CharonY

As with other forms of categorization it is obviously a bit arbitrary and at least theoretically based on genetic distance and/or fossil similarity. But obviously that is not trivial and fossils do not show linear progression. This article has a nice discussion https://doi.org/10.1098/rstb.2015.0237.

IIRC they didn't puzzle over it for long. Rather they were worried that found their could interfere with Curiosity's sampling and analyses.

Photosynthesis proteins as well as ATP-synthases arose a fair bit later. A common assumption is that substrate level phosphorylation was at the beginning. There are other hypotheses around which are based on how other reactions were potentially thermodynamic favourable, but i haven't looked at those for a while.

I think you are just fine. Binary symbols often have these ambiguity and often these things are not universal. Sometimes they have an indicator for the active state, so if pressing a button results in these icon being highlighted or appear it can provide more clarity. I think the the answer is yes. Ultimately many of these decisions are made to make things less cluttered and slick. At the same time it means that it conveys less information. The basic idea is probably that after trying it out once you get the idea. There are whole discussions about resolving ambiguity in UIs. Often the answer seems to be setting design standards, but if folks cannot agree on them, it will remain ambiguous. I also think that smartphones are designed to make us less smart, but I guess that is another discussion :).

I think exactly that make is difficult, though. If we try to quantify, we would start with e.g. creating categories. But what an experimenter create might be based on their own experiences. So let's say you have language that has, say 5 categories for drinking vessels, but only 1 for eating bowls and conversely one that has only 1 for drinking, but 5 for eating, and then you have one that has one or two for each. if you used drinking vessels to build your model the first and last would group together and if you used the eating vessels it would be the latter. If you used both they might separate differently, but adding yet another concept would change the model entirely again. Then some cultures or languages might have sophisticated categorization in areas that do not even exist in others and so on. I.e. whatever you select to look at will influence what your outcome will be. Finding a truly neutral ground where comparisons of divergent languages can be done with this is approach is seems incredibly difficult to me. That being said, I suspect the matter is sufficiently complex that I would require some serious reading (such as the Kemmerer, which I am not familiar with) to contribute anything meaningfully.

I suspect it is quite complicated. There attempts to map rough distance between language using a wide range of metrics and at least from what I understand there really is no good agreement on any overall methodology. In the above example I suspect that depending on what aspect is shown the differences are likely to be all over the place. Language is often context-driven and so are categories created in a given language. Even within speakers of a language there is inherent vagueness. While this paper from Hancock and Volante focusses on linguistic uncertainties, I think categorizations are not as static and/or discrete as they might appear. In the example in OP, depending on what item groupings you provide, they might invoke different contexts for the viewer which may be more cultural than linguistic. Also I am not sure whether the proposed measure handles certain ambiguities well. For example in the above example I am not sure why Germans would use fewer words than the Dutch, considering that equivalent words exist in both languages, though there are many local variations (e.g. Pott) or variations using contractions (Kaffee- or Teetasse/ becher) or more formal usages that are less common (Trinkgefaess). I.e. the measures would vary potentially wildly even within a language region.

Lorenz and Immelmann (Einfuehrung in die Verhaltensforschung) were folks who originally made me want to study ethology. Unfortunately the funding situation turned me off from it (I did learn how to catch finches with bare hands without injuring them so there is at least that). Sometimes I wished I had stuck with the original plan (greener grass and all that).

No worries, it wasn't meant as criticism (and I assumed that is what you meant), but just trying to adjust language a bit as I learned that in public discussions folks get hung up on such concepts and that it can lead to severe misunderstanding of health messaging. But I also found that explaining these things does seem to help to mitigate spread of false or misleading information to some degree. In the spirit of OP one could probably add that with Omicron the even vague hope of herd immunity is even more shattered (if that was even possible). While some folks start claims regarding endemicity, it is important to point out that we are not even there yet. We are still very much in the outbreak phase and it is rather unclear when transmissions will drop to a level where we actually enter the endemic phase. Moreover, given the reservoir of infected people, the risk of new variants remain extremely high and given the spread (Omicron arrived almost everywhere in less than a month) creating an even more uncertain timeline. This is a serious issue for health messaging, as folks demand some level of certainty about how things are going forward, but the current lack of clear answers drives folks to the crazy parts of the internet.

The relationship is a bit complicated, depending on the type of virus. IIRC some older studies on viruses similar to the coronavirus (mouse hepatitis virus is a common surrogate, for example) found that at either very low or high humidity some viruses exhibited better survival at various air temperatures than at moderate humidity. I remember one particular graph from a paper showing a non-monotonic relationship and I believe it it was published around 2010, but I cannot recall the author right now. But specifically for SARS-CoV-2 there was a review suggesting that warm and wet areas might actually reduce spread but the effects were not very strong: https://doi.org/10.1371/journal.pone.0238339

! Moderator Note That is on my, apologies, I thought I had posted a mod-note, but apparently did not. The reason why it is moved to speculations is because it appears that in OP some original assumptions were made that do not seem to relate to existing literature (or if so, no references were given). As such it seems to be original speculation, which can be further developed in the speculations thread as outlined in the guidelines. Speculations do not need to contradict established mainstream, but (as the name implies) allows for speculations in areas where the science is not established. However, if the hypothesis is grounded in mainstream science, it would be great if either references can be given or at least the context is outlined with respect to mainstream science. Some questions could be related to whether how categorization in the brain works and whether it is uniquely related to language? How does it relate to category learning in animals, for example?

You seem to interpret rather than read and forget what actually has been said. You said EHEC required a single cell, I said lit says 10-100. No one was talking about children at this point. I said the real value is likely higher as plate counting often underestimates cell counts (which applies mostly to dried or processed food). Then you came with an unreferenced wiki (which actually states to having quality issues) indicating id1 of around 8 for children. This introduced children for the first time. While it is unclear how they calculated this, as for EHEC you cannot make actually dose response curves and especially not in children, it does not provide evidence of single cell infection beside your gut feeling. I think I should stop taking it off-topic further, especially in the face of strong resilience to information. For those interested, one of my references above actually estimated the minimal infective dose in children as low as 2. But I also mentioned why the methodology (self-reporting) is problematic.

You mean the unreferenced wikipedia link vs the references I have given above? I mean, you do you, but it is funny that the link you provided actually does not support your claim (and it is actually in the range of the references given so no big discrepancy there, really). I will concede that the comment regarding underestimation based on CFUs is a bit technical and is more of an ongoing discussion in the community whereas safety regulations still rely on this method (the alternative techniques we have been using is based on flow cytometry, which is becoming more prevalent in food and water testing). So the estimate of 10-100 cells given above (but not 1) is a fair estimate, if you choose to ignore the above caveat regarding the limits of plate counting. And I do apologize to OP for taking it so far off-topic.

In the graph there were actually three periods when taxes went down. The clearly did not refer to the amount of reduction, but the fact that reductions happened. There are also economic reasons why taxes go up in certain countries in certain periods which is not caused by governmental desires to increase taxes: I am not sure what the graph you posted means. It appears that income is rising faster than taxes since the 2000s whereas taxes where much higher and rose more sharply with income until the 70s/80s? (by eyeballing it)? Also, it looks like the values are not inflation-adjusted, so basically any non-normalized monetary plot would go up over the years.

Could you clarify that? To me a claim of "always increases" would indicate that values only go up. If there are periods where it decreases it would invalidate that claim.

One can only hope. This pandemic has been a bit disillusioning. I suspect I should focus on the positive parts, but it is hard to see things opportunities to do something to slip through one's fingers over and over and seeing no willingness to change the approach.

I mean there were arguments that seatbelts were unsafe and similar things in the past: https://www.businessinsider.com/when-americans-went-to-war-against-seat-belts-2020-5 At this point I am almost convinced that in human history there are no original discussions left anymore. We just keep rehashing old things and convince ourselves that somehow we are making progress.

To me that sounds a lot like ideological waffling. If the issue is laid out as a health order and non-compliance is fined I do not see how blameworthiness is a principle. One could argue whether one should have health orders or regulations at all, as one would put blame on those who violate those orders. But that would seem a bit silly. I also do not see how fines for lack of vaccination lead to denial of health care. Folks have been fined for breaking various rules and I do not see vaccination as something fundamentally different from that perspective. Another example would be drug abuse. It is a behaviour that is under penalty, yet in Canadian law there are provisions that ensure that folks requiring medical treatment because of drug abuse are actually treated like everyone else. So while clearly drug abusers are blamed for their behaviour (and criminally persecuted, no less), the health care system survived it. As such it does look like another case of slippery slope fallacy. It is not to say that penalties for vaccinations may be a great solution and there might be better ways. I just find these specific arguments not very convincing.

Well, not mine, but that is exactly it. How the public act is a complex confluence of internal factors and includes but is not exclusively based on government responses. As you may have noticed, the USA did not suddenly became sane after the government switched. In contrast, the Trump administration likely did cater to anti-vaccination folks so much in part because they wanted to cater to their base. After all, pretty much the whole top of the GOP were first in line to get the vaccine, while questioning their effectiveness in front of their voters.

I suspect they might be referring to some misinterpretations that have been circulating in social media apparently (I have not seen the posts, but have been made aware of them). Basically a pre-print found that vaccinated folks who got infected produced fewer antibodies targeting the N-protein of the virus. In this context I think it is helpful if we get away from the notion of "strong" vs "weak" immune responses. The problem is that a "strong" response, can actually be harmful (cytokine storms are the most famous example). What we need is an "effective" response. I.e. a response that helps clearing the pathogen without or with minimal harm to the patient. Going back to the results, current vaccines target the S-protein of the virus. In other words, once an infection is detected, the vaccine-primed immune system will predominantly mount responses to this target. If effective, the response to the N-protein is going to be weaker than in folks who are not vaccinated, because, well, they don't need it. The virus is predominantly cleared using the S-protein as target. I.e. phrasing it as either a strong or weak response can create a bit of a misunderstanding of how things actually work and how effective the overall response is going to be to avoid serious illness.

No, I was referring to the minimal infective dose and I was also referring to adult dosages as unless I missed something we were not talking about children. But more importantly, for children the numbers are even less certain than for adults. A challenge is that to establish these values, the most accurate way is to feed people defined doses. But generally you cannot do it with children and also you don't do it in cases where serious illness is likely (as is with EHEC). There, we use a few ways to provide estimates, but obviously a large error bar is attached to those. While I have seen a study which estimated something between 10-100 cells, if you look a t more estimates, the values are pushed up closer to 500 for EHEC. For Shigella dysenteriae there is actually a paper with volunteers (very small cohort) where a dose of 10 cells caused symptoms but that is probably close to the lower limit. While the numbers might be reasonable and make sense given the reported dosages for adults (and obviously children are more susceptible), I note that they are still higher than one bacterium (and therefore significantly higher in adults) and perhaps more problematic, it is unclear where the values come from as no studies are cited. But given the issues I mentioned above, it is unlikely that one can establish ID1 or ID50 doses with EHEC in humans. There is one estimate that places the minimal infective dose in the area of S. dysenteriae (and considering the actions of the Shig toxin might not be entirely unreasonable). But to provide an example how these estimates are done. One of the lowest values I am aware of were reported by Tilden et al. (Am J Pub Health, 1996 86:1142-1145). Here they investigated bacterial titer in salami from which folks got sick and based on self-reporting of patients of how many slices of salami they consumed and the bacterial load they found in samples they estimated numbers between 2-45 cells causing the disease. As you can imagine, each step is rather prone to errors. Moreover the data is based on four patients, of which 3 were under the age of five. Another issue is that traditionally, bacterial titer is estimated from colony forming units, isolated from food. Newer analyses which focuses more on microscopic analyses indicate that these may often result in lower actual bacterial presence (depending on from which matrix you isolate and how you cultivate the colonies). I will say that due to lack of data the original estimate I provided (10-100) as lower bound might not be entirely unreasonable, but there is good reason to believe that it is at least somewhat higher. There is no data to support single-cell infections, however (which would be almost impossible to assess in either case).

One of the reasons why Japan had better outcomes despite lack of restrictions was that folks for example wore masks without mandate. Meanwhile, in Canada you see uptick in signal whenever such mandates are lifted. Behavioural responses are critical in a pandemic.

As with all bacterial infections, it needs to overcome defenses, find a niche to colonize and compete with existing bacteria. Every part in our body that can be colonized, already is. A lone bacterium arriving in the gut even after passing the stomach will face billions and of others already occupying the niche and denying them nutrients. Pathogens have nifty tools to carve a niche, by e.g. using toxins and/or effector proteins that mess with the host and remodeling the environment for them. Even so, a single cell has little chance to be successful in acquiring enough resources to compete. Therefore, often pathogens use quorum sensing to regulate pathogenicity factors. If they are alone, they try to stick around but cause no disease. But once there are enough coming in, they communicate with each other and start producing toxins and other factors, which make the host sick. BTW, my wife, who is more on the clinical side mentioned that infectious dose I mentioned was likely an underestimate based on an error in one early paper on EHEC. About 500-700 cells are more likely, which is still considered very low for a food-borne pathogen. In folks with stomach acid issues they might be lower, but just physically a single cell (except of in vitro, perhaps) is unheard of.

Actually, up on re-reading OP there non-government factor such as population compliance has been mentioned. And I believe I vaguely remember a short discussion in this thread regarding behavioural norms (though I might be confusing it with something else). Nonetheless given the scope of OP I think a broader discussion makes a lot of sense. After all, a great governmental plan is pretty much meaningless if the population does not follow it.

All of the ones mentioned are able are food-borne diseases, i.e. they are able to survive and multiply after ingestion (which is why I listed them, though intestinal infection with C. botulinum is perhaps less common). But as I mentioned, a single EHEC is very unlikely to establish infection (for a variety of reasons, some related to the pathobiology and expression of the mentioned Shiga toxin, which is partially regulated via quorum sensing and requires some cell density in order to establish successful infections and to compete with the existing microbiota, which includes other E. coli), though 10-100 is pretty much at the lower end of observed dosages for bacteria.

I do not think they can be as low as a single bacterium, but EHEC has been reported as low as 10-100 bacteria. However, much of its action is due to the Shiga toxin. Among gut infections I would probably be more worried about Clostridium difficile which is extremely difficult to get rid off (due to high resistance to antibiotics). The toxin of Clostridium botulinum is of course famously nasty though luckily not that common. Listeria are also nasty, with a case fatality perhaps around 5x that of EHEC. They can grow slowly at low temp, but typically do not exhibit gastrointestinal symptoms. Instead often unspecific symptoms of inflammation are found making it often very difficult to diagnose. One should also make sure that the lines are not e.g. leaching lead. One thing I learned from colleagues who are specialist for water safety is that in many first world countries (including Canada, USA and perhaps also Australia) there are often surprisingly few mandatory regulations. Now, I proceeded to put my fingers in my ears and pretended not to have heard it, so I am a bit hazy on the details but my faith in drinking water has been shaken a little bit. But from what I understand is that while the overall guiding principle is that the water is safe to drink, it can vary regionally what it means in terms of e.g. bacterial load or how frequently the sources are tested for such or other contaminations (or which contaminations are regular tested for).