I wish I could find a statistic on how much time is actually wasted in meetings. I work with some elite level companies now and I'm shocked at how much dysfunction they have that they don't necessarily have clear roles on their team and that their meetings are chaos. And that's a lot of stuff I just took for granted being around, you know, coaches that really understood, you know, how to create a winning type culture. So I'm thankful for an opportunity to be able to share these kind of nuggets with those groups. There's just too many meetings in general. I mean, some people hold meetings to plan the next meeting and it's like there has to be something more efficient than we could be doing and, you know, I pull a page out of my basketball playbook, you know, a coach at the beginning of a game is only given a finite number of timeouts and those timeouts are briefed by design, either 30 or 90 seconds. So they don't have the luxury of calling a timeout whenever they want or holding a meeting with the team whenever they feel like it. You only get a few of them so you have to use them wisely and you have to be briefed by design because that's how long the timeouts are and you best share something with your team that's going to put them back out on the court, you know, more apt to succeed. And I think businesses should follow a similar model. Like, hey, don't pretend we can have meetings whenever we want. I mean, imagine if I came into Lightspeed and said, you get three meetings this week or three meetings this month. That's all you get, Brad. So you better figure out how and when you want to use those. Oh, and by the way, when you have them, there's a 20 minute time limit on each. Not only is there a 20 minute time limit, there needs to be an invite list and the only people that are in the meetings are those that need to be there. We don't need this big corral of people and half the people are sitting in the meeting going, why am I here? Someone could give me a PDF with the bullet points from this meeting. This is a colossal waste of my time. The agenda of the meeting, what's the purpose of this meeting and who needs to have direct input, you know, so if you and I were going to have a meeting about how to create killermeeting.com, then who else besides you and I would need to be a part of this meeting? Who else would be able to add input to this? And if we decide that it's just you and me, then it's just going to be you and me meeting. We don't need to have anybody else in the room, but so many groups would have 20 people in this room, even though you and I are the only ones that need to actually have any input and that's wasting 18 other people's time. You should never hold a meeting if there's not a distinct purpose for holding the meeting. If you can't, you know, say at least in a clear sentence or a couple of bullet points, the reason that you're having the meeting and what is the outcome that you're looking for?  If you can't answer that, then you probably shouldn't have the meeting in the first place. So there needs to be something that they completely understand. This is the reason. Here's why we're going to the meeting. This is what Brad wants us to do. Here's why I'm actually invited to the meeting, whether it's for me to hear something or for me to share something. But I know crystal clear why I'm there and here's an agenda that and I know if we have an agenda and Brad sticks to it, he's unconsciously telling me that he respects my time. Because if he doesn't, if you just bring people in and everybody's talking and it's a free for all, then no one's being respectful of anybody else's time. So now I'm coming into the meeting. I know exactly what we're going to talk about. I know the reason we're having it and I know what I'm going to need to be able to do differently when I leave this meeting. And sometimes that'll take eight minutes. Sometimes it might take 90, but at least we know that every minute has been invested into something that's trying to get us where we're trying to go. And that's that's where I see a lot of folks. They're not doing that. One of the worst answers I think anyone can ever give to any question is, well, that's the way it's always been done. And I think that I hear that a lot. I hear that a lot as well. That's one of the reasons I enjoy going into the corporate world, even though I don't have a lick of corporate experience. I use that as to my advantage because I go into a company and say, I'm not going to tell you the way things have always been done. I'm going to come in with a fresh perspective and shake things up and do things differently. You know, but I think that people think, well, you know, when I was the VP here, we always held meetings and this is what we did. We have the month, you know, the Monday morning staff meeting is just the way we do things here. And no one's taken a second to step back and go, do we even need this Monday morning meeting? What's the point of it? Just because we've been doing it for five years doesn't mean it's of value. And I think that's why a lot of people do a lot of things in their lives. It's the way it's always been done. And they don't take time to question it.


Hello and welcome to this video explaining how to get started with the ST25-DV Discovery Kit. This demonstration kit is for evaluating the features and capabilities of the ST25-DV series. This board is part of the ST25 family NFCRFID Evolution board, which is an easy way to develop innovative devices and applications with ST components. This is the ST25 Discovery Kit, which has two parts, the mother board and the daughter board. On the ST25-DV Discovery daughter board, you'll find the ST25-DV in a DFN12 package, the ISO Class 5 antenna and a connector to the mother board. And this is the mother board that is used to drive the daughter board. It has a LCD display and touchscreen, a sterling USB to the bug, and an extension connector to plug the ST25-DV daughter board. And here is the view of the bottom of the mother board, where you see a STM32F405 room for the Bluetooth Low Energy module and room for the Wi-Fi module. In order to reproduce the demo, you need to download and install the ST25 app Android application. This Android application is developed by ST Team and available on our website on st.com ST25 app. Before starting, you also need to enable the NFC feature on your smartphone. Now, let's start with the ST25-DV Discovery NDEF demo. First, enter the NDEF menu, then touch the URL icon and store the URL in the ST25-DV 04K product. Tap your smartphone and it natively opens the stored web page of the ST25-DV series. In the next part of the video, I will show a firmware upgrade demo based on the Fast Transfer Mode feature. This feature is using a 256 bytes buffer of fast memory embedded in the ST25-DV product. First, the new firmware must be available on the smartphone in this specific folder. The firmware on the mother board is in version 105. First, enter the Fast Transfer Mode menu in the mother board. On the ST25 demo app, enter the firmware update menu. Pick a firmware to upload and click on start transfer. The MCU requires a password to proceed with the demo. And the firmware upload starts. After 46 seconds, transfer is OK. Press the LCD to boot on a new version of the firmware. Firmware upgrades through NFC will bring great benefits to the industrial sector as for machine maintenance as well as in the consumer sector for home appliance for instance. The picture transfer demo shows how to upload a picture from the flash memory of the MCU to the smartphone. Enter in the Fast Transfer Mode menu. Then select the picture icon and choose a picture by pressing it. Then on the smartphone, select the picture transfer. Then download the picture from the tag and start the transfer. So it takes about 9 seconds to transfer 16 kilobytes. The stopwatch demo shows how fast the smartphone can update the Fast Transfer Mode buffer. First, enter the Fast Transfer Mode menu on the mother board. Then in the ST25 demo app, enter the stopwatch transfer. And press Start. The latency is displayed on the LCD screen. And now for the Wi-Fi pairing demonstration. For this demo, we have equipped our board with an ST Wi-Fi module. On the demo board, first enter into the end-def menu and press the Wi-Fi icon. Select Write Wi-Fi Output Bond to store the Wi-Fi pairing and Def Message on the ST25 DV. Tap the ST25 DV with a smartphone. It asks confirmation to connect to the ST25 Wi-Fi network. Press Connection to complete the pairing.


for which we can submit papers and posters. So today, we will be having three speakers, Dr. Raj Keral, Dr. Ashish Shavland, Dr. Alok Jaju, followed by a quiz by Matusha Ma'am. So first off, we also have international speakers who are coming in for the international MRI teaching course, which is, as I said, on 2029 October. And that is Dr. Scott Flam. So he's a cardiac imaging pioneer, and he'll be taking lectures on cardiac MRI, importance of cardiac MRI to start imaging, and parallel imaging techniques and other efficiencies to enable high-through-portal cardiac MRI. The second is Dr. Manohar Shroff, who's professor and chair of pediatric radiology at Stix Kids Hospital in Toronto. These are the other few speakers who'll be taking cases, lectures such as pediatric cystic pelvic masses, pediatric solid pelvic masses, Dr. Haike Link, and Dr. Thomas Link, who will be taking on post-operative imaging hip and mimicry of intramural arteries. So this is the schedule for the MRI teaching course for day one, two, three. And today, we'll start off with the reload session now. So first is Dr. Raj Kedal. So he's a professor of radiology at the University of South Florida and radiology chief in Tampa General Hospital. So he's a director of body imaging and fellowships in MSK faculty, vice president of Florida Imaging Radiological Society, vice president of tower imaging centers, ventures. So he's also in the education course faculty at RSNA. He's got 100 plus publications and 300 plus presentations under his name, book chapters, editorial board members of multiple radiology journals. He got the best radiology, best doctors in America. He was nominated for them in 2016, 17, 18, 19, and 20. And he also has a teacher of the year award in the Golden Apple Award 14, program chairman of the Florida Radiological Society in 2018. And he's going to talk about the actualization of venal masses. Next is Dr. Alok Jaju. So he's the program director and of pediatric neuro radiology fellowship at St. Louis Children's Hospital in Chicago. And also the assistant professor at Northwestern University Fine Wing School of Medicine. And his topic today is going to be pediatric foster tumors. And last but not the least is Dr. Ashish Shabla. So he's done his MBBS and MD from KM Hospital. He's a senior consultant of department of radiology at Kutek Quad Hospital in Singapore. And he's got fellowship in abdominal radiology at the University of Colorado, Denver. Fellowship in cardiothalastic radiology from the University of Colorado. He's authorized a textbook on thoracic imaging titled Thoracic Imaging Basics to Advanced. But he's published around 80 articles in peer-reviewed journals and organized radiology courses for trainees. So his topic today is going to be imaging in Kuala Lumpur, Casinova. Again, this is just about the MRI teaching course, international edition, third, fourth, and fifth time in a month. Good evening. It's my pleasure and honor to be part of this course. And I would like to thank Dr. Potko and Dr. Verma for inviting me to talk about characterization of renal masters with MRI. Unfortunately, incidence of renal cancer has increased by 30 to 40% over the last 30 years or so. And this is predominantly due to incidental lesions due to increased imaging with ultrasound and CT scan. Although most of these lesions are less than four centimeter, increase in diagnosis has not resulted in better clinical outcome. In fact, they reported increased mortality from 1.5 to 6.5 deaths per 100,000. And this is predominantly due to over diagnosis and surgeries and aggressive management, even slow growing tumors, which may or may not show growth over the time. The cost effective strategies are necessary, especially to identify the clinically significant renal masses that could evolve into life-threatening disease versus the over treatment of benign or indolent malignant lesions that can be observed. As we know, ultrasound is very cost effective. It is very diagnostic for simple cyst. However, it has its limitations with smaller lesions, patients body habitus characterized in complex cystic masses, differentiating from complex cystic masses to solid lesions and cannot stretch the disease. CT scan is very sensitive and specific for renal masses for greater than two centimeter in diameter. However, it does have its own limitations in complex cysts, cyst containing hemorrhage or protein, lesion size, intraparent camel lesions that cannot be measured accurately as far as Hansfeld density is concerned because of volume averaging and misregistration artifacts. It can be limited with renal function. So that's where MR comes in. MR has got excellent soft tissue contrast due to which we can use multiple sequences and parameters to characterize the liver renal lesions. We do not need iodinated contrast. So some of the patients who have allergies can be still scanned with this in cases of renal insufficiency. Now with newer microcyclic agents, we can give IV contrast even in end stage renal failures. My learning objectives for this talk are to discuss typical and variable features of common renal tumors. How MRI can help as a problem solving tool to characterize the renal lesion by which the clinical management, planning intervention and avoiding unnecessary procedures. The plan for today would be to talk about different types of tumors, how we can characterize those with MRI. I'm not going to discuss port query of all renal masses. I'm not going to talk about inflammatory or pseudo renal masses or cystically agents. We are going to briefly talk about renal cell casinomas and its subtypes, some typical, and a typical AMLs, oncocytomas and other tumors. First of all, technique. Technique is very important. Our MR protocol is same for all abdomens.  Post contrast, we typically do all these sequences in with post contrast images in arterial venous, three minute delay, five minute delay in coronal and for all, we do subtractions as well. The many sequences that can really make difference in diagnosing renal, as well as liver legions is subtraction in and out of phase and fat side. Remember that for renal tumors, fat is your friend and diffusion-ready images. As far as subtraction technique is concerned, it is grossly underutilized. It drives me crazy when I see outside scans where subtractions is not done. This is very simple. You just had to push a button and machine does it for you. There is no extra table time or patient time. I think it's crime not to do subtraction sequences when it is so easily available and it makes a lot of difference in characterizing these legions. So essentially in this, you are subtracting pre-contrast images from post-contrast images. So it will subtract out the hemorrhage, hyper-intensity within the legion and it will just give you a pure enhancement within the legion, which helps you a lot. So for example, in this patient, this is a legion with slightly hyper-density. There's peripheral calcification following intravenous IV contras. There is no way of measuring how much this legion is enhancing. Same thing with MRI. You can see on T2-rated images, it is slightly, it is hyper-intense. So this is cystic legion on pre-contrast even. It is markedly hyper-intense, indicating hemorrhage or protein-ish material with IV contrast. You cannot exactly determine whether this is contrast or the hemorrhage within the legion. But when you do subtraction, you can see this ugly nodule within this cyst, which was a papillary renal cell carcinoma, which would have been difficult to diagnose either on the CT images or non-contrast or non-subtracted images. So subtraction technique is very important. Another legion, here on CT scan, without contrast, arterial phase, portal venous phase or nephrographic, corticometallia nephrographic phase. We don't know what is, whether this legion is enhancing or not. But on MRI, you can see that on T2-rated images, there is some heterogeneity within the legion. On pre-contrast images, there is area of hemorrhage. But with IV contrast, we don't know how much of it is enhancing. On subtraction, you can clearly see that it has got low-level enhancement. This was another papillary renal cell carcinoma. This was a 50-year-old patient. Shows an ugly-looking bilabilated legion with hyperintensity on T1 pre-contrast-rated images. Even on T2-rated images, the legion looks extremely ugly. But with IV contrast, you don't know whether this legion is enhancing or not. But on subtraction images, you can clearly see that this is just a hemorrhagic legion. There is no abnormal enhancement within it. We followed this legion for three years and you can see that there's hardly change in this legion. There's still some hemorrhage. It is still looking ugly. But there is no enhancement on subtraction images which saved nephrectomy for this patient. This was a high-grade papillary renal cell carcinoma. You can see that this legion has got extensive hemorrhage within the legion. This area, we don't know what is happening with IV contrast without subtraction. We don't know whether this area is enhancing or not. And on subtraction images, you can see really ugly looking papillary renal cell carcinoma which can be easily diagnosed once we subtract that hemorrhage. So subtraction, very important for diagnosing tumors. How about in and out of phase imaging? This is especially diagnostic for angiomyelipomas and some of the clear cell renal cell carcinomas. Let's see how we can diagnose those. Then angiomyelipomas come in different flavors. They can be very fatty like this where you are going to get this India ink artifact at the fat water interface. And this is diagnostic of angiomyelipoma. You can also see that there is fat here which is going to suppress on fat cell images. Another legion intra-parenchymal angiomyelipoma is going to show that India ink artifact all around it as well as chemical shift artifact. Some of the legions could be tiny which will completely show drop out on out of phase imaging. If there are legions containing less fat then that portion of the legion is going to show drop on out of phase imaging. However, the problem comes when there is a lipid poor AML or clear cell carcinomas on in and out of phase imaging. However, it has been shown that the lipid poor angiomyelipoma stained to follow signal of suase muscle on in phase and they will show areas of drop in signal on out of phase depending on how much fat contain is within the legion. Whereas in renal cell carcinoma they usually follow the perinchymal intensity on in phase and on out of phase due to intra-cytoplasmic fat that is microscopic fat is going to show uniform drop in signal which is very characteristic of clear cell renal cell carcinoma. This is a clear cell renal cell carcinoma in phase, out of phase. Although this tumor looks slightly heterogeneous you can see that on out of phase imaging there is uniform drop in signal and that's because of intra-cytoplasmic flat seen in this leisure, which is very typical. In lipid poor angiomyelipoma again we can see that it follows the signal of suase on in phase, on out of phase there are areas of drop in signal within it due to this small fatty tissue within the legion but it really depends on how much fat is within the legion. This is lipid rich angiomyelipoma which follows the signal of surrounding fat. You can see it is getting saturated on fat set sequences and out of phase imaging it shows areas of drop in signal typical for lipid rich angiomyelipoma. How about diffusion ADC sequences? This is especially helpful in differentiating cystic benign legions from cystic renal cell cancers can differentiate benign from malignant renal tumors maybe helpful in differentiating histologic subtype or grading the severity of the tumor DWI is also useful in patients if you cannot give gadolinium and that might be the only chance to grade the tumor. So here is a low grade, this is oncocytoma which shows hardly any restriction whereas this is a clear cell renal cell carcinoma you can see how much restriction is there and low ADC. So very helpful. This is a busy chart but let's tease it out. The RCC subtypes are clear cell which is by far the most common papillary and chromophobic. It's important to differentiate between these three as clear cell carcinoma tend to be very aggressive depending on its grade and stage and sarcoma test changes and one needs to be very aggressive in treating these tumors with nephrectomy whereas papillary and chromophobic tend to be relatively slow growing, especially chromophobic. It has got fire survival of 80 to 93 percent. So the management could be different here you put in papillary and chromophobic you can do nephron sparing surgery which will help in preserving renal function depending on patients age. So very important to make sure the type of tumor which you may be able to do with MR. There are four things that you can look to characterize this different types of renal cell carcinomas. One is T2 signal in and out of phase type of enhancement and whether there's necrosis or cystic changes within the region or not. So depending on this, we can see that in clear cell type renal cell carcinoma on T2 weighted images the region tend to be very high or intermediate in signal intensity compared with low intensity on papillary renal cell carcinoma and intermediate signal intensity on chromophobic type on in and out of phase imaging since clear cell renal cell carcinoma has got that intracytoplasmic fat it's going to show drop of drop in signal usually uniform on auto phase imaging which we saw earlier. Whereas in papillary renal cell carcinoma there is drop in signal on in phase not out of phase but in phase that's due to hemorrhage or hemorrhage within the region whereas chromophobic type is usually homogeneous as far as enhancement is concerned clear cell type shows avid enhancement which is similar to the cortex of the region whereas papillary shows minimal enhancement and chromophobic shows mild to moderate enhancement clear cell carcinomas tend to have necrosis within it papillary type may show some small cystic changes and chromophobic tends to be uniformly solid without any necrosis or cystic changes. So on our real phase you can see here that this is the clear cell type renal cell carcinoma which is showing avid enhancement similar to the cortex there are areas of necrosis within it this is partially exophytic more than three centimeter diagnosis whereas papillary is relatively hypovascular you need subtraction images to see the mild enhancement it is fairly well-defined and chromophobic it shows mild to moderate enhancement well-defined now necrosis within the region. So how does CT and MR perform in characterizing intermediate renal lesions? Margules and his group performed a trisor suspected study of 143 patients with indeterminate renal lesions detected on ultrasound 77 had CT, 66 had MRI and MRI showed definitive diagnosis in 95% of patients versus 78% on CT scan MRI recommended only additional studies or recommendations such as follow-up only in 1% of patients whereas CT recommended CT recommended more than 10% additional evaluation so MRI was more likely to give definitive diagnosis and less likely to recommend further imaging than CT. So let's go through a couple of scenarios to run through different types of tumors and where MR is going to be helpful in diagnosing this lesion. So scenario one, MR can be helpful to further characterize lesion where initial CT protocol was not adequate. So this patient had CT scan without contrast and you can see that this patient has got multiple renal lesions except one probably rest of the lesions are not characterized on this non-contrast CT scan. You can go ahead and do CT protocol with arterial venous phase. However, still there are going to be some lesions which are not going to be characterized as you can see on this MRI that all these lesions look cystic. Some of this lesion, for example, this one is hemorrhagic lesion, there's small hemorrhagic lesion here which would have any problem with CT scan with and without contrast. But on MRI, we can show that all these lesions are benign and this patient does not need to follow or any other study. MRI, in this patient at CTA examination which showed an indeterminate lesion here, we went ahead and did MRI in this patient and we can see there's this lesion which was not characterized on with contrast is in fact an angiomyeloperma. We detected another angiomyeloperma here. These two lesions showed gross fat within it. So there was no additional examination necessary in this patient. So summarizing scenario one, MRI can be helpful to further characterize lesions which are where the initial CT scan protocol was not adequate. So let's see whether MRI can be helpful in indeterminate lesion despite of adequate CT protocol. So here the protocol is adequate but still the lesions could be non-diagnostic because in homogeneous lesion, if there is intermediate change in density that is increase in density less than 20 harmful unit but more than 10 harmful unit, then those lesions are going to be indeterminate whereas if it is a heterogeneous lesion, then it's going to be difficult to exclude smaller nodular areas within the lesion. So this is a renal mass or renal lesion here. You cannot see it on pre-contrast but there was 90 harmful unit increase in density from pre-contrast to post-contrast which is non-diagnostic. So this is indeterminate lesion. We also have to remember that smaller cysts which are intra-parent chymal in central in location can give false reading because of partial volume artifact for those smaller lesions within the renal parent camera. In this patient, we went ahead and did MRI and we can see that on T280 images, it's a cystic lesion. There's some internal density on pre-contrast T1 but however on post-contrast images as well as on subtraction, there is no enhancement. So this is a lesion containing mild hemorrhage. So advantage of MRI in such patients is we don't have to worry about pseudo enhancement. We have subtraction images to subtract out the protein or hemorrhage within the lesion and we got very sensitive fluid sequences which can help us diagnosing this cystic indeterminate lesions. There was this study done for potential renal donors which is very important because we don't want to transplant any kidneys with renal lesions. There were 105 lesions which were with average size of 1.5 centimeter. 94, all this patient had CT scan with subsequent MRI. On CT scan, 94 of these 105 lesions were TSTC that is too small to characterize by CT. When they did MRI, in 99% of the lesions, MRI was diagnostic and no further imaging was necessary out of which 83 were simple cysts, eight were protein issues or hemorrhage exist, two were AML. So take home point is MR can characterize small lesions that are indeterminate with CT due to pseudo enhancement or partial volumine artifact. This was a indeterminate lesion as this lesion was kind of bioloped or trialoped and we can see following administration of IV contras. You can see some septations within it. Is there some nodularity within it? So this was at least two F lesions by Bosnay classification. On MRI, we can see this portion of the cyst has got dense hemorrhage. The other portion of the cyst did not have any hemorrhage and is an enhancing nodule which was diagnostic of early cystic renal cells carcinoma in this patient. So MR is sensitive for detection of enhancing nodules in cystic renal lesions. It upgraded 73% of patients on this study. It had 95% positive predictive value for malignancy with enhancing mural nodules. How about lesions with low enhancement that is difficult to detect on CT scan? The solid mass which is most likely to result in this conundrum is papillary renal cell carcinoma. As we can see it here, this is the enhancement pattern of clear cell renal cell carcinoma, chromophobic type and papillary type. And papillary type you can see it shows very low enhancement with IV contras compared with other two tumors. So if you suspect that there is very low enhancement or rule of thumb is if you have difficulty in deciding whether it is enhancing or not, they consider it to be a papillary renal cell carcinoma because in up to 30% of patients with CT, this enhancement is undetectable. This lesions tend to be hyperdense on pre-contrast CT. So it's difficult to measure the enhancement in many of these patients. This is a patient with, it looks like hemorrhage exist with IV contrast and on pre-contrast images, the density was around 28 harmful units following IV contrast on corticomedulary and nephrographic phase. There was enhancement of 16 to 17 harmful units. So this was, although the legion size is pretty large, it was still indeterminate whereas on MRI, you can see that this legion has intensity similar to perenchyma with IV contras. You can clearly see that there's some enhancement which on subtraction images, we can clearly see that this is a solid enhancing legion which was papillary renal cell carcinoma. So over half of the papillary renal cell carcinoma did not show definitive enhancement on corticomedulary phase with CT. On nephrographic phase, it did show some enhancement. So nephrographic phase is probably the best phase but MR did not have any problems detecting this legions at all. So take home point is when reading CT scan for hyperdense legion, nephrographic phase is key although you are still going to call some indeterminate legions with this, MR has better sensitivity and specificity for detecting enhancement of low level enhancing legions versus hemorrhage excess in this patients. Scenario number three, how about CT protocol is adequate, legion is enhancing but the diagnosis is uncertain. So in this, the legion is not fully evaluated with CT scan for example, this patient which was a fat poor AML but based on multiple sequences and enhancement pattern and diffusion weighted images as well as in an out of phase images, MR can characterize many of these legions. For example, this is a clear cell carcinoma, this is probably typical. It share with areas of necrosis within it, there shouldn't be any problem in diagnosing this on CT or MR. We can see that on nephrographic as well as carticum medullary phase, nephrographic as well as carticum medullary phase it's going to show marked enhancement especially in carticum medullary phase. It is going to show a drop in signal as I showed you before on out of phase imaging which is going to be uniform due to intraceitoplasmic fat which is also pretty helpful whereas in papillary nephrographic carcinomas which is second most common, they tend to be very cellular. They are hypointains on T2-weighted images. These are relatively indolent legions so it's important to separate these out from renal cell carcinomas. These tend to be bilateral and are more common in renal failure patients. Here in this patient, there are multiple legions. You can see one legion on right side which shows typical appearance of papillary renal cell carcinoma which is low enhancement and it is low signal intensity on T2-weighted images. Whereas this legion where we could see another legion in the other kidney which had similar features whereas third legion which was there was a simple renal cyst. So with help of MRI, we can easily diagnose papillary renal cell carcinoma which may be indeterminate on CT scan and you don't have to have aggressive treatment in these patients depending on patient's renal function, age and everything, you can do some other type of treatment. So papillary renal cell carcinoma commonly involves in-stretch care kidneys often contain hemorrhage or cystic degeneration. Usually homogenously hypoenhancing, they can show some restriction on diffusion-weighted images due to their cellularity which doesn't help. But unlike clear cell RCC, papillary renal cell carcinoma is frequently hypo intense on T2-weighted images whereas clear cell type, there are hypo intense on T2-weighted images. This is one of the ugly looking papillary renal cell carcinoma. We can see that it is hypo intense on T2-weighted images compared with clear cell which are going to be hyper intense on T1-weighted pre-contrast images. We can see some hemorrhage. We don't know what is happening here but on subtraction images with IV contrast we can see multiple labylations, fronds along the surface of this region indicating aggressive type papillary renal cell carcinoma. How about chromophobes? This is probably the least common and more indolent type of low-grade tumor. It shares morphologic features and histologic features of oncocytoma. They tend to be ISO to hypo intense on T1-weighted images. They show mild enhancement with IV contrast, no necrosis, their enhancement pattern is less than clear cell carcinoma. So they are something in between. So rule of thumb in this legion is there are usually slightly hypo intense compared with the cortex. There can be diagnostic challenge in diagnosing oncocytomas. However, with MRI there are certain features which can be diagnostic. This tumors tend to have central scar. They tend to be slightly hyper intense which is kind of unique for oncocytoma. They are slightly hyper intense on T2-weighted images and they show kind of slightly spoke wheel type of enhancement with IV contrast in corticomedulary phase. And on the nephrographic phase, they tend to be slightly hypo intense. The another unique feature of these tumors is these scar doesn't enhance initially, but on delayed imaging, this scar will show enhancement which will help you differentiate between the renal cell carcinoma and oncocytoma. The central scar, hyper intensity on T2 of central scar delayed and complete enhancement. Now, intravoxal fat that is out of phase is not going to show low intensity was 97% specific and 55% sensitive in patients with oncocytoma versus renal cell carcinoma based on these two studies. So very powerful feature to differentiate this from renal cell, clear cell type renal cell carcinoma. Another feature that has been described is segmental enhancement inversion in oncocytomas. So on corticomedulary phase, some portion of the tumor may enhance which gets washed out and then the other portion of the tumor will enhance on nephrographic phase which is kind of unique for oncocytomas.  Fortunately, these tumors tend to be the percentage of these tumors is less.  The key MR features in these patients is they are dark on T2. Unlike renal cell carcinomas which are going to be high on T2, they do show restricted diffusion which is a problem but they do not show any necrosis and they might show some areas of drop in signal on auto phase depending on how much fat is within the lesion. Sometimes you may not be able to distinguish this from malignancy and there is no shame in doing biopsy in these patients. Actually this study was just published last month which showed that if you see actually lipid poor angiomalipomas on T2A images show this uniform low signal and they show moderate enhancement on corticomedulary phase. And this is actually this is diagnosed. Actually this was kind of very useful feature in diagnosing lipid poor angiomalipomas. This was seen in 83% of patients with, sorry, the sensitivity was 83% and specificity was 90% in this patient. So maybe this feature is going to be very useful in diagnosing lipid poor angiomalipomas.  In those patients MR is also useful because here you can see that this lesion is clearly has similar intensity as surrounding fat.  So MRI confirms AML. Sometimes you might be able to see this pushing of fat into the renal perinchama which is typical for angiomalipoma from where it arises. So pretty diagnostic if you see it. So how about MR versus CT characterizing renal masses? This group did a study of 120 patients in leeches which were indeterminate on CT followed by MRI. The final diagnosis was based on pathology or followup. 39% of these lesions were benign masses such as angiomalipoma, oncocytoma or hemorrhage exist. The sensitivity of CT for diagnosis of renal cell carcinomas was 91% versus MR it was 94%. Specificity for CT was only 28%. Remember these are indeterminate lesions whereas with MR it was 68%. So using MRI in approximately 12.5% of patients with malignant diagnosis on CT could have avoided surgery whereas 2.5% of benign diagnosis on CT would have been appropriately recommended surgery which was not done with CT scan. So another study which was published in Abdominal Imaging which had 63 patients with indeterminate lesions which were smaller than two centimeter. And of the 63 patients MR was sensitive 100% of the time that means it diagnosed all those 63 patients. MR was 95% specific indicating benign versus malignant lesions of this 63 only three remain indeterminate following MRI. So MR take home messages MR has greater specificity than CT in distinguishing benign versus malignant diagnosis and fewer lesions remain indeterminate after MRI. So wrapping up MRI is indicated in evaluation of indeterminate renal masses on CT and ultrasound and provide additional diagnostic information which can be helpful in diagnosing and managing these patients. MR imaging is particularly helpful in distinguishing solid from cystic lesions when enhancement of renal masses is questionable especially for those where net enhancement on CT is between 10 and 20 household units. So we can either upgrade or downgrade Bosnack 2F lesions so that these patients do not have to go for follow-up examination every six months to one year for two and a half to three years. Diffusion weighted imaging and dynamic contrast in the imaging can provide specific information regarding tumor histology and the staging.  There are not going to be any lesions which are too small to characterize on MRI. Lesions with low level of any aspect hemorrhagic lesions and complex cyst. And that's all from me. Thank you. Everybody, it's a pleasure to be speaking at this MRI conference today. My topic here is congenital CNS anomalies. As you know, it's a very broad topic and in the next 30 to 35 minutes I'll probably barely scratch the surface. So for this case-based review, what I have done is I have focused on a few selected entities and I will start with showing an uncommon presentation of that entity and use that as a launchpad for a general discussion on that particular condition. So let's get started. So the first case is a 15 month old who presented with seizures. On these sagittal D1 weighted images, we can right away see absence of the corpus callosum and then there are these multiple cells which radiate all the way up to the ventricular margins. On the coronal images, there is absence of crossing fibers, abnormal ramps on orientation of the frontal haunts, a high riding and dilated third ventricles. Similarly on the axial T2 weighted images, there is absence of crossing fibers in the midline with a prominent inter hemispheric fissure. But the patient also has many other abnormalities including these multiple cysts in the lateral ventricles and possibly in the inter hemispheric fissure. Now you can also see those cystic structures on this sagittal D1 weighted image. Also the cortex and the gyral contours are very abnormal with broad gyra and shallow salsae in the right frontal region associated with this large mass like area of gray matter heterotopia. So what is this constellation of findings called? Is it a Cardi syndrome? Is it a Cardi Gutierrez syndrome? Is it a Clioneuronal tumor based on the cystic changes? Or is it Miller-Dyker syndrome? So this appearance is diagnostic of a Cardi syndrome. So a Cardi syndrome is one of the syndromes associated with corpus callosulitis genus cysts and it has the associated findings as we saw including gray matter heterotopia polymicrogyria cysts and sometimes posterior fossa anomalies as well. It is a real developmental disorder which is caused by an excellent defect. So it is fatal in males and only manifests in females. Clinically it is characterized by infantile spasms and on fundoscopic exam you may see corioretinal lacunae. A few words about corpus callosulitis genus. So corpus callosulitis genus is one of the most frequent plane malformation. It can be complete absence of corpus callosum which is called a genesis or partial absence or disgenesis. It is often associated with genetic abnormalities either trisomies or some single gene mutations or can be associated with extrinsic factors like maternal alcohol syndrome. And as you know corpus callosulitis genesis is often associated with other intracranial and spinal anomalies or craniofacial anomalies and part of them have syndromic associations. This is a companion case. This is a 17 year old male with developmental delay and seizures. On the axial T2 and T1 weighted images we see this lobular hyper intense mass in the midline in the expected location of the corpus callosum. Also there is parallel orientation of the lateral ventricles. On the sagittal T1 weighted images we see this lobular T1 hyper intense mass in the region of corpus callosum which completely suppresses on fat saturated sequence. This is an enhancing vessel through that region. So the findings are suggestive of a pericallosal lipoma with disgenesis or absence of corpus callosum. So pericallosal lipoma it's the most common location for an intracranial lipoma. It occurs in the inter hemispheric fissure and it is closely related to the corpus callosum which is often malformed. There are two morphological subtypes of pericallosal lipoma which include a tubular nodular which is the more common like in our case and it's often associated with severe corpus callosal disgenesis. The other subtypes is curvilinear where you have a thin band of fat along the corpus callosum and the corpus callosum may be either normal or only mildest genetic. There can be other associations with this including absence of tympilocidum, as it is ACI, polymicrogyria, heterotopias or sometimes dorsal cyst. Moving on to case number two. This is a one month old child with dysmorphic features. So on the axial T1 weighted images we see this abnormal fusion of the cerebral hemispheres across the midline. The inter hemispheric fissure is partly present, it's present anteriorly and a small portion is present posteriorly but it's obliterated in the midline. And you can see the continuation of gray matter and white matter across the midline as well as this abnormally long silviant fissure which continues across the midline over the vertex to extend onto the contralateral side. Same findings on the coronal images, there is fusion of the cerebral hemispheres in the midline, there is fusion of the ventricles with absent interventricular septum and on the sagittal T1. So what's the diagnosis here? Is it schisencephaly? Is it scintillencephaly? Is it semilobar holoprosencephaly? Or is it arinencephaly? So this is an example of scintillencephaly which also goes by the name of middle inter hemispheric variant of holoprosencephaly. So what is holoprosencephaly? So holoprosencephaly are characterized by incomplete separation of hemispheres due to abnormal cleavage of the prosencephalon. It's often associated with other midline anomalies including anomalies involving corpus callosum and the hypothalamic pituitary axis and also associated with craniofacial malformations. Holoprosencephaly is a spectrum with the least severe form being alobar and the most severe form being alobar and the least severe being lobar. Middle inter hemispheric variant is somewhere probably between semilobar and lobar. So in alobar holoprosencephaly, there is a single midline forebrain with a horseshoe shape monoventrical and a dorsal cyst. In semilobar holoprosencephaly, there is some separation of the hemisphere. The inter hemispheric fissure is partly present posteriorly and there is fusion anteriorly. There is variable degree of deep nuclei and thalamic fusion in semilobar. And lobar holoprosencephaly is the least severe form where there is only fusion of the most inferior portion of the frontal lobes, otherwise the hemispheres are separated. So this particular case is the middle inter hemispheric variant of holoprosencephaly, which is a relatively milder form and there is cerebral fusion in the posterior frontal or the parietal region with partial presence of inter hemispheric fissure anteriorly and posteriorly. There is a horizontally oriented sylvan fissure that extends across the midline over the vertex. The corpus callosum is usually abnormal with the body being absent and the genuensplenium are present. So holoprosencephaly are kind of the exception to the rule of callosal disgenesis in terms of its hemorrhological development. This is an example of semilobar holoprosencephaly where you see fusion of the frontal lobes across the midline. There is absence of interventricular septum, but the inter hemispheric fissure is partly present posteriorly. Again, you can see the same findings on T1 weighted images. There is this band of gray matter along the anterior aspect of the ventricles, absence of the interventricular septum and fusion of the frontal lobes across the midline. On the sagittal images, we can see absence of the corpus callosum in the mid portion, all the portion of the splenium and probably the genu or present. This is an example of alobar holoprosencephaly where there is lack of separation of the cerebral hemispheres. There is a single forebrain with a horseshoe-shaped monoventricle which widely communicates with this large dorsal interhemispheric cyst. Moving on to case number three, this is a child who presented with seizures. So on MR evaluation, we have coronal and sagittal T1 empirical sequence. So on these T1 weighted images, we see this abnormally thicken and lobular appearing cortex in the right perisilvan region as well as in the left perisilvan region. Also on the sagittal images, we see this abnormally deep sylvan fissure which extends all the way up to the vertex and is lined by these thickened and lobular appearing cortex. Same findings on T2 weighted images, you see abnormally thickened and lobular cortex in bilateral perisilvan region. Also, there is absence of septum pellicidum. So what's the diagnosis? Is it schizencephaly, polymicrogyria? Is it focal cortical dysplasia type two or is it gray matter heterotopia? So this is an example of bilateral perisilvan polymicrogyria. So polymicrogyria is characterized by numerous small gyri with bumpy appearance of the gray-white contour. It is caused by the arrangement of neuronal organization of abnormal cortical lamination. It can be sporadic or can be genetic or sometimes may be associated with inutrient infection or vascular incense. There are multiple syndromic associations with polymicrogyria and on imaging it can be focal, multifocal or diffuse. So bilateral perisilvan polymicrogyria is one of the common presentations. It can be sporadic or familial. It presents with developmental delay, motor deficits and sometimes seizures. There is a MR grading system for perisilvan polymicrogyria. So grade one is the most severe where you have involvement of perisilvan region as well as frontal or occipital lobes and the abnormality reaches all the way up to the, up to the frontal or occipital poles. A grade two is where the polymicrogyria extends into the frontal or occipital lobe but does not reach the poles. Grade three is purely insular and ocular in region involvement like we saw in our case. And grade four is the least severe form where you have involvement only of the posterior insular bilaterally. So these are two cases showing focal polymicrogyria. So the patient on the left side has this almost mass-like lesion in the left frontal lobe with multiple lobular areas of gray and white matter. So this is an example of a complex nodular polymicrogyria which can mimic a mass but it does follow gray meta-signal on all the sequences. This is another example of focal polymicrogyria where in the left parietal lobe we see an abnormally deep sulcus and a thickened lobular cortex lining the sulcus. So that can, again, this is something that can cause seizures and needs a careful evaluation of MRI for diagnosis. This is an example of diffuse polymicrogyria, a young child, a few months old, presented with infantile spasms. So on the T1 and T2 weighted MRI, we see this abnormal gyral and sulcal pattern bilaterally. The gyri are abnormally white, the salsa and shallow, and there is this nodular lumpy-bumpy appearance of the gray-white junction throughout. So this is an example of bilateral diffused polymicrogyria. Moving on to case number four, a three-year-old female presenting with seizures. So on the axial T2 and T1 weighted images, again, we see this abnormal gyral and sulcal pattern that is broadening of the gyri and very shallow sulci, and there is associated thickening of the cortex. If you look more carefully in the posterior region, there is this band of white matter with separates, somewhat normal appearing cortex with this additional band of gray matter-looking tissue. Defining is probably seen a little better on T1 weighted images where we see posteriorly a relatively normal thickness of the cortex, a band of white matter and then another band of gray matter. And T really looks more like diffused cortical technique. So what's the diagnosis? Is it polymicrogyria? Is it gray matter heterotopia? Is it focal cortical dysplasia type two? Or is it age area? So this is an example of subcortical band heterotopia. So subcortical band heterotopia belongs to the lesion-cephaly spectrum of disorders. So lesion-cephalys are characterized by smooth brain. There is positive of gyri and sulci and associated thick cortex. It's on a spectrum. So age area is the most severe form of lesion-cephaly where there is absence of a sulcation and the brain has a very smooth appearance with shallow silver and fishes giving it an hourglass appearance. Or the milder forms is called the package area where there is decreased number of gyri which are abnormally broad and shallow sulci. And package area can be associated with subcortical band heterotopia. So lesion-cephaly is caused by arrested neuronal migration and the cortical lamination is abnormal with four-layered cortex instead of five. There are two important genes which are involved in lesion-cephaly spectrum. The first one is the LIS-1 gene. It's the most common either deletion or mutation of this gene can result in lesion-cephaly. The other is XLIS or the DCX gene. It is an X-link disorder which causes lesion-cephaly in homozygous males but it causes subcortical band heterotopia in carrier females. So our case was a three-year-old female who had a package area with subcortical band heterotopia. This is an example of what's called the classic lesion-cephaly where you have a smooth brain with diffusely thick cortex and very shallow sylvanes fissure giving it a figure of eight appearance. This is another example of lesion-cephaly but in this case there is associated mycroftalmia and retinal detachment. So this constellation of finding is called the Miller-Dyker syndrome and this is associated with LIS-1 mutation. Another variant of lesion-cephaly which is sometimes called lesion-cephaly type two is the cobblestone lesion-cephaly. Again, just like any other lesion-cephaly there is reduction in normal sulcation but in addition there is a bumpy appearing cortical surface which gives the name cobblestone lesion-cephaly. This is commonly associated with the muscular dystrophy syndrome which also go by the name of alpha-dystrocliconopathies and these includes condition like Walker-Wartburg, Fukuyama and muscle-eye brain disease. So on imaging we may not be able to distinguish between these individual subtypes. So what we can call on imaging is a Walker-Wartburg imaging phenotype when we have all of these findings present. So let's look at an example. So in this patient, we have this diffused paucity of cells in both cerebral hemispheres with a smooth appearing cortex, with a smooth appearing gyri, but there is this lobular morphology to the cortex. So that's characteristic of cobblestone lesion-cephaly. You can see it a little better in the paritoxibital regions. There is associated marked ventricleomegaly and this characteristic kink appearance of the brainstem with associated cerebellar hyperplasia. Now there may be some mild cystic changes in the cerebellum as well. This patient also has abnormalities of the eye in the form of persistent hyperplastic primary vitria. So this constellation of findings of cobblestone lesion-cephaly, colosal dysgenesis, ventricleomegaly, abnormally kink brainstem, hyperplastic cerebellum and ocular anomalies is associated with the Walker-Wartburg phenotype. Next case is a five-month old who presented with nasal obstruction. So we have a sagittal D2 and D1 weighted image, which shows a bilobed mass extending into the nasal cavity. Superially, the mass appears to communicate with the subarachnoid space via defect in the cryptrefront plate. Same findings on the axial and coronal images and on the post-contrast images, there is enhancement of mucosa surrounding this cystic mass, but there is no enhancement within the mass itself. So pretty straightforward diagnosis. Is it a cephalosil, a nasal dermoid, nasal glioma or a inverted papilloma? So the diagnosis in this case is a cephalosil. So cephalosil is congenital herniation of one or more intracranial structures through a defect in the skull. And depending on the contents, it could be a meningocil, which contains meninges and CSF. Meningo and cephalosil or simply encephalosil, which contains meninges, CSF and brain parenchyma. Cephalosil is a more general term, which includes both meningoceles and meningo and cephalosil. And then there is a variation of cephalosil, which is called as atretic parietal cephalosil, which is typically seen in the midline hyperietal region and is characterized by herniation of meninges and some fibros or dysplastic tissue. Location, it can occur in the posterior location either in the occipital or occipital cervical region and this form of occipital cephalosil is more common in the Western countries or it could be frontoethmoidal, which is called the sensipital cephalosil, which is more common in Southeast Asia. So frontoethmoid cephalosil can also be classified into two types based on the bony defect. It could be nasofrandyl, as in this case, where you have herniation between the frontal bone and the nasal bone or it could be nasoethmoidal, where you have herniation between nasal bone and the nasal cartilage, like in our case. This is an example of occipital cephalosil. So we have a large bilobsistic mass arising from this defect in the occipital bone. There may be some herniation of brain pattern camera through the defect. Intracranially, we see a basement of the extra axial spaces, mild dilatation of the ventricles and abnormal morphology of the posterior fossa structures, including a small posterior fossa effacement of the cisterna magna, inferior herniation of the cerebellum and crowding at the foramen magnum. So these findings are reminiscent of a Kiari II malformation, but when you have a cephalosil, we're finding similar to Kiari II, it's called Kiari III malformation.  They are in the inferior occipital or the occipital cervical region, but in our case, it was more in the superior occipital region. This is an example of a broad-based parietal cephalosil, where there is a large bony defect in the parietal bone and herniation of both the cerebral hemispheres through the defect. There is also some cleosis in the herniated brain parenchyma. And this is an example of atritic parietal cephalosil. Like we previously said, it's most commonly seen in the midline parietal bone and it's characterized by a herniation of meninges and some dysplastic tissue, but there is no herniation of brain parenchyma or dural sinuses. There is typically abnormal orientation of the straight sinus, which is more vertical. There is a persistent phalosine sinus. And then there is this cigarship CSF cleft, which extends from the supracerebellar system all the way up to the defect in the calvarium. And also in this case on the hemorrhvenogram images, we see this focal splitting of the superior sagittal sinus, which is related to where the tract bisects to reach the defect in the calvarium. The next case is a spine case. This is a one-month-old child who presented with the sacral subcutaneous mass. On the sagittal and axial T2 weighted images, we see this, we see dysrefism of the sacral region and we see the cystic mass, which appears to be contiguous with the distal spinal cord. Here again, you can see the distal spinal cord with the cystic mass contiguous with it. There is no associated lipoma, although there is some continuity of the epidural fat with the subcutaneous fat. The important thing to note here is this is a closed defect that the cystic structure is completely covered by skin and the subcutaneous tissues. So what's the diagnosis here? Is it a myelomaningocele? Is it a myeloskesis? Is it a myelocystocele or is it a dermoid cyst? So the correct answer here is myelocystocele. So myelocystocele is a closed neural tube defect where you have herniation of the dilated central canal or the syringocele through a defect in the posterior elements. Here is a diagram illustrating the myelocystocele. So you have dilatation of the distal, dilatation of the spinal canal, which is called a syringocele and the syringocele extends through a dysraphic defect in the posterior elements. And since it's a closed neural tube defect, the cyst is covered by skin and subcutaneous fat. So it's a rare form of closed or occult spinal dysraphism present with skin covered subcutaneous mass, as in our case. It's most commonly seen in the sacral region where it's called the terminal myelocystocele, although it can be seen in the cervical thoracic region where it's called the non-terminal myelocystocele. This is an example of non-terminal myelocystocele where we have this dilated central canal extending into this fluid filled tract through a dystrophic defect in the upper cervical spine. So this is the meningocele component. So this is like a cyst within a cyst and the outer cyst is the meningocele and the inocytic component which is contiguous with the spinal cord is the myelocystocele component. So I find this chart very useful which classifies the neural tube defects and neural tube defects can involve the cranium as well as the spine, but we are focusing on spine right now. So spinal defects can be open or closed. Open defects are associated with Kiari malformation and ventricular megaly while closed defects are not usually associated with intracranial findings. The two open neural tube defects which you need to remember is the myelomeningocele which is by far the most common or myelos and the second is myeloskeesis or myelocyle. The most important closed neural tube defect which will present with the skin cover subcutaneous mass is lipo myelomeningocele and then you have the less common myelocystocele like we saw in this case. So whenever you are evaluating someone with a neural tube defect, the first step is to identify whether it's a closed or open defect and that will completely change your differential diagnosis. This is an example of lipo myelomeningocele where you don't have a cystic structure but you have a lipoma which is contiguous between the, between, we have a lipoma along the distal spinal cord and it's contiguous with the subcutaneous fat and again this is a skin cover defect. So this is an example of a fetal MRI with myelomeningocele. So these are fetal, this fetal MRI was obtained at 22 week of gestation and this was obtained at 25 week gestation after a region with the last cystic structure or crowding at the foremen magma. So myelomeningocele is open spinal dysrephism. It's characterized by a low-length spinal cord which ends in a neural placode and the neural placode extends beyond the level of the skin surface which causes expansion of the associated subarachnoid spaces. Intracranially it's associated with Kiari 2 malformation and when you could have medley like we saw in this case. In the recent year, our institution has done a lot of in-utero repairs of myelomeningocele and the data on that has been very encouraging. So the initial trial which established the efficacy of in-utero myelomeningocele repair was done in 2011, the mom's trial. And it showed that in... Sorry, please bear with us. We just so trying to sort out these technical problems we'll put the link for the registration for the International Edition of the MRI teaching course. So this starts on the 28th of October, 28th and 29th of October and then we'll see you in November on the 3rd, 4th and 9th 5th. We'll be covering various sessions in AI, neuro, body imaging, MSK imaging, cardiac as well as breast imaging. And we have an excellent team of international speakers who are joining us from US, Canada, UK, Singapore, Australia. We've already applied for emergency credit points and there are some activities which we've also arranged. So case of the day is somewhere where you can send us your interesting or a rare case from your institute and you'll be given a chance to present this during the conference. And the best entries will be receiving prizes for this. Also, you can send us your paper and poster submissions. You can mail them to MRIteaching at gmail.com. All the submissions will be receiving e-certificates and there are some prizes for the winners. So this is the excellent panel of speakers that we have who will be joining us for the conference. We have Dr. Scott Flam who's a pioneer in cardiac imaging who will be taking various topics and Dr. Manohar Shah who is a professor in chairing pediatric technology in hospitals in Toronto. Very well known for his pediatric lectures. Then we have Dr. Thomas Link and Dr. Haike Link. There's a team of speakers from Mayo Clinic who will be joining us in October as well. And the entire day where Dr. Dushan Sakhani and his team of speakers will be taking various sexual various lectures throughout the day for us on 4th of November. Sorry, I think we are ready with the lecture. So I will just share from my... I will discuss the imaging spectrum differential diagnosis of corangeocarsinoma and the limitation of imaging for pilari structures. Corangeocarsinoma is the most common primary pilari tract malignancy. It's second most common primary hepatic tumor after hepatocellular carcinoma. Seen worldwide, most common in North Thailand where it is due to association with liver flukes infection. And it is seen twice more frequently in males compared to the... These are the risk factor of corangeocarsinogenesis, parasitic infection, as the liver flukes I just talked about. Primary sclerosis in corangeitis, cholerythiasis, pilari disorders like polytocal cyst, hepatitis B, hepatitis C, and cirrhosis. As well as lifestyle related risk factors. I will go into the details of corangeocarsinogenesis. So these slides will be there in your PDF. Hepatitis B, hepatitis C, and liver cirrhosis, they are common risk factors for developing corangeocarsinoma and hepatocellular carcinoma. So be aware of that. Many times clinician will say answer whether the patient with cirrhosis has corangeocarsinoma or hepatocellular carcinoma. So that's the rule of the radiologist, become very cool. So coming to the anatomical classification, the corangeocarsinoma can be divided into peripheral intra-hepatic corangeocarsinoma, higher intra-hepatic corangeocarsinoma, extending from the insertion of the cystic duct to the second-order bile duct, and then the extra-hepatic corangeocarsinoma as shown in this illustration. What important for us is to know the morphological classification of corangeocarsinoma. These can be divided into mass-forming corangeocarsinoma. So the mass-forming corangeocarsinoma, they tend to invade into the liver parenchyma. They tend to oblate rate the partial vein without invading into it. Whereas the second type, peridactyl infiltrating type, they tend to grow along the bile duct. So they usually present with long structures and dilatation. The third type, the intradactyl type, it grows into the duct as a papillary mass, expanding the bile duct. This one has the best prognosis. Why the morphology is important? Because it decides the tumor's behavior, surgical approach, clinical outcome. Overall, prognosis of the patient is decided by the morphology. Workup of the patient, biochemical workup, serum CA-19-9, information is quite useful in differentiating the corangeocarsinoma from epitocelular carcinoma. As I said that the patient with corangeocarsinoma as services can go either way at the corangeocarsinogenesis or they can develop epitocelular carcinoma. But be careful, patient with benign biliria disease can also have high CA-19-9. So the mass-forming corangeocarsinoma, usually they are irregular mass, lobular mass with well-defined margin. In the periphery of the tumor, they are abundant tumor cells. In the central area, there are necrosis, fibrosis, and mucin, hyperintense on T1 and heterogeneously bright on T2-WGDM. Enhancement pattern is quite characteristic. In the arterial phase, they show peripheral thin-drain of enhancement with progressive centripetal enhancement in the subsequent phases. And the delayed phase, there is more intense enhancement. They are predominantly hyperintense on the epitopilary phase. And I'll talk more about it, some interesting signs on the epitopilary phase. The ancillary features are quite useful sometime in differential diagnosis. As I mentioned, the corangeocarsinoma tend to encase the hotel vein instead of invading as a tumor thrombus. They may be associated bilirialitation, lobariprofi, capsule attraction, and some other ancillary fee. This is very interesting sign, cloud sign. This is seen in patient with corangeocarsinoma in the epitopilary phase. So the central area of the tumor is bright in epitopilary phase and the peripheral is hyperintense. That is called cloud sign. Here is an example of a cloud sign which we reported in this journal. But this is not specific for corangeocarsinoma. It can be seen in metastasis from the musiness tumors. Another sign is the target sign, which is more specific sign of corangeocarsinoma. So in the high B value diffusion weighted images, there is bright signal here because of the tumor cells. Well, in the center area, there is dark signal because of the fibrosis or necrosis. This is seen only in the high B value images. This is quite useful sign practically to differentiate small epitocelular carcinoma from the corangeocarsinoma. So this is seen in the corangeocarsinoma. So in the first case here, T2-FatSat images show a heterogeneous mass in the liver and it shows heterogeneous T2-bright signals. The central area is more bright. The periphery is not so bright. In the high B value images and ADC images, clearly there's a cloud sign. So there is darkness only in the periphery of the tumor and in the central area, it's more of a T2-shine-through effect. So this is sorry, it's a target sign is present. It's hyper, the tumor is hyper intense on T1-white images. In the archival phase, classical peripheral rim-like enhancement and in the venous phase and three-minute and five-minute delayed phase, there is progressive enhancement. See the enhancement in this area becomes more dense with the time lapses and in the habitable biliary phase, what we are seeing is classical cloud signs. So this is how a Colenjo-Carsinoma looks like classical Colenjo-Carsinoma. Everything specific is present about it in the Colenjo-Carsinoma. Sometime even a single image is quite diagnostic of Colenjo-Carsinoma. So I'm showing that. This is a patient who has a mass which is showing heterogeneous enhancement. There is peripheral capsular retraction. There is attenuation of the portal vein. It's not invading. See there's compression of the portal vein. There is associated peripheral ductal dilatation. So one image quite confidently, I can say that this is probably most likely Colenjo-Carsinoma. Another example, 58-year-old man with hepatitis B and cirrhosis. CT scan shows in the photo venous phase a mass here. So the question again, whether this is Colenjo-Carsinoma or Hepatocelular Colenjo-Carsinoma, MR shows a lot of light on this case. Let's see that MR of this patient. So on T2 fat-sat images, the mass is heterogeneous, mildly bright in the periphery and dark in the center. And on the diffusion-vated images, it's bright. I'm not showing the ADC because of the lack of space here on my slide, but it was dark on ADC. So there is restricted diffusion. Look at this component of the mass. It is extending into a tubular structure, either it's a motorway or it is a duct. So see that it's bright. It's behaving same as some primary mass. On T1-vated images, this mass is hypo intense. In the arterial phase, there is barely any enhancement in the mass, but there is some heterogeneous enhancement. Very mild enhancement in the mass. In the venous phase and the delayed phases, there is progressive and more dense enhancement in the mass, as well as this component, which is extending here. So this is extending here. There is an ancillary feature here. The duct is dilated here and there is absolute retraction. Happy to be able to phase, the mass washes out. And if you move more cordially slices, this component, which we were analyzing, is not going into the portal vein as the portal vein is here on this side and the mass is here. And it's actually extending into the right duct. So all these features are favoring the diagnosis of cholangiocarcinoma. So quite comfortably, I can tell my clinician that this is not epitoma. This is cholangiocarcinoma. The differential diagnosis, as I said in clinical practice, is quite a common query, how to differentiate a cholangiocarcinoma from hepatocelular carcinoma. So in my, this is a chart I got it, in my experience, this presence of fat is quite useful. When the fat is present, it's more likely hepatocelular carcinoma because I have not seen fat really in cholangiocarcinomas in the literature they have described though. Then the capsule in the delayed phase is seen in the hepatocelular carcinoma and not in the cholangiocarcinoma. But if you invaded images, as I mentioned, is there can be target-like appearance if it's been present, it's quite useful. Portal vein involvement is typically in hepatocelular carcinoma. There is tumor thrombosis, whereas in cholangiocarcinoma, there's encasement of the portal vein rather than tumor extension. Then the duct may be dilated in cholangiocarcinoma, whereas in only large hepatocelular carcinoma, the ducts are dilated. Another example, a 54-year-old man with hepatitis B, again, the question is same whether this is hepatoma or cholangiocarcinoma. MRI, let us see the MRI, what it shows. So on MRI, this lesion is mildly bright, but quite well demarcated on T2 fat-fat images. There's a lot of information in the T1-mated images. So in the out-of-face image there, the tumor looks more darker. There is signal loss, suggesting that there is fat inside the mass. And this is bright on high-v value images. And I'm not showing the diffusion, but it was dark on diffusion, so there was presence of diffusion. And in the out-of-face, there is very mild enhancement compared to the unenhanced white images, not the typical enhancement pattern of hepatocelular carcinoma. But what is interesting is that in the three-minute delayed phase in the hepatocelular phase, there is a very subtle capsule formation. So we have two evidence to work, hepatocelular carcinoma, and then the further evidence comes from the biochemical. Workup of the patient, the patient. Alpha-phetoprotein level was more than 400, whereas the CA-19 was not high. So comfortably, again, we gave a diagnosis of hepatocelular carcinoma. This tumor was reflected, and the final diagnosis was well differentiated, hepatocelular carcinoma. A rare differential diagnosis of mass-forming carcinoma is hemangioma, not the classical hemangioma, but the sclerosing hemangioma. The classical hemangioma typically has peripheral nodal enhancement in the arterial phase, and which moves centripetally. Whereas in the sclerosing hemangioma, the same findings are present, but they are delayed. So in the arterial phase, there is nothing, but in the venous phase, there is peripheral nodal enhancement. And even in the quite late phase, there may not be complete filling of the tumor, of the hemangioma, because of the fibrosis element present in the center of the hemangioma. So in the clinical practice, again, it becomes sometimes difficult. This key is helpful. The hemangioma, they don't show any restricted diffusion. The bile ducts are never dilated in the presence of hemangioma. Epidupilates phase is not that useful. So an example here. 41-year-old man with incidental lesion in liver on the ultrasound. And the CT scan, single phase, photovine phase, shows there is a lesion with the heterogeneous enhancement in the periphery of the right lobe of liver. Amar was done for this patient. On fat-fat-tituated images, the lesion is heterogeneous, on slightly bright in the periphery, but dark in the center. In-phase, out-phase, at least confirmed, there is no fat, so unlikely, hepatocelular carcinoma, no clue for hepatocelular carcinoma. There is no restricted diffusion, quite useful evidence. And in the arterial phase, there is no enhancement. In the venous phase, there is peripheral mild enhancement. In the delayed phase, there is centripetal moving of contrast. And finally, in the tamiya delayed phase, the lesion completely enhancing. In the hepatopulmonary phase, there is some nodular patching enhancement in this patient. So again, it's more favoring the sclerosing hemangioma because there is no restricted diffusion and there's delayed sort of, enhancement is slightly delayed compared to the classical hemangioma. But in the clinical practice, the decision-making, it becomes difficult to call sclerosing hemangioma as sclerosing hemangioma. It's usually a hindsight diagnosis in my clinical practice. So we suggested biopsy. No biopsy was performed in this patient, but this remained stable over nine years when I was following this patient, almost same as appearance. So we concluded that this is probably a case of sclerosing hemangioma, definitely equivalent to carcinoma. It's out of question. And there is no ancillary teacher cell like absolute retraction or peridactal dilatation in this case to suggest as carcinoma. So comprehensive evaluation is important in such case. Okay, this is an interesting case recently encountered, but we have few more cases like that. A 51-year-old man with sigmoid, mucinous malignancy operated a couple of years back. So this patient had undergone a CT scan that showed multiple masses in the liver. We did MR for further evaluation. So on T2 fat set images, there are at least two masses in the liver, one here and one here. They are mildly bright, but not exactly T2 bright, but they have a margin quite well demarcated. There is restricted diffusion. And if you carefully evaluate the diffusion, it is the target sign. The target sign is present. There is the restricted diffusion in the periphery of the mass and in the central area is more of a T2 shine through an anus vibe, high point chance and look at the venous faces and the three major late and epitopillary face. There is progressive enhancement in both the masses. See this, here, here. And in the epitopillary face, classical cloud sign. So we knew from the history that patient has some use in the history of colinear mucinous sigmoid mass. So these are probably metastasis, but in the clinical also knew that this is metastasis, but we have to give it differential diagnosis that maybe these are multifocal colinear carcinoma, radiological differential diagnosis, but final diagnosis was confirmed as mucinous metastasis. So learning point is that the mucinous metastasis cannot be sometimes differentiated radiological from colinear carcinoma. You have, but that usually this is not a question because you always have a history of a mucinous malignancy in breast or colorectal cancer in such patient or with metastasis. Move on to the peridectal infiltrated colinear carcinoma. They arise between the second order bile duct and the insertion of the cystic duct. They spread along the bile duct. But in practice, a combination of peridectal infiltrative and mass forming tumor is more common. So they usually the MR features of peridectal thickening which is hyperintense on T1 that shows progressive enhancement typical signature imaging features of colinear carcinoma, hyperintense on T2-weighted images. They are usually associated with ductal dilatation and ductal narrowing that actually draw your attention towards the mass, the presence of ductal dilatation. And the most important in practice is the presence of restricted diffusion in the peridectal thickening and that makes our confidence high to call it a malignant structure. So here is an example of a patient 52 year old man presented with sepsis and abnormal level function test and this is how they usually present. So on the CT scan, single phase, photovenous phase, there is just focal ductal dilatation. Nothing else, focal ductal dilatation in the left that portal vein is not thrombose but it's adenuanted on colitis. It's compressed, it's narrowing caliber. It's not invaded by the mass. So the MR was done for this patient for peridevaluation on MRI. There is ductal dilatation in the left side and the duct are not as bright as they should be. They are very cloudy bright, but they are bright. See here, very difficult to make out. Most useful, restricted diffusion, it was present. I'm not showing it in the ADC here because of the lack of space on my slide but there is bright signals here in the diffusion weighted images. On the contrast phases, there is periductal thickening and enhancement, see along the duct here, along the duct involving a long segment of the duct. Typical example of periductal infiltrative collage carcinoma and this is how they usually present focal dilatation of the duct, either segmental or low bar, some territorial. So the take home message is one of the take home messages to never ignore focal ductal dilatation if you see on CT, do work up on this patient. So this patient came back six months later. Six months later, I have put up the initial CT and follow up CT side by side and you can realize six months later, the mass is not quite obvious. So initially it was a ductal, periductal infiltrating mass. Now it has become a combination of periductal infiltrating and mass forming collage carcinoma. This is usually a stage when we give the diagnosis, confirm diagnosis of collage carcinoma that is not good for the patient because by this time it's inoperable, it's good to diagnose, it's quite beneficial to diagnose the collage carcinoma at this stage and that is possible confidently only by a combination of MR and ERCP, as I may have shown with this example. So claskin tumor, everybody knows about it. This is the classification of claskin tumor. Difficult looks like complicated slide, but the slide is more useful to understand the classification. So in type one, only the common hepatic duct is involved without involving the confluence in the type two. The confluence is also involved in type three A, the right duct is involved, in the left duct, in the type three B, the left duct is involved, the right duct is paid and the type four is inoperable. Both the ductal systems are involved along with the hepatic duct. So this classification is useful for prognostication and for guiding the cell. So 56-year-old man with elevated liver function test and sepsis. There is a mass here in the hyalum with ductal dilatation. Bilaterally, the right duct is left duct on T2-Hase images. That's showing restricted diffusion. And in the contrast enhancement phases, there is typical signature of colon geocarcinoma progressive enhancement. No doubt this is a claskin tumor and the portal vein was paid in this patient. MRCP is quite useful in these patients in classifying into the PISMA categories. So in this patient, the left duct is well-involved and the main duct is involved. So this becomes type three B claskin tumor in this patient's surgery was not performed. Preparative treatment was given and due to presence of mobility. So this is how a claskin tumor looked like. Now we move on to a common scenario that we face in our clinical practice. Bilaterally strictures. So especially the extra hepatic pile that's strictured. I see it every, I mean twice or twice in a week. Here's an example, classical cases. 58-year-old man joined this. MRCP shows abrupt cutoff of the dilated duct while actual ducts are dilated. Three-minute delayed phase shows that there is some cuff of soft tissue enhancing at the level of cutoff. Axial post-contrast delayed images are useful showing that there is an eccentric soft tissue here, nodule in the region of the stricture, quite well-seen here. So in this patient, since they have presence of two evidence to suggesting the presence of malignancy. So you can uncomfortably call it cholangio carcinoma which is usually confirmed like MRCP. So this was confirmed after the dilated duct. So cholangio carcinoma. Now we move on to the opposite category of the patient. A 60-year-old woman with recurrent biliary colics or in this patient, an MRCP. You can see that the duct are dilated. Then our pulse duct calculate. Then there's a stricture. Post-contrast delayed images shows that there is a gradual tampering. So the gradual narrowing that is not abrupt cutoff. So in actual images there is no periductal thickening. What you're seeing here is calculus within the CBD. There is no convincing periductal thickening and there was no restricted fusion in this area. So there's no evidence for malignancy. So we'll probably benign, but again radiologist should be careful calling a benign lesion a benign. You never know, cannot exclude a mucosal cholangio carcinoma. But you can give, just whatever you see, you can describe and favor one diagnosis over other benign versus malignant. So in this case, we call it probably benign, but the patient underwent again. This patient was stable for four years. No MRCP was done. And we concluded that there is nothing no malignancy in this patient. So our problem here and question, our clinician asked whether the bile duct structure is benign or malignant. So final diagnosis usually is with the ERCP. We can suggest, we can look for the evidence. So the evidence for malignancy are presence of periductal thickening, usually eccentric, abrupt narrowing, presence of restricted diffusion, but the tumor tissue is so small in volume that very difficult to have a restricted diffusion in that area. Benign stricture again, it takes a lot of experience to call benign stricture, benign stricture, and it's better to leave this decision on the clinician. You can just leave it, mention it, you report what evidence you are collecting towards either of the nine. Move on to the third type of cholangio carcinoma, the intracutal cholangio carcinoma. So this is usually present like a polyp as a papillary growth in the lumen of the bile duct and there is no parent-kimer extension. This one has the best prognosis because it does not invades the liver parent-kimer. In clinical practice, you encounter them with as a focal or diffuse ductal dilatation with or without papillary mass and sometimes as an intracutal gas-like lesion with a mildly dilated duct. They have the signature of cholangio carcinoma or that how it looks like. So a classical example of a ductal type, on T2-Haste images, there is a mass-Haste, mildly bright on T2-weighted images, mildly bright on high B value diffusional weighted images. It was dark on ADC, so there is restricted diffusion and classical signature enhancement of cholangio carcinoma progressive in the faces. Three minute delay phase shows that the mass is growing within the duct, expanding the duct and there is upstream dilatation of the duct. MRCP, not the MRCP, this is T2-Haste, the mass is located in the duct. So this is how the intracutal cholangio carcinoma looks like. ERCP was done in this patient and cholangio carcinoma was proven. We, I couldn't follow up this case because of certain, because the case notes were locked. Sometime they can be seen on CT scan, like in this case and in this case, there's an enhancing mass in the CBT. Antionous proven, this has to be melignancy, but in this case, it came out as this plastic bilis polyp, so there are a few other pre-melignant lesion described in the literature very rare to pick up prospectively. It's usually the benignity is the hindsight diagnosis for us radiologists, clinical practice, everything. Enhancing in the CBT is cholangio carcinoma and channel is proven otherwise. And I follow that rule. Coming to the conclusions, we must be aware of the signature appearance of the cholangio carcinoma. The awareness about the differential diagnosis is essential as I mentioned the new synapse metastasis from cholorectal carcinoma. We should always seek help from the clinical and lab data and the radiologist, this is very important that you have high index of suspicion for cholangio carcinoma when you are assessing focal strict intra-herpetic or extra-herpetic bilareal strictures. Don't leave the patient alone, follow up those cases. If the clinician does ERCP brushing, even if it's benign, I will recommend if you know the patient, ask him to follow up maybe six months, three months and you may save some life. Thank you, sir for that excellent talk. So I think the questions will be coming up. So you can answer them on the chat box, sir, but I would request you to please... So Gauri, I think we can start with the quiz. Okay, Mithusha, please go ahead. So the quiz will be taken by Dr. Mithusha Verma. And so the two quiz winners will be receiving registration, free registration for the International Online Edition MRI teaching course. Also, Dr. Mithusha really doesn't need an introduction. She's a consultant radiologist in PET CT, CTMR at Nanavati Max Super Speciality Hospital. Her special interest in body imaging and radiology advances. Mithusha, I think we can go ahead with the quiz. Yeah, sure. Thank you, Gauri. And as you all know, the quiz is going to be prize winning. So the last two questions are the prize winning questions. And those who give the correct answer first in the chat box, so we'll win free registration for this upcoming course, which will be a five day entire comprehensive program from 28, 29th October to 3rd, 4th and 5th of November. So there are five questions this time. This is a short quiz we are having. And I'm going to share the first question now on your screen. And you have to just put your answers in the chat box. Yeah. So there are a set of images and this makes together one syndromic association. So what do you think it is? So even if you want to be partly correct, that is fine. You can just start putting your answers in the chat box. I can see one answer, juvenile nasopharyngeal angiofibroma. So there is something, vascular abnormality which is going on. There is something but intracranial also. So what do you think that is? This is, now let's see what the answer to this question is. So this is CAMS, which is a short form for cerebrofacial AV, so that is arteriovenous metameric syndrome. So there are facious, auspicious AV malformations and there is in this case, enhancing vascular malformation in the left basal ganglia as well. So combination of AV malformations in the brain parenchyma and in the facial soft tissue and nausea structure. So this is CAMS. Now we come to another next quiz question on your screen. So you have to identify the sign and what exactly this lesion is. So this is an easy one. So I think you can quickly put the answer in the chat box. Yeah, so as it's correctly mentioned by Dr. Sachin, this is T2 shading sign and this is endometriotic cyst or endometrioma. So the answer was shading sign. Now the next question, you just have to answer which sign does that picture depict? Only the sign. You can put the diagnosis. That's an additional point. But what is this sign? Yes, so this is T2 dark spot signs. So again, it is also seen with endometriotic cysts or endometriomas. So these are the two signs which help us to identify confidently endometriotic cyst when they are present as they might be sometime confusing with hemorrhagic cyst because both of them will have even bright content. But shading sign and this T2 dark spot sign, if positive, it means that it is a chronic ongoing hemorrhage which is happening and these are all clotted or chronic blood products which we are seeing as T2 dark spot and shading is because of the blood production different stages of degradation. So these two signs are important to identify endometriotic cyst. Now you have to assign ORADS category to this lesion. This is your case number four and as I mentioned, this is prize winning. So please read the question correctly. There are only five questions this time. So fourth one is on your screen. Give me the correct answer and you win the prize of pre-registration. So you have to assign ORADS category to this lesion. We see the correct answer is definitely dermoid cyst as Dr. Sachin Pathak has given the correct answer but we had asked for the ORADS category. So two of you have given correct answers. Dr. M Chandramolli and Harveen K and I think last quiz Dr. Chandramolli was a winner. Gauri. So we can consider Harveen K this time as winner for this quiz question. So the category which we assign as per ORADS to dermoid cyst is ORADS two category. These are benign lesions. Dr. Chandramolli have already won the free registration. So you are the winner but means twice registration to the same course will not make sense. So definitely we have two winners, Dr. M Chandramolli and Dr. Harveen K. Both of you please share your email IDs and contact details. Now the next question on your screen, the last question but again the quiz prize winning question. So quickly put the answer easy one. So this was an explanation. So ORADS two category for dermoid and endometriotic cyst both. So see this lesion, what do you think it is? Give your diagnosis on the screen. And one quick hint, give a LIRADS category to this lesion. Like we gave ORADS category, give a LIRADS category to this lesion. Somebody is asking for explanation for the last question. I will definitely revise that Dr. Preeti in a while. I'm just waiting for the winner for this question and we can get into the explanation part. So I think you people are missing on the LIRADS part. You can just refer to Google and the LIRADS table and quickly put the answer in the chat box. That's also fine, no problem. But just apply all the LIRADS rule and see where this lesion fits into. And the size of the lesion is 14 millimeters. Yes, so I think now you are on dot and after referring to your reference sheet. So this is Dr. Gauri. I think we can give it to Dr. Zubin for LR5. And again, Dr. Chandramolli, you are correct. So winner to this quiz question is Dr. Zubin. Please share your email ID and contact detail in the chat box. So I think we made this clear that the reference table has to be with us every time we are characterizing the liver lesions because otherwise it becomes difficult. So as you also saw, once you, the screen was with your question, quickly you had answered HCC. But when I asked LIRADS, there was a lot of confusion going on in the chat box. So just let us revise the LIRADS table. So LIRADS talks about how do we characterize liver lesion in a background of liver cirrhosis? For somebody who is more than 18 years of age, when there is a high risk of having HCC, that is chronic liver, parancampal disease, the background should be there. And orth cirrhosis should be there or the patient should be HPV or HCV hepatitis proven case. Then we apply this LIRADS and based on the size of the lesion and whether it is showing arterial phase enhancement or not, we have these categories assigned. So when we see this with our case and the table in handy position, we see that our lesion is definitely arterial phase enhancing. So we go this side of the table. Then it is the size criteria. Size is 14 millimeters which makes it coming into this category of LR3, LR4 slash 5 and LR5. Now how do we decide between these three? So there are major features which we have to look for. Is there an enhancing capsule? Is there a non-peripheral washout or third is threshold growth? So threshold growth, we can't comment because we don't have comparison but definitely the other two, enhancing capsule is there and non-peripheral washout is also there. So if two major criterias are present with a size of between 10 to 19 millimeters, it is assigned as LR5 category. So this is LR5 category and the lesion which is above 95% of chance of being malignant or HCC in a background of chronic liver disease. So always make sure that you characterize liver lesion using LIRADS whenever your patient is more than 18 years of age and there is a background, parankamal liver disease likes cirrhosis and don't try to kind of memorize the table because you might get confused while putting in the report. It is definitely allowed for you in your practice also. It's not an exam. So you can refer to it from the net and use this table easily and get into a diagnosis. So these are the major features to always remember non-peripheral arterial phase enhancement, non-peripheral washout, enhancing capsule, threshold growth and size criteria. Now as Dr. Preeti wanted to quick explanation to the dermoid question. So this is dermoid for sure, no doubt, T1 hyper intense, heterogeneous and fat suppressed sequence is showing that the lesion is now hyper intense on the fat set sequence. So there was fat within it. So ORADS if you read and go through you will find that dermoid cyst and endometriotic cyst. If it is typical dermoid or typical endometriotic cyst it is benign finding. The probability of it being malignant is less than 0.5% and the category ORADS assign is ORADS 2. So if you see here, so lesion with lipid content and no enhancing soft tissue is a dermoid and assign as ORADS 2. A lesion with that T2 dark spots line or shading sign which is like endometriotic cyst with blood or fibroma if it is completely T2 dark. These three lesions are ORADS 3 category. Now, sorry, ORADS 2 category. So benign lesions ORADS 2 category. So that was the explanation. And Dr. Chandramali, you will receive your pre-registration link before the conference actually starts. So don't worry. And thank you all for being there on a Sunday morning for the prelude session and making it a success. And we have a total six winner out of the three preludes. So congratulations and please do attend the entire course as per your feasibility of timing and schedule. It is on five days, 28, 29th of October and third, fourth, fifth of November. The recordings also will be made available for next three weeks after the course completes depending on the consent from the respective speakers. Dr. Gauria, I would request if you could share the screens again regarding the conference detail and with this, we can come to an end of the prelude. Thank you, everyone. And I've shared the registration link in the chat box. So those of you who want to quickly register, you can directly copy from there and register. Otherwise, just visit the Indian radiologist's webpage and you will get that link. Thank you, Madhusha. And thank you, everyone, for joining us today. And congratulations to the winners. We've shared the link for the registration for the conference in the chat box. And it is also available on the Indian radiologist's website. Also, please do send us your paper and poster entries and do participate in the case of the day contest. So hope to see you all on 28th. Thank you and goodbye. Dr. Amit, I think we can end the session.