Why do we essentially give that importance to the evolution of the Italian case law on the point? Because Italy is one of the few cases where national courts have actually given an answer to the point of the extent of the judges' powers in dealing with state law. And I refer to what Mr. Fiestra has said before concerning the different types of social control. So the object of social control is the point of essentially law and the point of fact. So this is a distinction that we'll see, as we will see later on, will be paramount in the analysis of the national judges. The Supreme Court has dealt with the problem of exo-official controls concerning state aid in Italy. And I must stress that exo-official powers in Italy are really an exception to a more general rule, as I said before. And so the attitude towards the question in the first place was a very conservative attitude. The Italian judges have been very reluctant to extend their exo-official powers, of course, also in light of not only the general rules concerning the management of the trial, but also in light of the questions of constitutional compatibility, so compatibility of exo-official power with the general rights of defense as set out in the Italian constitution. However, the ever-more pressing influence of European Union law has compelled the Supreme Court to question the rigidity of this conservative approach. And as I mentioned before, the most important evolution of the case law has dealt with essentially two fields, two of the main fields of law. On one hand, tax law, and I specifically refer to the case of banking foundations, but I will not dwell on this point because this will be the object of our next case study. And the point of the winding up of an enterprise, and especially the so-called literature on the extraordinary administration, what's here in Italy called grand in present crisis, so large enterprises that enter a period of crisis and they must be warmed up with certain procedures that I will not dwell upon because they take more specific points of our meeting. So the first question that has been put to the attention of the Supreme Court concerns the different degrees of judgment where state aid questions could be raised. Of course, the Supreme Court dealt with cases concerning its powers, the powers of the Supreme Court. So it must consider that the judgment before the Supreme Court is a judgment with a very limited object, at least in Italy. The Supreme Court of Cassation, Court of Cassazione, cannot reexamine factual evidence, cannot stand in the case from a factual point of view, but it is called to rule only on mistakes in law or other specific errors, mistakes that have been committed by the judges of the previous degrees. So it was relatively easy for the Supreme Court to state at an earlier time that the Supreme Court, Court of Cassazione, could not be called to express its views to judge a question of state aid if that question had not been previously raised in the previous degrees. Of course, one cannot in Italy, but I imagine also in other countries, cannot introduce a certain specific point of fact or law for the first time before the Supreme Court. So the first position of the Supreme Court was not only excluded the possibility of sufficient controls by the Supreme Court on the point of state aid, but also excluded that the parties could for the first time introduce the question before the Supreme Court. And I refer to my 10th slide, what I call the Supreme Court Step 1. The next step was to focus entirely on the point of ex officio powers of judges. The Supreme Court allowed four parties to bring before the Supreme Court the question of compatibility of a certain national provision, a certain national measure with new law, and specifically with specific regard to state aid law. So the parties were allowed to bring before the Supreme Court the question for the first time during the entire trial. But on the other hand, the Supreme Court excluded that it was amongst its powers to act ex officio. So I included in the slides some examples of the Supreme Court judgment where the question was specifically dealt with. The first judgment that I put in this slide concerned the litigation on large enterprises entering crisis. It said that the objection with which a party states that a state provision is in breach of new law concerning state aid law is an objection in the substantial sense, since it aims at demonstrating the lack of the conditions for the demand to be granted. Therefore, we included that the judge must assert an ex officio, they have the existence of such elements in order to verify whether the provision must be disregarded. So here the Supreme Court, yes, to the Supreme Court was very conservative. It's, in my opinion, it's also disregarded the distinction that we have made before between different types of ex officio controls. So one point is for the Supreme Court to pronounce on the interpretation of the law. On one another point is to examine ex officio sexual elements, elements that constitute only facts. This judgment sort of takes for granted that an examination of this sort concerning state aid is a factual examination. So this regards the fact that there is also, of course, an interpretation of the specific law that must be conducted. This is a point that will be then corrected by further judgment of the court. In the next slide, I put another example of what I call the step one of the evolution of the case law on the point. So always concerning the point of the law, the crisis entering crisis, if here the court, again, takes for granted that a certain kind of analysis on the point of compatibility of a national measure with European Union law always implies an ascertaining, in concrete terms, of a different treatment being put in place. So in my opinion, this is a point of view that is, of course, very conservative. And again, it starts from an assumption that is not actually right. There are cases where there are no necessities of a certain effect of this ammunition to understand whether or not a certain measure constitutes a state. Then this is something that has been then dealt with in the second step of the evolution of the Supreme Court case law. What is interesting in my opinion is also that, as you can see from the dates of the judgment that I put in this slide, that there are in the same year and also concerning the same question, very different positions taken by the judges with a few months of difference of them, which gives the exact measures of how much the question has been and the attention of the Italian judges and also the Italian scholars for the debate was very, very heightened. So step two of the Supreme Court, the first steps have been more careful. There will even be more open attitude towards the question. But it was explained not much as the duty of the national judge to directly apply the European Union law, but as an interpretation of the procedural rules. So this case that you can find in my 12th slide, the 2004 case, it concerned an interpretation of the rule concerning the appeal. So what must be the object of an appeal? And this here for the first time concerning state case was assertion that the analysis of the compatibility of domestic law with the community law is not conditioned upon the introduction of a specific question or demand since the point and be known by the judge also as a feature. Then, and I come to my 13th slide, again, the debate was so heightened that it was a high degree of attention on the point that the Supreme Court itself understood that there was the need to invest an even higher authority on the point. So it referred the question to the so-called session unit and joint sections of the Supreme Court. Briefly said, the most relevant questions are before the joint sections of the Supreme Court. And all there is a debate within the Supreme Court itself. The single sections of the Supreme Court can refer the question to the joint sections. So the joint sections were referred to the question of exo-feature controls in the field of state aid. And in 2006, they clarified that the exam of the implementation of state aid measures must be conducted also as a feature by national judges, even if a specific objection or request on the point has not been raised by the parties. And this judgment has been groundbreaking for Italian case law. And there was this point as being made by the Supreme Court, by the joint sections of the Supreme Court, by applying sort of analogic interpretation with reference to other similar cases, such as the case of the use of supervenants, so the case of a certification in the law during the trial, or questions of constitutional compatibility that afterwit a certain rule, a certain provision has been because it's incompatible with the contribution. So this has been the main point, the starting point of an evolution that has, in 2007, for the first time, led to the recognition of different types of exo-feature controls. So here in Italy now, case law has been quite constant in the latest year to divide the question of the types of exo-feature controls in two categories. So type one, exo-feature analysis of judges on point of law, and exo-feature control of judges on point of fact. I mentioned in the slide that the 2007 ruling of the Supreme Court, according to which the issue of the compatibility of a national provision with new law can be raised exo-feature by the judges on the grounds of the principle that I mentioned before, you are in Victoria, as it happens in the case of your super-variance. However, there is a distinction. So for now, the judgment of the joint sections of the Supreme Court was the first step toward the formulation of a distinction, depending on the issue requiring sexual scrutiny. So whether or not the issue before the Supreme Court or before the Supreme Court requires a further examination of factual elements. So if the unlawfulness of the entire discipline or one or more of its rules in questions, and when, of course, it is then clear that the entire regime, provisions at issue constitute by themselves. So without the need of a further factual analysis as stated, then the court can intervene exo-feature and pronounce on its compatibility, not much but on the need of further examination on the point of state aid. On the contrary, if the unlawfulness of the discipline comes into question in relation to its specific implementation, and so whether or not the subject in question enjoys a higher benefit than those granted to other of its competitors because of a state aid, the judge cannot examine the question if the parties do not specify and demonstrate the relevant facts. The judgment that I quoted does not specify this point, but, of course, this means that there are obstacles to the possibility for a court to present those relevant facts, which means that if the judge does not have all of its elements right in front of him, and according to the procedural rules of the Italian Civil Procedural Court that there is no more time to present those facts, then exo-feature control is impeded, is out of the question, cannot be upheld. This, of course, raises the other question of restubicata that I will not dwell upon because it was already mentioned by Mr. Fiestra. I have to say that this is now the case law on the point, and there are things, as you can see, in my last slide, number 15, that you can see that the position held by the Supreme Court in 1907 was then upheld even more recently, including the Supreme Court in 1916. There are not many cases, many more recent cases on the point of state aid. So the latest last case that concerned the point of exo-feature control was that with in 2016, and it confirmed that the distinction between exo-feature controls concerning factual elements and exo-feature controls concerning provisions that constitute exe by themselves state aid without the need of a more specific examination on the factual elements of the case by the court. So the case study that I thought would be interesting to examine the concerned banking foundations. For those of you, of course, who are not from Italy, I will briefly introduce the issue. Banking foundations were introduced with an Italian law, with an Italian foreign law of 1919, that separated the bank as an enterprise and the ownership of the bank. So the bank as an enterprise was given, so to speak, to corporations, and its ownership and the shares of that corporation were given to an entity, a new entity, called the Banking Foundation. So of course, the corporation, the banking corporation, continued to act as a bank, as an enterprise, and the foundation had certain limits that had been posed to its activity. Those limits will be very relevant in the examination of the solution to the case. So the law especially provided that the foundation could only have the act to attain purposes of the public and social interest, principally in the field of scientific research. Of course, this activity was not excluded by the fact that the foundation had to manage its shares, so the shares in the banking enterprise, so in the corporation. And initially, the foundation could also acquire shares of other businesses, either in the banking sector or in other banking sectors, in other fields that were not banking. With the only difference that they could not acquire a majority share in other banking corporations, they were under the control of the Ministry of Finance, and then I move on to slide number three of my second group of slides. They were under control of the Ministry of Finance and needed the authorization of the Ministry for operating on their shares of the banking corporation and other banking institutions. This limit was repealed later on, but that will not be as relevant for the solution of the case. Then in 1998, the Amitalial Law modified the limit to the foundation's activity. They could acquire shares in enterprises only in as much as such enterprises were instrumental to their purposes, so in their irrelevant sectors that were connected to their social services. So the contest here is that of an entity which does not have direct entrepreneurial activity and holds shares in another corporation that acts as an enterprise. And this foundation does not operate in a business area, but only manages shares. So moving on to slide 2001, the specific tax provision clarifies that banking foundations are non-profit-making entities operating according to principles of transparency and morality. For tax purposes, banking foundations are considered to be non-commercial entities, even though they pursue their objective through instrumental enterprise. This is what we have said before, a company that has taken care of operating only in fields that are connected to their social purposes. And this is the framework as far as banking foundations are concerned. The legitimate context with regard to taxing is that that you can find in slide number five, which generally, this is not the current regime. Of course, I referred to the previous regime concerning the corporation and the critical persons, which has now been repealed and substituted by the forces that is not relevant for the purposes of the study. And at the time, maybe those distributed by limited identity companies were subject to withholding taxes and advance payments. And maybe those distributed to entities that are not subject to corporation tax were subject to 30% withholding tax. The treatment for foundations are partly referred at the time. So corporation tax was reduced by half for entities of social assistance, foundations, and other nonprofit institutions. And there was an exemption from withholding tax as an advance payment on dividends. So generally, the treatment of those entities was partially different from the treatment of other entities. So moving on to the facts of the case, slide number seven, the banking foundations ask the authority for the exemption from withholding tax on dividends, stemming from their shares in the banking enterprise or in the corporation that I mentioned before. And the application of taxes reduced by half. Tax authority rejected such requests stating that the managing of the shares constituted a commercial activity, escaping the advantage regime. And this request was then denied also in the first degree of judgment. There was a second degree of judgment where the Court of Appeals, so to speak, requested the grant of the request in light of the foundation's purpose of public interest, the level of which the Court of Appeals stated that the banking foundation did not market such as other competitors. So the Ministry of Finance went to the Supreme Court. And the Supreme Court was then called upon to render its judgment on the point. It is important to stress, of course, that no mention whatsoever of any question concerning the compatibility of the tax measures with EU law and the political state law was made throughout the entire judgment. So nothing in the file ever mentioned the question of state aid. So now we must understand how the Supreme Court rules on the point. Of course, there are two different aspects of the question, a more procedural aspect of the case which concerns the specific object of our today meeting. So whether or not the Supreme Court and by law examine the question under state aid law, exorbitant, and then the more substantial question of whether or not the measure is issued if applied to banking foundations that could constitute a state aid with all that comes with it in terms of procedural rules. So we should try to apply here, in this case, the principles that I have mentioned before on the distinction between the two types of exo-feature controls. So whether or not an exo-feature control is possible by the Supreme Court and if it is possible, it is possible because of factual elements on the point of law. In general terms, Italian law allows the Supreme Court to examine exo-feature of the question of what ability with state aid law. Staying on the point of procedural law and going back to the distinction that we made before concerning two different types of exo-feature control. In this case, of course, the case was more complicated than that, than how I described, but I willingly simplified the fact of the case in order for you to see the point that I tried to make before concerning the difference between the two types of exo-feature controls between the two types of exo-feature control as being made by the Supreme Court in the 2007 judgment that we talked about before in Italy on the point that certain provisions constitute state aid access. So there is no need to examine the facts from a factual perspective because that provision constitutes state aid in also in, let me say, theoretical terms. So it is enough to just read and understand the provision to see that there is a difference in treatment and that this difference influences in a certain way the functioning of the market. This is the turning point for the Supreme Court so in the point that Supreme Court uses to distinguish between the first type of an exo-feature duty to control and the second type of exo-feature duty to control. The distinction between type one and type two of exo-feature control is a very movable distinction depending on the degree of judicial activism of the judge. In fact, that is precisely correct because the Supreme Court, based only on the fact that I mentioned earlier, decided that it had to refer the question to the Court of Justice. So it referred the question to the Court of Justice and found there to be in abstract a problem of state aid, a problem of measure constituting state aid with the two different sets of problems of procedural nature and substantial nature. This was not a state aid that had been notified to the Commission and then the Supreme Court referred the case to the Court of Justice of the European Union, which rendered its judgment and concentrated on the point of the exo-feature duty and the existence of a state aid in that specific case. The fact that I mentioned to you were actually the only fact that the Supreme Court, the Italian Supreme Court, deemed relevant to render its judgment and to act exo-feature in the case at issue. This goes to demonstrating in my opinion how the distinction between type one and type two of exo-feature controls can be actually kind of moveable and not so determined and not so defined. On the ground of those questions, the Italian Supreme Court actually in 2004 referred the question to the Court of Justice of the European Union, which rendered its judgment in 2006. How in your opinion, the Court of Justice would examine the question. So of course we cannot dwell on the more specific elements of the actual relevance of the case for the internal market. So we do not examine the question from the perspective of the minimis exception or the actual fact that such measure would have on the, on the, on the, on the, on the internal market. So in actual terms, would this measure according to new constitute state aid? So of course we have to examine if the banking foundation in itself can be considered as an enterprise operating on the market. And we come to the analysis of what constitutes its object. Again, the purposes of social public interest and management of its holdings in the banking corporation and possibility of acquisition of shares in other enterprises, banking or no banking. So the Court of Justice has, has to pronounce on the, on this question, how does it rule, how does the Court rule? Is, of course the first question is then is the banking foundation an enterprise? So a subject that comes to relevant from a point of view of U law on state aid. So is it the management of holdings and shares sufficient activity to acquire the nature of an enterprise for purposes of European Union law and state aid law? Basically, the Court of Justice stated that in abstract terms, the management of shares does not preclude the possibility for an enterprise, for an entity to be considered as actually conducting enterprise and it referred to the definition, to the definitions that are relevant in the field of VAT specifically with regard to this case. And so it stated that, in theory, the measure could, fiscal measure granting advantages so relevant such as the reduction by half of the tax debt and the exemption from withholding tax can be in itself considered as state aid being that the banking foundation can be considered as an enterprise operating in the market with and of course then there come all the necessary specification concerning the actual influence on the internal market and the Court of Justice stated that in theory, given the relevance of the banking sector in Italy and throughout the entire internal market, the measure could actually constitute a state aid. So this basically concludes the case study and I think it concludes the morning session if there are no questions from you.


What's good Josh boros back again with another video So I'm gonna check out WWE moves that were banned and the real reason why we're gonna check out some of these moves that WWE was like nah, nah, nah, nah, we gotta we gotta ban these moves for maybe Some sponsorship reasons maybe sponsors don't like the move being performed or maybe you know They're they're trying to get some more sponsors and they don't want to seem too violent Even though it is a wrestling show and the whole objective is to beat your opponent Which would entail some type of violence, but that's neither here nor there We're gonna check out some of these moves that were banned and the real reason why appreciate all love support Let's get right into this woman. Why did WWE banned the putt kick curb stuff GTS and chair shots I'll be sharing the real reasons to be had those and they banned them then they unbanned them And I love it But first let's start with the punch kick With the exception of the Rkl the punch kick is Randy Orton's most iconic move back So it looked vicious and that's actually what led it to being banned Orton has admitted that his boot connected with people's skulls will perform Oh, God instant is when Randy form the move I Understand why they they did ban it for a while and then they brought it back like around 2020 when he was punk kicking Legends again gave the chairman of WWE a concussion And it was the beginning of the end for the vipers signature move in 2012 The punk it was banned the safety of Randy Orton's opponents However, during the pandemic. Yeah, the fight did bring back the move The reason was that there was no fans and attendants So order could perform the kick safely while also making it look convincing Finishing move, but still pretty awesome is the vertebrator Shane Helms aka the hurricane used the move while competing in WCW and carried the vertebrator over to WWE However, he didn't get to use it for long surely after arriving in WWE Helms was told he was no longer allowed to use the move Even though Helms had never heard anyone with the vertebrator WWE deemed it too risky the move Perfect execution to pull off safely and the slaves mistake can result in the person taking the move laying on their head or neck Yeah, it has been banned in WWE ever since however, Seth Rollins and AJ Styles busted out the move in 2016 Oh, wow. Now the reason for banning them Yeah, I mean cuz the Looks like the opponent has to time it perfectly to raise up there They're they're they're headed neck so they don't you know land on their neck, you know I'm saying so but that is kind of a dangerous move The room for error is very very small there So I can understand why they would ban that this move was just straight up dumb when Michelle McCool started wrestling David B. She used a finisher called wings of love However, she'd be forced to stop using the move It wasn't because someone got hurt or because it was too risky The reason was that WWE felt it was too devastating of a move for a female wrestler Yeah, WWE banned a finishing move because it looked too powerful.  The ironic part is that after having wings of love banned Michelle McCool start using another finisher the face breaker It looks familiar. That's because it's the same finisher AJ Styles use the Styles Clash The Styles Clash is a pretty dangerous move very dangerous B for a while due to having a history of causing injuries Thankfully, nobody ever got injured when Michelle McCool used the face breaker But this has to be the first time a safe move got banned Bro, that move definitely looks brutal too Seth Rollins had a similar thing happen to him with the curbstop Yep Look at that one point. That was his move and then they took it back They took it away. He couldn't use it and then he was able to bring it back So Seth's first finisher in WWE the Skywalker looks good, but he didn't catch on. The curbstop on the other hand Yeah This happened actually because Rollins became WWE champion at WrestleMania 31 Seth cashed in his main the bank and won the WWE championship Classic cash in Rollins appeared on the today's show and footage of him hitting the curbstop was played Vince McMahon saw this and was worried about Shilin trying to imitate the WWE champion because of this McMahon had the curbstop banned and stayed that way for three years 2018 Seth had a talk with his boss and Vince McMahon allowed the move to be used again With the only difference being that was now simply called the stomp Seth Rollins had another move banned Which is crazy. They just took the stomp. They took the curb part out cause oh, that's too violent But it wasn't entirely his fault Seth started using the buckle bomb sometimes the curbstop while the stomp was banned for looking dangerous The buckle bomb was banned for actually being dangerous The first incident happened when Seth Rollins won Stain in 2015 Seth hit the stainer with a buckle bomb that caused the icon to injure his neck Stain later said it was a freak accident It was probably why the move wasn't banned on the spot However, about a year later someone else would get hurt at SummerSlam 2016 Rollins went down the first Universal champion Seth hit throw the buckle bomb into the crowd barricade Which caused Ballard to dislocate his shoulder while Finn won the match the injury forced him to be sidelined for several months The buckle bomb was still not banned. However, but an incident by another wrestler In 2020 Nya Jax fought Kairi Sane on Raw during the match Nya threw Sane into the turnbuckles The move caused Kairi Sane to injure her head leading WB to ban the move like with the stomp though The buckle bomb would return eventually A classic wrestling move is the pile driver The move was a staple of wrestling for years The band happened in 2000s a few years after Owen Hart infamously broke Storm Steve Austin's neck The Riles snake said that he could not feel anything from the neck down Thankfully that didn't happen and while Stone Cold did eventually return to the ring his career was shortened as a result of the botch pile driver This incident showed just how dangerous the pile driver was Most notably Kane and the Undertaker's Team Stone pile drivers. The shooting star press might be the most spectacular finisher in all of wrestling However, there was a time when the move was banned at WB Of course, the shooting star press is inherently risky But there are a few specific incidents that caused WB to slend the band hammer. The first was at WrestleMania 19 Brock Lesnar nearly killed himself Oh my god The near-death experience came as a result of Lesnar having already wrestled for 20 minutes and being physically exhausted That made it understandable why the shooting star press was botched. This on the other hand was much less excusable A little over a year after the Brock incident former cruiserweight champion Billy Kidman legitimately knocked out Chavo Guerrero while performing the shooting star Oh my god The shooting star press was just too high of a risk and had the move banned for several years The 450 splash got banned around the same time for a similar reason Who intubed Guerrero accidentally landed on Paul London's face and fractured several bones It wasn't till breasts like Evan Bourne and Justin Yeah, and then they brought it back with certain wrestlers being able to do it and perform it accurately Majority of the time will really all the time. I rarely seen like a ricochet Missed that move up or whatnot. So came along though the shooting star press and 450 splash were unbanned John Cena got a wrestler's finisher banned the fish I'm talking about is the burning hammer It's not been used a ton in WWE and there might be a very good reason for it The move is a bit dangerous to perform as it's difficult for the opponent to control Physicians that makes it easy for them to land on however, that is not the reason the move was banned Around nearly 2010 Tyler Rick start using the burning hammer as his finisher according to Rex John Cena got upset because Cena felt it was too similar to the Apparently berated Tyler Rex and Rex is forced to change his finisher whether you believe it or not Tyler Rex's story does make sense in the past few years the burning hammer has been used in WWE more and more And it comes as John Cena has been appearing in WWE less and less That could be some truth to that that could be some truth to that Politicking could be involved. I don't know how accurate it is. It does look similar You know, but it obviously is a different move and how it's performed, but it does look similar I get I get that but we don't know how true that is, but it could be who knows if CM punk returns to WWE He won't be able to use the GCS because it's bad Ironically both punk and the wrestler who invented the move are the reasons for it when Japanese wrestling legend Kent 2014 he underwent a few changes first He was given the name today with Tommy on top of that He wasn't allowed to use the GTS even though that was his finisher in Japan and he invented the move The reason was that WWE was worried to remind fans of CM Punk who had recently walked out which is wild Well, he invented the move and he can't even use it You know, he invented it The fuck However Unfortunately it was short-lived during a match against Brian Kendrick a Tommy hit Kendrick with the GTS But actually broke Kendrick's nose This was enough for WWE to take action and the GTS has been banned ever since as you've no doubt learned It didn't be tends to ban moves.  Let me see how these other people took it Tommy was allowed to oh, maybe you're not I don't know Unfortunately, it was short-lived during a match against Brian Kendrick a Tommy Yeah, I walked out of the company However, did we eventually gave in and a Tommy was allowed to use the GTS Unfortunately, I don't know maybe I guess you're not supposed to put your hands up a Tommy hit Kendrick with the GTS or maybe he's supposed to aim it a certain way This is enough for WWE to take action and the GTS has been banned ever since as you've no doubt learned WB tends to ban moves after an accident happens sort of the case with the brain buster And then they'll bring it back years later having a violent name The brain buster is The idea of the move is that a wrestler sends their points head crashing onto the ring mat and the line between making the move Look real and keeping a wrestler safe is very Actually decided to ban the brain buster because of a different botch move at Super Showdown in 2019 Goldberg fought the Undertaker Goldberg went to perform a signature jackhammer, but lost control and ended up delivering a Almost caused Undertaker to be permanently injured Terran the side of caution and banned the brain buster some moves are synonymous with on Russian have been out there They both shouldn't have been out there at that time Yeah, I was banning WWE for a while Buster for his entire wrestling career and had no issues with that We came to WWE though, that's when things changed in his third match for the company Joe fought Tyson kid When on the air Joe hit the muscle buster like normal, but Tyson kid did not get up It was a later discovered that kid had injured his spinal cord The situation was made even scarier when it was shared that only 5% of people survived the injury Tyson's a stand The muscle buster wasn't Wow transition to using the cookie in a clutch different type of move, but you won't see this that's crazy Five percent, bro. That's just look at that look look Only five percent of people survived the injury and of the five who do 99% are paralyzed The only reason why TJ Wilson survived was due to his top physical conditioning the four-hour surgery was performed where TJ's neck and spine Refuse and he received four screws 16 staples and a metal rod in his neck Jesus, bro. Oh So apparently TJ was told that he suffered a similar injury as Christopher Reeves he was told the C2 injury should have suffocated him to death That's just why Wow That's crazy. I get why they obviously banned him from doing that. Oh, I know he does it now in a w But and obviously it wasn't you know, it was just a freak accident, but damn Tyson's stand the muscle buster was actually banned and Joe transition to using the cookie in a clutch It's a different type of move, but you won't see this anymore in WWE Yep The chair shot are still used to the to the to the head See someone hitting their opponent in the head. The chairs used in WWE are the real deal Yeah, just imagine what it'd be like being hit in the head by one The full extent of the damage that chair shots to the head have wasn't known until years later as wrestlers develop chronic traumatic Incephalopathy or CTE what most people forget or don't know is that WWE didn't ban chair shots to the head until 2010 You can even see some matches from the beginning of the PG era where wrestlers hit one another in the head There is speculation that the reason to be finally ban chair shots to the head was because of it's fans white in September 2009 Linda McMahon announced used Ryan to be a US senator throughout her campaign Linda was criticized for a time with WWE and WWE indirectly got attacked as well Well, they would never admit it It does seem like they ban chair shots to the head to make their product of your safer and less violent Tell not only themselves, but also Well, the steel chair is definitely not the most dangerous sound about right to find out what is watch I mean, I'm all here's the thing There's a thing. I if you know how to do it, right? Obviously, there's a way to protect yourself We're not I'm not talking about unprotected chair shots There's an art to it. Crazy thing is there is an art to it.   No unprotected That's my only thing if they were to do that, but I know WWE just wants to stay away from that So I completely understand but yeah, it just once again It just comes to making sure, you know how to take the chair shot properly and know what to do The person who's giving the chair shot as well So but it's crazy most of those list is moves that they ban and then Somebody either got hurt or they saw multiple people get hurt or potentially, you know Have some issues with the move maybe investors or whatever and then there's like, you know what? We're gonna ban it and then years later. We'll unban it. That's literally what this list was man So comment down below. Let me know. What's your favorite move that was banned in this video? Or even if it wasn't in this video Yes, a move that you know was banned in wrestling, but you still love to see the move perform Let me know down below, but I appreciate all loves point guys shown on channel road to 150k I'm still here to speed you to wrestling champion world. Appreciate your keeping me. See you next one. Peace


We've done three stages this morning on Heat 2 of Rally of Canberra, very different stages yesterday at the service park at lunchtime, let's have a chat to the teams and see how they fared. We pressed on the first stage and just ran slightly wide on one of the real tight corners and clipped a rock or a stump or something in there and it's bent in the shock again, got a flat and limped through the stage and had to sort of get it back here and get it properly fixed so we'll do the Avo stages, just cruise through and get points. Walking back to your car, Park Fermi coming into service, good morning but probably not quite where you wanted to be. Yeah, I mean the first stage I really struggled to get any sort of rhythm, it was quite strange and the second stage felt better but just super, super slippery so the third stage again felt similar, just trying to keep it neat but I'm probably, that was my fault, I made a few little errors, nothing major but we just lost time where we shouldn't have so now we've got a little bit of work to do this afternoon but yeah as long as I just keep everything neat and don't make any mistakes I think we can get the time back. We pushed on in that last stage and we're able to just get a comfortable gap now so which was nice because I tried really hard through there and I got the rewards for it so just trying to get into a groove, we've got to make some shock-setting changes, probably got caught out a little bit, we tested with one spare in the car and now we've got two so the rear end feels like it's quite low and the car's pushing into corners so we've got to make some changes now, I've given the boys a list of things I need done just to see if we can get the balance right for this afternoon. This morning had a pretty good ride in that first one and you're like Molly was saying it was slippery but I thought it was pretty good but they just got us and then had a really good one on that Tim and Biller stage but started to back off a little bit towards the end because I felt it was, gearbox was bang and turns out we've actually got, we've spaced out four bolts, we've got one moment so boys got a bit of work ahead of them coming to the service but I know look again I think that's putting us in second with a little bit of a nice buffer to Molly now so consolidate that and come through some points. The first corner we really looked at, the second corner we went off over the hill and by the time I was there I was off into the bush and then the third corner did the same thing again and I just gave up after that and just drove slow for a while. It's certainly getting better, still a bit of fluttering in between corners and it doesn't feel like you're full of confidence because sort of hitting crest in fifth and sixth gear and then it'll cut out a little bit so sort of two or three seconds until you get some acceleration back but so I think we decided to pull the pin and we threw a belt off in one of the stages, lost power steering so yeah I think it'll spend some time on the dyno with the boys with you know with race talk and get it right for Queensland. Great battle we're down, pattern for full drive, very very close at the top. Yeah yeah we have had a good morning, really enjoyed the roads this morning a bit more tight and twisty so yeah we unfortunately had an overshoot in that last stage and dropped a bit of time but still right in it I think. We gave up fair too much on stage one, unfortunately took a little bit to get going and a bit untied in there but yeah clawed it back on stage two and I think we were dead or a dick on stage three so yeah look there's still you know we made a few adjustments in our notes we're still just trying to drive the lines that we're trying to achieve and and push on from there. It's very very tricky out there and we had a couple of spins in the last stage. To be honest I'm not driving very well I don't have a lot of confidence so we're just trying to get through as cleanly as we can and not make any more mistakes.


Okay, so we're going to get started here. So I'm talking to you guys about immune-related disorders of the N-nexa and ocular surface, and there are a lot of them. This is the list. This is not even the full list. I took off some like real zebras that I didn't think were as important, but I'm not going to spend a whole huge amount of time on each of them, but there's a few that I will spend a little bit of more time on, but we'll go through the rest pretty quickly. So this is the order I think they were in in BCSC, so it's kind of random to me. It's not even by severity, but we are starting with something not so severe, contact dermatitis, so this can be a type one reaction if it is occurring within minutes, and that is considered anaphylactic. I think more commonly it's a type four reaction, which is T-cell mediated, which is about 24 to 72 hours after exposure to the allergic agent. Symptoms are eyelid redness, swelling, severe itching. Signs will be erythema and scaling of the eyelids. Treatment is discontinuing the offending agent if we know what it is. Unfortunately, I think most of the time we don't know what they are, just because there's a lot of possibilities for things that touch your face if you think about it. But even if we can't really identify what the offending agent is, I recommend cool compresses and then some sort of topical steroid ointment or topical antibiotic and steroid ointment for a week or two. Atopic dermatitis is similar, but this is chronic and it does begin in childhood, and this is a type four hypersensitivity with increased IGE hypersensitivity and increased histamine release. Symptoms are itching. There are usually lesions on the eyelids as well as other locations such as arms and legs. And there's a history of other atopic disorders such as asthma and allergic rhinitis. Symptoms are scaling of the skin, some periorbital darkening, which is shown in the picture, and also some exaggerated eyelid folds. Treatment is minimizing environmental allergens and also food allergens, using moisturizing lotions. The acute lesions can be treated with topical steroids, but you don't want to use those long term because there's side effect of skin thinning. Long term, you might consider a tachrylimus ointment because that has fewer side effects. Consider oral antihistamines and then consulting a allergist. Allergic conjunctivitis, very common, this is an IGE mediated hypersensitivity reaction. Typically, this is going to be something airborne, so pollen, weeds, something in the environment, usually seasonal. Symptoms are itching, swelling, redness, and kind of a mucoid discharge. You can also see a chemosis, which is seen in the bottom picture, but the most common finding is going to be a papillary conjunctivitis. So treatment, again, decreasing exposure to allergens. Consider doing some massive cleaning of bedding, carpets, air filters, cool compresses, artificial tears, topical antihistamines or mast cell. Stabilizers, but you do have to warn people that if they do have concurrent dry eyes, that can worsen their dry eyes. You could consider a short-term course of steroids. You might consider topical cyclosporine like rostasis and systemic antihistamines, but again, warn patients about worsening dry eye. Next is vernal keratoconjunctivitis, which is bilateral, seasonal, most often in male children, but it could be year-round in tropical climates. This is type one and type four hypersensitivity. Symptoms, again, itching, photophobia. They can also have blurred vision and they can have a copious mucoid discharge, and the appearance is rather striking. So on the paleopubrolconge, they'll be pretty much almost like a GPC look on their upper tarsal congenitiva. They may have some hemosis present. And then along the limbis, you'll see this in usually in kids of African or Asian descent, where the limbis has this kind of gelatinous, nodular appearance, and hornartrantus dots is kind of a buzzword that you'll see on tests. So these are a little white areas of degenerated eosinophils and epithelial cells. So you'll see this typically on the superior limbis, but you'll see this all the way around 360. So for mild disease, topical antihistamines, mass cell stabilizers, usually, they do need more intensive therapy than this. So usually, topical steroids, they do respond quite well to topical steroids, but I usually like to start at a high dose and then rapidly taper down. If it seems like they're still flaring, you might consider topical cyclosporin 2% or tachrylimus ointment as well. You might also consider supertarsal injection of steroid. Haven't done this, because usually this occurs in kids who are not gonna be kind of sitting still for this as an outpatient, but that's something that could be considered for very recalcitrant cases. Atopic keratoconjunctivitis. So this occurs in 1-3 patients with atopic dermatitis. Again, this is type 4 reaction. It is depressal mediated immunity. They are susceptible to HSV and colonization of their lids with the staff. The patients who get atopic disease are gonna be typically older than those with vernal keratoconjunctivitis. It is your round. The papillae are smaller than what you see in vernal. And I'll show some pictures of all this later on, but they'll have kind of a milky congenitival, edema look with some sub-epithelial fibrosis. They can get congenitival scarring and simblaferos. So this is not a benign disease. They can also get PSC cataracts, shield ulcers on the cornea, which are kind of usually a response to the papillae on the upper tarsal conge. They can get cornea neovascularization. And there are associations of this with curatoconus and pollucid. So this is kind of showing some sub-epithelial fibrosis here and also papillae. This is some massive corneal neovascularization, very thickened eyelids, and there may be some simblaferon going here. And then this is an example of a shield ulcer, which is gonna be like a chronic corneal epithelial defect usually found superiorly. Treatment is again allergen avoidance. It's the same treatment as with vernal, so topical allergy medication, topical steroids typically. You do wanna watch for secondary herpes or staph infections. In very severe cases, they may actually need systemic immunosuppression like oral cyclosporin. Okay, I'll spend a little bit more time on Stevens-Joneson syndrome and toxic epidermal necrolysis. Just because this is one of the, if you see this acutely and you diagnose it, it's something that you can actually treat to prevent further complications on the ocular surface. So this is a rare, potentially life-threatening immune complex hypersensitivity disorder that's triggered by medications or infectious organisms. It's quite rare. The incidence is one to seven cases per million, but you will see it here at the burning occasionally. You'll have sloughing of the skin and mucous membranes, and they actually simulate partial thickness burns, which is why patients get transferred to burn centers. It can affect anyone of any age. Usually it's caused by medication, and sulfa is a, and like Bactrum are a big culprit, but also anti-epileptic meds, allopurinol, even something as benign as NSAIDs or Tylenol has also been in etiology. And 15% of the time it's from an infectious cause, the most common being microplasma pneumoniae, also HSV, adenovirus, and histoplasma. So when it first starts out, it's actually a very non-specific set of symptoms for up to two weeks. So there's malaise, fevers, a big thing that happens, and they have chills, they have headaches, and then usually at this time they'll get exposed to medication as well. So it's hard to really know, pinpoint what the exact etiology is. Is it a medication that they take because of brewing Stevens-Johnson or was it from something else? And then after this two week period, then they get a very diffused progressive rash. They'll get erythematous macules, that progress to baleian vesicles, and the epidermis is very easily separated from the underlying dermis. And then mucosal erosions affect 90% and affects all mucosal areas, oropharyngeal mucosa, ocular surface, GI tract, and GU tract. And so this is actually a spectrum of disease, depending on how widespread it spreads. So first is erythema multiforme, which is a detachment of less than 10% of total body surface area, and they may have localized typical target lesions. The definition of SJS, Stevens-Johnson syndrome, is detachment of less than 10% body surface area, plus widespread erythematous and propraric macules. Mortality rate is only 5%, but that goes up quite high with more progression of the disease. So SJS and toxic epidermonic analysis overlap is 10% to 30% total body surface area involvement. And then full-blown TENS is greater than 30% surface area involvement. And the mortality rate of that is actually 35% to 40%. So this is what patients will look like. They'll be sick, they're in the burn unit, they're on oxygen.  So that is her dermis that you're looking at over her whole face. On the right, this woman hasn't sloughed off too much of her face, but she actually has pretty severe oropharyngeal involvement. So her eyes are involved, and also her mouth is pretty involved. Acute eye findings. So there are ocular surface findings involved in 67 to 81% of patients. So we believe that pretty much all patients should be screened for ocular symptoms if they are diagnosed with Stevens-Johnson. But there can be variable presentation. Some people may not have any ocular signs. Some may have only mild, or they have a little bit of contractivitis, maybe a little bit of redness, and it can progress to severe, which is diffuse, extensive mucosal inflammation, pseudomembrane formation, which are these kind of membranes here, which are, it's basically their tarsal conventiva separating and sloughing off. They'll have epithelial sloughing of their eyelids and also lash loss. The late ocular complications are what we really kind of fear with Stevens-Johnson syndrome. They can have very extensive sim blepharone formation, eyelid deformities, ankle blepharone, where basically the eyelids kind of almost fuse together. Very severe dry eye, because you have destruction of the goblet cells and also the mybomian glands. There's limbal stem cell deficiency, corneal neobascularization, that can lead to thinning and perforation. Keratinization along the eyelid margins is something that happens a lot, as well as scarring of their tarsal conventiva. And if they have severe corneal involvement and you wanna do something like a transplant, it's a very high risk transplant because it's prone to rejection and failure. Even a cure to prosthesis or an artificial cornea is very prone to thinning, perforation, just because the ocular surface is so dry. So in mild disease, the medical management, there's actually medical management, so we recommend frequent preservative free artificial tears and ointment. Depending on how the eye looks, you could consider sweeping the foreign aces for pseudo membranes. I use a cotton tip. I mean, classically, they say use a glass rod, which I don't know where you find one of those, but cotton tip and just run it along the foreign aces to sweep for pseudo membranes. If there's large corneal epithelial defects putting an advantage contact lens, and then I'm using topical prednisolone and or rostasis. But then what's recommended, if there's more severe disease, is actually urgent amniotic membrane transplantation. So amniotic membrane is from the innermost layer of the placenta, and there are different forms of it. It can be dried or it can be cryopreserved. So when it's cryopreserved, we feel that it's really a lot more beneficial for these people, these patients. So it's actually acting as a substitute for the ocular surface. So these patients have sloughed their entire ocular mucosa, and we're trying to replace it. But we're not only replacing it, we're trying to get some anti-inflammatory treatment directly to the ocular surface. There are growth factors, anti-inflammatory cytokines found within the amniotic membrane, and there's various methods of actually applying the amniotic membrane to the ocular surface. Most commonly for these cases, it's sutured, could consider gluing it. There are not, there are suture-less ways to apply it to certain areas of the ocular surface as well. And it promotes re-epithelialization of the ocular surface, reduces inflammation, prevents symplophrone formation, and it naturally does degrade over one to two weeks, and depending how severe it is, after the amniotic membrane degrades, it may have to be repeated if there's still significant inflammation. So it's typically performed if there are corneal epithelial defects, if there are pseudomembranes, and if there's moderate or severe contactival injection. Perform within two weeks of the onset of symptoms, and I would recommend performing within one week if possible, just because the earlier you intervene, the better the outcomes are. Post-operatively, doing some topical antibiotics, prednisolone, rostasis, turbidex, ointment at night, and we also recommend QH saline flushes just to kind of flush everything off the ocular surface. And again, the amniotic membrane transplantation can be repeated later on. Actually, it was part of a study when I was at Loyola, where we looked at, it was a chart review of 128 Stevens-Johnson patients who were admitted and they were biopsy proven. And we had graded their ocular surface as mild, moderate, severe, and then these patients were either treated medically or with the amniotic membrane. And amniotic membrane hasn't really been used maybe only in the past, I think 10 years ago is when we first started doing it. So it was kind of a nice way to see how, compare how patients were, how patients did before amniotic membrane was employed versus after. And then the patients were graded as good, fair, or poor as far as outcomes. I'm not gonna go over all the results of the study, but this is one result that we had which was looking at patients with moderate to severe inflammation.  And we found that the patients who had early amniotic membrane transplant, most patients had the good or fair outcome. So there was only one eye that had a poor outcome after amniotic membrane, whereas patients who had no amniotic membrane transplant, there were eight eyes who did not do as well. So it would be these, were the eight eyes in the poor category. And this was within three months. And then after three months, the results were not as statistically significant. There was a higher P value, but the results were similar. But actually in, I think it was the last month's ophthalmology, there was a new grading system that came out for Stevens-Johnson. And it was a nice way to kind of help see what to do for certain grading diagnoses. Diagnoses. So mild SJS was defined as pretty much no staining of the lid margin, no staining of the cornea, hyperemia of the conjunctiva with no stain, and the treatment recommendation there is medical. Moderate disease was defined as staining of less than one third of the lid margin, no staining on the cornea, and then small staining was okay on the conjunctiva less than one centimeter. And this could also be observed and treated medically. And then there were severe and extremely severe, and both of these required urgent amniotic membrane transplants. So for both severe and extremely severe, it was greater than one third of a lid margin. Any epithelial defect, more than punctate staining, automatically put patients in the severe or extremely severe category. Staining greater than one centimeter puts you in the severe category. Multiple areas of staining greater than one centimeter was considered extremely severe. So again, both of these categories required urgent amniotic membrane transplantation, and the extremely severe may require repeat surgery. Do you like follow that, would you follow that treatment recommendation like that? I think so, I mean I, the way we had graded things at Loyola was we a lot, we would observe if there was a small cornea epithelial defect of less than 25% of the cornea we would observe. But with Darren Gregory, he's not out of Denver, he felt that you needed to be a lot more aggressive. So I may follow this now, that this is kind of the newer treatment guideline. So you really wouldn't consider doing like amnion until like, until they've got corneal staining? Yeah, corneal staining or extensive lid margin staining. This one doesn't really talk about pseudo membranes, but I think by the time you get to pseudo membranes, you are having massive staining of the conditiva. And then I'm starting to think it's like mostly conjunctival. Like would you, I don't know, I had a kid that's here this past week that had like a mycoplasma mechocytus and like had no corneal staining, but had like a decent amount of like conching. And so it would be like monitoring based on this definition, like would you ever do like a prokera for that? I don't know what would happen. No, cause prokera, prokera only covers cornea and like a little bit of the conch. So if their problem is mostly contantival, like probably have to do the full thing or you could watch them and then if they have any sign of any corneal involvement then jump to amniotic membrane. Okay, I think treatment guidelines we talked about, mild and moderate disease can be managed medically, severe or very severe should undergo amniotic membrane. And this new study that had come out, the severe cases all had outcomes the best corrective visual acuity of 2020 and mild or no dry eye symptoms. And then the very severe cases still did really well. Nine out of 10 had 2020 vision, seven out of 10 had mild or no dry eye symptoms. Three out of 10 had, did have moderate lid margin scarring and dry eyes and severe photophobia. So they weren't completely normal but they were a lot better than the patients who have very severe some blepharone who don't see well. So this shows that the treatment actually works. Yeah. I think once, so once the amniotic membrane dissolves or gets incorporated and if they're still, if they still like say fit into the severe or very severe inflammation category then retreat. But if they are calmed down where they're now like mild or moderate then you can observe. Okay, so that was SJS. So we're going to move to mucus membrane Pemphagoid. So this was formerly known as oculosicrificial Pemphagoid or OCP but I think a lot of people still refer to it as OCP because no one knows what you're talking about when you say MMP. So this represents a type two cytotoxic hypersensitivity reaction and it's a chronic psychotrizing conjunctivitis of autoimmune etiology. And it frequently affects other mucosal membranes, mouth or pharynx and genitalia. Difficulty swallowing is an early symptom. It affects women more than men in a two to one ratio and usually you'll see this in elderly patients. So the stages of mucus membrane Pemphagoid. So stage one is sub-epithelial fibrosis, which you see here. Stage two is fornoceal foreshortening. So if you only pull down their lid you'll notice that the fornox doesn't go down as far as normal because you'll see some scarring along the fornox. Stage three, there's simple forno formation and stage four there's extensive adhesions to the eyelid and globe. So this patient is stage four. She's got some blepharone. She's got some adhesions to the globe here from her eyelid to the globe. And she also has corneal scarring. So the diagnosis is to do a conjunctival biopsy. And ideally you want to take this from a non-scarred area. So what looks to be a non-effective area. So not a some blepharone area. When you send this off for direct immunofluorescent staining there's a special media they have to place the tissue in. And then you'll see basement membrane staining of IgG, IgM, IgA, and or a complement three to see along here. And then you do want to work with either dermatology and or rheumatology for systemic treatment. For mild cases this is just oral dapsone. For more severe cases this could involve psychophosphamide, rituxin, or other immunosuppressive agents. You want to really delay surgical repair until the disease is quiescent because it, because there's so much scarring that if you were to aggressively try and repair them surgically they're just gonna scar up more and end up being worse. Eyelid repair is often needed. These patients don't do well with any sort of transplant, they may need lumbel stem cell transplant even then they don't do well and they might need a carrot across thesis. And those also have a high rate of failure. Next is graft versus host disease. So this occurs in patients who have undergone allogeneic hematologic stem cell transplant. Ocular disease is the more common form in chronic forms of GVHD. And what happens is that the donor lymphocytes start to attack host histocompatibility complexes. And 40 to 90%, depending on the study, of patients with GVHD will have ocular involvement. So this is a T cell mediated process that leads to infiltration and inflammation of the lacrimal gland, congenitiva, and ocular surface. So they typically have very severe dry eye because of this. So that leads to decreased goblet cell density, scarring of the lacrimal gland and congenitiva, myobomine gland dysfunction in scarring and limbal stem cell deficiency. So these are just some examples. I mean, there's very kind of dry eye. You can see the diffuse punctate epithelial staining. Their ocular surface is very inflamed. And when it's chronic, it can lead to some extensive new corneal neubascularization. So treatment is gonna be just very, very aggressive dry eye treatment, very aggressive lubrication, punctal occlusion, topical cyclosporin, topical steroids. And then working with their hematologist or oncologist for increased systemic immunosuppression may be needed. Next is Tigason superficial punctate keratitis. So this is of unknown etiology and there are recurring episodes of touring, foreign body sensation, photophobia and blurred vision. And it affects kind of people of a very wide age range. It's usually bilateral, but it may be very asymmetric. And the signs are gonna be these small, kind of slightly elevated, corneal epithelial lesions that will stain with fluorescein and rosebangle with minimal conjuntival inflammation. So I've got some pictures here. So when we talk about SPK, depending on who you talk to, I mean really, to me, SPK really refers to this. So I was taught that SPK shouldn't really be applied to kind of dry eye in general because it's more specific for this particular syndrome. So you'll see these multiple very small dots in the epithelium that do stain with fluorescein. And sometimes you can have a little bit of haze around the dots as well. So it looks different than the dry eye punctate epithelial lesions because these are a little wider. They're a little kind of more elevated because in dry eye you'll see kind of excavation of punctate epithelial lesions whereas here they're a little bit elevated. They typically respond very well to topical steroids and you could also consider topical cyclosporine. However, it tends to recur multiple times over several years. So it's kind of something that keeps happening and people have kind of looked into viral etiologies but nothing's really panned out for sure. Interstitial keratitis is a non-supertive inflammation of the corneal stroma and it usually has neovascularization without involvement of the epithelium or endothelium. And it usually results from a type four hypersensitivity response to some sort of infectious agent or other antigens in the corneal stroma. Most commonly you'll see this in HSV, also Zoster, syphilis, and there are a lot of other rare causes such as TB and Lyme. But most cases you actually see it with syphilis and it will be with congenital syphilis. And this is kind of a later immune-mediated manifestation of congenital syphilis and it develops late in the first decade of life. And there's a stroma keratitis that lasts for several weeks. It's usually bilateral. If you have acquired syphilis, it rarely develops but if it does, it's typically unilateral. Symptoms will be pain-tiering, photophobia, some peri-limbal injection. You'll see some sectoral stroma inflammation and KP's. There will be a deep stroma new vasculatization seen later in the course and the cornea may appear pink and it's termed a salmon patch, just kind of another buzzword that you'll see on tests. Inflammation spreads centrally with a pacification edema and the sequelae are corneal scarring, thinning and ghost vessels in a deep stroma. So this is showing some extensive corneal neovascularization and scarring and then on the right, you'll see ghost vessels. So there were a lot of vessels there and then when they regress, you'll see the remnants of the prior vessels. Diagnosis and treatment, so you want to test for syphilis with blood tests. In the acute phase, you also want to apply topical steroids and cycloplegics. If it's untreated, the disease actually does burn out on its own but after several weeks. Systemic syphilis should be treated with penicillin as a neurosyphilis and you want to work with your infectious disease specialist for that. Next is Kogan syndrome. This is a rare syndrome but it's an autoimmune disorder that's characterized by stromal characteritis over to go and hearing loss. This is again, something that has an unknown etiology but it does share some features of polyarteritis nodosa and it typically occurs in young adults one to two weeks after a upper respiratory infection. So the signs will be, early on there'll be some bilateral faint whites of epithelial infiltrates in the periphery and later on there'll be some multifocal nodular infiltrates in the posterior cornea and then some patients develop a systemic vasculitis that presents as polyarteritis nodosa and there's no real specific diagnostic test for this. This is a diagnosis of exclusion. Treatment was with steroids for the vestibular auditory symptoms, oral steroids can enhance prognosis for normal hearing for very severe cases they might require some systemic immunosuppression. This is a very common thing that you'll see, marginal corneal infiltrates. So like I said, this is a very random order but this is what it was in BCSC. So marginal corneal infiltrates occur in the peripheral cornea where the basically areas where the eyelid margin intersects the cornea. So like at 10 and two and eight o'clock and four o'clock and they're typically very well-defined gray white anterior stromal infiltrates have a little bit of a clear zone from the limbis and there may or may not be an epithelial defect. The treatment is gonna be a combination of topical antibiotics and steroids. And here are some kind of classic appearances. This is pretty classic for a staff marginal infiltrate. This one is not as classic because there's so many but you can have multiple ones like this and you can have variable, I guess, distances of a clear zone. This one may be a little bit more central than typical and these may be just a little bit more peripheral than what is typical. Next is peripheral ulcerative carotidus or PUK. So this occurs in autoimmune disease. Most often with rheumatoid arthritis but it can occur with Wegener's lupus, polyarderitis nodosa and ulcerative colitis. You do need to work these up if there's no known autoimmune disease. It's usually unilateral but they can be bilateral. You can have paracentral thinning so it doesn't have to be peripheral but with rheumatoid arthritis it's actually I think more common to have paracentral thinning than it is to have peripheral thinning. And it's usually painless or they mainly just have mild discomfort. So this is pretty severe PUK that you can see in the periphery here. In this case there's some chronic PUK that's occurred inferiorly. You can see a lot of blood vessels growing in and then this is the area of paracentral thinning. So the treatment is they're gonna need some more aggressive systemic immunosuppression so work with their rheumatologists to do that. Increased lubrication, drops, ointment, puncto plugs. Oral, tetracycline, class antibiotics such as minocycline and doxycycline can inhibit collagenases and kind of prevent further thinning of the corneal stroma. Typically, classically you're not supposed to put on topical steroids because that can exacerbate thinning and delay epithelial healing. If you're getting to a point where there's a dysmedicine or a small perforation they may need to be glued and they may need a patch graft if they're perforated or if there's a larger perforation of corneal transplant but they typically don't do as well unless they have very, very aggressive systemic immunosuppression after their transplant. The Morin ulcer is a type of PUK but it's of unknown origin. It's a diagnosis of exclusion. There are some factors that might make you think that you have a Morin ulcer but the precipitating factors are going to be prior trauma exposure to parasitic infections because there's thought to be some cross-reactivity of the immune reaction to parasites with corneal auto-engines. In some cases may have an association with hepatitis C. So the signs are going to be a painful red eye and it usually is going to be starting in the corneal periphery and then spread circumferentially and then spread kind of more centrally and the classic sign, which I'll show you a picture of later is a leading overhanging edge in the cornea and it can be unilateral or it can be bilateral. So when it's unilateral, you'll typically see in older patients it's slowly progressive. You'll see an equal distribution between male and female. The bilateral type is more common in African males. It's rapidly progressive. It responds very poorly to treatment and perforations can occur. So it's a lot more aggressive. So here are a couple examples of Morin ulcers. So this is that overhanging edge and it'll be a very kind of well-defined kind of white edge and it's really seen here.  So there's very little success with topical steroids, cyclosporine, bandage contact lens. Patients may need to undergo a limbo-conjunctival excision kind of in the area where the disease is occurring. So excising the limbo-conjunctival area and then allowing that to recess. They often do need, or they might need a lamellar periodoplasty as well. They often do need systemic immunosuppression and consider systemic interferon if associated with hepatitis C. So again, this is something you'd have to consult your infectious disease specialist. Corneal transplant rejection. So this is something that can occur greater than one month after a transplant and up to 20 years after a transplant. And 80% of cases can be reversed with intense topical subconjunctival and or oral steroids. So this is why patients do need some sort of immunosuppression for their corneal transplant. So it's usually gonna be topical steroids but for very high-risk patients who are prone to rejection, they may need systemic immunosuppression. Corneal neovascular vascularization does increase the risk of rejection up to greater than 50%. And you could consider some topical and subconjunctival anti-vigorous agents. There are a few types of corneal transplant rejections. There is epithelial where there's an elevated kind of epithelial ridge that's caused by lymphocytes. Usually it's in the first year after a PK and this is more uncommon. Subepithelial, there'll be subepithelial infiltrates. Stromal rejection, not as common but there'll be stromal infiltrates. Some thinning of the stroma and that may need to necrosis. Endothelial is the most common and it's the most serious form because that can lead to a loss of endothelial cells which can lead to chronic corneal edema or graft failure. And the buzzword here is the kudaduce line which is inflammatory precipitates on the endothelial surface and it may be in a line under corneal edema and enter chamber cell is common. So I'll show a picture here. So this is a picture of a kudaduce line. This is in the endothelial surface and this is showing some stromal and subepithelial kind of diffuse haziness of the cornea. So there are different ways to prevent rejection. At the time of surgery, you can consider putting in a smaller graft that's further away from the limbis. I typically will recommend the patients are on topical steroids forever after the corneal transplant. However, you'll see a lot of people who are no longer taking topical steroids because they're, you know, they had their transplant like 10, 15 years ago. For those patients, I usually won't restart them if they've been doing well but if they ever have any sort of rejection then I tell people they need to be on steroids for life. You do want to remove any broken or loose sutures because that irritation can induce not only infection but also rejection. Okay, next is episcleritis. Common condition is usually self-limited. It's a benign inflammation of episcleral tissues. The minority of cases are associated with a systemic cause. So I don't usually work up patients with episcleritis unless they're coming in with like very recurrent episcleritis and I'll do a full workup. The symptoms will be some redness, usually not very irritated. There may or may not be any tenderness. That's very slight. It can be diffuse or it can be nodular. It's bright red in natural light and the redness actually blanches five minutes after the installation of topical phenyliferin. So that's a nice kind of diagnostic tool to differentiate between episcleritis and scleritis. So like I said, consider a workup if the condition is recurrent. There are some systemic associations but they're all less than 10%. So it can be associated with herpes zoster, collagen vascular disease, gout or syphilis. Episcleritis is something that will actually resolve without treatment. So even if you don't really do anything, it's gonna get better on its own. But if you do do something, you could consider a short course of topical steroids and oral NSAIDs to speed the resolution. Okay, so you wanna differentiate episcleritis from scleritis. So scleritis is severe ocular inflammation that's gonna have a high association with systemic autoimmune or infectious disease and it can lead to a destruction of scleral tissue in certain cases. Half of cases of scleritis are bilateral at some point during the course and this is not gonna get better if you don't do anything. It has to be treated to achieve resolution. So the symptoms are gonna be severe pain and redness. This will be a pain that's so severe that it often awakens people from sleep. And instead of that bright red that you'll see with episcleritis, this is kind of more of a purplish hue and it's got this deep, volatious hue and natural light. The globe is very tender to touch. So you can see this is very inflamed. So there are different types of scleritis. This is non-necrotizing scleritis and this can be diffuse or nodular. So it can be sectoral or it can be involving the whole entire segment. It can be nodular where there's actually a scleral nodule present. Necrotizing scleritis without inflammation and the other name for this is scleromalacia perforans. So this is a painless type of scleritis and there's a white, quiet eye but there's thin sclera and you'll see this in elderly patients. It's typically bilateral. 50% of these are from rheumatoid arthritis and scleral rupture is rare in these cases and it rarely needs surgical repair. Whereas necrotizing scleritis with inflammation is a lot more serious. This is painful. It's bilateral in most cases. It is highly destructive with vision loss in 40%. There's high association with systemic vasculitis such as Wegener's. The mortality rate is actually 20% at five years if you do see necrotizing scleritis with inflammation. So you can see this little photo montage of different very severe cases of necrotizing scleritis with inflammation. So very thin sclera and a lot of inflammation. Post-ear scleritis can occur in isolation or with anterior scleritis. However, with post-ear scleritis often even after a full workup, no systemic disease can be found. The symptoms will be pain, which may be referred pain. There may be some proptosis, tenderness, vision loss, and restricted motility. And the signs are coroidal folds on dilated exam. They can't have an exudative RD and they can also have papillodema. And then the T sign on B scan ultrasound is the classic sign in post-ear scleritis. So this is, I'm trying to get my mouse here, the T sign here. So this results from kind of a severely thickened sclera and then you'll see kind of the optic nerve coming back. This one is showing some coroidal detachment there. And complications of scleritis, whether it is anterior or posterior, can be significant. So you can get a peripheral keratitis, you can get uveitis, glaucoma, cataract, sclerothinning, a scleroceratitis, where you have actual opacification of your peripheral cornea that's associated with a neighboring area of scleritis. And scleroceratitis is more common in zoster scleritis. So the workup may have to be tailored according to the review of SIP systems. So you can check a CBC, ESRCRP, ANA rheumatoid factor in incas, uric acid, check for syphilis, check for TB, and check for sarcoid. So the treatment, some mild anterior scleritis may be treated with just oral NSAIDs. Usually though you want to use oral steroids and then refer to a rheumatologist for treatment for systemic immunosuppression. And they may start them on a variety of different agents depending on what the etiology is. And that is it.


Sorry about the salesman who was so good he could even sell a refrigerator to an Eskimo. It's not true, of course. Eskimos don't need refrigerators. They have nature's own way of keeping their food cold. But in warmer climates, refrigeration is part of our daily lives. We use it to keep ourselves comfortable, to keep our food fresh and our beverages cold. You might say that a refrigerator works by taking heat from the inside of the box and getting rid of it on the outside. Refrigeration is the transfer of heat from a place where it is not wanted to a place where it is unobjectionable. To do this, a refrigerator uses a unit inside the box that takes up heat and a unit outside the box that gets rid of it. These units are called the evaporator and the condenser. They are tied together by connecting lines referred to as the suction line and the liquid line. Also in the system are the compressor, which is a pump, the expansion valve, and in many systems the receiver, a kind of storage tank. A chemical substance called the refrigerant flows through the system. It's the refrigerant that picks up BTUs of heat from inside the box and discards them outside. In the process, the refrigerant changes from a liquid to a gas. Then in the condenser, it changes back to a liquid. At the same time, the pressure increases in the compressor and decreases in the expansion valve. Before you can understand how the system works, you must learn why and how these changes take place. That means learning some basic principles concerning heat. To begin with, take a swimming pool and Kathy, who was swimming in the cold water. After she has dried off, she finds the air warm. But Helen has just come from the steam room and she thinks the air is cold. The words hot and cold are relative. They're used to compare one thing to another. As the girls gossip together, Kathy gets warmer. Heat from the air passes to her body and warms her. But Helen gets cooler. Heat passes from her body to the air. Heat always passes from a warmer substance to a cooler one. If you put an ice cube into water, the water is cold, but the ice is even colder. By comparison, the water is warm. Heat will flow from the water to the ice. This changes the ice, which is a solid, to water, which is a liquid. If you heat the water, it turns into a vapor. This vapor is a gas. These three, solid, liquid, and gas, are called the three states of matter. All matter around us exists in one of these three states. Now, let's see what happens to temperature if you apply heat to the ice. The temperature of the monitor reads 32 degrees Fahrenheit. As the ice changes to water, the temperature stays constant at 32 degrees. The heat is causing the change of state from solid to liquid. Then, as you continue to heat the water, the temperature increases until it reaches 212 degrees. The water starts to boil. The temperature remains at 212 degrees. Heat from the flame is now being used, not for a change of temperature, but for the change of state. Remember, heat is taken in for the change from solid to liquid. Heat is taken in for the change from liquid to gas. Now, a change of state is always accompanied by a gain or loss of heat. This is a very important point. Any substance takes in heat when it boils or changes from a liquid to a gas. And, any substance gives off heat when it condenses or changes from a gas to a liquid. Here's a container filled with gas. We add a thermometer to measure the temperature of the gas and the pressure gauge to measure its pressure. What happens if you push in on the piston? Answer, the pressure increases and the temperature increases. Now, let the piston out. The pressure goes down and the temperature goes down. The role is, when a gas is compressed, the pressure goes up and the temperature goes up. When a gas is allowed to expand, the pressure goes down and the temperature goes down. It's true for any gas. Now, let's see how a refrigerator works. We'll begin at the receiver where the excess refrigerant is stored. It is in the liquid state and under high pressure. The high pressure forces the refrigerant through the liquid line to the expansion valve. This valve causes a pressure drop. The high pressure liquid becomes a low pressure liquid. This is like letting air slowly out of a balloon. The air in the balloon is still under high pressure. But the air that gets through expands and its pressure drops. In the same way, refrigerant that passes through the expansion valve expands and its pressure drops. The low pressure refrigerant flows into the evaporator. Now, if any of the food in the box is warmer than the refrigerant, heat will flow from the food to the evaporator. So, in the evaporator, the refrigerant takes in heat and begins to boil. Remember, any substance takes in heat when it changes from a liquid to a gas. The gas is sucked through the connecting line into the compressor. As the piston moves down, the suction valve opens. The gas is sucked into the compressor. As the piston starts up again, the suction valve is forced shut and the discharge valve is pushed open. On this stroke, the gas is compressed. Remember what happens when gas is compressed? Pressure goes up, temperature goes up. The gas, now at high pressure and high temperature, flows into the condenser. The gas is hot, hotter than the surrounding air. So, it gives up heat to the air. As the refrigerant loses heat, it starts changing back into a liquid. To complete the cycle, the liquid refrigerant returns to the receiver. Now let's review the whole thing. Refrigerant under high pressure flows from the receiver to the expansion valve. The valve causes a pressure drop. The evaporator takes in heat from the box. If anything in the box is hotter than the refrigerant, it gives up its heat to the refrigerant. As the refrigerant takes in heat, it changes from a liquid to a gas. Remember, any substance must take in heat in order to change from a liquid to a gas. The compressor sucks the vapor out of the evaporator and compresses it. This increases the pressure and temperature. The vapor is now hotter than the surrounding air. So, in the condenser, heat is given off to the air. As the refrigerant loses its heat, it changes from a gas to a liquid and flows into the receiver. Now let's consider some additional points that many refrigeration students have trouble understanding. In the evaporator, the temperature may be very low, perhaps 21 degrees below zero. And yet, the refrigerant is boiling. How can anything boil at such a low temperature? Water boils at 212 degrees. But other substances boil at other temperatures, some higher than water, some lower. The refrigerant known as R12 boils at minus 21 degrees. There's no mystery about it, it's simply a property of the substance. The refrigerant in the suction line is carrying all the heat it picked up in the box. But its temperature is only about 5 degrees above zero. If you touch the line, it feels cold. How can something that's cold be carrying a lot of heat? Remember, hot and cold are relative terms. You know when water boils, it's very hot. But refrigerant boils at a much lower temperature. So the refrigerant can take on heat, change to a gas and still seem cold. Again, the reason is because the two substances have different boiling points. You have seen the basic principles of refrigeration. Study the system until you understand it thoroughly. Memorizing isn't enough. You must understand what happens and why. Because all the rest of your work will be based on these same principles.