 Thank you so much for sharing your lecture with us, Dr. Salvatore. At this time, we will open the floor for any questions, so you can submit your questions to that Q&A feature. And we have a few in there already, so I will throw out the first one. Is NTM infectious? Should they get an antibiotic? It's a complicated course. A lot of patients that have MAI infections are not treated unless they are symptomatic or progressing on radiology. It's ubiquitous in the environment, so we don't always treat it. What is the difference between NTM and MAI? They are synonymous. They are alternative terms used. How much air trapping is normal on expiratory CT scan? I divide the lung into four quadrants, and I accept that if it's in one quadrant, I call it normal, and when I see it in two quadrants, I call it mild. If I see three quadrants, I call it moderate and four severe, just so that I say the same thing when I see a CT scan, so that I can be consistent. Thank you. What is the definition of traction bronchiectasis? Okay, so traction bronchiectasis is when we see, usually in the periphery of the lung, we don't see the bronchi. So when the bronchi become visible in the periphery of the lung, we call it traction bronchiectasis. It's really quite interesting why that would occur when the alveolite collapsed in the periphery of the lung. It pulls open the bronchis, giving traction bronchiectasis and it's associated with fibrotic lung diseases. I often see reports of bronchiectasis called, when you look, the dilation is only mild relative to the pulmonary vessel. And often on follow-up, the dilation is no longer there. Any recommendations on how to tell that the dilation is bronchiectasis or transient? That's a very good point. Otherwise, we're going to be over-calling bronchiectasis. The pulmonologist waits until it's 1.5 times the size of the pulmonary artery, but in radiology, we say bigger than the pulmonary artery for our definition. I guess we would have to retract the diagnosis if it became normal on the follow-up imaging. There are criteria if it's bigger on the CT scan, I would call it bronchiectasis, even if it's mildly larger. I think an interesting thing, too, is sometimes it's not that the bronchis is bigger, but the bronchis wall is thickened, which may make the patient have obstructive lung physiology. I think both things are important to report on the CT scan, but I differentiate bronchial wall thickening from a bronchis that has normal wall thickness and is bigger than its accompanying artery. The definition of bronchiectasis is permanent dilation of bronchi. Why is there then a reversal of dilation on treatment? Only with the treatment now that they're, it's new to us to be treating cystic fibrosis and seeing improvement of the size of the bronchis. This is relatively rare. Maybe the definition needs to be changed in the future to include reversible dilatation, which would help with the other problem that we had on one CT scan where the bronchis was bigger than the artery and on the second one it was not bigger. So we could say bronchiectasis on one study versus another, but for now it's considered irreversible by definition. Are the stages of circuit doses established based on X-rays or CT scans? Thank you for all these questions. On X-ray they were initially established, but because I think that we can apply those to CT scan because we can see the same things even more on CT scan. When we see fibrosis in the upper lobes on a chest X-ray and instead of, and it pulls out from the hyalum, that's very characteristic of sarcoid, especially if there's tenting of the hemi diaphragm, which indicates volume loss of the upper lobes. In contrast to tuberculosis pulls the hyalum, superior sarcoid pulls the hyalum out. So although they are based on chest X-ray initially, now that CT is available we can apply those the grading to the CT scan. Is there any benefit of low-dose CT to characterize bronchiectasis? Yes, I think we should be moving to low-dose CT scan and to MRI. We used to use, when you've been doing this for long enough, we used to use the highest possible dose to make the most beautiful picture and the pendulum is absolutely swung to use the lowest possible dose to see what we need to see. And I think the follow-up for that will then be going to MRI. And if we can see that the airway dilated there's no reason not to use the lowest dose possible, which I think that lung cancer screening has shown us that we can see dilated bronchi with a dose of less than three milligray. What is the normal thickness of the bronchial wall? It's barely perceptible. I tell my residents that if you can measure it, it's probably second. I don't think the cursor allows you to measure it when it is normal. But if you can measure it, I find that it is thickened to my eye, which has been looking at it for a long time. So I would just say that so if you can measure it, it is probably second. In a case where we have middle, super, and lower, low bronchiectasis, what may be the origin? So I guess common things happen commonly. When I see bronchiectasis in all the lobes, it's oftentimes a very bad case of MAI. As diseases advance, the best way to make a diagnosis is the earliest CT scan where the disease, where it starts. By the end, all types of bronchiectasis, all types of fibrosis can look have a lot of overlap because there's so much extensive disease. So because common things happen commonly, it's usually MAI. But any disease in its end stages can have bronchiectasis more extensively in all lobes. How do you differentiate cystic bronchiectasis from cavatory lesions of lung parakeima on CT? That would be very difficult. You're going to have to rely on coronal images and sagittal images to try to reconstruct the path to the central trachea. Sometimes that path is lost, is truncated. I think cystic bronchiectasis is clustered, and usually, cavatory lesions are, they may be multiple, but they're not necessarily touching each other. I think that that might be a helpful way of doing it. I heard you say you use a rortopulmonary ratio to assess for pulmonary hypertension. What happens when the aorta is ectatic? In my institution, we use 29mm as cut-off for main pulmonary artery. The literature says 29mm is the upper limits of normal, but I read a paper that said that 33mm was 95% confidence interval, so I went to 33mm. But I still think it's very hard to measure that exactly, depending on the position of the patient's pulmonary artery. I'm much more confident when the pulmonary artery is bigger than the aorta to call it pulmonary artery hypertension. I might suggest it at 33mm. I don't do it at 29mm. I wait till 33mm to be more confident. I make that higher. Can you have very small focal bronchial dilations? Very small bronchial dilatations. What is a lifeful question, too? The secondary pulmonary labial is the functional unit of the lung. It's shaped like a hexagon, and the bronchus is in the middle of it. The bronchus we normally don't see, so it's very, very tiny in size. When the patient has, oh, it's so interesting with, we'll take, for example, UIP, Usual Institutional Pneumonitis. The patient's alveolar epithelial type 1 cells stop working. The type 2 cells take over the function of the type 1 cells. The type 2 cells make surfactants, so there's no surfactant to keep the alveoli open. The alveoli start to collapse. If all the alveoli are collapsing, they pull open the bronchus. Now the bronchus is 3mm in size. It's not supposed to be 3mm in size, so that's the smallest little bronchi being dilated. When I see that, I know the patient must have fibrosis occurring when it's 3mm in size. Over time, as it gets more and more dilated from more and more adolescences, the bronchus takes up the whole secondary pulmonary labial and becomes 10mm in size. A dilated bronchus 10mm in size. And the secondary pulmonary labial here and the secondary pulmonary labial here are touching each other. These two 10mm size cystic structures, which are the airways now are dilated, touching each other, we call that honeycombing. Last question, please explain Williams-Campbell. Williams-Campbell is a congenital disease with absence of the cartilage that affects a specific part of the airway from the fifth to the eighth branch where there is no cartilage. So we have ballooning out of the bronchus and when the patient expires, they collapse. So there's short of breath because they're air trapping. So when you see this ant mini type of appearance where the central airways, where the trachea and the proximal airways are normal and the peripheral airways are normal but the middle ones are dilated, it's likely Williams-Campbell and they're going to do genetic testing to prove that.