Maps have continued to be green this week. You know what that means? Bitcoin to the moon! Well, not quite, but getting closer. An outer space-based mining rig mined Bitcoin at an altitude of more than 22 miles. The mission inspired talk of mining on the moon, which could solve the energy issues it has on Earth. But what if we get to the moon and a mining rig is already there? Here is your overview of the week. Bitcoin is often linked to the dark web and blamed for the opioid epidemic. Opioids like heroin and prescription painkillers like OxyContin and Fentanyl kill an estimated 115 people every day in the U.S. At least 46% of Americans are friends or relatives of these victims. But now, companies believe blockchain, the tech behind Bitcoin, may be the answer. Intel and Big Pharma want to help fight the opioid epidemic using blockchain tech. Blockchain could better trace drugs so they don't fall into the wrong hands and prevent patients taking out multiple prescriptions. It will also create immutable medical records. Currently, there is a software that looks through prescription records across America to detect opioid abuse. But records can be altered, not with blockchain. Using scanners and sensors in each bottle, even each pill can be immediately recorded on blockchain. The idea is being tried out by Johnson & Johnson and other companies. The experiment will see how easy it is to track pills for manufacturer to patient. However, a lot of opioids come from China so they're difficult to trace. Intel says, ultimately, it needs to go worldwide. We agree with Intel, blockchain will save the world. Don't have $85 million like the Secret of Pineapple Fund guy? Calling all crypto philanthropists on a budget. UNICEF is raising donations via crypto mining. Their Hope page mines crypto with the help of your computer's processing power. It allows visitors to select how much processing power they want to contribute to mine. The longer you stay on the page, the more crypto is mined. Any crypto mind is turned into fiat, then donated to UNICEF Australia and used to help vulnerable children worldwide. Nearly 2,000 people have donated computer power to aid the project so far. Bitcoin is becoming an increasingly popular way to donate to good causes, whether you are donating actual crypto or simply using computer power to mine. If you would like to donate to UNICEF Australia, visit their Hope page. What could bacon, crypto, and billionaire Warren Buffett possibly have in common? Warren Buffett is known for a healthy investment portfolio but not for a healthy diet. He drinks at least eight cans of coke a day and eats McDonald's. Check out what else he eats. The food giant Kraft Heinz has released the bacon, a token you can exchange for actual bacon. Buffett's Berkshire Hathaway is an investor. The McDonald's eating billionaire is not bullish on crypto, but apparently Kraft Heinz is. You can register for a bacon and trade it in for some real-life bacon or hodl for a better price and claim more bacon later. A cynical marketing ploy or a genius plan to get bacon-loving Buffett into Bitcoin? Big news coming out of the ether. Do you want the maybe good news or the potentially bad news first? Okay, bad news, but calm down. It's potentially bad news. Ethereum, the world's number two cryptocurrency, might be classified as a security. US regulators will be discussing it next week. If yes, then it has to register with the SEC in 2014, which is fine because if anyone convented Time Machine, it's Wunderkin Vitalik Buterin, right guys? If no, then nothing to see here, move along, keep hodling. All right, to see here, please disperse. Now for the good news. Good news, everyone. Vitalik is getting into sharding. What? Vitalik is gonna climb the shard in London? Um, no. He is hinted that sharding, a way of increasing transaction processing capacity, could be coming to the Ethereum blockchain. Stay tuned to his Twitter where we'll give away more hints, but no ethers. Repeat, no ethers. Last year, South Korea banned ICOs from being held in the country, and we were sadder than that time we missed out on tickets for K-pop sensation, BTS. But we listened, then translated, BTS' lyrics. In this black darkness you were shining so bright, we never gave up hope. This week, a new bill was introduced that could open the ICO market back up, albeit one now strictly supervised by government regulators. So hopefully less crypto fud and more crypto love. Want more aboard the crypto love train? Goldman Sachs will be opening a crypto desk after being inundated with requests from clients desperate to get their fingers in the crypto pie. This decision means that the company has officially decided that Bitcoin is not a fraud. Congrats to all Goldman Sachs clients who no longer have to be no-coiners. And finally, after deciding not to accept Bitcoin, Reddit doubled down on crypto and hopes to expand to Litecoin, Ethereum, and beyond. Like and subscribe for Bitcoin to the moon. Like, subscribe, and hodl for Bitcoin to Mars.


Welcome to UVitis Grand Rounds, this is our ongoing patient round series where we have a subspecialty that, subspecialty themed rounds, we are very lucky to have Dr. Alvi Talley chairing today's meeting and without further ado, Dr. Rai Talley. Thanks Jeff. Thanks for being here, welcome to UVitis Specialty Grand Rounds, I have this illustrious crew of fellows and residents that we would like to present some representative cases that kind of roll through our clinic to illustrate our approach to the diagnosis and treatment of UVitis to arrive at a diagnosis because the diagnosis really matters because it impacts the prognosis and the treatment of our patients. So just by way of introduction as you know, UVitis by definition involves inflammation of the UVL tract but in parlance it really, common parlance, it's intraocular inflammation of the eye, any part of the eye. It can be either infectious or non-infectious and those that are non-infectious are thought to be autoimmune or auto-inflammatory in origin. Importantly, there are masquerade syndromes particularly neoplastic masquerades and so all in all UVitis is not one disease but represents about 30 distinct entities with typical clinical features, course and prognosis. It is not a trivial disease representing between 10 and 15 percent of blindness in the United States and is the fourth leading cause of visual loss after diabetes and age-related macular degeneration making the personal economic impact of potential visual loss possibly greater than that of age-related disease given the fact that the peak onset is in the most productive years of life. So I would like to describe our approach to the UVI of this patient. As William Ossler said, you know, talk to your patients, they will tell you the diagnosis. So the history is extremely important beginning with the ophthalmic history, medical history and then eliciting things that may not come up in history through a review of systems. Then the ocular examination in which we grade the severity and stage of the inflammation and then assess the eye for structural complications in the front of the eye and the back of the eye including posterior sneakia, macular demenocroidal nevascularization. Then a general medical exam is conducted to the extent that it can be carried out in the clinic looking at the patient's skin, their joints for signs of arthritis or deformity and then based on this information formulate a differential diagnosis. So no labs have been performed. This is all history. So the differential diagnosis is formulated and characterized along several dimensions. One has to do with the anatomic location of the inflammation whether or not it is present in the anterior chamber, the vitreous, the retina or coreroid or all three compartments. The pattern of the inflammation particularly in the back of the eyes of pattern recognition is important whether or not the inflammation is predominantly in the retina or in the coreroid or both or whether or not it is a multifocal or a posipocal inflammatory condition. Whether or not it is granulomus or not granulomus by its clinical features. And then the presentation course in laterally. So is this an acute disease? Is it a recurrent acute disease or a chronic disease? Because this will help characterize the type of disease we're talking about, unilateral, bilateral or alternating. Then is this disease purely in the eye? Or what are the systemic host factors that are important? For example, is there a systemic underlying condition that may be associated with the inflammation such as we see in sarcoidosis, multiple sclerosis, spondylitis, AIDS or an iatrogenic immunosuppression? Is there infection present? What are the demographics? The world is shrinking. We see lots of patients from all over the world here in which a certain disease may be more prone in certain populations. And then the associated signs and symptoms. The laboratory is then used after this to exclude infection essentially and to identify systemic disease that may impact mortality or morbidity. And it provides actually important prognostic information for the physician and for the patient. So patient with HLAB27 positive anterior uveitis, we can tell that patient with a certain amount of certainty what the course of their disease is going to be like as opposed to say for example patient with Bay-Shet's disease or Serpigenus which will require a long-term treatment and immunomodulatory therapy. And then a treatment plan is formulated based upon the diagnosis and antimicrobial therapies in the case of infection, a stepladder algorithm employing non-steroidal anti-inflammatory medication with immunomodulatory therapy as needed as either first-line treatment or as part of a steroid-sparing strategy. And then to follow the patient closely to assess treatment and to monitor side effects of treatment. So we're going to kick it off with Dr. Zog who's going to show us one of the diagnoses that we never want to miss. So we're going to just start off by presenting a case. So this is a case of a 42-year-old. This is in 2006 when he first presented. And he's describing some floaters and some light sensitivity, not a lot of pain. He is HIV-positive and his CD4 count by his report is low with a high viral load count. His last CD4 that we could find was 231 at the time of presentation. His visual acuity is 20-40 in each eye, he pinholes a little bit better and his tensions are normal. On his exam he has an anterior chamber cell. He also has a cratic precipitates and then he has vitreous cell. So he has inflammation all over the eye. This is what is, sometimes these don't project all that well, but this is what we're seeing on his exam. So if we look at the right eye you can see that the details of the fundus just are not very clear. So he has some vitritis and then kind of some pigmented, some areas of depigmentation in the periphery and then kind of a circular depigmentation area sort of around the optic nerve, just kind of little areas that are kind of subtle on the fundus findings here. So you have some other imaging done, which doesn't project well again, but it sort of shows those areas where there was some pigment changes, kind of subtle but kind of some almost whitening here. And then on his fluorescein angiogram, this is kind of in the earlier phases of the angiogram, kind of see some patchy filling of the coroid, which can be normal as we go a little bit later. You'll start to see that you have, this is really late in the angiogram and you're seeing kind of this area here that's abnormal, kind of some patchy hypo and hyper fluorescence. This is highlighting one of those areas around the optic nerve. And sometimes these are pretty subtle unless you've been looking at a lot of these. This is an abnormal area that corresponded to the color photos in that eye. And then again here, kind of this area that's a little bit hyper fluorescent, really late in the angiogram. The optic nerve seems to be having some staining as well, maybe even some leakage. Listen, it's not a wide field view, but you can see kind of these almost circular plaque-like areas that are showing up late in the angiogram. So what do you do?  This patient has HIV. He's immunocompromised. His CD4 count is very low. So there's infection is really high on the list in those patients. You also have some infiltrative diseases that could present like this and inflammatory. But we're really thinking about a lot of these infectious things that could be happening to this patient. So what did he have done? He's a high-risk guy, so you kind of have to throw some high-risk things at him. So you do vitreous tap and inject. Try to figure out what's going on back there. He had some boscarnet that was injected into the vitreous. He's also put on the Valtrex. So you're treating CMV and you're also covering some of those herpes viruses as well. And then we did a lab workup. So his lab workup, CD4 count was 217. The biggest thing is that he had an RPR and an FTA that were both positive in him. His toxo was negative. And HIV patients, they can definitely have more than one thing going on. And so sometimes you have to treat multiple infections. But in this case, it looks like syphilis was the main diagnosis here. He had PCR in his vitreous that was done as well at the same time. And CMV and the herpes viruses and toxo were all negative. And anybody that you diagnose with syphilis, the next step is to get cerebral spinal fluid to see if they have involvement in their central nervous system as well. And his was negative. So his diagnosis was syphilitic choreo-retinitis. He was allergic to penicillin, which is the main treatment for this. The good thing about syphilis is it's very treatable. Dr. Vitale likes to desensitize patients and use penicillin. You can use alternative treatments, but this desensitization works really well. So the patient was admitted to the hospital, desensitized, treated with IV penicillin. We talked about his lumbar puncture results, which is important in these patients. And he actually resolved, which is kind of the rule in syphilitic uveitis, is that their vision usually gets better, especially if you can diagnose them early. And so he ended up 20-20 in both eyes. And that was after about a year of follow-up. So this is what his fundus looked like after treatment. So you can still see some subtle changes of pigment going on, but overall things look pretty quiet. The view is much clearer than it was before. So now this gentleman is three years older. Again, HIV is 45 now, in 2009. And he presents with a little bit of pain and decreased vision in his right eye for about four days. Yeah. So he had been off of his HIV regimen for about four months. Does it know why he went off? It's just a big problem. Yeah. I mean, these medications are not cheap, but very effective. So he comes in with hand-motion vision. He has 2-plus anterior chamber cellia, some posterior synechia, pretty extensive area, vitreous cell and haze as well. So again, kind of a pan-uveitis type picture. On his exam, we'll kind of see what his fundus looks like. So this is his right eye. So now he has this large optic nerve mass, essentially, and then really hazy inflammation of the retina as well. So again, HIV-positive patient, re-presenting with a really bad uveitis. Again, you have to step back and wonder what's going on here. Big hyper-autofluorescence here, lots of problems with the vessels, bleeding, haziness, vasculitis, lots of badness going on here. So you get an FAA here that kind of shows some of the same things. Kind of see that patchy kind of inflammation of the retina. This is actually in the uninvolved eye. In the left eye, in that right eye, just really not looking good. Really late in the angiogram. You go out over to the left eye, and he's got a little bit of staining around the disc, which is pretty normal, but he's got these little patches that make you wonder if the left eye's involved as well. So again, you have to take a step back, and your differential is still broad in this patient. CD4 counts now eight. He did have an RPR and an FTA that were again positive. What you do with these usually is you track the treatment of syphilis to make sure that they actually do clear the infection. So his titer had decreased down to one to two back in March of 2007. So his titer is back up with syphilis again. Everything else here was negative. His vitreous sample though, he had some toxo that came back positive on PCR. So he has kind of two things going on at once. But the key here was that in his history, he had a clear historical point that he had a reinfection with syphilis. So he was again introduced to another syphilis case here. So it looked like CMV retinitis. It could have been if you look at the appearance. You have syphilis based on the serologies. And then you have toxo based on the PCR. And then there's all the other different things that still could be involved here. So what do you do with a patient like this? You put them on everything. So valsyclavir for the possibility of any herpes viruses. The anti-toxo, so Bactrim is what he got. And then he had IV penicillin again after desensitization. And then a prednisone taper as well. Got him back up on his heart and then treated him locally also with Predforte, Cyclogell and Zymar.  So this is what he looked like a little bit later after some treatment. So he was looking a lot better. A lot of the inflammation is gone. He still has some hemorrhage and obviously the vessels are kind of attenuated from all the damage that had occurred. That was what he looked like when he first came in so you can kind of see the comparison of how much inflammation is down. So in this case this is now a syphilitic pan-Uviatus that was a reinfection in that right eye. And then we had to treat the other things there as well. His CD4 count remained pretty low. It took a little bit of time for that to come up. But he ended up with really poor vision in that right eye long standing because of the damage there. That's what he looked like at the last photos that I could find. So that large optic nerve kind of granulomatous mass was kind of gone there mostly. But still poor vision. I am not 100% sure. Sometimes I can't always tell on going back and looking at cases. But it was negative. It seems that just systemic penicillin really treats it all. And it really clears up the inflammation in the eye too. You can treat locally with steroids to help with that. But most of the time the penicillin alone will help to clear the vitritus and the cell and everything. Okay so we're going to show a couple other cases just to show how tricky syphilis can be. That it really is the great mimicry in the eye. So this is a 35 year old male with a 6 day history of decreased vision in his left eye. He's a high risk individual. He has IB drug use. He tells us that he had a recent HIV test that was negative. He's 2060 in both eyes on testing. This is what his retina looked like. So you can see a pretty clear view to the back of the eye. The vessels look fine. But the optic nerve is swollen here. And then his left eye again a little bit of optic nerve swelling. But you can see kind of this large kind of essentially right over the macula of some depigmentation there. You can see a little bit of hyper fluorescence here on the left eye. The right eye actually looks pretty good. The optic nerve might have a little bit going on in both eyes. On the early stages of the FA what you see here is some hypo fluorescence with some patchy hyper fluorescence. And then later in the angiogram you see that same area with a large kind of crescent shaped hypo fluorescence. And then the optic nerve seems to be staining here as well. So on his, he presented with kind of a classic syphilis is what we would say this looks like. On exam you could almost diagnose this. But you would still go to lab testing in this patient as well. So he had an RPR that was reactive and FTA that was positive. We retested him for HIV and it was positive. He had high CD4 counts. Had an MRI done that was normal. And again after treatment he improved to 2015-2020. So just a quick little case that shows patients can present with something completely different every time with syphilis. And again treatment to resolution of visual acuity is the rule in these patients if you catch them early enough. Okay so another one here, 50 year old Mel complaining of decreased vision. He has optic nerve swelling coming in. The bad thing for this guy is he's NLP in his right eye from birth. He's saying that he had a retinal detachment. He never saw out of that eye and so this eye is just kind of gone. His left eye is baseline vision is 2070. He's decreased down to 2100. No real significant past medical history that we can elucidate from him. He has an APD in that right eye and his eye is actually quiet. And this is what he looked like in his left eye. So you can see it's a little bit of a hazy view. Optic nerve is swollen here and then you've got this area of pigment changes kind of out in the periphery. So on his imaging the main thing that you're seeing here is a swollen optic nerve with some hemorrhages and then same thing here just a swollen optic nerve that kind of leaks late in the angiogram. Maybe even some potential CME there. So what does he have going on? He basically has an optic neuritis of some kind.  He ended up being treated again for neurosyphilis. Some of these cases I have limited information on. Dr. Whitelly probably has a lot more but that's another presentation. Just a patient with an optic nerve swelling. So you have to think about syphilis in that case as well. Another patient 29 year old came in with a week of a red pain fly. CD4 counts low. 167 with HIV. He's only had HIV for a week so this is kind of a new diagnosis for him. His visual acuity is down 2050. He has a really exuberant anterior chamber reaction so he has fibrin in his anterior chamber. 3 plus vitreous cell, 2 plus haze, retinal whitening. So again all chambers involved. This is a patient presenting with pan-ubitis. So the differential diagnosis again is very broad in HIV patients. Infection is sort of at the top of your list. This is what his eye look like kind of a bad photo sorry. But what you're seeing is over here in the periphery kind of have these like white areas that are actually above the retina. So kind of these pre-retinal infiltrates and one here as well. A little bit better picture of it. Just kind of some little whitening areas above the retina maybe some in here and up out here as well. So he had a vitreous biopsy and he was admitted for treatment of toxoencephalus and then kind of a workup for this source. And he ended up with CNS and systemic syphilis so his LP was positive and had another good response to penicillin. This is a case of a patient in the UK that was sent to Dr. Vitale. It seemed like it was sent to him as kind of like can you help us with this case? And this is a patient who had PRP and IVT for diabetes. And this is baseline visual acuity so 6 over 12. Essentially about 2040. 6 over 24 would be like 2080. And his vision was worse one month later. Clear to LP in his left eye. So vision just really tanked after this treatment. Had an afferent pupillary defect. Had a lot of inflammation going on in his eye. And he had this testing done over there.  HIV was negative. So again a patient with syphilis and this is just a really classic photo of what syphilis can present with. So it's these pre-retinol whitening areas with kind of a retinitis and optic neuritis. Really pretty impressive inflammation here. You see the vessels are not healthy. You get vasculitis with it. But it's really these kind of white pre-retinol infiltrates that are going on in this patient. Just kind of all over the retina. Alright this is probably my favorite one just because of the history that is the key point in this patient. So this is a 50 year old female. And Dr. Vitale will ask you this question in clinic. Are they a citizen? And at first I always thought that that meant, are they like a US citizen? Do they have their green card or something? I wasn't exactly sure. But it's that they're an upstanding citizen. So church going, upstanding citizen. She has a lot of systemic things going on. So she has polyarthritis. She's having ulcers, rash on her knees, ankles, all kinds of stuff going on. She had been diagnosed with I think bird shot initially. Oh was it mute? Sorry. She was sent to Dr. Vitale for a consult to see how to treat her. And she had some old vitreous cells on exam. Pretty good vision. But kind of a lot of systemic things going on. This is what her eye looked like. It actually looked pretty good on exam. Not a whole lot going on the fundus photo on the right eye. In the periphery maybe there's some pigment stuff going on. But pretty subtle on exam initially. Same thing with the left eye. Not seeing a whole lot on her exam. But her imaging kind of really shows some things that were going on. So what we're seeing on her angiogram is you're seeing kind of these patchy areas that are kind of filling a little bit abnormally. You see just kind of presentation things that are not normal as she's filling her retina here. Same thing. Kind of subtle things. Maybe there's a little bit of haze right in this area here. Kind of just pigment abnormalities and filling defects in the coroids. So it's not. So this is the key point is that she had a benign social history but her husband was having problems with same sex attraction. And they're currently separated. When I was looking up her case her name changed. And so it was like hard for me to tell is this the same patient. But I think we know why her name changed after this. She was RPR FTA positive. She had a positive LP and had IV penicillin treated for syphilis. So one of the issues with syphilis right now is it actually is on the rise from 2012 to 2013. It kind of doubled in rates. And it's mostly still young men having sex with men. And there are about 50,000 cases reported to the CDC a few years back. But there's no reporting that's required. Yeah. In Utah. It's mostly men having sex with men here. It's probably, is the prevalence less in Utah? It's hard to know. So there's different stages to syphilis. The primary stage is pretty rare to have ocular involvement. But you can have ocular involvement in secondary or tertiary. There's also congenital late and late latent syphilis. And again, those are all times that you can see syphilis affecting the eye. If you have somebody in these situations, a lot of times that your treatment may not improve the condition as far as the systemic things and maybe even some of the late things that are going on in the eye. But the key is to prevent further damage with it. So there's no formal reporting. There was a good study that came out from the UK that there were about 50 cases per million of syphilis. And there were about 0.3 per million of syphilitic uveitis. It kind of gives you an idea of how many cases of syphilitic uveitis there are. It's pretty rare. It's still less than 1% of our uveitis cases that are coming in. It's a lot higher in HIV patients though about 16% of them that came in and had uveitis from syphilis. So the presentation, really you name it, it could be anything. So that's why it's called The Great Mimicre. It can present with any sort of presentation. There are a couple of things that are classic, but it can really come as anything. So this just kind of shows we got cut off a little bit here, but every single system is involved. I was thinking maybe ocular plastics got out of it, but extraction motility you can have credular palsy. So it's just everywhere in any of the stages of syphilis. The most common things that you see are vitritis, iritis, KP and retinitis, but you can see again anything. So because of the extreme variability, it's really the history. You have to get uncomfortable with the patient and talk to them about their true risk factors for HIV and STD. STDs. There's two distinct clinical patterns. It's those superficial retinal precipitates. And then just a cute posterior placoid choreo-retinitis, which are two of the cases that I showed. If you had to profile a patient, this is what it would be, HIV positive middle-aged male. There are some classic OCT findings that show kind of disruption of the ISOS junction and then loss of the ELM in this left eye compared to the right eye on this patient. This shows kind of resolution of that with treatment. So you see the ELM come back and the ISOS junction kind of reform. On ICG, you can see early and late confluent hypo fluorescence, which is pretty specific for syphilis. On FA, you usually see this progressive diffuse leakage. And then the hyper-auto fluorescence is what we saw in that placoid type lesion. So the serology, you want to get a non-trepanemal test, a VDRL or an RPR, as well as a trepanemal test. So most of the time it seems like we're checking RPR and FTA. The CDC has this recommendation that they came out with that nobody really follows because there's extra steps in testing. It hasn't been widely adopted. You essentially get an EIA if that's positive, you get an RPR. If that's negative, you get a TPA. No one has really adopted this as of yet. You can do direct testing with PCR or the aqueous. Again, we talked about that a little bit. And then that dark filled microscopy is something that you can potentially do. Tracking treatment, you're using an RPR and a VDRL, the titers to see if they're getting better. So then a couple of key things. If you diagnose syphilis, what do you do next? So the key is that ocular syphilis is neuro syphilis. And so you have to get a CSF evaluation to get a lumbar puncture and always test for HIV. Treatment, there's a bunch of different treatments that you can do that are all approved for neuro syphilis. But IV penicillin is kind of what we do here. Don't treat with local therapy unless you have proper antimicrobials on board. So using steroids is fine as long as you're treating the underlying infection. And then just some take home points. Always consider syphilis in the UVitis patient. The pre-retinal to the acute posterior placoid choreo-retinase are kind of, can be diagnostic of syphilis. You can use enhanced imaging that is helpful. And then serologic diagnosis is really the way that you come up with a conclusion there. And again if ocular syphilis gets syphilis, get CSF and HIV testing. That's it. Okay. So Jim and I are going to present a case quickly. We have two cases left in a limited amount of time. So I'll move through the case presentation quickly. It's a classic representation of a diagnosis we see not too infrequently in the UVitis clinic. So this is a 68-year-old Caucasian woman in 2013 at an outside clinic. She was treated for a super temporal BRVO and related CME with intravitrally vastin. She responded well initially, but then returned to that clinic in 2014 with a recurrence of CME. And along with that was found to have a mild vitritus associated. She, before coming to us as a second opinion referral, she had had two separate approximately one month tapers of Durazol in both eyes. And by the time she got to us, she had been off of any topical treatment for one month. Her chief complaint is blurry vision more on the right than the left. And she also complained of worsening night vision. So these are medications. Most of them are over-the-counter supplements. She's on levotheroxin for thyroid and baby aspirin just for prevention of cardiac complications. Her past medical history hypothyroid, she had a recent mechanical fall from slipping on the floor at home. She has a history of miscarriage. She had knee surgery in the distant past with a complication of a pulmonary embolism afterwards requiring anticoagulation. And recently found out again she had another DVT requiring anticoagulation. She has no history of sex with transmitted disease and no known history of hypertension. Her family history is in non-contributory. She lives in Idaho. She's a retired teacher. She's traveled to Prague in April of last year when we saw her. She has no history of IV drug use and she does not smoke. And her review of systems is only notable for joint swelling, warmth, and redness in her hands. And when you look at her hands she has some sort of, some deformity of her fingers and hands almost like a rheumatological deformity of rheumatoid arthritis. So her vision is 2040 right eye, 2025 left eye. She does not have an APD or remainder of her initial exam as normal, pressures are normal. Enter segment, notably she has a deep and quiet enter chamber, mild cataract. The vitreous is notable for about half plus cell and one plus haze in her eyes. This is pretty equivalent. And then let's go through the photos. This is the funnest photo of a right eye. You can see that the view is somewhat hazy. The view of the optic nerve is a little bit obscured. The vessel is a pure normal. Remember she had a super temporal BRVO that was diagnosed in the past in this size. So there's some tortuosity to this arcade vessel and some collateral that are formed. You know, this looks like a hypopigmented blonde fundus. I'm not sure what to make of these at the moment, but these will be better characterized with further imaging. You know, these hypopigmented spots in the nasal mid periphery. Her left eye looks very similar. One plus haze, disc looks sharp, vessels look normal. Again, blonde fundus, but possibly some interesting hypopigmented lesions in the mid nasal periphery. So before we get to a differential diagnosis, there are other studies we can perform and so we got those. I'll shout out what you would get for this patient. Floricine angiogram, ICG, out of fluorescence OCT. Okay, so let's start with the OCT. So here's a right eye OCT. She's got CME. You can see that this vessel is more engorged than the corresponding inferior arcade vessel. Intra-retinal fluid. Left eye OCT is totally normal. Okay, so interestingly she's got the same amount of vitritis and haze in both eyes. The CME may be due to, you know, related to her BRVO in the right eye. Here's her FA. This is early transit. Right eye. 19 seconds. Vessels are filling normally. This is a wide, we got a wide field angiogram. So this is why it's so minified and zoomed out. A little later, 32 seconds. And then much later, 2.5 minutes. You can see that the optic nerve is lighting up. So there's some staining and leakage from the optic nerve. And interestingly, there is a retinal vascular leakage all over the place. Left eye is very similar. So 43 seconds, 4 minutes. Again, widespread retinal vascular staining with leakage from the vascular optic nerve also stains and leaks late. Here's her ICG. Right eye, 20 seconds. 32 seconds. Looks like, you know, the cord seems to be filling appropriately. Remember, ICG looks at caroidal pathology. 4 minutes. Okay. Now maybe you're starting, we're starting to see some interesting hypopigmented spots in the periphery. And then if you wait long enough, we can see that there is something interesting going on in the mid-periphery here. And these areas are, you know, they correspond to the whitish lesions, the whitish hypopigmented spots we saw on the color photograph. And same thing in the left eye. Early on, you don't see much, but as you get later in the ICG she has this interesting, you know, mid-peripheral ring of hypopigmented area. So let's just throw out some differential diagnosis. Remember, we can think of things that are infectious and non-infectious. Anybody have any ideas? So let's review the case. So this is a 60-plus year old woman, Caucasian. She has blurry vision, trouble with night vision, retinal vascular staining on her FAA, deep caroidal spots on her ICG, history of BRVO in the other eye, which may be a red herring. What are you thinking? Okay. Okay. This is also a bilateral disease, okay, presenting basically equivalent in both eyes, and she has a mild detritus. So any other ideas? Those are good. What's that? TB's on the differential. So good. So let's think about infectious and non-infectious. TB syphilis, you know, POHS is lower on the differential, but lesions don't typically appear like this. Non-infectious. So I don't actually have the diagnosis up here. We'll see the diagnosis in a second. So sarcoid, multifocal corditis, and panubiitis, lymphoma, VKH, mutates, PIC, tipps, etc., those are much lower on the list. So what would you do for workup? So throw out some ideas. Okay. Okay. Right. Okay. What are you thinking of with that? So, you know, the workup, her ANA is negative. We got the ANA and we got some rheumatological testing because of her deformities in her hands and, you know, just to rule out that this would not be a typical presentation for rheumatoid arthritis. Her ACE and lysozyme were normal. FT and RPR were negative. Her PPD was negative. ESR is normal. She had an interesting history of a miscarriage, a PE, and a DVT. So she sort of looked into that as well. Lupus anticoagulatory. So her hypercoagulability labs were normal. Test text area is unremarkable. But as Russell mentioned, her HLA-829 was positive. So what's our diagnosis? Burt shot. So Jim will talk a little bit about Burt shot. Anybody have any questions about the imaging and the workup and, you know, our approach to the diagnosis? So from her history, mild vitritus, trouble with the night vision, blurry vision, the typical features of the FAA, which are retinobascular staining, and then the fundus appearance of these hypopigmented lesions and the nasal periphery, which show up in, which are much more numerous in appearance on ICG, that led us to think about Burt shot. And that is a, this is a classic presentation of Burt shot, I believe. I can go through the utility of this. You sure? Thanks. Alright, so like Nick said, I want to give Brian time to speak, because he's got a good presentation. That's where they get the same. Exactly. So this will kind of answer some of the, of why we ordered the HLA-829 by Dr. Vitelli ordered it. So the classic symptoms with which these patients present include floaters, photopsias, and nyctalopia. I think those are probably the three main ones that you'll hear most often. They can also sometimes describe problems with color vision, and sometimes they will actually tell you they have a spot in their vision where they don't see as well anymore. Oftentimes you'll find that once you start testing, but they don't always notice that until you point it out to them. So blurry vision, our patient actually mentioned blurry vision. They don't always present with that. And that's sort of a key point here, is that visual acuity is not a great marker for activity of this disease. It's kind of like, I guess maybe glaucoma or retinitis pigmentosa in that regard, and that you can have a 2020 patient with really active disease that's rapidly progressive. And you got to look beyond the visual acuity to follow these patients. But this is what they'll typically present complaining of. It's about 1% of referrals to tertiary centers for uveitis. It's a little over 5% of cases of posterior uveitis that we see. It's more often found in women than men, but men certainly have it. Dr. Vitale follows a good number of men with bird shot. Their average age is in the 50s. They're most commonly Caucasian. And then HLA-829 is positive in 90% of patients. But it's also present in 1% of Caucasians in general. So you don't want to just order this test on everyone, because it's not going to be that useful of a test. But if you have suspicion for bird shot, or if it's something that you're worried about missing, this can be a helpful test, because if this is actually negative, that's when it's probably the most useful. If this test is negative, then you probably should start thinking about other diagnoses. So that's why we ordered it. The patient had sort of a classic presentation, and had this disease been negative, we might have had to go down different roads to look for other diagnoses for this patient. On exam, Nick sort of pointed some of these out, but there are yellow lesions that are deep to the retina. They're usually smaller than a disc diameter. They can be asymmetric between eyes. They're often clustered closer to the nerve and most concentrated nasal and inferior to the disc. There's not really, typically, any pigment clumping on them, and these often appear a little bit after symptoms. As Nick pointed out, our patient had a pretty blonde fundus. Sometimes these are a little more obvious on exam. If the patient has a darker fundus, they stand out a little bit more. Also on exam, you'll often see vitreous cell in haze. You can see a retinal vasculitis. You can see discodema and macular edema. So that macular edema might be related to that old BRVO, but it might actually be related to her diagnosis of bird shot. That's sort of up in the air. You can find epiretinal membranes in these patients pretty often. And I say a relatively quiet anterior chamber because you can have half to one plus cell in the anterior chamber in these patients. That's not a rule, but if your patient has a few cells in the anterior chamber that does not rule this diagnosis out, they can have a little bit of inflammation interiorly. The fluorescent angiogram, it depends on the source you read, but there are lots of different descriptions of the spots that you'll see on a fluorescent angiogram depending on the phase of the disease and how active the disease is. You'll often see some abnormalities sometimes correlating with the spots that you see on exam, but there's no consistent pattern with whether they'll be hyper or hypofluorescent, how many spots you'll see, and how well defined they are. Other things that you can see, which we saw, are vessel leakage, disc leakage or staining. You can see neovascularization, which our patient did not have, so that doesn't rule this disease out. You can have that with birdshot. And the classic boards or OCAPS question for those taking that in a little bit is that there's quenching of dye from the ventinal circulation a little earlier than you would expect. So just to sort of review, with our patient we saw the vascular leakage and the disc leakage as well. You see it in the other eye as well. You can sort of see this traveling into the macula and creating a little bit of petaloid leakage as well in the right eye where we saw the macular edema on the OCT. The ICG is really the test that gives this disease away. So if you're suspicious of birdshot, like we mentioned in HLA 829 is helpful and an ICG is always helpful as well. This is where you get the classic hypofluorescent lesions and the intermediate to late phases on the imaging. The lesions typically exceed the number of lesions that you see on exam. Even if they have a darker fundus and the yellow lesions are more obvious you'll often see far more hypo pigmented lesions on the ICG compared to what you saw at the slit lamp. And then you get this diffuse hyperfluorescence of the coroid late on the ICG. The OCT you can see macular edema and sometimes you'll see some outer retinal abnormalities which were not as prevalent in our patient. So just to review the ICG again these are those hypofluorescent spots and we certainly didn't see that many yellow lesions on the color fundus photos but we see a lot of them here. So with further testing which we'll go back to our patient in a minute. The patient can have a negative waveform on full field ERG which basically means that there's a greater decrease in the B wave than the A wave. Late in the disease the entire ERG can go flat. So the B wave tends to go first and the A wave follows. Treatment which we'll get into in a second can actually improve the ERG over time. It's not a change that you'll see after a week of treatment but it can improve a little bit. And the most helpful parts of the ERG are the scotopic B wave amplitudes and the 30 hertz flicker implicit times. Visual fields are also helpful for following these patients long term. They tend to have any number of different changes. They can have peripheral constriction arcute defects, multiple foci of field loss. But the abnormalities in mean deviation can be helpful to follow for these patients. And a 24-2 is not often good enough to really follow these patients long term. You want to get out to that peripheral field. So a 30-2 or a Goldman visual field are helpful. Most of these patients will actually get worse over time if they have no treatment. And the treatment does tend to decrease the chances of bad visual outcomes. What 20% of patients would do just fine without treatment is a good question and it's hard to identify them. So this is a bit of a controversy which will open up to the floor in a couple minutes. Is it worth treating these patients or not? And there's not a general consensus on that answer. If you choose to treat, steroids are generally not sufficient as monotherapy. They're good to start at the beginning and you can add them on top of these other therapies to take care of specific aspects of the disease like macular edema. And they can be oral subtenons or intraocular. But immunomodulatory therapy is really what's helpful for these patients in the long term. And you typically start with an anti-metabolite. And if that's not stabilizing the trick, if that's not stabilizing the disease and keeping it from progressing, you can add these other immunomodulatory medications below. The way you would determine if these medications are helping or not is again not by checking the visual acuity on each visit but by checking how the visual field is changing long term and how the ERG is changing long term and checking active disease at the slitland. For active haze and macular edema and those sorts of things. So you want to look at a lot more than just visual acuity with these patients. I think it's one of the take home messages here. And I'll turn it back to Nick. You want me to just finish this. Save time for Brian. So with our patients specifically we did get Goldman visual fields which shows some general mostly nasal peripheral field loss. Same with the left eye. And if we move on to the ERG, she did have some changes on her ERG with a 30 hertz flicker and the scotopic waves as well. But to get to the real discussion here there are some controversies with this disease which include what's the role of HLA A29. Thank you Dr. Valentine for that question because as I mentioned a lot of people have a positive HLA A29 and don't have bird shot. So when is the right time to order this test? Another question to be asked is should all patients be treated? Because as I mentioned some patients do just fine without treatment and the treatments that I mentioned do have side effects. They're not benign drugs and we're talking about putting patients on these for a very long period of time. They're not going to be on them for three months and then stop. We're talking about years of treatment. How long should patients be treated? And what's the best method and frequency for monitoring the disease? At this institution we tend to follow them with fields and ERGs and seeing them in clinic. And how is remission defined? At what point do you say this disease is stable? We're okay to stop treatment and just watch you. But I'd open it to the floor if anyone has comments on these issues or questions or anything. Yes, that's a good question. I don't know. Do people know that? I'll say on that from an anecdotal standpoint I think most of the residents and fellows here have seen patients from Dr. Vitalli's clinics who have gotten tired of the IMT therapy and have decided to go off of it. And then they come back three years later and you look through their chart and they were stable for a long time. They sort of disappeared for a while and they come back and their ERGs are flat and their fields are much more constricted. That's not exactly a prospective trial but it is kind of upsetting when that happens. You see these large changes when they stop their treatment. Yes, Dr. and Buddy. It tends to be systemic therapy. The intravitrile drugs that we use for these patients tend to be steroids if they're warranted. But no, not intravitrile, not the trixate. All of these are, that's a good question. All of these are systemic systemically administered. I'll turn it over to Brian. Never mind. Thanks. Thank you for your help.


Obesity has become the most devastating modern day plug throughout the world. Both in the developed countries such as the US and the developing countries such as China, more than 20% of the total population is obese. Obesity is a single risk factor which is inducing more than 50 kinds of different chronic diseases, including the type 2 diabetes and some kind of the cancers. Unfortunately, the rate of the obesity is still increasing, particularly in the children, making it the big public health problem in many countries. What can we do to stop or reverse this obesity trend? Where is hope? An emerging field called microbalm science and technology may help the human can to stop or reverse this obesity pandemic. Iron human beings have a huge number of diverse microbes living together with us, particularly in the gut. The cells of the gut microbalm can be 10 times more than our human cells. The gene encoded by our gut microbalm can be 50 to 100 times more than the gene encoded by our own human genome.   The gut bacteria can produce a lot of essential functions for the human host. The gut bacteria grows by using the undigested or non-digestible compounds from our diet as their nutrients. They also can grow by using the mucine and the loft cells from our intestinal tract. When their growth, the gut microbalm produces a lot of kinds of bioactive compounds. Some are beneficial, others may toxic or detrimental. These bioactive compounds can come into our bloodstream and impact the host immunity and metabolic metabolism. Many studies, including our labs, show that overgrowth of some bad bacteria in the gut, which can induce chronic inflammation, may lead to the development of obesity. We found that when endotoxin-producing bacteria overgrowth in an obese human gut can induce the obesity in the germ-free mouse. For following the cohort's postulate, this is the first example to show that some gut bacteria can be worked as a pathogen for obesity. If this overgrowth of this obesity pathogen is an important role for driving the obesity pandemic, can we do something to manipulate the gut microbalm as a new way to control obesity and related diseases? The answer is yes. We found that non-digestible but fermentable carbohydrates and some phytochemicals in the traditional medical food in China are potent ingredients for modulating the gut microbalm to a healthier structure. A new diet scheme which can provide the balanced nutrients for the human as well as for the gut microbalm, we call that phytochemical gut microbalm diet can encourage the growth of the beneficial bacteria and reduce the level of the bad obesity-inducing bacteria. Our clinical trial showed that this gut bacteria target diet can help the obese adults to reduce their body weight and regain the metabolic health. It can also help the morbid obese children as young as three years old to lose their substantial amount of body weight. It even can help the genetic obese children, such as the patient with Pran-Willi syndrome, to lose almost half of their initial body weight and regain the insulin sensitivity. However, it is not one magic bullet type of intervention. We need to regard our gut microbalm as a very complex ecosystem and manage it as such. It requires new diet and lifestyle management with rebuilding the health gut microbalm as the bioclinical goal. Now we have helped hundreds of obese patients to rebuild their gut microbalm and regain the metabolic health. So my question to you in the audience is how can you help us or how can we work together to make this new obesity management tool available for millions and millions of people, the rich and the poor alike? Thank you.


We got a good one today, boys. So you get 12 points for a 20-yard offensive touchdown. I've got a couple plays that I feel pretty confident I could do that with. You get three points on an interception or forcing a fumble. This cooldown is three. Literally, I have no idea what that could mean. Got a 95 overall team, but here's the thing. I know you guys see the same players for me every time because, like, Wheel-A-Mot, I always have this Tyreek. You know, I always have this Barry Sanders. And I always have Lamar Jackson. So I'm going to try some different stuff out today. And I'm probably going to expect some new players. So let's go buy some stuff. I'll open up a few packs actually first. See if we can somehow pack something new. I'm going to open a free agency bundle with four free agency packs. I highly doubt we will get anything, but it's worth it.  That's definitely not going to be a starter. I would basically need, like, Nidama can sue to come out on one of these. Carl Joseph, AJ Brown, probably just going to go straight to the auction house. This may just have been a waste of my time. Well, hey, boys, if I can leave with any information, it's don't open packs. Yeah, that could be good advice here. Okay, you know what we can do? This is guaranteed to get us something good. We're going to get a 97 overall theme MVP. Give me something dope that I can play. Ryan Fitzpatrick. I came back. I'll do it. Well, we're not scrambling, at least not much. I'll tell you that right now. Additionally, I want to give a huge thank you to Hustle Castle for sponsoring today's video. This game is so addicting, so I wanted to share it with you guys. To keep it simple in the game, you're the Lord of a huge castle. You can expand the castle, attack enemies, get warriors to fight for you, upgrade them, and go on boss fights. Honestly, there's so many things you can do, and I want you to see it for yourself, but I'm going to walk you through some stuff right now. Okay, so these are my three best fighters right now, and I'm about to go into a boss fight. So I want to upgrade my fighters so that when I go into this boss fight, I'm definitely going to win. So I'm going to open a Mythical Chest right now and hopefully get a new purple weapon. I got purple armor and a purple bow. Okay, perfect. So these are epics. They're super rare, and I'm excited to get one right now. Okay, so I'm going to give her this purple bow right now, and this is going to make her so strong. And this is the fight I've been waiting for, so I fought through 13 different waves of enemies, and I finally get to grab. Let's do it. He is huge. And dude, he's getting taken out. Dude, that archer is way too good. My archer is way too good. I can go through the whole game like this, I think. And I get a boss reward for winning that fight, and I just got a blue crossbow and new green armor. All right, awesome. Oh, also, I just made my own clan. Make sure to join. It's called MMG Boys. So, of course, there's a link for you in the top of the description. If you download Hustle Castle via the link below and enter your nickname, you're going to get a special bonus for all new players. It's 250 diamonds and 3,500 gold pieces, which is so helpful at the start of this game. This game's a blast, and has hilarious storytelling. I love the graphics and the color. All around, it's super fun. So you guys got to check it out. Hustle Castle, thank you for sponsoring. Enjoy the rest of the video, you guys. All right, so let's mess around with some X-Factors. I'm not really used to any of these. He gets protected. This ability is sick. Stronger pass blocking from all offensive linemen. I'm going to give him a hot route master for additional hot routes. Damn, he kind of gets some good abilities. This is actually really funny. I couldn't tell you much about Ryan Fitzpatrick, but we're going to try out pocket that I hot route master protected for this video. I want a new halfback. I want to mess around with the totally new halfback that I've never used. Just do something random. Something totally random. Damn, there's a lot of options. I want to love you on bell. Oh, but he's so damn slow. 91, really?  I'm going to MSU alumni, love you on bell. Statistically, he looks like one of the worst halfbacks on this board, but he'll get leapfrog, which we haven't used in so long.  Evasive leapfrog and outside zone guru. That's so weird. That's so weird, but we're going to try it. We just made this team so weird, so fast. I like it though. Is that my top three? Yeah, that's my top three. Let's see what he's got. Dak, T.O. I was going to say he has a Cowboys theme team, but I don't think so. All right, boys. Let's see what this Dak Prescott team has got. What's he looking for? You can't throw any of these, bro. What are you about to throw? I think he ran himself out of bounds. Oh, okay. Yeah, so the cooldown means that there's a three-play cooldown every single time you run anything, offense or defense.  Wow, this is really interesting. Second and 21, sending a big blitz. Um. I don't know what he's going to go for. Oh, that's a safety, safety. So the fumble gave me three points, the safety gave me two, and now it's my ball. We're going to pitch this out to Leveon Bell. We're going to get working on these X-Factor super early, okay? Evasive!  Literally every player is going to catch him at that speed. That's too bad. Let's see if we can get something. Oh, yes. Yes, Ray. Oh, he caught it. Ray Lewis rocked him, but he still caught that. Great job. I'm going to go to a peek zone bubble. I don't get to run it very often, so hopefully this is successful. You definitely have it. He's not ready. He's not ready. Let's go. Give me a spin? Yes! Leveon Bell's spin was so good, but it didn't get me enough. I got to go for it here. I don't have to, but punting doesn't make a lot of sense to me right here. I'm throwing it toward home. Got it! Let's go! Let's a touchdown! Wait! Is it a touchdown? He's so fast! Oh my God!  All right, we're going to go inside zone to Damian Williams here. Great blocking. What a drive. Cover two, playing underneath. It could be a run. I want Ray Lewis to be there if it is. It's not, he's looking for something small. Looking right here. Oh, he's going deep! No way! Tillman, how did you not get over to that? Wait, why does he have 12 points? Was that a 20 plus?  I did not realize that.  Get that pass, Fitzpatrick! Oh my God! What a bomb! Dude, Fitzpatrick is a God! He just tossed a bomb! All right, I'm just going to go straight into bench. Maybe I can hit him with a cheeser corner out of my own.  Oh my God, that's a pick six. Why would I do that? I never, ever throw that pass on the red zone. All right, I'm going to try this, where we just... Ooh, that's open. That's totally open. What a ball! I got a peak zone bubble back, so I'm going to give a rip at it. I need that 20 plus yard TD. Ooh, he's sinking to it. He sunk to it early. We're just going to go Damian Williams. Oh, that's so... Oh, it's not open.   And Shaz just hurdled me, and he's going to return it again. How is there no one there to get that? This game is harder when I can't scramble. I'll tell you that right now. All right, I see Leveon Bella open underneath. I hope you guys can understand that I'm going to concede this one and just try to do rope one. That was so bad. Pretty sure I was beating him 11-0 at one point in that game. Nate, Nate stir, 8,000. His team is not too insane, so I'm feeling pretty good about this one. All right, here's what we're going to do. We're just going to start this game out with a touchdown from Ryan Fitzpatrick. Wait, where are we actually going to? Oh, oh, I know what we're going to do instead. We're going to start out with an interception.  I'm blitzing everybody.  Oh, it's a play action. He got the pass off. I was in the backfield so fast. So this is going to be a run, third and two. He just wants the sticks. He can't get them. I'm going to press cover on this blitz. Does he throw out of the backfield? No, but he gets sacked. Let's go. Kind of was hoping he would throw it and throw an interception on accident. I'm going to try to get him again. I feel confident. I goofed at once, boys. I'm not going to goof it again. All right, I'm sending everybody deep. Fitzpatrick is going to get incredible blocking and Papamute is going to throw. Oh, he's not even, he, I think he left his Xbox or something. I don't know what he did, but he did not try to play that. First in 10, I'm sticking with the blitz package. I liked it. Let's see if he tries to throw. He does try to throw. Oh, I wanted my interception. I wanted my three points back. What are you doing, Nadester? Who do you want to throw this to? Oh, that's bold.  Let's go. Galomag gets it. Okay, I'm having a lot better of a game this time. Jeez, that last game was bad. I'm blitzing everyone.  Got him anyway. Good Lord, these blitzes are hot. I'm exactly on the 20. I don't know if this will count. It looks like it will. This will probably count as 20 plus. I'm going to try and hit Tyreek or somebody else if they're there. Tyreek, Tyreek, Tyreek. Oh, did he catch that? Oh my God. I thought I got picked off. Oh, they only gave me six for that. That's so not cool. That's unbelievably not cool, actually. All right, we're flipping it to the kicker. Grogg's got it. Aw. First in 10, keeping the blitzes hot. I got underneath covered. He's got nowhere to throw.  See if he ever adjusts to it. He runs the ball to Kyloos check, the fullback. Interesting adjustment. This is just an ego game. I just need to build my ego backup after last one. If he throws underneath, I'm screwed, but I'm blitzing. Let's go. Dude, this is rude as hell. Now I got it on the 17. I'm running the read option, but I can't really let Fitzpatrick have it. So pretty much just have to hand this off to Bell. Let's use the spin. Got him. Oh, but I spun a little too hard. All right, you want to see some absolute savagery?  It's first in goal from the five, right? If I score, I get six points. Here's what a true savage would do. Let me show you. I've got a touchdown, right? No. You pull it back. Now, when I get this touchdown, it's worth 12.  That's a blitz. You what? Got him? Oh, no, he switched on. Ah, damn it. It was going to be so cool, and now it's just useless. I have one play to renew myself here. Oh, that's the wrong pass. I'm bad at this game. Why am I so bad at it? All right, I'm going to take it very seriously in this half.  I'm going to get my points.  A third and 25. He has never thrown to his half back onto the backfield yet. Oh, he runs it. Fourth and 29 is going to go for it, not get it. And this won't count as a 20 plus. I'm coming off hot off the edge, Nitrene Lane. I finally get three points on a pick, and I could return this, but it actually makes most sense for me to stop it right there on the 21 and then throw it in. Let's see if one of these gets open.  Is it there? Doc fits Patrick with a doc. That's pocket dead eye right there. Never used that before, but that was sick. Defense is pretty much the same every time, guys. They just send a huge blitz and then he runs it and then gets no yards and gets sacked. So I'll probably skip as much of the defense as I can. Hey, props to this guy for sticking this game out, though, because this is a true massacre. Please throw it to somebody. OK, you know what? That's actually perfect. All right, exact repeat of last time. All right, so I liked what we did. We threw something weird that Ryan fits Patrick could dot up, right? I bet you we could do the same thing, honestly. Let's see how this sets up. Oh, yeah, that's there. That's totally there. Oh, they counted that! Dude, he was not in. I feel like he was totally out, but I will totally take my points. We got 49 now, and now can I actually get a two-point conversion? I can. Nice work. He throws. Wait, I'm being greedy right now. I know, but pick that off. Could not tell you what this is. OK, OK, but wait, but wait. Good tackle. First in 10. Where's he want to go? Hits the sideline. Good spin. Wow, he came alive here in this final drive. Can we get the red zone stop that we desperately want? Can we pull this off? He throws. Night train late, and he catches it and scores. I'm impressed. All right, we got some ground to cover. Uh-oh, uh-oh, I threw the belt. Nobody picked me off. I literally don't want you guys to watch this video. No way! And he caught it! Oh my god, I'm embarrassed. I'm so embarrassed. He's really about to score it again. I'm gonna throw the deep post on mid-high low. We're gonna see if Tyree Kil can just put the nail in the coffin right here. I'm bombin' it up.  Damn it.  Even in a game that I just shoulda won by so much, I really didn't even play that well. It was still fun though.  I had four TDs, but only 162 yards.   All right, boys, that was show off. I didn't really show off my skills at all. In fact, you probably think I suck, not after this, but that's all right. Thank you for watching. I'll see you in the next one. Peace out. By the way, guys, don't forget to download Hustle Castle. I talked about it earlier, but there's gonna be a link in the description and there'll be a link on the end screen of this video, so make sure you click that. Get the special bonus. Try it out. See you guys.


My name is Marcy Sklow, welcome to Going Deeper. Today I'm sitting with the Reverend Dr. Andrea Vazian. Andrea is a long time activist, social justice activist and a Reverend pastor and her latest big endeavor, very creative endeavor is the Sojourner Truth School for Social Change Leadership. Perfect. I did that very well. Perfect, perfect. So we're now embarking on part two of this interview. Welcome. Thank you so much. I'm so happy to be here. Yeah. So instead of asking you a question, a question, a question, this is the kind of thing I'd like to cover in the next 30 minutes. I wanna really hear a lot about the school. Good. And it is amazing what you all are doing. I wanna hear also about your work regarding being an ally. And I interviewed Irvin Stalb in the past and his work on active bystander ship was resonating for me a little bit in terms of the ally thing. And then if there's time a little more about the anti-racism work that you're doing would be fine. So I don't know where you wanna start with all of that because it kind of all feeds together. It does. Yeah. Shall we start with some comments about the school? Sure. And then we can get to ally behavior and ally shifts. Exactly. I'm delighted that you are a supporter and a fan of the Sojourner Truth School for social change leadership, which we often call the truth school. And I will tell you how it came into being and how we're doing briefly. I, as we talked about in the first half hour, was the pastor of the Haydenville Congregational Church for 12 years and announced my retirement from that church in the summer of 2016 and announced that I would be leaving in 2017. And it was the summer of 2016 that never occurred to me that Trump would win. It just didn't occur to me. I thought I would move into retirement and paint and write poetry and visit Sasha and Austin and have a nice life. It didn't occur to me that the world was about to shift. And then I had announced and then in November, Trump won the election. And I really became very depressed and very distressed. And in January of 2017, I made a long train trip for three days to Austin, Texas to see my son. And I was really very inside. And as Quakers would say, under the weight of it, I was under the weight of it. That Trump had won and I'm a lifelong activist. And I had lost my bully pulpit. I had lost my church and my community and the people with whom I had been so active. And I was very troubled. And I started saying a mantra to God, which was I am your servant, show me a sign, show me anything I am supposed to do in the Trump years that will make a difference. And it was on the train trip home that I received or I had the sense or vision or whatever of the Sojourner Truth School for Social Change Leadership. And it literally came to me. And I called Michael, my partner, my husband now, from the train and said, I've had this idea. And he said, run with it. He said, oh, you got zapped again. He calls it when I get zapped. He said, oh, you got zapped again. I didn't have the title then, but I had the idea. What we are is a nonprofit that offers movement building, very concrete, skill building, movement building classes in Greenfield, Northampton, Eastampton, Holyoke and Springfield. All the classes are free and we pay our trainers. And we use sites that already exist so we have no overhead of a location or an office or a building. So we use synagogues and church basements, lots of libraries, union halls, GCC, HCC. We use any place that'll have us that's on the bus route, on a bus route, is wheelchair accessible, doesn't charge us and welcomes us. And we teach everything from how to write an op-ed, how to write a great letter to the editor, how to speak in public, how millennials and elders can organize together, how we just, how to hold on to hope in hard times, how to sing songs of freedom and struggle, how to, we, this is our catalog for this fall and it has 56 classes in it, 56 classes between September 1 and the end of 2018. Oh my gosh, so that's only like three months. That's right, that's four months, three and a half months where we have 56 classes. And we meet on Tuesday nights, Thursday nights, Saturdays and Sundays. And the trainers are diverse, we have a very diverse pool of trainers. And a fifth of the classes are in each of the cities. What we're finding, Marcy, is that because the classes are free, we're just crossing lines, we're crossing boundaries of people who are middle income, people who are low income, people who are wealthy. Because we're in three counties, people are crossing county lines. So people in Greenfield are thinking, I really like that class in East Hampton and are coming, people in North Hampton are going to Springfield. People from Springfield are coming up to Holyoke. We're breaking down silos and we're finding that at the end of classes, people are taking out their phones and saying, now what's your name again and putting each other in their phones and saying, I'll beat your rally now, don't forget our fundraiser, that's happening. So the network is growing, the movement is building and the silos are sort of coming down. It's really a remarkable thing. We have a nonviolent army of volunteers, we have a lot of faithful people coming and we evaluate every class with a very formal evaluation process and people also tell us at the bottom of their evaluation sheets what classes we're not offering that they wish was there so then we can be very responsive and so we've added more on anti-racism, we've added more on cross-generational work, we've added more for teens, we've added teen and millennial trainers because people have asked for it. Sure, I also just need to put in a plug because I've started volunteering, haven't yet done a class but I've started volunteering as a host and I went and picked up my supplies and I never could imagine how complicated it is to logistically have all these classrooms in all these different places so I got a bag with a beautiful logo on it the True School and all my supplies and that was a whole other aspect of creative organization. And you know, what's really coming through is that I'm such a long time anti-racism workshop leader and trainer and nonviolent direct action trainer, I've done so many thousands of workshops that as a trainer I thought what do trainers need, what do leaders and teachers need and I thought somebody to pamper them. So we made the host program and you thank you Marcy and all these other men and women get there early, put the chairs in a circle, give everybody a name tag and frankly it is logistically complicated. We are using places we don't own so you have to get keys and show up and turn up the heat and lock up and so the host program is a huge hit because the trainers are being pampered. I was thinking if there is one person who gets some jolt of inspiration or some training that helps them move forward in making our world a better place, I'm all over setting up chairs and cleaning up the room and turning down the heat and sweeping up or whatever is needed. You know, it's all part of the work. There you go and we've heard stories already because I had the idea on January 29th, 2017 and we opened May one. We opened May one and have been running classes ever since so we've run 168 classes and we've trained almost 2000 people and what we're hearing Marcy is that people are coming back to us and saying I went to the peacekeeper training and three weeks later I was a peacekeeper at a marching rally in Springfield. I went to Michael Clare's publisher parish and then I wrote my first op-ed, it's coming out. We're seeing the results. So quickly. It's so, I've got chills right now because people are coming back to us and saying you taught us about effective consensus decision making and then I went to my affinity group and taught them. So we're hearing some of the feedback and some of the effects. That's amazing. I guess that in every way that you can let more people know about this is just gonna be important. How to market it in all these different ways. And that's the challenge because young people use social media so we're trying to use Twitter and Facebook and the things I don't do but some people in my generation really like a hard copy.  We leave these in bus stations. We leave them in doctor's offices. We leave them in lobbies. We leave them in bathrooms. We leave them in libraries. So there are people who are literally picking it up and there are people who are hearing about the school online. And also I'm imagining, you know, reverends and pastors and rabbis are announcing them. Totally, putting it in the bulletin. In the bulletins and in newsletters. Good, good. Well, it's so helpful in hard times to see that there is something we can do, you know? So I'm very happy about that. Thank you for being a host. We need you. Oh sure, I haven't done it yet but I will in a couple, like a week. Soon. Yeah, yeah. So talk about this concept of ally-ship, ally-ness and what that means. I mean, I think whites, also first of all, I just wanted to comment on your beautiful expression of your own history and your own background but it's interesting historically when all of these different sects, different cultures, all became white. And you know, like me too, you know, in different ways that in the past we weren't all seen as the privileged white. And now we kind of are all lumped into that and we have to own that. And how to talk to white people, all the different kinds of white people about their privilege and what they can do. So say some more about the ally-ship. That's such a great lead in because Irish, Armenians, Jews, other people who have been discriminated against and of course Jews by religion and anti-Semitism but when you think about people becoming white we remember that race is just a social construct that it has no biology, it has no basis in anything significant and it's a social construct for the purpose of exploitation. So a privileged group that became white through the various incarnations over time and a group that could be targeted or exploited that there would be a bifurcation and there would be a justification of that so that distortions and lies and histories, history was created, distorted misinformation, stereotypes and biases so a group or groups could be exploited and abused and depressed. But it has no basis in anything that is biological, sociological, anthropological that's completely gone, that's completely untrue. What I think is significant about allied behavior is that there are seven or eight forms of systematic oppression in this country. By gender, by race, by physical ability, by religion, by age, they're the isms, ageism, antisemitism, racism, sexism, homophobia, heterosexism, those are the isms. And what people tend to do is to identify very strongly with the place where they are targeted so that for me I'm dominant in every area except by gender. So to spend as we talked about in the first half hour to spend so many years talking about sexism in the only area where I was oppressed missed all the areas where I was dominant. I see. What allied behavior it does is it flips the script, it changes, it shifts the story and it says all the areas where you're dominant that's where you need to be active in partnership and speaking out in the areas where you get unearned advantage. And I get unearned advantage in six of the seven. So as a white, as a heterosexual, as a Christian, as a able-bodied person, I have privilege dripping from me when I walk in this room, when I drive home to Northampton, when I go to stop and shop any moment when I read The New York Times, any moment I am over-advantaged.  And the ally role is to see what has been made invisible to us for so long, which is our privilege. So that when you ask a white person to notice their privilege all day, it's like asking a fish to notice the water. What privilege? I'm in it all the time. But with training yourself to think how we are overly-advantaged as whites or as men or as people who are able-bodied or temporarily able-bodied as we say, tabs, or that we are able to see that we can speak out, we can notice who's not in the room, we can notice who's voice was silenced, we can notice who's safe and unsafe, and that we can speak to other people who look like us. So Marcy, you and I would be white allies able to support each other in swimming against the tide and in being outspoken people whose identity was allied behavior. I actually think that has been the biggest shift in my social activism to see myself as overly-advantaged, as having unearned advantage. It's not because I was so great, so smart, or so capable. It's because I was white and middle class and able-bodied and that advantages were just opened up before me. It's like I got a leg up everywhere I went. And whether it was housing or college or getting a mortgage for our home, people looked at me and Michael as a couple and thought, you're just what we had in mind. So I think it's very significant that we raise our kids to be allies at an early age. They get it, they can speak out, they are remarkable, and that we continue to work with people over time so people see their privilege, not just where they're targeted. And everyone can be an ally unless you are multiply, multiply, multiply, multiply targeted. There's some area where people have unearned advantage and can be outspoken as allies. And so that's why I think the concept and the identity and the activism is so important. So can you walk me through an example? I mean, you've been giving some examples, but let's take a white, let's take a coal miner from Kentucky. We just had this amazing Kentuckians coming to lever it and Paula was on my show and talked a lot about that. So let's think about Kentuckians who are in really a bad way because of the lack of work and how things are shifting in the economy. Yet they do have privilege. So how do you move them into this notion? I think we recognize and validate places where people are targeted and you start there. So you would start with somebody by saying you may be targeted by economic status. Poor people are targeted. They're targeted by classism. And that is difficult and presents every day of one's life challenges that in some days feel insurmountable. So people may, in using your example, feel targeted by class. They are targeted because they are poor. They may feel targeted by also that they're sort of geographic advantage that people believe that the stripes of the coasts that people are advantaged and they may feel targeted by regional biases and stereotypes. They also, I think everyone can recognize that white people in any setting, whether you're a coal miner or a CEO or in Hollywood or a nurse or a doctor, white people simply are treated with more respect, are safer in any interaction with the police, are underrepresented in prisons and on death row that even when one is targeted, one is advantaged if you are white. And that to ask people to hold the paradox and to hold the contradiction that we are targeted and privileged or dominant at the same time and that we have as Bev Tatum as Dr. Beverly Daniel Tatum would say, we have multiple social identities and to help people see the whole picture that we are targeted and dominant at the same time. And in the areas that we're targeted, we want people to be our allies. Your example, we want people to speak up for economic injustice for the huge gap between rich and poor. We want our allies who are middle class and upper class to stand with poor people. And in the areas even when we're targeted where we have privilege, we want to stand with others who are targeted. So any white coalmire can still be an anti-racist even though they may be multiply targeted in other ways. It's complex, however, it is a way of thinking and moving through the world and it is an identity. We want others to stand with us when we're targeted and we want to stand with others where we have the advantage. And white is always, always, always, always an advantage.  That's exactly the opposite. Racism is so old, so profound and so entrenched in America that racism is always present unless it's removed. So unless you have active anti-racist activity, racism has to be removed.  Which is what we've seen historically in Amherst schools, for sure. Exactly. Exactly, precisely, you said it precisely. Yeah, I've had a few people on the show talking about that. Absolutely. Specifically. I know you have. Yeah, yeah. Well, okay, so not to digress, but there is this movie that I really like called Pride. Have you seen this film? No. So the film is about these LGBT British young people who hear about the Welsh who are striking in their minds. I have seen it. And they decide that they wanna go and be allies to these Welsh coal miners. And they go there and at first, the Welsh are really mean to them. Really? And very discriminatory. And slowly, slowly, they accept them. One of the Welsh men admits he's gay. And there are these beautiful scenes of these two communities coming together. I did see it. And in the end, they go to a march together. To a Pride march. And there's the coal mine.  Absolutely. And they're completely, they're hugging. All these gay men are wearing pink boas. And the coal miners. And it is because people became real to each other. Because relationships break down biases. Because you can't hold a stereotype when this person is marching with you or lifting your cause. So when gay people who are targeted by homophobia and heterosexism, but are advantaged by class, team up with people who are targeted in other ways, there you have an example of targeted and dominant joining forces and becoming a voting block and a marching block for change. That, I have seen it. I forgot the name. It's so touching in the end when they're side by side in their arm in arm. It's a beautiful film. It's like we have an expression in my field as pastors, that's the in breaking of the kingdom. That the kingdom of God has moments when it breaks in to ordinary life on earth, when moments are perfect. When you have a perfect moment, it's an in breaking of the kingdom. When justice reigns, when peace is present, when people are safe, when kids are cared for, you'll have a moment that's an in breaking of the kingdom. The end of that moving when their arm in arm is in breaking of the kingdom. I love that expression because when we're looking for a movie to watch, we usually say we want it to be affirming, but this is much more specific to what we want, which is the in breaking of the kingdom. Wow. That's actually a very important concept for me to add to our interview. Because I believe it is what we are striving for every minute that the in breaking of the kingdom may be a moment today and two minutes tomorrow and an hour next week, and that we are creating, I would say, the kingdom of God on earth, even if there are just fleeting moments today, we are creating the vision we hold of people safe, of kids cared for, of the earth honored, of justice reigning, of peace present, that's the kingdom. And that we work towards it and walk towards it every day, all the time. And we have experiences of it that are tangible. You've had them. You've had them on the show with people speaking about their lives and visions and work. Sure, yeah, yeah. It's reminding me a little bit in 12 step work, the notion of spiritual awakening. So that in breaking of the kingdom is kind of like having a spiritual awakening or some sort of a epiphany or an enlightened moment. And there are religious leaders who say, it's not just something out there that we aspire to. We have those. We might have a dull period, but from time to time or multiple times a day, we do have those. Absolutely. And it goes hand in hand with we are the ones we've been waiting for. We are the leaders we've been waiting for. It isn't someday, it's now. The choices I make about the choices we all make about our time, about our dollars, about our energy, about our speech, about our activism, we are the ones we've been waiting for to make the change that is right around the corner and the in breaking of the kingdom today. It's a wonderful, wonderful image that I love, that I hold on to. And a wonderful place to stop. Yes. Our interview. Perfect. So thank you so much. Thank you so much, Marcy. Thank you for having me. Thank you so much. And thank you all for watching. I wanna do a shout out to Amherst Media. Thank you so much to the interns and the staff and everyone here who makes these shows possible. And also, if you'd like to see any of my shows, you can also go to marcysclove.com to see them there. Okay, thank you. Well, when I was a little boy, he said, son, let me tell you about that.