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Two rings I think depends on how you'd define a ring, since technically (for example) Saturn's rings have gaps in them basically splitting the rings into multiple bands. As for two rings on different planes, I highly doubt that's possible to sustain due to gravitational interference from any moons and the other ring. It maybe possible briefly due to an event, but will eventually stabilize onto the same plane

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Interesting question. Non astronomer here, I’d say unlikely because they would attract each others. And merge into one. But how could they even have originated as two separate rings, considering rings originate as spherical debris that floats towards a potential well that is always along the rotational axis? So the answer is no using basic physics.

Thanks for this!

Based on your bonus segment, I'm gathering that H5N1's ability to infect a diverse range of hosts is not that atypical or unique, and that many viruses have this property.

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"Zoonotic" is generally a term for a disease readily transmissible to humans or a disease that has a very similar human counterpart, and often that does not transmit readily from person to person -- though obviously there are a lot of exceptions, my definition is only a generalization.

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That said H5N1 does seem to be general enough that it can infect a wide variety of warm-blooded organisms, and to spread between many (though not all) of those species without birds - and that is very disturbing, because we know only one of two critical facts about H5N1 in people:

• We know we can get it, a number of people in close contact with birds have come down with it. I'm talking people who clean coops (read: barns) in chicken farms and that kind of thing, not a person with a bird feeder on their balcony.
• We don't know what keeps it from spreading from person to person. It can get you sick enough to need a hospital, if not kill you, but for whatever reason an ill person is not (yet) contagious to other humans. But it can spread in other mammals, eg. from one mink to another. Are we just not dense enough (population wise), the mink farm was loads of them all in an enclosure in constant close contact. Or a time factor, like it takes hours to acquire the load needed to trigger an infection, and the few minutes of contact human to human is not enough? Or is it biological, eg. it can't hijack the reproduction mechanics necessary to reach the level where it would be contagious? Or something else? We don't know, and considering how severe of a disease this is that is very troubling.

edit: to be clear, there are some solid information/fact-based hypotheses that posit why it may not be human-human transmissable (see the rest of this thread), but we don't know which one or perhaps some/all the possible reasons are the 'correct' ones; this is ELI5 not ELIdoctor

> Can the static tension of tectonic plates be quantified?

So, the way we as geologists would discuss this would be in terms of measuring the magnitude and direction of stress(es) within the crust. There are a variety of ways we can directly measure stress, e.g., borehole breakouts, overcoring, etc., which we can then use to produce maps of stress like the World Stress Map. Ultimately though, while maps of stress are useful for some aspects of assessing earthquake hazard, we cannot directly apply these to "predicting" earthquake hazards as this would require knowing much more about the stress history (as opposed to short term measurements), how stress changes with depth, the amount of accumulated strain on individual faults, the strength of individual faults, along with a whole host of other properties. Stress maps and estimates are one part of what we can do to assess hazards though.

> how are predictions about future quakes are made?

Here we want to be explicit about what we can and can't do and moreover what is implied by specific terms when used by professionals. Geologists, seismologists, and others who work on natural hazards often draw an important distinction between forecasts and predictions. This may seem pedantic, but these two terms imply very different things when being used by people like myself who works on natural hazards. Forecasts are hopefully partially intuitive from weather forecasting and we can use this to explore the implications of these two terms in this context. A weather forecast would be something like, "There is a 80% chance of rain today in this region", whereas a weather prediction would be "There will be exactly 1 cm of rain, falling at a rate of 1 cm / hr, starting at exactly 4 pm at this precise location." I.e., for something to be a prediction implies certainty in time, location, and magnitude. Generally, we can forecast the weather, but we cannot predict it and the same is true for earthquakes. The reason we cannot predict earthquakes is much the same reason we cannot predict weather, i.e., incomplete data characterizing a non-linear dynamic (i.e., chaotic) system. The utility of the two are also the same, i.e., even though we can't predict the weather in a perfect sense, the forecast helps us plan (i.e., if you saw the forecast from above, you'd probably bring a rain coat or umbrella with you, etc.). If you want to read even more about why we can't predict earthquakes in the true sense of the word, this FAQ goes into more detail.

For earthquakes, where do the forecasts from? Mixtures of basic mapping of fault locations and geometries, theoretical understanding of earthquake mechanics from both observations and modeling, a variety of geodetic measurements and measurements of stress (like from the first part), and records of earthquake histories from paleoseismology, historical seismology, and/or archaeoseismology. From all of these, we build assessments of how often particular faults have earthquakes, what the variability in style/size of those earthquakes are, time since the last event, and other various details we can glean from the geologic record. In the end, we end up with things largely similar to our weather forecast example, i.e., a probabilistic seismic hazard assessment, like the various ones for the US. These focus on different regions and consider different lengths of time (going back to the weather forecast analogy, largely equivalent to the difference between a daily forecast and the 10 day forecast, etc.). If you look at many of these, you'll see they are presented in a somewhat similar way to weather forecasts, i.e., the probability that a particular area will experience significant shaking in the relevant time frame covered by the map. Just like the weather forecast, while not a prediction, it provides a tool for us to assess risk and make preparations. I.e., much in the same way a forecast of sunny skies vs a chance of rain might determine your choice of clothes for the day, living in an area with a 20% chance of experiencing significant shaking in the next 10 years has very different implications than living in an area with a 1% chance of experiencing significant shaking in the next 10 years and you (and governments, etc) would/could/should respond accordingly.

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Oh, this is a good one!

What you're talking about here is tropism - what host a virus can infect, and not pathogenicity - whether or not it can make you sick and to what degree. They are related because the virus needs to be able to infect you in order to make you sick, but tropism is just one part of a much bigger picture.

Flu is even crazier than just sea lions, birds and humans. Check out this picture: https://www.semanticscholar.org/paper/Sialobiology-of-influenza%3A-molecular-mechanism-of-Suzuki/4bdb9bbce24fcc2dba5a37a65f5e33052119e4be/figure/0

Influenza can infect people, birds, pigs, cows...even whales!

Notice next to each one it has an indication of H or N with a number? That's the type of hemagglutinin (H) or neuraminidase (N) - two proteins on the surface of the fly virus that are important to the virus getting into a target cell. Notice the duck in the middle says H1-15 and N1-9? Yeah, waterfowl are the native hosts for influenza and carry all the different types in all the combinations. All the other animals are more limited. We name a virus by what H and what N it has and that's how we get H1N1, or H5N1. Hemagglutinin is really important to how the virus attaches to and enters a cell in your body. Despite it being the same protein in all different flu viruses, each number is slightly different. Each of these Hs binds to a modification on protein in your lungs called sialic acid. And... different types of animals have different sialic acids in different places in their lungs. So, for an animal to even get infected with a version of the flu it's sialic acid needs to match the virus's H.

H5 is one of the ones that scares us because it CAN infect humans, and when it does it's less than great. However, it seems like it's only possible to get an H5 virus directly from a bird and not from another human. (This is what public health people will monitor for - human to human transmission). The reason for this is where the right sialic acid for H5 is in our lungs... it's WAAAY down the bottom and you have to breathe in a lot of virus to get it there and start the infection, so it's not easy to transmit and probably doesn't spread to the rest of the lung where it could make enough of itself to infect your neighbors.

Vincent Racaniello has a good simple writeup on this: https://www.virology.ws/2009/05/05/influenza-virus-attachment-to-cells-role-of-different-sialic-acids/

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BONUS edit - there are actually more viruses than you might expect with a broad host range. Poxviruses can get around, you can share SARS-CoV-2 (COVID) with your dog and the deer in your yard, and arboviruses HAVE TO infect both insects and humans to be passed along successfully.

https://www.smh.com.au/national/bird-flu-is-spreading-among-mammals-how-worried-should-we-be-20230207-p5cig3.html

-Influenza viruses bind to certain sialic acid-containing receptors on the surface of cells, using them to get inside and take over. These receptors come in multiple varieties; human influenza viruses bind to alpha-2,6 receptors, while the viruses that infect birds prefer alpha-2,3.

This difference is important. Humans also have alpha-2,3 receptors, but they tend to be deep in the lung rather than in our upper airways. That makes it very hard for H5N1 to get a purchase, giving us good protection from the virus. The tradeoff is when it does take hold, that infection is deep in our body, often leading to severe disease. This explains why bird flu infections in humans are extremely rare but often lethal: the World Health Organisation has tracked 868 cases and 457 deaths since 2003.

...Indeed, the virus isolated from the mink in Spain had an uncommon mutation that allows it to more-easily infect mammal cells.

And it does not need to take many more steps before it is a danger to humans. Lab evidence suggests as few as five specific amino acid changes are all H5N1 needs to spread effectively in humans. Wild viruses with two of these mutations have been spotted. “It’s not really a big stretch for it to happen,” says Horwood.

Is this an imminent pandemic threat? “No,” says Professor Ricardo Soares Magalhães, director of the Queensland Alliance for One Health Sciences at the University of Queensland, “the situation is indeed concerning, but not a matter for alarm.”

The Spanish researchers tested all the people who worked with the mink but did not turn up any evidence of H5N1, suggesting the virus has not picked up a mutation that enables easy spread to humans.

And CSIRO bird flu expert Dr Frank Wong points out there’s no evidence the virus has a new mutation that allows it to spread easily in mammals. The mink, which are jammed together in small cages, may be a special case. “The risk of onward, mammal-to-mammal transmission has not really changed,” he says. “It’s still a bird-adapted virus.”

Nor is the situation analogous to COVID-19. That virus was (unfortunately) unexpected by health authorities; scientists have tracked H5N1 for years and have prepared vaccines and antivirals.-

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Step 1: start a degree in chemical engineering. By about year 3 or 4 you should have enough knowledge to design something bad but functional. After that you learn how to make it less bad, but never good.

Your use of the word "fluid" is the challenge. Now we have to consider the phase (gas or liquid), any chemical hazards such as flammable gases, pressures, compatible and incompatible materials, if you need pumps or compressors.

Distance and height differential are very important. For instance, a stormwater pipe from your roof to the ground is easy; an oil pipeline that goes up mountains and down valleys is much harder to design.

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No, don't think so. Many of the people who develop lymphoma have had mono, but not the other way around: the vast majority with mono will not develop any lymphoma.

Sure, but a dangerous situation for the 0.01% (or less) of people who play a sport at top competitive levels versus the easily double-digit percentage of people whose lives could be improved immediately with a more reasonable and scientific approach to what has become a vapid talking point.

And really, those athletes would probably be better off with a reasonable legal framework about PEDs instead of the black market and misinformation prohibition offers.

Not more than anyone else for the most part. 80% of the adult population has the EBV virus inside them whether they know it (by having had mono) or not (young people can be asymptomatic. EBV related cancers are more typical for people with immune suppression of some sort like drugs associated with an organ transplant, AIDS, or drugs used to treat autoimmune disease. That is when you see a higher incidence of these EBV associated cancers.

To be fair, the use of PEDs in sports creates a dangerous situation where people who wouldn't otherwise use them are forced to use them in order to compete. It happened in professional cycling with EPO doping and cyclists were dying of heart failure left right and centre.

Everything you say is a great explanation, and I agree that things are more complex in contrast to the "overdue" concept with an imaginery constant energy bucket that must be emptied in some event.

But if it was true that a constant amount of energy must be dispensed regularly, I think that there is some kind of sweetspot with semi regular Mw 4.0 - 6.4 events which have their centers kind of distributed, instead of one big Mw 8.0 event where everything gets damaged. At least to obviously see which structures will crumble with the next event and which most likely won't.

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The only thing I can think of here is because in the case where there is an open wound or anything at risk of being infected - you would want to avoid steroids. Steroids help inflammation but they can reduce your immune systems ability to fight infections. My best guess? But I really don’t know.