- Jake Hunter
- Jul 15, 2021
- 1 min read



A stream of consciousness from a few less-than-stellar modern philosophers


The Bucks dominated in their return to Fiserv Forum in Game 3 to the tune of a 120-100 win. Giannis was still great, but his supporting cast also elevated their games considerably. The saying about role players to home held true in Game 3, let's see about Game 4.
Speaking of Giannis, he has already entered elite territory with his production in these Finals. He has stolen Chris Paul's spot on the pedestal as the premier player in the series, and another monstrous game tonight might even put him on the inside track for Finals MVP even if the Bucks falter in the series.
We need to have a conversation about Devin Booker. Yes, he had 31 points in Game 2, but he wasn't even overly efficient in that game either. He hasn't looked fully right since his broken nose, but this team needs him to play at a higher level. People mentioning him as a "superstar" are just wrong at this point. He needs to string together a few strong games to win more people (me included) over to that side of the argument. Boo your TV with me tonight if you hear Mark Jackson call him a "superstar" again.
It was only one game, but I feel like the Suns are in a dangerous spot tonight. The Bucks have figured out that if Deandre Ayton accumulates fouls quickly, the Bucks will win. With no Dario Saric behind him (not that Saric is a world-beater by any means), the Suns need Ayton to play smart this game and the rest of the series.
Khris Middleton was solid if unspectacular in Game 3. I think he explodes for 25+ in front of the Milwaukee crowd in Game 4.
Cam Payne has been "Chicago Bulls Cam Payne" for about 6 straight games. That's....not good. Phoenix can be limited offensively if Booker isn't doing his thing, so they need Payne to recapture his form from early in the playoffs if they want to take a commanding 3-1 series lead.
Despite the raucous environment outside in the Deer District, the inside of Fiserv Forum was exceedingly average in Game 3. We need a better effort from the Bucks fans tonight.
Ratings Tracker: Game 1 proved to be the most anemic from a ratings perspective relative to the others. My theory for that being the case centers around the uncertainty that Giannis was going to play, though I've been somewhat surprised that nobody I know of brought that idea up at the time. They are still down considerably from 2019, but the Bucks' win on Sunday may bring some more interest to the series going forward.
In my opinion, Chris Paul needs this game for his legacy more than any other player on the court tonight. Be ready for him to bring his best.
Bucks Head Coach Mike Budenholzer looks to have figured some things out over the course of the series, and he had a decidedly better performance than Monty Williams in Game 3. Williams ended up benching Devin Booker for the final 13 minutes of play (granted, it was a blowout), so one has to question the status of their player-coach relationship in Game 3. It may be nothing. Booker had a poor night, and there don't seem to be any lingering issues brought to the public's attention. Keep an eye out for that storyline popping up in the broadcast, though.

Today I want to bring your attention to a disease that afflicts a part of the human body that is exceedingly important: your lungs. Most people know that the lungs are what moves air in and out of your body and allows us to keep living. Most people also have some familiarity with the idea that the things we inhale can potentially hurt the function of our lungs over time. In this post, I'm going to briefly detail a disease pattern that is caused by irritating molecules getting into the lungs: pneumoconiosis.
Ultimately, inhaling a lot of certain types of molecules can put someone at a higher risk of developing pneumoconiosis. Lots of things can cause this disease pattern, but here are a few major compounds that have been known to lead to this condition:
Asbestos
Silica
Beryllium
Coal Dust (Black Lung Disease)
Iron
I'll walk you through the pathophysiology (or, simply, how this disease comes about) of pneumoconiosis, but this picture might make what I'm about to say a little easier to understand. Understanding a little about how your lungs work goes a long way to understanding what pneumoconiosis really does to your body.

When you take a breath in, that air travels from your mouth down your trachea (or windpipe) into your lungs. The very ends of the airways in your lungs are called alveoli, which you may have heard described as little "sacs" that help us breathe. The importance of these alveoli to our breathing and, ultimately, our survival is that they are very effective at allowing oxygen to diffuse (or pass through) the layer of tissue the alveoli occupy and move directly into our bloodstream and for extra carbon dioxide in the blood to exit the body when we breathe out.
There's a lot of physics and chemistry that goes into this exchange that I won't spend time on here, but for our purposes, just think of the alveoli/bloodstream interface as a two-way street that keeps both ends of the road workin optimally. The important portion of the lung interface as it relates to pneumoconiosis is the layer that exists right between the alveolar layer and the capillaries of the bloodstream. This is called the interstitium.
The interstitium (sort of marked by that green arrow in the picture) is essentially a collection of support tissues and other cells that keep the lungs working their best, but because of its proximity to the air that is breathed in, it can potentially be very vulnerable to infections, autoimmune attacks, or diseases like pneumoconiosis. When this area is compromised in any way, it can become inflamed and, if inflamed for long periods of time, scarred. This scarring makes it difficult both for diffusion of gases across the alveoli and for normal expansion of the lungs when someone takes a breath in. This leads to what is called restrictive lung disease, which basically means that the lung has a hard time expanding and bringing in air while also having trouble with gas exchange even when the air makes it where it should be.
So now that we understand what is being affected, it's fairly simple to understand pneumoconiosis. Over fairly long periods of time, if a person is exposed to large amounts of irritating materials (like silica or coal dust), that person's lungs won't like that. There are defense mechanisms in your lungs to clear foreign materials out of places they shouldn't be in, but large amounts of dust can't be cleared in time and the lung tissue then becomes very inflamed. Long period of inflammation lead to scars, and these scars make it very hard for air to move through the lung into the rest of your body.
Typically, years of exposure are required to develop noticeable symptoms, but once they develop, they are fairly constant. Initial symptoms of pneumoconiosis include short, rapid, and shallow breaths as well as coughing and phlegm.
There are two stages of pneumoconiosis: simple and complicated. Simple basically means there is a small area of your lung that is fibrotic (scarred) enough to cause some loss of function, but that small area is the only one affected. The prognosis for this good so long as the person takes care not to expose themselves lung irritants any more than necessary. If someone did not follow this course of action, they could progress to complicated pneumoconiosis, which is much more severe and widespread. A person with complicated pneumoconiosis will likely have notable trouble breathing both at work and at rest.
Beyond just respiratory issues, pneumoconiosis left unchecked can cause lung cancer (particularly mesothelioma if the inhaled dust is asbestos) or even heart failure due to excess strain and pressure on the heart due to the fibrosis in the lungs. Pneumoconiosis is a serious pathology that warrants considerable action in order to prevent a sharp decrease in the patient's condition.
Unfortunately, there is no definitive treatment for pneumoconiosis once it is discovered. However, someone diagnosed can significantly improve their quality of life by taking concerted actions to limit their exposure to situations and substances that may inflame or irritate the lungs. For starters, if a patient has asbestos-related pneumoconiosis and works on a demolition crew that routinely knocks down old buildings, a good first step might be to wear a mask or find another job/task that does not expose the patient to even more harmful molecules that would exacerbate their condition. Another recommendation would be to discontinue or refrain from smoking, as cigarette smoke is the textbook definition of a lung irritant.
Think of pneumoconiosis similarly to a fire. If you don't want the fire (pneumoconiosis) to get larger, don't pour gasoline on it (breathing more irritants). While the analogy isn't perfect, it illustrates that pneumoconiosis is a disease that largely spreads only when more "fuel" is provided for it to do so.
Pneumoconiosis is a serious, but manageable respiratory condition with the right actions. If you work in a setting that has lots of dust floating around, maybe consider wearing a mask to protect yourself in general. I'd recommend reading online about occupations that might be at more risk for developing the disease. Here are a couple resources I found helpful:
Ultimately, stay diligent about any significant breathing changes you might have and make sure to let your physician know if you work in a place that has lots of dust or any of the substances mentioned in those links above. Take a piece of advice from my peer, Dr. BlendTec, when it comes to asbestos, etc. He wears a white coat, so he knows what he's talking about.
P.S. Pneumoconiosis is a fun word to say. Try to sneak it into your normal conversation this week
Thanks so much for your interest in Cogito Ergo Cogito! If you have comments, suggestions for us to write about a topic, or any questions about the blog, feel free to fill out this form and we'll be in touch with you as soon as possible!
