All right, hi, let's get started. I guess I know most of you. My name's Emerson Perrin and I've been here for a while. And many of you have heard me present about cell therapy in the past. And as a global perspective on this, we injected the first human with cells back in 2001 in Brazil. And so this is more in 2021. But it's a relatively young field. 20 years is nothing in the development of cardiovascular medicines. Aspirin's been around for more than 100 years. You still don't know exactly how it works. It took about 30, 40 years to get ACE inhibitors into ARBs into things that we use commonly now. So having something that is a live functioning entity that interacts with this environment is very different than a simple molecule. So that adds further complexity to it as well. Further, the cells that I'm going to be talking about today, we first injected in 2006 in Newcastle, Australia. So that's about 15 years we've been working with this cell. And as with anything, as you progress and you do trials and you learn things and you take steps, this is the latest step that we've taken. And for those of you that had followed along, you'll see that we have some new and exciting data and actually looks like we're getting somewhere. As with anything, whenever you have some kind of a new treatment, there's a lot of hype and hyper over inflated sort of expectations about what you do. And I remember back in the early 2000s, it's like, oh my God, cell therapy is fantastic and it cured the world. And it probably will. And everybody in this room has made a two stem cell. So there's no question that it works. The question is how do you get it to work? And so then that initial incredible expectation kind of goes away because nothing happens for quite a while because yeah, it's really cool, but you kind of need to figure things out. And then over the subsequent years, research is done. A lot of things are done. Things are better understood. And over time, you get to an understanding through research to the point that you actually then start catching up to that initial hype that you had. So this is kind of where we're getting here. So this trial is called a DreamHF trial. And I was the co-PI of the trial. And we let it, I see all my research coordinators here from Texas Heart is pretty much the leader of this trial. And so it's a great pleasure to now after six years, I'll show you the timeline after six years of work to have been able to present this. Let's see. I'm not advanced. Let's see. Oh, there we go. OK. This is actually over. I over disclosed. It's basically because I'm the PI. So DreamHF is multi-center, randomized, double-blinded. We'll talk about how this is done because it's quite involved, the sham control. And it's an event-driven trial, meaning it's not a trial that you have a predetermined end. You need to reach a certain amount of clinical events for the trial to be over because those events are calculated and then reach a point where either you have significance or not of what you're doing. The trial was actually quite an interesting history. It was initially sponsored by a company called Cephalon. And then Cephalon got acquired by Teva, who's a generic drug maker, who wanted nothing to do with a cell therapy trial that we had just written and gotten ready to start. And subsequently, then, Mesoblast, who is the company that has developed this cell and has a proprietary way of getting these cells, then took over the financials. And it was pretty interesting because we really had to do a lot of work to get the trial down to a smaller size from a financial standpoint. Originally, it was written as an 1,800 patient trial. Big pharma, 7,000, 8,000 patients is nothing. Well, you try to do something this involved.  This is a pretty significant procedure with a lot of things, as you'll see. So we, through changing endpoints and looking at things, we're able to get the trial more compact and down to a goal of around 600 patients is where we ended up. So there is a clinical endpoints committee that adjudicated every single meaningful clinical endpoints such as death and strokes and heart attacks and all these events that happened to the patients over time, and these events are delineated in a document. And there was a data monitoring safety committee that was headed by Dr. Roulou, who's the head of the Montreal Heart Institute. Really great group of guys that sort of monitored this study over time and made sure that we weren't causing any harm. And also in 2017, we had a futility analysis to make sure we weren't spinning our wheels and there was no chance of this being positive, which we passed, luckily. So this study was done across 51 sites in the U.S. and Canada. We're one of the top enrollers and you can see, here, let's see if I can get this error. So there's a heart failure team and there's an interventional team. And so because this is a kind of a phase three trial, it has to be blinded. And you really have to have a firewall to keep it blinded because we're doing procedures on people. So when you're doing a procedure, the guys doing the procedure know exactly what they did. And so we have this structure in which the procedure itself, when the patient came in to get the cells into the heart, that was done by a certain team. And then there was another team that then screened the patient, saw the patient initially, and then after that initial procedure in the hospital, then follow the patient for the duration of the trial. And so there was no communication between the two. I couldn't even go near the cath lab on days in which we had a procedure because I was the blinded part of the heart failure team. So that sort of guarantees that it's a blinded trial. And then a little bit I'll talk about what we did to actually blind the patients that were in the trial. And here's the continuing list of sites. So it's pretty involved and it's quite interesting having gone from doing 60, 80, 120 patient trials to doing a larger trial like this. So let's talk about the cells a little bit. So when we talk about cell therapy, okay? It's not one thing. So it's like cars, there's all different kinds of cells. And so it may be that one cell is really fantastic and another one is terrible and all the shades in between. So mesenchymal precursor cells are a very specific kind of cell. And we get these cells from the bone marrow. So these cells are selected with an antibody. It's an antibody against stro3. And these cells are characterized by having this receptor called stro1. And what they are is they're mesenchymal cells but which are the cells of the stroma of the bone marrow that have the ability to turn into different tissues. So they're true stem cells. And with this marker on it takes it back a step. So this is the cells that are like a generation before. So if the mesenchymal cells are like one in a, you know, 100,000 or whatever cells in the bone marrow, this is like one in a million. So it's a rare cell. And then once you get that cell, which is a very specific kind of cell, then you can stem cells have a property of cell renewals. So it's either grow. So you can grow these cells into cell banks. And so in this trial, for example, we had three different donors. So but we could have just had one. So you can have one donor provide cells for, you know, 1,000 people study. The advantage of this is so as it says here, they're allogenic meaning they're not from, you know, everybody's not getting their own product. That has been a real problem in cell therapy because when you give autologous therapy, especially if you're talking about your own cells, everybody's different. So if you take an 80 year old guy who's a smoker and sedentary diabetic, his stem cells are not that great. If you take an Olympic athlete who's 18 years old and super healthy, his stem cells are awesome. So using allogenic cells enables you to give the same product, that super healthy powerful cell to everybody. Now you can't do this with every kind of cell because not all cells are fly under the radar of the immune system. So these mesenchymal cells do fly under the radar. And that's real important. So if we get, for example, we took a biopsy of the heart and took a cardiac stem cell and multiplied those and gave those, you would just like a heart transplant, boom, you get rejection and you'd react and kill those cells. The mesenchymal cells, we inject them into the heart, they do their thing. They eventually probably go away. We could talk about that later. So there's a actually large animal work and sheep work in both non-eschemic and ischemic cardiomyopathy that show that these cells have, that they're very well studied, have anti-inflammatory and immunomodulatory, pro angiogenesis, anti-apoptotic effects. So they do a lot of good things. And they do these good things in models of large animals that are both ischemic created models and non-eschemic created models. So we performed a trial that got published in 2015, which is the phase two trial that's published in CERC Research that showed some really exciting things and it showed decrease in remodeling, improvement in remodeling of the heart and also less events in the patient that got these cells. And that was very important because it allowed us to negotiate with the FDA to be able to do this trial, the dream HF trial. So let's go over this a little bit. I know it's a kind of a complicated cartoon here but this kind of tells you a lot about the mechanisms because when I show you the data, we're gonna be referring back to what these cells do and it's all gonna make a lot of sense. This trial is beautiful and nothing else, it is extremely consistent in everything we see. I'm showing you parts of it but this is the stuff that a little bit more than what I presented over the weekend. So here we have the heart. Heart failure is something that is basically initiated by innate immunity and adaptive immunity. And there are cellular and non-cellular components but a major component of what makes heart failure, heart failure is that the inflammation that happens with heart failure keeps it going over time. And so you have cells in the heart and one of the main players are macrophages. And there's different, there's kinds of macrophages that this is a little simplified but there's kind of macrophages that come from the bone marrow, there's different kinds but they're the actors that do bad things given their stimulation from the environment and what's causing the heart failure. And so we'll just call these M1s, okay? So this is a simplistic classification into M1, M2, it's a little bit more complicated but basically M1 are pro-inflammatory cells, okay? And they secrete, as you can see here, TNF alpha, IL-1 beta and IL-6, these are three important inflammatory cytokines. And these are responsible for a lot of the bad things that happen. Well, if we then take an NPCs as a picture of the cell, let's say, and we put it in the heart, these cells have receptors for TNF alpha, IL-1 beta and IL-6 amongst other things. And so if you put them in that environment where these cytokines are all there, it's like if you throw somebody a fireman into the middle of a house that's on fire, these receptors, the cells get activated and they understand, oh, this is an inflammatory environment and they do what they're supposed to do which is counter the inflammation. And so then these cells secrete a bunch of different things which is kind of simplified here but they counter that inflammation, okay? And they do it at the local level and as you'll find out, they do it on a systemic level as well. So basically they have an action that polarizes these M1s into M2s which are not inflammatory, they're healing, okay? And instead of secreting all these bad actors here, they secrete things that have a lot of beneficial effects on the smooth muscle, on the endothelium, on blood vessels and on the heart muscles themselves that changes, you know, energetics, metabolism, versus apoptosis does all a lot of things locally at the heart muscle. But if you ever studied atherosclerosis, you know that atherosclerosis and development of plaques and plaque ruptures and heart attacks, that is a immune process. These cells are immune modulatory, meaning they modulate that stuff, mainly through these macrophages, okay? So they have an effect on the heart but they also have an effect on blood vessels. And just as an aside here, to note, it's important that IL-6, there's a soluble portion of IL-6 that leaves the heart and that induces in the liver production of CRP. And what we commonly measure CRPO, somebody's got a high CRP, it's an index of inflammation, you know, and that'll be important later, we'll talk about that. So this is a great, so you think, you look at this and you think, oh man, this is a great way to treat heart failure is to treat inflammation. So there have been, there are three trials of anti-TNF alpha led by Doug Mann, who we all know here. And actually the trials were stopped early for lack of benefit. So there has been a failure so far of therapy that we mainstream treatment to treat inflammation in heart failure. Now, an exception to that is this trial called the Cantos trial that was directed against IL-1 beta, but it wasn't really a trial looking at heart failure, it was a trial looking more at the sclerosis. But there are signals in there that there was some benefit in subsets of people with heart failure. So, okay, so let's talk about this trial. So the main inclusion criteria were that people had to have chronic, and it could be of ischemic or non-eschemic origin, because I told you these cells have been tested in both. And that's a fun thing to discuss later. And everybody was on optimal medical therapy. This trial was performed between 2014 and 19. So not everybody was on SGLT-2 inhibitors, but it was interesting to see in the beginning we had like 2% of people on intresto or 5%, and that went up to 50% towards the end of the trial. So all these patients are on the best possible guideline directed medical therapy. They had to be no option for other things or else you do those other things if somebody needs a standard bypass surgery if they're ischemic. They have to have a ejection fraction of less than 40%. And all of these patients that were either class two or class three, we enriched them for events. This is an event-driven trial. We want to see events. So how do you do that? Well, everybody that got enrolled had to have an admission for heart fader in the nine months prior to randomization or a visit to the ER where they got IV diuretics or IV treatment. Or they had a biomarker, anti-pro-BNT greater than 1,000. So these are things that selected out a population a little bit more likely to have events. Oh, and exclusion were basically we didn't want any acute patients or unstable angina recent heart attacks, things like that. We want a stable chronic heart failure population. Okay, so then how do we give the cells? So you can see on the panel here we took these patients to the cath lab and like I said, we needed to completely have them blinded. So as they go into the cath lab when we do an electrical mechanical map which is this structure is a three dimensional model of the heart that we create by touching the heart on the inside and that we color code for voltage in this case which tells us what's more alive and what's not so we can see scar, we could see good tissue, we could see normal and sort of intermediate tissue. But so to go in and do that we always take a picture of the pumping chamber. And so everybody that went into this trial they went into the cath lab and they got a stick of their growing and we did an LV angio on them.  So the patients and then they're sedated. If they were to get cells, we continued on with the mapping and the whole thing and did actually what we do in terms of injecting these cells Dr. Fishin, Dr. Chang are the guys that did the cell injections here. And if they weren't, if they were a sham control that's why we call it a sham control then after that they sat there and did master piece theater which is basically make believe you're doing an injection and we would have a script and people say, okay, now point number one and the voltage is this injecting did this and so you just went through this theater of and it would take approximately the same time so the patients couldn't tell oh, I was on in there for 10 minutes so I must not gotten the thing. So this is a very well thought out FDA agreed upon kind of thing in which then the patients that went to the cath lab were completely and plus we sedated them heavily. So with all of this, they had no idea they got a stick in their groin they felt some stuff in their heart and they don't know if they got a procedure or not that's very, very important. And it's also, as you know, very important for the us investigators not to know either because there's all kinds of bias if you know what your patient got even if you're trying to be the most the best investigator in the world you will be biased about things because you want your, we're not doing this because we don't think it doesn't work we think it's going to help people so we want to see it work. So for the people then that got randomized to getting cells, we perform this map. So here's the catheter goes back through the aortic valve it touches the heart and here so you create this shell that's color coded. So here, for example, let's say if there was a scar in the apex and then this intermediate and the colors were representing or the visible spectrum of light so it goes from red on the low side to violet on the top side. And so like this purple stuff would be normal tissue this would be intermediate this would be a scar. So you can look at the heart and you can see on a completed map you can see, okay, this guy had an LED in park. Okay, he's got scar here in the front of his heart. And here the black dots you can see where we did the injections. So there's a needle that runs through the catheter after we mapped it we had very specifically decided that we're putting these cells into intermediate voltage, not scar tissue. If you put it into dead tissue the cells are not going to get activated they're not going to see anything. If you put them into normal tissue that's not a good idea either. So this is, we've been doing this for a while and this is how we think it's the best way to proceed. So here you have a finalized map and there are the injections. The idea was to give between 15 and 20 injections and we achieved that in the majority of patients. Actually, here's the slide showing that actually 96% of the patients received the specified 15 to 20 injections. I talked about the duration of the trial. I had a symmetric slide. This wasn't in presentation but you can see here from the first patient visit in March of 2014 all the way to the last patient visit in February of 2020 we had to wait another year because the last patient and when he got treated we needed to be a year to go by before we could start closing down the trial and starting to get ready to look at the data. So it's a six year long trial that was decided to stop when we got a call from the data monitoring safety committee saying, we don't know about it we're just doing the trial, right? We're just doing this. So they're saying, okay you have reached the events number that is we think that you have a meaning for result you can now stop the trial. And I actually fought and I said, come on man let me, it was like December and I wanted to, I said we need to reinforce our end points a little more but they made it stop. Okay, so here is a flow diagram of how the study happened and here you can see a big miss that I won't do this again. So 1167 patients were assessed and screened and you can see here, 565 were randomized. Now there was an issue between, well so of the 565 patients you can see that 537 actually got randomized and treated. So I'm sorry. So these guys between when they entered into the trial there was a month gap between these things. And so patients violated the protocol. Let's say I told you you couldn't have an MI well that patient that got accepted into the trial had a heart attack, boom we can't put them into the trial. So nowadays what we do in every single trial and it's pretty much standard is you randomize usually if it's a procedure trial at the day of the procedure. So the guy's screen is ready to go he's in the cath lab you call the patient then gets randomized okay is a treatment or control. Now there's no time for the guy to have anything happened. So everybody that got randomized is gonna get treated or placebo, right? So and that's something I've had to explain. So this 565 patients is the intention to treat which is one way to look at trials. And then this set here the 537 is what we call the as treated or full analysis set. And it turns out in all the analyses there's no difference between intention to treat. I'll show you the full analysis because I think it's more meaningful to say this is what happened in the people it was defined by getting at least one injection. So if you got one injection you're treated and if you got no injections you're not. So then we have two groups 276 were controls and 261 are the NPC injected treatments. We stratified the patients in enrollment by class. So there would be an equilibrium between classes and then you say, oh, wait a minute there's 106 and 170. Okay later on during the trial there was an adaptive change that we did to just enroll class threes during the last year because as you find out if you enroll a bunch of class threes people start dying and having events and you run out of people that are having events because they've all had them. And if you do a time to first event analysis all your data has disappeared and you're sitting on nothing. So we needed to enroll more class threes. And so even though they were balanced in the first five years of the trial in the last year we enrolled just class threes. And obviously this is with blessings from the FDA, et cetera. Okay, so we'll look at the baseline demographics are basically the same in the two when you have this many patients you're really not gonna hopefully see a lot of differences. So here you can see the average age was like 62. The distribution of cardiomyopathy so there was a little bit more ischemic cardiomyopathy than non-eschemic. So it's about 60, 40, not quite 60, 40. And here you can see there were more class threes. I just told you we enrolled the last year just class threes. So wind up having a preponderance also like 60, 40 to the class three to class two, which is interesting. I'll show you some interesting things about that. And here you see about 40 few percent diabetics and amount of people around 55% that had revascularizations. And this is incredible. So 84% of the patients had either ICD or CRTD. So now we're dealing with a very modern well-treated population of patients all of which have defibrillators and to the next slide. If you look at the therapy they're all on very good medical therapy. So if you look at the RAS medications were over 90%, diabetics 90%, beta blockers over 95%, not the digits, but the digits in the 20s. And here, this is what I told you about in the beginning really SGLT-2s weren't even approved. So these are like a diabetic or two that maybe when it first came out got it for diabetes. And you can see statins here 65%. Again, the non-eschemics don't need statins, right? So they're not necessarily on statins. You can see that the overall ejection fraction was 28%. So we enrolled for less than 40 wound up with 28. And here you see the volumes about 150 endostolic volume, 200 endostolic volume. So that's a pretty compromised population. You start seeing events in people with endostolic volumes over a hundred. You can see the six minute walk of around 340. So that's pretty consistent as well. Here you have the anti-probium P's and the CRPs which are elevated. This wasn't in the presentation, just put it in here as a little extra color. It's kind of interesting to see if we look at class two and class three, there should be some differences, right? If you're enrolling correctly, there should be some differences. So if you look at the six minute walk, class threes walk less than class twos significantly so. The anti-probium P was significantly higher in the class threes. The CRP was higher in the class threes. I told you it's an inflammatory disease as was the renal function. So very nice and as expected, no surprises. Okay, so then we get to the wonderful part of this trial which is the primary endpoint. So the primary endpoint that I had originally made that the Mayan stroke, we changed when we did that reduction in the number of the trial to recurrent non-fatal heart failure events. So what that means is visits to the hospital for shortness of breath and to get diuretics because that's what the heart failure patients do. And as you can see, there is absolutely no difference. These cells are not a decongestive therapy and that's really not how they work. We thought that maybe on top of everything we might see an effect here. We were expecting to, we wouldn't have made this a primary endpoint but the primary endpoint is negative. Now that's a problem because the way rigorous science is structured, if you miss your primary endpoint, now everything after that is hypothesis generated, right? Now this is a new therapy. So it's very important for the, this is the largest trial of cell therapy by a lot ever done. So it's very important to kind of get your bearings and see if you have meaningful findings. And I'm gonna show you what I think are some very meaningful findings. So every endpoint that I'm gonna talk about though, this is not ad hoc post hoc analysis. These are all pre-specified endpoints with pre-specified analyses. And I'll tell you when they're not, there's just one. So heart attack and stroke, if you look at the overall population and you look on this panel right here, you can see over time, there's a separation, there's more heart attacks and stroke in the control population. There is a risk reduction of 65% in heart attack and stroke. So if you look at the numbers here, that's 4.6% of the NPC versus 13, 0.001. Okay, wow. Did I talk to you about a systemic effect of these cells on large vessels in the brain and in the heart? And this effect is due to a reduction in MI and a reduction in stroke, okay? So both of these things got affected. It's not one more than the other. So that's pretty interesting, right? If we look at the difference in then class two and class three, we see that this is basically present in both. So we have a 66% reduction in class two. We have a 65% reduction in class three. So this is a very nice time to first event analysis, by the way. Now, this bottom panel that shows these forest plots here, so everything on this side is benefit cells and here benefits control. But the reason this is done is this is a recurrent events analysis because the follow-up in class two and class three, remember I told you we enrolled class threes only for the last year. So the follow-up of class threes was shorter than class twos. So the mean follow-up of class twos was 35 months. The mean follow-up of class twos was 26 months. So what you do to make sure that you're not seeing crazy stuff is you normalize it for 100 patient years. And so this is looking at it this way, that difference in follow-up doesn't make any difference. So even looking at it like this, no problem. We have even a bigger effect, which is really nice. A 69% reduction overall in MI and stroke in the whole population. And you can see it's significant in both classes. Here's your P values and your hazard ratios. So that's kind of surprise number one. Okay, how about death? So we can divide death in a lot of things. So first of all, there's all cause death, okay? You died, suicide, got in a car accident, et cetera, et cetera. Then we can go to cardiovascular death. That's heart attacks, but also a vascular event, so strokes, okay? So, or not just heart attacks, anything that happens in the heart, okay?  And then you go to cardiac death with just things in the heart, okay? So we're showing you here cardiac death because it's kind of more meaningful, kind of separate out the vascular stuff from the cardiac stuff. But I have cardiovascular stuff in here as well. So this is, again, remember the primary endpoint, if all those recurrent events and everything, if you look at the whole population, there is no difference, okay? Interestingly, in class two, there is a very significant difference in death, in cardiac death, 57% reduction in death. In class three, no difference. So we can talk about hypothesis of which has happened, but I'm gonna show you what the real truth is in a little bit. It really isn't class two, class three, although you can imagine that class two patients have more viable heart. They have more heart tissue from which the cells to have an effect on, so, but we're gonna dig a little deeper in that and talk about that a little bit more. But nonetheless, this is a very interesting finding. And again, if we do, this is not recurrent events because death doesn't recur, right? It's only one time. So, but this is, again, normalized for follow-up over time for 100 patient years, and you can see it continues to be significant with a 58% reduction, and here you see the hazard ratios. Okay, this is the real story, and that's why in the beginning I was telling you about cells and inflammation, that's what these cells do, they're anti-inflammatory. So if we look, and so I'll take another endpoint, okay? It's a very commonly used endpoint. It's actually the endpoint that I think the FDA will want us to use moving forward. So it's a very significant endpoint, which is a composite of cardiac death, stroke, and heart attack, okay? So these are the big events happening to people. So if we just look at that, and if you look at this panel on the left here, this forget the right panels. This is in everybody, okay? So if we looked at death in mind, stroke, there is a 33% reduction when you've got these cells as opposed to being in control. That is a 0.02 p value, so it's very significant, 20% versus 30%. Again, that you could see the days here, I told you this is a mean 30 month follow up. This is a time to first event analysis. Okay, so then we said, well, and this is a pre-specified analysis. We thought ahead of time, well, we're gonna look at everybody according to their CRPs because a CRP is a good way to look at inflammation. And so we'll look at CRPs greater than two, greater than three, greater than four. Turns out it's all the same, and we used two. That's what he was using the Kanto's trial, and I think it doesn't make any difference, and two is kind of the cutoff, and that's what we had pre-specified. So look at this, this is amazing. So where is all the benefit of these patients from not dying, having heart attacks and strokes? It's in the patients that have inflammation. Is there any benefit in patients that don't have inflammation? No, don't give cells to people that aren't inflamed. Okay, so for the first time, we're able to nail the mechanisms and show this of how these cells work. They're doing their anti-inflammatory job. We know that heart failure is an inflammatory disease. We know that atherosclerotic is an inflammatory disease. And when you give anti-inflammatory treatment, that is more than one thing, that is a living cell that does a bunch of things, you get a significant effect. So this is the main story, but we'll look at some more stuff. Remember I showed you that a couple of slides back, cardiac death in class twos, right? So, and I told you, cardiac death, here's class two, but is it really class two or is it something else? Well, it's something else. Here's all the benefit, it's inflammation. So if this benefit back here was a 57% reduction in cardiac death, okay? Now we see, which is, this is incredible. This is a number needed to treat a four, okay? We see a 80% reduction in cardiac death in class two patients that are inflamed. If they're not inflamed, again, this is the same idea. There's no difference. Even in the class two guys, oh, well, but there, you know, no, if they're not inflamed, there's no benefit. It's the inflammation that does it and it does it in a very major way. This is an extra slide I had put in here just to show you the power of inflammation. So if you look at all, so all cause death is a lot harder to get a positive value in, right? Because you got people, there's, I can't remember the number, but people committed suicide and this and that and the other. Okay, so if you have a CRP greater than two, there was a 60% reduction in all cause death if you got treatment in cells in these patients. So I'm not trying to really cherry pick and show you this. I'm just trying to explain that inflammation is how these cells work and we consistently see this benefit across the board. Okay, then you say, well, okay, CRP, maybe this was wrong, right? Remember I showed you that CRP is produced by IL-6 and IL-6 is the real culprit and induces CRP production and liver. So guess what, we measured IL-6. And so this is kind of a complicated slide but basically this group that has all the events, this is the control with high CRP. So these are the inflamed patients, okay? And so they didn't get cells and they have inflammation. These three guys are either the non-inflamed patients that don't have events or they got cells and they're protected as I've shown you. Well, if you do the same analysis for IL-6, it's identical, it's the same thing. So it needed to be this way because if we have a difference in IL-6 doesn't show this, I'm in deep trouble. So again, it's very consistent one with the other. It is the inflammation and we've shown it. Okay, we'll finish up with safety. So importantly, there weren't any SAEs or treatment emergent adverse events associated with the cells, which is very important. And we've shown that before in NPC studies. And very importantly, and we won't go into this. I could do a presentation on this, is that there's really no immune issues. Everybody was tested. We did these tests to see if these cells, because after all their allergenic cells are from somebody else, are they causing any kind of problem? No, they're not causing any kind of problem. Okay, these cells really fly under the radar. And what I found incredible is the procedure, because you were, we took them to the cath lab, you're poking a catheter, and then when you're doing the injections, you're going, you're trying to appropriate the heart. Not really, but it can happen. And there was one perforation in all the treated patients. It's an incidence of 0.4%, which is the lowest incidence. So even though we did this at 51 sites, it shows that with good training and planning, you can really reduce the complications of a procedure. So it's a very safe procedure. And this is another interesting thing, is think about this. I'm talking about a follow-up of 30 months, and we did one procedure. Okay, you got to take intresto twice a day, every day, okay? So, and that's another point, that this benefit is on top of intresto and diuretics and SGOT2s, well, not SGOT2s here, but all the best medical therapy that we know how. So inflammation is different than congestion, volume overload. That's why we didn't hit the endpoint of recurrent non-fatal events, because that's not what these cells do. And so one thing that I've kind of come to a conclusion, is you kind of have to decouple this idea that in all these heart-fader trials, everything is always together. Well, if you're able to actually successfully treat inflammation, that's kind of a separate basket of things. So in conclusion from this trial, that we showed that the 150 million dose which we had gotten from our phase two dosing trial is safe, didn't cause any immune problems, which is very important. We showed that we missed our primary endpoint, that it doesn't help with non-fatal recurrent events, but we showed with a mean fall of 30 months, we had on top of guideline directed medical therapy, a decrease, a significant decrease in non-fatal immune stroke, a significant decrease in class two cardiac death, or with inflammation, and a significant decrease in the composite of death in mind stroke. And that the benefits of this therapy are really in those patients with inflammation. So, oh, this is sort of a summary slide that I had in here for like the press event. But, and it's, again, it makes the point about, here's the primary endpoint, it's congestion, we have no effect. Here are the other two endpoints, and it's really a local effect on the cardiomyocyte, on the microvascular. So we're having decreased intracardiac inflammation, neovascularization, things we haven't really talked about that cells do, cardiomyocyte survival, energetics, and then at the level of blood vessels, we're having a systemic effect where it was stabilized atherosclerotic plaques. This is likely due to the macrophage effect, I think both systemically and in the heart. Okay, so here I think I'll stop and take questions. Thank you very much.


Hey there, great to see you. Welcome back. We continue our journey into the nature of reality with a very important subject, something we've only touched upon briefly before, but one concept which is deeply significant to the evolution and transformation of our species. This is, of course, healing. To understand the nature of healing, we have to conceptualize two things, love and wholeness. The word heal etymologically derives from the word whole, which is the same root for the word holy and even hallow. So for instance, when you hear the Lord's Prayer and it says, hallowed be thy name, what that actually translates to is whole is your name. And since the name of the Supreme Spirit is, in actuality, a cosmic vibration emanating through all reality, hallowed be thy name literally means your cosmic vibration is whole and total. The bridge here from wholeness to love is also profound, as love is the vibration of creation which weaves itself into the fabric of reality from the source of all things. And so, at long last, in today's episode, we're going to explore this profound connection between love and healing and make sense of how deep and transformative healing can take place in every level of one's life. Here we go. Hey, really quick, on February 5th, we are going to be going live in Spirit Mysteries, hosting a special event, a brand new edition of the 12D Shield. This is a live group meditation for the purpose of activating our light bodies, protecting and cleaning our energetic fields, and creating a strong inner stability of mind, body, and spirit. If you'd like to attend, please use the link in the description to sign up now. If you're watching this after the event date, the recording is also available for you to enjoy, and I hope to see you there. Love is the source of all creation. It is the consciousness that actually forms the created universes, dimensions, and worlds that we live within. As we've discussed previously, looking into reality with a dualistic mind yields a perspective of three-ness. Time is observed as past, present, and future, space is seen as having the x, y, and z axes, and size is observed as the microcosm, the everyday world, and the macrocosm. This is the ever-present trinity of reality, but everything in this trinity, from atomic particles to the greatest of galaxies, are held together by forces that we have given particular names, which are sometimes seen as separate as well. Subatomic particles are held together by the strong force, molecules by electromagnetism, planets are held in orbit by gravity. But what if these forces are not actually so different? What if it was all the same force manifesting in various ways through different dimensions? This is actually described through something called the cycle of synthesis, which is a very elaborate diagram that demonstrates the process of creation from the supreme spirit into material reality and back again. It's very similar to the Kabbalistic Tree of Life in a sense, but also very different, much more scientifically minded, and less esoteric for the modern human mind. However, the cycle of synthesis is a very big conversation all in its own, and so we're going to have to save it for a whole episode later, but I promise it'll weave itself very nicely into this conversation. Now as mentioned, the primary vibration, if it could be described, that is imminent through all of creation, is love. Love is a particular vibration of consciousness that holds things together and binds them in the most beautiful of ways. Without love, marriage is just a shell that will usually break apart. Sometimes a marriage will stay together for the sake of the children. But in that case, is it not still love that holds the marriage together? Love for the children? Love is a bond stronger than any other.  In the Flower of Life books, Drunvalo explains how this works. Everything in the universe is a mirror of consciousness because consciousness is the first emanation from the Supreme Spirit. Matter itself is just consciousness crystallized, and consciousness is the light that reflects off the matter of the outer world and creates the material reality. What's more, the inner world of consciousness, such as our dreams, visions, feelings, emotions, sexual energy, kundalini, and even interpretation of the outer reality, are the source of matter and how this matter is arranged. Love is the binding agent within the equation. Love is the exact vibration that matter responds to. Love is the force that can change water into wine, or bring a person back from the dead. And love is the force that causes one to heal themselves and others. For this reason, it is love and love alone that will heal the world. To speak of healing without speaking of love is not speaking with the truth. In medicine, only certain things are possible, but with love, all things are possible. With love, the incurable disease is nothing but light, and the atoms of the body can be reformed into perfect health. The absence of love is the source of all disease, for it is love that binds matter into order out of chaos. And without love, chaos will always ensue. Disease then can be understood as matter in the body disorganized through chaos. Healing takes place only when love is present. Healing people, healing a city, or healing an entire planet is all the same. The only difference is simply the greater degree of love. The mind has the knowledge to manipulate matter, but love has the power to not only manipulate matter, but to effortlessly create matter from nothing. This is because when one is connected with love at the highest levels, they are connected to the source of all creation. No matter what the problem is that needs to be healed, love can always find a way. True love has no limits, and therefore our limits are only found in our belief patterns. If a doctor tells us that a certain disease is incurable and we believe them, we cannot heal ourselves because we become frozen in that belief. And then we must live out that belief even if it means living in great pain and discomfort for the rest of our lives. Only a miracle, something much greater than ourselves, can overcome a frozen belief, just as it is that the mind can stop healing from taking place. When our minds are in control and not our hearts, we will almost always suffer. To help conceptualize this, we might look at a few stories of amazing healings that have taken place. In Drunvolo's account, he shares that one time his wife walked into the kitchen and found a cast iron pan on the stove, which had been left on for too long by accident. She went and picked it up, and only a moment later her body responded with extreme pain. The pan had been searing hot. Now, these two had been practicing a lot of meditation and other spiritual techniques, and so he immediately ran in and said he would put her into a hypnotic trance, and she agreed. So he put her under, and the first thing he did was tell her that the pain would stop, and it immediately did. She became relaxed. Then he told her that the hand was going to return to normal on the count of three, and the moment he said three, he watched as her hand completely changed back to normal. It was at that moment that he said he knew that everything society and his parents had told him about reality was not true. The body was light, and it responded to consciousness. It responded to whatever the person truly believed. Drunvolo also shared some other amazing healing stories too. I particularly liked the one about the young boy who collected salamanders as a hobby, and was fascinated by the fact that he could pull off the creature's tail or legs, and it would just grow another back. But his parents never told him that that applied only to salamanders, but not people. So when he was 10 years old, when the boy lost his leg above the knee, what did he do? He actually grew another one back. Crazy, right? But there's one other story that I really want to share, which comes from Yogananda, and the story goes like this. A certain man was dying of diabetes. The doctors gave him three months to live, and he decided, well, if all I have left to me is three months, let me spend it in seeking God. Gradually, he disciplined himself to sit in meditation each day, longer and longer, and all the while he kept praying, spirit, please come into this broken temple. Three months passed, and he was still alive. Then a year passed, and he gradually increased his daily meditation to 18 hours a day. Then, after two more years, suddenly one moment in meditation, a great light filled his being. He was caught up in a state of divine ecstasy, and on returning from that state, he found his body had been healed. Oh Lord, he prayed, I didn't ask for a healing. All I asked was that you come to me, and the voice of the divine echoed within him. Where my light is, there no darkness can dwell. Now, we're almost done for today's episode, but before we close, there are a few important things that we must discuss. First, we must make a distinction between healing ourselves and healing others. All of the great spiritual teachers, including the ones we've discussed here today, say that we must begin with healing ourselves first, because if one cannot heal themselves, how can they expect to heal another? Further, even if one was a divine healer, they generally do not just go around touching people and bringing about miraculous healings, because each person has their own karma and their own story and beliefs that must be healed. It's not just about the physical abnormality, but the many dimensions of one's body of consciousness being brought into wholeness. In order to facilitate healing for another, one must have permission from the higher self in order to proceed. This is even evident with Yeshua in the Gospels. There were times when he denied people miracles, just like when he returned home to Nazareth, and they promptly tried to throw him off a cliff. So as you can likely tell, the scope of healing both oneself and others is a massive subject. We're only scratching the tip of the iceberg here, and the intention with this episode is to get the ball rolling for those who are called to go deeper and learn more. For those who are particularly interested, I have a few recommendations for reading. One is, of course, Drunvalos Flower of Life books, as much of the material we've explored today comes from Chapter 15 in Volume 2. I also recommend the books The Essence of Self-Realization and Man's Eternal Quest by Paramahansa Yogananda, each of which cover an exceptionally wide range of subjects that are relevant to the subject of both healing and the evolution of consciousness. Oh, and before I forget, a personal request, please hit the notification bell if you haven't yet. Then you'll be updated the moment that our next video goes live, as it seems many people are not actually getting notified about the new videos. And with that, thank you again so much for watching, and much love. We'll see you in the next video.


Okay, very good morning. It's Friday 23rd of July. So I hope you're doing well and hope you've had a great week so far Before I begin as per every Friday Don't forget to check out the latest market watch podcast on the Apple podcast platform Google or Spotify Slightly different change up because the head of trading peers who I normally talk to is away on vacation at the moment So you're gonna be joined by senior trader Tim Duggan and we're gonna talk about crypto currencies and some tips around trading Crypto because Tim as much as having spent the last several years trading the futures market is very active trading in that space as well So hopefully he can offer our community some advice about how best to tackle that more kind of volatile Asset, but otherwise let's get straight to it and let's talk about what is going on in markets this morning and Following on from a positive close on Wall Street the Nasdaq outperformed Technology really driving stocks back up We can have a look at some of these charts as well at the moment after we discuss general overall sentiment But the Nasdaq's tapping on record highs once again in the futures market the S&P 500 marked its best three-day rally now Since April and that seems a far cry from where we were on Monday, which when I was off I was reading headlines like equities Tanking the VIX was the biggest one-day jump since February oil was down in New York 7.5% and here we are end of the week talking about record highs So it feels like a bit of a broken record had to be quite honest But look, let's kick things off and look at some of these equity charts And then we'll look around the broader asset classes as well from a technical perspective Not too much for me to update you on from a news perspective And so we should be able to get through this fairly quickly. I know it's a Friday after all So looking at the Nasdaq here Technically as we've seen earlier in the week quite a nice technical response and the S&P kind of has a very similar setup And when you get these kind of synchronized technical setups across the major Equity indices it does tend to add then some more validity to the technical response that you see in these charts and yeah, certainly the Late June early July lows which acted as a bit of a flaw for that route that we saw Commenced at the end of last week and then hit the hit the floor on on Monday has been a decent target You can see here the Nasdaq back up retesting those highs and perhaps if we look at the world on a slightly More narrow time frame on a 30 minute chart You can really see here in the overnight apex session We actually hit that previous double top that we had going back to what Tuesday Wednesday of last week a bit of profit-taking so range bound for the moment now as we wait really for the US to come back into markets for the rest of the session and We've got a range of 14 965 to 15k now as the big target obviously on the upside Having been within two and a quarter ticks of that in the overnight session Yeah, but quite a phenomenal rally you can see here that we've seen over the course of the last few days and and as I said, that's the Nasdaq and The S&P looks fairly similar in its shape Certainly on the daily chart, which we'll look at first, which is that slightly longer term multi-month trend line We've been keeping an eye on the market obviously got close to that on the pullback that we saw back on Monday Which was quite a key inflection point for price over the last few months on the horizontal basis just above 4200 and the prices come all the way back up and here we are with insight again of all-time highs short term from an intraday perspective I've just got a trend line on from What was the overnight session from yesterday and that's been respected as resistance now turned support and just helping the price Squeeze up to the APAC highs now here in the futures as Europe has come in Just reacting to generally the more positive clothes that we had on Wall Street Asia overnight fairly quiet There's a holiday in Japan for sports day very timely because the Olympics kickoff tonight in Tokyo so Good luck team GB but The overall region was pretty flat the Hangsang was perhaps a slight under performer Still a lot of conversation about DD global, which is that card head car hailing firm Regulators in China weighing a range of potential punishments for the firm This is all to do with their cyber security in Beijing being uncomfortable that this company is just listed on a US exchange and They're considering things like a fine a suspension of certain operations or the introduction of a state-owned investor They've also considered possibly forcing a delisting or withdrawal of DD's US shares Although it's unclear at this point in time which particular Options going to be chosen but DD shares which do obviously now trade in New York were down around 11% Yeah yesterday and that's kind of just souring the notes over over seas in the Hong Kong market overnight Otherwise though the broader sentiment is generally positive Big thing for this week has been earnings, of course, and we did have a couple last night namely Twitter and their shares were up as much as 9% last night They actually settled more with the gain of round 6% or so They had a strong outlook and they posted the fastest revenue growth since 2014 On the flip side though the world's biggest semiconductor maker Intel didn't fare quite so well They were down around two and a half percent. They did beat on the EPS and their revenues Let me just transition here. They did beat on their EPS and revenues, but They're guided on their non-gap gross margins of 55% in Q3, which was down Quite a notable drop from around the 59 and a half percent that we saw in the prior quarter in Q2 Which investors didn't generally like that much So overall day on the week, you know, this is what it's looked like and as I said yesterday of all the companies that reported thus far About 85% of those have exceeded expectations with their earnings reports and thus has provided a bit of a More positive catalyst for equities amid then some of the Question marks over the spread of the Delta variant globally and what that could do in terms of impeding the speed and shape of the economic recovery That perhaps we were we were expecting Before the latest outbreaks that have been happening Terms of earnings today. You've got a couple slightly larger cap AmEx, Schlumberger, Honeywell, Kimberley-Clarke Probably the most notable names. Nothing really too much It's going to be an index mover or sentiment changer more relevant for the single stocks themselves Otherwise a quick look at some of the other charts in the FX space The dollar index pretty flat this morning But I'm quite conscious of just keeping a half an hour on the euro at the moment from a range perspective We are in close proximity to the weekly range Which is generally held through Tuesday Wednesday and Thursday Bit of volatility on the back of the ECB long story short great quote There you know, it's kind of a old wine put into a new bottle I heard someone write which is obviously a reference to the fact that they had their strategic review So there was some communication tweaks, but overall policy remained the same And so not too much a great deal has changed and thus We're kind of resuming back to normal trend here And I'd be quite keen to keep an arm the dollar today and that lower bound levels in the euro If we were to see any type of breakdown in price if we did then you've got the Early 5th of April lows seen not too far below the weekly low point that were coming at 1754 and the overall Low that was seen year-to-date came in late March, which would be at 1721 and a half So the euro chart still reflecting very much So the shift that we've had commenced from the 16th of June, which is this biggest red candle here Which is of course, you'll remember that memorable To height to hike dot plot. We saw surprise from the FMC Rate decision for cable at the moment. Yeah another trend line just keeping an eye on from Friday That's held both yesterday and in the overnight age of pack session as an area of resistance You could also probably stick a horizontal line here as well from what was yesterday evening's high to the APAC high with the trend line It's all working out quite technically quite nicely this morning. We're just drifting back down There after towards pivot You probably would have read a couple of headlines about the UK this morning already UK government is rolling out daily coronavirus testing for workers in critical services in England to allow them to avoid Self-isolation this is because of all of the the pinging that people are getting which is seeing a lot of people Not being able to attend work and then the knock-on implications that can have for things like food at supermarkets and so on and so forth Potential sectors that could be covered in this new program include food production supply Most notably energy waste water medicines emergency services order or border control and local government The process is only intended to run until the middle of August August 16th because as the government have already Outlaid when fully vaccinated people who come into close contact with someone with COVID-19 They will be exempt from self-isolation From after the 16th of August but the problem is is until we get to that point this latest rules now being Implemented to avoid the fact that the number of people in self-isolation on a week-to-week basis is going up very rapidly And that's having some consequence then on on the ability for the economy to to function And so is that important for the pound this morning? No, I don't I don't think so I think it's more of a political government slight mishap rather than it is that something that's Gonna worry markets because I would feel that the moves that they have now made is somewhat inevitable and has to be expected Otherwise then a quick look on the final charts to be aware of and let's have a quick look in the commodity space short-term just from pure technical perspective gold's been Just Respecting kind of more broadly arranged this week in the second half of the week That is from Wednesday between really 1795 which you can see was the low that we printed on Monday on Wednesday Had a bit of a rough break of that, but Unconclusive if you like on Thursday session And then you've got the s1 in close proximity to that surround the 1795 on the low side on the high side You can see here. We're just testing up at around the a pack highs again Which we're holding from late US session late European afternoon So worth keeping on 1808 and a half if we did see the dollar start to move lower Could act as a catalyst with a technical break wouldn't be surprising to see gold quite quickly run up toward the high that we printed Back mid-week and that would be up around the R1 and that high 1813 14 so you could see a pretty quick run of a couple of bucks if we see a technical Breakout of that range oil markets As I said down on Monday seven and a half percent Come back Friday up seven half cents This is the world we live in at the moment. It's a quite incredible price action really I mean you can see this kind of u-shaped movement again from a technical perspective Really nice respect of a trend line going back to Friday. You can see it really held nicely as a point of resistance on Wednesday and Thursday we broke out yesterday morning above that We came back on a pullback to that level before then seeing a pretty consistent bid through the US session into the Clothes and resistance being found at the previous highs that were printed back last Friday So technically from an execution point of view quite quite a nice setup Fundamentally, I don't think you really need to over interpret the moves too much I think the global moves are quite in sync at the moment from an equity oil perspective Obviously tied to some of the the COVID concerns and the the alleviation if you like of those concerns that then Happened thereafter in the second half of this week the OPEC kind of deal It's kind of done and dusted out the way now So that's not too much implications for the price here and now But the moment we still keep half an eye on COVID but the market seemingly from the price Activity here have kind of reacclimatized to the current state of the Delta situation for the time being so From a range perspective probably the pivot today I'd be keeping an eye on which brings into play that peak of yesterday mornings price activity And then obviously that resistance point and around the psychological as well 72 dollar hander will be quite key for oil in the intraday environment But that is pretty much it so quick look at the calendar We've already had the UK retail sales come out But they were pretty dull to be quite honest month on month 0.5 percent Which was basically in line against 0.4 expected. So hence the minimal movement seen in sterling And then just having a quick look at the rest of the morning There is some important information coming out today is the flash PMI day. So you get the eurozone This morning France 8 15 Germany 8 30 eurozone 9 UK 9 30 us at 2 45 These will really be the key data points generally speaking The the PMI's in eurozone at least have been particularly strong last time Some analysts looking for slight moderation just given the the Delta situation and how that's playing out in mainland Europe So you can see how that plays out But that's pretty much it as far as the calendar is concerned From an earnings perspective, we've already covered as I said Nothing really index moving or sentiment changing Just much more from a single-stop perspective to keep an arm for the likes of annex and honeywell and so forth So that is it. So I'm going to conclude and say don't forget to check out the podcast Whether today or this weekend when you're out and about and you need a little 15-minute blast in the year to get you up to speed and again Can it be quite an interesting chat with someone who trades crypto on a daily basis and hopefully he can pass on some Some good advice if that's a market you're interested in all right with that Enjoy the session ahead and have a fantastic weekend. Take care


OTAN Outreach and Technical Assistance Network. My name is Jen Grythin. I am the DELAC lead and GED teacher and lead teacher for Marina Valley Community Adult School and we're excited to be here today to present our project or a mid-year review for bridging the pharmacy tech gap. Before I introduce the rest of the team I do want to tell you in the chat I just put the link to a Google doc and it will take you to all of the links that you will you'll see as we go through our presentation so you can go and explore those on your own time. Our team members include Dr. Patricia Vizano, our principal, Lolita Anderson, our ESL teacher and ESL department chair. She's here presenting with me today. Cynthia Canchola is our CTE pharmacy tech teacher. She is not here but she worked in partnership and collaboration with us as we kind of went through this whole process and then I'm also joined by Jennifer McGrath our GED teacher and lead teacher. Go ahead and do the next slide for me because I can't change it. A little bit about our agency. Marina Valley offers adult basic education classes. English as a second language, high school diploma, high school equivalency or GED in our career tech ed department. Currently we have 696 students enrolled in a virtual 100 percent virtual program. Prior to the COVID pandemic we averaged about a thousand students who would come to either morning or an afternoon evening session and then COVID hit and we had to pivot. So prior to COVID we were 100 percent face-to-face. We had two programs, a high school diploma online and a GED online section that was sort of hybrid but not really. Those were the only two programs that we had that had any type of online component. The pandemic required that all of us really just pivoted and did everything that we were doing in the face-to-face instruction and turning it into a technology-based setting, which was a lot. So this D-LAT course that we took with Destiny Simpson and Dr. Porter and our coaches and OTAN, it really helped us address these issues and rethink how we were going to do this as we move forward. And we'll get more on to that in just a minute. And so to introduce our pharmacy technician program, we have had this program and assistance at our school for the past three years. It is a nine month course intern and includes internship, which where the students actually go out into the pharmacy and the pharmacies and learn more about and get on the job site experience and towards their hours for total certification. In order to be in this program, they have to have a high school diploma or equivalency and a balance of security number. And upon completion of this program, they are able to earn their immunization certification, which is where they're able to actually give shots in the pharmacies, which is helping out in the wake of the COVID situation. And as well as they get their state board certification for to be a pharmacy tech. And it is good for the state of California. There's also a national board equivalency of this as well, where they can go and travel to different states to be able to work as a pharmacy tech. And here are some pictures of some of our students. And this is pre COVID. So that's why they don't have their masks on. So these pictures were taken pre COVID. And you can see here, it ends up our classrooms, some of our cohort students and we have students that are practicing learning how to take the do their measurement of their accounts of their medications, and as well as how to weigh the different medications for compound medications where they have to put different ones together. So this is part of their training they do on site in the class, they take this experience out into the field. And part of our reason for doing this, we offer this course here in place because there is a high demand for pharmacy petitions in the area. And especially the next two years, there is a projection at least 2000 pharmacy tech positions that will need to be filled in the area. And this is for the Riverside and San Bernardino County area. So there is a great need for this particular entry level job for our students. And with that being said, and because of the fact that there is going to be greater demand for helping out our medical offices and helping to provide vaccinations, our pharmacy techs can be certified to give those shots as well in the pharmacies. And this is a picture of one of our students down here who actually graduated from our program. And she works in the field. And just a little quick story, she was one who gave my husband his second vaccine shot. So just about a month ago, that was pretty neat to have one of our former students giving a shot to my husband. That was pretty cool. So and how so basically what we're doing to help our pharmacy technician program is that in working collaboration with our pharmacy teacher, she has identified some skill areas where we need to help to grow our enrollment in the pharmacy program, we need to help our students to have to bridge these gaps. And so we decided to create what's called a bridge course. And in doing this bridge course, we've identified five gap areas that will help our students before they make the transition to go into the actual pharmacy tech program. So what this is, we are developing a customer service course, so they can learn a little bit about what it's like to be behind the counter and communication skills and whatnot. And they will also have a better background in medical terminology, anatomy physiology, and as well as strengthening skills in math and what the areas of medical mathematics they need for this particular course. And it's also going to align a lot more closely with our costs as math tests. And the last component is our computer and digital literacy skills where we need to help strengthen students skills and working with the computers because they're going to be online doing the computers quite a bit and as well as working with the pharmacy techs, the software that is being run in pharmacies. And so I've been taking off to you, Jen. So like many agencies when COVID hit, we saw a decline in our enrollment and they were scared of technology. They weren't sure how a class was going to work. They weren't sure how they were going to be able to do school when they couldn't come to the site. We did see a drop, but to combat that, we we recruited heavily on social media and our websites to get students enrolled and get them ready to go to enroll and recruit students for this pharmacy tech class. We plan to do class visits, be it virtual or in person, depending on how the fall rolls out in 2021. Our counselors are speaking to interested students as well as teachers and former students who went through the CTE program are coming back and talking to students who could be potentially interested to kind of recruit them towards it. We also noticed that we had some gaps in our students' digital literacy skills as far as how are we going to do school? Like all of you, when we pivoted to Zoom and online instruction, we really did struggle getting students into the site, how to get to Google Classroom, how to log into a Zoom. And there were several hours of myself and other teachers sitting down with students one on one going through how to do that. So to mitigate some of the frustration experienced by students and by teachers, we put together this technology orientation website. It's also on that Google doc that I just sent you. And here it houses just some basic how-to videos, how to log into school account, Google, the ins and outs of Google Classroom. And we use this just as a reference for teachers and staff alike to reference. And then they could give this website link to their students. And it's also synced to our school website. If you don't have YouTube, if you're not using it, I encourage you to. There's a lot of great stuff in here. But something that we are most proud about is not only did we make these as a staff for our teachers and students to use, but some of our students took the initiative and decided that they were going to help out. So with that, Lola, could you please talk about these student-created tutorials? Yes, of course. So by now, you are fully aware that digital literacy is a valuable tool for lifelong learning. So once you get your adult language learners to buy in, you know, it's important that you're conscious of the devices that they're using. And that brings us to the student-created tutorial. So I got my students to buy in. And I had over students, over 30 students joined on Zoom. As soon as I asked the students to use the annotation tools, I had students asking for help. I realized I was helping them based on the device I was on. Other students were trying to get, you know, trying to help based on the devices they were on.  Yes. Okay, so I asked the students to open up a new tab and basically search for tutorials based on the device that they're on. So we use Burlington English, you know, we're on Zoom and we use Google Classroom. So they started searching and I couldn't copy and paste from the chat fast enough. I mean, students caught on how to copy and paste onto the document that I was using.  And it was just very empowering for both for the students and extremely helpful. And it's okay that we have dupes because every student's effort is in there. And that's yeah, that's my testimony. And I believe we're moving on to screening and requires scores with Jennifer McGrath. Yes. So with that, and just a little sidebar Lolita teaches our ESL program is her ESL students that created all those tutorials. So it's wanted to give you a big shout out on that with I was really proud of that for ESL program. And so now moving on and making that transition to screen. So when thinking about how we're going to select our students to be part of this bridge program and where what this is, what are the type of students we're looking for for this bridge port that we can help better service them and give them a spark if they're interested in wanting to go into the pharmacy tech field. And so we are looking at our test scores for the ABE and ASC students, we wanted to target the low for the reading scores or low adult secondary education and risk levels five and six. And also we are going to go down to as low as the NRS level four, five and six in the math with the consideration that we are going to be providing a much more intervention in the module and medical math module for the course. We will be providing a lot more interventions to help fill in those gaps because most of our students may have high literacy but may not have as high level in skills and math. It could be because of literacy gaps there may be. So that's something that we want to take into consideration. And then of course for our ESL students, we will be looking at targeting the ESL students that are in NRS level six advanced level. And keeping in mind that these students will be probably in their current ABE ESL classes and also maybe doing their GED classes or high school diploma classes and finishing them up and they may take this course at the same time. So it's kind of like a natural chance for them to have a goal setting up. Oh, OK, I'm interested in risk and pharmacy tech, but I want to give my skills ready to go to that level. So working at this student foundation here to help tie in that and then they hope the goal is to have them when they're finished with their ESL and ABE classes and this course, they're ready to make that transition to enroll the actual pharmacy tech program and continue their pathway into a job. And so how do we bridge this gap? Lolita. Burlington English is an online learning management system the ESL department uses and also credits for increasing ESL CASAS test scores. So these students are meeting their benchmarks, payment points, but Burlington English also has a career readiness courses and one of those CTE courses is pharmacy technician. So having said that, our hope here at the Moreno Valley Community Adult School is to be in collaboration with Burlington English, you know, and get permission to integrate their curriculum supplemental material slash worksheets and embed them into, you know, some of our five modules that we're offering in intro to pharmacy. So I believe that and it's a star next slide. Oh, that's OK. I just wanted to add on to that as well. And is that in addition to using Burlington English as one of our resources, but just the Barbie tech soft skills component of it, we are also going to be blending in to a variety of different resources of curriculum. We're going to be using the actual pharmacy tech curriculum to build in for the medical for the term for the anatomy and physiology as well as for the medical mathematics components. We'll be using Aztec sources and a variety of creative resources. So it's going to be a blended of a variety of curriculum for these modules. And then with that, the whole goal is that we're looking at some outcomes, helpful outcomes here for this is the main ideas to increase and sustain enrollment in the pharmacy tech program. We want to expand that and create more enrollment for this course and also, of course, to support the increasing job market demand for pharmacy technicians in the entire region, which includes the city of Marina Valley. And with this in mind, we're hoping to expand our medical pathways and build further bridge courses to create and expand our medical pathways into medical billing and coding. Phlebotomy, we do have a phlebotomy program on our campus. We want to bridge do a great bridge course with that program as well and for hopefully a future medical assistant program in the future. And what one of the things that we would like to be able to do is because this is such a new and very unique adventure is that after we have piloted this course in the fall, this fall, we're going to be piloting this course. And over the next year, through refinements and evaluations and seeing how it works and everything, we're going to use the Moodle platform to create this course and put it in there. So we have a shell that we're going to be working with and we're going to build the course in there. And after it's all said and done over the next year, after this second year of our cohort, we would like to put this out on the public domain and put it out there and offer it for other adult education agencies across the country to have access to it to see if it's something that could be helpful for their programs as well. So kind of giving back to the community what we have gained from our D-LAC program. We want to give something back. So this is a very exciting adventure that we'll be doing. And Jen. The long and the short of it, I know we're running low on time. So the D-LAC process in the OTAN course without this program and these courses we wouldn't be here today presenting to you about the Bridging the Pharmacy Tech Gap. We wouldn't be able to do that. To date, we have developed our orientation materials and we have we've worked it into our master schedule for fall of 2021. This whole process assisted us in developing our leadership and presentation styles and communication styles. And the work that Dr. Porter provided allowed us to really see where our strengths were in different areas of ways we needed to approach tasks. And then all of our D-LAC trainings allowed us to learn and network with other adult agencies and pull ideas together because, you know, it's really better to use more than one brain, right? The smartest person in the room is really the room. So that's really how D-LAC and OTAN assisted us. Jen, if you could move it on to the next. Yeah, you go. Sorry. So a special thanks to Dr. Porter, Destiny Simpson, Netta, Penny and all of OTAN support staff and a special shout out to Coach Susan Greer. Development of this course would not be possible. And ideally, these resources provided valuable insights to what we need to consider and how we can build this course from the ground up. So thank you so much from the Marina Valley Adult School team.


Throughout history, a vast array of individuals who, for whatever reason, became figures idolized by their civilizations. Some even seen as godly-like figures, sentient, divine beings, whom, upon their passage into the next life, were believed to live on, often as deities, according to New World History. The most academically funded research practices in said preparations into the afterlife is undoubtedly that of the mummies found within ancient Egypt. The Valley of the Kings, impressive protective strategy against tomb raiders, yet the list of similar protective practices is long. The Sphinx even claimed as the protector of the pharaoh's pyramidal tombs by some, although we, like so many others, based upon a lack of evidence, is untrue due to the pyramids never having been proven tombs. Yet this theme of protecting the dead clearly permeated historians' minds, and, we suspect, this is due to its recurrence throughout history. The Curse of Tutankhamun, yet another relative story deriving from Egypt with mysterious goings-on during Howard Carter's incredible discovery of King Tut's tomb. The works of interesting motivations would often be left with these important figures. Not just solid gold death masks, thrones, coins, canes, and other jewels, but people of nobility have even been found buried within chariots, complete with eight horses sacrificed for the burial. We have also covered many other booby-trapped tombs, proof of the ancients' own beliefs in their own versions of the afterlife. But unquestionably, the most unique, and due to it remaining unsealed, the most enigmatic of them all, lay still guarded by an equally unique terracotta army, for all soldiers carved to depict an individual man, and the quantum phenomenon interdimensional pigment, Han purple, still visible upon many of this army. What makes this site so unique from all others is that an entire army along with other baffling technology guarded tomb clearly constructed over such an incredible amount of time and with such enormous effort. It must contain someone, or some thing, of unimaginable importance. Furthermore, as mentioned in a previous video, poison-tipped inexplicably advanced compound crossbows have been found still laying in situ protecting the entrance, though at some point coated in sediment, possibly why the terracotta army was found buried. Was this tomb pre-flood? Radar scanning technologies are advancing rapidly, and regardless of the Chinese strict forbitance to enter the tomb, technology is finally allowing us our first look into just what exactly such an incredible display of power has been guarding for all this time. It's an investigation we find incredibly exciting.