All right, good morning, everyone. Welcome to Grand Rounds. I'm Sean Collin, one of the chief residents. I'll be moderating today. We have three riveting cases and very interesting titles as well. We have two of our chief residents presenting, Cole Swiston and Allie Simpson, as well as one of the pediatric neurology, PGY3 residents, Mary Glenn View presenting. We'll start with Cole Swiston. And a fun fact about Cole, Cole is an avid fisherman, as most of us know. He recently bought a secondhand drift boat and hopefully we'll be able to take that out at some point this spring and he'll have to row the rapids that have been a nemesis for us for the past three years.  Instead of shoveling my driveway, I've been shoveling said boat. Okay, so I have a couple of cases that I saw as a PGY3 on primary call that I'm titling 12 beers and a PB and J with a unifying diagnosis, but just kind of a challenging thing to see. So jumping right into it, I'm not gonna give it away, but I'm just gonna present both faces first. First one was an 11-year-old nonverbal boy with autism. He presented, actually he had three exams over the course of a week, one in clinic, one in the ER and one formal E-way. Before ultimately it was discovered the diagnosis. Parents were concerned that he had progressive vision lost both eyes over three or four months. He'd been bumping into walls, falling downstairs more often and had difficulty with his iPad that was uncommon for him. And they noted some intermittent tearing and redness in both eyes. He has some atopic history, including eosinophilic esophagitis allergies, but no known past ocular history up until this issue. They've been using an allergy eye drop for this tearing and then he takes Xeritech and Flonase for his allergies. This was from my exam with him in the ER. Him being nonverbal, going to tell that he was intermittently fixed and following no pupil issues and normal pressures. And then most notably on his exam he did have trace to one plus injection in both eyes with a keratinized appearance to superior conge and then scattered fluorescent uptake to the ball bar congenitiva. The cornea had three plus diffused punctate epithelial erosions in both eyes which were confluent in the right eye with an FB defect, although he did not have any concern for ulceration or infiltrate. Thinking about other etiologies or vision loss in a nonverbal patient with autism, maybe self-harm behavior, there was no cataract, no retinal detachment, though the view to the back of the eye was fairly hazy due to the cornea. And these were pictures from the EUA that you can see just with the ret cam photo there that that superior ball bar conge is quite wrinkled and kind of a very rough keratinized appearance with fluorescent uptake and then an inferior affluent FB defect there. So that's case one, not going to give it away. Similar but separate case was actually just a month later on primary call in the university emergency department at 36 year old male with eye pain, both eyes but right worst than left for five days. He had the same symptoms a few months ago and was treated for an eye infection with some drops, no recent illness, no contact lens use, no trauma for him body and really no prior ocular history up until this issue. It takes no medications. We're able to get a vision on him. It was four, 2800 at the phase in the right eye, 2100 in the left, no improvement pinhole, no pupillary issues, normal fields, extractor movements in the normal IOP in both eyes. Exam for him also had injection of both eyes, right, worst than left, rough, variably staining, keratinized congenitiva, bulbar conge. His right eye did have an inferior infiltrate and ulcer with an overlying FB defect with some thinning and diffuse stromal haze, no ulceration in the left eye yet but did have rough appearing epithelium with diffuse punctate erosions. In that ulcerated eye did have a underlying fribrous reaction in the anterior chamber and then the rest of the exam was limited due to cornea but normal. And so what I did mention for both of these was the importance of social history and diet. So patient one, the boy with autism, his entire diet consists of peanut butter and jelly sandwiches. It refuses to eat anything else. Patient two is very gaunt in appearance. He drinks 12 years a day and eats primarily fast food. And so I did not pick up on this in the first patient in the pediatric ED but with the EUA with Dr. Hoffman, I almost immediately recognized that we should draw serum vitamin A level which was lower than the lower limit of the assay for that patient. And then when I saw this second patient, I said, that looks pretty similar. And with the alcohol use, drew a vitamin A level which was also reduced. I wanted to talk a little bit today about vitamin A deficiency and the ocular manifestations of that which is zero ophthalmia. As far as WHO estimates globally, it's the most common cause of blindness in children with over 250 million children affected and then almost three million with the ocular manifestations. And as we probably know, that's most commonly due to malnutrition in developing countries but in the US, we don't usually think of that as an etiology as most of our foods are fortified with vitamin A, milk, margarine, cereals, some other foods all have vitamin A in them. And so in the US, it's usually a malabsorptive process or a GI tract disorder that will get you to this point but I thought it was interesting that both these cases, both these patients ate their way into or drank their way into vitamin A deficiency. So where do we get it? In the diet, you can have vitamin A in two forms. The preform of the vitamin A, retinol and retinolasters come from animal products, primarily liver, fish, eggs, and then fortified dairy products or from usually plant-based products. You can have pro-vitamin A, crotinoids, alpha beta-carotene and beta-cryptozanthin, comes from leafy green vegetables, sweet potatoes are very high in vitamin A, tomatoes, fruits, and then some vegetable oils. Importantly, in the US, 75% of our vitamin A is consumed in the preformed version and up to 40% of that comes from enriched foods, kind of highlighting that importance in our diet. While globally, depending on diet, usually it's consumed in the pro-vitamin A form and up to 100% of this preformed vitamin A can be absorbed in the duodenum but only 10 to 30% of the pro-vitamin A-crotinoids, hence another reason why we see it less commonly in the US. Vitamin A is a fat-soluble vitamin absorbed in the duodenum. It's kind of oxidized to its retinol and retinoic acid, main active metabolites, and then stored in the liver. It's transported throughout the body for its various needs on retinol-binding protein, which requires zinc, so if you have poor zinc, you can also have low vitamin A, so whenever you're drawing a serum vitamin A, it's also good to draw a serum zinc. In the eye, it serves two very different but important roles for the ocular surface. The congenit corneates needed for maintenance and differentiated of stratified scrimaceous epithelium and the retina. It's very important with the visual cycle, as we know, it's needed for the creation and regeneration of radopsin and that's preferentially in rods. And so as far as symptomatology, and we've all heard of night blindness from Xerophthalmia, that's the most common presenting symptom in 71% of patients, and then the other findings are ocular surface-related. So congenitival cirrhosis, buttoe spots, and corneal cirrhosis are the next most common symptoms. These last four categories, according to WHO, are all just complications related to Xerophthalmia. The corneal ulceration, Trata Malaysia scarring, and the Xerophthalmic fundus is due to longstanding vitamin A deficiency, you can see some posterior pole changes, which will show as well. The nyctalopia can be very subtle, especially in pediatric patients where you might have to observe for a behavior change and in this patient with autism. It's usually the earliest presenting symptom, and the ER changes actually may precede clinical symptoms, and these ERG changes as well as the symptoms can resolve as early as 24 hours after initiation of treatment. So this is a table from a recent paper with a patient with vitamin A deficiency. You can see the first four roads are all dark-adapted ERGs, and then compared to the green representative, normal wave form, quite flat throughout, especially the oscillatory potentials, and then light-adapted, not as affected, and then proceeding after treatment one week, one month, and two months, you can see almost near normalization by one week. And the surface changes actually thought that our patient had a pretty good representation of that caratinized appearance of the condom type, and this condom type will wrinkling in dullness, but toe spots will always be on boards. They're usually these triangular-shaped white to yellow plaques, peri-limbo in the intrapalpibral region, and they just represent a buildup of caratinized debris over an area of a divided-lized conge. Corneal cirrhosis can be mild, as we saw with our patients with PEK, but can progress to crata-malacia, ulceration, secondary infection, and then scarring, which is gonna be the main cause of irreversible vision loss for xeroaphthalmia. Long-standing low-vitamin A can give you this xeroaphthalmic fundus, which is represented by pale white and yellow seed-like spots along the vessels and in the periphery. These are also reversible changes that go away with treatment. And so, like I mentioned, really the only way or what was thought to be the only way that you get irreversible vision loss was corneal scarring. However, there is a rare etiology related to long-standing vitamin A deficiency of optic neuropathy. From what I've been able to see, there's only been about 10 reported cases of this, and the pathophysiology is not fully understood, but we do know that vitamin A plays a role in bone growth and hematopoiesis, and they've looked in animal studies. I think it was cows, and they showed that vitamin A deficient cows had an increased osteoblast activity, including in the optic canal. So narrowing of the optic canal led to subsequent ischemic necrosis of the nerve, and then irreversible vision loss from optic neuropathy. And so, in developed countries, malnutrition is not the most common risk factor. It's usually poor absorption from bariatric surgery or a short guts syndrome bowel resection. Cystic fibrosis, as most of these patients commonly have, pancreatic insufficiency, and lead to poor fat soluble vitamin absorption, chronic diarrhea from inflammatory bowel disease or celiac, and then any sort of chronic liver disease where vitamin A is stored. I put alcohol use disorder on both sides of this. As was illustrated with our patient, he, in all likelihood, had a component of alcoholic hepatitis that was not storing vitamin A, and then, you know, because of the alcohol use did not have a broad diet as well, so had poor intake. And as for poor intake, our patient with autism fits on that side as well in the developmental delay category. And they've actually looked at this. Autism is an unrecognized, relatively common cause of xeroephthalmia in developed countries, and that's because of their propensity for a very narrow diet. And this is a table from a case series of a variety of autism patients with vitamin A deficiency, and this column is their diet, and not just part of their diet, this is their exclusive diet. So it's french fries, rice balls, bacon and blueberry muffins, so it doesn't sound terrible, but you're not gonna get any vitamin A. There was a group in Australia that looked at the most common causes of vitamin A deficiency in children. So it developed country, and while two of these celiac and cystic fibrosis were due to poor absorption, autism was actually in the top three etiologies. As far as diagnosis, this is really a clinical diagnosis of special attention, like I mentioned, to the past medical and social history, looking at the risk factors in resource poor settings, or in the US, you can treat empirically. It's fairly low risk, and especially in patients with really refractory dry eye, it may be a diagnosis to consider, but you can also draw serology, like I mentioned, includes zinc levels, as that's needed for transport throughout the blood, and then supplemental studies, like we saw ERG, or dark adipotometry, and you can do impression cytology of the conjunctiva, which will show you representative pathologic changes that are not completely diagnostic, but suggestive of serothalium. The WHO recommends these various repletion recommendations for vitamin A deficiency, 200,000 international units at days one, two, and two weeks, so three doses. You cut that in half based on the patient's age all the way down to less than six months. If there's a concern for a malabsorptive process or any corneal involvement, it really should be IM. In fact, some patients or some hospitals will admit these patients for intramuscular repletion. In adults, this is the repletion recommendation here, and then support the corneal surface and treat the complications with antibiotic vitamin or drops. Promote corneal healing with doxy or vitamin C, then do not use doxy in children. So our patients, the 36-year-old with alcohol use disorder, he had a right corneal ulcer, which puts him in WHO category X3A. He did have his vitamin A repleted. He had a culture, was started on fortified bank and Tobra drops, and then as well as vitamin C and doxy was told to use erythromycin in the un-ulserated eye. And then I talked to him for a long time. He had quite severe vision loss with risk of corneal scarring without using the drops in close follow-up. And given the opportunity to potentially detox as well, we did offer him admission, but he ultimately felt like he could follow-up and reliably use the drops. Unfortunately, he did not. He forgot the drops in the emergency department, but he did follow-up two days later and then three more times over the next two weeks. Vision did improve somewhat. The pain in the infiltrate did improve. The ulcer was consolidated, but then he was ultimately lost the follow-up, so I don't know his eventual outcome. The patient with autism was category X2 because of the corneal involvement. He was referred to GI as well as his PCP for repletion. He was given large doses. I couldn't find the exact dose that he was given. And then was also given supplements to use long-term. His mom would crush them up and sprinkle them on his peanut butter and jelly sandwiches, which seemed to work. He had a full vitamin panel to look for other deficiencies which only showed vitamin D, deficiency, no other issues. And then within a month, his vitamin A level was low normal, but still normalized. He did end up undergoing a subsequent exam under anesthesia with photos ERG and a VEP with ophthalmology, which I did wanna mention. By that point, as expected, his ERG had normalized, but what we found was that the patient or the parents didn't really feel like his vision was improving at all, just by treatment. And he had reduced P100 amplitude in latency periods for on his VEPs, indicating a possible optic nerve issue. And during that EUA, he did that fundus photos. You can see both nerves are quite pale on both eyes. And then he didn't have a true RNFL OCT, but on these Mac OCTs, you can see that the retina kind of ends at the interplexiform layer. And there's very, very little retinal fiber layer remaining. So here's a representative normal of what we should be seeing. And so he underwent a optic neuropathy workup with an MRI brain. And then the other metabolic studies that I mentioned, but it was ultimately thought that this was one of those rare cases of irreversible vision loss from optic neuropathy related to zero ophthalmia, which was kind of sad. And so kind of some take home points. This is not just a disease of developing countries. You need a keen history to reveal the source of malabsorption or malnutrition in these patients and keep by many deficiency on your differential refractory dry eye. Learn from your mistakes and your mentors, like I mentioned, when I saw the first patient in the ER, I had no idea what was going on. I knew he had very dry red eyes, but I did not think about vitamin A deficiency. I wasn't until I was with Dr. Hoffman in the OR during the EUA that it really clicked. And then when I saw the patient about a month later with alcohol use disorder, I said, that's gotta be vitamin A deficiency. And while 12 years in a PB and J may get you through a primary call shift or a Wednesday night, if you're Catherine who you're not, you're not getting any vitamin A. Happy to answer any questions. Thank you guys. Dr. Olson. But time just briefly, but this is one that can sneak up on you. And when it doesn't make sense, I had a cataract surgery patient that just the vision, he just kept complaining about things even though his vision on the chart turned out that this was this, that he had a bowel absorption syndrome. But the worst I had was a cult where the guru thought that the secret of life was daily LSD and only brown rice. And a person died. So this is a lethal disease, even though it was finally caught, the person was already going into general systemic failure. The corneas were essentially melted down to decimates membrane and the person never recovered. So this is one you gotta have in the back of your head because it could really fool you at times. Just real quick. Yeah, mortality rate, I think it's quoted between five and 25%.  And that, you know, again, this being lethal, not so much due to the vitamin A deficiency itself, but just the overall nutritional deficiency. Yeah, it's, I mean, it's needed for a lot of our immune function. So they can be pretty profoundly immunocompromised as well and get a variety of secondary systemic infections which can all be lethal. Great. Thank you. All right, thanks Cole. Oh, Srav says, great topic in review after seeing an autistic patient in fellowship on a french fries diet for several years with severe optic atrophy and permanent vision loss. I've started screening every autistic patient and developmental delay patient for poor diet. I ask about multivitamin and suggest starting one if they're not doing it. Thanks for discussing. Thank you, Dr. Bagunta. All right, well, thanks Cole. Up next, we have Allie Simpson who's another one of our chief residents. She's going to be one of our cornea fellows next year. Allie currently living her best life on elective rotation, which is a great rotation to be on the month before your wedding. And she's expecting that Cole and I will be in our best behaviors at her wedding. Her case is not all that is pigmented. I don't think I have any dietary recommendations but we'll see where we go. Okay, so I'm gonna start off with a case as well. The 20-year-old female, no past medical history. Presenting to retina clinic with chronic floaters in the left eye. Visual acuity 2020 in the right eye, 2025 in the left, normal IOP, normal slit lamp exam in both eyes and a normal fundus exam in the right. However, in the left, she kind of had this purple, darkly pigmented lesion, pretty far peripheral. And you can see this optose photo at the time that I don't know if you can see my mouth. That area, inferiorly, is not an artifact. That is actually the tumor that we're talking about. Oh, I put it in my mouth. So the initial ultrasound in 2017 with Dr. Harry showed this large mushroomy tumor of the celery body. And the ACE scan at that time had showed this kind of really regular, high reflective lesion that was about a centimeter in all dimensions. I won't quiz the residents because we just went over this last Friday with Dr. Harry, but this configuration is concerning for melanoma. I think they'll nod their heads and agree, but that this ACE scan does not necessarily correlate. You'd expect something much lower reflectivity for melanoma. And so that allowed us to kind of expand the differential. So a melanoma is a nevus, an adenoma of the pigmented celery body epithelium, which is similar to a chirpy, but of the celery body, meduloepithelioma, melanocytoma, hemangioma, not because of its appearance, but just because of how highly reflective it was on ultrasound were part of the differential. It was recommended that she follow up in four months for repeat exam, and unfortunately she was lost to follow up for three and a half years. So she represented in 2021, she's 24 at this time with progressive left eye pain and vision loss that had been worsening over the past few months. At this point, she's hand motion is centrally in the left eye. She's got an eye pressure of 42 in the left. She's got some mild congenjection, but no specific dilation of any vessels to be concerning for a feeder vessel. Mild corneal edema and a lot of posterior synigae, lots of deposition on the anterior and posterior lens capsule. Unfortunately at this point, there is no red reflex or view of the fundus in the left eye. She saw Dr. Harry again in 2021 where at this UVM, you can kind of see this large mass coming from the celery body. It's a budding the crystalline lens, but it's not fully captured here. And actually a standard B scan couldn't actually characterize the size of this thing either. So this is actually an immersion B scan ultrasound, which you can see this really large celery body lesion. At this point is about a centimeter and a half in all dimensions. It maintained its high reflectivity on A scan, but there was some more vascularity at this point in this exam. So while the A scan continued to be inconsistent with melanoma, there was overwhelming concern that this could be a melanoma. At this point, she's demonstrated there's growth, the tumor, there's a lot of intraocular pigment deposition. And while her work up systemically with imaging and lab work was reassuring, the ambiguity of this possibly being malignant lesion was kind of unacceptable to her. She had just gotten married, she was wanting to start a family. I think there was also some concern about her lack of following up for three and a half years that they didn't want to take any risks. So the patient was offered a nucleation and she elected to proceed. So then I got to see the path with Dr. Ramilas. It was nice to kind of have some continuity, but as you can see, this is a really large tumor. This is actually six fields of view combined together to fully capture this celery body mass. And it is impressively pigmented. A little bit larger, a higher magnification. You can see again, really densely pigmented cells. It's difficult to understand what's going on with the nuclei. This image does show kind of the pseudosys formation within the tumor. So there's no real epithelial lining, but there are cysts throughout. So this is a once bleached histologic section in which you can kind of be able to see some of the architecture.  You see some macrophages kind of in the center part of the specimen. But again, it's still a little bit difficult to actually see what's going on with the nuclei. So this is a twice bleached section and now you can really convince yourself that these are bland nuclei, small nucleoli and low not nucleus to cytoplasm ratio in this specimen. That was throughout the entire thing, which is really reassuring for benign lesion. And also helped us make the diagnosis of a celery body, melanocytoma. So melanocytomas, you might also hear them be referred to as menocellular nevi or melanocytoma of the optic disc. They were first just arrived around 1930, but the term melanocytoma started to be used more around 1965. It was coined by Zimmerman. And you'll see melanocytoma of the optic disc a lot in the literature. And the reason is it's most commonly located there. So these lesions can be located anywhere in the UVL tract, just like our case. They have this really common appearance, darkly pigmented. They can just involve the optic nerve or they can kind of spread out and avoid the adjacent core rate and retina. They were rare. I tried so hard to find an incidence to report for you guys, but I couldn't find one. Just know that a lot of this data is coming from case reports and analyses where there's maybe 10 to 20 patients in total reported. These are usually unilateral and they're slightly more common in women with about a 60 to 40 split. The mean age of diagnosis is 50 years, which you can imagine that's the same age that you're starting to worry about more of melanoma in your differential. In one study, they found out about 8% had an association with ocular melanocytosis, but that there were no other ophthalmic diagnoses that predispose someone to developing one of these. These are quite stagnant lesions. The growth is actually quite rare, only about 10 to 15%. One study showed growth over several years. The thought that these may be congenital and that they are amelanotic and then gain their pigmentation throughout life, which is why you're diagnosing them at 50 years, but they don't seem to be growing after that. I always find this surprising that there's not a lot of visual impact for these melanocytomas. One study found about 75% have preserved vision and 26% experience at least mild vision loss and snelin acuity. What is interesting is about 90% of them did have visual field changes and this ran the gamut from a large blind spot, nasal step to arguments. What is visually impactful for these patients are kind of the secondary consequences. So retinal exudation, optic dyskidema or optic nerve ischemia, subretinal fluid and then RVOs like I'm showing here, obviously do have an impact on the vision. There is not a lot of, sorry, a malignant potential for these lesions. Fortunately, so malignant transformation was reported in about one to 2% of cases. However, profound vision loss and growth of these lesions made one concern for malignant transformation. Pathologically, you're gonna expect your classic spindle-shaped melanoma cells among like the parenchyma of our oval melanocytoma cells. So these are typically diagnosed clinically. Fundus photography is really helpful in following them serially and getting measurements, obviously visual fields to kind of gather whether they're experiencing any visual field defects. Unfortunately, FA just kind of shows hypochlorosins throughout the whole angiogram. So it's not entirely helpful, though if you're looking for some of these other consequences like fluid or RVOs, it will show that. Similarly on OCT, again, if you get an OCT through one of these lesions, there's nothing specific, but they can be helpful for looking for retinal pathology. And then of course, ultrasound. So most melanocytomas are small, less than two millimeters, which certainly wasn't our issue in this case. You can imagine trying to infer the internal reflectivity on ultrasound can be quite difficult with this. To the point that in the literature, you're gonna find some reports that are gonna report that melanocytomas are high reflective, while others are gonna say that they're low reflective. I would say most of the reports do all them high reflective though, just like in our case. Prior to the use of ultrasound lesion simulating melanoma, so this was all comers, mevi, melanocytomas, medulla epithelialomas, et cetera, were responsible for about 20% of the nucleations, but now nucleation specimens from melanocytomas are really quite rare. And just to review the A-scan. So what was interesting, these densely cellular lesions, those that have a very homogenous structure like a melanoma are gonna have low internal reflectivity just because of the lack of interfaces, whereas those with multiple interfaces are very heterogeneous, they have cysts or necrosis or pseudosis are gonna have high reflectivity. So things like a homangioma would make me think of that. So the A-scan on the top is one of a melanoma. You can see it has low reflective waves where I've just copied below the A-scan of our lesion that's showing high reflectivity. So in our case, the microscopy showed multiple pseudosis which cause high reflectivity on A-scan. And to our knowledge, this was the first correlation between the histopathology of a large melanocytoma with pseudosis and high reflectivity on A-scan. So we have now reported this and it's in a case report now. My takeaways. Not all of that is pigmented as melanoma. It's not lost on me, especially that I'm going into cornea that this will probably be the only time that I see this tumor, but it was a good reminder to keep the differential broad to share decision-making with patients is key. I think about what the outcome would have been if the diagnostic ambiguity of this lesion hadn't been shared with the patient and how ultrasound kind of helped introduce some of that ambiguity because to her, when the pathology came back benign, she was relieved that she didn't have a malignancy. She had just gotten married. She could start having a family and she no longer had a blind painful eye, but I could imagine if someone was expecting that this to be a melanoma and they were enucleated for a benign lesion that the conversation would probably look a little bit different. And then lastly, Dr. Harry's parting words with us on Friday at our mole lecture was ultrasound is important. And I feel like it was really displayed in this case as well. These ultrasound is important for helping broaden the differential diagnosis. Like in our case, it's helping us gain measurements. It's helping us even tell internally what these tumors may be doing. And I think it was really well demonstrated in this case. Those are my sources. And thank you, Dr. Harry, Dr. Mamelis and Dr. Guy and of course the awesome path fellows who put together the photos for this case. I'm happy to take any questions. There used to be ultrasound fellowships and people who subspecialized in ultrasound. It's another example of a kind of a dying subspecialty. We're lucky to have Dr. Harry. He has expertise, but most places in the country, ultrasound, good strong diagnostic ultrasound is just hopefully what maybe one group has taught the other that expertise doesn't exist in a lot of the country anymore. Can we learn that these are benign and relatively slow growing? Like you said, only like 15 and 20%. Did you see anything in the literature that when they do grow, they're aggressive? Like in this case, 3.5 follow-up years, you can see that almost the entire eye is tumor. Like that's pretty impressive. Yeah. So even if I think diagnostically, if we would have known right off from the start that this was a melanocytoma, that interval growth during that three and a half years, I think we would have still been concerned for malignant transformation. And maybe she would have ended up with an enucleation or at least the biopsy to start, even if we had not considered melanoma in the differential for sure. We have a comment from Dr. Mamelis so we'll unmute him here. Okay, thanks. Can you hear me? Yes, I can. Sorry, I'm moving really slow on crutches. And so I'm just sitting at my desk here. This was interesting for a couple of reasons. First of all, the sheer size of this lesion and the melanocytomas that we usually see granted, they're very rare. So we don't usually see these are quite small or just medium size. And so this one was very large. The other thing that was interesting about this was the fact that there was the high reflectivity on the ultrasound. And that was because of the cysts that were in there. And usually when you see these, the reflectivity is low, which then makes it difficult to discern these from a malignant melanoma. And that's where the difficulty comes up in trying to diagnose these is to discern the melanocytoma, which is benign from a melanoma, which is potentially aggressive. Now, there have been rare cases reported where a true melanocytoma has then turned into a malignant melanoma. And in fact, Dave Apple reported one from here. It was right after I had left my fellowship with David and he reported one here. But these are extremely rare that these go on into melanomas. And so this one was very large. It had high reflectivity. And it's less commonly seen arising from the ciliary body than it is from the optic nerve head, which is where you most commonly see these. But this is only the second ciliary body melanocytoma I've seen in 35 years. So very, very rare lesion. And nicely presented. It really made a very nice case report. Thanks, Dr. Manlis. Any other questions or comments? All right. Well, thank you, Allie. All right. Up next, we have Mary Glenn Veyu. She is again a pediatric neurology, PGI3 resident. Mary Glenn, fun fact, she is from Montana and her favorite activity there is kayaking. She's going to be talking about myelin ligandendrocyte lycoprotein or MOG optic neuritis. All right, everyone, thank you for having me.  I'm on my adult neuro year. So this is an adult case of MOG optic neuritis. So the patient is a healthy 39 year old female who came in with a week of painful eye movements and progressive bilateral vision loss. And the first symptom that she'd noticed was that pain with eye movement didn't think much of it initially. And then she started to develop a central scatoma that spread outward. She described her vision as walking into a dim room after being outside on a sunny day. She saw a local ophthalmologist early on who didn't really notice anything significant on her visual acuity, visual fields or a fundoscopic exam. And she had an MRI brain without contrast done as an outpatient, which was unremarkable at the time. But over the course of that week, her vision continued to decline and she then had complete loss of her color vision. She described everything as seeming washed out and she could only make out big shapes. So really in terms of her past medical history, there was nothing too significant. She hadn't had any surgeries, trauma, or other ophthalm problems, no similar episodes in the past, no significant neurologic or autoimmune history. And the only medication that she took was Benjamin for weight loss and then no significant travel or exposure history, notably no preceding viruses or vaccinations that she reported. On her exam, as you can see her visual acuity was significantly impaired in both eyes. She did have a RAPD on the right and her visual fields were globally affected. Her color vision was also severely reduced and she was noted to have grade two discadema bilaterally. Her neuro exam, including cranial nerves, her motor exam, sensory exam and coordination were all normal. And she did note full range of motion but pain with extracurricular movement. So we admitted her and obtained MRI brain, face and orbits with and without contrast. And it did show diffuse enlargement and abnormal enhancement of her bilateral optic nerves consistent with bilateral optic neuritis and notably greater than 50% of the optic nerves were enhanced and her MRI and T-spine were normal. There's no other lesions seen on her. So in terms of her diagnosis, she was atypical in terms of her optic neuritis because she had bilateral involvement but the classic tryout of typical or demyelinating optic neuritis involves this variable vision loss, periocular pain, worse with eye movement and color blindness. So in thinking of your differential and what to work up demyelination is obviously a high concern as well as other antibody media processes such as NMO spectrum disorder, MOG, inflammatory autoimmune diseases such as sarcoid, SLE, et cetera, infectious causes, post-infectious or post-vaccination and then it can just be idiopathic as well. So given our high index of suspicion for an inflammatory or autoimmune process in her, given her age, her absence of other infectious systemic signs or symptoms and really no risk factors in her medical history, we started empiric treatment of optic neuritis with one gram per day of IV methyl prednisone and we chose to do five days followed by a six-week oral prednisone taper in her while we awaited further workup. So the lab workup we got on her when she was inpatient, we did CSF studies and her opening pressure cell counts protein glucose bands were all negative including flow and cytology. Her inflammatory markers and other autoimmune labs such as ANCA, ENA, ANA were all unmarkable as well. Her serum aquaporn IV antibody resulted negative and while she was admitted, we did get the results of her CNSD myelinating panel and she was MOG antibody positive. She had a relatively low titer but we did consider that to be positive. We also sent a Mayo encephalopathy autoimmune and perineoplastic panel that eventually did result negative as well. So we diagnosed with MOG optic neuritis and one of the most impressive things to me was to see her dramatic improvement. So on day of discharge her vision was 2040 bilaterally, she'd no longer had an APD, normal visual fields and her color vision was still impacted but was significantly improved. So MOG optic neuritis, in terms of MOG antibody disease optic neuritis is one of the most common clinical manifestations and presentations of this disease. You often see the pain precede the vision loss and the vision loss is typically more severe than in other optic neuritis disorders such as NMO or MS and it typically involves more of the optic nerve. So as in her case, we saw a greater than 50% of the optic nerve affected. You often more commonly see optic disc edema as well than in other causes of optic neuritis. It is more commonly bilateral than in other causes of optic neuritis. So in 50% it's bilateral. It's more likely to be a monophasic course but it does still recur in about 50% of patients. And the best news is that the prognosis is good. So typically most of their lesions resolve over time as opposed to MS lesions or NMO lesions. You're less likely to have CSF bands and the treatment is IV steroids which typically patients respond well to. In the duration of treatment, it doesn't seem like there's a very clear consensus to this but generally three to five days of IV steroids followed by a six to 12 week oral tapers, generally what's recommended. Interfractory cases, plasma exchange can be considered, IVIG can be considered and the length of this course varies as well. So as I said, one of the cool things about this case was being able to have an answer the same hospital admission and be able to provide some prognostication for the patient which rarely happens in neurology. So her five days stay, we were able to say you have MOG optic neuritis and that was very satisfying for me and I think gave her some peace of mind too when she's wondering for this BNMO am I more likely to have recurrent lesions, spinal cord lesions, et cetera. So I think it's awesome that in the past 10 years we've started to identify these discreet antibodies implicated in optic neuritis and they can give us some guidance and give patients some guidance about what to expect. So obviously she'll follow up with neuroophthalmology and autoimmune neurology as an outpatient and continue with occupational therapy until her vision is totally recovered and that's my case. So you think about the underlying problem is metabolic and obviously then there's a strong autoimmune component associated with that but what are some of the other, I mean it can't just be optic neuritis what other presenting symptoms do these people have or is this really just mainly optic neuritis? With MOG antibody disease, well in kids we more commonly see ADEMS so this diffuse demyelination pattern that usually also is monophasic. It can present with spinal cord involvement alone so it can be really highly variable. So it can be a fairly profound problem associated with the nervous system elsewhere but this is the most common and why do we think that it tends to be monophasic and not recurrent? That's a really good question. I tried to look into that too and it seems like if people stay seropositive they're more likely to have relapses but that's really the only thing I can see that's a risk factor for relapse versus just having a monophasic course. So still a bit of a mystery then? I think so, yeah. So that great case and it is very gratifying to see these people. I think that the wonderful thing is that they tend not to have other neurologic conditions like multiple sclerosis and they're not really at risk of becoming paralyzed like neuromyelitis and optica, which is just great. And their visual recovery tends to be really terrific and often not nearly as much optic nerve tissue loss like on OCT as a lot of other optic neuritis is. But the spectrum of presentation is extremely broad as Mary Glenn was saying and in kids they could present like basically in a coma because their entire brain is inflamed and yet they recover. There can be very profound cerebellar and brainstem inflammatory conditions pretty much anywhere that there's white matter can get inflamed. One of the interesting things that has come out with MOG optic neuritis is cryon, chronic relapsing inflammatory optic neuropathy which has always just been a, well I don't know, you just keep getting optic neuritis I don't know why. But as these people keep coming back for follow if we test them for MOG and it turns out I'd say at least half maybe two thirds of those folks actually have MOG and now we have a test for it and now we have some sort of guidance as to where, how to treat them. That has been hugely gratifying. And then also slightly buried was that 50% of these people do recur. So relapsing optic neuritis is not uncommon probably more common than multiple sclerosis. I mean you don't see people with regular multiple sclerosis having relapsing optic neuritis again and again and again whereas somebody with MOG they can 50% of the time.  So the Mayo is the one, they're the ones who developed this antibody test which was terrific. They just have everybody's serum in the entire world who's ever had anything wrong with them. So they are constantly searching for stuff, useful stuff and it's been so great. But when a test gets licensed then other places can do it. So ARUP can test for MOG. So we just learned on Friday at the Wynow meeting Western Intermountain Neurologic Organization meeting there were a couple of folks talking about MOG and of course it turns out that there is a difference. So there is a cell-based assay and turns out that the dead cell-based assay which is what ARUP does is not as sensitive as the live cell-based assay that Mayo does. So if you're kind of thinking about the diagnosis and you've got this equivocal level it's enough to make a diagnosis but if you really wanna know, you still have to go to Mayo. Great case Mary Glenn.


It's time we're introduced you to some intriguing prospects then twenty-three NFL draft who are you looking at Jackson Smith and jig Bah from Ohio State He's a wide receiver and you need to know a couple of things about him He's a very interesting case Okay, because if you look at the numbers are kind of like what happened here five passes you caught just five passes in all of 2022 here's the deal. He missed the entire season with an injury. It was a hammy, but he's still universally considered a top three receiver in this draft because of how Spectacular and eye-popping he is when he is on the field. So let's go back to 2021 for just a quick sec Ohio State's receiving core loaded. They had newly minted offensive rookie of the year Garrett Wilson They had Chris O'Lave, Jackson Smith and Dugba is just sort of in that world. He led guys He led that trio in receiving right? Well, so we're talking about the Garrett Wilson's We're talking about the Chris O'Lave's his fully healthy game His last one was the Rose Bull against Utah that year he put up 347 and three touchdowns in that one It was bananas Garrett Wilson He has not been shy about calling Smith and Dugba the best of that talented group. He calls him the best Think about that. He actually went as far as to call him quote the most natural athlete I have ever seen that's super impressive and eye-popping if you ask me in the praise It doesn't get much loftier in the ceiling clearly is about as high as it gets But some GM's Probably have him a little down or maneuver him on the draft board a little bit because he missed nearly the entire 2022 season So it'll be very interesting to see how he's viewed who's willing to take a swing on the potential Just as a reminder though, the last top tier receiving prospect to face these kind of questions was of course He wears number one Jamar Chase he opted at LSU as we all remember I'm gonna just say fair fair to State that he has done pretty well for himself. It's worked out for him in this case So hopefully that sort of sets the precedent for Jackson's favor come April There's one thing you need to know about Jackson Smith and Dugba of the Ohio State Highly talented teammates love him and he's got all the potential in the world. We'll be back


Hey guys welcome back to Tech Talk. My name is Chase and today we're going to be discussing the battery select switch system on both our premium and sport fish model boats. So today we're on the open 262 which is the smallest boat in the sport fish lineup. Take a look down at the battery select switch. This boat has twin 200 Yamaha's on it. So on your engine bank that's going to control those two batteries. Your house switch is going to control its own two batteries designated for all your electronics for the house. The unique thing is this system has a voltage sensitive relay in it. What that is is it's taking power from the motor and sending it directly to the battery bank for whichever battery needs it most.   Once they get to the charge level it'll then alternate and start sending current back to the engine batteries or whichever battery needs it the most. And from that point this will be the system that will never let your batteries get below 12 and a half volts which is a really unique system while you're running the engine. So another great feature is being able to combine these circuits in an emergency situation.  This would be a good time to parallel over stealing power from your engine batteries to then run all your electronics. So while you're running the motor this will allow the house bank to be charged and while it's charging you can stay in that combined mode until your house batteries are at an optimal level. Once they reach that level and you can come back simply go back to your normal running on position. We've also carried this design down to our premium models again installing a VSR. A VSR stands for Voltage Sensitive Relay. This device takes the voltage from the motor's alternator and sends it up to the battery that needs it the most whether it's your starting or your house battery. We hope you've enjoyed this short video on some of our new battery select switch features. If you have any questions or comments please leave them below, like and subscribe and we'll see you next time.


From Seattle, Washington, extracting the signal from the noise, it's theCUBE on the ground at OpenStack Day Seattle 2015. Now, here's your host, John Furrier. Hello everyone, welcome to theCUBE on the ground here in Seattle. We are here for the LinuxCon, which happened yesterday, but here, OpenStack Innovation Day. I'm John Furrier with theCUBE. Our next guest is Shiram, at Cloud Don on Twitter. Thought leader, influencer in the OpenStack community. Great to see you again. Thanks, John. Great to see you again. It's nice to have you back. I really appreciate our foray to the Pacific Northwest with theCUBE. It's not live, but it's on the ground, which we love doing, and captioning the thought leaders. I gotta ask you, OpenStack's having an innovation day here at the Washington Athletic Club. Great participation. This is not just a meetup. It's a mini event, and a lot of folks here right off the road from Taipei, and you've got Tokyo right on the corner, OpenStack SV coming up. What's happening right now? Sure, that's right. I want to stress it did. This is the first time we are having a one-day OpenStack event in Seattle. It's kind of surprising to know that on a cloudy city like Seattle, we never had an OpenStack conference. So I'm pretty excited to bring that here. And this is also the first time that we are having a fully loaded track on telcos across any other city on OpenStack days. So those two are really good. And what is happening about OpenStack, you just got out of LinuxCon, and of course there was a lot of buzz about containers, right? So the three things that I'm seeing that two combined essentially towards enterprise, but one out on telcos, right? So there's a big push on making containers native on OpenStack. Make OpenStack the native platform for containers. There's a big push there. And that kind of ties in with how to make enterprises happy. So OpenStack enterprises, and then the second major pushes that enabling telco applications, and our free applications.  Well, the continued mission of stability, obviously one of the core tenants we're hearing over and over again, but yet run faster, more functionality. Keep the stability, but add the innovation. Kubernetes, you've got a bunch of stuff going on around container, container management. It's gotta be easy to deploy. But now the wrinkle in the equation is not just developers and partners, it's operators. So talk about the role of the operators. You mentioned telcos. What's the status of the operators? Are they happy? Do they want more? What are they, what's going on right now? Sure. I think the right way to answer this is like they're happier, right? And you mentioned on stability part, and I would take it for any projects, right? So yes, Kubernetes can scale too, but generally like speaking, it's when the rubber hits the road that's where the problems will be, right? But one good thing is OpenStack has taken operators feedback much more seriously, and then we have a better loop of feeding back the operator feedback into OpenStack product development.  So bottom line is operators have more say in how OpenStack is gonna be, and it's much more clearer now than last year. And they're participating more. We just interviewed eBay, and we heard Walmart mentioned by Jonathan Bright.  Any new names you can share? What's the key operators up here in Seattle? What's, give us some more data. Oh, nice. It's interesting in operators here, right? I think the Blue Box crisis is the biggest players in OpenStack. Their model was interesting because they own the operator spot, right? The clients are not really, because of the managed product model. So they are the biggest operators per se, even though they're one of the vendors and a part of IBM.  So there's a little bit of operators, sorry, users community here, even though there are two big vendors, it used to be three big vendors, but with Nebula going away, it's just HP and IBM on Blue Box, right? Thank you, Bram, to a good point about Blue Box. We love Jesse, you know, it's a Blue Box big fan, but now they're part of the mothership at IBM, I wish we cover all their events. So IBM, the big push in here. Is there an opportunity for a new operator? I mean, we're seeing huge opportunities, obviously Blue Box was a great example of some entrepreneurial creativity and growth, and self-funded, they took some outside financing, ultimately had a great exit. But there's more opportunities, or is there more opportunities? So interesting thing is, I think, I want to tie this conversation into, we have startups hard in the OpenStack ecosystem, right? The first round of startups are all about installations and make the distributions better. And then now the big players getting in, Red Hat, HP, Canonical, Suzie, so they are having a good handle on how to make the distribution solve some of the problems that operators face, that enterprises face, right? No, that's kind of settling down, but interesting thing to look at is now, we're talking more about applications, right? Whether enabling the containers, or it's not exactly a past there yet, but think about what kind of applications I can run on, right? So, and I'm seeing a lot of more startups working on solving those problems. So, that's what I want to say where the OpenStack ecosystem is going, but it doesn't mean to say that there is no role for operators. Still, it is, the infrastructure will be largely like operator dependent, right? So the one thing that we can hope for, which is good for OpenStack would be like, how to make it much more easier for operators? I am not seeing the operators role completely going away, which as long as we stay at IAS level, right? How the customers are consuming it? Are they gonna consume it like how managed private cloud is? So they are not, they are oblivious to the infrastructure layer, or they are just only talking about past layer or anything on top of it. That's still like, it's a different consumption model. Someone is gonna still deal with operators, and as long as they are there, we need to make their life easier. If there's opportunities, entrepreneurs will sniff it out, but you bring up the question about entrepreneurial opportunities. We were just talking earlier here on theCUBE, on the ground, is that it's a software problem, not an IT problem here at OpenStack. So that's a big opportunity. What software opportunities are you seeing or white spaces? Do you see entrepreneurs focusing in on? We've heard portability from Swarm to Kubernetes, making Kubernetes easier, making container management easier.  No, I agree with you. I think with everybody talking about containers and orchestration, right? There's definitely a lot of opportunity. There's also a lot of good players there, right?  So it's interesting to, I'm not saying it's a white space that I'm not saying there's no innovation possibly there, but definitely we can make it easier. But I also want to look at something more, right? So the customers really care about their LOB applications. What can we do that? Can we make running the applications easier? Can we get more monitoring better on that? Can you make your life, can you make your application life cycle management easier, right?  And then the other side of the equation is like, what is the security story, for instance, right? How does the compliance story? There's still white spaces out there. From a developer point of view, we can say that, hey, just everything is in the log, I can just check market, right? But that's not how customers want it, right? So what is a good package solution there, right? So, and then again, like, there are other kinds of innovations too, right? We talked about NFE a little bit, right? Now, there was a lot of innovations on like storage and networking. We had a lot of solid fires, SAV, ink tank, big M-brain, big switch, those kind of startups, right? But what would be the next one, right? So Acanda, for instance, so they are moving a level above, still like solving the problem of virtualized networking, but instead of the level two and below, right? They're doing at the level above. So those are some of the opportunities that we are, they are looking at it, but of course there's more. And one more thing taking is like, I think there's a talk about hyperconvert solutions are like entire, so how can we do it better? Can you have, I hate to say the single pen of place, I mean, it's a very cliche expression, but you know, like anything that just don't do it just a piecemeal computer storage and networking, but can you do it at a much higher level? So those are the some spaces that I'm seeing actually happening and expect to happen more. The good news is we heard from Cebu from eBay is that it's an engineering opportunity, it's not just so much write some code and you're off the races, it's a combination of software plus some engineering. So that's cool. So great opportunities for entrepreneurs. Obviously they can get involved in meetups, local environments, but it's this local scene, OpenStack, certainly we're in Palo Alto and in Massachusetts, but we're seeing it there. But here in Seattle, you're here, you brought this together, this event together. Are you happy with what's going on here? Do you want to see more? I mean, Blue Box is sold to the dark side with IBM, they no longer a standalone venture. I mean, I think I'm more cashed to work with IBM, but I mean, what else is out here? I'm excited, you know, like what else is out here? Like of course, like it is, it just shows like what is the awareness of OpenStack in this city? Like it's a home time of cloud computing. We have Amazon and Azure here, right? But you know, as much as there's a mind share for them here, we do not have a lot of mind share with OpenStack, but it's definitely increasing, right? The Blue Box guys and HPKs were like doing a lot of OpenStack meetups, creating a lot of momentum out there. This is just like, I would say this event is kind of establishing the flagpole of Seattle into the OpenStack roadmap and then say that this is a significant presence here. And then not to mention this, there are at least couple of startups here working on like stealth mode, I've been talking to them. And then one of them is working on storage, making storage much easier based on using OpenStack, right? So it is going to be interesting to see whether like we have the big players here, who's going to be next as an interesting question to ask. But I would say that like we are at a much more state, which is more hopeful for OpenStack and more positive for OpenStack. And this event is a demo of that one. We were a little bit hesitant, I was a little bit hesitant to have like 150 people here to have the event. I scaled on from 200 to 150, but we were sold out. And then like we got 175 registered and we got 30 more waitlisted. So I'm very ecstatic. And I would like to thank all the sponsors and specifically thank the OpenStack Foundation. And I also want to thank the next Foundation who allowed us to be a co-located event. So with all their help, this event is going to be a huge success. Well, OpenStack certainly has been resilient. I've been following it since it was a glimmer in the eyes of a lot of folks and then watched it turn into a marketing event. Then it really became real. And since that point, it's always survived the rhetoric of OpenStack is dead. I mean, it always moves faster, always gets stable.  Share your perspective on that. No, absolutely. So the community is very resilient, right? I would say it's more than resilient, it's more agile. And then the developers, of course, are the key. And then now the users and the equation, right? So there was a little bit of mismatch between what developers implemented that brought in for the users and then users were not very happy with it. Now that the loop is much more tighter, you know? So we are in a better shape to handle anything anymore. So kind of stepping back from the, stepping up from the software part of it, right? It really, what matters? Like how many users are going to adopt it and then what happens at the customer side, right? You can talk a lot about like this cool new toys, containers, missiles and all those things. They will also face the same problem when they go sell to the customers. And then select what two years ago was OpenStack. Now we are seeing with the container ecosystem, right? But when you go take to the data centers and put down in the world production, that's where the issues are gonna be. So taking that, combining with where OpenStack is right now, OpenStack is at much more better state to handle those things. We have been getting a lot of feedback from real users. Of course, I would appreciate, I would like to have much more users, much more larger deployments. And one more thing is like, we should not treat OpenStack as an isolated entity, right? Like it's gonna be, realistically speaking, users are gonna have multiple abstractions there. So how much well that OpenStack is able to adapt to these new things, that's gonna be successful at OpenStack. And the indications are correct. It's going in the right direction. I want it to continue in the right direction. And in Seattle, great tech community here. Obviously a lot of smart people. Obviously, well-educated, Microsoft, Amazon, OpenStack, a lot of developers. You know, they got a football team that's competitive now. So, you know, you know. Yeah, we just thought a little bit, but yeah. If you look at, you know, San Francisco, the Silicon Valley, Seattle, and then obviously New England with Tom Brady, very competitive environment here, technology-wise. Yes, it is very competitive. I think what could be a little bit lacking from an entrepreneurship point of view is the VC funding, VC pull of money, right? So, a lot of Microsoft millionaires and Amazon millionaires are not there yet quite to give it back, but it's improving. It's a lot. I've seen the last five years that it's improved a lot. There's a lot of activity happening around the... There's a generational DNA established here in Seattle, going back to Microsoft. Now you have Amazon exploding. Now you have OpenStack exploding. A lot of great stuff. That's true.  We are Dan Bay area. I would say the Seattle community is a little bit more... People are chill here. They seem relaxed all the time. Yes, it is. Everybody who comes here. So, you know, but it doesn't mean to say that we lack entrepreneurship here. The Seattle tech community is improving. It's entrepreneurial shows. So, you can expect to see much more startups and making more names soon. All right, we're here in Seattle. This is theCUBE on the ground. We're exploring all the data out here in Seattle. OpenStack Innovation Day meetup here in Seattle. I'm John Furrier. Thanks for watching. This is theCUBE on the ground. Thank you so much, John. And I would like to add one more thing. This particular event, we had stress on including diversity and inclusiveness. So, that has shown off. We have a lot more female participation and then people of minorities participating here. And anybody who's watching here, I would like to say that please think those two things and try to include that in your tech events. Tech is very inclusive here in Seattle. And obviously great community. Thanks so much for organizing this. This is theCUBE on the ground. Thanks for watching. Thank you.


Freedom! Today I wanted to talk to you about, what is, what is, oh, it's New Year's, isn't it? Didn't we just make like a video about a holiday? I am so over this. But I do hope that you in your content, your content strategy, I hope that you have somehow worked in the new year and you have capitalized on this in some way because it's something that is shared globally. There aren't too many global tentpole events. If you don't know what a tentpole event is, I think I might have a video in what there's an I maybe on screen talking about what tentpole videos are that I made a billion for ten years ago, and that should catch you up. Now, there aren't too many of these. I hope that you have capitalized on this, but that's not what each video is about. I don't know why I'm rambling. Why am I rambling? Anyway, our, our staff wanted to take a break and say Happy New Year. So, guys, take it away. I'm Steph from Staff Shorts and Happy New Year Freedom. Happy, Happy New Year Freedom Family. Happy holidays and we wish you a Happy New Year. To all of my Freedom family, wishing you a happy and prosperous new year with the help that you will have many blessings in the year to come. My name is Perry McGuire and Happy New Year Freedom Family. I hope you guys have an amazing new year. I'm sure you've got loads of different, you know, plans for your new year and things like that. So, yeah, I hope you have an amazing one, guys. From all of us here at the Freedom office, Happy New Year and me, you guys have a wonderful 2017. Happy New Year Freedom. I wish everyone in the Freedom family a Happy New Year. I wish Freedom family a Happy Happy New Year. Happy New Year Freedom Family. Happy New Year to everyone from Freedom. Happy New Year Freedom. Hi, Freedom. I'm Jaycee, also known as Julius, video editor for Anthony and I'm wishing you all a Happy New Year. Hi, Freedom. This is Gilbert from the QC team, wishing everyone a Happy New Year. Hello, Freedom. Happy New Year. Happy New Year Freedom Family. So, hopefully you've gotten all of your various holiday songs out of your head and now you can be prepared to go back to work or back to school or back to whatever it is that you do with your normal everyday life because it's over. But that's not that big of a deal. Like, you know, there's other stuff around the corner. There's all kinds of holidays and stuff. But I do want to take a moment to say that all of these holidays that we celebrate this time of year, the deeper meaning is community, family. And that's what we are here at Freedom. We are the Freedom family. So, do take time if you have it to stop by the forums, say hi, be a part of the community. On Twitter, don't forget to use hashtag Freedom Family anytime you see something that is YouTube or digital media related. Share it with the Freedom Family so that others can see it. Or maybe you just share out your own videos using hashtag Freedom Family. That way, other people can discover those as well. Anyways, until next time, don't forget to like, subscribe and do all those things that make us love our jobs. Also, be awesome to yourself and amazing to each other. Bye, Freedom Family. Whoa!


James welcome to Brooklyn Ryan good to be here. Thank you. Yeah James I gotta say I think one of the things that has always stood out to us is your physicality your toughness how would you describe the importance of that you bringing that to a team that has championship aspirations. It just allows me to be who I am you know I don't have to no pressure of being the guy or the score or just going there feeling my role and do what I'm supposed to do. Yeah well what is it like for you coming to a new team and of course every player that has sat down talked about championship and chat championship aspirations for you to integrate yourself and acclimate yourself what is that process like. It's different you know everybody always says when you're going at the end of the year is that to be in a championship or to win a championship or win it when it's really realistic and you have guys a group of guys who really sacrifice everything to win this year you know you can just feel it in your heart that you do whatever it takes to get that done. James when you look at you know the stars that are on this team with Kyrie Irving and James Harden and Kevin Durant what are the things that excite you most about their games and getting to be on the floor with them. The floor is gonna be spaced you know it allows everybody to operate that easier rhythm level everything. What about your presence defensively some other guys Sean Mark sat down with us it was talking about areas that he has tried to short up the gaps in the roster looking at it the way the team played last year and defense was a major part of that you being one of those guys how much whether it's your voice by example the way you're playing how much can you help bring the level of play on that end of the floor whether guys are in the lineup out of the lineup whatever the road rotation looks like just to have that be in added mainstay for this group to keep improving on. I was fortunate to be coached by some really great coaches and you know the defense aspects always been the reason why I got on the floor you know to even show my offensive presence or whatever so you know I think the knowledge of knowing where to be makes the game a lot easier I feel all of us are veteran players we know the game pretty well you know we know when Steph is coming down he's gonna come out one of the wings or one of the corners you know just things that you have to play to know a little bit how about James when you have you know a lot of veterans and we talked about this earlier with I think we talked about with Paul Milsep it was one of the or maybe Lamarcus one of the veterans here who's accomplished like yourself and you go in and you look at the roster you know okay like I'm not gonna play 30 minutes a night I know that how much of an adjustment is it meant to lead to know my role what I may need to do on this team is to give them seven good minutes or or I may not play for a week or maybe some nights I'm playing 25 how difficult is it to accept that or or how do you kind of you know process that I mean eight years seven years AJ would have been a little bit more disappointed but thirteen years James is good spirits happy blessed to be here and like I said fill any role that needs to be filled in for any game what does that mean to a team I mean you've been on so many different iterations of teams and groups and I'm sure some had different levels of chemistry and connectivity but to have so many guys and you're not the first to sit down and just say whatever the team needs to win when when that is real in a genuine feeling what impact does that have on the ultimate group or through the season when when you are going through some of the highs and lows I think I think that kind of attitude just contagious you know when we're not playing or that we don't get the miss we want you know I feel we're older mature enough to know we have to work get that extra conditioning in it's something that no one's gonna have to tell us you know it's gonna be an easy piece of mine I feel you talk about playing for some great coaches in this league Eric spulster obviously is a coach who has a wonderful reputation has been at the helm for a long time in Miami if you were gonna think to your time there and say what's one thing that stays with you that you learn from coach Spoe what would it be you taught me how to act like a champion before I was a champion interesting and what about that specifically when you drive home I mean off court on court the way I work the way I eat now everything is about becoming or being a champion before I'm a champion the cuisine has changed a lot the dietary choices I've been I've been paleo for about two years but it gets harder in New York man you just said the buzzword are you still paleo no no no I it's hard like James I know it's hard in New York maybe you know what you just you get that stretch of three or four days off and you go not paleo for a day yeah you just got to pick your spot right well James we are we're so excited to have you here congratulations on joining the Nets looking forward to the start of this season thanks for joining us for sure thank you