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Of course, this is Louis XIV. This is the magnificent palace that he built when the French Empire was at its peak. And this is the main entrance. This place, like, you know, sets the bar for oculance, I guess you can say. And, of course, there's always all kinds of works with the stonework, with the latticework, with the metalwork. This is the famous Hall of Mears. And so this is where the Treaty of Versailles was designed, which ended the war to end all wars. You know how that one went after World War I, 100 years ago. So this is the famous Hall of Mears. You just have to say it's a busy place. You don't get to get a private tour. You don't get to have it yourself. But pretty spectacular place, if I do say so. And there's the, so I couldn't quite get the roof in. Focus there, there's the Neurals of the Roof, of course, the Grand Chamber of Deers. All right, so what are we going to talk about today? We're going to talk about glaucoma. And any path lecture regarding glaucoma starts with the trabecular meshwork. And so this happens to be a particularly beautiful piece of meshwork. When you guys do your path rotations, you'll see when we get trabeculectomy specimens, they do not have traps on them most of the time. And they're often just sclera. This happens to be a beautiful one. So when we're talking about the trabecular meshwork, there's different ways to break it down. And the first way is you can do the anatomic way of looking at the angle as you're looking at it with agonium here. So when you're looking at it with agonium here, you're looking into the anterior chamber angle. We're going to go ahead and start, say, Catherine. What denotes the apex of the angle? What is the first thing that you'll see when you look in with the agonium there? You'll see the Schwabbi's line. Schwabbi's line. What is Schwabbi's line? It's the end of Decimates membrane. Exactly. So where Decimates membrane terminates, there's a little, sometimes there's a bump, sometimes there's a little line, but Schwabbi's line. And so that denotes the beginning of the trabecular meshwork. If you look, the trabecular meshwork is triangular. This is the apex. And here's the base down here. It's so triangular-shaped. So when we're looking in with the agonium there, also, Sean, there's a couple of different ways we denote the meshwork here. So first, from Schwabbi's line, what's the next part of trabecular meshwork posteriorly? The non-pigmented meshwork. The non-pigmented meshwork. And because it's kind of thinner at the apex there, you don't have a lot of chance of pigment gathering this. When you look in, it'll be a paler line. Theresa, what's the next area here? The pigmented trabecular meshwork. And so that's where sometimes where you get liberated pigment granules. They'll gather up right there. And Rachel, what is the base of the meshwork here? The scleral spur. The scleral spur. So when you look in, you'll see a little line that denotes the scleral spur. Now, when you think of the trabecular meshwork, you've got to think of it in three dimensions. And so the apex is here. The base is here. The scleral spur acts as a little lip. It goes around 360 degrees. And the meshwork sits in that scleral spur. And it almost like a little shelf that the trabecular meshwork sits on. So if you're looking in with agonium here, sometimes underneath the scleral spur, you'll actually see this structure right here. Ariana, that's actually the root of the iris. So you can actually sometimes see that part of the iris are part of the ciliary body when you're looking in. So the other part of the trabecular meshwork we can do is you can also divide it vertically, if you will, for the corneal and the uvial scleral meshwork. But then also, this part of the meshwork right here is particularly important. Allie, what is that called? The juxtacanalicular. And therefore, that means this is what? Schlemz canal, all right? So when you think of Schlemz canal, it's not a round tube. It's kind of an oval area, and this is it right here. And again, you think of the trabecular meshwork in three dimensions, Schlemz canal runs all the way around. And so this is Schlemz canal. It's this juxtacanalicular tissue that is important, because a lot of people think that's where the impedance to flow of aqueous is, and that may be what's involved in open-angle glaucoma. So it's the juxtacanalicular tissue that's important. And here's a close-up. Let's talk a little bit about the flow of aqueous, all right? So we're graced with a senior today. Wow, this is so special. All right, so tell us, where's the aqueous humor made? The ciliary body. Made in the ciliary body. And then how does it get to the trabecular meshwork? So it's made the ciliary body wraps around the iris through the pupil and then into the trabecular meshwork. So here's the meshwork. Here's that juxtacanalicular tissue. Here is Schlemz canal. Chris, good evening. Hello. So it gets into Schlemz canal. Where does the aqueous humor go after that? So it goes to the juxtacanalicular tissue, and then it'll eventually get into the veins. Aqueous veins will go to the veins. Exactly, so here's the aqueous veins, and it will eventually make its way out to the circulation. Here's a close-up. There's that juxtacanalicular tissue. Now, the trabecular meshwork's not just a wide-open meshwork. There actually are endothelial cells lining it, and there is both active and passive transport of aqueous through there. So it's not just passive flow through this meshwork of tissue. All right, so here we're showing that nicely. Here is the trabecular meshwork. Here's Schlemz canal. Here's one of those aqueous veins. And then you see it drains out right into the plexus here, the episcleroplexus. And so I always tell you this every year. Your mission is when you're at the VA or in clinic looking at patients, find an aqueous vein, because we never think about these. We never look for them. So if you're looking with a slit lamp, just beyond the edge of the limus, deep in the episcleroplexus, you'll actually see some aqueous veins and it'll look like there'll be a vessel with bloods in it, but then you'll get box-scarring of the vessels. So you get aqueous flowing there with the little red blood cells in between. So your mission today, find one of those aqueous veins. And you look at it, you go, oh, yeah, they're there. God, why haven't I seen that before? So they're really there. So that's your mission for today. Find them. That's just with a slit lamp, not with gonia. Slit lamp, no, it's actually outside because remember it's on the episcleroplexus. And so the aqueous veins drain it through the, trabecular meshwork through Schlemz canal and then through the sclera to that little plexus that's on the surface of the sclera. All right, so when we're looking right here at an angle, what I wanted to show this is that if you look at a trabecular meshwork and you're patient with open-angle glaucoma, it looks the same as an age match control without glaucoma in light microscopy, meaning that we cannot see the pathology of open-angle glaucoma on pathology. Now the meshwork is different in a 20-year-old as opposed to an 80-year-old, but if you take two 80-year-olds, one with open-angle glaucoma, one without, on light microscopy, I can't tell the difference. And so you really can't tell when you look at that. All right, so when we break down glaucoma, we break it into several different anatomical features. So the first thing we look at is we look at open-angle glaucoma. And then when we look at open-angle glaucoma, you have primary run-of-the-mill open-angle glaucoma not associated with anything else, but you've also got secondary open-angle glaucoma. So we're going to circle back to Catherine. What do we see in here? So you see multiple trans-illumination defects, 360. So this would be concerning for pigment dispersion. Exactly, so there's an entity called Pigment Dispersion Syndrome. And so people used to argue about where does the pigment come from and why does it occur? And if you look at this picture, this tells you you look at the trans-illumination defects in the iris and you see that it has a radio appearance to it. And when you go ahead and you look at the back surface of the iris, you see that that lines up directly with the zonular bundles. So you know the zonules, remember when we talked about lens, they come along here and then they insert onto the cylinder body. Well, this is the back surface of the iris. And so when you have a posterior bowing of the iris, those little zonular bundles will scrape on that pigment epithelium and release pigment, giving you a secondary open-angle glaucoma, what we call pigmentary glaucoma. You know, for some reason this occurs in younger myopes, males more than females, why I don't know. But if you do an OCT of the anterior segment of the eye, you'll see there'll be posterior bowing of the iris. And then you get the scraping of those zonular bundles releasing the pigment. And so when you look, here's a really nice path specimen here. Here's what you're making our measurement. Look at all that pigment. So you can imagine what that pigment's gonna do. It's gonna come up that measurement and cause a secondary glaucoma. Right here, here's the iris. And you can see right there where some of those zonular bundles have scraped off that pigment. So it goes through the pupil, comes around. Predominantly, it's in the inferior angle. Yes. A lot of people have heavily pigmented TM. How can you tell on path that versus pigment deposit in the TM? Yeah, you have a lot of pigments, especially in a darkly pigmented person. You do have a lot of pigment in there. But when you look at the person who's got pigment in the mesh work from just the eraser from normal pigment, it's uniform. Whereas if you look at pigment dispersion, it's usually inferior. Because remember those aqueous currents, they carry the pigment around. And also that pigment deposits on the posterior surface of the cornea. What do you call that? Catherine, the pigment deposit from pigment dispersion on the cornea. Kuchenberg spindle. Kuchenberg spindle. So it's this triangular shape area in the inferior third of the cornea. So the aqueous carries it. So when you go in the ozone with pigmentary dispersion, you'll actually see that the inferior angle have more pigment than the superior angle. And also you'll see the trans-elimination defect. So that's real helpful. All right, there's other reasons for secondary open-angle glaucoma. Sean, what's going on here? So in this picture, there is a big mass kind of growing right across or right below the angle, kind of pushing the iris away. Wrong button. What would you be concerned about? Melanoma. Exactly, so don't forget, if you have a malignant melanoma arising from the ciliary body, it can actually invade forward into the trabecular mesh work. And you see that widely separated area of the iris root and the mesh work as this tumor pushes in here. So that's another cause of secondary open-angle glaucoma is invasion from a tumor, from a ciliary body tumor. And here you can see another one. Here's the cornea, the marcation, the end of dissonance membrane, and here's the iris root. And look, here's this pigmented tumor coming from the ciliary body growing into the trabecular mesh work and the angle causing a secondary open-angle glaucoma. It's open angle. All right, what are we looking at here, Teresa? The picture of the anterior segment with the iris dilated. You can look back and see the lens. There's a deposit more peripherally that kind of has like a scallops edge, so pseudo-expoliation. All right, so pseudo-expoliation or now we call it exfoliation syndrome can also cause a secondary open-angle glaucoma. Why do we have this pattern here, this kind of a bullseye pattern of deposition? The iris acts like a windshield wiper. Exactly, so you get this little deposits on the surface of the lens and as the pupil moves in and out, it scrapes it back and forth so you get a lot of exfoliation material here and you get some in the center and then it's clear in between where the pupil scrapes it off when it goes. And here's a nice close-up view of that scalloped appearance. So you get this exfoliative material and now people have really worked out the genetics. It's the loxal one gene and it causes a defect in how the elastic tissue and the matures and in any event you get extra material that deposits on the surface of the lens and you end up getting this exfoliative material and then of course that can cause a secondary open-angle glaucoma.  In the angle, Chris, what's that? Well, she said angle, where else does this stuff deposit? We saw that one, that doesn't count, saw that? It can deposit in the endothelial cells of the cornea. It can deposit in the sphincter and dilator muscles of the iris, it even deposits in the iris pigment epithelium and it can deposit all along the zonules and so unfortunately exfoliation is a triple threat when it comes to cataract surgery. You get deposits on where the zonules insert to the capsular bag along the zonules themselves and where the zonules insert in the cellular body so it makes the zonules triply weaker. Also, it makes the capsule more brittle and makes you more susceptible to glaucoma, makes the pupil so it doesn't dilate as well and it gives you more susceptibility to corneal edema so we see a ton of this here. There's a whole pocket of exfoliation in Utah because it's a disease most commonly seen in people of Northern European ancestors where a lot of Utahns come from. You open the Salt Lake phone book, you see a lot of Sorenson's and Petersons and all that in there so you see a ton of exfoliation here so you guys will see that a lot in surgery and this just shows you nicely on retroalumination that scalloped border. Okay, so this is Arianna, what is this called, this pattern of deposition on the lens capsule? This is showing iron filing. Iron filing, so when you were a kid in shop class, did you ever have some iron scrapings and put a magnet on them and it all stands up on there? Sorry, I come from the non-enlightened era, boys did shop and girls did home act so it was a very non-enlightened thing. Girls were supposed to learn how to cook and clean and things, yeah, see now that you do both and guys did shop manly things, cutting and hammering and manly things so this is the so-called iron filings pattern and of course what we worry about is this exfoliative material deposits in the trabecular mesh work and so it gums up the mesh work and these people can get in trouble relatively early, you can watch them and they're doing fine, doing fine and then suddenly the pressure will really shoot up and so what's interesting is if you do cataract surgery, the intraocular pressure and exfoliation patient will actually drop by three to five points eventually and so I think the reasoning first of all is you widen the angle so that helps a little bit but then you remove all that exfoliative tissue that's sitting on the lens capsule and when you're doing your irrigation and it's floating through there you're actually flushing out a lot of stuff in the angle so even though people with exfoliation you gotta watch them real carefully cause they can have a pressure spike the first day in the long term, especially the first few months after surgery that IOP actually drops so you end up un-gumming the mesh work if you will. All right, yes? Is the exfoliative material more like an epithelial on pathology? No, it's actually a protonaceous elastin tissue, yeah. All right, so this is, I guess who did we end up? Did you answer it? I think Ariana, you answered one, didn't you? Okay, Allie, what the heck's going on here? What do you see here? Okay, and what does that cause? Okay, good, so at least you guys are reading it cause you know I go through this systematically and I'm gonna start like going out of order just to confuse you but at least you guys are reading ahead of time.  Oh, it's been there for a while and then of course the spouse always says oh, he's been blurry for years, he hates doctors and so by the time they come in, their pressure's 50, they have corneal edema and what ends up happening is you have a hyper mature cataract, the cortex will actually liquefy oh, the capsular bag is intact, protein will leak through that intact capsule and these are, what kind of cells here, Allie? Macrophages, so you see these macrophages and look, they're just in gorge, they're just stuffed with this protonaceous material and so you can imagine these big fat macrophages can clog up the mesh work but also just the protein can too and so these people can get a pretty significant glaucoma and the treatment is to remove that lens. So that will actually cure this secondary open-angle glaucoma what we call phacolytic glaucoma, it's not really a lysis of the lens but they call it phacolytic glaucoma and this is just a tap of the anterior chamber when people weren't sure what was going on there and you see again, big fat macrophages sitting here. All right, so when we think about glaucoma we've been talking about open-angle glaucoma now where you've got primary and secondary but don't forget there are other causes of glaucoma you can have narrow or closed-angle glaucoma you can have the opposite which is angle recession, dramatic angle recession where the angle is actually wider than normal. All right, so what are we concerned about here? Concerned about angle closure probably. Yeah, look at the, what's the tip off here in this picture? Why would I show both eyes? That's mid-dilated pupil. Exactly, so you look, there's the pupil with light shining in it, constricted pupil. Here's a mid-fixed dilated pupil so these patients who come in with acute attacks of angle closure they'll often have a mid-position iris but it doesn't move well. And of course when we look at with the slit lamp the tip off is you can actually see the forward bowing of the iris. There's the beam on the cornea, there's the beam on the lens and then look at the beam here as the iris narrows in the proofy.  So it comes forward and really what it amounts to is you get a relative pupillary block. And so when people have an angle at risk they've got a narrow angle to begin with. High hyper-opes, big swollen lens, then you dilate them and the pupil dilates fine. It's when the dilation is just beginning to wear off that you get maximum apposition of the iris to the anterior lens capsule and there you'll get a relative pupillary block. So what's the treatment of this condition? Exactly, so you do laser peripheral adectomy, make a hole in there, it allows the aqueous to bypass the pupil and go straight in. And so for those of you who are younger and haven't done a laser PI on someone with an angle closure, it's pretty cool. You hit that iris and man, you'll get this gush of fluid coming through there and the iris will recede right before your eyes, pretty satisfying. All right, now if you don't treat an angle closure right away, Catherine, what can happen? Exactly, what do we call that? Well, anterior sony. Exactly, so we abbreviate it as PAS. You'll have all the abbreviations in ophthalmology, peripheral anterior synechia. So when you get apposition of the iris sticking to the peripheral cornea, look, here's the measure, we're clear back here and the iris gets stuck. So if you don't break off an angle closure if it just chronically keeps getting worse, you actually can get synechia closing the angle and then those are much more difficult to treat. So this is actually synechia, peripheral anterior synechia closing the angle there. So a secondary angle closure glaucoma. And here you can see again, apposition of the iris to the peripheral cornea and there's the measure, we're clear back there, closing it off. So Sean, what's another cause of secondary angle closure? I'll give you a picture of it right here. Neovascularization, what can cause neovascularization? Those are the top two and you can get a chronic ischemia to the eye just from bad circulation in general, severe carotid disease. And so when you get chronic ischemia, these ischemic factors will go ahead and diffuse into the anterior segment of the eye and you get abnormal blood vessels growing on the surface of the iris. And eventually these blood vessels can grow on the surface of the iris and they'll grow all the way over into the angle so you'll get a secondary angle closure glaucoma due to neovascularization. So it's a neovascular glaucoma. And there you see, here's the iris, iris pigment up thin, you've got vessels in the stroma, that's normal. But you shouldn't have vessels on the surface of the iris here. And so that's called rubiosis eridus, you know, red iris. And so you see these little vessels here and as they grow into the angle, you get a secondary angle closure. And here you can see this is an area where you've got the iris actually stuck to the lens capsule. So what kind of glaucoma does that cause, Teresa? The posterior synechiae. Exactly, so this is now a posterior synechiae. Posterior to the iris, not anterior. And that iris sticks on there. So you can get posterior synechiae, which give you a blocked angle right there. It'll actually, but it's not just that a narrow angle moving back and forth, it's actually the iris sticking down to the lens capsule. So you'll get a secondary glaucoma from pupillary block. And here you can see sometimes you'll even get an inflammatory membrane going all the way across. So they call that an occluded angle. So if it zippers up all the way around, they call it pupillary seclusion. But if you get a membrane growing all the way across, which blocks it off, it's pupillary occlusion. So this is an occluded pupil and you see an inflammatory membrane sticking the remnant lens capsule to the iris causing a secondary pupillary block. And eventually you'll get an angle closure glaucoma. Now, what's going on here, Rachel? And so here's what's left of the mesh work here. Here's the iris root way down here. What's going on here? Exactly, so this is kind of the opposite of the narrow angle of the closed angle. This is an angle that's way wide open. And so this is now an angle recession. And what's the most common cause of this? Trauma, exactly. So it can be automobile accident. Usually this can be secondary to the two dudes. You guys all heard this, how all trauma is two dudes. Never one, it's two.  That's the classic story. They're usually drunk and belligerent when they're telling you this. So they had to run in with a fist or a foot or automobile accident. And in any event, you get a severe blunt trauma to the eye. What is associated with these initially? What's the history, or what do you see on findings often initially associated with this? Hythema, so you get the eye filling with blood. So you really want to be careful once the hythema clears and everything's stabilized, wait a month or so, then go near them and look. So final bonus question. How soon after a severe trauma like this does angle recession glaucoma occur? Yep, seven to 10 years is the average.   And so it's a redundancy to say that. You could say that about your own kind. And so these guys just won't show up for follow-up and we see these periodically in the clinic. Someone will come in when they're 40 with blurred vision. And you look at them and their pressure's 45 and they've got a temporal island of field and that's all that's left in that eye.   So I put the fear of God in these guys. I tell them, you know what? You could develop glaucoma and it's really sneaky.  And so you never say blind to a patient with macular degeneration or optic neuropathy. You say loss of vision because blind is a very limbic word. And so if you say blind, it has a pretty good connotation. So these are the guys you say blind to because you really want them to come in because they can lose vision very slowly as their pressure creeps up over seven to 10 years. This just shows you just the differences. Here's a normal angle. There's the iris root. So technically it's not so much that the iris root tears. It's almost a tear in the face of the ciliary body. So you get a tear that goes, here's the mesh work here. It goes all the way back here. And then eventually over the years that mesh work can become sclerotic and cause you to have a secondary glaucoma. And here's that mesh work. Look at it. It just kind of sclerosis over over the years. You just don't see a good mesh work there. All right. This just kind of shows you, it's a nice picture because we cut it in half. And so here's a patient that's had, look at that angle. Angle recession, cataract surgery. Look at that nerve. Totally cut down there slowly over time. All right, so since we're talking about glaucoma, obviously the place where glaucoma causes its damages at the optic nerve. So what do we see in right here, Chris? You were seeing a nerve that has pretty large cup to disc ratio, which makes us concerned about glaucoma this thing, which is something like this. So where do you think the edge of that disc is? The edge of that cup is, I mean. Kind of hard to tell, maybe right there. This is where you obviously want to look with three dimensions. But boy, that's a pretty suspicious looking cup right there. And this one I think would be a little bit bigger.  There's still an argument to this day. The pathology is in the axons of those ganglion cells coming into the cribriform plate and coming into the laminocrobrosa. Some people say it's block of axoplasmic flow. Other people say it's chronic ischemia and maybe both. And so in any event, you get chronic damage to the axons as they're passing through, then you get secondary death of the ganglion cell. And that's what causes the cup to get bigger. And if you don't treat it enough, you get death. So this is a cup to disc ratio of one. And so this is a totally wiped out, totally wiped out cup with untreated glaucoma. Now oftentimes you can even see an excavation of the cup. So that's even more than one. That's even if you're calling cup to disc ratio 0.6, 0.7. This is like 1.1. So it actually excavates, and this person had a trauma. There is a corneal scar, we call it a glaucoma. And you can see it had a ruptured lens, summering ring there, and then severe glaucoma with cupping. So when you look right here, you'll often see temporarily, look at that nerve fiber layer, completely gone. There's a single fiber left. And then nasally, you'll often get this vessel going in and then it'll dip down. And so it'll often disappear. You see it go into the disc, and then it disappears as it goes down in. And so this is what we call the beam pot. Those of you from Boston, you know the beam pot. And so it's actually got a wider atrophy from the edge of the rim than there is actually the rim itself. So this is a severe end stage glaucoma. And if you look, you'll see that the laminar crebrosa is really bowed backwards. And then of course the fibers in the optic nerve are markedly disrupted secondary to this chronic glaucoma. And there you see another one where, I mean this is totally cupped out, total beam pot. And it's kind of cool looking. It almost looks like those cliffs that Jeff Tabin climbs up and kind of dangle over the edge and climb your way up. All right, this is interesting. This is an optic nerve seen in cross-section and it's got some focal areas of damage. What the heck is that? There you go. And what causes that? Well, this is often an effect from a severe sudden glaucoma. So see you've got someone who goes in and a cute, popular block and their glaucoma goes way up. So you get this kind of cavernous atrophy. They call it schnobbles. Cavernous atrophy. It sounds like something that you would like, you know, used to shoot when you were a teenager. Oh man, let's do schnobble shots, you know? Come on, humor. So this is schnobble's cavernous atrophy and it's usually the result of an acute high-pressurizing. If you do a special stain, you'll actually see that that's hyaluronic acid in there. So people have speculated that the high-pressure literally drives that hyaluronic acid from the vitreous into the optic nerve head focally. The other thing that can happen with acute pressurized alley, what part of the eye are we looking at here? Yeah, so those who are damaged to the lensopathelio cells and eventually they vaculate, what are those called? Glaucomflechin. I love that word just because it sounds cool, you know? Glaucomflechin. And so it can actually with an acute pressurized cause ischemia to the anterior lensopathelio cells and then you get these focal opacities that they call glaucomflechin. It's a great word. Now all right, so what does glaucoma do to the optic nerve? Mix it atrophic and what part of the nerve gets atrophic? Exactly, so the ganglion cell layer, look at the ganglion cell layer here. Totally wiped out, nerve fiber layer. So next week we're gonna do retina path and what do retina ogres and onions have in common? Layers. And so you guys really better know the layers of the retina and there's a lot of them. So know the layers of the retina cause we're gonna talk about glaucoma. The only difference is a CRAO, remember the central artery brings blood to the inner two thirds of the retina. And so you would actually not only wipe that out but you'd wipe out the inner nuclear layer and even part of the anterior part of the outer nuclear layer. Whereas this just gets ganglion cells and then secondary nerve fiber layer. So not quite as extensive of damage. And now here you can see this is an area where they've got damage here. This is the macula of a normal eye. You see the ganglion cells are multiple thick. This is the macula of an eye with severe glaucoma and look how it's even wiped out the macula. So the macula is the last to go and that macula or papillor bundle is really the last to go. And so people will often have that temporal island and that central vision and the periphery gets wiped out and end stage glaucoma, even the macula gets wiped out eventually. All right, we're going to talk about a couple of other different entities that can cause glaucoma that you need to know about. So this is something that you may see with the peed's people. This is congenital glaucoma. And so back in the olden days when I was a resident, they called this Barkhans membrane and they said, well, there's a membrane that grows across the angle in kids with glaucoma and the way you treat it, we used to do what's called a goniotomy. And so now these guys, people have discovered the angle again because the glaucoma guys are putting all these little chunks in and these mixed procedures.  The idea would be you cut Barkhans membrane and then magically the glaucoma would go down. And as we study it more, we discover that it's not so much, it's a membrane growing across the angle in kids with glaucoma. It's that the angle just doesn't form normally. So you get this connective tissue here but you don't have a normal angle behind it. What we were doing in essence is we were just cutting a big swath that allowed aqueous to go into either slump's canal, even if it was there, maybe even just the face of the cellar body. So we were just given a way for fluid to go, kind of like people are doing now with migs. So we were just 35 years ahead of our time and didn't know it. And so this is a congenital glaucoma. You get this membrane-like structure over it but you don't really get a normal angle developing. And there you see it. There's the angle, there's Barkhans membrane, there's the angle in congenital glaucoma. So the angle just doesn't develop well. It's just not normal. All right, so there is an entity that we want to talk about today and that is the ICE syndrome. Katherine, what does the ICE stand for? Something to do with filial syndrome. Yeah, irritable, corneal, endothelial syndrome, so ICE syndrome. Sean, bilateral or unilateral? I just mean unilateral. Yeah, it's very, so again, I got to teach you guys now because for oral boards, you say it with conviction. So even if you're guessing, you say unilateral. If you go unilateral, then they know you're guessing, you don't get credit for it. So just put it out there, okay? So it's usually unilateral, it's very interesting. All right, Teresa, so there are three parts of ICE syndrome depending on if you're lump or a splitter. And so what are the, what's the first one? What am I showing here? So essential iris atrophy. All right, so it's called essential iris atrophy. If you look here, they've got what's called corectopia, the pupils abnormal. You even get what's called polychorea, multiple pupils. And so you see a moth eaten iris, multiple pupils here and they can get a severe glaucoma from this. Rachel, what is the common final pathway of all of these three different entities of ICE syndrome? Exactly, so you get this abnormal endothelium growing into the angle which causes glaucoma, but even growing onto the iris. And so the first one, most common one is called essential iris atrophy. Chris, what's the second entity of the triad here? The second one is Chandler syndrome. Chandler syndrome and so these all have common things. Chandler syndrome, you still get polychorea, you still get glaucoma, but what does Chandler syndrome get in addition to that? Cornial edema, so here you see the cornial edema, hazy cloudy cornea. So Chandler syndrome has very similar to essential atrophy, but with corneal edema. And then the third one, Marianna, all right, so you get, it's called coganry syndrome or iris neva syndrome.  So coganrys or iris neva syndrome. And when you look at the pathology and all of these, it's the same and it's called the desmetization of the angle. So abnormal endothelial cells grow all the way across the angle. They close off the angle completely and they start laying decimates membrane even on the iris. And you look right here, look at that decimates membrane. Goes all the way over to the angle, but right there on the surface of the iris. Alley, what stain is this? PAS, why? Why would we do that? Exactly, and that is what decimates membrane is. So you see decimates membrane really thick, covering the angle, covering the surface of the iris. So that's kind of the common denominator in all of these ice syndrome patients. And here we have, this is actually perfilaridectomy that they did. So this is pretty cool. A patient had ice, a perfilaridectomy. The AS stain again, look, here's decimates membrane on the anterior surface of the iris. And then we go to higher power, sure enough, there's the iris, there's decimates membrane right there. And if you look carefully, you can see melanocytes popping through, forming that little iris nevus that you see in these. And so this was cool. This was the cover of the Archives of Ophthalmology. And so it's my only archives cover, so I made the cover with this gulica syndrome. There you can see again these iris nevi on the surface in Cogonry's. All right, now there's another entity you need to know that can be associated with, well, a group of entities that you need to know that can be associated with glaucoma. And the way I like to memorize these, there's a paper George Waring wrote literally 40 years ago about the stepladder classification. What are we talking about here, Becca? Like Peter's anomaly and like... What do we call the whole category, though? Wrongly, by the way. Well, that's what this is, but what's the whole umbrella called? That's another string of the umbrella. So these are called the anterior chamber cleavage syndromes. And so wrongly, we thought that when the eye was forming you'd get this wave of mesoderm coming out and that it improperly cleaved and then left you with these syndromes out here. So they called it the anterior chamber cleavage. Now we know that it's not mesoderm, it's actually neural crest and it really isn't a problem with cleaving. But that name is stuck to the literature. So the anterior chamber cleavage syndromes. And so what is this, Sierra Becca? That's a posterior... Postural embryo toxin. So the first thing you see in these is you see a thickened anteriorly displaced Schwabbe's line. So you see it's thickened and instead of having to look with the gonium or you can actually see Schwabbe's line in these kids, even with a slit lamp. And so you see this anterior displaced Schwabbe's line it's called posterior embryo toxin. They thought this was due to some toxicity during the growth of the embryo and so that's why they called it that. And here you have a close-up. It's the Schwabbe's line. Okay, now what's the next kind of step in the stepladder, Catherine? So you see the posterior embryo toxin. There's posterior embryo toxin real nicely. What else are you seeing here? Scarring over the angle. Yeah, so you've got scarring over the angle. You start to get some thinning of the iris here. What do we call this? Exactly. So we used to split them into two, axon, fel, rigors, and homily. And so the now people just put it together because it's kind of the same thing. So the next thing in the stepladder you still have posterior embryo toxin, but then you start to get these little fibers growing from the decimally membrane all the way across the angle. You start getting thinning of the iris. Now, there is actually a rigors syndrome, if you will. And so these kids are just funny kids that got weird teeth and skeletal anomalies and other funny things with them. And so, but in the eye, axon fel used to be just the things across the angle and then rigors was when you started to get the iris at you. But now they've lumped that together to axon fel rigors anomaly. Now, this is a little bit different. Sean, what is this one? What do we call this one? This is Peter's Anomaly. So Peter's Anomaly is characterized by a central dense opaqueness in the cornea. And they still have the other things with it. But in addition to that, you start to get this. And what Peter's Anomaly is characterized by is you get, for some reason, the posterior cornea just doesn't form well in the center. So you don't get endothelial cells. You don't get this membrane. So you get this dense scarring in the center.  You've still got this, you know, synechia there. And so what I like, and what these people also have is they'll have a funny anterior polar cataract. And so I like to think of it. It's like the lens went up and took a bite out of the central cornea and pulled it down with it. So there's this little opacity in the lens and then there's this bite in the center of the cornea. And you see Destiny's Membrane, she's gone in Peter's Anomaly and endothelium in the center. So you get this opaqueness in the center and that's called an internal ulcer of von Hippel. And so if you notice a theme here, virtually all iterms were described by Austrians and Germans in the late 1800s. And so von Hippel as in von Hippel Lindau syndrome. And so it's an internal ulcer of von Hippel and that's a characteristic finding in Peter's Anomaly. So again, if you're trying to learn these and memorize these and know them for boards, I find the step letter classification a good way to do that. And everybody's brain works differently. My brain is, I'm not a lump or I'm a splitter.  Every entity has a little box in there and that's how I keep track of them. So if you think of this, the whole broad umbrella is Antioch chamber cleavage syndrome but you remember the little boxes of the posterior embryotoxin, atcifal rigors, Peter's, then it helps you understand what's going on with these. Okay, and there's the gardens behind Versailles. This is a huge garden. I mean, it could take half a day to walk through these and there's ponds and beautiful flowers and all, but they had a horrible storm in Paris a couple years ago and it took out 10,000 trees in the area around Versailles from the winds. Hurricane winds took them out, so amazing what weather can do. So this is Versailles. So next week, layers. Okay, questions on glaucoma, angle pathology of glaucoma. All right, great.


T.E.F.L. San Diego, California The course in San Diego takes place in a real English language school, giving candidates the perfect opportunity to hone their skills with real ESL students. The school's five classrooms are equipped with everything that you will need while completing the course and students will have use of photocopiers, a resource library and Wi-Fi internet, which is available throughout the building. The school also provides tea and coffee to students and there is a small shop where snacks can be purchased. The training center is situated near the downtown area and is well-placed for access to the city's many attractions including the museums, gardens and zoo inside the famous Balboa Park. The San Diego trolley system, considered an attraction in itself and main line train services mean that travel within the city and to the outskirts is never a problem. The San Diego course usually runs during the first week of each month from Wednesday to Sunday and is time to fit around your other commitments. Classes run from 5.30pm to 10.30pm on Wednesday to Friday while Saturday and Sunday classes are 9am to 6pm. There is an average of 10 to 12 students on each course so you will have plenty of individual access to our team of professional teacher trainers who are on hand to guide you through the course.


I have a briefing on the status of nuclear power plant decommissioning. The safe and effective regulation of decommissioning nuclear power plants is an important, and I think timely, topic for us here at the NRC, seeing how over the past few years we've had a number of plants announce decommissioning. There are different issues that surround the closure of nuclear reactor plants. These include several license amendment actions to reflect changes in the plant, exemptions needed to multiple emergency planning and security requirements, or requested anyway, a focus on decommissioning and spent fuel management funds, an increased interest in the involvement of communities and states surrounding nuclear power plants that are decommissioning. Many of the regulations that we have in place at the moment are actually designed for operating reactors and don't consider the different nature of the reactor once it goes into permanent shutdown and defueling. So efforts to address these challenges were initiated actually by the commission previously, about 14 years ago, but were delayed due to higher priority work. So today I'm very interested to hear from all our panelists and both the panels that we'll see their views on this topic. So the first panel is an external panel which includes Kathleen Fox, who's Deputy Assistant Administrator for the National Preparedness at the Federal Emergency Management Agency, Chris Recchia, Commissioner who is from the Department of Public Service from the State of Vermont, Ralph Anderson, who's the Senior Director for Radiation Safety and Environmental Protection at the Nuclear Energy Institute, Dan Stoddard, who's the Senior Vice President for Nuclear Operations for Dominion Power, Wayne Norton, who is the President and Chief Executive Officer of Yankee Row in Connecticut Yankee, and the Chief Nuclear Officer of Maine Yankee and the Chair of the Decommissioning Plant Coalition, and David Victor, who's the Chairman of the Santa Nofre Community Engagement Panel. After the first panel, we're going to have a short break, and then we'll have a second panel which will be the NRC staff. And I will turn things over to Mark Satorius, our Executive Director of Operations. Good morning Chairman and good morning Commissioners. I know I don't have to swing my head so far for the Commissioners that we have here today. I need that exercise, thank you Commissioner. The staff is here today to brief you on the status of the Power Reactor Decommissioning Processes at the NRC, with a special focus on the four plants that, within the last year or so, have opted to cease operations and move into the decommissioning phase. Next slide please. The decommissioning program at the NRC has a long and successful history. After the 1997 issuance of the Licensed Termination Rule and associated reactor decommissioning regulations, the staff invested a significant amount of time in the late 1990s and the early 2000s, developing improved guidance for implementing the new regulations. The staff's investment produced a more efficient and effective process for both licensees and the NRC, and resulted in significant increase in the number of license terminations and active decommissioning work as shown by this slide. Decommissioning activities involve several NRC offices. The level of involvement depends on the stage of decommissioning and decisions made by the licensees regarding the immediate dismantlement or the entrance into a safe store mode where major decommissioning activities are delayed for some period of time. The decommissioning process will be more fully described later during this meeting by my colleagues here at the table. But efficient interactions among the multiple players during all phases of decommissioning is important to continued success of the program. Slide three. These efficient interactions have never been more important than now.  To address this, the staff has taken several actions to deal with the current as well as the future potential for additional shutdowns. These actions include consolidating the project management responsibilities for all reactors transitioning to decommission into one branch in the Office of Nuclear Reactor Regulation before being transferred to the Office of Federal and State Materials Environmental Management Programs or FSME. Forming an inter-office decommissioning transition working group to identify and prioritize current and future challenges as well as to improve communications across offices and act as a focal point for decommissioning improvements. Third, developing interim staff guidance in tandem with ongoing licensing reviews for security and emergency preparedness issues. And finally, identifying potential regulatory improvements and past lessons learned that could be implemented in future rulemaking activity or through enhanced guidance documents. This continuing level of effort by the staff should ensure that the four prematurely shutdown units currently transitioning into decommissioning will do so successfully building on the experience of the past using the tools currently available to make the process as straightforward and efficient as possible. Thank you and I look forward to the remainder of the meeting as well as from your questions. I now turn it over to Andrew Prasinko to my far right from the Office of FSME. We will further discuss decommissioning processes and improvements implemented as a result of earlier experience with power reactor decommissioning. Drew? Thank you, Mark. May I have my first slide, please? Okay. Thank you. Good morning, Chairman. Good morning, commissioners. As Mark said, I'm going to be discussing this morning the decommissioning process, some process improvements as a result of earlier reactor decommissionings. And also I will be discussing FSME's role during the transition from an operating reactor to a decommissioning reactor. Next slide. This slide shows the decommissioning process including opportunities for public involvement which is defined in 10 CFR Part 50 and it's further described in several decommissioning procedures. The major steps include the licensee submits two certifications. One certification is a cessation of operations and that has to be done within 30 days of permanent shutdown and a certification that the fuel has been permanently removed from the reactor vessel when that activity is completed. A decommissioning report follows, more formally known as the post shutdown decommissioning activities report, and here's where I'm going to use an acronym, P-S-D-A-R, is required to be submitted within two years following permanent shutdown. As required by regulation, we will have a public meeting near the site normally within 60 days of receipt and the purpose is to discuss the licensee's overall plan for decommissioning. The licensee can commence major decommissioning activities after 90 days after submitting the P-S-D-A-R and the decommissioning must be completed within 60 years. In at least two years before the planned termination of the licensee, the licensee must submit a license termination plan. We will then hold a public meeting, again as required by regulations, and to offer an opportunity for hearing. At the completion of the decontamination, the licensee will conduct final radiological surveys to verify that the facility meets regulatory requirements for release and R-C will perform independent verification surveys to confirm the licensee's results. Finally, we will terminate the license at the completion of the decommissioning process. Staff's levels of effort during the process are influenced by the licensee's decommissioning approach with increased licensing and inspection activities occurring during transition and active decommissioning, as well as when spent fuel is being transferred to dry-cast storage. As already mentioned, the decommissioning process involves several NRC offices and the interactions among the offices is governed by office procedures which dictate the roles of the various offices throughout transition and through the decommissioning process. The decommissioning process also offers opportunities for public involvement and stakeholder interaction. In addition to the required public meetings related to the submittal of the PSDAR and the license termination plan, staff has participated in additional public interactions related to Kiwani, Crystal River, and Songs 2 and 3, which will be discussed a little later. Next slide. The decommissioning process has been used successfully to decommission seven power reactors since the implementation of the license termination rule in 1997 and 10 reactors overall. The decommissioning activities at these facilities included decontamination and dismantlement of radiologically contaminated components or structures and remediation of the surrounding site to levels acceptable to NRC. In some cases where required, licensees also met more restrictive state requirements. All of the facilities were released for unrestricted use according to the license termination rule. In many cases, though not required by NRC, the licensees also removed structures and equipment at the facility. Next slide. As of today, staff is managing 17 permanently shut down power reactor units that are in various stages of decommissioning. Specifically, progress is being made at three reactor units that are actively being decommissioned. These units are Zion 1 and 2 and Humboldt Bay. Ten reactor units are in safe store, not counting the four units that recently shut down. And the four units that recently shut down in 2013 that are transitioning to decommissioning are doing so in a physical configuration as well as through licensing. Crystal River and Kiwani plan to enter safe store according to their PSDARs. While Songs 2 and 3 is not expected to submit their PSDAR until later this summer, so their strategy is still being developed. Vermont Yankee has announced its intention to shut down by the end of 2014, and Oyster Creek has indicated that it will shut down in 2019. In addition to these 17 units, additional permanent shutdowns could be expected over the next five years based on publicly available information, which the staff will then manage as needed. Thanks to the long history of the decommissioning program, staff has implemented several improvements based on experiences during previous decommissioning activities, including several ongoing guidance document updates and implementation of a new rule focused on decommissioning planning during operation. Some highlights of the other lessons learned include operators should work with the stakeholders to establish expectations for the end state use of the site, maintain communications throughout the decommissioning process, keep records of any spills or other contamination during operation, which will improve site characterization upon decommissioning, upon cessation of operations, and include flexibility in the decommissioning plans to allow for changes. These lessons learned have been incorporated into several guidance documents and will be continued to be integrated across the decommissioning process. For the four transitioning sites, previous industry lessons learned were leveraged into the creation of some type of community outreach program to engage locally affected parties throughout the process. The activities range from the formal, as you've heard, the formal community engagement panel at SONGS to the more informal decommissioning open houses hosted by Crystal River. The interactions seek to keep the public engaged and informed throughout the process. Next slide. Until the project management function transfers from NRR to FSME, FSME's main role has been to support communication among the various stakeholders during the decommissioning transition process. As mentioned on the previous slide, today NRC has sponsored several public meetings, including the end of cycle and annual assessment public meetings at Kiwani and Vermont Yankee, PSDAR meetings at Crystal River and Kiwani, and a public meeting at SONGS to discuss the decommissioning process. In addition, during the last year, the staff has supported numerous congressional staff briefings at centered hearings and has met with state and local government officials, as well as with non-governmental organizations to discuss decommissioning issues. Our intent is to make sure that all parties have a clear understanding of the process, are given an opportunity to have their opinions and their heard and their questions answered, and to ensure that a path forward is well established for successful completion of the decommissioning. We feel that the goal is achievable thanks to a decommissioning process that is well-defined and has been successfully used in the past, the dedication of the NRC offices involved in the transition efforts, and the ongoing efforts to engage and interface with the public and other stakeholders throughout the decommissioning.


Hi folks just a little update video here. I didn't intend to go a whole week without posting a new video I should have posted my next book review already. That'll be coming up in a couple of days But right now I want to invite you to take a look at the stuff that I've been doing over at 50th Street First of all, it's my visit to a wizard world in Richmond back in the September I made one of my little convention montage videos. You should especially look for these cosplayers. There's Tina Belcher thinking about butts and This Star Trek Gilligan mash-up group take particular note of the phasers made of bamboo and Then there's the Mario Tennis Doubles team On that same trip I made an interview with Bob Camp. He's one of the co-creators of Ren and Stimpy There's a link to that video here This picture is his opinion of Pokemon Go and then there's the new regular show on The 50th Street channel called the Oh Look show which I started last month with my Cosplaying host Beth Love. We attended the Megacon in Tampa Bay and One of the things we saw which people aren't viewing and I think you should it's these handmade dragon eggs from a local Artist who calls herself the ungeneral store They are just as amazing in person as they are in these pictures and they look fantastic in these pictures So go look at that video This past weekend Beth and I attended the Repticon a Reptile and exotic pet show in Orlando and that video will be coming up soon that same evening. I alone Visited this Halloween show called the what's it called silly kingdom? No spooky Empire I Just posted that video yesterday. There's a lot of neat stuff there including this really impressive Gomez and Morticia couple the Oh look show Publishes a new episode every Tuesday and Friday and you can see them by subscribing to the 50th Street channel The other thing I have coming up and I've had three people ask me about this is My visit to the Chamberlain bookmine or the infinite bookstore that I've published some teasers about I'm going to publish episode one of that adventure tomorrow I should have published it today, but it turned out to be a longer edit than I was expecting They're gonna be three episodes and you'll see the big walkthrough on episode three. That'll be We'll see there's an old look show on Friday, so it'll be Saturday or Sunday. Maybe Monday depends on how long it takes me to edit them Anyway, it's coming up soon So visit the 50th Street channel and subscribe to it once I get a hundred subscribers at 50th Street I'll be able to pick a custom URL for the channel and I won't have to send people that long nonsense link and coming up here on my channel is a new book review and Some more cheap stuff to look at and a few other things. So see you then


Today, we shall discuss chemical vapour deposition of carbon nitride coating significance of carbon nitride coating. Now, we know that TIC that means, this titanium carbide coating that is known for its extraordinary hardness and which means, enhancements of abrasion wear resistance. And on the other side, we have also titanium nitride which is better known for its anti welding property and also anti hydration property. So, when titanium carbide is used then the domain of application is well defined that means, where the functional surface is subjected to abrasive wear then we put TIC coating. However, when the application demands a coating which should be capable of combating the wear at a higher temperature in that case the wear resistance is not just abrasion, but there could be also welding or adhesion adhesive wear that also come in picture. And in that situation titanium nitride or the nitride of any particular transition element is it appears to be much more effective and durable than that of carbide coating. Now, if we consider the transitional element we can quickly have a look these are from group 4 B. Now, 5 B is tantalum, niobium and vanadium 5 B this is 6 B chromium, molybdenum and tungsten. Now, if we pay our attention on this here we have titanium, zirconium and hafnium and they are carbide. So, the chemical stability of carbide that goes in this order that means, hafnium carbide is more chemically stable than zirconium carbide and zirconium carbide is will be more chemically stable than that of T i carbide titanium carbide. Similarly, we can also have hafnium nitride, zirconium nitride or titanium nitride. If we now choose titanium as one of the strategic material in that case we have T i c and T i n having their well defined domain of application, but there are situation where we may need a balance of property between titanium carbide and titanium nitride that means, the functional surface need both resistance to abrasion and resistance to adhesion that means, more of chemical stability and the welding property and in that case a balance between T i c and T i n is found out to be quite effective and that is why for application carbon and nitrogen are brought together to make a coating a composite coating or a multiphase coating which is known as titanium carbon nitride. And this titanium carbon nitride one of the major application is in the area of manufacturing that means, the tool for manufacturing where one can use titanium nitride carbon nitride coating it is an intermediate between titanium carbide and titanium nitride giving a balanced property of abrasion wear resistance and also anti welding or adhesion wear resistance. In addition to that it can be also noted that if we like to have a top layer of T i n and it is to be done on a tungsten carbide being one of the most strategic material for cutting tool and all wear part in that case the high temperature CVD does not allow direct deposition of titanium nitride. So, in that case that first layer just in contact with the substrate is titanium carbide and the top layer is titanium nitride, but in between to graduate the property slowly from the interface to the top surface titanium carbon nitride is also used just like a bridging layer or a buffer layer. So, this is T i c n coating because titanium carbide is well known since the cutting tool came into being and also titanium nitride it is known for its chemical stability. So, it is titanium carbon nitride coating which can have also well strategic application and some of those strategic areas carbon nitride coating can be found out to be one of the very best candidate. Now, characteristics of T i c n coating that is already known to us that means, this titanium carbon nitride is more chemically stable than that of titanium nitride while resistance to abrasion will be better than that of titanium nitride. So, this is something in between two extremities that means, titanium carbide and titanium nitride. Now, this concept of putting carbon and nitrogen together that can be extended to also incorporating oxygen and here we get titanium oxycarbonitride the whole idea behind this combination is that T i o if we put T i n and T i c in terms of chemical is chemical stability this is the order in terms of hardness this is the order that means, when it is a temperature sensitive where involving the chemical stability of the material then it is of course, T i o which can have a very overriding influence. However, if we consider alone the abrasion where resistance in that case T i c would be the best candidate. So, titanium nitride we find somewhere in between. So, chemical stability of T i o that is the highest T i n is in between and T i c at the lowest n and when it is the hardness it is T i c best then T i n and T i o is that is the last choice. If the situation demands that we must have some blending of all sort of requirement that means, hardness what does it mean abrasion resistance anti welding property and chemical stability because of the wear which is actually temperature sensitive like chemical reaction or diffusion wear in that case we find that T i o would be the better candidate than T i n or T i c. Now, following the same logic which was behind this coupling of carbon and nitrogen one can keep on mixing also oxygen with carbon and nitrogen giving a new phase which is called titanium oxycarbon nitride and it has been found to be one of the effective coating particularly in those situation where temperature can be quite high promoting or inviting diffusion wear or chemical reaction type wear and in that case it has been found that T i o is playing a decisive role in combating the wear. However, it has to be also understood in clear terms that alone chemical stability cannot serve the purpose or serve the requirement of the cutting tool it is also abrasion wear resistance or hardness that is also desired in the cutting tool. So, we can keep both the extremities together in right proportion and we have titanium nitride in between and putting this oxygen, carbon and nitrogen in right proportion we can get a titanium oxycarbon nitride. Now, CVD reaction for titanium carbonitride. Now, CVD reaction for titanium carbonitride in that case we have to take if we consider the conventional CVD conventional CVD means high temperature CVD this high temperature means around 1000. So, here what are the basic reaction which can be illustrated by this equation T i C l 4 C h 4 here we have temperature pressure and excess H 2 as carrier gas and also to prevent reversal of the reaction. So, that gives us T i C plus H C l it has to be properly balanced and also we can have in simultaneous reaction N 2 and H 2 that can also give with pressure temperature and with hydrogen also here we can get T i N plus H C l. So, these are the governing equation now if we put them together we are going to get this T i C N in right proportion. Now, the problem with this is the requirement of high temperature. Now, we can have a look quick look in this diagram the Ealingham diagram. Ealingham diagram means we have on one side delta G 0 T this is plus this is minus and that is the temperature. Now, this Ealingham diagram will give us a clear guidance how the temperature can be determined or what will be the threshold temperature for to carry forward the reaction in the from the reaction reactant to the product. So, it should be a product favored reaction. So, in that case we can find two lines may be something like that this is just illustration this one may be T i C l 4 plus C h 4 which gives us T i C plus H C l with proper of course, with proper balancing and this one that will be for T i C l 4 N 2 H 2 that gives us T i N and H C l. Now, here what is important this delta G 0 T or delta G T because we have a pressure which mean not to be standard atmospheric pressure. So, this is T and P and here also T and P. So, what is important what we understand from these two diagram that we have to really target these two points. So, this is for T i C and this is for T i N. Now, these are the two points from our experience we know that if we like to conduct the classical CVD of T i C and T i N this temperature is around 1000 degree and this is around 900 degree centigrade. Now, this 900 and 1000 that is exactly what we understand as limitation of high temperature CVD straight forward H s s tool steel die steel or any structural material steel cannot be a good candidate as a substrate for this CVD because it will be metallurgically damaged it will be annealed there can be grain coarsening. So, lot of post CVD processing has to be taken and this is a really a challenging task. On the other hand if it is on carbide tungsten carbide this tungsten carbide being a very good candidate which can support this temperature it is free of any problem. So, one can look into the limitation of this CVD in that this temperature does not allow this substrate to be used for receiving this coating though there is tremendous demand for this carbon nitrite coating titanium carbon nitrite coating which is a blend of T i C and T i N. So, that is why what we need to do we need to shift this point on this side what we can see from this diagram further that this reaction is also not spontaneous that means, we have to raise this temperature and so that the whole delta G 0 T corresponding to a temperature that can be well below this side. So, that the reaction can proceed spontaneously in this in the direction of the product and exactly for this reason we find that there are certain materials which are actually the source of carbon and nitrogen which can allow us to go down with the temperature that means, we can bring down the temperature lowering the temperature this titanium carbon nitride that can be conducted in the zone which is of immediate interest that means, the zone say 500 to 600 even if it is lower than this that will be also most welcome, but considering the limitation of this chemical reaction one can fix a target of a range of 500 degree to 600 degree not above that and if we can conduct this CVD of titanium carbon nitride by following another path then that would be something quite advantageous and say CVD can have a widespread application. Now, what is this moderate temperature CVD the key factor behind this moderate temperature CVD is the source material for carbon and nitrogen these are actually organic materials materials for C and N that means, this acetonitrile number 1 CH 3 C N number 2 trimethyl amine this is CH 3 trimethyl amine then we have the third one dimethyl hydrazine this is dimethyl hydrazine and then hydrogen cyanide. So, some serious investigation has been carried out to look for certain source materials for carbon and nitrogen which can be a effective donor of carbon and nitrogen and at the same time titanium will be supplied by the conventional source that means, titanium tetrachloride and putting them together perhaps we can see that the reaction can be conducted in a temperature lower than that which is required to have T i C and T i N by the conventional CVD. So, if we follow the reaction then acetonitrile that means, CH 3 C N plus what we have T i C L 4 plus H 2 that gives us T i C plus T i N CH 4 and H C L this is one mode of the reaction which can be carried in the forward direction and we get simultaneously T i C and T i N and with some byproduct of CH 4 and H C L. So, this is acetonitrile we can also look for the possibility of using trimethyl amine. So, in this case we can also write and we have to put T i C L 4 with hydrogen and that gives us T i C T i N, but it has been found out and proved that it is it leads to production of methyl chloride and also H C L. Then we have dimethyl hydrazine and this is exactly NH 2 which can straight way participate in this chemical reaction plus H 2 and in this case we have T i C plus T i N plus H C L and the last one which can be also a good candidate for this chemical reaction. So, this gives us straight forward T i C plus T i N and H C L. So, we can see that at least there are four chemical roots which can lead to formation of T i C T i N and exact requirement will be served by this Ealingham diagram that means, if we see here this one. So, this is temperature delta G 0 T at that means, at the standard state plus and minus. Now, here we can put this one say for normal change of free energy for reaction leading to T i C. Then we have another one which is also delta G 0 T for the reaction T i N. Just now we have concluded and here we have around 1000 that is the threshold and this is around 900. Now, if we put them together we can find out that this is shifted quite remarkably on this direction and exact line that will depend upon the delta G 0 T and that will be that will depend on respective enthalpy of formation and entropy of formation and that will be guided by the governing equation say what we can write here governing equation means this delta G 0 T that is actually delta H 0 minus T into delta S. Now, here this should be the actually summation of delta H product minus delta H reactant minus T this sigma S product minus sigma S reactant. So, one has to really using these two here these terms for product taken all the product putting it here taken all the reactants and putting in this second place of this parenthesis and then respective value of entropy of the reactant and product one should be able to find out that what is the threshold temperature because at the threshold temperature means this is the point. So, this is the point and for this if we put it to 0 then from this thermodynamic property T can be found out. However, if the reaction is conducted at a pressure other than standard atmospheric pressure then we can write further to this. So, this is actually at the particular pressure in question where the CVD is conducted is equal to delta G 0 T plus RT into ln k where k is the equilibrium constant. So, this has to be taken care of considering the coefficient stoichiometric coefficients and respective thermodynamic property and with that we can find out what is the temperature and as per the documentation it is confirmed it is reported that around 500 to 600 all these reactions which are explained here by this four equation that can take place within this temperature of 500 to 600 and which will be not only of academic interest, but will be of theoretical or industrial importance. So, this way we can see that this use of organic source material which are supplier of carbon and nitrogen instead of conventionally chosen methane or acetylene for carbon and molecular nitrogen or methane for nitrogen instead of that if we use acetonitrile, trimethylamine, dimethylhydrazine or hydrogen cyanide there is ample opportunity of conducting the same CVD and this can be done well within 500 to 600 degree centigrade which will be of immediate interest in that it will be an useful technology process for depositing this material in the wide range of steel family starting from HSS, die steel, toll steel and many other light alloy steel. So, CVD reaction with organic CN compound that has been narrated and here we find out the role of this delta G of the reactant which is an organic compound of carbon and nitrogen and its value is so strategic and each can have a real overriding influence in bringing down the temperature required for this CVD reaction. Now, factor influencing the growth rate of TICN coating. Now, naturally one would be interested to know what are those factors because there are certain operational parameter once the CVD is established we have to control those operational parameters and those parameter can be summarized as follows. Number one immediate of immediate attention is temperature then comes the process pressure and finally, it is TICL 4 to hydrogen ratio. Now, we understand that temperature the role of temperature can be well understood because the graph of delta G variation with temperature we understand that this reaction is not spontaneous and we have to really cross this threshold value to have a substantial negative difference so that the reaction can proceed in the forward direction and it becomes really a product favored reaction. However, it is interesting to know from the research result that particularly this is true for trimethyl amine and this dimethyl hydro hydrazine if we go beyond certain temperature of course, here the one interesting point is to keep the temperature as low as possible, but if somebody is interested in higher growth rate and to use this process for certain substrate which can allow little rise of the temperature little rise of the temperature then he can elevate this temperature and the reaction can go at a faster rate. So, that provision is already there. However, if we cross that limit what can happen that in that case instead of heterogeneous reaction we may end up with homogeneous reaction. One precondition of severity is that for all this coating process is that coating should be synthesized on this substrate. However, may be the reaction the reaction should take place on the substrate surface on the substrate surface and the product should also synthesized its nucleation growth and lateral growth vertical growth everything should takes place on this solid surface and it should not be a homogeneous reaction, but as we have mentioned that if we go to that temperature that may be counter productive in that reaction may not no longer be heterogeneous, but it becomes homogeneous and then the whole purpose of CVD is lost because in that case in the gas phase reaction takes place and we get dust powder flex of titanium carbon nitride instead of a coating a uniform well adherent well coherent coating on the substrate surface. So, the temperature rise should be also considered with that particular care then comes the pressure. Now, definitely pressure has a role now with increase of pressure it has been found that the growth rate increases with pressure. Now, this can be some thing like this, this is a typical nature it is typical nature of any synthesis process. Now, this is actually a point which gives the maximum yield and on this side if we have a low pressure high stream velocity on this side and this is pressure and that is the growth rate. Growth rate of the coating it can be milligram per hour or it can be micron per hour increase of mass or increase of the thickness. However, if we go beyond that point what is going to happen because of this high pressure then mean free path will be shorter and that will invite collision and reaction in the gas phase. So, in that case not only the growth rate will fall that means, there will be no reaction on the surface, but reaction will take place in the space above the substrate surface and the coating growth rate will fall. Then comes this TICL4 H2 ratio this is already known that if we like to increase supply of titanium by increasing titanium tetrachloride mass flow then proportionally H2 has to be also increased if it is not done then we may have excess of HCl and this HCl may revert the reaction and then the reaction instead of being product favored it becomes reaction favored. So, there also we have to pay attention that how to increase that TICL4 with the increase of H2 if we like to have enhancement of the growth rate of this coating. Now, coating composition one thing will be very important and interesting here is that TICN, now more generally we can express this as TICNY. Now, for all practical purpose it is also the experience that if we have like 0.5 and 0.5 it is some kind of a equal blending of carbon and nitrogen in that lattice side with titanium. However, this percentage of this 1 is to 1 of carbon to nitrogen that also depends upon the basic composition of the carbon nitrogen source. That means, those organic materials which are used for deposition of this carbon nitrite coating there we have to look in what is basic composition of carbon and nitrogen and that basic ratio of carbon and nitrogen which is present in the source material that will also influence the final outcome here in the value of X and Y. So, this point can be taken into consideration in selection of the source material apart from the fundamental consideration or most important consideration is the temperature threshold temperature where we can initiate the reaction and that temperature is obviously, of immediate interest considering the temperature sensitiveness of various substrate. Another thing is also in our observation that if the temperature is raised little bit in the in the CVD process then the percentage of this X, X goes up in comparison to percentage of Y that means, that high temperature promotes formation of TIC more carbon and in proportion to nitrogen and as a result we have a titanium carbon nitride where it will be more than 50 and that will be less than 50 and this is also another experience that with slight increase of temperature of deposition hardness of the coating also increases and this can be explained by the concentration of higher concentration of carbon on this in this coating because titanium carbide is basically harder than that of titanium nitride. Now, pressure can also have some influence, but with rise of pressure what is the experience that coating becomes porous less adherent and in that the influence of pressure should be also considered if one has to make a good quality on the coating in terms of high density good adhesion and adequate hardness of the coating. Now, this is very important aspect of this coating that means, the performance of the coating the performance of the coating depends upon number one wear resistance of the coating. Now, here one issue can be raised that what is the thickness of the coating? Thickness of the coating this is very important issue because of the simple reason in conventional CVD using the temperature in the range of 900 to 1000 our experience is that hardly we can keep the coating more than 5 micron hardly it goes to 6 to 10 micron. The reason is as follows that coating is conducted deposition is conducted at a very high temperature and when it is brought down from high temperature to the room temperature because of this delta T high value of delta T residual stress generated at the interface is quite high and there is every chance of separation of the coating from the substrate and failure of the interface it is not the cohesion not the density of the coating, but it is just the separation at the interface because of this high stress build up and that is why we have to keep it within that range, but here the situation is little different because of the simple reason that this deposition now can be conducted in the range of 500 to 600 degree centigrade. So, this gives us a clear edge or a leverage of increasing the coating thickness by our common sense we understand if we have a thicker layer obviously, life of the coating will be longer and if it is a thin coating life of the coating will be also shorter. So, thicker coating means high performance coating provided it can be retained with adequate adhesion with the substrate and there this high temperature is the greatest obstacle, but for this moderate temperature coating that obstacle is clearly removed. So, one can very reasonably make an attempt to look how this thickness of the coating and the life of the coating they are correlated. Now, performance of the coating clearly means here that this coating of TICN it has to compete with the conventional coating that means, conventional TIC coating or conventional aluminium oxide plus TIC coating. Now, this coating can be put in from a coating thickness of 2 micron to as high as 50 micron without any difficulty at least after the deposition there was no such visible mark of failure at the interface from the visual inspection. So, the coating has been deposited in steps of 2 micron from 2 to 50 micron. Now, conventional TIC coating which we normally deposit at 1000 degree that is 4 to 5 micron and this TICN has been deposited using acetonitrile as the source of carbon and nitrogen. Now, when it is aluminium oxide and TIC that is a multi-layer coating we have here 1 to 2 micron and here also 4 to 5 micron. Now, if we now display the tool life versus thickness of the coating some interesting observation can be made. Now, this is the case of continuous turning this is continuous turning in a lathe it is a ductile material and industrial speeds feed depth of cut that has been chosen and here if we put tool life that is in minute and here the coating 3 coating that means, one is this TICN with different thickness and then we have TIC and this multi-layer coating. So, the plot is something like that let us try to illustrate if this is a 50 minute tool life we can have a thickness of this this is about 24 micron. What does it mean a coating of TICN which is a product of this moderate temperature severity and if it has a thickness of 24 micron then it can give a life of 50 minutes in continuous turning. Now, if we have a coating of 2 micron just 2 micron this life will be very low if it is even less than 10 minutes. So, these are the two thing what is quite interesting. So, it is even just 10 minute, but if we have a coating thickness of 50 micron then of course, the coating reveals its weakness here the life is just it is 50 minute it is 15 minute. So, this is about 5 minute 2 micron 24 micron give 50 minute and 15 micron give 15 minute. So, we also find here that even in this coating which is deposited in the range of 600 degree centigrade they are also if we increase the thickness of the coating then also we have this premature wear on the coating first wear on the coating delamination of the coating and it is not just gradual natural wear of the coating, but it should be flaking delamination and premature separation of the coating from this surface. That means, with the thickness of the coating the stress at the coating substrate interface has gone up and that was responsible for early separation of the coating from the substrate and that leads to shorter life of the tool. But when we put 4 to 5 micron coating of TIC then its life is just 10 micron 4 to 5 micron TIC and in that case it is just 10 minute. However if we put this multi layer coating of aluminium oxide that means, this is Al 2 O 3 plus a bottom layer this is top layer that is the buffer layer in contact with the substrate this is 1 to 2 micron and this is 4 to 5 micron this is high temperature. So, this is actually the low temperature coating. So, this is actually the low temperature coating this is moderate temperature at 600 degree centigrade, this is at 1000 degree centigrade this is also at 1000 degree centigrade. So, what we find this is around 45 minute. So, what is interesting thing that a coating of 1 to 2 micron aluminium oxide with a buffer of TIC 4 to 5 micron it can give a service life of very close to 45 minutes. Whereas, a coating of TICN which is less where resistant than aluminium oxide which can give offer a service life of 50 minute and this is possible because of the larger thickness of the coating and this larger thickness of the coating means larger thickness of the coating means actually here it offers wear resistance over a large thickness and as a result the duration of the coating it lasted to 50 minutes. Now, when it is interrupted cutting why we can see another interesting picture it is an interrupted cutting that means, it is just like a cross shaped job which is allowed to rotate and it gives an impact on the surface of the tool and in this case what we find that this a 4 micron thick TICN coating and then we have 4 to 5 micron TIC coating and then 1 to 2 micron AL 2 O 3 plus 4 to 5 micron TIC and if we see their performance number of heats it receives here it can go up to straight forward 60,000. This can go up to 40,000 these are some indicative figure and this is just 10000 that means, what happens this is a test of toughness of the coating. Now, you can find out that since it is aluminium oxide naturally toughness will be less than that of TIC and that is why we find that this can receive 40000 impacts and then only it shows the fracture or a chipping whereas, this 4 micron of equal thickness which can go straight to 4 micron and in this case it can receives shock up to 60,000 times 60,000 impacts it can receive before it shows some sign of a chipping. So, from this it is also evident that this coating which is a low temperature coating deposited at 600 degree centigrade this is 1000 and this is 1000 and which are comparable in terms of thickness, but this has a clear edge over this high temperature coating and it shows its strength in machining situation in machining environment where the material has some non-symmetry in its geometry and while rotating it can give some kind of interruption in cut and the coating with the cutting edge can survive more number of impacts compared to the conventional high temperature coating. Another figure performance figure can be also shown here and this is simply this is simply it is a it is in the milling where we have 6000 it is a fly milling with 1 milling insert we can also conduct this test and here when it is 2 micron thickness it can go to 18000 impact, but when it is 4 micron it will receive only 6000 impact and when it is 24 micron thick it can receive only 1000 impact, but when it is an aluminium titanium carbide coating this is 4 micron and this is TIC that is also 4000 impact and when it is aluminium oxide it is actually 2500 impact. So, this is high temperature coating and this is a low temperature coating of equivalent thickness, but when this inserts are used in milling action with a fly milling mode then also this low temperature coating shows its strength and this is at 4 micron, but when it is 2 micron it is 18000, but when it is 24 micron it is very low to 1000. So, from this performance test also we can see that the strength or durability or capability of this coating is much better than the conventional coating and it is going to be one of the best candidate for all sort of machining application whether it is continuous cut or interrupted cut or in also milling operation. So, we can summarize this discussion in that it is possible to deposit titanium carbon nitride coating at moderate temperature of 500 to 600 using organic compound as the source of carbon and nitrogen. The ratio of carbon to nitrogen in the coating is found to be proportional to C N ratio in the source material. Relatively thick coating of titanium carbon nitride can outperform aluminium oxide coating in continuous turning. The set coating is also a better candidate in interrupted cutting.