Live from Las Vegas. Expecting the signal from the noise. It's theCUBE, covering InterConnect 2016. Brought to you by IBM. Okay, welcome back everyone. We are here live in Las Vegas for IBM InterConnect 2016. This is SiliconANGLE's exclusive coverage. This is theCUBE, our flagship program. We go out to the events and extract the signal from the noise. I'm John Furrier with two great guests here. Really great story. Jason Jacobs, who's the founder and CEO of RunKeeper, fitness application platform. Just recently sold. Congratulations. And Simon Weecroff, adventurer, among other things. Been legally blind since 17 and has done some amazing things. Quite an interesting story. We're going to talk about how technology enables the spirit of happiness and pursuit for people to do stuff. Great story, Simon. Thank you for coming on. Jason, thanks for coming on. I really appreciate you sitting in the time. Thank you. Thank you for having us. So everyone wants to know that I want to go to the next level. Then we had a lot of athletes at this show talking about technology, technology innovation to augment their life. And we see augmented reality, you see virtual reality, all these things happen.  They can actually see the screens. Yeah. You're having trouble seeing. So how has this worked for you? Share with your story, with the audience, where you were and how the fitness app helped you and your story. Well, Runkeeper came along at a real ideal moment in my life. I was in a point in time where I was incredibly frustrated with losing my sight. I felt I got to a point where I was beginning to limit what I was doing because I couldn't see. And I felt that wasn't really a way to progress. So around this time I was looking for a way to go out there and challenge myself and really push. And I lived near some football pitches, some soccer pitches in my house. And I positioned myself between the goalposts. I just went up and down a soccer pitch. And at the same time, I began using Jason's app. And Jason's app was the first one to give audio cues. So rather than having to look at a screen, for the first time I got the information to audio. So it would say how far I'd run and how fast. And then I took that information and decided to see if I could pair the distance cue to what it felt like underfoot and just begin to memorize a route on the open road. So you basically have a route, you basically routed the data on cues.  Yeah, you make a few mistakes a lot of the way. The open door. I used to run into lampposts and road signs and things like that, but then you'd remember where those were, sort of pair that with a distance marker and one keeper and then just continue to build up the route. So it took me a couple of months to build up a three mile route with the aid of one keeper. That's awesome. Great inspiration. And Jason, I'm sure this is not a use case on the startup pitch, but this is a great example of some of the things that you're passionate about in your entrepreneur. You just recently sold your company to ASICS. Congratulations. Thank you. Super validates. You got to know your young family too. It's good as well. Keep them fed in college, make some money. But more importantly, talk about your story because this is not how you saw it or was it? How did you see this happening with your app? Yeah. So I mean, I think one thing about Runkeeper is that a lot of people assume that it was started by a competitive, serious ultra performance runner and was built for people like that. But the reality is that I'm just kind of a regular guy. I mean, I played a year and two games of Division III hockey in college and quit and played intramurals for the rest of my time and was always into things like lifting weights. And when I stopped playing sports, I started running as a way to just kind of hold it all together and actually after college, I'd only worked in small high-growth technology companies and was addicted to building these small high-growth technology companies and said, I know this is what I want to do my whole career and ultimately I want to start and build a company myself. And I was looking in areas that I knew but not necessarily areas that I was passionate about and I didn't really know what I was passionate about other than building these technology companies and it all just kind of came full circle because I signed up for my first marathon as a way to basically like spark my creative juices because I was so frustrated with this grueling process to try to figure out what kind of company to start.  Fitness is what I'm passionate about. I've been passionate about fitness my whole life. It's a huge part of who I am. I want to build a fitness technology company and I want to help regular people like me to get and stay motivated around fitness and sport. So, I mean, on the one hand, Simon is just what we, an example of just what we set out to do in terms of helping people to get and stay motivated around sport. But did we know that we could enable someone to overcome the kind of hurdles that Simon has overcome on that quest? We had no idea and it's just absolutely amazing to see and really humbling as well. And Simon has been a big inspiration not only for me but for my whole team as well. When we have hard days, we just think about what Simon is able to do and it's very motivating for us. Simon, the mindset of a growth mindset, I always, when I talk to my kids, I try to give advice with them because they're not listening to their teenagers, but be a growth mindset.    I mean, that's, there's a lot of reasons to tap out of that. Yeah. Take us through some of those. I suppose one of the really important points was the point where I quit doing something because I couldn't see. I was trying to climb half-dome in Yosemite and the idea was to get to the top before it's my girlfriend. She'd say, yes, it'd be a fantastic romantic. But it turned out climbing half-dome was harder than I thought. I'd never tried to climb a mountain before. And I was beginning to sleep and trip. And yeah, I quit doing something because I couldn't see. And that was really difficult to live with. So then returned to the UK and realized and I'd quit because I couldn't see. It was so hard. And I'd told myself that, you know, I'd never quit again. Even if it was because I couldn't see, that was just nothing. So you had it inside your soul.  I'm gonna, I'm not gonna lay down. Absolutely. And then I sort of applied that more generally, saying even if, you know, in times get hard, you know, it's no reason to quit. You know, gotta keep pushing, keep moving forward. And it was difficult the first few times. I went out and I really can't sort of point out just how much the app made the difference because it was a real lady's voice. Cat, is it? Cat, is it his voice? Is that helpful? The new revenue we've given feedback? Yeah, just hearing her voice every sort of couple of minutes was a real motivator in it. Filming full of confidence and I'd wait for the next sort of update from Cat, which really made me believe even more. And yeah, you know, I did run into the lamppost. I really did hurt. You did run into a lamppost.  And then when I went for my first ever ultra, there was a really difficult moment where I'd trained on a pancake flight airport. So I'd never run a hill in my life because there's just no hills where I'd memorized. But unfortunately I'd picked out a race that turned out was really hilly because I couldn't see the elevation gain map on the website. So I had no idea it was hilly. I thought it'd be flat, it's a road. So I turned up to this race and after 50 miles my legs were just destroyed. Emotionally I was falling apart, I was just crying and I sat down and I thought back to when I'd promised myself that I'd never quit. But there's a difference between quitting and failure. And I told myself that I'm happy to fail and the only way I was going to fail is if I could no longer stand. So I stood back up and 33 more miles until I could no longer stand. And then I got to be moved from the race. But then I just saw that as any other failures except for all the lessons learned. And from that point on, you know, I've never had to...  So you got up after 50, ran another 30. 33, yeah. 33. And all on the hills. So like you had like your body felt the hills.  What's going to stop? Will you have those motions going on? Yeah, you know, it really is an emotional roller coaster. You're up and down and a lot of the time when you're doing the bigger distances, it's all about managing your emotions and staying in control. And, you know, it's the same when I'm doing the training. You know, I've got to stay in control all the time. So if I make a mistake, go like two steps to the left, I'm going to get hit by a car. And the cars are going like 70 miles an hour. So I've always got to really manage emotions, stay in control, try never to make any mistakes. So was the technology the augmented reality for you was compelling, obviously? What's there a moment where you knew right away with the app? Did you have like, oh, I'll just try this out. Tire kicking? Was it like? Yeah, it was a definite moment because it started on the soccer pitch and the soccer pitch was essentially easy. It's, you can't really go about, just run up and down. But the only reason I stopped is because of the dog walkers. So I just couldn't see them.  They thought they'd move. It was a strange chicken with someone who can't see them. Yeah, someone did that to me the other day. I just won't have that one in. I was absolutely plowed into them because they didn't move. You go to New York, no one's moving.  But the definitive moment with the app was on a closed road. And I was using double yellow lines and I could feel the lines underfoot. And the app, I just so happened to configure it to do three minutes. And now my pace perfectly matched 0.3 miles. I'd hit these greats underfoot. And it was at that point in time, I thought maybe I can take this and really go with it and memorize the rule. So you saw the pattern, okay, wow, this is actually workable. Yeah. And then from there it was just, you're in. Yeah, there was a, I suppose another definitive moment where you're running this closed road and then at the stop, it's a dual carriageway, which is like a freeway interstate sort of thing. So I was running the closed road and then there was this one day where I knew I just had to step onto that road and just keep on going. So I was running up and down, trying to build up my confidence, waiting for Kat to tell me how far I'd gone. And eventually I did build up the confidence and I just told myself in my head that cars move, they will not want to hit you. They will move. So then with that sort of, as a mantra.  No one wants to hit you. Yeah, I know. That's a good leap of faith. Hope the parachute opens and you jump off that of the plane. Well, no one does want to run you over and I just told myself that, because no one really wants to do that. As long as you're paying attention, that's not going to happen. So I just told myself that that's what's going to happen. That is what's going to happen. And I just went out onto the road and I did it. But then, you know, you can always stay in this invincible mindset for a very small amount of time. So I think it's probably about 0.5 miles where it like turns around the corner a little bit. So I got to that bit and I just burst into tears because the mindset could only stay real for a short space of time. But then the mindset doesn't need to exist anymore because then you've built up on confidence in your ability that you no longer need to believe that you need to be invincible and things move because you're so confident and you practice the rule. You get used to the software. So it really was an immersive augmented reality for you. Certainly, you're there. What's happened since? I mean, any new updates, any new innovations to your usage and new adventures that share some thoughts around what you're doing now? Yeah, well, the next big step is something that I've been contemplating for years now. And I learned to train solo, which was a fantastic achievement. I did go over to sort of the ultra distance and my favorite adventure was I ran from Jason's headquarters in Boston all the way to the start line of New York, Madison and around the Marathon. So that still remains one of the best adventures just because it felt like a bit of a pilgrimage to get into. I feel like home. Yeah, for us too. Get into me, the team, because I've never met these people in real life. I'd heard Kat's voice so much. I'd never met Jason, which was okay. Is Kat a real person on your team? So Kat, so when she created the audio cues, she was the girlfriend of our CTO and they're now married, so. And Kat is still Kat, so she's a real person. She got license on a whole row. She signed that. A Siri voice. I mean, that's the voice in your ear. That was a helpful thing for you. That was a real compelling reason, wasn't it? Yeah, and I think perhaps it was a human voice made it more real. Yeah, and I don't want to tell Simon this, so Simon cover your ears, but at some point we might have some voice alternatives, maybe some other options besides Kat. So Kat will still stay, she'll still be there. She'll still be there. She'll stay with the girls. We'll get her on a freelancing basis. She'll come in, do some personal control. She'll just call me, we'll just talk. How's it going, you know, coaching? Yeah, he doesn't need run cupries. He's just going to call Kat when he goes out and she can be in his ear. But the next step is to now compete solo. And that's just a case of finding the right location. The right location is the desert. So I'm heading out to the Namibian desert in May, and I'm going to try and do it on guided solo, just me. And I'm developing an app with IBM Bluemix and we're going to see if it's possible for me to compete solo. I mean, all this new technology around real time and streaming is actually going to help, I think, a lot. Jason, I got to ask you, your team, obviously the motivational factors of what Simon's done has probably been an inspiration for everybody. I know it's for me here in the story of others watching and you mentioned this for you. How has it impacted your team's growth, their mindset, new product development? Has there been an impact to that? Yeah, I mean, to be honest, I think when we started the company, we kind of had, we had a germ of an idea that we wanted to just help people no matter where they are on their journey to get out and stay motivated around the sport. But we didn't really have a clear sense of brand and self. And over the years, we've really kind of tightened and figured out who we are. And what we stand for as a brand is that, I mean, our mission is to get the whole world running. And as a brand, what we stand for is helping regular people do exceptional things.  And you're doing exceptional things. So it's like you couldn't possibly be more representative of the brand we're trying to build or how we're trying to inspire people. And so we think about that all the time. Like we, and I, I mean, even as an entrepreneur, this is my first company, I'm seven and a half years in, it has had ups and downs and highs and lows. And it's been a long journey and I love it, but huge sacrifices and things like that along the way. And I personally think about your journey all the time as an inspiration to me. Not so much in my running because you kick my butt at running, but when I'm, you know, building the company because that's the only thing I can even, that even scratches the surface of the hurdles that Simon's had to overcome. So we had Neil Henderson on, he was with the performance cycling team with Apex coaching and they have the device, the glasses. So you're running solo with Blue Mix. You could be not so solo, by the way, you could be, they could be tracking your every move. I think maybe, I don't know if that's on the horizon, but you know, there's other ways to also help you. Yeah. That's also pretty dangerous to go out solo in the desert. Yeah, you got to survive in the desert as well. So I've got to take all my own food and sleeping equipment and everything. So it's not just a case of running solo. I've also got to try and... How about half dome? You're going to go back to half dome? I mean, it is a very beautiful place, but it's dangerous. It's very grueling, by the way, too. Yeah, I would like to go back and I think I'm going to wait because I've got two sons now. So I think I'm going to wait until they're a little older and then try... I wouldn't do half dome solo. Now El Capitan, that would be, that's your next one too. You can get, you know, free climbing El Capitan. Is there a nap for that? There are a few blind climbers, but yeah, I'm not very... No, no, don't. You've got two kids. My wife won't let me climb El Capitan. I've got four kids or jump out of an airplane. So there's things I can't do. I'm the anti-adventurer. You know, you've got two kids. Jason, where did you play hockey? Well, I played in high school and I went to Wesleyan University. I played for a year and two games. So you can kind of count that as playing college. Are you from the Boston area? Yeah, born and raised in Boston. Just at a suburb of Boston called Newton. Okay, yeah. I used to live in Redding. Dave Vellante lives in Harvard. Guys, thanks so much for sharing your story. Simon, I'm going to give you the last word. Share with the folks out there who are watching who look at your story and say, wow, it's an inspiration.  I bought Google Glass right off the first line. The guys in there at Google I.O., I love tech. But there's people like, hey, you know what? I'm not, I don't really want to be on Facebook. I don't like tech. How can that help them? So one, the inspirational piece of never give up your thoughts on that whole mindset. And two, how technology can help them. Yeah, never giving up is a pretty important mindset. It was something that was intuitive. You know, I didn't just all of a sudden have it. It was a slow gradual process and then the ups and the downs. And you do build on it.  It's moving forward to make a big difference. Soon as you start, put your life on pause. You know, that's where it all starts to fall apart. Keep moving, keep moving. Keep moving. How about technology? Not worrying about the technology for the phobia folks out there. Technology for me has been the ultimate enabler because essentially I can't even read a book. Now, there's a lot of things in my life now that without technology, I wouldn't even be able to function. You know, imagine not being able to read anymore and not look at your computer and read a website or pick up a magazine or a newspaper. You lose contact with the world. And it's only thanks to sort of apps being accessible and phones that, you know, I can now communicate like using things like WhatsApp. Because WhatsApp for me has been a fantastic step forward. Could you send audio messages? Because typing can be quite difficult when you can't see. So technology is a fantastic enabler and it's definitely not something to be scared of. It's something that can be adapted and really change your life. That's awesome. Well, thanks for coming on theCUBE. Really appreciate it. Jason, thank you for much for your story. This is theCUBE telling the stories here inside theCUBE here at IBM Interconnect 2016. Moving back with more after this short break.


All right, well, thanks for sounding out guys. We'll try to cover some, hopefully how you'll retina stuff. A lot of these slides are actually from Becca Genture. So you should all text her, thank you. But we can get into it here. Try to have it interactive and have just a lot of pictures and naming things, but sometimes that's hard in the morning, I get it. All right. All right, so we'll start with some posterior segment trauma stuff that they often like to ask about. So young patient, blunt trauma, you see whitening another retina. I'll start with this one, because I think it's pretty easy. So this is commercial retina. It's also been called Berlin's edema. I don't think they would ask that though. It's transient, although can leave some visual deficit in the area that's affected, especially if it's in the macula. One thing they do like to ask about it is kind of where is the damage? And it's in the outer retina, it's disruption of the outer segments and then can result in some atrophy down the road. Here's another type of trauma that's actually pretty common. Anyone recognize this one? Brutal rupture. Yeah, exactly. So this is gonna be blunt trauma. And then what's the most common cause of secondary vision loss after coronal rupture? Which is the exact same view? Yep, definitely. And I think most likely they'll ask you to recognize the coronal rupture and then you'll have to answer something about CNV. Yeah, all right. This one has been on OCAPS as well. This is optic nerve evolution. This is gonna be a bad injury, of course, NLP. How about a history of head trauma or intracranial hemorrhage? And then you see this. Turcans. Turcans. Yeah. Starting out on the East, it's good. This is dialysis. This is most commonly gonna be in kids and blunt trauma. They often like to ask about dialysis presenting late. So this kid will have a distant history of trauma and then they'll come in with the big RD. You may have to recognize that it's due to a dialysis. This is due to an evulsion of the aura at the vitreous base. Again, almost always gonna be associated with trauma, especially on OCAPS. And more likely they'll ask you where this will most likely happen. This is kind of one of the things where there's actually not very great data on but OCAPS really likes to ask you about it. And so the answer is the infertemporal quadrant. And then super nasal is the second most likely. And kind of the theory of that is that there's less protection of the globe in the infertemporal quadrant with the orbital bones and everything. All right, how about this injury will usually be associated with a bullet that does not result in a ruptured globe? Cool, bacteria, something I remember, perhaps. Yeah, scope area, yep. These patients are really high risk for secondary retinal detachments and primary PVR. So kind of by definition, they don't have scleral rupture but they will often have chloride rupture and retinal rupture and just a bad looking eye. How about this one? Oh, wait, Joe for scope? Yeah, yeah. Sculpt area, is that just due to, like it's almost like a more, since there wasn't direct injury from the bullet, is it just like kind of a more intense commotion or what's the? Kind of, it's from like the shock wave. So this is high velocity projectiles. So this is almost always like a bullet from like a real gun. In my mind, commotion is kind of blunt trauma, counter-coup, thing like on the opposite side of the eye. So I guess in some ways similar that they're trauma but one is always going to be blunt trauma. One is always going to be penetrating bullet trauma and certainly scope area is a lot more destructive. Gotcha. How about this one? Perchers. Perchers, yeah. And kind of a defining feature is these pertur fleckin. They look like little cotton wool spots but they're almost geometric and they have like little lines of clearing between them which defines them as pertur fleckin. And so obviously this is associated with a lot of things if you group, people have split it into perchers or perchers like retinopathy. It looks the same. I don't think that that is really a important differentiation but head and trunk injuries is probably the most common one and most likely what you'll see it associated with on a test but also things that cause like embolic processes can cause this a long bone fractures where there's fat emboli is at least the proposed theory. Pancreatitis and then eclampsia in the study of childbirth have also all been linked to this perchers retinopathy. Pretty much always gonna be bilateral and it's usually pretty symmetric looking too but obviously this is one that you need to be thinking about other things that cause whitening and the retina, infectious, CMD, porn, iron stuff like that too. Okay, moving on from trauma just have a couple of slides on AMD. I think you guys probably have a really good handle on this already but just a couple of facts that I think they've asked about before. So kind of population-based only about 10 to 20% people have wet AMD. Druzen are markers of kind of unhealthy RPE but you do see Druzen in normal retinas so occasional small Druzen does not count as AMD. That's just kind of regular aging. Usually they're between RP and Brooks membrane but we have other things like pseudo-articular Druzen. I doubt they would ask about that. Kind of the higher risk types of Druzen or the larger soft Druzen and then pigmentary changes are both kind of the highest risk factors for developing CMD in the future. They definitely like to ask about size of Druzen and kind of how that contributes to stages of AMD. Anyone to remember the cutoff for either intermediate or large Druzen? Like 64. Yeah. And probably the most important one is distinguishing a large Druzen. What's the cutoff size for that one? 125. 125. Yeah. And who knows why or why they picked that number or I guess rather what else in the retina is that size that you're supposed to compare it to? And? Yeah. And it's a vein at the like optic nerve crossing. Perfect. So yeah. Early AMD is multiple small Druzen or a few intermediate. Intermediate AMD is extensive intermediate Druzen or one large Druzen or GA not involving the fovea. So just because they have GA doesn't mean it's advanced dry AMD. It has to be GA in the fovea. So that's also important when you're thinking about who should be on ARIDs, which they like to ask about just because they have geographic attribute does not mean that they don't qualify for ARIDs. And if it's not under the fovea, they probably should be on ARIDs. And then of course advanced is either wet or GA under the fovea. All right. Original ARIDs formula, decrease the risk of progression to advance AMD from intermediate AMD by about 25%. This is the formulation for the original ARIDs, but of course that's generally not what we use anymore. They switched beta-carotene for lutein and zeozanthine and they almost for sure ask you this, but why did they make that switch? Lung cancer. Yeah, specifically in smokers. There was a slight increased risk that when they looked back at the data there. Perfect. Okay. Some basics about little detachments. So what type of detachment do you think this is? Just based on first impressions. Very metogenous. Good guess. Do you see a break? Exited. Perfect. So remember that the OCAPs, they're not gonna give you all the information out there, but they're supposed to give you enough information to make a decision. So they could show you a picture like this and then you kind of have to assume that if you're not seeing a break or they're telling you that on exam there's no break, even though it's not showing you all the retina, sometimes you have to make assumptions, which is probably the most frustrating part of OCAPs. But so Exited have already defined by kind of no break, this bolus smooth elevation of the retina. We'll see how that looks different in metogenous. I think this one's tricky because it's superior, which is where we usually see regemetogenous. You also get the shifting fluid, which I think is not the best descriptor because you can also see that in regemetogenous, but that might be kind of a buzzword that they use can be associated with lots of things, tumors, hypertension, especially eclampsia, childbirth types of stuff, any inflammation in the eye, especially in the forms of posterior uveitis. And then like anatomical defects in the eye kind of cause exited RDS to so optic pits, nanophthalmos, morning glory syndrome, those things that can for some reason allow fluid under the retina or kind of like nanophthalmos will increase the outflow resistance and therefore kind of be a contributing factor of why fluid can build up under the retina. So regemetogenous looks different. Usually it has this corrugated kind of wrinkly appearance and then of course you're gonna find a break. Sometimes they ask you about these Linckoff rules. There's four and they're all designed to help you find the break or nowhere to look to find the break. I don't really like these rules because I think it can be simpler if you kind of just summarize it. It's just that the break is at the most superior part of the detachment. So I think that kind of covers, definitely rules one through three. So you just kind of look at all the clock hours that are involved in the detachment and then the break is most likely to be in the one or one and a half clock hours that are most superior of the detachment. The kind of the tricky one is rule three. So if it's inferior, you figure out which side of the detachment is highest and then it's gonna be on that side. Rule four is that you can have this little kind of strange configuration where it's bolus inferior and there's kind of the sinus of shallow subretinal fluid coming from a superior break. Joe corrugated means wrinkly. Corrugated means wrinkly, yes. Yeah. I think Catherine knows that better than anyone here now. Okay, treatment, these are just the principles of treatment of retinal detachment. You have to find the breaks, treat the breaks, plug the breaks. So all the ways we fix detachment do these three things. A buckle is just another way to plug the break and that just allows time for the cryo or a laser to help. The buckle really doesn't do much down the road once you have good adhesion from the treatment besides kind of help save you if there's new breaks that develop but really the gas, the oil, the buckle, those are all just, we use those just because they temporarily close the break as the cryo or the laser helps seal the break which is the long-term solution to the retinal detachment. They're generally not gonna ask you like details about like vitrectomy, surgery, repair or really detailed like buckling questions on OCAPs. But they will ask you obscure things like this. So chronic RDS are usually gonna present with low pressure clinically but they're more likely to ask you about ways they can present with high pressure. So one, of course, just kind of for chronic RDS it's a lot of ischemic retina, they can get NV and NVG or there's this kind of theoretical shorts, Matzoo syndrome where detached retinas allow outdoor segments to shed and break off and they're not getting eaten up by RPE cells like they usually do. And then they float kind of to the angle and plug up the angle and cause glaucoma. I don't know if that's like ever really been documented but they like to sometimes ask about that. All right. Which one of these are not associated with detachment or tears? With arrow. Yes, great. Oh yeah, and what is the third picture? It's kind of hard to tell. Is that a meridian fold? Yeah, perfect. So OCAPs will also give you blurry pictures but so left to right, so this is lattice. This is kind of paving stone which is not associated with tears. The third one, I'm pretty sure is a meridian fold which you'll only see if you're looking at the aura. See, and these are often nasally where you have kind of more of those dentate processes which are normal. A lot of people have meridian folds too but you can develop a little hole or tear at the posterior tip of it. So technically they can be associated with detachments. The final one I think is kind of a vituretinal tuft which again also can progress to a tear. Retinoschesis, so most commonly this is infertemporal. So same as dialysis. It's bilateral and most people, they can be associated with pretty nasty detachments but in order for that to happen anatomically you have to have an inner hole and an outer hole. I think that makes sense. Those detachments also associated with a high rate of PDR. That's something that it would maybe ask about. Lots of ways to differentiate schesis from detachments. Schesis will have absolute scatoma. So you can test that I guess with a visual field test but also with your indirect lens and like cotton tip or depressor you just kind of put it above the lens and they can see it moving around on their retina. The schesis reacts to laser because to get laser uptake you need retina touching RPE. So in a detachment you don't have that schesis you do. And then kind of a little more subtle and probably less likely to be on OCAPs but more clinically useful is when you depress it. Fluid doesn't come out of a break. It kind of just stays bolus and elevated and then ultimately ultrasound and OCT if you can get it are super helpful too. All right, this is attraction of detachment. Of course from diabetes, from PDR. If they ask about PDR they'll probably ask you in the setting that it's the most common cause of recurrent RD. And then they may ask you about this gradient system which is also not super health, not super clinically helpful but grade A is kind of just some little vitreous clumps or cells in the vitreous. B is more rolled edges especially on break. So they'll show you a picture of a horseshoe break that looks kind of chronic and rolled up. And then C is pre-retinal membranes or sub-retinal membranes. And then it's kind of relevant whether it's anterior or posterior to the equator and kind of how much of the retina is involved. You guys remember indications for pneumatics, I'm sure. It's pretty simple. No PVR, the break has to be relatively superior. So kind of the superior 240 degrees and all breaks have to be within one clock hour because you're treating them with a small gas bubble. Again, the macula on and off doesn't matter and the distribution of the tet detachment doesn't matter. You're just treating the break, the sub-retinal fluid will resolve. So the indications only have to do with where the breaks are, okay, drug toxicities. So I'm not gonna go over all of them. You kind of just have to stare at a table and remember these, but how about this one? This is probably the one we see most often or at least look for most often. Black window. Black window, yeah. And of course, they're not actually just gonna ask what drug causes this. They'll ask what is this patient being treated for? Something like that. So you have to know what the drug is for. So rheumatoid arthritis, lupus, kind of different autoimmune diseases for black window. How about this one? So pigmentary retinopathy, there's kind of one drug they like to ask about for that, even though there are lots of different things could cause this picture. Like some of the phenothiazines. Yeah, so this is gonna be someone who has like a underlying psychiatric disorder. So yeah, phenothiazine is the drug family and then thyroidazine is the specific drug that's most commonly seen with this. Obviously we don't see this much anymore but they definitely still like to ask about it. How about this one? Like what's the defining feature in that fundus photo that you should recognize? It's not the most typical picture. And the picture does not go with the OCT. Crystals. Crystals, yeah. So this is tamoxifen. That's gonna be the most common drug. It's gonna be associated with the crystalline retinopathy that they'll ask about. So of course breast cancer in the first picture shows kind of pretty extensive crystalline retinopathy but you can also get this just little focal foveal excavation there, which can look a little bit like mactel too but if they have breast cancer then you gotta blame it on the tamoxifen. It was talk too, right? Yeah, so talk can cause crystals. Generally they're gonna be inside the arterials because that's an involunt process. They're mixing talk with their injectable drug of choice. But yes. I've also had the mask like they're already on plaquinil and then what drug puts them at higher risk for toxicity and it's using tamoxifen. Also tamoxifen, yeah. Oh, that's a good question. So other like risk factors for developing plaquinil toxicity. So of course time and dose are probably the biggest ones but I think it's also renal dysfunction, tamoxifen or any underlying maculopathy. That's probably just cause we can't differentiate underlying other maculopathies from plaquinil but those are all reasons that you need to screen them earlier. All right. Rifabutin is not something we see anymore either but it's something that causes a hypopion, a sterile hypopion. It's used for patients with HIV for prophylaxis for Mac. So something that could be confused with endophthalmitis and something that they still occasionally ask about. All right, some pediatric retinal diseases. First just a little bit of anatomy which they definitely ask about as well. So one of the trickier things is kind of what is the vitreous doing while the eye develops and kind of this primary secondary tertiary vitreous. So that's something I think kind of just got no cold that they'll quiz you on. So the high load artery kind of fills this embryonic fissure in the second month and then it regresses in the fourth month and then kind of that high load system completely disappears in the eighth month. We'll see in a second what we get when that doesn't happen and kind of that tertiary vitreous that's, or sorry, so the primary vitreous is that high load system. I wanna make sure I'm saying that correctly which completely disappears. The secondary vitreous is the vitreous that we know in the adult and then the tertiary. The only thing that it forms in the adult eye is the lens zonules. So this is persistent fetal vascular sure. So that high load system can stay around and completely connect the nerve to the lens. It's also the most common cause of unilateral cataracts in infants. It can look a little, it can look a lot like retinoblastoma when you first see it.  And then they also have persistent fetal vascular eyes elongated ciliary body processes which is something that has been asked before that probably has to do with because those are also, like we talked about kind of related or at least attached to the zonules and therefore a type of vitreous at least during development. You got to worry about glaucoma in these patients and we treat them generally surgically to remove their cataract and then treating their underlying amblyopia is something that OCAPS likes you to not forget about. You can have this to a smaller extent. So this is really the same process that forms a Midendorf dark dot or the Bergmeister papillae. I think you guys know about these anatomically and they're due to the same process of not having complete regression of that primary vitreous or hyeloid or artery. All right, this is ROP over a little bit. Some of the confusing things are things that I find confusing about ROP. So sometimes they may show you just a picture and ask you what this is. You're noticing that there's no vasculature peripherally past that demarcation line and there seems to be a little bit of a ridge at that. So this is probably like stage two. There's not really new vasculation on that ridge as far as we can tell in this picture. So important to know kind of the risk factors or who you need to screen. So these are babies that are 1500 grams or less than 32 weeks of age or if they use supplemental oxygen for a long period of time and this is why ROP has the highest rates in kind of developing nations where they're still relying on a lot of high oxygen which we do less of in the U.S. now. So we... Is it 32 or 30 weeks? I'm sorry? Is it 32 or 30 weeks? I think it's 30. Is it 30? I could definitely be fact checked there. Thanks for catching on. You can double 15 for 1500 and that's your second one. That's a good memory tool. Perfect. I'll have to update that. All right. So we grade these within zones, stages and plus disease. So these are the zones. Zone three doesn't... Your zone two goes all the way to the nasal retina and then zone three is kind of that crescent of temporal retina. And then the radius of zone one is double the distance from the disc to the fovea. And that radius is about the diameter of the 28-diopter lens when you're looking in the eye. And then we also do stage. We're kind of... Stage one is just that demarcation line. Stage two is a ridge. Stage three is new vascularization growing from the ridge into the vitreous.  And then plus disease is just torturous vessels, which is a pretty subjective thing. And people are trying to develop more analytical diagnoses based on imaging and AI now, but plus disease is something that we still use a lot clinically. So I think the most confusing thing for me was treatment of ROP because you learn like kind of this threshold cutoff, but then you also learn kind of the stage one and stage two ROP. And it was always really confusing if those were like related or different or whatnot. So to try to clarify that, so this threshold disease cutoff came first. So they initially just had this threshold disease cutoff to help define which eyes, which babies had a 50% risk or higher of having a bad outcome, meaning like total retinal detachment. So this is what gives us this definition of either five continuous clock hours or eight non-continuous clock hours of essentially stage three. So new vascularization and the in zones one or two. So this came first and defined kind of the worst eyes before they go on to have an RD. So in this study also said that all of these eyes that means that the special should get treated, of course. But then a little later, they said, well, maybe we should be treating eyes with less severe disease. And so that's kind of where this pre-threshold or type one and type two eyes or criteria came in. So when you hear type one or type two, that's all referring to pre-threshold or eyes that do not meet that initial threshold criteria. And so kind of in the e-drop study or early treatment of a ROP study, they looked at treating eyes that met some of these earlier criteria and showed that treatment of type one ROP, which again is less severe than threshold disease was still a good idea, meaning it prevented bad outcomes. So again, type one, again, all of these do not meet threshold criteria. This is either zone one with any stage of ROP and plus disease, zone two, stage three, with or without plus disease. Same with plus disease is kind of repetitive because that was already covered in the first one or zone, in zone two, this is probably the most relevant one. Zone two, stage two or three, so that's any type of ridge with plus disease. So seeing all of those when they're not meeting threshold disease criteria should still be treated. Zone type two, which is kind of anything but type one can be observed until they meet either type one or threshold disease. Any questions about that? Cause that really didn't click for me to be honest, like until fellowship. You guys got it perfect.  Some people don't operate on stage fives because it's really hard and they usually have bad outcomes anyways. Okay. How about this? If this is not ROP, what do you think this one is? Toxo. Toxo, could be toxo, especially if it's fever. Yeah. So this one's fever. Toxo is gonna have some inflammation, vitritis and then this kind of stock is gonna be going to a peripheral granuloma. So this, the most common gene is FCD4. You get exactly this kind of, this draging of the retina. This is a pretty kind of extreme picture of what we can see with fevers. A lot of times it's more subtle but they can develop new vascularization, vitreous hemorrhage.  So it's not true strabismus. They call it a positive ankle kappa. And then distinguishing this from ROP, it's gonna be a full-term baby. There's gonna be family history typically of fever. How about if you see fever like disease with detachments, it's really bad. It's in both eyes and it's a male. What does that make you think of? Coats. Coats, so coats will cover that too. Coats will almost always be unilateral but it's definitely, pretty much always in males too. This is kind of a little more obscure one but something they will sometimes ask about. So this is- Nori? Yeah, exactly. So this is nori disease, it's X-linked. And in my mind, it's just really, really bad fever. These people get bad detachments and proliferative stuff and it's bilateral. It's really rare, but again, Ocapsule Center likes to ask about that rare stuff, especially when we know the gene. So this is a coloboma. They're most likely to ask kind of like what causes a coloboma anatomically? And it's incomplete closure of an embryonic fissure. That happens at week five. That's why colobomas are generally kind of inferior or more specifically, infranasal. In the, so you can have this, this is of course a coriorentinal coloboma but you can get them in the iris, in the lens. Sometimes for the lens, it's just your missing zonules in that area and most commonly, infranasal. And a lot of times they're bilateral. So this is Coates disease. So there's lots of kind of things to recognize like the Talaeontic Tatic vessels, kind of the light bulb vessels, which especially you see on FA. Again, this is almost, this is mostly in boys. It's almost always unilateral. They like to contrast it, especially to retinoblastoma. So kind of thinking about how you can differentiate that kind of family history with the retinoblastoma, genetic testing, ultrasound is going to be key. You'll have calcification for the retinoblastoma. You generally won't for Coates disease. And really the light bulb aneurysms is kind of their biggest buzzword for this. How about rapidly progressive vision loss, nice stagmas in a six year old, bad ERGs and Ocaps is absolutely, yeah, exactly. So Ocaps wants to ask about stuff that causes permanent vision loss and death. So they're going to favor stuff like that. Oh, I'm sorry. I said yes to labors. And this is Batten's disease. It could have totally been labors too based on the I presentation. And so this is recessive for Batten's. They sometimes want you to know the gene. It's CLM3 and it's important because it's lethal and because they usually present to ophthalmologists first. So their vision symptoms start like kind of age six, usually they'll have profound vision loss and then the thing is caused by profound vision loss like nice stagmas for business, a bad ERG and then they'll develop seizures, cognitive decline and then it's fatal by at least the early 20s. Okay, moving on to some tumors. Are we doing time? Okay, I'm going to speed up a little bit. Okay, so cordial tumors, let's go through these. So this is a melanoma. You can see it kind of breaking through Brooks there causing that mushroom appearance. This is also a melanoma. Sometimes they can have portions which are not pigmented. I think you guys know this pneumonic for things that are suggestive of melanomas especially when you're trying to decide if it's melanoma or just a nevus. So I think the most important ones are thickness based on B scan and then fluid is probably kind of the things that most likely suggest that it's malignant and then of course growth is really the biggest thing that you'll see over time. They can get big, they can break through Brooks and cause that mushroom appearance on B scan. This can look like a melanoma, but this is a melanocytoma. It's always going to be right on the optic nerve and it's super darkly pigmented. It generally does not have malignant potential. This is just another one. Cordal mets will look yellowish. They'll be multifocal. They'll often be in both eyes. They're kind of lumpy bumpy, is a buzzword. And they importantly have high internal reflectivity whereas melanoma has low internal reflectivity on B scan. Coral hemangiomas will be kind of orange and red. They can cause exudative detachments kind of most commonly compared to any other tumor. These also have high internal reflectivity. And this is Sturge Weber. It's going to be probably most commonly seen in the setting of Sturge Weber where they can also have these either circumscribed which the first picture showed or these diffuse coroidal hemangiomas which can take up the whole coroid. They can look a little different. They don't have very well-defined borders at all. And when you see these eyes, what they're going to be asking about is probably glaucoma. So these eyes have high risks of high rate of glaucoma. Retinoblastoma. So you're just going to present as leukocorea. They're going to have calcium on the B scan which is key. They might be multifocal like this. We'll talk about the genetics here in a second. So, and then also important to know that these kids have a high rate of secondary malignancies. I think sarcoma I believe is the most common one but they also have pinealomas and melanomas. And the trickiest differential is comparing these to Coates disease which I think we talked a little bit about. They do like you to know these two pathologic findings. So Homer right. I always thought of Homer donut with a jelly donut in the middle. Although that's kind of confusing because the other one looks like a donut too but the Homer right rosettes are less mature. So you can also see them in like embryomas or some types of other tumors. The flexiner winter steiner ones are specific to retinoblastomas. They're more mature photoreceptors. They have central clearing. You know they're more mature because the photoreceptors are functioning. They're making outer segments and that's kind of why you have that central clearing and why you know they're more mature. Genetics of retinoblastoma is tricky. So it's a tumor suppressor gene but it's inherited like an autosomal dominant process which again is not typical but it's because the RB1 gene is so big and so prone to sporadic mutations that if you inherit one mutated copy you're almost, you have a very high rate of developing a second sporadic mutation and therefore getting the disease. Genetic counseling and kind of thinking about the inheritance is also tricky and something they test a lot. So if you're looking at the patient they have multifocal tumors or bilateral disease they're almost for sure have a germline mutation and can therefore pass it on. If you know the parent has bilateral retinoblastoma or therefore you know that the patient has risk of inheriting the RB1 mutation. They're not quite 50% for having the disease because penetrance is only 90% meaning there's a chance that they might not develop it and then those patients will be mostly bilateral if they're inheriting the disease but a 15% will have unilateral disease. And then if the parent has unilateral retinoblastoma then that's a little trickier because you don't know whether they're that 15% that do have, that does have a germline mutation it could therefore pass it on or the higher rate of 45% let's see I think I'm confusing myself. So if it's unilateral disease in the parent you're not sure whether it's a germline mutation or not. So there is a 15% chance that the kid will have retinoblastoma. If they do have, if the kid has retinoblastoma then you automatically know that it is a germline mutation and therefore the second kid kind of just falls into the initial algorithm of that 45% chance of developing it. And if the parent is unaffected then you have kind of just your sporadic risk of developing retinoblastoma which is far less than 1%. Again, most of those are gonna be unilateral but sometimes they can have bilateral disease. So that's a confusing topic probably helpful to sit down and like look at the charts to understand the genetics there. This is a astrocytic hematoma associated with two diseases that we know about which is tuberous sclerosis in neurofibromatosis. If you see this, you gotta think of on Hippolindal syndrome it's a retinal, a capillary hemangioblastoma. Also important to know what you also see in VHL so that's renal cell carcinoma, Pheos and CNS hemangioblastomas. Sometimes they want you to know the mutation is on chromosome three so VHL three letters chromosome three. This is a retinal cavernous hemangioma. You see these fluid levels where there's kind of clotted blood and then fluorescing that flows above it. If you see this you wanna think about hemangiomas in the brain because that's kind of the combination of Wyburn-Mason which is one of these diseases that does not have a gene and is not hereditary. And there's an association with bleeding with dental procedures because they might have hemangiomas under their teeth. We're gonna, this is vasopriliferous tumor. I don't think they're gonna ask you about that. The chirpy have lacunae. Again, this is hypertrophy, not hyperplasia. That's what differentiates it from anivis. So the same number of cells, they're just getting bigger and swollen. This is anivis with drusen which are, if you remember, you're two fine small melanomas. Acronym drusen are a good thing because they are a sign of chronicity. If you see this combination of just lots of pigment on the sclera and in the coroid, you think about ocular melanosis and if they have pigmented skin too, then this is ocular dermal melanosis which is associated with glaucoma and high melanoma risk. B-dump is really uncommon. They will, if they ask you this, I think it'll be in the setting of ovary cancer which is kind of the most classic association but it can be associated with other cancers too. This is bilateral uvial or coroidal thickening and pigment, usually with kind of some of these funny patterns. Coroidal osteoma, the key thing will be that it'll be hyperechoic on ultrasound and have a shadow because there's calcification there. Running through some of the white dots syndrome. So ampy, classically, this is gonna be block early, stain late. Young women, good prognosis. Mutes can look kind of similar but they have that brief like appearance to the fluorescein lesions. It's more commonly unilateral where ampy is usually bilateral. They're gonna complain of photopsias especially on OCAPs associated with mutes and this can come after a viral illness. Birdshot I think is easier for you guys to recognize. I think the important thing here is that vision loss is often from CME in the kind of acute phase and then just kind of a scheming and atrophy in the long phase and that you wanna treat these patients aggressively with kind of immunosuppressive therapy. Multi-focal cortis and panneviatus and PIC are essentially the same disease. Just one has vitritis, one doesn't and here the key for OCAPs is that vision loss is due to secondary CNV. Pose is probably the most, the key thing is that there's no vitritis or pose. Blow syndrome is pretty obscure. It's kind of pediatric sarcoid disease where they have kind of a multifocal corditis type of look to it. Okay, so we got like 13 minutes to run through some random things for retina. So this is blood associated endothelmitis. It can be staff and strep, but in OCAPs it's probably gonna be hemophilus which is unique to blood associated endothelmitis and these eyes do bad. The endothelmitis vitrectomy study is for cataract surgery does not apply to these patients. Usually we try to take these patients to surgery a little earlier, but it's tricky because sometimes the view is horrible. Post-surgical endothelmitis. So blood related is the highest rate cataract surgery. We have the EVS study to guide us. So it's not important to know that if they have light perception vision or worse, they should go straight to vitrectomy. If they have better vision than that they can go to vitrectomy or you can do a tap and inject. Post-traumatic, I think the only thing to know about this is that bacillus is kind of that key one. Kind of like hemophilus is to blood related. Bacillus is to traumatic endothelmitis and having a foreign body in the eyes is a bad risk factor. If you see this and they have no visual complaints this is asteroid. One thing they might ask what asteroid is that if you need to see through the asteroid the asteroid disappears on fluorescein angiogram.  I don't think they'll ask you about the pathology of the asteroid. Wait, really? That's so cool. It is pretty cool. And it's something we don't do too much, but yeah, it works. I've seen it work. Cholesterolosis can look like asteroid, I guess. I don't think I've ever seen this before, but apparently you can get it in the anterior chamber which asteroid does not go in the anterior chamber. So I guess if you see this, you wanna like test for systemic chai systemic cholesterol levels. Car and mar. I don't think they'll get into too much details of this but recovering is kind of the first antibody described in car. There's more now. Car is classically cones and rods. Mar is just rods and mar will kind of, we think attacks like the bipolar cells so that therefore has an electronegative ERG. That's you get the first inflection, the A wave from the photoreceptors but then you don't have functional bipolar cells. So you don't get the second, you don't get the B wave. That's what defines a electronegative ERG. They'll probably ask you about this.   So which will be used for viral hepatitis is an important kind of drug effect as well. Lasers, you don't have to know any of this except I think twice for me, they asked what does laser stand for and they gave different fake acronyms. So it's important to know light amplification by stimulated emission of radiation. I think I remember it being kind of like the only one that made sense. So you guys can probably figure that out if they ask you that question. See, this is a horrible acronym. Don't remember the acronym. Lots of things can cause CMV. I think, or I'm sorry, CME. You guys know all these. Niacin is a tricky one that they will ask for. That's used to treat high cholesterol. Niacin is the same as nicotinic acid and it doesn't leak on fluorescent angiogram. Chlorofolds, another horrible acronym. Don't remember that, but it's essentially like low pressure, inflammation or things pressing on the back of the eye can cause chororhenyl folds. Ischemia, so you guys may wanna, I'm sure you'll be able to recognize retinal whitening in a vascular pattern that's gonna help you differentiate it from infectious stuff. So most importantly, you gotta think about emboli. You guys know how to work that up. You see that a lot. Then of course, you can't forget about GCA and patients. This is over than 60. Some say over than 50. And then kind of just other random things that can cause arterial occlusions in the eye. I think you guys know these. This is Android Streaks. You guys know the Pepsi Mnemonic. Probably Pseudocentrum Elasticum is the most, definitely the most common association and probably the most important one because you should get an echo to look at their heart. There's some cardiac things that they have to worry about. And then similar to lots of other things, the most common cause of vision loss in these patients is secondary CNV because Brooks membrane is damaged. These are lacquer cracks. These can look really similar, but they're in high myopes. That's kind of how you're going to differentiate them. Macular hole, I think. Oh, Pijoo. Yes, yes. Real quick for lacquer cracks. Are those also associated with CNV? I always forget or- Yeah, it's tricky because high myopia is associated with CNV. And so these patients are gonna have really high myopia. So they'll have like myopic CNV. Will the CNV come directly through the lacquer cracks? I don't think so because I don't think they're breaks in Brooks membrane. Actually, I don't know anatomically exactly what they are, but you can definitely see CNV in these patients because they're high myopes. Right, okay.  And all you have to know is that once it becomes a full thickness hole, that's when we take them to surgery. That's really, there's all these stages but really it's just kind of, once you hit stage two, then it's full thickness and then you take them to surgery. And surgery has generally a high success rate. This one, oh, who can recognize this one? I make me really happy. It's my favorite diagnosis. Is it retained PFO? No. There's a yellow spot. Popper one. Oh, I like popper that I think- Or is it laser? Yeah, it's laser. So laser or solar you're gonna spray in the phobia. This one, the fondest picture is pretty bad here, isn't it? But you're gonna see generally like a yellow grayish spot in the phobia or if it's laser, you can see, you know, obviously more. They will not show you laser. That's too like modern for them but they can definitely show you solar retinopathy where it's just gonna be a single spot in the phobia. And then they probably won't show you that CT either but if they do, it's gonna be outer retinal, hyper reflectivity, whether it's laser or solar, it's gonna look kind of the same. It's just in laser, it can be more non-central. And then something that they might ask you about is kind of, so drugs that photosensitize you, usually we think about this like for sunburns but can also make your, theoretically, like your retina more sensitive to solar retinopathy. So sometimes it's usually like either someone like on acid or someone who took a lot of like tetracycline in the vignette who's gonna get solar retinopathy.  So you can see the C-fan configuration, the top one, these kind of salmon spots which are kind of like, I think they're just kind of like older hemorrhage and then the black sunburst is kind of, is like dead RPE from ischemia, all changes you can see in sickle cell. Probably the one important thing to know is that unlike systemic disease where SS is the worst, SC and S-thal are actually the worst for retinopathy. It's a kind of a weird association there. We treat these patients generally with laser, sometimes with anti-vegeta. How about this finding? I had this on O-cap splints. What disease is this in? Susak. Yes. Susak. Beautiful. They're not Dawson's fingers. Right. Yeah. Dawson's fingers I think is above the corpus callosum, but you guys probably know that better than me. So this is going to be a young woman with confusion, vision loss for multiple BROs, hearing loss, and then these spots in the corpus callosum, they get treated aggressively with IVIG and steroids. They also have these kind of weird gas plaques. They won't ask you about that. They're essentially just things in the retinal arterios that are not at the bifurcation, which is obviously the more common spot for emboli. This is just some foveal anatomy that you guys know about.   I think that's about 20% of people. Couple more minutes, retinal trials. So I think the only ones that are actually important that they'll ask you for are comms. The conclusions are small melanomas are okay to observe. Medium melanomas are okay to plaque. And then large melanomas, you don't need a radiation before you enucleate them. Those are the major outcomes. And then these are the sizes. There are also, these are the thickness sizes. That's the most important one. If you're going to remember any of the size cutoffs. You guys know clinically significant macular edema. Again, this is not based on OCT. This is a clinical exam finding. This, the DRS just showed that PRP works and defined high-risk PDR. So that's any PDR with vitreous hemorrhage or if you have a lot of NVD or if you have NVI. That's who we PRP. Nowadays we PRP really anyone with PDR, but this was by the study answer. EVS where we talked about that. These were kind of some random factoids that after taking OCAPS for many years was seemed relevant and are kind of random. I don't think I have time to read them all, but I think this is being recorded. See, if you want, you can come back and look at these random but high yield facts. Let me show them on the screen. VKH, the recurrent stage is anterior UVIS. The chronic recurrent stage, the last thing where they have exacerbations are anterior UVIS. It's more the acute first presentation that they get the more classic posterior effusions and all that, that can be a high yield fact factoid. This is CSR, you get that expansile dot more common than the smokestack pattern. This is juvenile santhobranium loma they present with hyphemas in young babies. And it's a two ton giants cell on path. Okay, thanks for sticking through it. I know those reviews are tough. Good luck guys, you're gonna crush it.


Hello friends, welcome to the session. I am Alka. We are going to discuss matrices. We have to compute the following Our two given matrix are minus one four minus six eight five sixteen two eight five and the second one is 1276 805 three two four we have to add these two matrices. So Let's start with a solution Some of these two matrices equal to minus one plus twelve four plus seven minus six plus six then eight plus eight five plus zero sixteen plus five then two plus three eight plus two five plus four This is equal to eleven eleven zero sixteen five twenty one five ten nine Therefore the sum of the two given matrices is equal to 1111 zero sixteen five twenty one five ten nine. This is the answer Hope you understood the solution and enjoyed the session. Goodbye and take care


Good morning everyone, we are from team analytics and we are working on sunbird analytics here is my team I am Siddharth, Aleksha, Shivam and Tanmay. So starting off with our objective our first objective was to install sunbird portal on our local machine followed by playing around with the code getting our hands dirty and understand each of the controllers views workflow between them and then use various sunbird APIs in order to generate analytic reports and in case we do not have such APIs and create our own data APIs based on our requirements install sunbird server on our local machine and testing our own created APIs on the server. So let me give a overview of what we have done we have successfully installed sunbird portal on our local machine we faced some challenges in the beginning but they were easily fixable they were just the problem with the version of node and the dependencies and we went through the entire scripts what was nightmare for us was there was no comments in there. So we had to figure out everything on our own how each of the component work and especially ma'am helped us a lot in this phase and we successfully added an analytic section which generates four different kind of reports in there first one is content consumption followed by location wise course enrolment gender and education wise course enrolment and we tried installing sunbird server for more than 26 time failed every time except one sent over 100 emails to team sunbird and except without getting any proper reply we did not get the required API key in order to test their API so as suggested by team sunbird we created our own APIs in order to test the front end and in the end our only working server stopped working so we had to map everything from Cassandra to my SQL because we had a software which generates random data for us so in so rather than again and bring data into Cassandra we had a software to do that for us and now I will ask my friend to tell about the technologies we have used. Yeah coming to the technologies part the technologies we are we use in our project are the Cassandra, AngularJS, NodeJS, cluster module in NodeJS and ExpressJS the Cassandra the database used in the sunbird is the Cassandra and this Cassandra driver is used to access the database coming to the AngularJS AngularJS is we used to use AngularJS to create a report step that is in the front end part NodeJS and the NodeJS we used to create the data APIs cluster module in NodeJS the cluster module in NodeJS we used to increase the throughput of the system. ExpressJS is a library which is used which we created a server to accept the to get the request over to my friend Shivam to continue the session. So this was the part that took like we did this part over 26 times and just succeeded once so it is the sunbird server installation. So initially we generated the xstep API key from the jwt.io website then installed and updated the git and clone the sunbird devops folder and then we updated the config file based upon the information provided on the documentation of sunbird server installation. This step includes eight different stages of installation the first was the sanity check it just checks the prerequisites if they are prerequisites softwares if they are properly installed or not and it also checks the RAM if it is compatible. The second was the config so it installs the config and the host files the third is depth it installs all the dependencies dbs installs and configures the kasandra database APIs was used to install and deploy the cong API proxy was used for installing ngx server key clock install server key clock installs so this step used to install key clock which is used for authentication purpose and this eight stage core so all the other stages were third party of the third party but this was of sunbird and sunbird software. So we have developed some error guide and IIT Bombay X team also helped us in this. So the first error was that SSH connection failed so we will have to develop the SSH connection the RAM not enough so initially we took a local system which had 4GB RAM but we didn't check at the initial step that what was the RAM and then we faced this error. So actually the RAM should be of 8GB. Second was the refuse to connect so the database was refuse to connect so here we had to add a host in the etc slash host files. The third was this error was coming at the API stage so what we advise that it should be done before that API stage so here we had to change the pg underscore hba.config file and do the necessary as described here and in the report and final was that IP address was unreachable. So here we added host name and the IP address to the ansible slash host files. So this was the steps we did and only once we had succeeded to successfully install the sunbird server but then eventually at the end that also stopped. Good morning guys I will be explaining about the front end so this is just a flowchart for the workflow and when the APIs are called. So I will be explaining through this video so we have made this video so first you log in. So let me point out here that initially there were only this as you can see there are six tabs right now initially there were only five the analytics tab the last one is what we have added. So we had to go through a lot of code as Siddharth said earlier it was very painful and as he already said that we had added four tabs content consumption education wise and location and gender. So yeah let's start with the content consumption as you can see there are like three drop downs here. So the first drop down is for this all the courses that the user has created. So the user who is interested in seeing the analytics will choose the course for which he wants to view the analytics and as soon as he selects a course let me add this the list of courses is fetched to API that we have written it is called the get courses API. So once you select a course another API is used to fetch all the contents within the course. So the second drop down is for that so all the contents are fetched as soon as you this select the content for which you want to see the graphs and you can see the graph there are two things there is a graph and there is also table we have provided here and you can change the third drop down is for choosing the graph type you can for content consumption we have line graph and area graph and one more I can't remember. So yeah so this was content consumption the rest of the three are very similar to each other and so I will be explaining only one. Yeah so this is the area wise distribution. So yeah here we have only two rounds so the first one is again for the selecting the courses again it is fetched through get courses API and again we can select the graph type. So I like to add that we have used this Google charts for doing all these graphs and these things because I really like Google charts all the width adjustments and all it can be done very easily using Google charts and also they provide very beautiful charts. So yeah changing the graph type is also very easy so yeah so that was the front end part. So this is the education and after that finally we have the gender one. So over to Siddharth he will explain about the data APIs these are the screenshots of various reports which are being generated and then coming to the back end which is working behind all this. So first of all let me give you a little overview of how it works so basically I have created an express based Node.js server which accepts all those requests all the API calls are post which takes the user ID and when we log in into Sunbird what we get after handshake is a session token. So this should also be sent in the header along with the ID course ID and the session token which we get so generally it should be a very easy task but the problem with Cassandra is it does not provide any joints any group buys or any kind of aggregation so we have to do everything programmatically and the Node.js is a synchronous programming so before even we can fetch the data it was free processing it and we are we were getting a null response so how we managed to do this synchronous programming in a synchronous environment was something using callbacks so it is function under a function under a function it goes till D level till we get the required response and in the end we send the response to the server and first API is get course gender distribution it basically based on the course ID checks the course enrollment gets the user ID of each of them use that user ID to determine the gender and in the end performs aggregation and returns array of JSON objects in which there is a gender type and the count of the number of course enrollment belonging to that category and it is same for education area the content consumption is a little different because we had to convert the timestamp and all so the in content consumption each content has an ID followed by user ID and the timestamp when it was consumed so we had to convert the timestamp into required format and it performs aggregation over a period of a year so it shows a consumption pattern in the last year how it is basically number of times that content was viewed in that year so we just it is a simple query we just give the timestamp along with the content ID and it gets all the all the number of times it was being viewed and then the response is the JSON object array of JSON object with month and year and one thing I would like to as in the beginning you said that we do not even know how to use each course of our machine so we finally figured out how to use that so basically there is a module in Node.js called cluster Node.js was designed to use only one core of your PC so what this cluster does is it copies the program and it runs on each server so it increases your throughput it does the load balancing and it increases the stability so even if one worker goes down other are other are still responsive and what I have written is if one by any chance if one crashes one worker crashes then it creates a new folk I get folks a new one and so it basically increases the throughput and the stability so that's all so any queries. So when you wrote the API did you have a sample API to look at? Yes sir. You had and that was useful. Yes sir. How long did it take you to write the complete API test it and confirm that it is working? Lot of time sir as I said. The second point is when you are writing an API why did you not make it more generic by saying that the user can actually request a time interval during which the user wants the data you are fixing it to one year. Yes sir. It is not always that I would like a one year long history or something. Yes sir that's something which can be fixed. Because that is rather easy to fix. Yes sir. And that would make your API more generic. Was this your first time handling Cassandra and such things? Yes sir. So you learned something useful? Yes sir. You did not use Angular also? Yes sir. Even the Node.js was used earlier? Yes sir. It was time to figure out how to do this synchronously because even before our... The key for future is such new things will keep emerging. These were not there ten years ago. These will be replied by something else ten years ago, ten years later. What it means is in each of your professional career be prepared to keep learning new things. And if a new useful thing has not appeared on the horizon should keep your brains polished by just attempting as an experiment learning something new trying it out and dirtying your hands. Never let that practice go away from you. Because having done this once second time you will do it faster. But with something else. And that is why we always say learning how to learn fast is the important take away from our entire education system. It's not exactly what this or that you have learned. Good work you enjoyed I suppose. Yes sir. You unfortunately have no exposure to Open edX right? Yes sir. So there is a comparison that ought to be done in terms of the API richness of Sunbird servers versus Open edX. And there is a feedback that the Open edX architect has requested. When I mention to him that over the next year we will be examining this. So that would be useful thing. Okay thank you.


Thank you Alex for that warm introduction. I was privileged to know Barry and honey And I'm so pleased to be here tonight among so many of their friends And it's so moving to see you Alex carrying on the example of community leadership set by your parents Hello, everyone. Thank you for coming out tonight. It's wonderful to see so many friends here. Good to see you here, Mayor Tory Thank you for being here. Thank you all for gathering this week We were delighted to welcome President Rivlin of Israel to Canada as Of course, you know the president had to cut his visit short because of personal reasons We wish him and his family and especially Nahama very well. I Also like to thank Adam Minsky CEO of UJA Federation of Greater Toronto and his entire team for organizing this event I cannot think of a better way to celebrate the ties that unite Israel and Canada Ahead of tonight have been given some thought to this idea of friendship between nations About what binds us together In 1948 Canada was one of the very first countries to formally recognize Israel and more than 70 years later Our friendship endures our understanding of each other deepens our affection for one another grows That's not a coincidence It's a choice and to understand why Canada continues to make that choice Why our two countries are so deeply committed to standing with each other one must first look at Israel's leaders President Rivlin has not only dedicated his life to the people of Israel He has been a leader who brings to life the words of Israel's declaration of independence By advancing the vision of a democracy based on freedom Justice and peace with equal rights for all under his leadership the Canada-Israel Relationship a natural partnership rooted in shared values and a shared vision for the future has continued to grow and thrive But our ties are also made stronger by Canadians and Israelis who've long nurtured our friendship Indeed Canada's Jewish community has played an essential role in this journey From raising awareness about the challenges facing the Jewish homeland to giving young people the chance to visit Israel To creating more opportunities for greater cooperation You have given countless Canadians the ability to better understand Israel the Jewish community and its importance to Canada But beyond that the Jewish community has played and continues to play a pivotal role in shaping the Canada that we know today It's been more than 250 years since the Jews are here in Israel It represents more than 250 years of contribution to our country And growing up in Montreal, I was lucky to discover and appreciate the Jewish culture all over my city The music of Leonard Cohen, the mood of Mordecai Richler, the streets of Côte-Saint-Luc or the Hampstead These examples are numerous and we can say so much about Toronto and many other communities from one end to another in the country Jewish Canadians are our friends, our neighbors, our colleagues, our fellow compatriots Helping the most vulnerable Repairing the world Jewish values are Canadian values Through our relationship and friendships, we've gained a better understanding of Jewish identity and the unique challenges facing your community But as Alex mentioned, it hasn't always been this way Indeed, we have grown to be much more compassionate and more supportive than we once were There was a time when we let anti-Semitism take hold in our communities and become our official policy A time when we turned our backs on the Jewish people in the most desperate of moments Canada's ill treatment of the Jews before, during and even after the Second World War Is well documented And while this is a dark shameful chapter of our history, it is one Canada needed to confront Last November our government issued a long overdue apology to Jewish refugees and the passengers of the st Louis we turned away during the Second World War That day we vowed not only to remember But also to act on the painful lessons of our past Something we must do every day Today anti-Semitism is a tweet inciting hate It's a threat in the comments section It's graffiti on a high school, near high park It's an abhorrent attack this past November on Jewish teens wearing kippas It's the horrific murder of Jews in Pittsburgh, in Paris, in Jerusalem, and around the world Anti-Semitism is on the rise And a hallmark of its latest iterations Is a deep-seated hatred for Israel Or as my friend Erwin Kotler, who has done incredible work on this subject Put it well to me a number of years ago and continues to- Erwin, are you here tonight? I heard Erwin might be- no, not here tonight, there we are As he told me a number of years ago The new anti-Semitism features the 3Ds Demonization of Israel, a double standard around Israel And a de-legitimization of the state of Israel That's why a movement like BDS or the so-called Israel Apartheid Week has no place in Canada When Jewish students are made to feel uncomfortable on campus because of their identity When people don't feel safe dovening in shul That is unacceptable, period, and it's un-Canadian And I can assure you that this is a message I proudly bring wherever it must be heard Canada will always condemn hatred of any kind against any community And Jewish leaders have echoed this message time and time again Any movement that calls into question Israel's right to exist Or the right of the Jewish people to self-determination is promoting anti-Semitism It is an attack on our Israeli friends, on Jewish Canadians, and on the values we share An attack on the foundation of the Canada-Israel friendship And on everything we stand for That is why we will continue to stand up against anti-Semitism To raise Israel's voice and stand alongside her, including at the United Nations A group of terrorists like Hamas and Hezbollah who target civilians Canada has also sought to increase cooperation with Israel through many bilateral initiatives From trade to innovation to science to technology to security Ambassador Lyons often jokes that her mission is the most visited of any mission around the world And it's easy to see why Countless Canadian groups, from business leaders to civil society organizations To community groups visit Israel every year And since November 2016, 13 high-level visits have been held by Canadian leaders Of all orders of government I myself traveled to Jerusalem to attend the funeral of the great Shimon Peres I've had the chance a couple of times now to see with my own eyes Why the city has been so central to the religious, national, and cultural identity of the Jewish people For thousands of years, and it's a place I very much look forward to visiting again My friends, Canada and Israel share a special bond One rooted in mutual respect, a shared history, and common values But our bond is made strong by people like you who seek to bring us closer You do tremendous work to sustain and promote our partnership And Canadians are better for it President Rivlin's visit this week attests to Israel's desire to deepen our ties We know that we have more than an ally in Israel We have a real, trusted friend on whom we can count And who can count on Canada to continue to stand by its side through thick and thin Thank you all for inviting me here tonight to join with you Merci d'être ici tout le monde Merci beaucoup


Obviously, without John Masters, you can't have the airborne operation. As a John Masters instructor here at the United States Army Advanced Airborne School, I'm part of a small team that is tasked with ensuring that we train our John Masters, as well as our new jumpers here in the division. The 82nd Airborne Division is America's strategic response force. It is the only full airborne division inside the United States Army, and it is one of the highest guardians of standards inside the United States Army. Our entire purpose is to make sure that we can place paratroopers anywhere in the world on short notice to make sure that we can continue to defend all the things that our country holds near and dear. I think what makes me the most proud to be a Jump Master is it is by definition what it means to be a good leader. Lead by example, nothing is more important than leading my jumpers out the paratrooper door. Here at the schoolhouse we have an influence outside of the 82nd Airborne Division. As John Masters leave and go to other airborne units or even other non-airborne units, by teaching those Jump Masters how to be good leaders and how to run a safe operation, we can affect change in other airborne units, allowing them to safely execute the operation based off the standards that they learn here.


what the Narcissist fears most, what they see as their greatest threat of danger or harm. Before you watch the rest of this video, I would like you to take a moment and type what you think is the Narcissist's greatest fear in the comments below. If you guessed that the Narcissist's greatest fear is being exposed, you guessed right. They fear people seeing them as they actually are, as bad people, as people who are narcissistic because they fear rejection, they fear being dismissed, they fear being treated as unworthy of serious consideration, they fear that people will see through the illusion and realize that it isn't real, which is why they can often seem so defensive and passive-aggressive, they're trying to defend the illusion, they are indirectly resistant to the demands of other people, they are avoidant of direct confrontation because that is the only way that they can maintain the illusion and they need to maintain it because it serves them, it gives them fuel, they strategically position themselves in a way where they cannot be manipulated in the same way that they manipulate you, they control you but they position themselves in a way where they cannot be controlled using the same methods that they use to control you, whatever they are criticizing you for, they will do everything in their power to not be that, to not be associated or identified with whatever it is that they are criticizing you for, if they're saying that you're not good at something, whether it's cleaning, cooking or something else, they will go out of their way to portray this image that they are good at that, they will portray this image that they are efficient and capable of doing something, that they are criticizing you for, I'm sure you can remember many things that they have criticized you for and I'm sure you will notice that whatever they want to be good about them will always be something they criticize you for, it will always be something they say is bad about you, they use their perceived deficiencies of you to make them look like they're superior to you, to make them look like they're better than you, but why would they even feel compelled to demonstrate that they are better than you, unless they felt like they were beneath you, their desire for superiority comes from a place of inferiority, they secretly feel like you're better than them, but then this is clearly evident in their behaviors, they just don't realize it, they don't realize that this is what they're communicating, they are dependent on you, their self-esteem depends on what they can get you to believe, so that they can then feel a certain way about themselves, their entire image is dependent on what they can get you to believe, which means that it isn't even real, it's an illusion, it's a false self, and once you take away your belief it all falls apart, because their image is dependent on what they can get you to believe, whatever you reflect back to them, which is what they then reflect back to you, which means that it is your reflection that sustains the illusion, so even if they do manage to manipulate you, you're actually just admiring a reflection of yourself, there is no way to give your attention to admiration directly to a narcissist, it's only ever going to be a reflection of yourself, because it's a false image, it isn't real, and that's why no matter how much you give to them, it's never enough, they can never be satisfied, they always want more, they feed off your reactions, because it is your reaction that sustains the illusion, that's what gives it power, you are fueling something that doesn't even exist, but you make it real, which is why they are so dependent on you, they have this desire to be something or to feel a certain way, but they can never make a reality of it, because they have no identity, they have nothing of any value or significance to actually communicate to you, they lack confidence, they have no values or principles, but they have this childlike desire to be something, and this is what they transfer onto you, by manipulating or abusing you, and pulling you into their realm, so that you can then reflect it back to them, and then they can feel a certain way about themselves, they can feel like they're somebody, they're heavily dependent on you, because they wouldn't be able to feel that way on their own, they wouldn't be able to generate those emotions from within, because they lack the central most important part of being a person, they have no co-identity or values, there's nothing that is central to their existence or character, this is what the narcissist fears most, they fear being exposed, they fear being rejected or dismissed, they fear being treated as unworthy of serious consideration, they fear that people will see through the illusion and realize that it isn't real, they fear there's so much, that they will often try to turn your character inside out, the first thing they go for is your self-esteem, they want you to lose confidence in your qualities and abilities, they want to devalue and degrade you, they want to discredit you, and then they will even assassinate your character, they will smear your name, and try to get everyone to see you in the same way, they try to destroy everything in you that they don't have, everything that they are envious and jealous of, they have black and white thinking, they see it as though something is either good or bad, right or wrong, real or fake, so if they can make you out to be a fraud, they believe that must make them real, which is why when they think you're onto them, the first thing they're going to do is try to destroy your character, they will provoke you to react to them, they will try to entice you, they will try to turn you into something you're not, because they believe that will minimize the risk of their exposure, they believe that will prevent people from uncovering something damaging about them, whatever a narcissist is trying to take away from you, it's always going to be something that they don't have, or something that they're insecure about, these people are banded who they really are a long time ago, because they couldn't hack it in life, they lacked the qualities needed to do a task or put to the situation, they traded their legs for a wheelchair, and now they expect you to push them around, they are dependent on you for attention, admiration and validation, they need you to sustain the illusion that they are real normal healthy people, when the reality is that they are not, these are damaged people who can only elevate themselves at your expense, they have to step on you to get ahead, they have to destroy you to build themselves, they cannot generate anything from within, because they lack the central most important part of being a person, they have no co-identity or values, which means that they're not really a person at all, they can only sustain the illusion of being a person for your reactions, which is why they are so dependent on your reactions, because if you don't give them any attention, they will quickly die out, it would feel like life or death to them, which is why as soon as they feel like you're onto them, they will pull out all the stops, they will do whatever it takes to capture your attention, they will smear your name and try to get everyone to think there's something wrong with you, because deep down they know exactly what they are, they know that they cannot generate anything from within, and it scares them, they don't want anyone to know about it, because they know there's no future in something that started out as a game, so they just carry on with the illusion, they go from one person to the next, whoever buys into it, whoever feels it with their belief, but deep down they know that it isn't real, they're lying to themselves, which is why all they can do is manipulate you, the best you will ever get from them is an illusion. Thank you for watching, I hope this video resonated with you, please like, comment, share and subscribe, if you would like to donate, my PayPal link is in the video description, coaching enquiries, you can email me at coaching.naxtvivert.uk, thank you for watching and I'll talk to you soon.


The study investigates the effect of water absorption on abrasive wear performance of jute glass carbon reinforced composites, finding that hybridizing with jute and or carbon fabrics improves wear resistance, while stacking sequence has a slight effect, fibers relative amounts have a visible effect, and water uptake induces a noticeable decrease in wear resistance. With increasing normal load and sliding time, the wear resistance decreases, displaying fiber matrix debonding, multiple cracks, fiber fracture, fiber pull-out, debris formation, and wear scars through SEM observations. This article was authored by M. A. Abdel-Bakey and M. Camel.