Very Interesting!

Well, what it mainly comes down to is that PCs of the time didn't have dedicated 3D hardware the way they do now, or the way that the 1994 Playstation did--it wasn't until the release of the 3Dfx Voodoo 3D card in 1996 that this capability really started to become mainstream in gaming PCs. So, any 3D in a game had to be rendered entirely using the machine's CPU, and ray casting engines like the ones used in Doom were simply a far more efficient way of rendering 3D, albeit they took some shortcuts in order to do that.

I actually remember playing through the whole of the original Tomb Raider (1996) on the PC in software rendering only, and the huge difference it made once I got a 3D card and ran it via that instead.

Doing true 3D polygons requires a lot of floating point operations (the PS1 did use intermediate integer shortcuts on top of dedicated floating point hardware which is why PS1 games have that distinctive warped perspective and shimmering) but in 1995 the target for PC games was still the 486. The fact that the makers of Dark Forces demanded a whole 8MB of RAM when there were still many people with only 4MB drew some interesting complaints at the time.

Unfortunately the big performance difference between the existing base of 486 users and the new Pentium adopters was the processor's floating point performance. That's why Quake (1996) required a 75Mhz Pentium and even on a 100Mhz 486 would run at about 10fps (I know because I only had the 486 at home so it was easy to compare just how big a difference the Pentium's floating point unit made). So the two advances that allowed for 3D games where processors with strong floating point performance (Pentiums) and dedicated accelerators cards that could do many floating point operations in parallel (even better than a Pentium).

By comparison 2.5D games required no floating point operations and could use small integer based lookup tables. 2.5D games are based on a very simple ray casting. For each vertical line on the screen the game projects a ray along the 2D overhead grid until it hits a wall. It then takes the distance to the wall to determine which scale lookup table to use and draws an appropriate vertical strip of pixels taken from that walls texture, which unlike 3D texturing aren't from arbitrary points but rather a simple vertical line using that lookup table to know when the duplicate (stretch) or omit pixels to draw it at the correct scale.

Most of the answers so far are talking about the lack of 3D rendering hardware at the time as the cause. This actually wasn't the issue at the time.

The issue wasn't how quickly to render the polygons; the issue was how do you determine which polygons you need to render. And that is not a graphics card issue; that is a CPU issue. In all games that have a moving viewpoint, from way back in Battlezone all the way to today's best looking games, the computer needs to rapidly filter out what it can ignore and not even send to the video card.

Carmack and iD made the breakthrough of using Binary Space Partitions to *instantly* know the exact list of walls they had to consider rendering based on where the camera was located. Ars Technica has a great article going in depth on it, probably at a higher-than-ELI5 level...

At an ELI5 level, what is Binary Space Partitioning in a 2.5D game?

Simply, the level is looked at from the top, so processed on the basis of the "floors" of the model. The computer splits the the floors into triangles on the basis of what walls can be seen when the camera is on the triangle. Depending on how varied that list can be, the triangle can be cut into further smaller triangles, so the list is as close to totally accurate as possible. (Imagine one giant rectangular room with 10 hallways coming off of it. Depending on which hallway you are looking down, the walls will be vastly different. So the giant room gets cut into many many triangles rather than just 2). This processing takes a very very long time, and is saved with the level. It is not done on the player's computers.

Additionally, the use of triangles mean the game never needs to calculate "which triangle am I on?", because when the triangles are built, they also save what triangle is on the other side of each edge. So when you move from one triangle to the next, the game already knows "crossing edge B of Triangle 12 moves you to Triangle 16".

Oh yeah, and additional ELI5: What does Binary Space Partitioning mean?

Complex word and complex science, but actually very easy conceptually:

• Binary: Means two options, "on or off", or "yes or no".
• Space: On the map/level
• Partitioning: dividing

So, Binary Space Partitioning means "dividing up your level so you know if you are in front of or behind each wall"

When the first "3D" engines were created, there were no 3d acceleration. So doing actual 3d were not possible.

With the ID Tech 1 engine, they basically made a 2D engine but flipped the textures for the walls to make it look 3D.

There are a bunch of videos that explains how it works and why it was revolutionary. It is thoroughly fascinating.

What I loved was the 2D background with 3D characters on top kind of games that worked around the early limitations in processing power. Games like Final Fantasy VII and Silver.
Silver can be bought on GOG and has aged very well in my opinion.

Wait this is 2.5D? I thought 2.5D was strictly games rendered in 3D but with 2D movement like platformers. Wikipedia says it is both, but it seems confusing to me since they're very different and only one of them is still commonly used.

I always call it original Doom or Wolfenstein 3D type graphics but that is not concise.

Sometimes it doesn't, people have been known to wake up with snot all over the pillow. When it does stop it is normally because the nasal passages swell which prevent both snot and air from going through them. The nasal passages tend to swell completely shut when you are laying down. When you treat a cold with advil + sudafed you are dramatically reducing the swelling in the nose so you can blow the crud out of your nose more easily.

Because if you're laying on your back, you are now drinking your own snot and boogers all night.

It doesn’t stop. For most people it just runs down the back of their throat into either the stomach or lungs where it lodges unless you are able to cough it up in the morning. If you can’t cough it up it may become pneumonia.

It dont. The mucus drips backwards to pharynx and you swallow it like swallowing the saliva produced in your mouth. It stops when the virus is under control again.

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The logic is: if you don't use it why allocate it to you this much money if it could be used elsewhere?

The issue: this logic is faulty and doesn't take into account large bulk expenses (for example, when launching a new project or upgrading infrastructure)

Doesn't this promote frivolous, wasteful spending?

Yyep.

Michael: Why don’t you explain this to me like I’m five. Oscar: Your mommy and daddy give you ten dollars to open up a lemonade stand. So you go out and you buy cups and you buy lemons and you buy sugar. And now you find out that it only costs you nine dollars. Michael: Ho-oh! Oscar: So you have an extra dollar. Michael: Yeah. Oscar: So you can give that dollar back to mommy and daddy, but guess what? Next summer… Michael: I’ll be six. Oscar: And you ask them for money, they’re gonna give you nine dollars. ‘Cause that’s what they think it costs to run the stand. So what you want to do is spend that dollar on something now, so that your parents think it costs ten dollars to run the lemonade stand. Michael: So the dollar’s a surplus. This is a surplus. Oscar: We have to spend that $4300 by the end of the day or it’ll be deducted from next year’s budget.

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Imagine you're a master blacksmith. You have to heat up your iron to the right temperature to work with it. Too hot and it turns to pure liquid. Too cold and it won't bend when you hammer it. Once you've been doing it long enough, you can probably tell the temperature pretty accurately based on exactly the color of the red-hot glow, right?

Well, all objects are glowing just like hot metal does. It's just that most objects aren't hot enough that the glow is in the visible spectrum. You glow in infrared, which is slightly lower energy than red. This is also how thermal cameras work.

The thermometer can measure how much you're glowing in infrared, and just like the blacksmith, can tell your temperature.

The laser is just a thing for you to use to know where it's measuring, to aim. It's just like a laser-mounted gun sight.

The laser is just used for aiming and is not used as part of the measurement process.

The sensor itself is typically a thermopile that is composed of thermocouples (edit or something similar) to measure the heat and uses a lens that can pass longer wave IR like a germanium based lens. The lens might give like a 12 to 1 distance to spot ratio, or something close for example, so that at a distance of 12 inches a one inch spot is being measured.

https://www.senbasensor.com/products/infrared-thermopile-sensor/

https://www.te.com/usa-en/products/sensors/temperature-sensors/thermopile-infrared-sensors.html?tab=pgp-story

One tricky thing is that objects with a low emissivity like shiny aluminum could give a false reading in certain instances.

edit added some sensor links

A contact thermometer will warm itself up through conduction. With an infra red thermometer, the surface you're measuring the temperature of is radiating heat. The sensor in the thermometer picks this up. It effectively measures temperature the same way a digital camera could be used to measure brightness.

The laser dot just helps with aiming.

To add to to the other answers here: the general name for this type of instrument is "pyrometer" and there are actually a few different subcategories that offer better accuracy. They all use the same basic principle of measuring the blackbody radiation coming off of an object, described by Planck's law. The cheap ones measure total power coming from an object over a narrow frequency range, but are affected by anything that would change how much power is received (field of view, obstructions, emissivity). The next level measures the ratio of power received over two frequency ranges, which should not change even if the total power intercepted does, so it fixes obstructions/field of view but still has issues with temperature and wavelength-dependent emissivity, as well as any materials like gas or glass that have some absorption spectrum and modify what reaches the pyrometer. The last level is basically a full spectrometer, measuring a bunch of frequencies and fitting the curve to Planck's law, which can account for pretty much anything with the right calibration.

Historically, pyrometers have been used for measuring high temperature things because (a) it's difficult to measure with other techniques and (b) they release a lot more power (visibly glowing!). However, the same principle applies to lower temperature objects, it's just harder to get a good signal.

All objects at finite temperature emit electromagnetic radiation. Very hot objects like stars, oven heating elements, and old school light bulbs emit some radiation that is visible (light). Closer to room temperature, objects radiate mostly infrared light which we can't see. Materials like silicon or InGaAs will produce a small electrical current if illuminated by infrared light. By measuring this current, knowing the materials electrical response to radiation, and by knowing how temperature and wavelength or radiated power are related (see Wien's displacement law or Stefan–Boltzmann law), you can calculate a temperature.

you get an adrenaline rush, adrenaline makes your body go into fight or flight mode. it pulls blood to more important places. you become cold in your hands and feet where it narrows arteries. your glucose processing goes into overdrive to create more energy for the muscles. adrenaline also makes your sweat glands go into overdrive. makes your face become red from the extra blood, makes it very hard to sleep and makes it very hard to eat because blood has been pulled away from your digestion. afterwards you get to have a nice low blood sugar crash.

Don't forget that sweating is the body's way of cooling itself down. Water is pushed onto the skin's surface where it can evaporate, taking some of the body's heat as it moves from the skin to the air. Your body can sometimes tell the skin to produce sweat even if it's already at a good temperature. If too much sweat is produced, you will feel cold.

In general, price levels should go down, not up. It was hard and difficult to make the first iPhone; now, it's much cheaper and easier. As things improve - from machines to software to experience - the price of goods should decline. This causes a problem though, that John Maynard Keynes put this way (approx:) If people believe prices are going down, they will put off buying today to buy cheaper tomorrow. Makers won't buy raw materials, figuring they'll be cheaper in the future. Left unchecked, this 'deflationary spiral' can cause recession and depression.

Keynes' remedy was a 'little inflation'. If people believe that prices are going up, they will buy today instead of waiting. Similarly, makers will bid up the prices of raw materials and labour, with the expectation those will be more expensive in the future. The net result is more economic activity than in the deflationary case.

"Stable" prices are very rare, in the sense of all things staying the same, instead of the general price level. Some things go up, and some things go down, according to fashion, supply, and technology. The general price level can stay relatively stable for long periods of time, though.

In the US, from 1813 to 1913, the general price level fell by 38%. In other words, it only $0.62 in 1913 to buy what cost you $1 back in 1813. The decline was an average 0.48% per year. This is obviously good for people trying to live on savings or small incomes.

In 1913, the US got the Federal Reserve. What you could buy in 1913 for $1 would cost you $25.53 in 2013. Or, put another way, $1 in 1913 would only be worth $0.04 in 2013. Not very good for savers or people on fixed incomes.

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You really have two questions here. One is what causes inflation, which someone else will probably answer, but a bit on the value of goods and services:

The world has a certain amount of goods, land and stuff in it. There's also only so many working hours people can perform. The "Real Economy" in a way has a certain amount of physical things and actions.

Let's say the world has 10 000 cash, that transfers between people, is used to pay for goods and services. In a way, that cash describes or applies, is spread out in a way, across the goods, land and labor.

And the price of things really comes from the RELATIVE value between them. A bread costs 5 and an ipad costs 500, because of the work involved and how much people want each of them.

But let's say someone waved a wand, and all cash doubled.

Adam used to make a paycheck of 100, and went and bought a bread for 5. But now Adam instead has 200 in his pocket. So he decides that - hey- he's going to buy TWO breads, and eat particularly well.

But so does everyone else who usually buys bread. But the bakery does not have any more bread than before. There's only so much grain being farmed, so much flour made from the grain, so many loves of bread made from the flour, and this remains the same.

So suddenly there's the SAME amount of bread, but TWICE as many attempts to buy bread at 5.

Through various processes (like: people bidding over each other, the bakery raising prices until there's no longer excessive demand), the price of bread will rise to 10. At this price, Adam only wants to buy 1 bread, just as before, and the demand for bread matches the supply - so it will not happen that the amount of money increases and prices remain the same.

In a way, how many "currency units" a country has in their daily life is completely arbitrary. In the sense that in the US, bread could be 5 and ipads 500, and in another country it could be 50 and 5000. What matters is the amount of real stuff. The money just describes the real stuff.

About inflation, things are set up so that as the economy grows, the amount of money grows just a bit faster. Due to machinery, processes improving etc. the number of actual things grows over time, but the amount of money grows just a bit faster, causing a small bit of inflation. This is considered a good thing.

If the amount of money grows too fast whilst the physical economy is the same or shrinks, inflation will be high, and this is bad, it causes small-scale economic disruption and chaos in various ways

If the amount of money grows too slow or shrinks, whilst the physical economy is the same or grows, prices will actually decrease (deflation), and this is also considered bad.

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edit: changed "fixed amount" to "certain amount"

Ugh. Can y’all ELI4?

How inflation works and the role of central banks in containing it is one of the most politically contentious questions out there, so unfortunately if a 5 year old asked me this I'd tell them 'people don't agree, and they can get really upset about it'.

Many proteins undergo conformational changes and have different properties in the different conformations. "Moonlighting proteins" are ones that have multiple distinct biological functions, and many moonlighting proteins accomplish this by conformational changes.

One of the best examples is aconitase, which is an enzyme in the citric acid cycle. In order to fulfill its enzymatic function, it uses iron as a cofactor. However, under conditions of low iron, it changes conformation and acts to upregulate iron uptake genes.

See: https://royalsocietypublishing.org/doi/10.1098/rstb.2016.0523 and for more on acontitase in particular: https://pubs.acs.org/doi/10.1021/cr950040z

Yes. Part of the protein folding problem is accurately predicting how a protein will change in its 3D structure under different environmental conditions.

One classic example of dramatic differences in protein function based on their folded shape is prions. We generally don’t know how prion proteins get “mis”-folded to begin with, but their presence catalyzes other properly folded proteins with the same sequence to also misfold in the same way, essentially becoming a transmissible disease to anyone exposed to those prions.

It is likely that misfolding happens relatively frequently and biological systems just deal with them except in the rare case of prions where the changes propagate and spread their effects to other proteins which causes enough distribution that we actually looked into the root cause to discover those specific examples of misfolding.

CJD prions are a pathological example.

Folded one way they perform their normal structural function in the brain. Folded another and they don’t work, and cause nearby proteins to also refold the same way, turning your brain into a useless sponge.

Yes, there are many many examples of this. Post-translational modifications lead to changes in protein secondary and tertiary structural changes (eg. voltage-gated ion channels). Protein misfolding diseases (AD & prions) are another group of examples of this.

In a way, haemoglobin does this. with decreasing PH, the structure of the protein undergoes a physical conformational change and a few alpha helicies rotate, having the eventual effect of releaseing any bound oxygen. When the ph returns to normal, the protein reverts to its inital conformation, sequestering any oxygen. I guess this is technically a difference if you are asking that? If you want to find more, I think a good place to start will be looking at proteins with multiple stable confirmations at different PH levels (like pepsin, although I dont think inactivated pepsin acts as a signalling molecule!), or proteins that change in different charged enviroments (things like gated ion channels).

The SARS-CoV-2 spike protein binds to the ACE2 cell surface protein, but the two structures are completely different. You can think of the ACE2 like a doorknob and the SARS-CoV-2 spike protein like a hand. The normal substrate of ACE2 is angiotensin, which also has a very different structure from the spike protein.

So, there's no risk of the immune system mistaking one for the other. And as others have mentioned, if it did happen, it would have shown up in clinical trials.

There are multiple reasons why this would be unlikely. First off, a healthy immune system undergoes a mechanism called self-tolerance. Through a complex interplay between your immune cells and you regular cells, any antibody that is created that targets your own cells is not propagated and cells that make that antibody undergo death. So unless a person already has an autoimmune condition, they are unlikely to develop one from a regular protein challenge.

Secondly, gaining immunity from a vaccine is not very different than gaining immunity from the virus. All viruses utilize some kind of surface protein to bind and eventually enter cells. Everyone is constantly infected with dozens of viruses. People don't generally develop autoimmune conditions from it.

Thirdly, immunity is highly specific. On the molecular scale, there is an immense amount of variability in what a even a short peptide sequence can look like. Something that is selected to bind the specific spike protein is highly unlikely to bind anything different unless its really really close in structure. The ACE2 receptor is not at all close in structure to the spike protein, there is just an interface through which they interact. It's kind of like saying "my key ring holds my key which inserts itself into my lock, shouldn't I be worried that my key ring will unlock my door?"

Lastly, the vaccine has been tested in animal models (the immune systems are not that different) and on people. I guarantee that immune system response was very very well studied in every phase trial. No serious auto-immune conditions have been reported in the thousands of people tested. Is it possible that some very small population may have other adverse effects and was not chosen for the trials? Yes, absolutely. However, scientist on the whole have a pretty good understanding of the immune system by now and it is very unlikely. Even so, the potential benefit of eradicating a disease that can kill \~1% of the population probably outweighs an the risk of a previously unseen complication in <0.01% of the population.

Nearly nil. We'd see it early if it caused direct targeting on angiotensin or other familiar human proteins.

However most infections has a chance to trigger auto-immunity, and inherently, in theory, so does any vaccine. We don't have any examples of this yet, nor any real indications any current vaccines increase incidence of auto-immune disorders (to my knowledge).

However this is looooong term stuff. If one of the vaccines, for one reason or another, slightly increases the chance for some auto-immune disorder or something else, we probably won't know for years.

As an aside I find all the people not being skeptical at all a bit dangerous. We're all right to be skeptical, that's healthy, especially with a vaccine on such a fast track and almost no clinical long term examples in history. However we must also temper that skepticism with the fact that we do know for a fact that the long term effects of Covid-19, even in people not badly affected of primary disease, can be debilitating for a long time. And I can almost guarantee there'll be even more insidious after effects found much later considering how this thing spreads in vivo.

Immunologist/Vaccine Researcher here
Short answer.. no.. Couple points

1. Think of it this way. The ACE2 receptor is like a certain type of lock on some our cells (thinkof the cells as buildings). The virus basically has a spike protein/key that can specifically bind to these receptors and open the door to get in. What a vaccine does is train the immune system ( an e.g. would be antibodies = beat cops, B/T cells = patrol squad cars) to look for the type of key/spike protein and NOT the lock/ACE2 receptor. So a vaccine won't teach the immune system to attack the ACE2 receptor
   1. Secondly, in normal healthy immune systems, by the time the system is mature, it has trained not to look at proteins that are normally produced in hte body - called self-antigens - to avoid your question exactly. That's a different detailed convo for another time - but the analogy above holds.

On the contrary to most replies, the answer is yes, the vaccines can induce B-cell autoimmunity, but this is far less likely than a SARS-CoV 2 infection itself.

Many who have replied seem to be unaware that B-cell autoimmunity is often induced through B-cell sensitisation due to complexes between self and foreign antigens.

This would include complexes of spike proteins bound to ACE2, outside the cell (as a consequence of cell lysis for example). But also note that the spike protein has been documented to bind to a wide variety of cell surface proteins, through neu5ac residues. The sialic acid residues of gangliosides for example could explain the Guillain-Barré syndrome association with COVID-19.

The mistake arises when the B-cell receptor is sensitive to the self-antigen, and internalises the receptor bound to the self/foreign antigen complex, but mistakenly only presents peptides from the foreign antigen on MHC-II to T-cells. Thus autoreactive B-cells can be activated even when there is no T-cell receptor autoimmunity. T-cell autoimmunity is far rarer than autoreactive B-cells due to robust negative selection processes in the thymus.

edit - a paper investigating this process in vivo:

"Cocapture of cognate and bystander antigens can activate autoreactive B cells"

https://www.pnas.org/content/114/4/734

Of course this B-cell mistake needs to occur multiple times in B-cell germinal centres for a serious illness to develop, and the kinetics depend on the antigen availability.

Hence why in the case of a viral induced autoimmunity (Guillain-Barré syndrome for example), the influenza virus is much more likely to induce the disease than a flu vaccine. The good news is, at least as far as GBS is concerned, is that it is rare. The incidence in Norway during the 2009 H1N1 pandemic was one in \~58,000 documented cases of Influenza and the incidence following Flu vaccination is at least an order of magnitude rarer than this.

Oversimplified answer: There are different nerves that sense pressure, heat, and pain. Internal organs don’t have the pressure kind but they do have the pain kind.

In addition to what others have said, it's also the same reason why you didn't feel your socks touching your feet until I just mentioned it. Our brains are designed to filter out the vast majority of the stimulus that we receive so that we can focus on the important things.

You can hear your own body, it's just never ever quiet enough no matter where you are. Watched a video only a few weeks ago and cannot for the life of me find it (Think it was a Tom Scott video but could he wrong).

The video was about precisely this and was only a few minutes long, but told the story of a man who was hiking through the desert and had been told before he left that he will reach an area so quiet he will be able to hear his body functioning, and he could. There is also a superficial room where you can experience this but this was a completely natural phenomenon. I hope somebody else can find the video or some information on it.

Not an answer, but kinda on topic; as a woman that's had a child, I learned about round ligaments because of the pain of them being stretched. See, a woman's uterus is held in place by these ligaments. And when she gets pregnant and her uterus gets bigger and heavier, it puts more strain on them. (Makes sense, right?) If you get up too fast or move quickly in the wrong way, you get these sharp pains (kinda feels like a leg cramp, but deeper) in your lower abdomen. And because they've already been stretched, they never really go back to the way they were before. (Like a rubber band, once stretched) so 8 years after pushing out my crotch fruit, I can still get up too quick and get the stabby uterus pains. Never knew they were a thing before I got pregnant.

You can once you learn what they feel like. It took me five years of fairly dedicated qigong and breathing practice before I could feel my kidneys.

The easiest organ to feel is the lungs. You can close your eyes and feel those when you breathe. After the lungs comes the heart, you can feel it beating in your chest. From there you get into the kidneys, liver, and other internal organs.

The generally accepted reason is the diffusion of (and the resulting collapse of) gaseous bubbles in the fluids between your bones/cartilage.

The debate is still out on whether it’s the bubble forming that makes the sound or the bubble collapsing that makes the sound.

However you’ll notice you can only crack joints that you haven’t moved in a while, which allows the gasses to diffuse. Then you can pull the joint apart creating a void which is promptly filled by the gasses diffused in the fluids surrounding the joint as the pressure drops in that area. Eventually pressure returns to normal and the bubble collapses.

Again, generally it’s accepted that the collapse of the bubble is the cause of the sound but the debate is still out on that.

There are two types of cracking or popping. The one we do with fingers backs etc that’s cavitation of solute gasses in the synovial fluid.

The other one is tendons that have some sort of scaring on the sliding inside their fascia causing a snapping sound.

Sorry eli5s

Your fingers pop like by little bubbles of air bursting.

Your knees crack because tendons and ligaments snap like guitar strings.

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My jaw does that clicking sound too every time I open my mouth wide and I experience lock-jaw almost every morning. My left shoulder’s bone clicks too every time I raise my left hand up.. Is this normal?

Most of the answers here are correct, but not for your specific question. The air bubbles coming out of solution is true for most of the joint "cracking", but the noise some people's knees make during a squat or going up stairs is caused by "knee plica". It's a band if tissue that forms in some people that slides over the bone and causes a snap noise as the knee is straightened under a load. Where joint "cracking" is not immediately repeatable, knee plica snapping can occur continuously.

It doesn't cause pain because the tissue is not being irritated. In some people it does get irritated and painful, which we call synovial plica syndrome.