CharonY

It is tricky and in open discussions we can also see that some labels are getting outsized attention. But ultimately I think everyone uses labels knowingly or not, because that is how humans think. This does lead to a certain bias, as some groups will use different codes and labels and these are then considered identity politics, whereas the categories oneself uses are most invisible as they are part of the way we see the world. The issue is that one needs to make a conscious effort to not remain on the superficial level in public discourse, but the increasing reliance on short bits of information makes it increasingly difficult. And while there are folks who weaponize it to spin, I am increasingly worried that folks are also just less well trained to go beyond these superficial aspects. I.e. it is not necessarily a well orchestrated manipulation, but more a general lack of competence in processing, understanding and presenting information (and I say that as someone who is working on a regular basis with the next generation of thinkers).

Perhaps, "Trump is a real man, he does all the harassment and rape himself".

There is a bit of grumbling regarding a settlement for sexual harassment in Shapiro's office. As the perpetrator was an aide and no himself it might not be that critical, though there is a (highly hypocritical) vector of attack.

Just putting things next to each other is not drawing parallels or informative. You need to establish a) what you think the link is and b) provide context and interpretation. Rather than providing a long list of such things, how about just taking one aspect out and elaborate on what you mean and try to foster a discussion on it. For example, how is it different from other calls for ethical AI implementation? Is there anything that we can discuss. This here is a discussion forum and not a "here is my random thought" forum.

A couple of good points mixed with some not so good points. Generally speaking it is not binary, but a matter of grade in terms of prediction. Even something like a simple mechanic model (throwing a ball) can be difficult to use if the situation is sufficiently complex. Not everything is a spherical cow in vacuum. In psych, the idea is often to develop categories and use large observations in order to identify patterns. As such, it is not that different from other complex sciences. But what is true is that because things are complex, reproducibility is often an issue. But to various degrees that is true also for natural sciences, depending on the complexity of the system. Empirically, we have seen that even imperfect models yield results (medicine is such an example).

This is a good example how erroneous and/or simplified assumptions invariably lead to wrong conclusions. As mentioned above, there is a difference between link and active causative agent. Infections can trigger certain (long-term) issues down stream, but there are two things that are important and you seem to have missed. Especially the loose use of all (i.e. generalization) is very problematic here). a) just because infections can trigger some potentially unrecognized issues, it does not mean that all of these issues are in fact triggered by them. So while it may be fabulous that all diseases are caused by infections, we know that it isn't the case. b) you confuse trigger with the active cause. The reason why some folks (myself included) think that some chronic issues are related to infection but have not recognized as such is because certain symptoms manifest after the infection is cleared. You need to read Ewald in the context of Koch's postulate more carefully. If there was an ongoing infection the link would be far more trivial to establish. However, we are aware of conditions like post-viral syndromes (such as long-COVID). Just based on this, the argument of antibiotics does not make sense. First, depending on the pathogen and their interaction with the immune city, the trigger for later issues can arise early on in the infection process or at symptom onset. Therefore, antibiotics would be too late to the game. Second, even if they weren't some of the best understood interferences with the human immune system are viral (some bacteria also do odd things, mostly intracellular ones, but they seem to be fairly different as a whole). Antibiotics don't work on viruses. Third, your argument that we just need to develop new antibiotics itself is problematic. We are running out of them as resistant bacteria (which again as a whole are likely not that relevant to the current discussion), are taking over. In the last ten years only 20 or so antibiotics have been approved and they have been very long in the development pipeline. In some cases, within months, resistant bacteria against new drugs have been detected. Far from being a panacea, we are increasingly unable to treat simple infections.

There is some harm as simplifications are inherently more attractive than the more accurate, but far more complicated answers. If phrases carelessly, folks might actually come to wrong conclusion and challenge existing (and effective) treatments. Especially in the area of vaccinations misleading information have shown the impact of how poor science has led to real harm The issue here is that there are common but also very different pathways involved in antiviral responses and certain auto-immune diseases. The latter are incredibly varied and at best superficially similar. Yet, infections are known triggers for many autoimmune diseases with different manifestations. Now, the important bit are really these differences, but despite having a background in infectious diseases, I wouldn't be able to draw up the involved pathways without significant time investment on my end. And even for the same diseases, viruses can have different routes. The viruses HTLV and EBV have both been associated with rheumatoid arthritis, for example. But while the former seems might impact it via proinflammatory responses at synovial cells, EBC seems to mess up something with T cells. I am not quite sure what you mean here, the non-immune driven apoptosis has multiple triggers, including the presence of certain dsRNAs intracellular, others via detection of viral RNA extracellularly via receptors (and more). Immune-induced activation of killer cells relies on detection of viral antigens. So at least at that point does not mess with self-recognition.

My equally valid counter points are: - Pisces - Helical - Star-aligned - Mind-driven - Geolocality - Dave A broader discussion on this topic would be how we arrive at certain classifications of natural phenomena. Ultimately, they are based on arrangement of properties we are looking at. Mainstream science has arrived at a range of categorizations in various disciplines that are based on overarching theories. Depending on the disciplines, the categories can be more or less stringent and also more aligning with theoretical or with empirical assumptions, depending on how much we understand the respective system. That all being said, the most important factor is how useful these categories are for a given research direction. Again, in mainstream sciences certain categories survive because they have proven to be useful, others (e.g. the elemental categorization originated from Empedocles) eventually vanish as they are not really helpful, even if popular for a given time. In other words, this question has to be answered before anything else:

What I meant is the link is established, and not unlikely as per your post. But hypertension also has many other non-infection related causes, so the reverse is not true. For imune response, the underlying mechanism are too complex for this forum. Infections can push the system to a state that triggers an autoimmune response, but so can for example prolonged stress and metabolic syndroms. Simplified generalized explanations of complex biological processes tend to be only applicable in a very narrow way, if at all.

Not unlikely, infection-associated inflammation is known to be associated with hypertension. You just cannot make the assumption that ll hypertension is related to infection. It is unfortunately way more complicated than that.

I don't think that he postulated it as aggressively (in part because it is trivially false). What I believe he has argued (and it does align to some level with what my line of thinking) that a) the role of prior infections in disease development are often overlooked and the the current paradigm of looking for current active infections might be too limiting and related to that that b) especially for chronic diseases, folks assume a too elevated role of genetic factors. It is a while back where I read a little a bit about those arguments and I do think that the research field has moved a bit along based on data of the last two decades. But again, the quote above is clearly inaccurate.

Cancer cells are our own cells. Antibodies against them would target healthy cells, too. Only some cancers are associated with e.g. viruses and there are vaccines against e.g HPV.

I would argue that this depends on the timeline. If we talk about species, we implicitly project long time lines (such as, until extinction, for example). Conversely societal benefits can be short-term. But if we add sustainability to the mix the timeline for what we consider societal benefit gets extended (i.e. it should not only be good for the current, but also for future generations). At which point what one might consider beneficial would converge. Edit: I should also add that one should not assume that selective pressure are all to the benefit of the species (as in creating a more successful species as implied by some comments). After all, a lot of species went extinct following highly successful and specific adaptations. It is possible to specialize oneself into a corner, for example.

Well, the group is a PAC (which is one of the weird US monstrosities) and from the looks of it might have been more anti-Trump rather than pro-Haley. Depending on who organizes that PAC it might be less about party, but I might be wrong.

1) yes, or more precisely we have the interconversion of NADH <-> NAD+ + H+ + 2e- 2) Not quite, it is the initial donor. The chain is basically a redox gradient, starting with NADH and ending with the terminal electron acceptors. 3) Also not quite, NAD+ is regenerated during the first step of the electron transport chain, following the reaction shown in 1). The electrons then continue to move through the chain, which powers the proton pumps. That is not part of regeneration of NAD+ per se, but just the process necessary to ultimately gain energy from the whole ordeal (the gradient in turn powers an ATP synthetase). 4) Simply put, yes. When there is oxygen, cells can use respiration to get more energy rather than having to rely on fermentation. That being said, under the right conditions (e.g. very high glucose surplus) some cells also conduct fermentation even in presence of oxygen. Here, cells prioritize rapid energy generation via glycolysis over the more efficient, but slower process of respiration. But this is only possible if glucose is not a limiting factor (as it is often the case in nature).

I think that is not entirely wrong but also (in my mind) not very helpful. A more specific way to think about it is to view fermentation as a means to regenerate NAD+. During glycolysis (as well as during oxidative decarboxylation of pyruvate and the TCA cycle under oxic conditions) NADH is generated which can power an electron transport chain, which we refer to as respiration (with the ultimate purpose to generate energy). In aerobic respiration the electrons are ultimately transferred to oxygen, but those able to respire under anaerobic conditions can also use e.g. sulfate or metals and so on. But if respiration is not an option, and the cell e.g. only uses glycolysis for energy generation, it will accumulate NADH that it has to convert back to NAD+, otherwise glycolysis will stop. This is where fermentation kicks in during e.g. ethanol formation NADH is converted to NAD+. Perhaps that is also not very intuitive, but if you look at the mechanisms, it is quite a bit more precise.

When she ran for presidency there were mixed perceptions on her record, but also the fact that she is from California. The latter paints her too elitist for the Mid-west crowd, and her former job as prosecutor (and associated track record) might have soured her to the left.

I think that is fairly anecdotal. In my field of work, and especially in the lab, I do see that on average women are better requiring focussed tasks (but of course there is a bit level of self-selection in terms of interest). To my knowledge, there are studies looking at task-switching and I think there is no clear evidence for differences. It might depend on task or there might be cultural factors and so on. That is very true and I see much in that especially among older colleagues (who likely had to fight very hard for their positions). Indeed. Acquiescing to a diminishing assumed centre (and defining it is pretty difficult to begin with) is likely not feasible. It is the reality that the less and less is found in the centre now and I will note that many of the sane GOP folks are very far away policy-wise. They are not center politically, they just happen to mostly acknowledge that there is an reality. Catering to that is supremely difficult and almost certainly a losing ticket.

No I am not making an argument about morals. But about efficiency. If saving the weak increases your reproductive success, that is what is going to happen. I.e. there is no prejudgment of what is weak and what not. What survives survives, and it can be alone or in collaboration with others. Protecting the young is a prime example of supporting the weak. Another is the behaviour of buffalos which have repeatedly being observed to try to rescue their members from predation. Not only species are doing it, but for those that do, it obviously provided benefits. Likewise there is emerging science suggesting that many social animals exhibit some form of empathy, which likely is necessary for social behaviour. In other words, animals (and humans) don't help each other because from some moralistic stance, it is because there are mechanisms in place, biologically, that makes us want to help each others. Otherwise we would be solitary animals. And this behaviour clearly has reproductive benefit. Therefore, using your clarified stance on what you describe as "strength" it means that in many species helping the weak actually promotes strength (aka reproductive success). Solitary animals or those that do not care for their young are not automatically stronger than those that do not. It has nothing do with morals, it is just a different strategy. And considering that either strategy still exists, it means that they are not better of worse as a whole (though a particular social animal has been very successful so far).

That's fair. But I suppose that Phi alludes to the fact that old white guys have dominated this (and other) positions of power for quite a long time. I.e. any divergence from that would more likely add perspective as a whole.

In other words it is all about reproductive success in whatever form, which would include collaborative behavior, rather than the original notion that suport leads to weakness?

Again, that is not necessarily true. Predators are not necessarily the key selector in a given species. Many species have virtually no defence against predators, but rely for example on high reproduction rates or life cycles that minimize overlap with predators and many more. I.e. the "strength" here is just being one of the lucky ones to reproduce before predation (or anything else happens). And if you broaden it up to be more accurate in having any traits that helps with reproduction, the argument of taking care of the weak kind of evaporates. For example, some may have large testes and high sperm load increasing likelihood of reproduction. But they might run slower. Parents that take care of that "weaker" one to fertility suddenly gain a higher chance to influence the gene pool. It is indeed not a complicated argument. Just not a scientifically accurate one.

The issue here is that I don't think that there are any studies out there that really are able to investigate e.g. which genetic factors could lead to prey escape. As you can imagine that would be incredibly difficult to do. What has been studied to my knowledge are specific elements with a genetic basis (e.g. coloration) and detection by predators. While it makes intuitive sense, I just don't think that we have the data to establish that as fact. And biology has many ways to be really counter-intuitive.

Likewise, group protective behaviour (i.e. regardless if it involves exclusively your offspring) can improve overall reproductive success. And conversely, risking "weaker" (however they might assess it) offspring can backfire dramatically. Though again, that does not make much sense to me in the context of predation as used in earlier posts. After all, even the strongest offspring is unlikely to survive a predator and survival would be more a matter of luck than individual strength (assuming lack of protective behaviour).

The last part is the important bit, as it can lead to traits and behavior that make a species less suitable for the environment (but for example more attractive to their potential mates). The tricky bit here is that extrapolating this to general behaviour is a bit like using anecdotes to apply to human. We could take footage from a stampede during a terror attack or some other mass-incident and then claim that humans have the propensity to trample each other to death. Individual animal behaviour takes a long time to explore, something that the field is has only started to recognize very recently. Not only for that reason it is silly to try to apply these vague narratives to human societies (either for or against certain elements in society). And also, if predators get to the injured and sick ones, it does not mean that it has any effect on the quality of the gene pool. After all, even fit folks can get injured or sick. Though especially for the latter there is no need for predation, it would be between them and the pathogen.