm hungry for it. I want the games. All right, come on, Cell. One, two, two, one, two, two, bang. One, two, two, one, two, two, bang. Double three, hard knockdown, you know you gotta rely on Cell. I wish I learned the corner loops. Damn it, pick him. I think we do have to make the responsible decision and switch or not here. Yes, what a roller coaster.  Ah, I should have done having that for sure. That would have been great. Hello, keep the knockdowns coming though. Keep them coming. Just go for it, Cell, just do it. Just do what you gotta do, Cell, it's that easy. Didn't back dash far enough. Not nearly far enough for the old God 2H. Oh my God, the mortals beware. Ooh, okay, never mind. We gotta take a hard knock down here. Now, this is a situation where early sparking might not be as useful, at least in my opinion here.  Okay, this is gonna get him someone next to the corner, I guess.  No, that actually hit, that was kind of nice though, I'll give it up. I did not think it was hitting from that angle. Okay, this is gonna give us a hard knockdown, but with who is the question? I'm gonna go with Cell. Cell's been doing it off all game, I wanna at least let the character maybe finish it off.  Okay, well, we didn't get the full combo, but the reset was still an option. Cell takes the 3-0, definitely a good win for me. I don't know how long, I might cut out the middle set there if the video's too long, but regardless, I hope you guys enjoyed it. If you did, make sure to go down below, let me know all those things. Also while you're down there, leaving me a comment about your thoughts, make sure you hit the like button and subscribe to the channel if you do enjoy what you see here. We do a ton of fighting game content, including a full week of Broly coming up here very shortly, so definitely stick around and look forward to that. Other than that, if you wanna watch even more videos right now, there should be some up on your screen, so feel free to check those out if any of them catch your eye. I have been Dr. Joy though, I'm gonna get out of here now and I'll see you in the next one.


The study presents a SARS-CoV-2 subunit vaccine candidate that has been shown to be immunogenic in baboons and protective in mice using matrix M adjuvant. This article was authored by Jinghui Chen, Nita Patel, Robert Horped, and others.


So I'm just going to kind of give you the 30,000 foot view of what's going on in kidney cancer and feel free to stop me and ask questions. And some of these slides are pulled from decks, you know, that we give at sort of professional presentations. And I'll try to break it down for you since it's in a lingo that we're used to, that you may not be used to. So I'll try not to insult your intelligence, but really just let you know. Thank you. Sort of how we look at therapies on a big picture level for groups of patients and for individual patients, et cetera. So a lot of new therapy in kidney cancer, as many of you are aware of and many of you have been treated with, is these checkpoint inhibitors. And the way I explain it to patients, as some of you have heard, is basically removing the brakes on the immune system. So it goes like this. All of our bodies obviously have an immune system to fight infections. In part, that immune system also presumably would try to eradicate cancer cells, right, as being foreign. So immune system is meant to eradicate foreign substances, foreign cells, viral cells, fungal cells, et cetera, but also cancer cells. And that sort of basic interaction, this is even better, that basic interaction is listed here. So here's a tumor cell, in this case a kidney cancer cell. And antigen is just another word for protein. So cells express proteins on their surface. It's like their characteristics.  It's sort of the defining features of that cell. And normally a T cell, which is one of the immune system cells, not the only one, but the most important one, basically the way that a T cell fights a tumor cell is through this interaction right here. The protein expressed on a tumor cell engages this T cell receptor. This is called a ligand. This is called a receptor. And that engagement stimulates the T cell, right. And it stimulates the T cell to fight this tumor cell, to kill this tumor cell. So this is sort of, we'd call it T cell recognition of tumor cell. And the way it recognizes it is through this specific interaction. Now, normal physiology would dictate that you need sort of a positive and negative balance to anything, right. To blood pressure control, to anything in your body needs a positive and negative balance, including this interaction. So one of the ways that this is regulated is through this PD1, PDL1. So PD1 stands for Program Death 1, and it's called that because it's sort of a negative regulator. It would turn down this immune response. And so we talk about PD1 being expressed on T cells and PDL1, or the ligand, the Program Death Ligand 1 being expressed on tumor cells. So it's sort of a positive interaction and a negative interaction. And it's the balance of those interactions that determine whether or not this T cell is going to actually kill this tumor cell or become what we call anergic, sort of dead and lifeless and not able to do its job. And obviously, again, for normal physiology, you want a healthy balance of that. We'd all like these T cells to be stimulated, right. We want the balance of more positive than negative, but just as sort of a general look at this interaction. But it's important because it really underlies a lot of our therapy. And so I think I have this on the next, oh, I forgot my animation. Again, positive signals and negative signals. And again, we're trying to, in essence, accentuate the positive, right. So if we remove the negative, if you remember your math days, right, subtracting a negative is like adding a positive. So if we remove the negative, we're going to accentuate this positive T cell response, and that's everything. That's what we're trying to do. And now we have drugs that can basically block either PD1 or PDL1. And here are some names we'll be talking about specifically, and there are actually more on here. These are the ones in advanced clinical development and kidney cancer. It's not clear whether blocking this or this is better. Does it, should you block A or block B? We don't really know that yet. It doesn't appear to be a difference. Or should you block both of them? There are some trials that will come up in the next couple of years that will block both of them. And just to mention it, I won't talk about it, but this is not the only negative signal, the negative interaction on these T cells. There are a number of other molecules, a number of other checkpoints we would say, and there are drugs being developed against them. But this is just what has been clinically developed to date. So let's talk about specific data. So the only checkpoint drug approved in kidney cancer is this nevolumab drug. And I just told you nevolumab blocks PD1. So if it ends in AB, it's an antibody, no matter what the drug is. If it ends in AB, it's an antibody. So nevolumab is a drug that's an anti-PD1 antibody. So instead of allowing this negative interaction here, it covers this receptor. I don't have a picture, but basically this antibody binds the receptor, prevents the negative, again accentuating the positive. So there were a lot of preliminary studies with this drug. I won't go over it. This is what we resulted in this, what we would call a registration trial. That's a term that just means it's a trial meant to lead to FDA approval, which happened in this case. So these were patients who had advanced kidney cancer. Stratification just means making sure there's an equal number of patients with certain characteristics in each group. And they were randomized to either get nevolumab. It's a drug given intravenously every two weeks. In the trial, it was given as weight-based. It's now just given as a flat dose. Everybody gets 240 milligrams, but the dosing isn't important. Or a drug called Everolimus or Affinitor, which is an older drug that was commonly used in this setting, in this what we call refractory setting, meaning patients have been on one or more drugs and the drugs have failed them, and so now they're moving on to another therapy. And this was the main result of the trial. So there are a lot of ways to measure benefit of the drug. How many patients have tumors shrink? How much do they shrink? How long do they shrink? But obviously the ultimate way is, are we helping patients live longer? And so this was the primary endpoint of this trial. And as you can see, what we want to see, ideally what we'd see is a curve that does this, right? It goes straight across, right? That's what we're going for. So up and to the right is good. So when you see a comparison of curves like this, you know, the lighter-colored curve here is for patients who receive this Everolimus drug, and the darker one is for patients who got nevolumab. We commonly call it NIVO. The brand name is Optivo. You've probably seen the commercials. And basically, there was an improvement in survival of six months. So what that means is that, you know, on average, how long are we making patients live longer with this drug? It doesn't guarantee that benefit for all patients, and it doesn't limit the benefit, right? So you could get that drug, and it could make you live longer by years. Or you could get the drug, and it could not help you, right? That's true for any drug out there. So again, that's the difference between sort of average numbers and averages for the group and how it's going to affect an individual patient. The other way to look at it is this hazard ratio, which is a little more abstract. We always talk about medians as well, because it's a concrete number. It's an interval we can get our head around. Hazard ratio, what the hazard there is, in this case, is risk of dying. So if the hazard ratio is 0.73, what that means is that, instead of looking at a median, so a median is exactly the midpoint. So it's a comparison between the midpoint. A hazard ratio compares the lines across their whole length. Basically, what's the gap between these lines, not at any one point, but at every point along those lines. And a hazard ratio of that means there's a 27% reduced chance of death with this drug at any point in time. It's another way of thinking about the data. Again, it's actually, frankly, probably a more accurate way, because it takes into account all of the data, not just one point. So different ways of thinking about it. But nonetheless, this was really one of the first times that a drug had been shown to improve survival and kidney cancer. And it was the first time in this particular setting, to my knowledge. So this drug was approved almost exactly a year ago. I think it was November of 15. And it's commonly used as our second drug. Again, that's how it was studied. I mentioned there are different ways to look at effects of drug. Another one is called progression-free survival. So overall survival is obvious. Progression-free survival means how long do patients live without getting worse, without having their tumors get worse by a certain amount. So this is a little more interesting. So again, these numbers aren't nearly as impressive, right? So progression-free survival, or we commonly use the acronym PFS, was about four and a half months for each drug. What's a little bit interesting here, and I think we're still sorting out in clinical practice, is you can see these curves are really overlapping until you get to about 12 months, and then they start to split. And that may be for a variety of reasons. One is immunotherapy can have a bit of a more delayed effect than, say, drugs like Sutent and the like, which have a more immediate effect. And the other, and I think I have slides on this later, is part of what these drugs do is induce inflammation, right? We're trying to induce inflammation against the tumor. And so that can make tumors look bigger on a scan, when in fact that's actually a good thing. They're bigger because of tumor cells, excuse me. They're bigger because of immune cells, not because of tumor cells. And so some of these people who quote-unquote progressed and got worse actually didn't get worse. They were actually getting better. And that's just that our scans aren't perfect, right? When we look at a scan and we're looking at a nodule on there, there's no arrows that say, well, this much is tumor cell and this much is immune cell, right? It's just a white blob, right? You've all looked at scans with me and others, and you can see they're relatively imperfect. And so that's probably what's going on here as well. The other side of the coin, obviously, when we're talking about drugs is side effect or risk. So, sorry, this is a really complicated table, but basically it looks at the first three columns are nivolumab side effects, so to focus on that. When we think about side effects, we think about grade. So we grade from one through five, sort of mild, moderate, severe, life-threatening, and a grade five side effect is one that caused death, okay? So we want to see obviously low numbers on this page. This is the percent of patients who experience these side effects as related to treatment at some point while they were getting drug. And you don't really have any context, but I can tell you these numbers are pretty low. So we worry most about grade three and four side effects. Those are likely to be what bothers patients most. That's not entirely true. And if you've had grade two side effects, they're not terribly fun either, but in terms of sort of the more severe side effects, you can see they're really in single digits, you know, one or two percent. And that's really low compared to some of the other drugs we give. So the drug's really well tolerated. Even if you look at all grade side effects, even the most mild side effects, it's really pretty low. What I usually explain to patients is that, again, these drugs are meant to cause inflammation around the tumors, but they can cause inflammation around any organ in your body. And they commonly cause it around skin giving a rash or itchiness of the skin, diarrhea, sometimes lung inflammation, fatigue, sort of a generic side effect.  It's much lower. I don't think I have any slides on Sutent. We have a little bit of a comparison with this drug, which is probably better tolerated than Sutent. So, but, for instance, this top red box here, these are individual side effects, obviously. The top one is just saying, big picture, 18 percent of patients who took this drug had some grade three side effect. For Sutent, that number is probably 50 or 60 percent. Yeah, just sort of off the top of my head. It's somewhere in that range. On paper, actually, drugs like Sutent cause the same type of side effects, right? Diarrhea, fatigue, hand foot syndrome, right? All the stuff that you're familiar with, but the severity and the frequency is much less, is usually how I explain it to patients. And the mechanism of how it causes it is totally different, but that's sort of neither here nor there. All right, so this is what I was talking about with this sort of tumor flare. So, again, if we have a generic collection of tumor cells here, and if we did a scan, let's say this was a nodule in the lung, a kidney cancer nodule in the lung, and we did a scan and we measured, the way we measured tumors is just unidimensional. So I put a little electronic ruler here and I drag it across and I put it here. Not perfect, but it gives us a rough estimate of amount of tumor. And let's say this was two centimeters for the sake of argument. And then we give some immune therapy, nebola mabor, other therapy. What we're trying to do is induce those T cells to kill the tumor cells, right? By removing the negative, we're trying to stimulate those T cells to fight the cancer cells. But you could see if I put a ruler here and dragged it across and put it here, it would be bigger. It could be three centimeters, right? So that's a 50% increase if you do the math. But in actuality, it's a good thing. And again, there's no way to know this on a scan, but it's just a phenomenon. It doesn't happen quite as often as people talk about. So any of you who've read consents, right, know it's definitely going to happen. You're definitely going to get worse before you get better. That's not the case. It does happen. We're aware of it. But it's just sort of an interesting phenomenon that I think gets talked about more than it actually happens. And this text is really just saying the same thing. So this drug was, on the base of the trial I showed you, approved a year ago in previously treated kidney cancer. You have to have gotten at least one drug, like Sutent, to move on to this drug outside of a trial. And actually from melanoma, I think I showed this last year. So basically what happened is when these drugs, when drugs get developed, they're often developed broadly across diseases. And you do these trials and treat a lot of different people, and then you figure out, G, it's disease A, B, and C that responds, so we're going to continue development in those diseases. So melanoma has always been sort of linked with kidney cancer as a disease responsive to immune therapy. And so this drug was also developed in melanoma. In fact, that was really the first, first drug. And this is just a chart I'll explain it in a second that shows combination therapy. So not only patients got not only this nevolumab drug, we got another drug called ipilumumab, which inhibits a different checkpoint molecule. Not shown on that one schematic slide, but inhibits sort of basically two drugs to inhibit this process as opposed to one. This is what's called a spider plot. So basically each line is an individual patient and it measures their tumor burden over time. So they all start at zero, right? They have whatever disease they have going into treatment, and what we want to see is what's shown here for many to most patients. Their tumor burden goes down, this is percentage, so it goes down by 20, 40, 60, 80%, you know, when they get their first scan, and then it stays there.  So it gives you sort of a bird's eye view again of how the group did, more than curves can do, because it tells you about individual patients. Again, so a lot of people who had a response, obviously not everybody has a response, and some people who have more stable disease. So they don't have tumor shrink, but they have stability over a period of, you know, this is about a year or so.  We did this trial. This was a trial looking at different combinations of these drugs, just different doses. And the way this regimen is given is two drugs every three weeks for four doses. So there's four combo doses, and then they get nevolumab by itself as what we might call maintenance therapy. And so this was a preliminary trial that showed activity, I might have it here. I don't think I have the activity, but it showed activity, not quite as dramatic as melanoma, but clearly an active combination. Of course, as I have on the next slide here, two drugs are always more toxic than one, right? As oncologists, we love to put drugs together. It's sort of what we do. We love putting drugs together. And in many other diseases, combination therapy is what's led to cure of those diseases. Lymphoma, testicular cancer, there are many examples where one drug is not curative, but two, three, four drugs is. So that's the background of why we do it. This is a similar one of those tables. And again, I don't have the other one up here, but these numbers are higher than what is seen with the nevolumab alone. That's the end in this designation here. So again, getting these two drugs while maybe more effective, we don't know that yet, certainly causes more toxicity. And I bring it up because this large trial was done, has been completed, and we're waiting for results. So basically this said, okay, we know nevolumab by itself has activity. We know in a small trial that if we combine it, there could be more activity, although with more side effects. So let's use this combination as sort of an upfront initial immune therapy combination compared to good old Sutent, which is the standard of care. So this trial was ongoing. We accrued several patients that accrued, I don't know, maybe 800 or 1,000 worldwide. And the results probably should be out in the next one to two years, I'm guessing. And this may change the standard of care, right? Sutent is a standard, not the only one, but the most commonly used standard, certainly here. And again, this is now in patients who are treatment naive, right? So they haven't gotten any prior treatment. They just walk in the door and they're getting their first treatment. And so we'll see whether this combination has advantages over Sutent. But again, in the next year or two, that may really change how we approach, our sort of standard approach to patients. Obviously, this was done in the context of a clinical trial. And then I just have a few slides, sort of rapid fire about all the other trials going on. That one is sort of an example. And it's sort of the leading example, just because of the timeline over which it happened. But there are many others going. And they all have sort of a common theme. So these are all big randomized trials where you take patients and you allocate them, you randomize them into one of two or one of three groups. Sutent is often the control arm, right? It is the standard drug right now. So we use that to say, well, how would patients do on a standard therapy and compare them to how patients do on experimental therapies? This drug now has a much better name. It's called a tessellizumab. Oh, there it is. I think I spelled it wrong. Tessellizumab, it's actually approved in bladder cancer, but being studied in kidney cancer as well. And this trial looked at sutent versus getting that drug by itself versus a combination. The tessellizumab is also called a vastan. It's an anti-blood vessel antibody. It's been around for a long time, approved in kidney cancer. So, again, starting to mix and match drugs from different categories, if you will. Targeted therapy and immune therapy together, alone, et cetera. That was a phase two, which actually will get reported in next February. And then a large phase three is ongoing, again, very similar to the other combination looking at a combination therapy compared to sutent. So this trial is actually completed accrual as well. But it's behind in terms of timeline from the other one. And there are about five of these trials. Two, I guess, are done. Three are ongoing. This is an example of a combination that's going to be in a trial we have coming up. So, and again, it's an example of a combination of an immune antibody. Remember AB, antibody? Pembrolizumab is approved in lung cancer and probably some other things I'm forgetting. But it's also an anti-PD1 antibody combined with accident, which as you may know is a VEGF targeted therapy used commonly in the refractory setting. And so, again, a combination of an immune therapy and a targeted therapy. This was a phase one study. And there was some updated data presented a few weeks ago at a European meeting. This is on just a handful of patients. But you can see the spider plot here. Remember from the other trial, pretty much all patients had tumors get smaller. Super tiny amount of patients. But the response rate to this regimen in the updated data of about 50 or 60 patients was like 70%, which is about twice what we get with, say, a drug like Sudsen. Now, you know, drugs and combinations always look good in their initial data, right? If you treat a small number of patients, and so things generally tend to settle down if you will over time. But that's a really high number. It's as high as has ever been reported in kidney cancer, to my knowledge. So it looks like some of these newer combinations, you know, could have enhanced activity. Now, whether that'll play out into making patients live longer, right, which is the important outcome we don't know yet. That's what we're waiting for these big, large trials to do.  Should be open here soon. Again, very common theme. Combination of existing drug plus new drug versus existing drug is one way to think about it. Anti-blood vessel therapy, plus immune therapy versus anti-blood vessel therapy would be the other way to say it. And just yet another example. This is the trial that is just sort of finishing up now, again, but just to give you a sense that there's a lot of work going on here that is probably going to change the standard of care in kidney cancer. So right now it's Sudsen, but it may very well change in the next two, three, four years as these results become available, assuming that there's benefit, right? We don't know if there will or won't be. That's why we do the trial. And then just to tell you sort of what we're doing here on a local level, so this kind of trial is what we call a sponsored trial, right? The company who makes these drugs wants to do this trial and spend the money, which is about $125 million, because they'd like to get this approved, right? So it's a sponsored trial that we participate in. This kind of trial is what we call an investigator-initiated trial. That means we have an interesting kidney cancer in these drugs, and we have an idea, and we're not going to test it in 800 patients, but let's test it in 40 or 50 patients and see. And this is just the idea of giving this nivolumab drug intermittently instead of continuously. So one question with immune therapy. If you think about it, if we generate an effective anti-tumor immune response, just like if we gave you a flu shot and generated immune response, you don't need a flu shot every month, right? You need it once per season, or if you get a pneumonia vaccine, right? It's basically a lifetime. So if you're generating an anti-tumor response, excuse me, an immune response, it should be durable, ideally. And so maybe if we can induce an immune response with this drug that we could stop giving it at least for a period of time. Why would we do that? Well, to spare people side effects, right? So if you keep taking drugs, eventually you'll have side effects, right? And so if we can keep people off therapy, and I won't explain this whole complicated schema to you, but basically it's a way of treating people up front, and then if they have tumors get smaller, to basically hold the drug. And we did this actually with SU-10 and some data that's about to be reported, but basically extending this concept to newer drugs. So this is not yet open. It will be in a few months. And then the other sort of other end of the spectrum, neoadjuvant is a term that means giving drugs before surgery. So this is a study that's just about to open that's basically using some of these new checkpoint inhibitors in patients, not who have advanced disease, but who have localized disease. So they walk in the door with just a tumor in their kidney. They do not have advanced disease. And we're giving them these drugs and cohorts just means different groups of patients treated differently, the details aren't important, giving them before they get their surgery and a little bit after. And this is really more of a scientific study, right? So we can look at the tissue and look at those T cells and get smarter about do we need one drug or two drug or one dose or two dose or, you know, so just different things that we're interested in with the idea that this could have applicability to patients with advanced disease. So we would say this is just a platform to study the drugs for use in other settings, not that ultimately I think these drugs are necessarily going to be used in this setting. They may or may not, but it's really just a way for us to study it and obtain tissue to get smarter. So as I think about sort of the future of immune therapy and kidney cancer, what I hope is that, you know, we'll be able to sort of dial up and down again. We can give more drugs to more patients, but that's going to have more side effects and we're waiting to see if there's benefit. Ideally we could give patients as little therapy as possible, right? We could give you one drug that has barely any side effects. We induce a response and it's there forever, right? In an ideal world. It's not going to be possible, of course, for all patients. But if that one drug doesn't work, then we could add another. And so it takes a lot of years to figure all that out, but that's how I think it's going to sort of play out over the next five to 10 years. Not forgetting about our good old friends, Sutana Xitinibic Center, that VEGF therapy is still the standard of care as we stand here today. It will still have a role. The disease didn't suddenly become a different disease because these new drugs were introduced. So they're additive to what we have there. I don't think they're going to replace. And then I just wanted to mention some other new data that came out. So this was at this European Cancer Conference a few weeks ago. So a totally separate topic. So again, in patients who have non-metastatic kidney cancer, they walk in the door with the kidney tumor in place, they see the urologist, they get it cut out. So for those patients, there's no standard therapy, right? We basically just keep our fingers crossed and hope it doesn't recur. There is no therapy that's common. But there have been a number of trials to test what were, at the time, newer drugs like Sunitinib in that setting. Can we prevent your disease from coming back or can we delay it? And this was a large trial that was reported recently. Again, it was clear cell kidney cancer that confined to the kidney. They got surgery and then were randomized to get either Sutan or placebo. The reason there's a placebo in this trial is because doing nothing is the standard of care, right? It's advanced disease, but in this setting it's appropriate. And more confusing curves again, but basically if you look up here, this is sort of where the main result is, if you can see that, basically giving Sutan in this setting delayed the recurrence of disease by about a little over a year. Let me see if I have anything else in here. Yeah, and these are just the specific rates at different points in time. So, you know, it's not clear whether the drug will get FDA approved in this setting. It's not clear whether people will use it. It can have side effects. So, you tell me, I mean, as a patient, you're saying, well, I'm willing to put up with side effects for a year in exchange for delaying recurrence of my disease for a little over a year. And obviously that's a different equation for each patient. To tolerate it wonderfully is no big deal. If you don't tolerate it well at all, then it is a big deal. So, these data are really hot off the press and we're sort of waiting to see how it unfolds. Importantly, if the FDA approves it, which I think they will, but I don't know. And then how people actually use it in practice. But just wanted to mention it because it's some big, big new data that just came out. So, just to wrap up. So, immunotherapy. Nevolumab currently is approved after at least one treatment, but a lot of clinical trials are ongoing and this will change how we approach patients. There's no question about it. And then just briefly, the suit and after kidney surgery it does delay recurrence. But again, we're waiting to see what the FDA does and sort of that risk benefit, you know, I think is perhaps in question and I'm happy to get your input about it and talk about it. And it's also true that a lot of these immune therapies are now going to be studied in this setting. So, you get surgery and then get an immune therapy and those trials are just starting. So, that data is here as a way. Thanks, I'm happy to take any questions. So, the question was the brand name of this drug is called T-centric. It's this one. It's the Atezzolizumab. This one? No, not that one. This one? So, in kidney cancer it's still investigational. It's not FDA approved. So, you get FDA approval for a specific disease. So, the drug, it is approved in bladder cancer. It is still investigational in kidney cancer pending the result of this trial. Or maybe this trial. This trial might do it, but I have a feeling that the FDA will wait for this trial that's on the screen right now. So, this smaller trial will be reported in February. The issue is that, you know, the question really is sort of a big picture of the development questions. How much evidence is required to lead to drug approval, right? That's a big question. So, 300 patients seems like a lot, but it's really actually a fairly small number of patients. So, I don't know that the FDA will approve on the basis of this trial on the screen. The separate trial, which has completed a cruel, probably will be another probably good two years until it's reported. So, that's the sort of the good and bad news of these kind of trials is that they're big complicated trials. They take a while to do. They take a while to read out, we would say. So, again, drug development is slower than we'd all like, but it's just the nature of having to do these kind of trials to make sure there's benefit. So, I think it's going to be a couple of years. Answer your question. Stunned silence is falling over the crowd. Yes? Right, yeah, no, fair enough. So, a lot of those commercials you see for rheumatoid arthritis and plaxoriasis and all stuff, those are anti-inflammatory drugs. What I've just told you about are pro-inflammatory. So, we use some of those anti-inflammatory drugs to treat side effects. So, they're related and, you know, I don't know if that was your question, like, yeah, why is it exploding, is that the question? I don't know exactly. I mean, I think it's, you know, you just get it, you know, creating antibodies is a science and so, sometimes that science advances and then the science of understanding the disease. So, all these molecules I talked about 10 years ago, I mean, we knew about them, but they weren't even close to being clinically relevant, you know? So, you can know a lot about a disease and not have drugs to treat those targets or you can just not know the targets, right? And so, you know, the advances happen when you understand the targets, they actually matter and you have drugs to inhibit them and that's basically what's happening. Why is it happening now? I don't know, just basically because all those things are connected together. I don't know that, I guess maybe your question is the development of the anti-inflammatory related to the development of the pro-inflammatory? I don't think so, not to my knowledge. I don't know much about the anti-inflammatory drug development story, but I don't think they're related. Yeah. Say that again, I'm sorry. Patient. So, the median age of kidney cancers, yeah, about 62, median meaning half-older, half-younger. Yeah, I don't know about that. It's a good question. I have no way of knowing. I mean, the hypothesis is, well, gee, your immune system is getting weaker over time and that's why, but I don't know that that's the case. Age isn't really an important factor in outcome for patients. So, a patient who's 40 or 60 or 70 can do just as well, vice versa, so that would sort of argue against that. So, it's a good question. I have no way to ask it. We don't have a good way to measure the immune system, right? So, all those commercials of these products that boost your immune system, right? I mean, that's marketing, right? We have no way to measure it. I mean, you can't really measure immune competence. You can measure T-cells. You can measure a lot of stuff, whether it's actually related, you know, to reality is a different question. So, there is no good way for me to measure and say, aha, your immune system has this score and five years later it has this score. I don't know how to do that. All right, come on, more questions. So, for all comers, it's about 30%. If you take everybody who has their kidney removed for kidney cancer without other visible disease, about a third of people will have recurrence, depending on the size and the grade and the stage and if you have tumor cells in the renal vein and depending on a number of factors? Somewhere. Somewhere, anywhere. Yes, just recurrence in general. Yeah, usually not the other kidney. So, yeah, general. There was some more. It's a difficult question for a Sunday, I mean. So, the moonshot is a, you know, it's obviously a federal program, basically to pump money into cancer research. So, I don't know.  You know, money is a good thing, right? We need money to do all these trials. There's no question about it. And so, on some level, more money means more progress, but they're not directly correlated, right? We can pump a bunch of money into something and it fails, i.e., see the public school system. Right? I mean, we can, so money isn't, it's necessary but not sufficient. So, I'm all for any programs that can give money, you know, to fund cancer research and prioritize that over other things, right? I mean, it's pretty early to know whether it's happening or not. You know, I think the initiative is fairly early and I don't know that I know enough to answer that question. There aren't.  It's not like we're hoarding stuff and keeping secrets here, right? So, I guess it depends on what the specifics are. So, I mean, I think it's a good thing, but a lot, like a lot of big programs like that we'll see at the end of the day if it makes a difference. You know, there is definitely a marketing element to that, right? Calling it moonshot and we're going to do this and we're going to do that and it's great, but you know, for those of us in the trenches, reality is just slow, right? I mean, it's just hard. If it was a matter of writing a check, then great, let's do it, right? But it's harder than that. You got to understand the biology. You got to have the drugs. You know what I mean? So, there's some inherent things that you have to have or you won't make progress. And frankly, a lot of the recent progress with all these agents came well before moonshot, right? So, patients will be living longer with these drugs, having nothing to do with that program. So, it makes it hard to assess the impact, I guess, is my point, right? So, the spider plot where the only published data, the only public data is from a previous trial in like 10 patients or 20 patients, very small, so it's not terribly meaningful. It looks similar to the other ones I showed you, but, yeah, until those big trials are reported, that's when you get those nice charts to look at. Yeah, before that, I mean, I don't know the data. People up too late watching baseball last night? Sure. Sure, my pleasure, thank you. Okay, any other questions? Last chance. Yeah, exactly. That's true. All right, thank you. Thank you. Sure. Thank you.


No, I've never seen, I've seen a couple of clips on the old Instagram once in a while and have throwbacks of, you know, this guy or that guy and Rebels rocking the special teams unit or something like that.  So, you find the mistakes and you find the good things. Going to be weird seeing Jonu on the other side and just, I guess, kind of getting to see him again. Every year there's turnover in the league. Every year guys come from this team that go to different teams and different guys from other teams come here. I'm happy for Jonu and the contract that he signed. He's an extremely talented individual and I'm sure our defense is a plan for him. Like you said, you're used to an ever-changing lockdown, but has this year been played to hear as far as you guys come in every week, team meetings, or guys that get introduced, have you ever seen anything like it? No, I mean, I think we're, it's very close. Well, I think we're on the verge of saying NFL record of most guys played, you know, every week come prepared to win. That's, I mean, as cliche as that is, it's what we have to do. We're also present there. But you look around, got a path to the locker room tonight. Very good job. We got a team meeting on Wednesday. Introduces guys. Tell us about the transactions that Jon made. And so I try to make it a point to go and introduce myself to all those guys. And I mean, if you're here in this building, you're here to try to help us win. Taylor, on the offensive line, you guys have all been battling through different injuries and issues this season. It seems to be getting, you know, some more continuity and time on the line. And you're starting to feel that. How much, how might you guys be able to build off of that and improve down the stretch? Yeah, injuries happen. They, guys, you know, we don't plan for it. It just, it just happens. And so I know we're missing Nate right now. And I think Bruce did a good job stepping in. He plays a lot of effort, very athletic guard. I think that us as a unit, you know, every week is an opportunity to gain more confidence and gain more chemistry, a good game, more battle. You mentioned first and second down, boy, that could be this week. Did you feel like before the second half when you had to get away from it, that you were as close to getting the running game going without Derek back there as you've been? Yeah, I thought, I mean, we ran the ball efficiently in the first half of that game. And based on unfortunate circumstances, we weren't able to do that in the second half.  Every defense is different. And this defense does a great job of stopping the run, stopping the pass, creating turnovers, and not letting teams score. So we have to worry about everything this week.


All roles lead to the property show brought to you by the private property.co.za. The show is happening on the 27th to the 28th of August 2022 at the Santon Convention Center. Remember you can also join virtually from anywhere you are in the world. Tickets are available at thepropertyshow.co.za. And thank you so much for joining us for the Private Property Show podcast tonight. My name is Stumi and tonight we are talking saving and investing in the time of rising interest rates. But before we jump into our conversation, remember to engage with us and interact with us, send us your comments, your questions, anything that you would like to know or something that you may be struggling with currently in the property space. Send us those questions and you can stand in line to win 500 rand cash and the winner will be announced tomorrow. And also remember you can scoop those tickets to the to the property show that is happening in Santon. So tonight we are talking in interest rates and that they're rising and in fact I have somebody who is going to take us through this. I'm sitting with Tammi Kaile who is the head of savings and investments from Apsa Bank. Tammi, thank you so much for joining us, good evening. Thank you to me and thank you and hello to the listeners as well and the viewers. Thank you. Let's let's go straight into the conversation and talk about our interest rates. You know interest rates have been rising at a rapid rate in South Africa and a lot of people are asking themselves why is the Reserve Bank doing this? Do you maybe want to take us through some of that rationale? Yeah, thanks. Thanks for this. I think what what we need to do is, you know, as as viewers and as people look at what's happening globally, you know, first and foremost, I mean, I think you can see, you know, that the interest rates are rising all over. And that's also being informed, you know, by the level of inflation going on, you know, globally as well. I mean, I think as you can see today, you know, it does announce that the inflation rates inflation rather went up by 7.4 percent. You know, whereas the previous month, it was 6.5 percent. You know, this is out of the of the reserve Reserve Bank's mandates and their mandates generally is to is to maintain inflation between 3 and 6 percent. You know, already at six and a half and then seven 7.4 percent. It's already quite significantly high. Now, the banks mandates generally is driven by making sure that they contain inflation and interest rates is one of the levers there. Many that they utilize, but then one of the major ones is is interest rates. You know, so so where inflation goes up, interest rates tends to go up, you know, and also as inflation goes down, then, of course, interest rates will also tend to to follow that particular trend. And that really is the driver. I mean, I think everybody can see, you know, if we talk about why inflation is going up, you know, because that's that's what's what's really is happening.  I think they're also making matters a lot more worse than than we all anticipated. And as a result, you know, you know, economies are trying to to contain this inflation and interest rates, you know, increases usually would be the one that gets to be utilized most. Sure. And with all that is happening, what is the best way one can save and make sure that they have some even savings that they can use in times of need? Yeah. So I guess with interest rates going up, it really is depends on depends on which side of the fence you are you are at.   I think that will be the starting point that you will have to look at, you know, as a consumer. And then of course, you know, looking at where the interest rates are best positioned, you know, for you and the amount that you have and also in terms of accessibility of those funds as well, does play a significant role in where you would put the funds, you know, as well for us. Yeah, and talking about putting the funds in different places, if someone has disposable cash currently, where would you say is the best place to put them? Would they maybe put it in a house loan or a home loan, rather, savings or investment account, or even maybe try and acquire new properties and maybe a new investment? What would you advise someone to do in these times? Well, firstly, it's a good problem to have, you know, so when you when you have extra cash, I think, you know, consumers are really struggling right now with the rising as I think we've spoken about the rising in in petrol prices, you know, and and just the living costs, you know, generally, you know, have been on the increase, you know, in the last last while, you know, so that's the that's the first thing.  It's important that you put it away for for some rainy days, you know, I think what we normally call emergency funds. Now, in terms of that decision, you know, around where do you do it? And again, back to those who are sitting in the middle of the fence, who have a bit of borrowing, but also have a bit of savings.  You know, I think these things depend, you know, I think we always encourage both that you must do, you know, servicing of your debts whilst you're also doing a bit of saving, because saving really is a is a is not easy, you know, it's not easy to save. And so it's important that that behavior of saving gets to be encouraged and gets to be, you know, adopted fairly early on, as soon as you can. At the same time, if you look at the APSA, you know, home loan as an example with, you know, with the flexor reserve, what it does help you with is that you can actually put extra money that if you need to access it at a later stage, you will then, you know, have access to it. Now, the good thing about that is because, you know, as you put extra more money into that home loan account, you are reducing the capital that is utilized to calculate, you know, your interest rate. So what it does is it saves you a bit more interest, interest costs or interest expense. But what it also does is that it reduces, you know, over time, of course, you know, the time it takes for you to repay or settle your your home loan as well. So there is the benefit of putting it into a home loan account, you know, so that you almost, you know, benefit as I've just indicated. But at the same time, putting it into a savings account, a bit in a savings account, you know, so that you've got something on the side that will help you for some kind of images that you might be experiencing. Sure. No great tips there. And thank you so much for sharing that. And one of the other things that you normally hear people do is using a credit card as a savings account where people now put money and then use it at a later stage. Would you say that this is wise? So two things to that.   That's a huge benefit already. You know, it means that you get to use those funds for free. That's a starting point, a very wise and savvy approach to using credit.  You know, so they will encourage, you know, consumers and customers that they actually look at the alternative, you know, which is to put it into a separate savings account where you get to end interest out of as well. Sure. And where can one get a prime rate in terms of investing and savings? And if what, how does one even qualify for it? How can how can one make them make sure that they are ready and they are a good candidate for it? Yeah, so, so I think, you know, with prime, you know, prime is currently at point 25, as we speak. And, you know, if you, if you were to put it into an investment account, you'll have to just really think about, you know, where you can get a return that is that significant, you know, and I think there are a lot of options that you can have.  You know, so I think, you know, it might be worth a while to, you know, for a consumer to look into that as an option.  So, so again, it all depends firstly on the, on the consumer's appetite, you know, for risk. But I think if you want something that's safe and secure and capital guaranteed, you know, a fixed deposit, you know, is one of the products that you could really consider. And I think you would need to consider somewhere between, you know, two years and above and as well as three years, you know, so I think it will give you a very sizable. And what's nice there, you know, just maybe if I may add to me is that, you know, those are above inflation, you know, so what you're getting, you know, at fixed deposits, you know, at 8.25 as an example, you know, you know, you're getting far better than what inflation is sitting at 7.4. So you get real growth, you know, because that's one of the things that consumers would want to look out for as well. Line, so Tommy, we were talking about some of those factors to consider when you are investing. You were going? Yeah, yeah, I was I was saying, you know, I think time is quite an important thing that people tend to understate. And I think give yourself time to view your investment, making sure that it's still giving you what you're looking for.   But if you if you're wanting something that's secure like capital guaranteed, but also with an upside, you know, of interest benefit that you would get, then you would look at things like our fixed deposits, you know, and and our tax receivings, savings account, you know, as well, which are easily accessible on our websites, you know, and our banking app at the same time as well. So and of course, you know, I think if you want to do anything that's you know, further than that, I think what we generally do encourage, you know, consumers is to engage with our financial advisors, you know, I think people tend to shy away from speaking to a financial advisor, assuming that it is quite costly.  Ultimately, it's your decision, but you do need to get guidance that the last piece for me would be, you know, an assessment of whether you've got any emergency funds, you know, so it's no use, you know, taking all of your money that you already have and putting into investments that might end up not being too secure. And you don't have, you know, emergency funds and should any emergencies happen, now you need to go tap into that investment as well. Again, you know, so we want, you know, we do tend to encourage that consumers do look into that as well. You know, so those there's a couple of things that you can look at, but those are the core that I think, you know, would be important for anyone to start to considering, you know, before they make a lifelong, you know, decisions around their money. Yeah, and just speaking about financial advisers, would it be wise for somebody to look for an independent one or should would would absent be offering some of these services and how would one go about procuring services like that? Well, I think it's important that you get a financial advisor that you are comfortable with. I mean, as a consumer, you know, somebody you are, you are comfortable to open up and provide them as much information as they are asking, you know, in order for them to be able to give you the best possible assessment and and maybe still or guiding, you know, so I mean, I think ourselves as APSA, we have financial advisers available across the all of our branches in our branch network, and they actually even, you know, be in a position to come to your location to have conversations in our around this as well. You know, so I think we do encourage and they come actually free of charge, you know, there is no fee for an engagement point, you know, so when assessment needs to be done, I think it's important that, you know, as I've indicated that consumer take and fund consumers take advantage of this. And and I think a decision thereafter can be made. But I think to your question is it important? I think it's super critical because there's so much information that's out there and it can be overwhelming, you know, for me as a person who works and I do not necessarily have the time to consume all the content that's available on on on the websites, you know, around investments, you know, and I do need to speak to someone. You know, if you're not calling us directly, you can even engage with the advisers in as as I've just indicated. Sure. You know, talking about education, it's very important that we we teach young kids as well to start this from a young age and are they any maybe young children or even young adults tailored products and how can maybe parents, you know, educate their children in terms of how not to succumb to to brand pressures and, you know, peer pressures on how they they spend their money and really just contribute to to building the family wealth and building wealth, you know. So so it's interesting you bring that point to me because I think children and and, you know, and kids are really impressionable right, you know, at a very young age and and when they look at their parents, they they see heroes, you know, you know, I think, you know, yes, there is a lot of pressure from peers and at school and wherever that they they engage with with with their peers. But I think at home, there is an even more significant, you know, influence that can that can be achieved.  And I think that's important, you know. And then the second thing for me is is really just, you know, encouraging them and also making them aware that money is not infinite. It is it is finite.  So we think that that's important. It's important also to make it fun, you know, if you don't make it fun.  And I think it's important that we do apply those principles. And then, of course, it's important that you almost create a separate account, you know, specifically for them. Let them have experiment and experience the use of a card, the use of of an account.   And and I think that that in my mind is a starting point to making saving a culture in their lives, you know, as a as a way of living in their lives was, you know, to to leave it and they start when they are older. I think there's a lot more difficulties, you know, that you in that you would encounter, you know, as an adult, you know, in in starting to save when you had not been used to to it.  Great stuff. Thank you so much for that. We've spoken extensively about the investment vehicles that apps are offers for saving an investment. So any last words or advice that you would give anybody who wants to get into the space of investing or even maybe pivot the investment journey because they've been investing and now they really just would like to take it to to to a new level or new horizon altogether. Any last words? Yeah, so the reality is the cost of living is really escalating, you know, someone thinking might not have enough, you know, money to save.  I think that's at the at the level of, you know, wanting to get yourself from one paycheck to the other. I think as a starting point, but someone who already are saying I've invested, I've got enough, I've got a surplus, you know, that I really want to see what I can do. I think again, Apsa offers the ability to buy property for investments, you know, and I think that that also can be taken advantage of and and be done, you know, and also other alternative businesses that can be done. But I think the key thing for me is that, you know, we've got products that allow us to invest for long term. You know, I think about tax free savings products that, you know, we have in our space that allow you just to invest, get the returns, but at the same time, you know, not pay tax out of that, those returns as well. You know, I think it's almost a double benefits that you get to achieve. And I think that consumers must think about that, you know, but actually the last part, you know, that for me is even more critical is that have a look at your at your financial, you know, situation and review it with the aim, you know, to see whether there are any opportunities to open up capacity for saving. You know, I think we always talk about just have a look at your bank statement, you know, just see whether is there anything that you think, you know, you should be not be paying for that is actually in your statement.  Tommy, thank you so much. Such great insights that we have received from you tonight. Thank you so much for joining us and sharing your your wealth of knowledge because it's definitely a wealth of knowledge. Have a good evening. No, thank you. Thank you to me and thank you to the viewers and listeners. Thank you so much. So review your spend and look for that opportunity to save as well as invest some of that disposable income. Thank you so much for joining us for today's episode, right here on the private property podcast till the next time we see you every week day, 7 p.m. Have a good night.


Everybody forced to it rip in 2022 top transcendent collection baseball case number 11 random hit style So we have 58 hits inside this case right here I'll get it open and bring it over here just like we have been this is 11th case So you guys have pretty much seen it by now But we're gonna have a wander Frank or Vlad jr. Through the years 50 card base at this day sealed It's number to 99. It's about to change that Transcendent gold deco auto one-of-one oversized caught auto or tool caught auto or letter patch auto As an item transcendent chrome four card pack with least one super fracture. That's gonna stay sealed One-of-one auto patch or bat knob nameplate book Bat knob or slash nameplate a 1958 top super factor auto a Transcendent VIP party invitation number to 99 and then 50 framed autos with at least two one-on-ones in the full set Those are all individual hits. So here we go. Y'all. Good luck. Maybe I'll save the Babe Ruth for Kyle What if that actually happens what if it isn't the one you open very kind of you I'm gonna bring that back up and be like look How nice I was I'll just Everyone I saved the babe Every time that's for a favor. That's for a favor. That's for a favor. All right party invitation RCP by April 26th. I believe it says What's everyone's favorite hit today so far through 10 cases I'm gonna be biased and say the David Ortiz patch auto one-of-one I'll just I'll just be biased We went we went against the grain Nobody thought we would pick those Kyle 78 of non-yarn. All right. There's their oversized cut Letter patch auto or dual caught auto top transcendent pack gonna stay sealed with one super factor inside at least four chrome cards The Super Fractor 1958 design Super Fractor auto 50 card base set gonna stay sealed also numbered 78 of 99 Through the years Vladdy or wonder one-of-one there the Deco gold one-of-one and this isn't a book So it's gonna be a patch auto one-of-one Then last thing in here. Oh Look at that. They got the freshness thing. That's not some of this. She ran that off the end I 50 Framed autos one redemption. I can only imagine who that's gonna be 50 framed autos. Those are all individualized open those up and go through I'm typing out control I think I think I saw Brad pull a Helen Keller out of this Think Brad pulled a Helen Keller cut auto you also pull the Stevie Wonder and someone in chat asked how do they sign it?  Framed autos. I think it was a Helen Keller. I think it was Or maybe I just saw it pulled somewhere else. That'd be a really good one Paul revere Russell Wilson dual cut what? Oh, let's Yeah, I like that. I'm in Let's totally let's totally get a Paul revere cut auto and put Russell Wilson's right next to it What an idea you want to make people hate the sports card hobby. Let's do that All right, so our judge of Belcher who we started with Judge seven to ten purple auto That's awesome. Always good to start with with the judge low-numbered at that All right green to 15 is an Adrian Beltray auto 9 to 15 If that's correct we're sold out What I just saw is correct and we're sold by what what just happened I just confirmed us 58 spots on all we're sold out guys Holy crap. What just happened? Who bought what? I I didn't see I deleted the orders I think it it's just a lot of orders Appreciate it guys Although Michael has bought a few Yep, Michael has bought a few Let's see that thank you Michael very much Best of luck later, man And our pool also to 15 out of 20 the machine It wasn't it wasn't it wasn't them Ernie if someone else but we are sold out for the night. Oh my goodness Every little bit of space for personals later on everybody a little bit Alec Thomas work you out of 11 to 15 Alec Thomas 11 to 15 Barry Larkin auto nine out of 10 Barry Larkin nine of 10 Bobby Whit jr. Three of 10 10 minus three jersey number Let's go Bobby Whit guys get your group break spots for tomorrow as well Starting off with prison premier league court Kings contenders and there's a full divisions case of prism tomorrow during the day as well And I'll be here tomorrow for some hockey baseball basketball and football In the evening Bobby Whit three of 10 big time Bobby Big hit Bob Bo Jackson 12 out of 15 on the auto Bo knows Rookie Otto Brandon Marsh 10 of 15 Brandon Marsh 10 of 15 rookie Otto Bryce Harper six of 10 Nice Bryce No way man ruby One of one rookie Otto Bryson Stott pulled a vertical last time right? Yeah, we pulled both ruby stott rookie autos one out of one the Phillies are flying right now in this That's a monster That's big card Shoo, Brian stoot Need to stop what you're doing right now Buster pose the auto seven to 20 buster Cal ripkin jr. Auto three of 20 california ripkin jr Hey, Carl Yastremski Carlifornia Yastremski 13 of 15 on the auto doesn't work does it? Yeah What's your uh, what is it again? my ypm y tpm yastremski's typed per minute How is it getting worse? I can't figure it out My name is ridiculous cc sabatio auto bookend 10 of 10 The struggle is becoming greater Get some water Man, it's killing me tonight. It's all like yelling and talking Dude, I don't know what I'm gonna do when I'm over there and you're breaking. I'm gonna have to like type and top of it I don't know what I'm gonna do Chipper jones auto one of 15 Chipper jones by the time it's time for the random we switch. I'll just you're just gonna have to do so much work over there Chipper jones one of 15 To 15 again now is a cody bellinger 15 of 15 cody bellinger Where do you go to the cubs former MVP ruby one of one corey seager auto That's a lane card right there corey seager one of one former World series mvp one of the transcendent boxes Got a derrick jeter auto jersey number two of 10 We're cooking with the frames here. We're cooking with the frames um, I'm sure some other shops have them but uh We are sold out of hours Got 15 breaking them all jeter two of 10 Holy cow, man Next is a donny baseball eight of 20 Oh the empty case, um, I'm not sure. We did we we did we don't sell them. We don't uh Sell or ship them eight of 20 don mattingly auto Tatis auto four out of 10 Cooking with the frames sounds weird four of 10, but it works Tatis Frank thomas the big hurt auto 13 of 20 Back-to-back mvp winner what 93 94 I think Frank thomas George springer auto two of 15 I think everybody's exhausted chat's quiet I'm worried myself out green auto greg maddox five out of 15 Mad ducks angry birds greg angry birds purple to 10 Hunter green seven to ten rookie auto reds Guy throws 105 We break again tomorrow. So kenzie's during the daytime. I'll be here in the at night Life's hunter green there next up is a rookie auto jaren durand six of 20 soundly waiting redemption I we've only seen one today Uh image variation again jeremy panya. That's the third base image variation. Oh no purple parallel this time purple nice to 10 on the panya Good luck on this one Good luck on the panya to 10 purple parallel variation auto so horizontal to 10 Yeah, and sam will be sunday With the old switcheroo this week Joey vato auto one of 20 Joey vato vato vato Johnny bench auto 14 of 15 Johnny bench 14 of 15 Shipping is free worldwide Re-shipping jonathan india auto four of 20 Uh, we have pulled no cardinals yet, right? Pulls us into this one Oh, he was here. What yeah, we pulled the pools of 20 I'm just looking at the list because I didn't remember it jonathan india there Yeah, steven. We're all sold out Someone came in and grabbed I think everything that was left in case 15 That's all that's all the spots right there guys Still personal tonight group break starting 10 a.m. tomorrow with kenzie starts with prison premier league I've certainly been enjoying prison premier league same with kyle Got a jose abrey u auto 12 out of 15 We're on case 11 Shipping is free prestige worldwide For why why why so after bray you Green nice julio radriguez for a 15 rookie auto Best of luck everybody 415 julio radriguez Mariano Rivera 18 at 20 with the mean mug Awesome moe went on to a miguel cabrera 17 of 20 nice miggy Yeah, maybe steven I don't know man. It's always so tempting. There's so many good things to be had in these cases Gonna miss rustle mania It's not too busy, man. Mike piazza auto 16 to 20. I might be able to watch some on sunday at least Today is do they air it on peacock like the whole thing like live So I have peacock. I don't have tv or is it just all day tomorrow Mike schmidt auto 5 out of 20 Schmitty Then I will miss it I'm too busy What's that for mike? Mike Mike and mike ruby mike ruby mike One of one the one of ones you've hit have been unreal tonight In the framed autos color match Mike trout here on a heater with some of these On fire good luck on that everybody jeez jeez Oh, man Nicoladolo rookie auto 11 to 20 What's up, dan and we're we're cooking we're cooking They let us cook they let kyle and I cook No one ryan auto 3 of 15. It has kind of been silly though.  I'm missing O'Neill cruise two of 20 rookie auto O'Neill cruise hit a tank yesterday After that the wizard ozzy smith auto 9 of 10 The wizard also known as dr. Strange Next up paul gulchman auto 20 20 back-to-back cartinals legends nlmvp paul gulchman How many of you guys took advantage of the top scrum buyback program? Oh lsc 11 3 run Well, man It's all I know about that game. I haven't watched any of it too busy too busy Peter Lanzo auto 9 at 20 polar p with a smile is cheesing How much dan you're ripping any scarlet and violet today? Randy johnson auto 10 at 20 the big unit robin yant auto 13 of 20 count on yant holla famer rod caru 17 of 20 on the auto Well, I mean now you should because The buyback program's over But if you had base, yeah, you you should definitely hopefully Got your uh 20 bucks a pop on those right 20 bucks for the base I think that's what it was I'm sorry, dude. I'm sorry, man No way platinum one of one Ronald akunya jr Trout and akunya the one of ones in the frame set this time scooby-dooby karoo Goodness gracious. I didn't realize that illegal. Thank you Ryan sandberg auto 6 of 15 rookie auto spencer tokelson 14 of 20 It wasn't in this one. All right, this is a spencer. Yeah, trade turner auto 12 of 20. This is the first time we haven't had him but 61 names so trade turner auto 12 of 20. I guess this trade off for getting a drowning community of one of one and like In like eight other mags on the frames Don't throw a whole clip. There might not be a wander then in this Let's see the wander Okay, there is a wander here 20 to 20 rookie auto so that we didn't we didn't get a vlad didn't get a show Hey, there's a big big names that I that I can think up top of my head Wander franco 20 of 20. That's not going to sleep. It's going to the mag Illegal so smart and glad he's here in channel every time contributing so much This through the years is just a vlady jr. Get a lot of vlady for us in these This one is 1997 tops vlady jr through the years auto one of one Some of those late 90s or 2000 designs are some of my favorite. I think Deco Deco gold auto one of one Dodger helmet old Dodger helmet Piazza, maybe Oh, yeah, piazza Mike piazza one of one Take sure it is a Dodger here on the deco gold auto man piazza Everybody likes piazza. Okay patch auto one of one patch auto one of one Astros Jordan alvarez Hit a mammoth shot dude. He went like 450 yesterday. I think Dude's crazy three color game use patch auto one of one.  Give us a healthy season of buxton. I should just save these for the next Took me it took me uh Six cases to figure that out to just save these instead of using the fillers So it goes I guess we're getting there again. Yeah, we're making progress case by case Okay Now we've got an oversized cut auto dual cut auto or A nameplate patch auto Yeah, I knew Anil Cruz did too. Yeah, there were some guys that hit some monsters yesterday a couple a couple of big lefties This is this is a dual Okay, it's it's a cut. I see an old Like a black and white photo Grover cleveland Whoa grover cleveland Cut auto one of one 22nd and 24th u.s president. What a guy What a guy grover cleveland oversized cut auto one of one The guy who invented the cleveland browns. I think that's what I named him that She never just ragged on cleveland now Ragged on cleveland. Oh boy. I didn't mean to start this. Yeah, the dates on it pretty cool I mean with a lot of those guys 1896. When did he die? He died pretty shortly after that, right? 98 or something. So I'm pretty crazy So we had four one of ones in the frame so I didn't realize that But it's it's it's always two sometimes is three. We've only seen two all night tonight So that makes sense. We would get an extra one there and they were really freaking good This is what you got either one of these. We don't know Piazza Okay That's fine. All right random time. Good luck everybody names hit same amount of time Put them side by side to see who's get what? 10 Well a pair of fives names first one two three four five six seven eight nine and 10 Jason c is on the top and bottom there and the hits 10 times best of luck y'all one two three four five six seven eight nine 10 Johnny bench Down to the yard on alorez one of one Jason c with the bench the peña redemption and the abray you john a the Bryson's start one of one Jason c the corey seager one of one The ladolo and the sabatia john a another pack he had a pack at earlier too Yeah Hey john pack magnet jason c wander franco john a buster posi john c with a Glad jr. One went through the years cal ripkin tautis o'neill cruise Greg maddox chipper jones brandon marsh Derek jeter two of ten jersey number bobby wit jr Acuña platinum one of one auto Goldschmidt bullholz randy johnson grover cleveland oversize cut signature nullan ryan Mike piazza deco one of one a trade turner 17 out of 20 jonathan india Aussie smith john a with the uh invitation congrats john Jason c sandberg bell tray And hunter green steven l with a jaren durand rookie out of 20 jason c the superfactor biren buxton don mattingly frank thomas spencer torkelson harper piazza springer steven l with the mariano out of 20 Jason c pita lanzo cody bellinger julia rodriguez alex thomas rod caru erin judge carlie stromsky mike schmidt bow jackson miguel cabrera thomas b with the joey vato out of 20 and jason c with the larkin The trout ruby one of one robin yount the basset and the one-of-one jordan alvarez auto patch That'll do it for number 11 12 is up next everybody


Productivity is a key component in making ourselves viable. And we need to wake up to the fact that it is at competitiveness globally that's going to allow us to succeed. And productivity starts at micro level in your office space, even in your home. Are you generating the greatest output with the resources you have? But resources are not just money. And so why wouldn't it be the interest of every government to want to see its people as productive as possible? Because that's going to add to the wealth of our country. The wealth of our country is what's required to generate the necessary resources to pay for our social services. Health care, education, infrastructure, sporting activities, all are important. For life, thank you for being a wrong person. Our country cannot be sustained because it makes it productivity. Our things are important. It's important to look forward to the country's growth. It's important. Thank you very much. You're welcome. You're welcome. Because of these themes.


What's up everybody, Jason here for jaspyskatesrace.com We just sold out the last four boxes of 2023 certified football. Four box break, number four. And let's see what we have hiding here in the last four, guys, good luck. So here's the customer names. Nathan got Dolphins last spot mojo. And here we go guys. For the Seahawks. John with that one, straight up. I had a Nick Chubb rally to $199 for the Browns. We have a DK Metcalf to $199 for the Seahawks. And then we have a Brandon Sheriff for the Jaguars. It's a 75. Jaguars, that is Nathan. And nice, beautiful patch there. Out of 50, Jackson Smith and a Jigba. Three color patch and autograph, nice. Eagles, our sorry not Eagles, Seahawks, John. Matt Junon for the Patriots. Justin Fields to $275. Keishaan Booty. And we've got a Jared Goff rally to $199. Lyons is Nick. Next one out of 75, Will Anderson, Jr. Josh Downs for the Colts, Luis, with that one. And more, the second to $199 for the Colts. And then we've got a Cedric Tillman to $199 for the Browns, John. Hopefully we just get Clifford some hits then. He can steep a little comfortable at night. Saquon Barton for the Giants, James. We've got Josh Jacobs for the Raiders, for the Jerry. And we've got a Jaren Hall to $349 for the Vikings, Clifford. We've got Young Hoku to $249. Falcon's going to Chris. And we've got Derek Henry, Garellik to $199. Ty and D.A. with the Cedric Tillman. Gary's Davis for the Charges, Luis with that one. All right, two more boxes, guys. Mirror signatures to $125. That's for the Falcons, Chris. We got Miles Garrett to $50. There's a Dak Crest, got to $199 for the Cowboys, calling cards. And then a Bijan Robinson, Relic to $249. I haven't seen an autograph of his yet, so hoping an autograph at some point. Nice one there for Chris. A.T. Perry for the Saints. And a Jaren Hall, Relic again there. For the Minnesota Vikings, Clifford. We've got Gary Wilson for the Jets, Chris Butler, Gold Team. To all the Gino Smith for the Seahawks, John. And Jalen Hyatt, Freshman Fabric Mirror Signatures. That's for the Giants. James with that one. We've got a Tanner McKee for the Eagles. Nick with that one. And a little Jordan Love to $99. Give me a package, Jeff. To $3.99 for the Saints. Saints that we got for the Jaguars, Branson Strange. Nathan. And we got a Miles Garrett, or sorry, not Miles Garrett, Garrett Wilson. Jets, Chris Butler. We got a Rodney Hampton for the Giants. That's James. We've got Immortals there with Dan Hampton to $1.99. And Sean Clifford. Looking good packers. But a Trevor Lawrence to $50. These are the game for the Jaguars. Tajah Spears. Kendrae Miller for the Saints. Nathan with that one. Stake on Barkley to $50. And there you go, guys. So all these numbered cards will be top loaded. And then here are all the hits here. Little T-Law Relic, Relic, autograph there. Kendrae Miller-Auto, Jaylen Hyatt. He's on Robinson Relic, Desmond Ritter autograph. Jared Henry, another Jared Hall, Cedric Tiltman, Kenny Moore, Chubb, Sheriff, Jared Goff, and Jackson Smith and Jigbar up here with one of the nicest ones. So there you go, guys. Another case is posted. First case number five, JaspysCaseBricks.com, guys. Thank you.


So first and foremost the important question I have to ask who gets the joke You know one no one has ever seen Christian Slater's epic gleaming the queue All right. Well, that's lost on all of you and I feel bad about that So a couple of months ago. I guess it was a couple of months ago I was down at the Red Hat user group down near the Red Hat tower and Jason Hibbet says hey Do you want to come talk about Kubernetes in five minutes? And I laughed and I said no, you can't do that. That's just quite simply impossible. So, okay, cool. I'll do that so Me not being a very smart man So you can't do how Kubernetes in five minutes We can talk about it being written and go and we can talk about it being a Google project And we can talk about at CD and we can talk about all the other components and bits and stuff And I'll run out of time way before we get to anything meaningful But the one point I can make in five minutes at least I hope I can try to make in five minutes We can know why Kubernetes? I mean Kubernetes is a tool that exists. It's part of atomic. It's part of core OS It's part of most most modern application centric or most modern container centric app tools out there Why why why does it exist? Well, and and I this next slide This is the one that I hope gets the docker guy not to want to beat me up But containers are really just kernel parlor tricks And I say that and I say that earnestly and but I say that to try to make the point What containers are are things that live only inside the kernel. They only live inside the Linux kernel That's the only place they exist if you were at Thomas's Container and security talk if you were the core OS talk yesterday. You had a really good Really good introduction into what containers are containers a kernel control groups containers or SC Linux and containers a kernel namespaces So if they're everything that a container is is inside the kernel How does it know when I want my application to span three servers or three data centers or three planets or whatever? How does it know what's past that and the answer is it doesn't? Containers only exist inside the kernel. That's it So to have to be able to scale out a modern highly resilient all of those fun buzzwords application We have to have kubernetes We have to have a tool that will take my kernel and take four other kernels or 40 other kernels and Glue them all together and let me see them as one abstracted out whole That's what it does and that's in the rest of it is bits and in their fun bits that I wish I could get into We get I have two minutes and 19 seconds left So we're not gonna be able to do that. So kernel containers are awesome kernel parlor tricks. They really are The core s guys not here today is he did he leave? He was if good because he's probably gonna want to beat me up after I say that So what kubernetes does do is it takes all of those kernel constructs? And it lets you make the highly available apps and do all sorts of fun things and that's what it's there for So I guess in if I had a summary and I really don't have a summary that um, but In the how we can't get into but the why kubernetes is one of the most important tools out there. I think today Containers are parlor tricks, but they're also revolutionizing the data center Containers are changing how we think about technology and I'm not gonna say dev ops, but I'll go ahead and say dev ops They're really making us rethink There is a new mode to it and the whole bimodal thing people kind of cringe and especially in this room probably people cringe a lot But it's making us rethink how we do software and it's making us rethink how we deliver software So we have to have a tool that's gonna get out there and let us Let us make that next step and that's what kubernetes is. I think it's a really good. I think it's a really good start to it So so that's the point I wanted to come up and make That we have to have kubernetes because we have to have containers and containers can't think outside the kernel And that's what I've got. I have 50 seconds left. I wish we could have questions, but if anyone wants to rough me up I'll be outside


Alright, I'm a bit worried about our boy episode four of our mob cycle 100 watch through inside evil spirit and last episode Kind of left off on a somber note I guess maybe some foreshadowing for the future in terms of mob and the decisions He might have to make and how that's gonna take a toll on his mental because he has to choose sides one way or another Because of how powerful he is. I think he's kind of just scared of that power that he has doesn't really trust himself yet We're gonna hop right into this one of you knew the channel drop us up and hit that big blue bell and let's get started Hey Dimple What is temple up to? Wait that guy okay first off what is going on? But that guy looks like the guy that Reagan lied to about like putting a curse on who he wanted to put a curse on I'm gonna guess they have no idea what dimples up to wealthy Let's go Yeah He just says nothing about it. He'll pay for our taxi. We're taking a train.   This rich person has gathered them all here Lying Doesn't even deny it. Okay, so this guy's a big deal. Oh Shoot I don't run a legit business now.  Oh Well what happened to her Oh, this seems like a hunter hunter. What's her name's room? Is she like possessed?  Maybe that was a flash into the future and that hasn't happened yet at the beginning What's the reward aside from money, there's no way Reagan is volunteering first Yeah, dibs ease Good idea brother It's mind games He's playing crazy mind games. Yeah, this guy knows Reagan Okay, did he kill them Psychological warfare dog Reagan really is the greatest anime character of all time Get in there buddy Confidence is key gotta make her feel comfortable Wait, oh my gosh her fingernails Did that actually What wait is he the possessed one did he gather them here for another reason?  Oh Wait, no, no wait. I'm like 5050 now. I don't know I mean how they go you saw Hey, Joe do sama says that's the word And what's up with the dad is this what the dad's seeing right now Reagan Reagan Oh, there's no way Reagan sees past it, but all these other psychics don't Damn, he said that's that's rookie stuff. Oh Oh my god Reagan saw pass them, but nobody else did even I believed her. Oh What What is going on these all of them trying to rid the demon from her? I Like a mob's little jacket winner 49. Is that for the the Rock Paper Scissors? Dimple scared of this demon that's in her I Was he a big deal demon oh he was a psychic before Oh my The psychic that went down a dark path Geez, I feel like that's referencing like oh Oh It was a flashback.  I guess I feel like that's kind of referencing the path that mob could go down It's just hatred and evil because of how powerful he is Ogami keiji oh Oh, dude, this is a match-up for mob All right, yeah, let's let's see what what kind of big deal this guy is What an interesting strategy a god dog. I'm genuinely afraid from even mob Do not a process person conscious Oh mom's gonna have to step in now Yeah, why I mean maybe the dad is evil stop punish him Trying to reach his actual daughter in there oh Shoot damn it's getting serious man. Oh my goodness. They're trapped.   He looked like reached you there for a second mob did This is gonna be a battle of Titans, isn't it refusing into one? Yeah, what's Reagan's take on this dog someone stronger than mob So creepy.  Hey, we got Reagan temple. You can try to defend it, too Oh my gosh, he's giving devil his body Wow Oh Yeah, that takes a lot of trust holy the original temple would have kept it It's kind of naive, but I think temple even kind of feels bad about the naivety of mom Trying to change himself there he goes.   Oh shoot. It's funny seeing mob with temple's facial expressions like mob isn't that expressive usually Here he goes That's a bold plan. Oh So does they fight inside the body to try and push the other out Welcome I get you some tea Please why is mob naked, but he's wearing a suit.    He wanted mob to come It makes sense it's harder to build up a strong positive feeling just sinking into negativity I'll just pull the it was all a nightmare Oh Altered your memories What I feel like he's going to be very surprised though by who mob is as a person Because mob doesn't see his powers in any way or want to use his powers in any way now So as a regular person, he would still be the same mob, right dog this popped off hard It's insanely powerful psychic just come at no where I like how it did loop back around from the very beginning the intro But dude dimple mob might have been the highlight of the episode like I said seeing mobs character with those facial expressions That of which we haven't seen before because usually he's pretty expressionless. It was kind of a tree So now he's he's kind of is this like a dream? I state I guess from mob and mobs reliving through his memories, but without ESP It's gonna be interesting like I said though I feel like this spirit is going to be very very very shocked by who he sees as a person because mob is not your typical Esper not your typical kid in general either though because it's been if episode four drop a comment down below And I'll catch you in the next one. Peace peace