Good to see all of you again. We are back with corporate governance and in our previous sessions we basically were talking about the globalized contextualization of corporate governance, its different contextualization from a national context also and the different schools of thought which basically exist around the historical aspect of corporate governance. Today, ladies and gentlemen, we are going to talk about the theories of corporate governance. Now, when we talk about the theories of corporate governance then naturally we are opening up a Pandora's box. In the coming sessions, we'll be looking at the different theories and we'll be understanding how they are similar and how they tend to differ from each other. When we are talking about the different theories then, ladies and gentlemen, we talk about the various variables and the various disciplines which merge together to create that framework of corporate governance. Now, when the subject of corporate governance is based on a strong theoretical foundation then it is derived from several disciplines such as finance, such as economics, such as accounting, such as management, such as law and organizational behavior. This multi-dimensional governance system prevails in different countries. When we see this different multi-disciplinary approach towards corporate governance, it basically is an all-encompassing subject and it has this overlap between these different subjects that we are talking about and disciplines that we are talking about and therefore it makes corporate governance even more interesting. So, sometimes the connotation or the interpretation that maybe corporate governance is confined primarily to finance or corporate governance is confined to law is wrong. Actually, it is an amalgamation of different disciplines and different theories which tend to overlap with each other to create a corporate governance framework which then is stipulated by law and is practiced throughout different organizations. Now, when we are talking about the practice of law, of rules, of regulations in different organizations then definitely the context of social behavior also becomes very important. And when we are talking about organizational behavior then we are looking at why is it that in certain countries or in certain environments the framework can be practiced in a better way while in others that framework faces a lot of problems and also there is an issue of implementation. So, we are going to be looking at these different theories. We are going to see how these different disciplines are interrelated with each other to develop different frameworks which are practiced from different dimensions in different countries. So, that is what we are going to be looking at ladies and gentlemen. But even before that we are going to be looking and following aspects play a significant role with regards to the types of corporate governance. The legal system of the country. Now, this is extremely important. The corporate structure, the shareholding pattern and the cultural and value system, the economic system, political system and governance, path dependency, resource dependency and institutional environment also play a dominant role in corporate governance. So, again ladies and gentlemen, boys and girls, what we are seeing is that when we are talking about corporate governance there are so many perspectives, so many aspects, so many building blocks and these are some of the very important ones. For example, when we talk about Pakistan and because Pakistan is the Islamic Republic of Pakistan, therefore we have a dual legal system. We have the common legal system or the common law system and we have the Islamic law system. And it is absolutely independent of each other. The common law system has its own judicial structure, has its own laws which tend to emanate from the common wealth legal system, from the common law system while when we are talking about the Islamic law system, then that basically emerges from the Quran, the Sunnah and the Hadith and again that is something which is universal. So, both interpretations and both laws are independent of each other, have their own judicial framework and setup and again have their own set of judges and sometimes they can be in contradiction of each other and that is where many problems do arise. But again that depends upon the texture, the fabric of the nation. We also look at the different corporate shareholding. Like in a country like Pakistan, the minority shareholder is not given his or her due place within the corporate system even though it is there in law but by practice the minority shareholder is not properly represented. We also look at the cultural and value systems. That is again very important and because we have a rigid hierarchical system within our families, therefore even in the corporate sector, we have a comparatively rigid structure which exists in the corporate governance mechanism of Pakistan. So, all of these things become extremely important with the resource dependency and the path dependency and again the different political issues which tend to sometimes become very unpredictable. So, within this unpredictability, we see that the corporate governance framework and the corporate governance structure gives more stability and more predictability. Now, when we are talking about theories, then that is also very important to understand that theories are different from rules and regulations. Theory is a supposition or a system of ideas intended to explain something, especially one based on general principles independent of the thing to be explained. So, again, it is not something, theory is not a definition. Theory is not something which is absolutely specific but a theory is a generalized approach of understanding a particular phenomena or particular concept, a particular word or a particular environment or a particular law. So, again, when we are looking at theories, they are not straight-jacketed, they are not permanent, they are not something which are absolute but they have more flexibility and are based upon the different dispositions which have been taking place within a specific set of variables. So, again, in other words, a theory is a set of principles on which the practice of an activity is based or it can be defined as a set of assumptions, propositions or accepted facts that attempts to provide a plausible or rational explanation of cause and effect, the causal relationships among a group of observed phenomena. So, again, dwelling upon the theory in more depth, then these are the different variables and these are the different contexts on which a particular theory is based. And ladies and gentlemen, theories in corporate governance are defined based upon the cause and effect of variables, such as the configuration of the board of directors. That is very important. It would vary from country to country. And therefore, based upon that configuration, we would be able to adjudge or we will be able to determine the level of implementation of corporate governance within a particular organization. And then we can collectively also ascertain the state of corporate governance in a particular country based upon an extensive survey of studying the board of governors, its composition, its texture, its implications and its working also. So, that is a very, very important variable. We talk about the audit committee, which is the strongest committee within the corporate governance framework, the role of top management and the social relations beyond the legal regulatory framework. So, that also tends to determine the fabric or the implementation and the transparency of a particular corporate governance framework in a organization. Effective corporate governance requires applying a combination of existing corporate governance theory. So, again, it is not an isolation. It is overlapped. And what we see is that in real life, it is never one, but a combination of different theories, which tend to enable organizations to become more corporately sociable and also corporately responsible, which enables them to safeguard the interests and the rights of different stakeholders and shareholders and create a balance or develop an equilibrium between the different aspects of corporate governance. And that is very important. So, what we are going to look at are the different theories of corporate governance. And we are going to go in detail in our coming session. So, there is a sociological theory. There is a stewardship theory. There is a transaction cost theory. There is a resource dependency theory. There is an agency theory. And there is a stakeholder theory. So, we have these different theories which exist within the corporate governance framework. And in our coming sessions, we are going to be looking at each one of these and see what their implications are and how they tend to interrelate with each other to create a corporate governance framework. So, thank you again, ladies and gentlemen, and see you in the next session. Good office.


I have parents that call me or message me, you know, behind their kids and say, you know, say that they feel so comfortable having their kids at our place. And that just makes me feel great. Hey guys, thank you for joining me. So I'm starting a new series where I want to interview local businesses, especially during the pandemic, during COVID, who can use our support or help, whether that's showing up and making purchases at their establishment or donating money, whatever we can. So today I have with me, Gio, who are the general manager of GymSports Bar, what's now going to be GymSports Bar and Grill. Okay, great. Tell me what happened and how did we get into the place where you even were going into a new location? Well, we closed the old location when the pandemic started. It was actually four or five months after the pandemic started. Was that by choice or were you in a situation where it was just no longer feasible? I really don't want to talk about that situation at all because there's no, that's the past. And I would like to live in the now and go with that. And the new place, the new place we found is a better place. It's bigger. It's more in the middle of everything. It's now a restaurant and bar. And even though it's going to be the same GymSports Bar, it now has food. And the menu is pretty much set, except we're going to be adding some wraps to it and stuff to make it healthier for the West Hollywood crowd. And you've been pushing to have food for a while now, right? Even before? Yes, we actually wanted to have food before we were thinking about taking over the old coffee bean, but that was becoming too pricey. That was going to be way too expensive to do that. So, I mean, unfortunately, COVID happened and stuff like that. But to me, it's kind of is a blessing in disguise as far as the movement of GymSports Bar in real.   We had menus. We were handing menus to people. You want to order a pizza? You want to order this? There's Chinese food that you can order. And then the whole bar, I mean, it was just, it was just like, yeah, it was something I was like, so you would see, you would see like, especially some of the kids coming in with boxes of pizza from down the street and stuff like that. But now, now you don't have to go anywhere. Now we have food and it's going to be good food. And it'll be healthy, or most of it will be healthy. And the drinks will always be the same. Delicious and strong. People come to the drinks, so the drinks will always be the same. So, so you've started to go fund me, your fundraising, is it 75,000? That's correct. We started that to help us to help build you a new home in the area that we are building. It's just something that we have to make sure that everything goes according to plan. It's a little cushion that we need. And we're very thankful for whatever anybody can give, whether it be $1 or $1,000, whatever, whatever. We're very thankful from the bottom of our hearts. Thank you so much for anything that you can give. It's been going on for about two weeks now, I think. Yeah, two weeks, it's going pretty well. I mean, 75,000 is a good goal. And I'm hoping we can reach it. And so, tell me a little bit about, I mean, you referred to it as a home, the kind of culture and energy and environment that you've created in this place that's very unique in comparison to all the other bars and restaurants in West Hollywood. I love when I call it a home because it is a home for everyone.  It's a home. I love when somebody comes in there for like the first time and you see them and like about 10 minutes of after being there, all of a sudden they let their guard down, they drop, you can see the like release from them because they feel that they're in a comfortable environment. And I love that. I think it's great. And that's what we want to create at the new Gym Sports Bar and Grill. It's a home. And the kids that have been coming to Gym Sports Bar for the last 10 years, they know that this is their new home. And everybody is welcome at this Gym Sports Bar and Grill. I have parents that call me or message me, you know, behind their kids and say, you know, say that they feel so comfortable having their kids at our place. And that just makes me feel great. You know, I love one, I love one that if you're new and you come into our bar and you see me and you want to come up and say, hi, please do, you know, I want you to feel as comfortable as you can. Customer service is my main goal. It's my it's my co-workers main goal to make sure everybody is comfortable at that.  Have you been here before? Do you know this person and that person introducing me? So they definitely have taken on that kind of, you know, family energy as well. Yeah, the people that come there are super, super great people.   I'm very protective. I'm very protective of my of the people that come into the bar, my my customers, as well as my employees co-workers. And it's just it's just a great place to relax, you know, and now it's a great place to relax and have food, which is even better.  And speaking of your co-workers, I know I'm sure it's had an impact on them not being able to work at the establishment for a while. Are you able to to bring a lot of them over to the new location as well? A lot of them are coming back. Yes. Unfortunately, some have moved because they couldn't afford to stay here in LA. So they had to move back home and they're probably more comfortable there. So we have talked to a lot of them about coming back to the bar and grill now the restaurant. And hopefully most of them will be able to come back. We did lose a few employees to COVID, unfortunately, but you know, and they'll always have a place at our place in our hearts at the bar and grill. I mean, it's yeah, it's I it's a great team. And it has become a family within itself with not only just the people that work with but with the customers. And that's what makes it great. What makes you want to come back there. Yeah. Okay, give me a quick little, you know, two, three sentences about what you want to say to people as far as donating and helping support your opening.   We're not we're not blind to that. But whatever you can give, we are very thankful for that. Very thankful. Perfect. Thank you. All right, Geo. Thank you so much for doing this with me. I know you had some technical difficulties. This is take three, but we got it. And I would I think this one was better, but why didn't the second one work? I'm just trying to think why didn't okay, I think I had my husband on there. We were talking about it was it was a user error. Didn't hit the record button. Yeah. Okay, so I definitely want to revisit this and I want and touch base with you and the progress of construction and you guys opening. So we'll definitely do that. And then we'll we'll get Gary in there too. Let's let's plug a show since he's got a new show. Oh, great. Great. His show is called Headliners. It's a virtual show. His next show will be in March, March 15th, I think it is. He's been working. He's been working with amazing talent all over the country.  And the first show was really great. Such great feedback from the first show. Because the people who bought tickets were not disappointed at all. It's called Headliners. Please like the page on Facebook. Follow him. He's Gary Thomas at Gary Thomas and he's on Instagram. Okay, I'll put links. Yeah, I'll put links to everything down below in the description as well as the bill for me and the yes, please Instagram page for for Jim Barr. Okay, great. Yeah. Yeah, the Jim's Worth Bar and Grill Facebook and Instagram pages. We're fixing that up now and making the Jim's Worth Bar and Grill. And then yeah, if you can plug Gary's show as much as possible, that's awesome too. All right, guys. Thank you for watching. Please again, donate help support for this local worthy community home for everyone. Like this video if you liked it, please subscribe if you haven't already and then share this. The more we can get this word out, the more we can get people to hear about it and donate. All right. Thanks guys. Thanks. Thank you very much. Thank you.


Okay, so secondary open-angle glaucoma, and I'm going to start with a little bit again just to review. You guys have been hearing this nonstop, but multi-factorial progressive optic neuropathy with characteristic loss of retinal ganglion cells and atrophy of the optic nerve. And then we usually think about IOP dependent and non-IOP dependent, and IOP is just a risk factor. So characteristic patterns of optic nerve damage, and we went through this last week, and visual field loss. Who couldn't remind everybody what type of visual field loss you get? Arq. What else did I hear? Paracentral scatoma. Paracentral scatoma. That's a classic. Nasal step. What's the top three causes of nasal step? Glaucoma. Glaucoma, glaucoma. Very good. Paracentral island also, you know, keep that in mind when you see these patients. And you can even get, you know, a lot of times too, you can get almost a, basically a hemifield defect as well, but superior arc and inferior arc are also pretty classic. What other things would you want to look at? So they've got identifiable contributing findings of secondary open-angle glaucoma. What does secondary mean? What's the difference between primary and secondary? Nico, you'd like her about to talk. Yep, secondary.  In primary, it's a wide definition of idiopathic, where we can't find anything. We can't find any underlying cause. So, dysfindings, anomalous vessels, remember, keep in mind, you know, the disc can look asymmetric because there's anomalous vessel pattern. During embryogenesis, the way these central artery and central at the vein end up basically being formed and then diverging. And that can give you very different looking optic nerves. Does a small cup to disc rule out glaucoma? So can you have glaucoma with 0.1 and 0.3 in the other eye? Absolutely. And can you not have glaucoma with 0.7 and 0.8? So you have to look at the rib. You have to look at the whole, it's the totality. And obviously with secondary, it's really that history and it's going to be that clinical exam and angle findings are really important. So dischanges, we talked about this the other day, and again, cupping or what we refer to as cupping, deep, large suspicious cups. You can have normal cups, you can have not a deep cup, and it's really the progressive loss or change to the neurofiber layer. So it's the rim. Notching, nasalization of vessels, but none of these are all really pathodemonic. I think the way we're starting to think now, it's adrense hemorrhage or neurofiber layer or diskeying hemorrhage that really becomes more pathodemonic. What do you think about if you see a hemorrhage? What's the first thing you should think about? Really simple. No pressure. No pressure? What about the pressure's fine? Basically, Pat, what? Still uncontrolled. You see a hemorrhage, their glaucoma's still uncontrolled. So what's happening? What's changing? And we've changed from, when we see a hemorrhage, we've changed our work up a little bit away from just IOP to what else is going on? Do they have sleep apnea? What's their blood pressure? What other contributing factors? And it's always good to ask, are you on an anticoagulant? What else could give you a hemorrhage in the retina? Diabetes, what else? Hypertension? Vain inclusion. Vain inclusion? You know, an impending vain inclusion. You may be able to see a few other hemorrhages along the way and then say, OK, this is a vascular vent. Mastrofe? Also, somebody is coughing, sneezing, you know, and if they're on an anticoagulant, they can get hemorrhages anyway. So it's just another thing to keep in mind. But generally, a neurofiber layer hemorrhage on the disk is uncontrolled glaucoma, even if their pressure is 16. And what else do I have here? Just some progression of optic nerve damage over time. How long do you think this would take to occur? So the first thing you should ask me is, well, Dr. Roscoe, is it a pressure of 20? Or is it a pressure of 40? So let's say it's a pressure of 20. Think about the studies we talked about last week. They started to see neurofiber layer changes and visual field changes and optic nerve changes over. How long? Board question, 1 to 5, 5 to 10? What do you think? How many think this would progress at a pressure of, say, 20 over five years? How about over 10 years? Generally longer. It's a slowly progressive optic neuropathy. But if that pressure was 40, then maybe it could be over, I would hesitate to say maybe a year, two years, three years. But it's going to be much more rapid. And then again, up in that first photo, in photo A. So that optic nerve on the right-hand side could very well be glaucoma. You may look at it and say, oh, that looks normal. But that could be a glaucoma's optic nerve. Morning, Lee. So again, visual field changes. We talked about all the different things you could see. So you've got your paracentral scatoma. You've got your nasal step. You've got your hemorrhage, central island. The other thing too, and I think I talked about this the last time, if you see a hemorrhage, definitely do a central 10. Because you may miss a neurofiber layer hemorrhage. So the large studies that were recently completed, the adage study, showed that if you had a disc hemorrhage and did a 24-2, that visual field was normal. But if you did a central 10, you actually did see some early damage. And you did see damage within the central 10 degrees, which I also thought was really interesting. So secondary causes. Well, let's go through some of the secondary causes. So Nico said we have to have, it's a reason to have the glaucoma. It's a reason to explain why you have elevated IOP, or optic nerve damage. So something I love, exfoliation or pseudo exfoliation. Pigmentary dispersion. Lens-induced glaucoma. We'll go through some of these. I personally still get them confused. Every time, I just got to go back and memorize them. But they like them on the boards, because it does kind of confuse you. Basically, when I look at these fecalitic lens particles and fecal antigenetic, I mean, the key thing to me is got to get rid of the inciting factor, whatever that is, whether it's the cataract, whether it's the remaining lens particles. And there's a lot of times an inflammatory component. Tumors. Always think about tumors. If you see, OK, we'll get to that. I'm going to give you guys some ideas. Inflammation, trabeculitis, fuchs, posnarslasmin. I've actually seen one case of that. That's really cool. Posnarslasmin, we really don't understand it. It's really interesting. Elevated episcleral venous pressure. Think about that as well. Look for dilated torturous episcleral vessels and trauma. Hyfema, angle recession, steroids. Always ask about steroids. Always ask about trauma. Were you ever on steroid drop? Did you ever have inflammation in your eye years ago? Did you ever have surgery years ago when you were on a topical steroid? And then trauma, angle recession. Always goneo. How do you make the diagnosis? What's the one thing you need to do to make a diagnosis of primary open angle glaucoma? Confirm the angles open. Absolutely. Goneoscopy. So secondary. Also, sneak thick facade can be insidious. When would it not be insidious? When would it not be slowly? When would a patient notice that pressure is going up? Symptoms. OK, what would give you? So I guess the question is, when would you have symptoms of high pressure? And when wouldn't you have symptoms of high pressure? Yep, exactly. That's exactly it, when the onset is more acute. So if you have somebody that comes in, so could a patient have a pressure of 40 and not even feel it? Yep, no corneal edema, right? So it's been a slow creeping. And that's exactly what we were just talking about, Beck. You know, the case of somebody who's had a PI years ago. In fact, explain, I think that's a great case. This patient comes in, had a PI in the past. Yeah, she had PIs in both of them. Well, she did have symptoms, though. She had symptoms, yeah. She had redness and pain. How high was her pressure? It was 35. It wasn't terrible. The year told me 80, but I don't know what they were mentioning. But yeah, she had PIs in both eyes, but she still had an ever-natural lens. And it was, you know, enough to cause a problem. And she just had the lens out like a year ago. But now this time, she actually won't. Did you have corneal edema? No, actually, the corneal was pretty clear, yeah. And 35, generally, if she's got good endothelial cells, they don't get a corneal edema. Pressures in the 50s and 60s, yes, absolutely. But I think the key thing there is when you have a pain in PI, you want to go to your own. You want to make sure that that angle doesn't have angle closure. I shouldn't say angle closure, but chronic angle closure or creeping PAS, perfylentyrsineakii. And if she did have that, then she may have not been symptomatic with a pressure of 35. The other thing, too, was she did, I don't know how she thought of it, but she had a bag of drops at home. She told me she gave herself a pink drop that was chloride, but that was all that I knew about. It was one of those bullets that we carry around like to clean out the PI after we do injections and things like that. Oh, really? She's sort of chloride. Yeah. But then she picked up this other drop, which was COSOFT. OK. It's so good. She gave herself a drop of COSOFT. Interesting. I'm a little better. That's pretty interesting. Good for her. So slowly or rapidly progressive, we talked a little about that can be painless. Again, if it's a slowly increasing IOP. And secondary open angle. So by definition, it is open angle. So secondary open angle, and you've got a dugonianoscopy, and you have to confirm that. We talked about can be asymmetric, but also can be bilateral, depending upon the etiology. And I guess what are some of the things to consider if it's asymmetric? Sort of went through that list of secondaries. Will it be asymmetric? What? Psyduck's filiation. Psyduck's filiation? Is it truly asymmetric though? Or I should say, is it truly unilateral? That's the question. So on the boards, they will ask you, what is the most common, I remember this from God, my board's 20 something years ago, what's the most common cause of asymmetric? Secondary open angle glaucoma, and it is pseudo exfoliation. But I don't know if they said secondary if they just said open angle. They may have just said open angle. But it's, in a sense, bilateral, but it does present asymmetric. What else would be asymmetric? Trauma. So always think about trauma. Fuchs, ice, those would all be asymmetric. And ask about the history, so family history, medical history, trauma, surgery, and medication history. And those are some of the things we talked about last time. So back to our list, exfoliation, pigmentary, lens-induced, tumors, interocular tumors. Again, always go near, look at the iris. Think about, so how would tumors actually give you secondary glaucoma? I'm sorry, what, Lee? The lens diaphragm effect would kind of... Okay, so if it's pushing forward, right? So would that be secondary open angle? Or would you see distortion of the iris and almost perhaps some angle closure? Right? So that's a little bit of a mix, but no, absolutely. Look at that iris. Look at that iris contour. So something behind the iris, ciliary body, cis, ciliary body, tumors, masses, absolutely. What else? Distortion or anatomical changes? No, but good thought. Could be causing bleeding or increased oxygen demand, which is the abascurization. You can have the abascurization, yeah? Absolutely, yes. Tumor cells are being involved. And tumor cells, yeah? Think about tumor cells too. So if you see more pigment in an angle, okay, so here's a good question. You see more pigment in an angle. What should we be thinking about? Pigment dispersion is one. Pseudoxfoliation? And tumor. Yeah, very good, huh? And trauma, trauma can do it also. So four things. So different reasons for having pigment released from the eye. But look at that angle. So if you see asymmetric pigment, definitely start to think about, well, what's giving you that pigment? So fuchs, what about fuchs? Fuchs is a cool one. The boards like fuchs, they like fuchs. I don't know if I've ever seen a fuchs. I've questioned fuchs. What would you see in fuchs? It's usually unilateral. What's a telltale sign? Heterochromia. Heterochromia, which eye is abnormal? Not gonna tell ya. Let's keep going. Oh, so totality of the workup. So we're gonna do anything different. You're gonna do anything different for your secondary open angle glaucoma than you would for your primary. Okay, right? So if you see something abnormal, the iris, you're gonna send them to Harry and have a mask and look at his, and look at the angle. Trying to think what else you would do differently. So let's go back to all our causes. Let's go through each one. Exfoliation, what would you do differently? Anything different? So what we're learning, we know it's genetic, right? So you wanna know more about a family history? Maybe you're gonna ask them. We now know that there's other elastoid type abnormalities. Actually, the work that's coming from here. So you may ask them. I always ask my patients about other things. COPD, asthma, AFib, pelvic organ prolapse, hernias, vasculopathy, things like that. Pigmentary dispersion. Yes, Lee, go ahead. For exfoliation, they're saying that the thyroid. So you would always, and all these patients do an OCT. We don't yet know if the lamina crevose is actually different in exfoliative patients. We also don't have any clues to why one eye gets the exfoliation and the other one doesn't. Because if you do conge biopsies, you will actually find, well actually, if you do biopsies anywhere in the body in these patients, you will find exfoliative material. So lungs, meninges, heart, uterus, gallbladder, vasculature, conging type of skin. So this elastoid material is all over their body. Just doesn't necessarily cause any problems unless there's some sort of stressor, is what we think. We think the stressor actually may be ultraviolet light, but that's a whole other discussion. So you would do an OCT in your head? You would always do that, yes. So in any patient with glaucoma, you're gonna look at their optic nerve, right? You're gonna do an OCT. What about pigmentary dispersion? What would you do differently? Okay, so always look at translumination defects. And we'll show some pictures of those. Always transluminate. If I can't tell you anything. Goniogonio, goniogonio. My second thing is transluminate. Transluminate. Look at their iris before you dilate them. Otherwise you will miss things. What's, so good translumination defects. What else would you do with this patient? What are you gonna look for in the anterior segment? Pigment. When would you see the pigment? When the iris has friction, so when the iris is moving, so after you dilate them. When else may you see pigment in these patients? What do you wanna ask them about? Huh? I love these exercise. These are the coolest patients. These are so cool. I remember I had a girl, she was 16 years old. She came in to see me, she was a gymnast.  Every time she went on the trampoline. Runners, basketball players, soccer players. If you are, it's not, I shouldn't say lucky enough, but because it's unfortunate for them. But they can disperse pigment. Do you think they always have elevated IOPs when they disperse pigment early on? No, no. So you can see an anterior segment full of cells and they may not have an elevated IOP.  So you're gonna hear stories of, oh yes, after I run, my vision gets blurry and I get a bit of a headache. So then what you wanna do with that patient, and I just had a patient the other day do this. He's in the 60s, actually 50s. He looks like a, he looks, he's classic for a pigment dispersion, but I couldn't get him to actively disperse. You want to try to get these people to actively disperse when you wanna check their pressure. And your management is going to depend on what their pressure does when they actively disperse. So if they throw off pigment and their pressure stays in their teens, you may not do anything.  And there's a whole big discrepancy with, you know, whether or not to do a peripheral iridonomy. And I think a lot of us would still do a peripheral iridonomy if they're actively dispersing and their pigment's going up. Now you would say to me, well, why are you gonna do a PI if their open angle and their pigment dispersion? So why would you do a PI? Yep, so Bob Rich, probably back in the 70s and 80s, has shown, and actually there's some pretty cool ultrasounds now. When you do a PI in these patients, the thought is that there's a buildup of anterior segment pressure pushing the iris back, and then there's friction of the iris on the zonules because you get translumination defects in mid periphery. So if you do a PI, you're actually going to relieve that pressure differential between the anterior segment and the posterior segment. Or anterior chamber and posterior, yeah, posterior segment. And allow that iris to come forward. Does that make sense? So it's not bowing back. The other thing that's interesting about these patients, they tend to be males and they tend to be myopes. So always like, oh, and what else do, are they more predisposed to? What do pigment dispersion, what are they more likely to have if they're myopic too? Lattice. Lattice and retinal detachments actually. Retinal detachments is the key kind of keyword. And what's interesting too is it's disproportional to their myopia. So in and of their myopia, so their myopia increases them through retinal detachments, right? But if they've got pigment dispersion, it puts them at a higher risk. So we think that there may be something that's genetic that's different about their eye. So these patients also, you want to warn them about retinal detachments. Lens-induced glaucoma we'll get to, intraocular tumors we talked about, fuchs, positive schlassmen. That's a really cool one too. How do these patients present? What? Redness. Redness? Actually pretty quiet. They're always pretty quiet. But eye pain, what else? Just a genilateral. Genilateral? Men or women? Tends to be a little bit more on younger women. I always think of my pigment dispersion as my middle-aged man or younger man, although my 16-year-old gymnast didn't fit that bill. And positive schlassmen I think of more women. And maybe it's just because I saw a girl. But, and they tend to be generally younger.  They're pretty quiet. But they have a little bit of discomfort, a little bit of blurring and really high pressure. Fairly high pressure. 30s and the 40s. How do you want to treat them? Steroids. It's an inflammatory cause. You're going to see these fine sort of stellate KPs, but they're not even classic KPs. But, and if you go any of them, sometimes you say that you can see, you know, some inflammatory cells in the trapeculum ashwork. But they're actually really, really pretty quiet highs. They're really interesting. And then surgical trauma. We'll talk about an angle recession. Go through this. So again, a little bit about exfoliation. It's the most common identifiable cause of glaucoma worldwide, cunning for majority of open angle glaucoma in some countries. Progression is anywhere from 15 to 40% of cases. And it's estimated that 80 million people worldwide. So where, oh, this is actually cool. Where was Lindbergh? Anybody know who, I'll talk about him in September, actually, when I present about exfoliation. John Lindbergh. There's actually a John Lindbergh society. And it's been resurrected by Bob Rich. And it's pretty cool. So he first discovered it in 1917. And he discovered it in Helsinki, Finland. And he was an ophthalmology resident who found the material, went to present and do his dissertation at that time. That's how they got their degree to practice. And he presented it as a resident to some of his professors. And they also sort of perpued him. And one of them actually took his idea and took his discovery and then went on to talk about it. And basically say that he was the one who discovered it. So came back, then it turns out, so then John actually got the recognition for the discovery. And it was in 1917, so it's been 100 years. And the other thing that was really neat, it was in Helsinki, Finland. And I recently met his grandson. And I thought that was really cool. Distinct disease, very specific mechanisms of development. But we don't know what's the contributing factor. And we know that there's a genetic predisposition. The majority of people say, oh, what gene is it? What's the gene? LOXO1, LOXO1. And what does LOXO1 do? I don't expect you guys to know this details, but. So it converts tropolus into elastin. And these patients have, they have a genetic abnormality within the LOXO1 promoter. It's actually for the messenger RNA. And it's a suppressor gene. And we're not quite sure what's going on with LOXO1. So these patients have LOXO1, but it may be dysfunctional. And in the material itself is LOXO1. So it seems like something is wrong or dysfunctional with the LOXO1 enzyme. And it collects. And you get these microfebrile or deposits that are almost kind of gluey that can't dissolve. And we also think what happens is, if you think about AGV trauma, anything that damages tissue, if the tissue's damage, if the elastin's damage, it wants to repair itself. And we think that's what's happening is because there's damage, the LOXO1 gets activated, but then there's something dysfunctional about the LOXO1. So the elastin tissue is not repaired properly. That's sort of the hypothesis. And it holds with UV. UV damage is elastic tissue. Genetic predisposition, as we talked about, most patients actually have a lot of it, something like in Iceland, it's like 98% of the population actually has the genetic abnormality or the risk allele. But yet they don't go on to present with exfoliation. Largely overlooked, especially in the US. What's the, you have any idea what the percentage is, actually, in the US? Kind of rough estimate. It's age-related also. So if you're older, greater percentage of the patients will have it. In Utah, it's about 3%, 3% to 6%. So over 60 is about 3, over 80 is about 6. And that's consistent with the United States. Other parts of the world, it can be as high as 30 or 40%. And then Bob Rich always talks about it being potentially reversible or curable if we can figure out what causes it. Increase in prevalence with age. We used to talk about it being Eastern European, Scandinavian. Do you think that's true? No. So it was first discovered there. But it's actually prevalent in Turkey. Huge population, probably about 30% of the Turks will have exfoliation. Guatemalans, Mayans, we have a big population actually down there that was discovered. Actually, Alan Crandall was the one that picked up the exfoliation in his patient population. So we're actively looking at them. Africans, Indians, Japanese, large patient population in Japan probably runs about 20% to 25% in Japan. I think the key thing here is you need to look at these patients before you dilate them. You need to look at translimination defects.  Because exfoliation can be very easily missed. Why is it important to know that this is their cause of their secondary opening glaucoma? What's different about exfoliation patients? Whatly? Zonulatahisins, OK. If you're doing cataract surgery, you may want to do cataract surgery early in them. What about their glaucoma? Going back to that optic nerve that's going to take 10 years to progress, are these patients going to follow that rule? No. These patients can go blind rapidly. It's really scary. It's really scary how quickly these patients can lose vision. And sometimes it could be really young. And then on the other hand, you could have an exfoliation patient that never develops glaucoma. And they do perfectly fine. And we still don't understand why. And what's the difference with that? What's unique? Why some patients and others and not others? And one of the things we think about, too, is just because you have the material doesn't mean you're going to get glaucoma. And maybe the patient with exfoliation who's developing glaucoma would have gotten glaucoma anyway. So maybe they have a genetic predisposition just to open angle glaucoma. And now on top of it, you put this material and they've almost gotten a double whammy. Sort of the way we're thinking about this. Here's some of the prevalences. Greece, Turkey, Navajos, US, average is 3%. As we said, Chinese, Spain, Japan. That actually is a little bit higher now. It's closer to 20. But yeah, sort of all over the place. I don't know about the Eskimos. I don't think anybody's gone back and studied them again. A lot of patients with open angle glaucoma will have exfoliation. That's another thing to realize. You guys are coming out of a phenomenal training department. So you have a patient with open angle. Always go back and think, did somebody miss something? Never take someone's diagnosis for 100%. Go back and question that. And obviously in Iceland, the majority of patients with open angle have exfoliation. It's a really high number, 74%. Glaucoma, much more rapid progression. And we don't know. You brought up something, too, Lee. That's a good point. Is it the laminocrobosa? And that's why. Is there something genetically abnormal about the elastin in the collagen and extracellular matrix within the laminocrobosa that makes them more susceptible to IOP fluctuations if they have exfoliation? Because again, this is a genetic abnormality throughout their whole body. Or is it just the extreme fluctuations? These people fluctuate all over the place. They don't follow the book. Their pressures are all over the place. Tons of fluctuation, rapid progression, and just worse overall disease, greater medical failure. One thing that's interesting. So I thought this was really cool when I heard this. And I work really closely with Bob Rich. And I go to, there's think tanks every year that we have just on exfoliation. We get all the people from all around the world. Japan, Turkey, Iceland, Finland, the people that originally discovered this when we sit around and we talk about exfoliation. And Bob Rich always tells about a case where he had a patient who developed exfoliation but had a sector erudectomy very early on. And that area where that patient had a sector erudectomy never developed exfoliation on zonules. I thought that was really cool. So there's some sort of dynamic interaction between the iris, zonules, the lens. And also, if you take the cataract out sooner or earlier, I should say, you may slow down the production of the material. So there's this push now to take the cataract out earlier. Even if they don't necessarily need it, you may have better outcomes because those zonules are not as traumatized and as abnormal. But maybe it's affecting the material and the material production itself. So somehow the zonules are not as disrupted. But you may have less material and less block hormone progression. It would be a cool study to do. Yes? Do you know why it's peripapillary? So they always talk about peripupillary. You can see peripheral as well. But classically, they talk about it being peripapillary. And it has to do with peripapillary rough. And it may be. So the other thing with exfoliation is there's more ischemia occurring to the eye. And we're not quite sure if it's because the blood vessels are not, they're stiffer because the material in the smooth muscle of the vascular wall or they're actually occluding the microvascular. The other thing that's really cool about these patients. So Lou Pasquale at Harvard did a study. He published this if you guys are interested. But he looked at capillaries in the nail beds of patients with exfoliation. And their nail bed capillaries in their nail beds are much more tortuous. So there's something abnormal about their vascular system because of the elastin. And these patients with exfoliation, back to your question, have more iris ischemia. So also keep that in mind. And that's perhaps why we see it's basically an end vessel right at the iris pupillary rough. But we may be having pupillary defects because of ischemia as well. And you get ischemia in these eyes. Which also may be the reason why they've got worse glaucoma. So it's sort of a chicken and egg what's coming first. There was a little bit of a tangent. Material, what do you call these? What do you call this? What do you call this ring sign? What? A bullseye? A bullseye, or they call it three ring. I don't know if you hear one, two, three. But it's a three ring sign. And you can get translimination defects definitely in the heart periphery as well as a pupillary rough. Always look at the pupillary rough. Always look really carefully. Sometimes the material can be very difficult to see, very difficult to diagnose. You can see capsular contraction as well. That's another thing to think about. You see a patient who comes in. They have a history of open-angle glaucoma, come from an outside dock. They have a cataract extraction. And you see thymosis. And you see contraction of the capsule. What should you think about? Exfoliation. That patient may have exfoliation, and it was never diagnosed. They're also more likely to go on to have lens dislocations. And I think the interesting thing is we've been trying to figure out if doing cataract surgery earlier prevents the later lens complications from lens dislocation. And nobody's been able to actually quantify that. It's sort of a, again, a thought. Iris pigment in the angle. We talked about unilateral heavier pigments. What do you call this? What does this patient have? Policies line. What gives you a sample leases line? What? Exfoliation? What else? Pigment dispersion. So it just means, why do you get sample leases line? What is that? Where is it? Tell me where it is. Where is sample leases line? Antirdeshwabi's line. Yep, right there. Antirdeshwabi's line. And where do you tend to see it? Inferior angle or superior angle? Yeah, inferior angle. Why? Gravity, conduction flow. What about over time? Let's say this patient's pigment dispersion. So here's a good question for you guys. Exfoliation and pigment dispersion. What's going to continue to have more pigment over time? And which one's going to continue to get less pigment over time? OK, pigment. Why? Is it the iris or is it more the lens iris dive from the cataract? Well, that too. Yeah. So I always think of the cataract coming forward. And the iris basically gets pushed forward and you don't have that friction. So over time, a patient with a heavily pigmented angle due to pigment dispersion is going to get less pigment. So over time, where is that pigment going to be? So here's another interesting question. Where are you going to see more pigment in a pigment dispersion patient who's, say, 75 years old? Inferior angle or superior angle? You may see it in the superior angle because the inferior angle may clear. So because of convection and because of aqueous fluidics, the thought is that the inferior angle is going to clear faster over time. You also should think about pigment dispersion in patients who may have very little pigment in their angle. And again, just because of that reason, that angle has been cleared. But the damage, and they also may have normal IOPs. So don't be fooled if your pressure is normal and you've got damage, but you've got translimination defects. And you still may see some asymmetry between the eyes in terms of pigment. Ghost cell glaucoma as well is another one. And or trauma, hyphema, clearing blood. But you're not going to see a sample these days. You're going to actually see blood then in Schlem's canal. What else do you think about if you see blood in Schlem's canal? Another cause for secondary open angle glaucoma? Episclerol venous pressure. Yes. Think about elevated episclerol venous pressure. Can you have blood in Schlem's canal and have a pressure of 12 and not have anything wrong with you? Can you have blood in Schlem's canal? So does everybody with a little bit of blood in Schlem's canal need to be worked up for glaucoma? I had a patient at the VA like this a few months ago. No. Sometimes you can see it can't be normal. Just reflux. I mean, it's a dynamic vascular system. You can see some blood in Schlem's canal. It doesn't mean anything. Yes, Lee? Along the same lines. That's a good question. What do you guys think? If you see blood vessels in the angle, are they always pathologic? Why Niko? The Pyros vessel? Yeah. That are more tortuous and more on the anterior surface. So correct. So yes. And it's the pattern of the vessels. Again, it's not too dissimilar to the retina. If you see collateral, you guys are going to see collateral vessels. And you're going to see shunt vessels. And these are not the fine sort of spidery vessels that are consistent with ischemia and neovascularization. So when you see neovascularization, it's going to look very different. And you also want to look at the configuration of the angle. And then you take the whole patient into the picture.  I mean, this isn't in this talk.  What gives you neovascularization of the iris? Ischemia is the number one thing. So you worry about carotids, ocular ischemic syndrome. What else? Diabetic retinopathy. Tumors. Tumors can absolutely give you iris. Neovascularization. Uveitis, also, and sort of congestion, chronic inflammation. And then, obviously, all the normal ischemic CRVOs and CRAOs, et cetera. Pigment dispersion, your younger male myopes, wide IOP fluctuations, up to 40 to 50 with symptoms. So again, and you want to get them in an active state of dispersion. So that'll be the difference between pigment dispersion syndrome and pigment dispersion glaucoma. Do they have elevated IOPs, and are they having optic nerve damage? Burnt-out pigmentary. Again, you look, and you see these trans-elimination defects. And maybe they've got a faint sample E.C.'s line. They've got normal pressures, but they've got optic nerve damage. And is it symmetric or asymmetric? What do you guys think? Could be asymmetric. Actually, could be either. Really depends upon their myopia, too. But you may see it tends to be this, I would think of more as being a little bit more symmetric. Because generally, they're going to be about the same. If they're minus 4 and 1, they'll be a minus 3 and 1⁄2 or 3.50. But it can actually present either way. Reverse pupillary with block, we talked about. Treatment. What's the zent male line on the capsule in the back? So you'll actually see pigment also on the anterior hyaloid face. And you can see it where the anterior hyaloid face actually comes up to the lens posterior. So if you can, if you can, oh, and this actually was really annoyed. I have to take my boards again. And I was at a board course. And they showed a really wide dilated eye. And they showed the zonules. And they had some pigments. They had some schmutz, couldn't even tell it was pigment, schmutz on the zonules. And on the anterior hyaloid face as it comes up to the lens. And my mind always thinks exfoliation. So they were like, what's giving you these changes or this debris on the zonules? And I said exfoliation. And I was wrong. And it was pigment dispersion. So they were talking about the zent male. So if they happen to show you they like pigment on the back anterior surface and on the zonules. And pseudo exfoliation, they like, people are rough. But this actually could be either. This is sort of classic for pigment dispersion. But I've seen patients like that with exfoliation as well. Oh, we didn't talk about this. What did they get on their cornea? Croukenberg, Croukenberg's Bendels. Oh, yeah, and here. What's this? There it is. Yeah, it's an IR line. Heavily pigmented angle. And this is the reverse. Oh, we were just talking. I forgot I had this in my slide. The ultrasound after a PI. It's really cool.  It's really neat. I always thought this was a really, I like pigment areas really cool. It would be neat to look at the genetics. Fakolitic, fakolitic glaucoma. So fakolitic glaucoma, large cataract macrophages. And again, I wish there was an easy way to sort of remember this stuff. It's just memorization. But macrophages, plugging the trabecular mesh, wear a hyper-mature cataract, what do you need to do? Take it out. Take the cataract out. Lens particle glaucoma. So different from fakolitic. Fakolitic, the cataracts there. What's lens particle? Part of it's left over, so there's some cortical material. So lens particle glaucoma, too. Do you have to have this right after the cataract surgery? You can, but you don't have to. What about 10 years later, you do a yag cap and you disturb the cortex that's there, l-schnick pearls, and you break up this material. Did you then get lens particle glaucoma? Sure. Yeah. It's sort of a reaction. The material clogs the trabecular mesh work. What do you want to do for this one, too? Steroids, aqueous depressants, clean up the material. So I have a question. It really depends upon the presentation and it depends upon how much of this inflammation. Because don't forget, you can have a really hot red eye because of the elevated IOP as well, and not so much from the inflammation. So again, it depends upon the presentation. I don't think I can give you a Pozner-Schlossmann. Hit them hard with steroids. Don't be scared of the pressure. These patients, it's tough to say. You can also have goniome, do gonioscopy. You may also have a component of angle closure, too. If this is a complicated cataract and they've got a lot of cortex material, a lot of manipulation, maybe the capsular bag is not intact. The rye may be hot and red because of. But it's usually, it's not so much inflammation as a pressure spike because of this material that's there. It's not like the FACO antigenetic, which we're going to talk about as well. That's really an anaphylactic inflammatory process. So FACO-lytic glaucoma, hypermature cataract, lens particle, white fluffy cortex in the anterior chamber, generally capsules not intact. Again, it's just, you know, it's more complicated. I always think of these as the more complicated cataracts. Treat the inflammation, treat the IOP, and you may need to go in and take out the material. And that really gets to your point, Lee, is, is this going to resolve over time? If it's a little piece of material and eye's not so inflamed or pressure's not so high, you may not have to be as, it may not be as critical to get into that eye and take the material out. But if it's a really hot red eye with a lot of inflammation, even all the steroids in the world is not going to help you get all that material resorbed in an appropriate time span. But keep that in mind, actually. Even like I thought that was a really, I forget who presented that case. It was really interesting to think about a YAG capsule years out, you know, 10, 15 years out. And the patients got, you know, inflammation in a high IOP because the material got disrupted. And then phacoanalytic, anaphylactic. So, again, that's really more, that's really more inflammatory as well. And that's when the lens protein. So I think of that always as the bag that's not intact and that lens material's leaking out. And then there's an inflammatory reaction. So there you've got to take the lens out, actually, as well. Ocular inflammation, glaucoma, steroid responders, gonioscopy. Oh, so why no myotics? Why don't you want to put these patients? Actually, myotics work really well in pigment dairy dispersion also. But young myopes, you really don't want to use pylote. We don't use pylote as often anymore. We used to use pylote on these patients. But increased risk of retinal detachments and also the headaches and the symptoms. Why no prostaglandins? Why don't you? I mean, we do, but traditionally speaking, you always want to think that your prostaglandins can be aggravating inflammation. Leaky, it breaks down the blood aqueous barrier. Prostaglandins break down blood aqueous barrier. And they give you CME as well. That's very, very well documented. The other thing they can actually do is reactivate herpes. So they're pretty benign, but there are cases where they actually can throw you a curveball. So what is this? Poshers-Lassman up front. Fuchs heterochromia. Oh, Fuchs heterochromia erudiciculatus. Also on gonioscopy, what do they have? They may give you pictures, photos like this. Yes, yes, very, very fine. So that gets back to your question. That's another case where you can have very, very fine. And they're not crossing the trabecular mesh work. They're sort of this low line. And they just look, their angles just look a little bit different. Recurrent bats of elevated IOP, mild iridus, trabeculitis. We talked about this. What is this? That's classic actually. That's the Poshers-Lassman. They get these fine, fine, fine. They're not even really stellar. It's really not KP's. They're just this very stellar, yeah, sort of little inflammatory. Do you keep these patients on long-term anti-inflammatories? No, no, not at all.  And it actually, they outgrow it. So it's generally younger patients, middle age. Middle age women, again, is what I think about. And possible causes. Do we know what causes it? Yeah, I think there may be a viral etiology underlying it. You gotta see them. Yeah, you absolutely have to see them. But if you, you may have one or two cells in the anterior segment, it's really not an iridus. So it's gonna be different than an iridus. In your differential, always consider herpes. But again, it's this sort of fine. What would you see if you had a herpes? Do you get this sort of fine? Generally, herpes is much more of an iridus. Any sort of infectious etiology is gonna have larger KP's. This is very, very fine. And a very quiet anterior segment. And they're not really red. They're blurry, a little blurry, their pressure's high. But it's really the trabeculitis. But you gotta see them, yeah. And you know, and some of these patients too, if they really know their disease, you can always, you never wanna give anybody a standing prescription for steroids. But the ones that really know their disease will also know to start it and then come in and be seen. Oh, and then aqueous suppressants because you are dealing with elevated IOP. Trauma, high incidence of rebleed, larger hyphemes, greater likelihood of elevated IOP that's pretty intuitive, compromised angle.  Think about sickle cell, higher risk of rebleeding. When do they tend to rebleed? How many days? Three to seven. Three to seven, generally within the first week. So you wanna immobilize them. Gonioscopy, you know, it's, you wanna know if there's an angle recession component, you're not gonna be able to see it, especially if they've got an active hyphema, but at some point you wanna get that patient in and you wanna do a gonioscopy and you wanna see where that angle's torn. Angle recession is going to, down the road, five, 10, 15 years. You know, it's really hard to speculate but that patient needs to know if they've got angle recession there at a higher risk of glaucoma over time and they need to be followed, basically for the rest of their lives, which is a hard thing to tell a young kid who's got an high hyphema. You know, keep going. You know, when you're 50, 60 years old, don't forget about the fact that you had trauma to your eye and keep getting examined. Hemaletic, ghost cell glaucoma, these patients will have, ghost cell glaucoma's pretty cool. It's this khaki looking, red blood cells with no more, you know. And you know what's actually cool too? You can see ghost cell glaucoma. What do you wanna look for in ghost cell glaucoma? What's another telltale sign when you think about ghost cell? What? Yep, look at the anterior vitreous because you may still see some ghost cells there or even some, you know, RBCs but if they had a vitreous hemorrhage, think about ghost cell glaucoma. Angle recession glaucoma, tear in the ciliary body, longitudinal ciliary muscle fibers, unilateral secondary open angle, talk about when does it occur, other eye developing POEG. And they can always have mixed mechanism too, you know. They can have angle recession and they can have POEG. Risk factors for progression, pretty obvious. Elevated IOPs, diurnal fluctuation. Which study? Which study talked about diurnal fluctuation? That was last week's lecture. It was here. Chris, Mike, Nico, Becca, you guys here last week, I think so. Ages study. What are the two things the ages study taught us? Two things. I don't remember, two things for ages. What? Yes and no, but that wasn't what that taught us. 18, yes, 18. 18, patients had less progression if they were under 18 and diurnal fluctuation is bad. So patients went on with more progression if they had diurnal fluctuation. And if they had IOPs that were over 18. So now when you look at studies, it actually reports that as a separate outcome. Percentage of patients that had IOPs of 18 or less at all time points. And that was because the ages study. Think about nighttime IOP, sleeping position. We talked about all these. These are sort of the way we think about glaucoma now. Blood pressure, hypoprofusion, ischemia. Recommendations and treatments we went through. And then prognosis. Prognosis really is the cause of the glaucoma. Any questions?


Okay, good morning. So, I guess you've all had a chance to express yourselves on the essay on what you make of all this. So, today is our last day in the causal theory of reference, and I'm just going to, in the first two sections today, wrap up on some relatively technical things about causal chains and informative identities. And then I want to look a bit at the broader implications of this. There's something about the causal theory of representation that really changes, it really affects your picture of the relation of the mind to your knowledge of your surroundings. I want to try and catch some of that in the last section today. I've been trying to restructure the class quite a bit, and after moving all the pieces around quite a lot, I realized that there are actually quite good reasons for keeping it the way it is. So, not for the first time. Okay, so on Friday, we'll go on to Putnam's article, brains in a vat. Okay, oh boy, okay, brains in a vat on Friday. Okay, so where we got to last time, we're talking about the function of language and why you'd want a language at all, and maybe the basic function of a language is to let you transmit knowledge from speaker to hearer. Then, if you're thinking of reference in that context, reference in the context of having a system that you can use to transmit knowledge about the things in your surroundings, then what reference to the object is going to require is that if you're going to refer to the object, that's the same thing as being in a position to transmit knowledge about that object. And if you think that knowledge is a causal notion, that in general knowledge of the object requires that you be causally connected to it, then that's just going to imply that reference to the object demands that you be causally hooked up to it. There'll be a causal connection between the thing and you. So putting that around the other way, reference to the object is going to require a causal connection to the object in virtue of which you're in a position to transmit knowledge of the object. I know obviously not any kind of causal connection is going to do for knowledge.  Yeah, I mean, I'll be unconscious. So not any kind of causal connection is going to be good for reference. So this suggests that the kind of causal connection that's going to matter for reference is one in virtue of which you're in a position to transmit knowledge of the object. Evans's formulation was the item you're trying to refer to is the item that's a dominant source of your associated body of information. So the idea there was there might be two objects, one of which is your dominant source, the other of which is getting some information into the pool of information you associate with a term, but it's not the dominant source. That's the model of that Napoleon example is whoever's a dominant source of the information you associate with the term. That's the one you're referring to. Or I gave, I tried to do a photograph of two different people where you're mostly getting information about one of them, but some information from the other is getting in there. You'd say that's really a photo of the person who's a dominant source of the information in the photo. So in the case of perception, the dominant source of your current perceptual information, that will be the object that you're seeing. So you can refer in perception using terms like this table or that table, but if you think a little bit further about the way it goes in perception, if you take a term like this table or that person, then when you or I are looking at the table, there's a whole bunch of things that are actually causally involved in perception of it. For example, there's the sun, right? Our friend Mr. Sun is involved in here because it is light rays from the sun that are bouncing off the table and striking your retina. The window is involved because if it wasn't for the window, then there couldn't be that causal process of the light getting in. The lamp overhead may be causally involved. There might be lots of stuff, lots of things that are causally involved in the generation of your perception, but you wouldn't say just as you look at the table that you are seeing the sun or that puts you in a position to refer to the sun. The lighting might be kind of hidden, so you don't even know where the lamps are. You don't know what the illuminates are, so these things are causally involved, but you're not seeing them or in a position to refer to them. And when Evans talks about dominant source, it's not obvious that that really helps sort out why that is. And why is the causal connection that matters, the one between you and the table rather than the one between you and the sun? Every bit of information that you get from the table, well the sun is causally implicated in you getting that information. You see what I mean? So just saying it's the one that's involved in generating most of the information, doesn't disentangle the sun and the table. Have I stated that plainly? I mean you see there's a problem here that we want to specify more exactly, which causal connections matter for reference and which don't? Solutions? It's not that hard. Frankly, as you'll see in a moment, yes. Dominance source. Dominance source, yeah. Dominance source, the thing about that is that it depends exactly what you mean by dominant source, but in the face of it it sounds like something like quantity matters, yeah. But the sun, the table is involved in you getting lots of information, but every bit of information you're getting from the table, if it's only the sun that's allowing you to see the table, then the sun is causally involved in generating every bit of information that the table is involved in generating. So it's not clear why the table rather than the sun counts as dominant. It's not just quantity of information being generated. You see what I mean? There must be something right about that, yeah. And that's very intuitive. You're focusing on the table in a way that you are not focusing on the sun, yeah. But the trouble is to spell that out a bit, but I agree that that's the intuitive answer to this puzzle, yeah. The sun could be replaced for that. That's really an interesting idea. It depends what you mean by replaced, though. I mean, if the table was replaced by a duplicate, yeah, then I don't know, in some sense things would go on as before. If the sun was replaced by a duplicate, all right, but if the sun was just taken away, you wouldn't be able to see anything at all, yeah. Right, and if you take away the sun, you wouldn't see the table at all. Yeah, they're both involved. You see what I mean? Yeah. The causal immediacy of the table. Yeah, yeah, the sun was way downstream in the table, yeah. That too is an interesting idea, I mean, but what about our old friend the mirror, the unexpected mirror that you don't realize is there? Yeah. Reflection, yeah, right. Yeah, but you know, if I've got the mirror here, right, the unexpected mirror, then it's causally in between you and me, yes. But I don't even realize there's such a thing there, but I can see you in the mirror. If you wave to me and I wave back, that's not crazy, because I know it's you, right? I see reflection, yeah. I was trying to wave to you, if you see what I mean. I see you reflected in the mirror. Okay, one last, yeah. I'm sorry, I don't mean to make too, I think this is interesting, and all of these ideas are chipping away. Figure ground, yeah. Yeah, that is a bit like that focusing idea. You know, it's when the thing is lifted out for you as figure from ground, and you can choose what to focus on, yeah. Right, right. Let me try this on you. So this is just stating the puzzle I just gave. There are different causal roles for the object you're seeing, the thing illuminating it, and if you see it through a telescope or through a mirror. I see the force of saying you might just see the reflection there, but it's also equally colloquial to say I saw you through the telescope or I saw you in the mirror. Yeah, I mean, if you're looking at yourself in the mirror, you're looking at because you want to see how you are. You don't want to see how your reflection is. If you see what I mean, it's not just but you're interested in how your reflection is this morning. You want to find out how you are. Okay, so what about this? I mean, I don't know that this is a comprehensive answer to the puzzle, but something like when you're making a judgment about the table and you're saying the tables are brown or the tables rectangular, then you're responsive to the brownness or rectangularity of the table. You see what I mean? Whereas you can't make a judgment like that about the sun just by looking at the table. You see what I mean? And actually, there's a range of characteristics the table has. How big it is, just where it is. There's a stack of things you can find out. Is it shiny? Is it matte? There's a stack of things you can find out about the table just by looking, but you can't really do that with the sun just by looking at the table. So there's some sense in which your verbal reports about the table are differentially sensitive to the characteristics of the table, but they're not differentially sensitive to the characteristics of the sun. If the sun turns up or turns down, then you can see the table better or worse, but you're not varying your judgments about how the sun is. Flawed visual perception. Yeah, very good. Okay, so this way of putting it implies that perception is always accurate, which is probably a bit too strong. You're trained philosophers who live in a world of hallucination and illusion and madness and so on. Okay, but I make the following claim. In ordinary perception, if you're going to be able to talk about the cup at all, it's got to be pretty much the way it looks. What I mean is, if I seem to see a badger there, then it's not that I'm looking, I see the cup all right, but I'm just having some illusions as to what, it's not like straight or curved. Straight or curved are pretty, how should I say, they're pretty subtle distinctions compared to that kind of thing. If it really looks like a badger, then that's a hallucination. I'm not seeing the thing at all. I'm not able to refer to it. So unless I'm getting it mostly right about the thing, the thing I'm seeing in the distance, I'll write straight or curved as one thing, but roughly what size, what kind of thing, is it a fleet of aircraft or is it a car or an elephant? Vision can't be completely useful about these things and still leave you in a position to refer to the thing. Well, we have some ability to keep track of objects perceptually through changes in their characteristics. What I mean is, just as a person waves their arms and so on, there's change in the position, I can demonstrate this for you now, there's change in the position of the arms, but you have no trouble keeping track of the object through those changes. Whereas some changes in an object, you have trouble keeping track of the object through those changes. So with the case of the flowers over a period of days, it seems to me the spectrum of cases, if you're just looking at a bunch of flowers and they're, let's say, withering before your eyes or just waving in the breeze, then you're changing all right, but you have no trouble keeping track of them. So you don't need an identity judgment, that's the same flowers again, but sometimes you do, I mean, if you come back after a period of days and they're all changed colour, then you really might be a bit puzzled what have they been replaced or what? I'll say more about that kind of case in just a moment. Yep, very good. Let me give you another, can I put that in hold just a second, because I want to give an example that I think might be an example just like that, okay, and then come back. So you see how this works for proper names, but if you get all your information about Sally down a telephone line, I keep telling you about Sally, then I'm implicated, the telephone line is causally implicated, but the role that's a causal connection that Sally plays is different because it's Sally's various characteristics that are responsible for all the judgments you make using that term, whereas variations in the telephone line don't make a difference as to whether you're going to say that Sally is tall or not, that's okay. So there's something systematic about the role that Sally plays in that kind of case, the telephone line or your informants don't play, but this is what I think might be an example of what Dylan was talking about. Suppose we go back to our old friend, the sinister Goodle, so when you're making your judgments about Goodle, you might say well look my judgments about Goodle are all about the theorems that he proved and the proofs he gave of them, so I make judgments about how innovative Goodle's use of a recursion theory was and that is actually systematically reflecting what Schmidt did, you remember the story? The Schmidt did the proof and okay, but then my judgments about Goodle, using the name Goodle, are systematically varying with what Schmidt did. You see what I mean? Is that your kind of case? So why are we going to say isn't this guy really just the conduit through which all these different characteristics of Schmidt, the mathematician, came to be causally affecting our verbal judgments and in that case when we say Goodle, we'd be referring to Schmidt, that's the wrong answer because Goodle stole the credit. Do you see what I mean? That is Dylan's kind of case. Do you want to supplement that with another case? You're talking about reflections. Yeah, so this is a case where Schmidt is it where stands behind Goodle, so here you have Goodle, here you have Schmidt and here you have the verbal reports and Schmidt's causing Goodle to talk and Goodle's causing our verbal reports, but we're differentially sensitive to the characteristics of Schmidt, who we're talking about in the maths. And your kind of case is one where you've got Goodle, you've got a mirror reflection of Goodle and that's causing the verbal reports. Yeah, and you might say well we're systematically sensitive to what's going on in the mirror. Yeah, these are puzzling cases. You might say well this is Kripke's revenge, this is where Kripke comes back in because really to look at this, you can't address this kind of distinction in terms of dominant source or differential sensitivity because they're equally dominant, they're equally differentially systematically sensitive. So you've got to actually look at the details of the chain and in this case say but there was some funny business here, if you see what I mean, when Goodle stole the credit that blocks the reference from going all the way back to Schmidt or the mirror reflection is somehow transparent in a way that means that the reference does go all the way back to Goodle here. So Kripke might say well this just means you've got to look back at this historical stuff that Evans was saying forget about that. You see what I mean? Yeah, this is a homework exercise. I don't have a crisp sorting out of this yet. Yes, that's right. Yeah. Okay, suppose we take the Napoleon case where the swapover happened very late. Is that the kind of case you're thinking of? So we've got, as you put this mature, the mature imposter takes over very late. The thing is in the Goodle-Schmidt case, Goodle is really transparently transmitting, I mean conducting all these characteristics of Schmidt because whatever Schmidt does, Goodle just does that, replicates that and it's proof. So when we make the verbal judgments as to what we say Goodle was doing in his proof, we are actually causally sensitive to what this guy was doing. In the Napoleon case, there's the imposter and there's the emperor, the mid-period emperor and there are our verbal reports and they are being caused by the late imposter and the mid-period emperor. But one's not acting as a conduit for the other. You see what I mean? It seems to be a different, maybe you're reading it some different way but my picture is that here you're getting a lot of information from this guy coming down here and here you're just getting a little bit of information from this guy coming down here and that's what makes the distinction. You don't have that same kind of sneaky kind of structure as you do here. That's very good. I mean if you're going to say it's a way of transmitting knowledge of the thing, let's take that very seriously and now you've got Goodle, you've got this figure who is an imposter, a fantasist, one of the flotsam and jitsam of Vienna in the early last century. What he's doing is he's hijacking this sober series of mathematician stuff and projecting this fantasy onto it. Then you say, well is he a reliable source? No, he is not a reliable source. He's a kind of guy who goes around pinching mathematicians ideas. Although he might actually have just written it all down, so in fact it's all just the same way as Schmidt had it, he's not a reliable source so you can't get knowledge of what Schmidt was doing from this but you could get a knowledge of what Goodle was doing from this chain. Although this is a causal chain all right back here from Schmidt to Goodle. It's not, how should I say, epistemic. It's not, it doesn't have to do, it's not a chain through which we can get knowledge. You see what I mean? So that's lost here but this bit of the chain we do get knowledge and that's why we'd say we're referring to Goodle rather than Schmidt. That's really powerful I think. There's something right about that. I think from an Evan's point of view there's something about this though that is, it's against the thrust of Evan's account. Evan's idea, so this is a very good way of, I think something peculiar about the causal chain going through, back through Goodle to Schmidt in virtue of which you're differentially sensitive to Schmidt's characteristics. Yeah, it's not the right kind of causal connection to give you knowledge. Evan's I think when he's just talking about the dominant source of your current information, the idea was forget all that stuff about going back into history. So it's alien to the spirit of Evan's account and I think within Evan's own account you'd have to be saying something like, look what we know about Goodle is after all not just the mathematics. What we know about Goodle is something about where he was born, was he married, where did he live, did he have children. You have this picture of someone with a life and the mathematics is just a little bit of the life, I mean with all due respect and what matters is that Goodle was contributing, this person here was contributing to covering most of that biography rather than just the mathematics. So I don't know, these are two different lines and I think they both have something to them. So I don't know, I guess that's my idea of wrapping up, is to raise a lot of loose ends. I'll leave them as homework. Okay, anyone else want to take a shot at that? Okay, I think that is actually pretty much the state of play today. I think we don't have a tight necessary sufficient causal account of reference but something like that gives you a picture I think of where we are today. If you can think of something which you might well be able to or that this sorts out some of this then that would be great. Okay, so I want to just review where we are with informative identities, where we began. So where do we got to an informative identities? Remember, Frege, this is where we began in about, I don't know, a long time ago. A equals A holds a priori and according to Kantus to be labelled analytic while statements of the form A is B often contain very valuable extensions of a knowledge and cannot be established a priori. So then I showed you these distressing photographs. Yeah, when you say well that's informative alright and then you think about it a bit and you think well those are informative too. Yes, because it's informative. If you have a causal theory of reference then it's informative to be told that it's the very same thing that was causally responsible for this photo as was causally responsible for that photo and if you think that's a model of reference in general then it's very hard to see how if you have, if signs have their references fixed by causal chains, how could you ever get an uninformative identity? The same as the sign isn't going to be enough. So how are you ever going to get an uninformative identity? But it seems like we need uninformative identities and if you take this inference and you say well that needs an extra premise, does that need an extra premise class? Yes, what is that extra premise? Okay, so we got the morning star is the evening star. Okay, so now we've got an inference of three premises right? Is that valid or does that need another premise? Sorry? Is it good the way it is? Put your hand up if you think it's good the way it is. Yeah, you really have to say that. Put it in your hand if you think it needs another premise. I don't think that's a daft response if you think it needs another premise. The thing is if you said it needs another premise you'd really be in trouble. If you took seriously the point that it's very hard in a causal theory to see how the identities can ever be uninformative, yeah? Then what you say is well I don't after all, this is like the case of the photographs when I have the morning star here and the morning star up there. It's like the case of these photographs because I don't know if what's causally behind this use of the phrase the morning star and that use of the phrase the morning star is that the same thing? You see what I mean? So you might say this, I mean it's not a daft thing to say well you do need another premise because after all the causal chain back here might be going back to something different to what the causal chain up there goes back to. So in that case you would need another premise, namely something like the morning star is the morning star and similarly for the evening star, yes? But can you see the problem at this point? Because are you done adding premises? No you are not done adding premises, in fact you have only just begun, right? I mean you're really in trouble at this point because it's just going to keep exploding and the board is not going to be big enough, yeah? So at some point you just have got to be able to say that inference is just valid as it stands. We really need these uninformative identities. You couldn't have any kind of inference involving names unless you had, you could at some point stop and say I'm just going to use the fact of identity here in the inference. But then how do you ever get to that? I mean how could that ever be valid? If it's not ever valid then we really have lost the use of singular terms. We really can't use names for gossip and so on anymore. We should be tragic. But on the other hand this thing about how is it the same causal chain? That seems very powerful. I mean how do you know a priori that the causal chain is going back to the same thing? Well again this is like another loose end. I think there isn't a canonical answer to this. It is something that's still discussed as a kind of open problem in the literature. That's what I mean when I started that Frege's puzzle really looks obscure and must be fairly straightforward when you start. It is by no means straightforward. But let me just say something about how far I think we've got. It's something like this. What certainly seems a priori and maybe analytic is if you say this general form of argument a is f, a is g, a is f and g. Arguments like that. You can say this schematically the general form and it could be a priori that arguments of that general form are analytic. Just the same way you can say something like p, if p then q, so q. That general form of argument is valid. Now here I'm not talking about any particular argument. I'm just saying if you've got an argument of that form then it's valid. So here what Frege is right about is if you've got an argument of that form then it's a priori that is valid. But when you're arguing this table is f, this table is g, this table is brown, this table is rectangular, so this table is brown and rectangular, yeah? Then that is not a priori there that you really have an argument of that general form. And I'm not saying it's very unlikely but in principle it's possible that just as I talk some force from outside is zapping the table and replacing it with a qualitatively identical counterpart. I don't say it's likely but it's not a priori that it's not happening. And of course there are all these illusions and tricks and so on where people do substitute one thing for another and you don't realise, yeah? So this goes back to this thing about the flowers, actually changing. What seems to happen is that in perception when you're talking about the same person it might be that you and your evil twin are both in the class, yeah? But that you just move in and out so the two of you are never in the class at the same time, right? That's a possible scenario, yes? And then if people talk about you and say that person's f, that person's g, that person's both f and g, then that's not actually a valid argument, yeah? So when somebody does put information together from different sources, sorry, does put information together from different premises about you as true of the same thing, then you're assuming that that's not happening. There aren't being substitutions you don't notice. So you could say, well, what's happening is the general form of argument, what is this general form of argument require?  Well, what that requires is that you have the same sense for A every time, right? It's not just the same sign, it's the same sense. But what does same sense require? Same sense requires that you've got the sign A and you've got a causal chain back to a particular object. So think of sameness of sense not as a matter of sameness of description or something like that. Think of same sense as a matter of your way of causally locking on to the object and keeping that the same so that if I say to you, watch this piece of chalk, watch this very carefully, right? You can do that, you can lock on to the piece of chalk and keep tabs on it over a period of time. That's what sense is. It's a way of causally locking on to an object and keeping tabs on it over a period of time so that if you've causally locked on to the same object in the same way all the way through here and you're just expressing that, then you've got a valid inference. It's not a priori that you write because you might have made a mistake. You might think you'd causally locked on to the same thing but not of causally locked on to it.  You're putting together information over time and you're using this perceptual ability to keep tabs on the sameness of the object over time. And something like that seems to go on in speech too. If you're talking about your friend Sally, you might say, Sally the singer, Sally the singer and just use a tag like that to so I can be sure it's the same Sally you're talking about over the period of time. It's not a priori that you're really managing, that I'm really managing to keep tabs on one in the same object but if I am doing it then I have the right, if I am managing to keep tabs in the same object, then I have the right to make this kind of inference without any further premises. I think something like that is where we are with informative identities. If you say that does not sound like a neat and tidy theory to me, I think you're right. It does not sound like a neat and tidy theory to me either. But something like that is a state of play. I don't know, maybe the GSIs, there's some cutting edge stuff that I don't, but I think that is where we have got to. Does that make sense anyhow? You see what I'm suggesting? That was the right answer. Okay, let me talk a little bit more broadly now about how this way of, these ways of thinking about reference affect your knowledge of your own mind. We talked about this earlier that you can have, it's very tempting to think if you just shut your eyes, close out the world, you can have authoritative knowledge of your own thoughts. You know whether you're thinking and you know what you're thinking just by inner reflection. It doesn't matter what's going on around you. But if you buy a causal theory then that kind of claim really doesn't seem so good anymore. You know what you're thinking. You know when you're thinking the same thought, when you're thinking a different thought, right? So it's not just that I know that I'm thinking. I know which things I'm thinking. But if I know which things I'm thinking, then I must be able to tell when I'm thinking the same thought or a different thought. And the trouble is that a causal theory seems to threaten this kind of idea. We came upon that earlier. But I want to just put this round another way. Suppose you say, look, let's suppose the causal theory is correct. I don't see why we can't hang on to the idea that even in splendid isolation I can know whether I'm thinking and know what I'm thinking. Yeah, let's try and do that.   And you have a thought, as one does, about Goedl. You think, is that really right that Schmidt stuff? Goedl is innocent, you think. Goedl was framed. So what happens is you're struck by a particular thought about Goedl. And then you say to yourself, I'm thinking about Goedl. Okay, you can do that. Right there you are. That's you. I'm thinking about Goedl. And then you think, well, if I'm thinking about Goedl, then by the causal theory of reference, there must be such a person as Goedl. And Goedl must be causing me to think this very thought. So since I'm thinking about Goedl, Goedl exists. Right. And if you've read Kripke, then you know that. Okay. So there you are, locked away, thinking, and suddenly you've established the existence of Goedl. How do you do that? Right? I mean, of course, if it doesn't just work for Goedl, I mean, it will work for water, too. You are locked away with your own thoughts. You have a thought about water. You think, I'm thinking about water. Therefore, there is such a stuff as water. And you know that just by reflecting in the contents of your own mind. How did that happen? You realize now the benefits of knowing about the causal theory of reference because it's knowing about the causal theory of reference or lets you do this, right? Well, again, this is, it's not that I'm suggesting a tidy resolution here, but let me suggest a way of thinking about this. Suppose you've got it that you're thinking about Goedl and you get from that to Goedl exists. Well, maybe that transition is all right. I mean, if the causal theory of reference is right, then that is a kind of a priori transition, right? You couldn't be thinking about Goedl unless Goedl existed. You couldn't be thinking about water unless water existed. I mean, that's it's quite intuitive anyhow. But how do you know that you're thinking about Goedl? Well, maybe you could only conclude that you're thinking about Goedl if you already know about Goedl's existence. So maybe that thought justifies you in saying you're thinking about Goedl. But does it only if you already know about Goedl's existence? I suppose you didn't know whether Goedl existed. Suppose you thought that Goedl was just someone who figured in a thought experiment of cookies, right? Then it could happen that you were actually having a thought about Goedl, but didn't realize that this was a thought about Goedl because you thought it was a thought about an imaginary person in a thought experiment of cookies. Yeah. So only if you have knowledge of Goedl's existence, the first thing there justifies you in thinking the second thing. So you've got here an argument, a set of transitions that are correct, but they don't actually generate knowledge of the conclusion because you had to know the conclusion to make the transitions. Yeah. So that might be one thing that would block that kind of inference. And if it is, it's an example of a much more general phenomenon. This is in the trade. This is called transmission failure, where you start out with something you know, and you make valid correct transitions from that. And you get to a conclusion, but you don't know the conclusion on the basis of these three transitions, because you had to do the conclusion already in order for these transitions to be correct. So the reason I say it's quite general is you might think that something like that goes on with Descartes' Kajito. How about Descartes' Kajito? You guys all seem pretty clued up about Descartes' Descartes. Doodle Descartes. Okay. So Descartes' Kajito is kind of like that if you think about it. It's only these inferences point you from the thought out to the world, right? And that's what's weird about them. Descartes' inferences point him from the thought back to his own existence, right? That's what he was doing, I think, therefore I exist. But they seem vulnerable to the same kind of complaint, because what's going on here is Descartes has a thought. He thinks, that's me. I'm doing that. Look at that. That was me. I'm thinking. And then he says, so I exist. And then people said, well, can you just do that again? How did that prove your own existence? Didn't that in some way presuppose your own existence? And you could think that's got the same kind of structure actually. If you think how you get from just having a conscious thought to the judgment I'm thinking, well, if you already knew you existed, if you already knew about yourself, and then you have the thought. And then you can say, that's me. I'm doing that. I'm having that thought. Therefore I exist. But you had to know of your own existence to get the conclusion out. Do you see what I mean? Yep. If you didn't know of your own existence, and you're just struck by a thought, you wouldn't be able to tell it was you that was doing it, because you wouldn't know there was any such thing. Just as here, if you didn't know of Goedl's existence, then when you had a thought, you wouldn't be able to say to yourself, well, I'm thinking about Goedl. One other, I mean, I think this is, I guess what I really want to get at is, these inferences might strike you as pretty weird. And in a way, they are pretty weird, right, from your own thoughts to where the external world is. But they are part of a family of really interesting and that have the same structure. And they are really interesting and it's hard to diagnose exactly what's going wrong with them. Here's one other last case. I don't know if you'll know about Descartes, I guess. What about GE Moore? This is one hand and this is another. GE Moore gave the following proof of the existence of the external world. The skeptic questions the existence of the external world says there are no material objects. GE Moore gave a very long talk in which he discussed the nature of material objects and so on. And then said, look, here I can prove the existence of material world. This is one hand, this is another. Hands are material objects. Therefore, there are material objects. Therefore, there is an external world. That's a common reaction to all of these arguments. Hands are material objects. Therefore, there are material objects. Therefore, there's an external world. And his point was you can be a certain of the existence of a hand as you can of the premise of any skeptical argument. That's just where we come in. But you might think this argument too has that same structure. You get a perceptual experience. You make the judgment this is one hand and you say external objects exist. But your perceptual experience only lets you draw the conclusion this is one hand. If you already know that external objects exist, yeah? So Moore is trying to get from the experience to the external world and he faces that same structure of problems. So whatever you think of the particular diagnosis I'm giving in terms of transmission failure, I really want to just end by highlighting these kinds of inferences. These are really interesting inferences. Okay, so Putnam on Friday. Okay, thanks.