So I'm going to continue the talk on rheumatologic, ophthalmologic diseases, and this one is probably much more common than the one that Tom was talking about. So I'm going to talk about temporal arthritis. And in recent times, the residents have been getting quite a few calls from either the primary service or the ER regarding whether or not their patient has temporal arthritis. And I've discovered that sometimes this patient may or may not even have any ophthalmologic symptoms or neurologic symptoms. So at first, I was kind of annoyed. But in preparing for this talk, I've confirmed that temporal arthritis is a disease that's, at least in the literature, shared between rheumatology and ophthalmology. And so my job today is to equip you with some information about temporal arthritis and hopefully to make sure that you're not annoyed when you get called about patients, possibly with temporal arthritis who don't necessarily have eye symptoms. So we'll review the basics of temporal arthritis or giant cell arthritis, review some ophthalmologic presentations of giant cell arthritis, and then finally give you some updates on the antibiotic treatment study. In terms of the history of temporal arthritis, it is a relatively new disease described mostly in the last 100 years. And the only hint of some description of this disease in ancient times is this picture on the tomb of an Egyptian pharaoh who has a picture of, well, the tomb has a picture of a harpist who looks really sick and may have some thickening of his temporal artery and may be blind as well because of his kind of looking into space glance compared to the other people. And so that's kind of a stretch, but it does reflect the fact that this is possibly a newer disease. It was first described a little over 100 years ago by Hutchinson.  And then 50 years later Horton described two cases of patients with giant cell arthritis systemic symptoms and he described it in a weekly Mayo Clinic conference. And then later described five more people and interestingly none of them had eye vision symptoms. So he and his colleagues, well, there's multiple names that have been proposed and probably the only one that's stuck is giant cell arthritis. But he and his colleagues ended up trying to find out there's an infectious cause. They ground up bits of positive biopsies and injected it into five healthy controls. They were aged matched and none of these controls ended up getting the disease. And then the last patient that they injected it into it wasn't in the scalp. The other five were into the scalp. The last patient, they injected it into her vein. And she did develop symptoms of fevers, malaise, elevated ESR. But because the other five didn't develop the symptoms, they concluded that it wasn't an infectious process, but rather some type of autoimmune process. By definition, temporal arthritis is an immune mediated vasculitis of the medium and the large vessels. And the vessels that are most vulnerable are the vessels of the cranial bed. And these include the superficial temporal artery, the vertebral artery, which is not depicted here, the ophthalmic artery, and the posteriori artery.  And so as I said before, the most common vessels affected include the superficial temporal, the vertebral, the ophthalmic artery, and the posteriori artery. And you'll find that this high incidence of occurrence in the vessel actually stops abruptly after it hits the dura. And the same thing happens with the central retinal artery. There's a medium amount of vulnerability, and then once it hits the dura, she loses some of its vulnerability to the vasculitis. And so the question is, why does this occur? And it has to do with histology. So we can kind of look at the artery and see that there's different layers to the artery. There's the intima, the median, adventitia. And arteries actually contain elastin. There's, I think, elastin in all three layers. And so in the vertebral artery, before it hits the dura, it actually is thicker, and it has a lot more elastin. So a lot more elastin in the tunica media and the tunica edentition. Here the elastin is darker staining. And then once you hit the dura, there's a lot less elastin. And so the amount of elastin actually correlates with how vulnerable the vessel is to vasculitis. And when you talk about temporal arthritis, you have to know that age matters. And there's a peak prevalence between 70 and 80. It is much more common in northern Europe. It's well-described in Scandinavian countries. And when you look at Europe, when you go from north to south, there's a decline in incidence. There's also a higher prevalence in women, so the ratio is three to one. And in population studies, and so this is a population study from Olmsted County, Minnesota, they not only found that the rate of giant cell arthritis is increasing over time, they also found this kind of cyclical pattern to things. And this average is out to be every five years. And because of this cyclical pattern, they have proposed that there could be some environmental trigger that is going on. And they have tried to match it with flus that have kind of a cyclical pattern. So there's a lot of viruses like perinfluenzovirus, EBV, chlamydia, other things that have been proposed to be a trigger for these cycles. So I just wanted to take a jab at the pathogenesis. And so thinking is that there's some type of virus or antigen that is triggering inflammation of the arterial walls. And the first thing that happens is that there's activation of dendrocytes. And then the dendrocytes, once they're involved, they spit out chemokines. And then the chemokines in some way actually causes fragmentation of the elastic lamina. So it brings us back to this elastin issue. And then once this fragmentation starts, this cascade starts with hyperplasia and then ultimately occlusion of the vessel. And when you occlude the vessel, you get symptoms. And so when you're taking a history, most common symptoms in giant cell arteritis by far are a new headache and jaw claudication. And the new headache can be this temporal artery, temporal pain, but the headache can be elsewhere in other places as well.  And then also PMR symptoms are basically kind of arthritic symptoms in the proximal joints. And I was surprised to find that there are a couple of symptoms that are super high yield in diagnosing temporal arteritis. So common symptoms that have higher likelihood ratios of suspected temporal arteritis was diplopia and jaw claudication. That's come up multiple times in the literature that if there's good clinical correlation, if there's double vision or jaw claudication, that really helps you out. In terms of signs and exam findings, everything revolves around the temporal artery. So there's high likelihood ratios if they've got a beaded temporal artery, they have a prominent or enlarged temporal artery, they've got a tender temporal artery or they have an absent temporal artery pulse. I don't think I've ever palpated somebody's pulse. And then of course, one of the signs that's very helpful is an elevated ESR above 50. And the upper limit of normal for ESR usually is defined at 50 millimeters per hour. But to be more accurate, for men it's actually the age divided by two, and for women it's age plus 10 divided by two. Unfortunately, the ESR isn't always helpful. And approximately 5 to 10 percent of the time, you may have biopsy-proven temporal arteritis, but actually have a negative ESR.  And there's other markers that can be helpful, including a CRP, which is more sensitive. And IL-6 is technically the most sensitive, but it's not commercially available and probably not as specific as the other two. In addition, you can have temporal arteritis without an elevated ESR based on the American College, the American College of Rheumatology criteria. So this was made in 1990. And all you need is three of these. So any three of this, you could potentially have three knots with elevated ESR and still have a yield of sensitivity of 93.5 and a specificity of 91.2. So I talked about diplopia being a very important question when somebody has good reason to have temporal arteritis. In terms of vision loss, by far the most common etiology is anterior ischemic optic neuropathy. So in this study of 63 or 64 eyes, by far people had swelling of their optic nerve indicative of an anterior ischemic optic neuropathy. And not only does this anterior ischemic optic neuropathy have swelling of the nerve, I tried to find one that showed pallor of the nerve. So there's a pallid swelling to it, not just plain swelling. And about 50% of people with temporal arteritis with anterior ischemic optic neuropathy will have this milky, chalky, white appearance to the nerve. So treatment of this disease, as you all know, includes steroids. And up front, it is IV or high dose PO steroids. And this is a long term treatment. So you start at one meg per gig per day for at least a month. And then as long as the patient is stable, they're tapered slowly over a course of six to 12 months. And I think this range is even wider, meaning that a lot of rheumatologists drag this out a lot longer. The prognosis from a vision standpoint, lots of numbers or big range, but the prognosis is between five to 34% can have recovery of vision. And this is recovery of two lines on the Snellen chart. However, if you start out at NLP, your recovery is probably pretty minimal. And so now I want to present some things that I think Dr. Katz had presented on earlier this year and what had been presented at NANOS. So the data that was presented previously was that there has been a strong association between giant cell arthritis and the strain of bacteria called Birkeldaria. And so previously it's been described that the Birkeldaria DNA has been found in the walls of patients with giant cell arthritis compared to controls who don't have the DNA in their walls. And so we've also found that an ELISA-4, this bacteria is found in patients with temporal arthritis and not in patients with control. And then this is another graph that depicts patients with giant cell arthritis and they're ELISA-titer for the strain of Birkeldaria. And you can tell from here that they have a much higher level than controls. And I think Dr. Kenig actually tested his blood and his value was about 50 picograms per milliliter just to give you a reference. So although I don't have time to go into some of the basic science research, we have been able to isolate the organism in vitro and show that it can activate giant cells and then activate giant cells by activating dendritic cells. And then Dr. DiDomenico, who's a hematologist and did a lot of this research, was able to induce a vasculitis in mice with this bacteria. And then she treated them with steroids and antibiotics. And treating them with both steroids and antibiotics seemed to help the mice do better than having them just be treated with steroids alone or without anything. So I want to describe a pilot study and the purpose of the pilot study was number one to find out if treating patients with antibiotics was safe and to use this information to build upon a later larger study. So inclusion criteria for the pilot study on human subjects was that they had to have a positive biopsy for giant cell arthritis. And they were enrolled either through the rheumatology or neuro-ophthalmology clinics. And they had to have a positive Birkeldaria, ELISA titer. And if they met the inclusion criteria, they were placed on minocycline or doxocycline for 30 days and then put on a steroid taper. It was either an individualized taper or a six month long taper. And then they were followed for whether or not they had relapse and if they had any side effects from antibiotics and then their inflammatory markers were followed as well as their Birkeldaria lipopolysaccharide titer. So in all we've enrolled six patients, I'll describe five of them because one of them is still getting treated. So in total there's been three males and three females and their average age is 80 and they've all had a biopsy that confirms giant cell arthritis. The first case was an 84 year old man with a new diagnosis of giant cell arthritis. His presentation was central retinal artery occlusion with light perception vision only alongside headache and jaw pain. And just take note that his initial titer was 538 which is high. So because of that he was enrolled in a study in place on an antibiotic for 30 days. And he's been followed for 16 months and in that time he's had no relapse and he's been tapered off his steroids completely after a total of 10 months. But he did have one side effect from steroids and that's avascular necrosis. He's been asymptomatic but this was found on bone studies. So this is a graph that depicts his ESR levels in red and his Birkeldaria lipopolysaccharide titer in green. And then this gray bar represents his treatment, the time frame that he was treated with minocycline. And you can see that both the titer of the bacteria and the ESR drops in conjunction with his remission status and after treatment with antibiotics. Case two is an 88 year old woman. She presents previous enrollment with a left frontal stroke and scalp tenderness. She actually had some question of whether or not she had genital arthritis in her past. But her presentation prior to enrollment was basically a stroke and scalp tenderness. And she had elevated ESR in a positive biopsy and again her titer was elevated at 521 picograms per milliliter. And she was treated with antibiotics. At month four after enrollment she did have a relapse and that's this asterisk right there. Her relapse with scalp tenderness, weight loss and elevation in ESR as you can tell from the rise in ESR right here. And so her prednisone was promptly increased from 10 milligrams to 20 milligrams. And because her Birkeldaria lipopolysaccharide titer never really dropped, if you remember the other patient dropped a lot lower, it never really dropped because of that Dr. Curry, her rheumatologist actually gave her another course of minocyclin. Just to see if it could come down and it did and it seemed to also match her ESR level. So next case is a 61 year old woman again presenting with the genital arthritis relapse. Her presentation was actually painful in cold hands when driving and she was found to have bilateral subclavian occlusions. And because of that she needed a write-up or extremity bypass and her carotid and brachial artery biopsies were sent to pathology and it showed up with giant cells. And so her, before enrollment, her Birkeldaria titer was also elevated at 513. She was put on minocyclin and she's been followed for about 10 months and in that time she did have a relapse that included jaw pain. And because of that her prednisone was increased. The interesting thing about her story is that number one she never really had elevated ESR throughout the time that she's been followed or at presentation. And she kind of constantly had left upper extremity pain with exertion. So it's kind of hard to tell if she was, you know, having smoldering disease. And so here with this ESR in red it just kind of reflects, so it's about 20. We just have to take off 1-0. But the ESR has been about 20 to 8 to 10 the whole time. And despite her relapse right here the ESR kind of stayed the same all the way through. However the Birkeldaria lipopolysaccharide titer has always been high. So it started out at 500. It didn't drop too low. Dropped about 300. And then you wonder if this number right here before the relapse was trying to hint at potentially her potential to relapse. But it's hard to say. And so case four is an 80-year-old man whose presentation was anterior ischemic optic neuropathy. And he was followed by Dr. Warner for about nine months where there was multiple attempts made to bring his steroid dose below 20 milligrams. I think there were like three trials to get him below 20 milligrams and every time he would have recurrence of vision symptoms. And he unfortunately also had severe osteoporosis with compression factors from the steroids and a bout of pneumonia which could have been from being on the steroids as well. So nine months after multiple attempts to get him below 20 milligrams for prednisone he was enrolled in the study. And he was enrolled because his titer was elevated at 590. And he was put on menocycline. And in about seven months he actually finally went below 10 milligrams for his prednisone. And at 17 months follow-up he has not had another relapse. His prednisone does his currently at 1.5 and he might be on that for a long time. And this is his graph of his ESR in red. And you can tell that his ESR also wasn't all that elevated for his age. So 32 was his presentation ESR. And his ESR kind of oscillates in different areas but kind of within the normal range. But his lipopolysaccharide titer drops and then stays low and is more reflective of his remission status than potentially ESR. And this last case is from the VA. He's an 87-year-old man with a new diagnosis of giant cell arthritis and he had sequential anterior schematic neuropathy. And here's that pallid swelling. He had a very elevated ESR with 74 and he had a positive temporal artery biopsy. And it sounds like within a week he had both eyes affected. His case was a little different because he got some heparin because he had such a severe course of the giant cell arthritis. But eventually he was placed on steroids. And again, his Burkle-Daria titer was elevated and so he was treated with 30 days of minocyclin. And at eight months' follow-up he did have a relapse while he was on a little dose of prednisone at one milligram. And his relapse was jaw pain and headache. And his steroids were promptly increased to 20. And once they increased that he had hallucinations and agitation and delirium while at a skilled nursing facility. And then this is his graph. This is his treatment with minocyclin. And you can tell that both the lipopolysaccharide titer and the ESR rise right at the point of his relapse. So this graph shows basically the peak Burkle-Daria titer for each case and the trough Burkle-Daria titer. And in this graph you can kind of tell which ones had relapse. So it was case two, case three, and case five that had relapse. And the two that did not have relapse were case four and case one. And they seemed to have the steepest slope of drop in this Burkle-Daria titer. And then also if you look at the cases that had relapse, the person who relapsed the fastest was the one who had the least drop in the Burkle-Daria titer. So we'll probably need more numbers to kind of sort that out. But the overall conclusions in this pilot study is that there have been so far six patients enrolled. And I guess five of them have completed the antibiotics. And out of those three have had flares. And so you might think that this is quite a lot of flares. And it might be, but when you look closer into how they were treated, they were actually treated with a really fast steroid taper. And most of them were tapered on a plan that was 210 days to be off steroids. And that's quite a lot. And when you look at rheumatologists, they kind of drag things out sometimes to one to two years. So this was a very fast taper. And that's probably why we got some of this signal. And it seemed like the ones that had flares had the smallest drop in the lipopolysaccharide titer after antibiotics. And none of these flares in these three people resulted in a serious complication. None of them had new ophthalmologic involvement. And none of them had any side effects to this antibiotic minocycline or doxocycline. Three of them did have steroid side effects like the avascular necrosis, delirium, and then the compression fractures. And then it seemed like even though the titers dropped, they still stayed elevated after treatment. They never went down to a normal controls level, which is about under 100 or 50 picograms per milliliter. So in conclusion, it seemed like adjuvant antibiotic therapy in patients with giant cell arteritis is safe. Perhaps this Berkel-Daria lipopolysaccharide titer could be a novel marker for monitoring disease. And then many patients with giant cell arteritis suffer from complications, severe complications from long-term steroid treatment between 58 to 86 percent. And perhaps therapy directed at Berkel-Daria, the strain of Berkel-Daria, may help some people taper off of steroids. And in order to answer that question, we definitely need a future study. And the goal is to have a prospective placebo-controlled multi-center trial of patients with steroids and antibiotics versus patients with steroids and placebo. And that's it. So I definitely want to thank Dr. Katz and Dr. Kenig for involving me in their research. And then Dr. Warner and Dr. Degree for helping me with everything. And then I don't think you've met Ivana. I kind of wanted her to talk today, but I don't think we had enough time. So not yet, but their steroids, their titers are high. But I think some of that still needs to be analyzed. Some of them, I don't think I went into it in too much detail, but Dr. Kenig, the rheumatologist, had extended their minocycline for 60 days. So I don't really have the results of that, but he's starting to do that. It's really hard to analyze because they were treated by outside rheumatologists. A lot of them were on methotrexate. And so that has to be accounted for, I'm sure, in the future study. I think just reviewing the charts, none of the rheumatologists here, because we have some of the controls that are treated elsewhere, those have been. But I can't tell you if they're doing worse or better.


Hi, everyone, Joe for Jaspy's casebreaks.com with 2023 Bowman's best university football. Yes, football in that Topps Bowman style. It's the eight box break, random player break number two. One spot gets you three players. It's a 25-spot break. Any dual multi-sign cards are going to be randomized between the players on the card, right? So the Bryce Youngs, TJ Stroud, Caleb Williams, triple, that would be a randomizer between those three. Because actually, Bryce Young and TJ Stroud are under the All Other Players Not On List. Nick Jaspy was letting me know that Bryce Young and TJ Stroud do not have base autos or parallels. So I think they're only like the specialty or insert autos like this. So they're in all the All Other Players Not On List. But most everyone else is, including the players that we'll probably be looking for next year, like Caleb Williams. All right, so big thanks to this group. There's the original 25. That's what we're going to use for the promo, too, the original 25 as we always do. And then we'll triple you up. So there are all of the names. Let's get them into the first list. And there are all of the players. Let's get them into a different blank list. And then we'll use the first tab right here for the randomizer results. Let's roll it, randomize it, six out of four, 10 times for names and players. One, two, three, four, five, six, seven, eight, nine, and 10th and final time. 10, right? Yes, 10. Got Jeremy all the way down to chat. Six out of four, 10 times for the players. One, two, three, four, five, six, seven, eight, nine, and 10th and final time. Six out of four, 10 times, 10 times. We've got Clayton Toon down to Nick Singleton. So I'm not going to read all of these names. Too many names. Got to preserve my voice for tomorrow. For Thursday. Tomorrow's my Friday. All right. Geez. Week went by fast. Here's the first part of the list right there. Jeremy Port without all other players. Spot. So I'm going to show you just the list as is just because I want to get it on this recording. Put it on Wax as they say when they used to put things on Wax. Do they still put things on Wax? I guess they're still vinyl records. There's everybody right here. And now I'm going to alphabetize by your first name so you can see all your players grouped together. So Chad Cromwell, you got a bunch of players there. They are nice. Bonix, Caleb Williams, it might be, could be some first round picks next year. Dorian Thomas Robbins from PCLA was drafted this year. You got Hendon Hooker, Ed P. They're your players, right? You got some Kool-Aid right there. He does have a Kool-Aid NIL deal. I think that's what Gabe said yesterday. Anyway, you got Will Anderson. There's Eddie with your players, Jason Kaye, Jameer Gibbs in there as well. There's Jason Parker with his players, Nolan Smith, Jeff Han with a bunch of players right there. Who jumps out of it? Madison, BJ O'Jallari, Stetson Bennett, Jeremy Port, they're your players right here. Got the all other players not on list. So that does include Bryce Young, CJ Stroud, got Yerkovich, Joe among the others. There's Anthony Richards in Matt's group. Graham Mertz, Cameron Warden, Scott's group, Stephen Kaye with a Bijan Robinson in his group. Got Aiden O'Connell, Veraders. There you go. More than Aiden for my Raiders. There you go, gang. I'm going to pause the video. When we come back, we're going to see if there's any trades. Then we'll have the breaks. Stick around. BRB. All right. Welcome back, everybody. No deals were done, so the list remains the same. I've re-alphabetized it back to player names, so it's easier for me to spot right there. I appreciate that chat. Yeah, I know you'd be all in on a million dollar bounty. One day, we've got to move more of these best university cases if we're going to save up for a million dollar bounty. Get that bounty money going. More of these best university cases. All right. Good luck, boys and girls. Each mini box will contain one auto. The usual best format. Bowman's Best has two autos per mini. Baseball, doesn't it? I think it's finest, which just looks like the same shape boxes has one. Anyway, two autos a box in this set. We haven't kept track of baseball scores today. Let's whip around the league while we're doing this football break. Celtics. There's only one playoff game, basketball playoff game today. Celtics smoke the Sixers with Joelle Embiid, so I don't know. That's interesting. We'll see what happens there. Series is tied 1-1. Rockies beat the Brewers 7-1. Royals beat the Cardinals 6-4. I think Ohtani had 13 strikeouts and like five innings or something like that.  Red Sox beat the Blue Jays 8-3. White Sox beat the Twin 6-4. Yankees and extras edged out the Guardians 4-3. Nationals beat the Cubs 2-1. Rays beat the Pirates, the 20-win Pirates, believe it or not. Braves beat the Pirates 8-1. Tigers beat the Mets 8-1. Braves beat up on the Marlins 14-6. Padres 1-1. One runs the Reds 7-1. Dodgers on a Max Monti walk off Grand Slam beat the Phillies 10-6. They sweep the Phillies and then they go on the road to face the Padres. Go down the road to face the Padres. Giants beat the Astros 4-2. Diamondbacks beat the Rangers 12-7. Tigers beat the Mets 6-5. And the A's are currently leading the Mariners 2-1. Bottom of the A's. Jalen Carter. And all-card chip in this as well. Xavier Hutchinson to 1-50. That will be for Stephen K. What happened in that game, Nick? What happened to the Brewers? They shouldn't be losing to the Rockies, right? A 4-on-4. That'll do it. Fight song Will Leviss. Bass Will Leviss. Milwaukee only got 5 hit by Kyle Freeland among others. That's a decent season for Kyle Freeland. Not a bad start for Eric Lauer, but their bullpen really didn't help him out. Rough train ride home for Nick and the crew. There's Trenton Simpson. T. Simp. Simp 22. That will be for... For Joe. For Joe Uber. There's a speckle, Hennan Hooker. There's a Bryce Young. Jordan Addison. Jordan Addison. Going to Jeff Hennan. Just had 2-50, Jeff. Bryce Young going to the All Other Players spot. And there's Tavionne Thomas. That will be for Jason K. This could be one for the future, Chad Caleb Williams. He's got the hype now. But, you know, obviously, one season can go by and that could change everything. I mean, this guy pretty much only played one season, right? So the stock can rise and fall really quickly during the call of the season. Rex has some trivia for us. How many walk-off grand slams in MLB history? In MLB history? Regular season walk-off grand slams? I did. I had a four-unit play on the Red Sox yesterday, Jason. I had one of my best baseball betting days yesterday and I pretty much... And I was doing very poorly in April. And I think that one day kind of made up for it. So I didn't do anything today. I might have some plays for tomorrow. But I had a four-unit play on Boston. It made me sweat out a little bit. I think I have to thank Connor Wong for a late inning home run that broke the tie and ultimately gave him the win. It was close. They won again today, too. This is from 1876 to May 2nd, 2023, so it does not include Max Muncie's today. I mean, I wouldn't even know where to start, Rex. Is it over or under 10? And maybe I'll try to guess from there. Thanks for asking, Jason. I appreciate it. I do have my April record posted on the Joe's Picks tab. I will keep that updated as much as I can. I haven't really done the daily updates as well, but I got through April... That record is just through April. Through April, I'm only 40 and 64 with a 38.46 win percentage. I don't mind the win percentage. As long as I'm plus units, I was minus 8.28 units. But I think after yesterday's play, and I won a bunch of other games, too, I think I'm now plus, like, two or three units now. So, now one day, making up for the month, it was kind of nice. Got to pick my spots, though. Dave Barros, what up, man? Guessing 27. It's between 200 and 300? Wow, that's a lot more than I ever thought it would be. Walk-off grand slams? Yeah, I don't know. 206. Where are you getting this information, Rex? Sometimes you have to fact-check, Rex. From the first opening day Major League Baseball history, back in 1876 through May 2nd, 2023, there are 278 instances of players hitting a walk-off grand slam according to baseball almanac. Wow. That just seems like a lot. There's Peyton Thorn. That's for Jeremy Port and Peyton. I guess it's 150-some odd years of baseball and I guess that's about two per year, Scott saying, good math. Yeah, so I mean, I guess that makes sense. That's an average of two-ish per year, so I suppose I should have used logic, but I didn't. I should have been like, how many seasons of baseball have there been between those years? I would have just guessed one a year. I probably would have guessed 150 or something like that. All right, good trivia, Rex. Good trivia. This is a radar right here. Marcelo Meyer? No, that's a baseball player. Michael Meyer. Michael Meyer is not on this list. It goes Mason, Mitchell, Nathaniel. So that goes to all other players. It goes to Jeremy Port. So to CJ Stroud, Will Anderson will go to Ed P. There's another Tevion Thomas that goes to Jason K. Nick, they're not always very good. So we gotta really appreciate when they are good. Credit where credit is due. Good trivia, Rex. Well now we want more. This is good trivia. It would have related to the Max Muncie Grand Slam walk-off, pertinent to the conversation, in the right lane. Good timing on it. Fooled everybody. Everyone learned something. David, what did I guess? I was saying, is it over or 10? Over under 10? Bear is only guess 27. But I guess if we thought maybe one a year, we should have been able to logic our way out of that. Should I bust out a... I should bust out a... trivia. A bit of trivia that I have not... that I have not asked this question in a little while. But after Rex's next trivia... Who has the most Grand Slams in how many? I could tell you who has the most Grand Slams in a single inning. That would be Fernando Tete Sr. Against the Dodgers' Korean pitcher Chan Ho Park. Park Chan Ho. Two Grand Slams. One inning off the same pitcher. Fernando Tete Sr. And David says, what was the year that had the most walk-off home runs? I say most Grand Slams. Jim Tomey. James is guessing Manny Ramirez. There's Ramon Davis. Aqua Lava at a $1.99. That will be for... Jeff. Caleb Williams for Chad. Any other guesses for the trivia questions in the chat? And what was the year that the most walk-off home runs? I would say somewhere in the 90s. Jaron Hall. Jaron Hall will go to Jeff Hennan. And how many Ultimate Grand Slams in baseball history? Well, I would say like... I would say a thousand Grand Slams in Major League Baseball history. A-Rod had the most Grand Slams at 25? Wow. What about the year? What about David's trivia question? And what about Chad's Ultimate Grand Slams in History question? Oh, and a Hennan Hooker autograph. Ooh, that's kind of a cool... I don't think I ever realize what Hennan Hooker's autograph is going to be. For a two-letter autograph, I think that looks pretty sharp. That goes to Chad and the Hennan Hooker spot. We'll also get this base card. Oh, how many... Sorry, I missed that chat. How many Ultimate Grand Slams in Major League Baseball history? I've never heard of Ultimate Grand Slams, by the way, is defined as a team down by three and hitting a Grand Slam. Man, he had 21. Here's a Bryce Young speckle, not numbered. I have no... Well, if there were... What did Rex say? How many walk-off Grand Slams were there? If there was 278... Ultimate Grand... I feel like that situation can't be too common. Or as common. Or would it be more common than a walk-off situation? Maybe it's more common than a walk-off situation. So I'd say... 400 Ultimate Grand Slams. In 87, Don Mattingly set the record for most Grand Slams in a single season with 6. And they were the only Grand Slams of his career. Wait, Ultimate Walk-Off Grand Slams? Alright, so if Rex was saying there were just 278 walk-off Grand Slams in general, I would think the number has to be less than that. So then I would say 195. Specifically, the situation where a team was down by 3 and walked it off with a Grand Slam. 32. So all other situations were 2 runs. A 2-run difference or less to walk it off. 2-1 or tied. No, in one inning, Chad. Yeah, Rex is talking about how Ventura charged the mound and got 6 hits from Nolan Ryan's fist. Very ill-advised. Ventura, at the time, I think was a young punk. And Nolan Ryan, yeah, he's ornery. There's 158 out of 199. Henry, 2-0, 2-0. Henry's going to go to Matt.  Another Hendon Hooker. And a Justin Ademiola. Justin's going to go to this list. He's going to go to Chad. It's a 75, Chad. Yeah, Chad, do you not remember the video? And Nolan Ryan won that handily. And Payton Thorn, gold autograph. Another Payton Thorn for Port. 10 out of 50. How was Hendon Hooker the QB of the future when he was only three years younger than Jared Goff? As Indiana Jones says, James, it's not the years, it's the mileage. Less mileage on Anthony Richardson. And how long's Goff's contract? I don't think that long. Did Nolan Ryan actually say in the game? That's another bit of trivia. I don't think he got ejected, right? I feel like the ums were like, well, he charged first. Yeah, it was... Today, the story is the reason why I think Nolan Ryan even threw at Ventura was because Ventura had kind of pimped a home run off of Nolan Ryan in spring. I don't think it was even off Nolan Ryan. I think in spring training Ventura had admired a home run or kind of pimped a home run a little bit. And I think Nolan Ryan was like, he didn't like it. And he was determined that he was going to plunk the kid or kind of throw at him if he ever saw him. And he did. And then Robin Ventura was taught a lesson. Ah, was it White Sox pictures constantly hitting batters so the Rangers had retaliated? Yeah, there was history there. It wasn't just an isolated incident. So here's some trivia.  There's a baseball diamond. The reason why lefties are called south paws is because most stadiums are oriented where a left-handed pitcher this way his arm would, his left arm would be pointing south. So most baseball stadiums are kind of oriented where home plate is either pointing south to southwest. Right? For the most part there are only one two three four. There's only four NL ballparks where they don't point south or southwest. What are they? Let's see how many people know their ballparks. So there's only four ballparks in the NL. We'll go AL later. Only four ballparks in the NL. I've done this trivia before so for you long-time listeners, forget it, but I feel like we got some new people here. Four ballparks that don't point south or southwest where the, where home plate isn't pointing south or southwest. No NL stadium goes southeast, by the way. No stadiums are oriented this way. But there are four that are kind of like this way. There's Jermaine Burton from Alabama that's going to go to chat. James is saying Braves Reds Pirates. Yes, Brave Stadium points this way, northwest, like that. Did you look it up, James? Reds Great American Ballpark also pointed like that. Pirates, PNC is also pointed like that. There's one more. Yep, easy note has got it. And James got two. Brewer's Miller Park is oriented like that. All other stadiums, either that home plate's pointing directly south will point south or in between south and southwest anywhere around there. In the AL there are one, two, three stadiums. Yeah, the giant stadium the giant stadium points straight west like that. But there are three stadiums in AL that are pointed not southwest that are pointed northwest like this. No stadium goes this way, by the way. All stadiums are oriented either south to southwest. A few are this way. Three AL stadiums. And there's Doran Travis. The reason I think they're pointed in that direction is the sun in your eyes. There's Doran Travis to 99. That'll be four Chad.  One, two. Yeah, three AL stadiums are oriented a little weird like that. Don't look it up, try to think of it. James looked it up. James is right though. Camarica for the Tigers. Home plate points northwest. Guaranteed rate field for the White Sox. Home plate points northwest. And the Rangers stadium also points northwest. We're trying to play trivia, James. Trying to test your knowledge. Not seeing who can look it up the quickest. Jayden Reed. It's all good. It's interesting, right? I don't think people would have gotten it right away anyway. Jayden Reed that goes to Ed P. Three boxes to go. Yeah, actually, globe life points northwest. I'm looking at baseball almanac. So, globe life does not exist anymore. So, I don't know where the new Rangers stadium points the same way. But see, I think if you're in a dome that's a lot of times those dome stadiums will kind of point in a different way. But usually, most games are pointed that way because of because of sun issues. You don't want to get sun in people's eyes during day games. But yeah, most baseball stadiums are naturally oriented where southwest. So that's why when a lefty's on the mound their left arm is usually south. Southpaw. Now, for instances like I think for like the for like the San Francisco Giants stadium the home plate shoots directly like home plate to second base that line is directly east-west which which may create a sun issue when the sun is rising the sun sets in the west. So I guess the sun would be behind the stadium so it wouldn't be in the pitcher's eye because that's where the rest of the stands are right behind there. But I guess there could be a point during the day where the sun would be right in the pitcher's eyes. But I think the reason for that it's not common but the reason for that is because they were building the stadium right along the water. So I think the geography kind of dictated the stadium there.  So does the sun get into the pitcher's eyes? Zach Harris into 75. It's probably not a good thing. Like during a day game that runs late. I guess games don't run late anymore. Here's Zach Harris in Lava. He's going to be for Trevor. So if they start a one o'clock game that it'll be done by three anyway so that's not going to be a problem. And even national games will probably start like at five o'clock Pacific. I think that could be a problem if the sun sets at around seven. Caleb Williams speckle for Chad. Here's his rival Dorian Thomas Robinson. And here's a Caleb Williams autograph. This is what Chad was asking for. He's like hey while we're serving you can you pull me a Caleb Williams auto? Sure. Why not? 14 out of 50. You need to hold on to this one Chad. Tull around this point next year. And hopes that he has like a Heisman award-winning season. Here's Ramon Davis to 150. That will be for Jeff. I got you. So Barrows is also saying they built it in a way that helps block the wind as well.  Do I see him? I need to look up some tiktoks of that. Need a choo choo for Caleb Williams? Train whistles are for out of fives and under. Here's another Peyton Thorn for Jeremy Port. And as a UCLA fan I don't know if I could give Caleb Williams a train whistle. I don't know. I've told the so-called expert and I don't watch enough college. I'm obviously not a football scout. A lot of a lot of the so-called experts seem to think that Caleb Williams if he does, you know, what he's expected to do in this year of college is supposed to be top 5, top 10 pick or first quarterback off the board. What if the Dolphins draft Tua's brother? That'd be kind of funny. Which I suppose is possible I guess. We don't know. I mean I'm hoping for the best for Tua's health. Candlestick. The wind was crazy there. Ah Chad's, is that trivia Chad? Per the CDC research which sport expands a person's life expectancy the most will help you live longer live stronger and longer than all other sport activities. I say I say walking. Speed walking. Swing is a good one Dave Varros. I like that. I want something low impact and higher heart rates. That's what I'm going with. A light jog. 30 minutes a day. That sport. Yeah. American football. Jess James I guess. I don't know about that one. Wow. Racquet sports? Tennis? Badminton? Racquetball? That's my score. I grew up playing a lot. I still play some tennis not as much but there's Tizwan Harry Tizwan Tizan Harry. That goes to Joe. Joe you. I do enjoy the tennis. I suppose that's because it's what yeah. Racquetball is a mini court. High bursts of energy running around swinging swinging something. A lot of short bursts running. Not a lot of sustained running that could damage joints. There's a Hinden Hooker 149 out of 199 Aqua Lava going to Chad. I enjoy the tennis. I just don't know a lot of people who play a lot of tennis in my peer group. A lot of golfers though. Where's golf on the list? Will Leviss If you don't take a cart we'll have a speckle that's going to go to it's going to go to Trevor. And Cade McNamara Cade McNamara will go to Cade will go to Chad. I'll guess by how many years tennis to add to your life? On average person on a casual basis only what's casual like? What a couple hours a week? It is a good exercise. Short bursts of running and then rest. Short bursts of running rest. There's like interval training. Golf is not considered sport. So it's not a what? Golf's a sport. I said 10 which I feel like is a lot. But I'm shooting the moon. 9.7 Look at that. Giving myself the hit on the bell. There's more tennis players out there. Let's go play some tennis. See this is what I do with a box check so I don't lose a pack. Did Tennessee release Malik? Well it's no not at the moment. I feel like they're more inclined to release Ryan Tano before they release Malik Willis. I have 2 QBs under 2 QBs under rookie contract. 3 is soccer. 4 cycling. 5 swimming. 6 jogging. 7 just general calisthenics. I do like swimming. I enjoy the swimming. I could do that. Weather needs to get a little warmer though. Soccer I played a lot of soccer too but I feel like I definitely gonna pair an ACL playing soccer. Rob Lowe was a great tennis player back in the day. I feel like I feel like that rings the bell. Rings a trivia bell. Was he like ranked in Southern California? I think he's from California. Was he like a ranked youth teenage tennis player? Masterpiece is Speckle C.J. Stroud Young Refractor for all other Jeremy. I can't believe they kind of unless Tennessee is thinking they're gonna have a Tray Lance Brock Purdy situation here's Nathaniel Dell it's for Jeff. I was a little surprised that they I was a little surprised that they went with I don't know what they maybe they end up trading Malik Willis. They always take more sugar and calories and they lose in no cardio. What about what if like no cart no cart all walking carry your own bag kind of golfing. See most people just drink beer and ride a cart all day long. 78 out of 99 Dontavian Wicks that'll go to the all other player spot. What was the case hit? Looks like an outlaw poster. No that's not a case hit. Those die cuts we see a lot of like these. Those are pretty common.  That goes to Jeremy Port. Name that tune. It's Clayton. And there's another Henden Hooker right there as well. Scott can see them trading Willis when some teams QB goes down. Actually that's a good point. And just keep hanging out to Malik Willis until a team loses a quarterback which happens every year someone and then you make that call. All right gang here's the recap. There's the Caleb Williams which is pretty nice even though he's a USC guy. Some Bryce Young's got a Henden Hooker as well. Not too shabby. Hopefully these guys if they're drafted hopefully they become pro all pros. If they're not drafted hopefully they're future first round draftees. There you go ladies and gentlemen. I'm Joe for jaspyscasebreaks.com Thanks for watching. Thanks for breaking with us. I'll see you next time for the next one. Bye bye.


When you are in the hole, the way starts in the hole. It could be changed. When you are in the hole, the way starts in the hole. You add H-O-L-A, add W to H-O-L-A-E. To express the fact that we have to start with what we are. With the total day of our being, with all we have. But what we have is often defined by our personal history. And this personal history becomes fully useful only once we are ready to integrate it, accept it, and let go of it. With every new experience, I have the power to redefine my past. I am alive and well. The past has brought me to good place. The present is mine. My past has brought me here to the threshold of a new life. Blessed be my past. The future is unfolding its new path. Blessed is the promise of life. I now release my past and all its judgments. I am now ready to embrace the present and receive its gifts of life. The past is not a burden. It's a scaffold which brought me to this day. The path is now open to my full express of life. I now release everyone in my past. I am free to go wherever I want. I am free to become who I am. I am giving myself permission to redefine myself beyond my past history into the fullness of life. The past is past steps to a fuller life for me. The past is gone. Blessed be I can now close the door and move on to the other ways of being. I am not my past. I am not my present. I am that which I am becoming. I now create my own life out of past, out of the present. I have the power to reach into the past according to my own needs. It is good for me to remember all that I am, to harvest the blessings and knowledge of my life. Drivers are to be perfect and allowers are to be yourself. Drivers are to hurry up and do things, take your time, allowers. Drivers try hard, allowers to do it. Drivers please me, allowers consider and respect yourself. Drivers be strong, allowers be open and get your needs met.


Thank you all so much for coming here and to Peace Action Maine for so graciously inviting me So as you probably know, or perhaps you don't the topic I'll be speaking on progress the idea of progress and specifically What is the measure of progress in everyday language and understanding? Progress is taken to be a self-evident good Desirable by all humanity The very idea of progress its practice its implementation its power has been justified Indeed made a necessity by the conviction that its spread will herald a new era of peace and prosperity in the world Despite the reservations that have been articulated more recently and for all its imperfections and failures It's full realization is the goal to which we ought to aspire If one is to assume then indeed self-evidently that this is true What is it that progress has brought in its wake that is indeed self-evidently good? As many point out of course correctly humankind is today at the historical peak of its possibilities in the sense both of shaping the world and directing its trajectory Economic resources are greater than ever before Material extreme poverty has been substantially reduced in much of the world There have been massive advances in scientific technical knowledge most notably in medicine and its curative possibilities and effects Human rights law universally applicable has for decades granted formal equality between and among individuals of all races genders and among those with other differentiating ascriptive characteristics and Finally though of course not exhaustively relatively seamless communication and engagement with people's all over the world has now been made possible on a scale previously unimaginable So yes progress has been all that of course Yet it has been much else and has brought about much else This lecture will address that remainder the much else which remains largely unspoken the world and most recently and in the present moment what is referred to as the third world or The global south which exists of course also here in the north has been subject to this Imperative the imperative to progress the necessity of progress as a means to Emancipation if not Liberation the term developing countries is in fact an indication of precisely that These countries are developing along a continuum whose ultimate objective is to become developed So what has this involved? What have been its harms hidden and revealed? What has progress brought about for millions even billions of people across our shared earthly terrain as Many will recognize in much of the world the march of progress has also entailed an extraordinary violence across several registers cultural temporal psychic and material This propulsion forward or is it backward has in the most generous interpretation unintentionally led to the eradication of Hundreds of languages societies ways of life cultural practices Simultaneously or indeed as a consequence the peoples of the world now inhabit life forms more uniform almost Indistinguishable on a scale Unprecedented in its global reach though here one hesitates to use the word Unprecedented so banal has it become in its sheer repetition We would do well to recall that progress and its gift Modernity has swept everyone in its wake and the ravages of modernity Precisely in its completeness is made the most apparent in the places of the world where we perceive mostly its absence One thinks for instance of the assumption that parts of the third world remain pre-modern or primitive It is here after all that the majority of the excluded billions live as Though somehow they have not caught up with the time in which they find themselves as though in fact it is possible to live in this time and Simultaneously outside it in a parallel or perhaps even backward temporal universe an Assumption that fails entirely to consider that not a place on earth has been left untouched by contemporary systemic forms of power and coercion intervention and subordination violence and exclusion To take only the most obvious example No, people have been spared the experience or minimally the effects of colonialism or that most modern of forces capitalism So whatever failures or insufficiencies indeed perversions of modernity We witness have perhaps to do with the place to which such areas have been relegated in the contemporary hierarchy of power not in fact their position outside of it and Yet the triumph of progress its conquests and successes are what we are told what is insisted upon Its damages are less evident its casualties even less so Among the least violent instances One thinks of the linguistic hierarchies produced in much of the formerly colonized world Which have resulted in nothing less than class apartheid From Algeria to Pakistan Fluency in the colonial language French and English respectively is a mark of distinction Enabling membership in the elite classes comprising of course only a tiny Minority far above the millions or even billions who speak the native language or even worse The languages referred to with only barely veiled condescension as a dialect or vernacular No longer even dignified with the appellation language or In another instance the designation as native or traditional the garments worn in these societies for centuries as Though to have progressed sufficiently to have become fully modern people must adopt and routinely wear so-called Western attire only Resorting to traditional wear on special occasions the occasions themselves Often the sign of a culture soon to become obsolete the last vestiges of which relegated to those who are doomed to never so to speak catch up To illustrate using one more approximate example in His insightful book radical hope ethics in the face of cultural devastation Jonathan Lear tells the story of the crow nation In giving an account of what occurred when his tribe was confined to a reservation And the buffalo had been led away The chief of the nation says quote The heart of my people fell to the ground and they could not lift them up again He concludes by saying somewhat enigmatically quote after this Nothing happened What does such a phrase mean after this nothing happened How could anything not happen? Did history or perhaps life come to an end even as it continued There is something more to this confession The disclosure possibly of a form of dispossession that empties the world of meaning in This reading progress may be interpreted as a rather cruel desertion an abandonment of those not able to keep up with its pace or demands or not fully inhabit its potential on Whose part after all and in the name of which power Should we not be forced then to at least also speak of loss Or at least take a moment to reflect on what costs have been exacted on whom and Where and perhaps to recognize that progress has never looked especially Promising for those who find themselves in its way Indeed the idea that there is no limit to what human beings are capable of may now sound to some More like a threat than a promise All this is not to say before the charge is even made that these other forms of life Indeed other life worlds were idyllic much less an untainted innocent paradise It is however to say that too much remains obscured from view That perhaps to sever some forms of attachment is injurious possibly fatal Including those attachments which appear irrational and possibly even self sabotaging and that this too must be taken into account in any narrative of progress as pure liberation and It is also to say more essentially that these peoples and worlds did not have the hubris or perhaps only the means To inflict or bestow their cultures practices languages traditions on the entire planet and That too in the name of good of universal emancipation It is also to point out that the wiser thinkers of the ancient world did not profess faith in progress as a temporally chronologically determined improvement in the conditions of human life Think for instance of the Roman stoic philosopher Seneca who believed in progress as the human capacity for the Expansion of knowledge, but did not expect from it any improvement in the general community of humankind Such humility if one can even call it that or helplessness is worthy of reflection What makes our moment our world such that we believe unequivocally that the world must without resistance or a resistance made futile submit to it or ideally fall enthusiastically into its embrace with the conviction that such submission will enhance the well-being of all the world Given its dominance and more importantly its implicit hierarchies For the billions left out of this triumphant March Those who remain insistently or without a choice on the peripheries or for those who have Insufficiently moved along this hapless yet quite clear trajectory. We have little left, but derision or even worse pity We can only think or to be certain as a matter of historical fact That those who live in this moment who exist however precariously in this time Do not in fact have a place in it these people the benighted Majority uninvited to join this exalted mission who live in this time Where else indeed would they live? belong elsewhere in a history long lost or relinquished as Though they are suffering from a lack an absence as if they no longer Correspond to this time or that time is hurtling towards an end to which they can never hope to arrive It is to treat living people as if they were their own ghosts as good as already dead Haunting the modern present as if already banished from the world Hoping in the manifest destitution of their condition for their own exorcism The structures of the modern world perhaps like the pre-modern, but we all know how terrible those were Seem routinely to produce such superfluous and marginalized communities These are not exceptions as we often think or are told but rather the consequence of a structure of power that necessitates subordination on the part of majority populations it matters very little what form they take within developed or developing societies as Effects or products of an increasingly voracious capitalism a system itself predicated on Untold exclusions or within broader systems of total control and Given the means at our disposal these people and countless others can be dispensed of in unparalleled numbers in The most spectacular example World War two which occurred principally of course in the most modern and developed of all societies World War two resulted in as many as 80 million deaths 80 million to say nothing of the manner of those deaths as Original and stunning as unspeakably horrifying One would like to say inhuman But sadly they are perhaps and only all to human in More recent memory the Cold War so terribly and misleadingly named is The perfect example of the hierarchy of power and of life that seems so Indelibly etched in our collective consciousness This period of several decades from 1945 to roughly 1990 Widely regarded as a time of peace because the two then most powerful countries Managed to resist mutual destruction and seemed instead content to wage their wars elsewhere Where perhaps the absence of peace was incidental or maybe irrelevant This period was among the most brutal in much of the developing world Against received wisdom and very much on the contrary These decades were marked by widespread and devastating war the so-called proxy wars and not only those Waged between the two superpowers Resulting in millions of casualties even more refugees and displaced persons and Before we dismiss this as ancient history We need to recall the enduring legacy of these wars Consider for instance the landmines that still kill and maim Thousands from Laos to Afghanistan most of them children So how are we to evaluate this period and its characterization? Disgracefully referred to by some historians as the long piece What allows such an appellation and how even in the abstract does this have to do with progress? and its valuations There are other examples One thinks of those who bear the costs of one of the signature if collateral consequences of accelerated progress We are living now in the Anthropocene In other words our present geological age is the first in which Human activity has been the dominant influence on the climate and environment This has had the effects it has with which we are now all too familiar Despite the insistence of some in this country that it is a fiction or to quote one presidential contender Climate change as a hoax invented by the Chinese to undermine the US economy Such a dismissal is only possible in a context that is spared the most brutal effects of this scientific fact It is the world outside Structurally and repeatedly consigned to irrelevance which suffers its worst consequences as In India to name only one of literally innumerable examples Where over? 300,000 farmers have killed themselves in the last 20 years 300,000 farmers have killed themselves in the last 20 years The causes as with everything are complex But have minimally to do with repeated droughts or conversely excessive rainfall Both leading to successive years of crop failure with farmers having no option but to resort to bank and private loans resulting eventually if predictably in crippling debt and For all the talk of India as a rising power of having progressed at a marvelous rate Agriculture remains the single largest employment sector with 70% of India's 1.2 billion people living in rural areas Areas that have long been made uninhabitable for reasons apart from climate change of course But with climate change too as an effect of the rampant modernization spawned and implemented over decades of development policy Then more visibly there's the story now haunting the world of Syria of Iraq Though the latter given our chronic historical amnesia has faded virtually entirely from memory Despite its almost complete ruin In Syria then Aleppo One of the world's oldest continually inhabited cities The mention of which left one third-party candidate utterly mystified in Aleppo then suffering from the misfortune of its geographic location Modern warfare has done what successive invasions failed to do throughout the ages Laying waste to half the city This ancient world heritage site as it was designated by UNESCO is Now threatened with total Annihilation We have come so far that one is tempted to say that this inexorable advance of progress has no end in all senses It will both continue and also have no definable goal We see now some of its less benign effects The proliferation of means making possible the destruction of the world and that too many more times than once Structural enduring inequalities in wealth opportunity inclusion the total conquest of nature The almost complete devastation of social relations communities and bonds a Denuded morality a concept which appears now in anachronism Insistently lingering somewhere in the shadows associated only with the worst conservatism as a relic from another time once Defined by a sense of restraint a time that must urgently be left behind The collapse of any substantive politics or the possibility of participation in the political process No matter how democratic a term itself that has long been evacuated of meaning and yet remains one of the signature marks of progress The hierarchies of life Human life above the world of nature of course, but also of certain human lives certain forms of living above others So in light of this not to mention colonialism total war genocide totalitarianism, etc Is it possible to be consoled by the thought that progress will one day in the indefinable future? Close yet so far Free us all entirely from what apparently constrains our full human potential Should we not instead conclude that the brutal violence inflicted by human beings under any name? Torture slavery genocide Cannot be consigned to the past like exhausted theories in science They simply return in a different guise and Given the means now available to us It may be easier to imagine the end of the world than any significant improvement in it There is also not the ancillary fact that the idea of humanity itself seems a fiction Composed as it is of billions of people for each of whom life is singular unique and naturally final So what would it mean to speak of a general progression of a general progress? Encompassing every single one of the seven billion human lives now present on earth as Appears increasingly true Human beings have been blessed or cursed depending on the moment with a seemingly limitless capacity for enhancing knowledge While being chronically incapable of learning from it or from experience One such edifying realization might be that there can be little progress only an Unending struggle with our own obstinate nature Paranthetically psychoanalysis which is both an intellectual project and clinical method has largely fallen into Disrepute no doubt in part because of its avowed admission of the limits of human agency Nevertheless psychoanalysis wisely though in what now appears to be a wholly futile gesture Tried to inform us that human beings can scarcely be masters of their destiny We might instead come to view the idea of resignation as a virtue Though resignation has long been considered a form of weakness and even worse submission as if through sheer will Itself hardly a constant or even definable force We might alter the conditions of our own existence or even more brazenly Imagine that we can change those of humanity at large Freud suggested that we come instead to understand the determining role of fate and history in our lives While also affirming a more modest ambition Namely effecting a minor change in our orientation Toward that fate as also toward our place in the social world Finally a Few words on the link between progress and peace if indeed there is one or maybe one Quite apart from this only very partial chronicle of warfare and dispossession Peace is invoked by everyone Not least those governing affairs of state national and global who repeatedly tirelessly profess an absolute commitment to peace while inflicting the worst atrocities in its name There are of course countless others with less cynical more benevolent intentions but given the ubiquity of the word in the mouths of everyone Should we not be at least a little suspicious at every moment of its enunciation Should we think instead in light of what has occurred and more of the same likely to come That even if we assume human progress is an evolutionary process a movement of space within time of time within space of which peace may be a part that Progress is a process that may well be going nowhere and Still as John Gray reminds us in his remarkable book the silence of animals To suppose that the myth of progress could be shaken off would be to ascribe to modern Humanity a capacity for improvement even greater than what it ascribes to itself I'd like to end with one of the canonical readings of progress Which seems only to become more prescient with the passage of time Though it was written at the very pinnacle of human debasement the mid 20th century The German Jewish essayist and philosopher Walter Benjamin writes then of the angel of history Whose face quote is turned toward the past Where we perceive a chain of events he sees one single Catastrophe which keeps piling wreckage upon wreckage and hurls it in front of his feet The angel would like to stay Awaken the dead make whole what has been smashed But a storm is blowing from paradise It has got caught in his wings with such violence that the angel can no longer close them This storm irresistibly propels him into the future to which his back is turned While the pile of debris before him grows skyward This storm is what we call progress


Hi everyone, I'm Arianna Longley and I'm the Chief Operating Officer here at the Patient Safety Movement Foundation and I am here today with Dr. Benjamin Wang to do an interview around ventilator associated pneumonia. And so we have a great interview set for you all today to learn a little bit about Dr. Wang and also around some of these policy issues that we think that we might be able to achieve and we hope that you all who are listening in today might have an idea how we can push this forward and we know that in order to improve patient safety we have to get everyone involved and if you're out there listening and have an idea put your ideas in the comment box below here on YouTube, send us an email and get engaged. We really need to think about this in a new way and really pleased to be with Dr. Wang to get some of his thoughts. So Dr. Wang thanks for being with us today. It's my pleasure. Thank you so much for the warm introduction Arianna and please just call me Benjamin for you know for the sake of personability please. Sounds good Benjamin. Well thanks for being with us.  So I'm a physician and a biochemist by education and training but about 10 years ago I was taking care of patients in the ICU and a young 19 year old young lady came under my care and because she had just given birth and some complications had occurred she ended up on a ventilator and my team and I watched this young lady basically get worse on the ventilator and over the course of the next couple of weeks catch a pneumonia and ultimately pass away and something about her I mean maybe it was the age or the point in which my training but it didn't seem right to me that these things were happening to patients that were otherwise healthy and young and had you know their whole lives to look forward to um and as kind of the junior physician on the team my job was to go into the literature and and see if we could have changed that and lo and behold I discovered hey wait a minute she caught a pneumonia she got ventilator associated pneumonia because of the device we were using in these patients and and that's kind of an interesting theme along with many of these hospital prior infections they're not because people are sick or they come into the setting necessarily but they're often device related and at that point I said you know um somebody should do something about it if we don't do something about it more of these kind of stories are going to happen and um I I just didn't feel like I could live with myself if I didn't try and do something so I started a little company to make better devices to prevent those pneumonia. That's awesome Benjamin and you know I think it just shows how many people out there can make an impact right you know you started off your career in critical care as an MD and now we're taking that knowledge that you learned while in medical school and training to be a physician and now are turning that into an entrepreneur entrepreneurial project and company that can impact patients and I think that value of all that knowledge that you have from your training can now really extend much more broadly. Well I appreciate that and you know we we do the best we can here at Neatham. Yeah good well um we're excited to kind of get into VAP as this issue now and you know I love that we started off with this patient example right it's all about how how this affects people these aren't just statistics these are you know women men black white you know it really impacts everyone so anyway I'd love to kind of get into the second question which is really why don't you kind of give for the audience listening in background around VAP as a patient safety issue so they can understand why this is important. Yeah so the story really starts decades ago when we started to realize when you put a breathing tube into a patient for a longer period of time the breathing tube is a foreign object that really doesn't belong there and then when you put them on anesthesia and they can't call for themselves the breathing tube will end up being a nitis for infection which means basically the device causes these infections down down the road um we we knew decades ago that when you put a breathing tube into a person their risk of an ammonia increases 600 to 2000 percent and it was it it was so common in these longer-term mechanically ventilated patients that we started to give them give these entities a name and we started to study them and and we called them ventilator associated ammonias because for some reason when people got put on a ventilator they develop these specific types of mnemonias now they're they're an interest this is an interesting condition because it's unlike any condition you see anywhere else you don't see the types of bacteria and fungus that that like to cause these infections in the community and you don't even see it outside of the icu the types of bacteria and the types of infections that are caused in these patients are unique but they are also very hard to treat and many times they're antibiotic resistant just by the nature of the types of bacteria that they grow so um you know while we as physicians we learn that if somebody comes in from the community they're likely to have you know a handful of these types of infections the types of infections that you see in the icu are just dramatically different difficult to treat and deadly many cases now before 2009 the whole world was looking at this and basically saying this is the biggest infection problem we have in the world you can't provide normal medical care without running into this infection and it was true but at the same time it was very hard to diagnose different parts of the world and different institutions had different criteria and if you weren't looking carefully you missed it and patients were worse worse for wear because you know we lacked surveillance and this was such a big problem that you know the United States government basically the Centers for Medicare and Medical Services said you know what we can't tolerate these kinds of infections hospitals have to do a better job and so since 2009 they've instituted penalties for having these infections but what that also did was hospitals because they couldn't solve this problem because patients were still coming in with these infections as a response to those penalties many hospitals decided to call the infection something else that was if that was a first kind of a bad thing that happened because now hospitals were just calling the infection something else avoiding the penalties and patients were getting sick and and hospitals weren't doing doing the job so the government intervention in this case had quite the opposite effect that had in other places like bloodstream infections and catheter related infections and and you know IV infections and that such but for ventilator associate ammonia it had the opposite effect it pushed the problem under under the radar now the CDC and and and CMS got together and they said you know we are we know this is continues to be a problem we know when we survey the hospital length of stay and the problem you know the mortality rate from these ICU patients that we see from the very outside of it from 50 000 feet and none nothing has changed so we have to figure out a way to create better surveillance so they got they brought a group of very smart people together put them in a room and said come up with a better surveillance criteria and they created a new surveillance criteria called ventilator associate events or VAE and the idea was the ventilators have these our electronic devices and they record the the settings on the ventilators so if you want to catch changes in ventilator settings then you can do that fairly automatically because it's in the medical record that way you can hopefully get away from the subjectivity of one doctor calling it one type of pneumonia and one another doctor calling another in a hospital saying you know we have a lot less of these infections and that way hopefully the surveillance will get better so they did this they brought these people together and they created this definition but it turns out that years later um researchers started to investigate these definitions and see if they really worked and it turns out the definition for ventilator associate events only covers about 12 to 15 percent of ventilator associate moneys which means the vast majority of these moneys number one were not being surveyed were not being recorded and instead we were trying to measure something that had no correlation in terms of cost control or patient safety so after enough data came out in 2019 the Center for Medicare and Medical Services basically said we're going to do away with this VAE definition in terms of surveillance so hospitals don't even have to survey or report the number of VAEs they they are seeing now you can imagine that's probably not good if you have no surveillance or reporting requirements for hospitals to do this all the while patients are patients are the ones that are are the ones um um dying and suffering from these conditions um now not all the hospitals listened during the pandemic and actually the CDC came out with a report about two weeks ago that showed the number the incidence of VAE that was reported to the cdc from 1400 hospitals during the pandemic increased every quarter for 2020 sometimes by as much as 45 percent now we knew these criteria were not good people were not very honest about reporting them but what we are seeing in terms of ventilator associate pneumonia that is that it is one of the leading causes of sepsis and death in covid patients and when we look across across the pond at our counterparts in europe they're seeing rates of ventilator associate pneumonia and covid patients that are 45 50 percent and responsible for law you know an additional average stay of two to three weeks so if you're wondering um why this is a big problem it's it's because this is the reason why hospitals are doing so poorly during the pandemic if we could get people off the ventilator sooner and healthier we'd be in a completely different situation with the pandemic today wow benjamin yeah that's you've clearly shown that this is a huge issue and that you know although we've been trying to make changes and there's been you know additional research now we have the research to show what we're doing isn't really working so i'd love to just move on to the next kind of session section of the interview and talk about you know coming from this world where you spend probably nearly 100 of your time thinking about that every day you know what are these attempted solutions to mitigate the prevalence of that um and if you can talk specifically around potential policy solutions or reimbursement measures that would be great yeah so for the most part i mean many of the innovative solutions i've seen out developed in the community are basically trying to again mitigate the fluid and bacteria from entering into the lungs there are really three things that we can do judiciously in this fashion to improve the situation and number one is that number one is to find ways that we can reduce the the number of pathogens that are necessarily in the airway in the mouth the nose and in the trachea leading into the lungs while a patient is intubated number two is we can remove the the fluid that facilitates the the passage of these pathogens into the lungs and and really number three is we have to find ways to get people off ventilators faster because the sooner you get them off the less ventilator associated ammonia you see you see in them and these you know for the most part are not they're not rocket science and and can be done it's simply when you go and talk to customers the end clinicians you hit a wall because it's not a problem if you can hide the problem from from the payers now from a policy standpoint that's that's what's really holding back a lot of innovation is if you allow hospitals to cover up that they have this enormous problem they don't want to solve it they're not going to solve it um just like climate change you know um for us you know in medicine antibiotic resistance and infection and these kind of complications are our climate change if we do nothing and we allow the status quo status quo eventually we're not going to be able to do the things that we want to do in medicine a lot of our advances in our technologies rely on the fact that we can do surgery that we can anesthetize a patient that we can help them breathe for them when they cannot do that if we lose that ability a lot of what we do in medicine in modern medicine disappears and is not safe to perform but from a policy standpoint i mean the negative incentives that that government has put in place are not working you know they haven't worked from the beginning they haven't put the focus on these infections but have basically incentivized hospitals to run the other way and decide that they don't have any of them so if if there's one policy change that needs to begin um it has to do with surveillance and and penalties hospitals are not going to come clean and look for a solution if they think they can hide um but at the same time they only want to hide this problem because there are negative incentives in place you know um the first thing we should do is ask um cms to remove the penalties for these types of infections so that hospitals can begin to um estimate and and come clean with the fact that there are these complications and that will have ripple effects in terms of innovation too uh we're not solving the problem today as it is but that's not to that's not to say that in the future solutions can't appear to address this problem um if they if it's necessarily necessary to do better surveillance the key with ventilator associated pneumonia and some of these other hospital acquired infections is the fact that they are unlike things that we see in the community if if the government really wants to quantify and survey the problem carefully all they have to do is carefully look at the types of infections and the antibiotics prescribed in these cases and i know for a fact that it's in everybody's interest to have better antibiotic um surveillance but also stewardship because these are the only drugs that we have in modern medicine that the more we use the less effective they become and and we have to look at them more as a resource rather than a way to avoid um addressing real systemic problems in our healthcare system absolutely um you know i think you bring up really good points that you know here at the patient safety movement we bring up all the time that we can't continue doing the same thing over and over again and expecting a different result we have to get new minds together get get new conversations to happen and so we've been so thankful to talk with you today benjamin because you're planting these ideas for everyone who's watching now maybe there's something that everyone can do and so i'd love to just kind of end with what you know if if someone's watching who is caring for a loved one or might have been a patient themselves uh or might be a health worker in a similar situation to you they just want to do something to hopefully change the outcome for future patients or administrators who are collecting that data um you know what are if we focus on maybe those three first and can leave the policymakers last what what can these people do that are watching today to try to help i think they can um you know i'd love to tell everybody that they could do something different and i'm sure they everybody has a place to play in um a role to play in this in in the movement to change this um situation um i mean one of the best ways is to basically be an advocate and to look where other people aren't looking i mean from a patient standpoint or even a clinician standpoint when you see something that you don't understand if you see if a loved one or a friend gets sick and you've never even heard you you can't imagine the bacteria that you hear that's that's growing or the infection problem that's growing read a little bit learn about it and and be an advocate go out there and and say something to somebody about it because you know the more that we kind of gloss over and accept that this is something it's a problem that we're not willing to understand the more uh the less attention will be brought to these problems um quite frankly many of these patients who are in the ICU right now are are the ones who are are there because they got ventilator associated pneumonia we know that from the data um from a clinician and and then administrative level i mean yes you know we can we we can see these problems very clearly and we should listen to um the research and be attentive of of what is um what is happening in our healthcare system because um you know i i tell this to to people who are trying to be leaders in healthcare all the time you know it's great to put in hard work and to inspire other people along think about what is your legacy when you leave that hospital when you leave that room with that patient when you leave and retire and go on to do do whatever it is you want to do what is the legacy that we leave for future generations or even just the patient that is going to be discharged from the hospital you know i like to think that we should all strive to leave something better than it was before and and one of those ways that we can do that is we can prevent more of these infections and save more lives um that's what i would tell people you know just just be attentive watch the look at the details yeah i love that and you know when i think about hopefully people from the public seeing this video it is it's the speak up listen and observe and and ask those questions i think there's still so much um so much work we all have to do to make sure that patients and their family members know that they can speak up and ask those questions and if they don't understand something that it's okay and and you know step step back a bit and ask that provider you know hey use language i can understand um so beautiful well thank you so much uh benjamin for joining us today any last minute thoughts before we close no no um i i just i'm i'm always very hopeful and optimistic i really do believe that we can solve this problem together um we just have to make it our priority to do so absolutely so thank you so much benjamin and uh for everyone who's watched leave comments below and let us know what you think and how you can help how you think other people can help so thank you very much


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Hit parade high risk high reward There's been some really nice rewards popping out of here.  What a nice break. I Don't know too much hockey, but I know guys like this you know Guys like that some pretty nice stuff this guy too We started off with Jack Hughes Solid break, thanks everyone for getting in I'm Joe for jazzy's case breaks calm We'll see you next time the next time we have more hit parade up jazzy's case breaks