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Why is livestock bad for the climate?
It is always told that eating meat is bad for our climate. This is most often explained by mentioning following reasons (Source):

Methane is produced when digesting the food and also the faeces of cows produces greenhouse gasses afterwards
Fertilizers produce greenhouse gases
The processing of food with machines produces CO2
The farming of land with tractors etc. produces CO2

The last three points I can understand. But I have some problems understanding the first. My questions in this regard are:

Cows emit methane. But the methane is produced by digesting plants. The plants themselves got the carbon from the atmosphere. So at least this is a closed cycle and no net greenhouse gases are emitted. Isn’t livestock therefore climate neutral?
It may be that especially for factory farming, forests are cut down. This produces a lot of CO2. But I also heard that the plants that are grown may store more carbon then the trees that were there before. Is this true? If no, is this really the only reason meat is not carbon neutral?
How is the carbon footprint of livestock even determined? Is it really determined by the forest which was cut down in order to produce food or is just the methane exhaust of the livestock measured?

Own research
In this source it is stated that grass feed cows may be carbon neutral in the long run (under optimal conditions) and may even increase carbon capture in the short run. Nevertheless, nothing is stated why this is not true for crop feed cows (how do crops and grass differ in this regard?)
On this site it is stated that “[Only] In a stable climate, trees store more carbon than grasslands”. But what’s about crops like wheat? They have more biomass and deeper roots than simple grasses. Also there may be several wheat plant on the area one tree takes. I found nothing regarding this on the web.
Ps. I am not a biology professional so please forgive me if I misuse some terminology and do not cite scientific papers.

Short Answer
I'll address the first two of your three sub-questions:

Livestock are not climate neutral because different processes of the carbon cycle create different carbon-based molecules at different rates and that linger in various "reservoirs" throughout the globe for different lengths of time. Given these details and the fact that the underlying chemistry of the different C-based molecules varies, each carbon-based molecule has varying degrees of effect on the climate.

For example, CO2 (e.g., from decomposition of grass) has less radiative forcing than methane (CH4) (which can be created in excess by cows fed a starch-rich diet of corn).

See "Would fewer cows mean less methane emission?" for more details.

Croplands have drastically lower carbon storage ability than forests, natural grasslands, and wetlands. You can compare global measures of aboveground and belowground biomass to determine this.

The model-driven analysis of the paper your link cites is taken out of context and its comments on resiliency are not generalizable in understanding absolute carbon storage capacity. The paper comes with many caveats.

Long answer

You're inappropriately assuming that all carbon molecules are the same.

There is a finite amount of matter in the universe, including carbon. You probably know this from the Law of conservation of matter. However, one carbon-based molecule does not necessarily (and in fact does not) have the same physical and chemical characteristics of other dissimilar carbon-based molecules.

Importantly, not all carbon-based molecules are greenhouse gasses, which have unique reactivity and physical structure to function as re-emitters of infrared radiation. See here for an explanation and here for a simplified YouTube video cartoon explanation by "Minute Earth".

Carbon returns to the atmosphere typically via combustion or decomposition. (See comments about the carbon cycle below). Much of the carbon released by these processes are either CO2 or CH4.

The carbon cycle reflects the law of conservation of matter in the recognition that carbon transfers from one object to another via biogeochemical cycling; however, how it transfers varies both in the chemical and physical processes occurring, in the time spent in one "place" (i.e., a nutrient/chemical "reservoir") vs another, and in how readily it "comes"/"goes" from one place to another (i.e., its flux rate).

The timing of residence times and flux rates (i.e., movement from one place to another) dictate whether a reservoir acts as a source or sink.

CO2 (carbon dioxide) and CH4 (methane) are quite different in the reactions from which they are generated (see Would fewer cows mean less methane emission?), the rate at which they are generated, and ultimately in their chemistry. This last point has drastic impacts on residence times, flux rates, and ultimately their their climate warming impacts:

Both molecules differ in their residence times in the atmosphere as well as their magnitude of radiative forcing. From MIT:

methane immediately begins to trap a lot of heat—at least 100 times as much as the CO2. But the methane starts to break down and leave the atmosphere relatively quickly. As more time goes by, and as more of that original ton of methane disappears, the steady warming effect of the CO2 slowly closes the gap. Over 20 years, the methane would trap about 80 times as much heat as the CO2. Over 100 years, that original ton of methane would trap about 25 times as much heat as the ton of CO2.

Note, also, that some of the atmospheric methane will eventually be chemically converted to carbon dioxide. From here.

Methane enters the atmosphere and eventually combines with oxygen (oxidizes) to form more CO2. Methane converts to CO2 by this simple chemical reaction.

Regarding methane production of cows and rates of release of greenhouse gasses, please see my other recently-answered BIO.SE post: Would fewer cows mean less methane emission?

Regarding carbon storage:
As stated above, understanding the carbon cycle requires both an understanding of residence times and flux rates. To determine the carbon storage ability of one biome or environment vs another, we typically measure the biomass of the organic matter (with interest in determining the C:N ratio) as well as flux rates in/out of our target carbon reservoir (e.g., plants such as crops or trees). Regarding flux rates, of particular interest are rates of carbon sequestration.
Ultimately, any community of plants that is capable of sequestering more carbon into large amounts of high-C:N biomass will result in larger carbon storage. The longer-lived those plants (i.e., the less labile their carbon), the longer that community of plants acts as a carbon sink.

Also note, that different climatic conditions (e.g., see Gallardo & Merino 1993), plant-cell chemistry (e.g., C:N ratio as well as % of lignin; again see Gallardo & Merino 1993), plant anatomy (especially root structure; see Poeplau et al. 2021), plant age (e.g., see Peichl & Arain 2006), and plant diversity (see Chen et al. 2018), etc. can impact the degree of carbon storage in the organic matter of soil: soil organic carbon.

So two questions of interest are:

which plant communities store the greatest amount of carbon-rich (i.e., woody) biomass in the smallest area (or volume) of space for the longest amount of time?

Which plant communities have the least disturbed (least labile) organic matter sinks?

We can approach this in two ways: per area or across the globe:

Across the globe: see here, here, and here for depictions and explanations. Many have tried to quantify this, so various values show up. Below are some examples:

 Carbon (Gt C) stored in ecosystems (based on Scharlemann et al., 2014); source: U.S. Forest Service

 Source: IPCC

Per area:

 Source: FAO
If we take the carbon mass numbers from the IPCC table in the section above and divide by total area, we can get estimates of total biomass. visual Capitalist did so conveniently, which I copy below:

 Source: Visual Capitalist; original data from IPCC 2000
Do note, however, that the per-area storage of carbon of any one of these biomes (especially forests) would be greatly impacted by the age of a given patch of vegetation. As such, the numbers in the above table only reflect current biome statuses vs maximum storage of these plant communities under ideal (i.e., non-anthropogenically degraded) conditions.  Of particular note, is that temperate forests vary greatly in their biomass based on the age of the stand: old-growth forests have much greater biomass per hectare than secondary forests or managed forests. However, the majority of temperate forest land (i.e., the numbers captured in the table above) currently is managed or secondary in nature and therefore does not fully capture the carbon storage ability of less-anthropogenically-modified versions of temperate forests. This explains why these numbers are much lower than other forest types.

Some estimate that <10% of forests in the US (as low as 1%, see Davis 1996's Old growth in the East: a survey), are old-growth in status. (You can ignore references (e.g., here) to studies like DellaSala et al. 2022 which show much higher numbers because they are defining mature forests as 80 years or older -- hundreds of years younger than is typically used to define old-growth status and certainly nowhere near even the transition point of many temperate forests).

Also note, that total carbon currently sequestered vs. rate of sequestration are different. Large woody biomass is a huge sink of carbon but not necessarily quicker at sequestering new carbon. For example, see Heinrich et al 2021 ("Tropical secondary forests sequester carbon up to 20 times faster than old-growth forests").

Croplands (especially those managed by modern high-throughput industrialized agricultural practices) are constantly losing organic matter in soil due to tilling, erosion, etc. Undisturbed forests essentially have little to know organic matter loss (though this depends on climate and local hydrologic cycling).
Your reference to grasslands being better carbon sinks vs. forests is taken out of context (or at least inappropriately generalized). The study (Dass et al., 2018) out of UC Davis -- influenced by the propensity for large California wildfires due to years of fuel buildup negating their typical long-term storage ability -- used a set of models to predict future change. I'll leave it to you to read the actual paper, but at the core of their claims is that "extreme heat-waves, drought and wildfire have increased tree mortality" in California while grasslands are more resilient to these issues given their propensity to store most of their carbon underground. they built their models assuming these risks continue, and thus claim that grasslands are more resilient carbon sinks in the state of California.

From their conclusion: "Our study demonstrates that, in the absence of aggressive mitigation of global greenhouse gases, forest management strategies to reduce fire risks, or both, grasslands will store more C for a longer period of time than forests in California." they also note that their results reflect "dryland" forests, but as we can see above, most of the carbon is stored in tropical and boreal forests as well as wetlands. They also note: "our results indicate the potential direction of change as opposed to predictions that consider the full ensemble of ecological, physiological and management factors that can alter pathways and responses of ecosystems to climate change."

In other words, their model-based prediction study is not meant to be a generalizable nor understood-to-be-factual study, but another piece of thought for California policy-makers...

Short answer
Two factors playing a role in livestock's contribution to the greenhouse effect have to do with methane being a more potent greenhouse gas and the fact that the conversion of plant materials into meat comes with low efficiency.
Background
Up front - I'm not a climatologist. My 2 cents worth here are two points:

Methane is a potent greenhouse gas, and way more potent than CO2. Quoted from UN Environment Programme's website:

Methane is [...] a powerful greenhouse gas. Over a 20-year period, it is 80 times more potent at warming than carbon dioxide. Methane has accounted for roughly 30 per cent of global warming since pre-industrial times and is proliferating faster than at any other time since record keeping began in the 1980s.

and

Livestock emissions [...] account for roughly 32 per cent of human-caused methane emissions.

Another issue is the food pyramid, which consists of different layers: organisms higher up in the food chain consume biomatter from lower layers. Every layer dissipates heat, because of efficiency being less than 100% (Fig. 1). Often live stock is fed on crops specifically produced for the meat sector. If the production of all this animal fodder would instead have put to use to grow veggies for human consumption, a lot more food would have been available than when it is inefficiently cycled through live stock first to turn it into meat (and methane).

Fig. 1. Transfer of energy through an ecosystem. At each trophic level only a small proportion of energy (approximately 10 percent) is transferred to the next level. source: Encyclopædia Britannica

To illustrate trophic level loss for the OP: What would feed you longer? One rabbit? Or the vegetables you fed that rabbit over its lifetime to raise it? You feed a lot more people with less resources eating vegetables than eating rabbits.

@DKNguyen that's the point, yes

I have found an answer for your first question. The Global Warming Potential of methane is much higher than that of carbon dioxide. Because methane stays in the air for a shorter period of time than carbon dioxide, the GWP is higher for a shorter period of time: over 20 years it is approximately a factor 70. In 100 years the factor is approximately 30. And in 500 years, methane has still 7 times higher warming potential.
Note that the GWP compares the warming potential of one tonne. If we assume that one mole of carbon dioxide is converted to one mole of methane (since both contain one C atom), then it follows that 1 tonne becomes 0.36 tonnes. This follows from comparing the molar mass of carbon dioxide and methane. Taking this into account, it would still be better if carbon dioxide is not converted to methane.
Therefore, a closed cycle which converts carbon dioxide to methane contributes to the greenhouse effect.


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Correlated evolution of discrete traits: do traits need to have phylogenetic signal?
I'm doing a phylogenetic analysis using the Discrete program in BayesTraits. Of the  traits I am testing, one of them does not show any phylogenetic signal (using the Fritz and Purvis d-statistic).
Does this mean that a test of correlated evolution using this trait is actually not appropriate? I was surprised that there is actually some support for correlated evolution between this trait with no signal and three other traits (Bayes Factors of 4-12).
Some of my colleagues, who know more about this than I do, think that Discrete analysis can be used if only one trait shows phylogenetic clustering.
I would be very grateful if someone could let me know whether or not this is the case, or point me towards any references for this! Thanks in advance

I have a gut sense that you might be able to learn something even in the absence of phylogenetic signal in one of two characters. I don't have a reference, but I expect that simulations could sort it out.
I'd recommend using data of similar shape simulated on your tree to experiment with how frequently you would expect BFs of that magnitude even with independent evolution.
For example, you could shuffle the state of the non-signal character at the tips of the trees, and see how frequently you get a similar BF from Discrete. This is a heuristic Monte Carlo approach without a strong formal basis, but you could at least evaluate whether something about your phylogeny's structure is pathological and confuses Discrete. This Monte Carlo approach is implemented in Mesquite, providing some methodological precedent.
I'd also recommend running Discrete with MCMC rather than ML, if you have only used ML. For your actual trait data, I'd examine the rate parameters late in the MCMC chain using Tracer. If there are a lot of modes of the rate distribution, then it's possible that the internal reconstructions are too noisy to draw much of a conclusion.
I'd also consider whether you are encountering a multiple testing problem. How many total phylogenetic correlations are you examining? If the answer is "a large number of bivariate correlations", then you do expect to find what appears to be a strong association at some rate even when there is no association.
It would also help to know more about the size of your phylogeny and how the different characters look when mapped onto the tips, or on a sample reconstruction.

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Would fewer cows mean less methane emission?
Rotting grass produces the same amount of methane as cows that digest grass (see this source). So if cows did not eat the grass, it would still emit methane. Therefore, if there were fewer cows, would the total methane emission change at all?

AFAIK methane is only produced by anaerobic fermentation. Grass rotted i.e. by funghi produces a lot more CO2.

Couple of thoughts:

(The OP's article is a low quality source of info with either an interview taken out of context or an inappropriately vague or under-informed interviewee. Reasons why will become apparent throughout my answer.)

Much of the world's grasslands are maintained for and by grazing livestock. Without dedicating so much of Earth's surface to livestock, we would almost certainly have less grass.

Though, much of the world's livestock are fed corn vs non-cereal grasses more commonly referred simply to as "grass". It's unclear if the OP's question is referring to grasses taxonomically (i.e.,inclusive of cereal crops) or in a general sense regarding grass leaf blades only. Regardless, my initial claim applies to presence of both pastoralized grasslands and croplands. The distinction is more important for a later point I'll make below.

See here for more info.

Grass does not always "rot." Methanogenesis is an anaerobic process. The bacteria in a ruminant's stomach are anaerobic, as are bacteria in various wetlands (or in landfills). However, the large majority of grasses do not grow nor die in these anaerobic conditions, so methanogenic bacteria would not be responsible for breaking down most grass. Instead, most decomposition produces carbon dioxide. See here for more info.

Relative abundance of various bacterial types in a ruminant's gut is dependent on that particular livestock's diet. Methanogens (i.e., methane-producing bacteria) only become dominant when the cow consumes a high-sugar feed (vs. a high cellulosic feed) -- e.g., corn vs other grasses. See here for more info.

A quick review of the methane cycle might also prove beneficial. Methane is broken down both by UV light and by methanotrophs (though the latter is more important for preventing CH4 from entering the atmosphere -- e.g., in places like wetlands -- and the former is more important for breaking down existing atmospheric methane). Folland et al. (2001) estimated that the "lifespan" of methane in the atmosphere is ~9.6 years. As such, the rate of methane production is important, as slower production will result in less accumulation. This is important when one considers that decomposition of plant matter in wetlands, for example (though quite variable based on conditions) can take years (vs hours/days in a ruminants stomach). From EPA:

Decomposition of emergent macrophytes in lacustrine wetlands may take from about 200 to 1000 days for 90 percent weight loss (Hill 1985). Breakdown rates (per day) range from 0.0008 for woody plants in bogs to 0.0190 for non-woody plants in riparian wetlands (Webster and Benfield 1986)

I'll try to update later with more thoughts, but this is a good enough starting point to post.

 Folland, C.K., T.R. Karl, J.R. Christy, R.A. Clarke, G.V. Gruza, J. Jouzel, M.E. Mann, J. Oerlemans, M.J. Salinger and S.-W. Wang, 2001: Observed Climate Variability and Change. In: J.T. Houghton, Y. Ding, D.J. Griggs, M. Noguer, P.J. van der Linden, X. Dai, K. Maskell, and C.A. Johnson (eds.). Climate Change 2001: The Scientific Basis. Contribution of Working Group I to the Third Assessment
Report of the Intergovernmental Panel on Climate Change. Cambridge, UK, and New York, NY: Cambridge University Press.

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Can the genetic sequences for CRISPR components be inserted into the host genome so that the cell perpetually produces CRISPR components?

Theoretically speaking, can you insert the gene sequences for cas9, sgRNA, and promoters into the host genome so that the cell perpetually produces CRISPR components?

In this scenario, I'm guessing there would be no way to have the host cell produce DNA templates for HDR?

How long do CRISPR plasmids last in the nucleus and is there any way have them persist for 10+ days?

Quick answers/comments: 1) yes 2) why not? 3) stable transfection/genomic insertion using retro or lentiviruses. If the insertion is stable, it can last the life of the organism.

Comment to 1:
Yes. Many labs have integrated Cas9 stabely into their cell lines. E.g., for CRISPR/Cas9 screens (forward genetic screens). It's very useful, since then you can avoid double transfections (of Cas9 and sgRNA) which lowers the efficiency.


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Mutation profiles for Corona viruses in non-human hosts
In this question Mutation rate breakdown by original and mutated nucleotide for Coronaviridae mutation profiles for SARS-CoV-2 in humans are given. It is a known fact that mutation profiles are dependent on the host species and it was speculated that the Omicron variant of SARS-CoV-2 evolved at least partly in a non-human host based on its specific mutation profile.
My question is: What are some mutation profiles for SARS-CoV-2 in non-human hosts? All known non-human hosts count.

So, what have you found so far?

@bob1: No published numbers so far, some PCA plots showing different ellipses for mutation profiles for different species is all I have seen yet.

You should add the information you found to the question - prior research helps keep your question from being closed. Note that serial passage in animals in the lab is generally considered "gain of function" research, so won't have been done!

@bob1: There are data from natural occurring outbreak among animals (mink farms and white tailed dear come immediately to my mind), and also infection in other animals show typically mutations specific to that animal (hamsters are the animal model for Covid-19, to mention another species.

I second bob1: add the data to the question and explain why it is inadequate for your purposes within the question.


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What species is this white thin shell? Santa Cruz, California
These shells (see in green circle) are empty inside which look like very flat marble donuts/coins.
The small ones are like dollar coins; big ones can be cup coaster-sized.
It has beautiful five-fold symmetry (see the top one) on its back and a whole on its ventral part. Must be related to sea urchin?
What's more interesting is that some of them (see the one at the bottom) have a tiny shell of a different kind anchored on them.

In your second photograph, are you referring to the white conical shell or the little black thing?

sorry for not being clear. Trying to refer to the same thing - flat white shells

They are definitely sea urchins, specifically a type of sand dollar called the Eccentric Sand Dollar, which is found all along the Pacific coast of of the US. Here's what they look like when they're alive:

They're filter feeders partially buried in the sand.
If you're referring to the white, conical shell attached to the sand dollar, that's a barnacle, probably a California Barnacle, but the species is easier to identify alive (or newly dead) than bleached and eroded (to me, anyway.)

you are amazing!

@Code42 - Thanks, but I just happen to like sand dollars and I'm good at searches. :)


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What is the highest known trophic level for a consumer?
Or rather, what's the longest known food chain between a producer and an apex predator?
I've found a few similar questions and answers online, but none of the questions clarified some of the nuances of the question meaning all of the answers I've found are rather vague (e.g: 'about 10' or a more specific value without a specific chain, "we don't know", 'it depends', 'in the ocean' or 'infinitely long') or just random guesses (x2).
You might be able to consider the food chain of cannibalistic species or two species which consume each other to be infinitely long, so I'll assert that a food chain can not contain the same species twice. Also don't consider food chains that are only theoretically possible, I'm interested in what food chains actually exist and actively occur between widespread species. This also means not including species which eat just about everything, unless the species being eaten is one of their primary prey.
There probably isn't a definitive answer to this or a way to prove that one food chain is the longest, but I'm just interested in how long a food chain can get.

Hi and Welcome! You may not know that this site requires evidence of prior research (quote and link to source/s) in an attempt to answer your own question (this is a Q&A site, but one with slightly higher expectations.) For example, have you searched for the role of environment on food chains, etc.? If so, what have you found? Showing evidence or research greatly increases your chances of getting an answer.

you might have an easier time by making the trophic level version of the question the title, the food chain one all but unanswerable.

@anongoodnurse I wasn't sure how to site my sources properly, since StackExchange seems to just treat Markdown references as links but I used some sources multiple times or had multiple sources for one point, but I've done my best

That was an excellent edit to include sources. Since you did your part, I'll try to find out. I fully expect, though, not to find one definitive/reliable longest food chain length. The more complex the ecosystem, the more likely to be more "steps" in the food chain (E.g. a desert is less complex than a salt marsh.) I'll avoid the ridiculous or artificial. (E.g. coyotes > ospreys > ship rats)

OK, I did try. The common answer is "unknown", one reason being that food webs are seasonal, another is that the same species can be lower or higher in the food chain depending on size, population, etc., and oof!!! The most complex ecosystem on earth is the tropical rainforest, but I found more trophic levels in the ocean. But none were fixed; they change and are interconnected. Ugh. I'm sorry; I would have liked to have given a better answer.

@anongoodnurse Don't worry! I was fully anticipating there to not be a definitive answer thanks to the many variables involved. And you've clearly done far more research than me haha. Since it seems most of the variables relate in some way to time, maybe it be possible to identify a worst-case and best-case scenario?

I just decided I don't know enough to say much of anything. I read a number of papers, but I'm still kinda flummoxed. See here for an example of how complex oceanic food webs are. You should see the tables, some with hundreds of superimposed webs.


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How are ray finned and lobe finned fish are sister clades?
I think my previous questions may have been misinterpreted (I honestly was too tired to formulate what exactly I was confused about), so I’d like to elaborate on my confusion about the phylogeny of Osteichthyes.
Ray finned fish (actinopterygians) and lobe finned fish (sarcoptertgii) are classified by the shape of their fins. Their common ancestor obviously had some type of fins, so either one of the groups is paraphyletic (in the sense that their common ancestor belonged to or evolved from one of the groups), or the common ancestor had fins that didn’t resemble either rays or lobes
Despite my efforts I can’t find a straightforward source saying the latter is true, so how are the 2 groups sister clades?

Or Osteichthyes have intermediate fins with characteristics of both. there are actually quite a variety of fin types in extinct fish. just because their descendants have evolved drastically different fins does not mean the basal forms did. Imagine if the two surviving group of mammals were ungulates and bats and you asked did there ancestor have wings or hooves?

Please re-read the title of your question and remove one of the instances of “are”. Also take out the first paragraph: I have no idea what your previous question was, and it is irrelevant to this question, which should stand by itself. If you need to explain anything of this sort do it in a comment.

The misunderstanding here is the difference between phylogenetic classification and character evolution. Essentially, just because an organism has one certain trait it doesn't automatically belong to some group.
Words like paraphyletic, monophyletic, and clade, are descriptions of groupings by ancestor-descendant relationships. Clade and monophyletic, for example, refer to an ancestor and all of its descendants. Paraphyletic generally refers to an ancestor and most of its descendants, but excluding some portion. Talking about "bony fish" but excluding tetrapods would make bony fish a paraphyletic group.
Character evolution is the study of how characters have evolved among a group of organisms in light of their phylogenetic relationships. Textbooks often talk about clades having synapomorphies, or characters that have evolved in some ancestor and are present in its descendants. Some clades have clear synapomorphies that do indeed strongly match a clade (e.g. all the members of the clade have the character, and other organisms do not). However, it's not uncommon for synapomorphies to only be mostly true. Perhaps some members of the clade lost the new trait, or some species outside the clade independently evolved the same trait. These exceptions, however, don't change the group membership of those organism.
It's not the character that defines a species' clade, but the ancestor-descendant relationships. It's not exactly true that Actinopterygii and Sarcopterygii are "classified by the shape of their fins." It's just that fin shape is a really good synapomorphy for those clades because it's both consistent and probably has important evolutionary consequences. Because of this people adopted the common names ray-finned and lobe-finned fishes, giving the implication that that's what defines those groups.
The misconception is understandable because we use characters (previously morphological characters, recently increasingly genomic characters) to craft our hypotheses about what we think are the true ancestor-descendant relationships.
All that is to say that the most recent common ancestor of Osteichthyes is just that—it is an ancestor of both Actinopterygii and Sarcopterygii, but doesn't belong to either clade, regardless of its fin morphology. Actinopterygii and Sarcopterygii share that common ancestor to the exclusion of other groups, which makes them sister clades.

Here's a pretty nice resource from Berkeley relevant to this topic. I'll also recommend the Understanding Evolution site that it came from.

to be fair those groups are also both clades and taxon, as groups they are robust enough to have survived the transition in methodology. so you also get a confusion of cenvention.


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How selective are wolves about the size of their prey?
For an animal that lives and hunts socially like a wolf, is there a lower threshold to the size of prey items they will hunt? A pack wouldn't have much trouble with catching say a rabbit, but would the food provided be enough to actually make the hunt worthwhile? What is the limit in which a prey item becomes too small to be worth catching?

Hi and Welcome! You may not know that this site requires evidence of prior research (quote and link to source/s) in an attempt to answer your own question (this is a Q&A site, but one with slightly higher expectations.)  Did you google this? What did you find?

I will say that hares make up a large part of a wolf's diet in a certain season. What's too small for a wolf to bother with? That depends.

You should not post here until you've demonstrated your own research effort. Given this stipulation -- and the rich literature about this very topic -- I will keep my answer cursory so as to act as starting points for your search. A simple Google or google Scholar search on your part will reveal many more details/studies.
You should review the following ecological concepts: prey switching, optimal foraging theory, principle of allocation, and others.
Some accessible articles on Prey-to-predator-size ratio include: Henriques et al. 2021, Tsai et al 2016, Cohen et al 1993, and Vézina 1985
Regarding wolves:
According to Becker et al 2018:

[Wolf] Prey selection is influenced by the absolute and relative abundances of prey types, the life history characteristics of predators and prey, and the attributes of the environment in which these interactions occur.

Smith et al. 2010 demonstrate that diets vary with season -- their focus being on winter diets.

Huggard 1993 shows the impact of environmental variables such as snow.

Herd density plays a significant role:

Sand et al. 2016

Davis et al 2012 showed that lower density of secondary prey mattered more than heightened density of primary prey.

Huggard 1993 (Canadian Journal of Zoology) showed that density of herds (vs herd density) mattered more in Banff National Park in Canada. Herd size and habitat also mattered -- with wolves avoiding some habitats and seemingly choosing places that optimized preferred habitats and large herd size.

Wolf scat/diet studies showing smallest species in their diet:

Sin et al 2019: smallest for Sandanavian wolves = domestic dogs

Nowak et al 2011 showed the following small prey made up the stated percentages of wolve's diets in Poland:

brown hare Lepus europeus (2.5%) and Eurasian beaver Castor fiber (1.4%). Domestic animals, exclusively dogs and cats, made up 1.0% of food biomass.

Works cited:

Becker, M.S., Garrott, R.A., White, P.J., Gower, C.N., Bergman, E.J. and Jaffe, R., 2008. Wolf prey selection in an elk-bison system: choice or circumstance?. Terrestrial Ecology, 3, pp.305-337.
Cohen, J.E., Pimm, S.L., Yodzis, P. and Saldaña, J., 1993. Body sizes of animal predators and animal prey in food webs. Journal of animal ecology, pp.67-78.
Davis, M.L., Stephens, P.A., Willis, S.G., Bassi, E., Marcon, A., Donaggio, E., Capitani, C. and Apollonio, M., 2012. Prey selection by an apex predator: the importance of sampling uncertainty. PloS one, 7(10), p.e47894.
Henriques, J.F., Lacava, M., Guzmán, C., Gavín-Centol, M.P., Ruiz-Lupión, D., De Mas, E., Magalhães, S. and Moya-Laraño, J., 2021. The sources of variation for individual prey-to-predator size ratios. Heredity, 126(4), pp.684-694.
Huggard, D.J., 1993. Effect of snow depth on predation and scavenging by gray wolves. The Journal of wildlife management, pp.382-388.
Huggard, D.J., 1993. Prey selectivity of wolves in Banff National Park. I. Prey species. Canadian Journal of Zoology, 71(1), pp.130-139.
Nowak, S., Mysłajek, R.W., Kłosińska, A. and Gabryś, G., 2011. Diet and prey selection of wolves (Canis lupus) recolonising Western and Central Poland. Mammalian Biology, 76(6), pp.709-715.
Sand, H., Eklund, A., Zimmermann, B., Wikenros, C. and Wabakken, P., 2016. Prey selection of Scandinavian wolves: single large or several small?. PloS one, 11(12), p.e0168062.
Sin, T., Gazzola, A., Chiriac, S. and Rîșnoveanu, G., 2019. Wolf diet and prey selection in the South-Eastern Carpathian Mountains, Romania. PloS one, 14(11), p.e0225424.
Smith, D.W., Drummer, T.D., Murphy, K.M., Guernsey, D.S. and Evans, S.B., 2004. Winter prey selection and estimation of wolf kill rates in Yellowstone National Park, 1995–2000. The Journal of Wildlife Management, 68(1), pp.153-166.
Tsai, C.H., Hsieh, C.H. and Nakazawa, T., 2016. Predator–prey mass ratio revisited: does preference of relative prey body size depend on individual predator size?. Functional Ecology, 30(12), pp.1979-1987.
Vézina, A.F., 1985. Empirical relationships between predator and prey size among terrestrial vertebrate predators. Oecologia, 67(4), pp.555-565.

Also of interest: "Wolf Pack Hunts A Hare | The Hunt | BBC Earth" 4:05 min YouTube video by BBC Earth.


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Estimating Weight of Human Skeletal Muscle?
Is there a way to measure the weight of skeletal muscle?  I understand body fat and lean body mass can be measured by: skin fold calipers, electrical impedance, table lookup based on formula of weight, age, and height.  I have not seen a method to determine skeletal muscle.  I asked an endocrinologist and they were not aware of a method.
I suspect subtracting the weight of the skeletal bones, skin tissue and organs from the lean body mass weight could determine weight of skeletal muscle.  It seems this number could vary greatly be the person unless perhaps people who handle deceased people have accurate measurements of the above for age, weight, height, etc...
It would be useful to know the weight of skeletal muscle because it could be used to determine body energy expenditure, as lean muscle uses more calories than fat.

You probably know that evidence of prior research is required on this site. It's a good question. Editing what you've found so far would make it better. :)

Updated with research references.  Are my categories ok for this?

Did you search "how to determine skeletal muscle mass"?

I did and the calculations are for Lean Body Mass (LBM) = Total Weight – Fat Mass which includes Organs, Skin, Bones, Body Water, Muscle Mass.  I think I'm looking for Muscle Mass, which will allow me to multiply it by 6 kcal/lbs and fat, 2 kcal/lbs to get a more accurate calculation of BMR.  I don't think the 6 kcal/lbs is supposed to include organs, skin, bones and body water... I suspect this factor is for muscle tissue only.

Hmm, I see that you're correct that the first few hits do refer to lean body weight, but on the first page of hits (for me) is a good article specifically on skeletal muscle estimation, which discusses the method with which I'm most familiar.

What link are you referring to?  I see https://www.healthline.com/health/muscle-mass-percentage, which uses a estimated chart and the numbers don't add up to the correct BMR.  There are some formulas here, but again it is rough estimate and don't measure if a person has lifted lots of weights https://www.frontiersin.org/files/Articles/505707/fendo-11-00031-HTML/image_m/fendo-11-00031-t001.jpg.  There is suggestion of using an MRI, water displacement.  There is a formula using impedance https://journals.physiology.org/doi/full/10.1152/jappl.2000.89.2.465.

Also, Creatine ( methyl-d3) dilution in urine for estimation of total body skeletal muscle mass.  The only problem here is if a body builder is taking creatine supplement, it will throw off the results.  Are you referring to this?

This was the article I saw towards the bottom of the first page of hits. It compares two methods of estimating skeletal muscle mass. The method I'm familiar with is that using a DXA scan, although I'm passingly familiar that one can use MRI, but have not ever bothered becoming knowledgeable about it, because DXA scans are so easy and so much less expensive. Good research on your part, btw.


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Butterfly Raises Abdomen Like A Scorpion
Since a few weeks I am observing a little butterfly in my living room and normally I put insects out but it's cold outdoors and I thought it's secure inside. It occassionally flies around, especially since last 2 days and now I saw it is behaving differently. It has raised it's abdomen rectangularly (90 degrees) and it looked greenish with white stripes. When I tried to make a picture with flash on, it lowered it's tail and the color has also changed to a brown. The picture shown is just a couple minutes later taken without flash. I'm worrying if it's afflicted by a worm and I am thinking about if it's better to put it to rest in that case!?
As I am writing this line, it has lowered its tail further.


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What's the purpose of using more than one culture medium for bacterial isolation?
What's the purpose of using more than culture medium for bacterial isolation?
Why not use just one?
If this is not generally used in isolation of various types of bacteria, I'm concerned especially with Acinetobacter spp. isolation, which grow well on blood agar and MacConkey agar.
Examples of research which include the isolation of acinetobacter spp.:

In this study, 200 (9.5%) Gram-negative, non-fermentative strains were
selected among 2108 Gram-negative isolates identified at mega
laboratories over the Suez Canal and Nile Delta regions in Egypt (1044
urine culture, 108 pus, 537 sputum, 322 blood, 23 cerebrospinal fluid,
and 74 wound) from August 2017 to October 2018. The 200 strains were
preliminary inoculated on MacConkey agar, blood agar, Acinetobacter
agar, and CHROM agar media. [1]

The samples were collected from patients of all age groups, both
sexes, who were critically ill and suspected for pneumonia, urinary
tract infection, septicaemia, skin and soft tissue infection and
meningitis. The samples were inoculated on Blood Agar and MacConkey
Agar plates under strict aseptic conditions. [2]

All the samples including bland pus, respiratory tract samples,
fluids, swabs and urine samples were surface streaked onto BA [Blood agar] and
MacConkey agar plates. [3]

https://doi.org/10.3390/antibiotics9090603
Oberoi, A., Aggarwal, A., & Lal, M. (2009). A decade of an underestimated nosocomial pathogen - Acinetobacter in a tertiary care hospital in Punjab.
https://doi.org/10.22159/ajpcr.2018.v11s2.28590

Edit:
There is one species in the genus Acinetobacter, Acinetobacter haemolyticus, which causes beta hemolysis on blood agar, however, not a single research that mentions using both MacConkey and blood agar, mentions this as the reason for using blood agar.

I think this would be more appropriate on Biology.SE and would be more likely to receive good answers there. I can migrate it for you if you have no objection.

Please do, thank you.

A good start would be to look at the purposes of each medium, and to realize that not all the bacteria that fit the category Gram neg, non-fermetative are Acinetobacter...

Were the people receiving the samples trying to urgently identify unknown pathogens? If so they would grow on several different media.

I am not sure I get your question, Do you want to isolate a sepcific type of bacterium or in general isolate most bacteria from a sample?
If you want to isolated a specific bacterium from a samples, there various "selective" media you can use. Now, I never saw a medium that is really selective, meaning other stuff will grow on it as well. But in general you can be confident that the diversity of colonies you get on these media is lower than what you get on a general medium.
If you want to isolate as many bugs as you can, well then you have to try as many media as you can. Not all bugs will like the same medium. Also there is this misconception that bacteria like rich media. This is not necessarily the case and often rich media are actually highly selective for fast growing bugs that are able to tolerate well stress, carbon overflow, and ROS/NOS.


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Boundary of a cell and its membrane - position definition and jargon problem
Can extracellular be extramembrane/intramembrane?
Definition of Extracellular here:

Extracellular matrix: The extracellular matrix is a complex network of material such as proteins and polysaccharides that are secreted locally by cells and remain closely associated with them to provide structural, adhesive and biochemical signalling support.

Another definition here:

The extracellular space is the space outside of the cell membrane but part of a multicellular organism. The term is typically used for a secreted protein that remains associated with the cell, e.g. as part of the extracellular matrix. It is not used for a protein that is secreted into the blood stream (or other body fluids) of eukaryotic, multicellular organisms, such as insulin or fibroblast growth factors.

Not really helpful in clarifying. On Google, various sources tend to give rather conflicting definitions.
This is one definition of Extramembrane found here:

In this study, we find that over 60% of the extramembrane domains were structurally related to proteins of known structure.
There's no definition or figure of what makes up extramembrane, yet it's been used over in journals.

Consider following scenario in terms of domains of integral proteins, membrane proteins, for e.g. loop-1 of A-protein is inside cell but outside membrane(?), helix-1 is inside membrane but outside cell(?), loop-2 is outside cell and outside membrane.
Can we refer to loop-1 as extramembrane and intracellular since it's not within membrane but within the cell? What is the correct reference to this domain?
Can we refer to helix-1 as intracellular (as well as transmembrane)?
Can we refer to loop-2 as extramembrane? extracellular?
What is the corrent way to refer to these 3 positions?
Asking this question becasue there's a real dilemma around holding an accurate understaing understanding and definitions of cell components references/positions and use of the above jargon.

Neither of those definitions are definitions of "extracellular". One is "extracellular matrix" one is "extracellular space". I think overall you're not really asking a very goal-directed question, what's the problem to solve here? Can you give a specific example where conflicting terminology is used in different places?

@BryanKrause goal is to know clearly what defines extramembrane and extracellular of a cell, membrane, that consists membrane proteins. e.g. a figure/image showing exactly what comprise of these definitions.

They are adjectives that mean "outside a membrane" and "outside a cell". Do you know an example where these terms are used inconsistently based on those meanings?


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CRISPR/Cas9: How can inserted DNA be used as a donor for the homology-directed repair if Cas9 only creates blunt ends?
The CRISPR/Cas9 method allows new genes to be inserted. After Cas9 cuts the Target-DNA, it can use a homologous piece of DNA as a donor template for homology-directed repair. But HDR only occurs when there are sticky ends, and Cas9's cuts end in blunt ends.
What did I miss?

According to this Addgene blog:

There are four different HDR pathways to repair DSBs. Here are  three
central steps of the HDR pathways:

The 5’-ended DNA strand is resected at the break to create a 3’ overhang. This will serve as both a substrate for proteins required for strand invasion and a primer for DNA repair synthesis.

...

Essentially, this resection process generates the required overhangs through partial degradation of one of the strands.
To understand the mechanism of resection a bit better, this is a good read:

Huertas, Pablo. "DNA resection in eukaryotes: deciding how to fix the break." Nature structural & molecular biology 17.1 (2010): 11-16.


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Emotions in Animals Based on Neuroscience
I know very little about the subject, so please forgive any misunderstandings in the question. First of all, by emotion, I mean feelings of pleasure and suffering and not merely just sensory recognition of damage to the body or things like that. If I understand correctly, the consensus among scientists is that all mammals can feel pleasure and pain based upon all of these animals having similar brain structures to humans that have been correlated with feelings like pleasure and suffering. https://www.emory.edu/LIVING_LINKS/publications/articles/deWaal_2011b.pdf.  The way I'm hoping to potentially find an answer is by asking if it's known that there are certain structures in the human brain that are necessary for feeling pleasure and suffering and if it's known that are any animals that do not have these structures or similar structures?

Hi and Welcome! You may not know that this site requires evidence of prior research (quote and link to source/s) in an attempt to answer your own question (this is a Q&A site, but one with slightly higher expectations.) For example, you can search using terms like "dog emotion and MRI", and quote from the article. Showing evidence or research greatly increases your chances of getting an answer.

look up the amygdala

What is it about the paper that doesn't answer your question? A link alone gives us no information.

It is so broad that I wrote my thesis on it! The evidence is also inconclusive and dividing. I think this is too broad for this site. Here is a fairly recent review on the subject https://www.sciencedirect.com/science/article/pii/S0149763419305391


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Primary charge separation in Photosystem II
I was reading through an article about primary charge separation in Photosystem II when I came across the following graphic:

I assumed that the axis is measured with respect to the unexcited system, which implies that the primary excited state (ChlD1*) has energy of 2 eV more than the baseline PSII-RC. However, I also know that the light absorption of PSII peaks at $\lambda=680$ nm, and light with a wavelength of $680$ nm only carries $1.8$ eV. So how is it possible that the incoming photon seems to excite the Photosystem II reaction center to a higher energy than the photon itself carries?

Did you consider the quantum efficiency (QE)? The absorption peaks - yes, but nevertheless it's a distribution over wavelength (energy).

Oh please — "an article". If you reproduce a figure from the article, please do it and us the courtesy of citing it, preferably with a link.


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What is the easiest way to determine the species of non-tuberculous mycobacteria?
We have isolated a mycobacterium strain from patient sputum using an NTM Elite plate.
When inoculated into an MGIT tube, we observe fluorescence when observed under UV light, which means it is highly likely to be a mycobacterium.
We have assumed it is M. abscessus since M abscessus has been grown from the same patient in the past. But what would be the easiest way to verify that?
Would the answer be different if we needed to know the subspecies, like M abscessus bolletii?
We are a small lab with limited equipment, so if the best solution is to use a service provider, we would also be open to that.

From this paper [Ref. 1] as well as this one [Ref. 2], it looks like PCR, potentially combined with genetic sequencing, is a good way to go.
In the first paper, they used 16S rRNA sequences to identify samples of non-tuberculous mycobacteria (NTM), and PCR restriction fragment length polymorphism analysis (PRA) of hsp65 to determine species. This method has the advantage of running on a standard PCR setup, then sequencing products of interest as needed (either in-house or via a service).
In the second paper they used a different method - multiplex real-time PCR with high-resolution melting (HRM). This method was performed on a RotorGene 600S instrument. It's not clear whether this particular instrument is necessary, or if the method can be adapted to any real-time PCR machine. This group also sequenced some samples.

References:

Moghim S et al. Identification of Nontuberculous Mycobacteria Species Isolated from Water Samples Iran J Basic Med Sci. 2012 Sep-Oct; 15(5): 1076–1082. PMID: 23493797; PMCID: PMC3586926
Peixoto ADS et al. Identification of nontuberculous mycobacteria species by multiplex real-time PCR with high-resolution melting. Rev Soc Bras Med Trop. 2020 Nov 6;53:e20200211. doi: 10.1590/0037-8682-0211-2020. PMID: 33174954; PMCID: PMC7670742.


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Human Fat Adipose Tissue: Maximum Energy Transferred out per Day?
The article "A limit on the energy transfer rate from the human fat store in hypophagia" states that subjects with moderate activity levels are found to have a limit on maximum energy transfer rate from human fat stores of 290 kJ / kgd. This results in 31 kcal / lbs.
Question: Does anyone know (possibly with access to the full article) if above numbers are kJ/(kg body fat) or kJ/(kg body weight)?  Optional, the article mentions moderate activity, what happens in the case of high activity?
I asked because if its kJ/(body fat), then this limits a 185 lbs male with 27 lbs body fat to 837 kcal/day metabolized from fat adipose tissue into energy, limiting his weight loss to about 2 lbs/week.  If it's kJ/(body weight), then a 185 lbs male can transfer 5723 kcal/day from fat adipose to energy and lose about 13 lbs / week.  Rough calculations made where 3500 kcal deficit = 1 lbs weight loss.
I have information that suggests a person without any food, only water, performing moderate exercise of 6 miles walking per day, for three weeks, loses about 4.3 lbs/wk (accounting for the loss of 11 lbs material in colon). This data suggests:
They either:

This examples uses energy from breaking down muscle tissue over the 837 kcal/day limit (fat store max) suggesting this article calculates using kJ/(body fat weight).
This examples uses energy over 837 kcal/day, which was 2344 kcal/day from the fat store, not including muscle tissue, suggesting that this article calculates using kJ/(body weight).

If I understand correctly, what you actually want and need is the access to the full article. There are various ways to do this: either contact your library, a friend working at the university, directly request it from the authors, or ... well, there are also other ways which should not be publicly promoted, but are available online.

I have full access now and my suspicion is that the result is a max of 837 kcal/day/lbs body fat can be transferred from fat adipose tissue per day.  This suggests that maximum weight loss of adipose tissue before using energy from free fat mass (skeletal muscle) is about 1.6 - 2 lbs/wk.  I suspect people dieting should know this..

Paper
From the conclusion: "The main thesis of this paper is that the FM is able to transfer energy to the FFM up to a maximum rate of (290±25) kJ/kg d."
Where FM is fat mass and FFM is fat-free mass.
So (290±25) kJ/kg d or (31±3) cal/lbs d is the maximum rate of energy transfer possible from FM to FFM where the kg or lbs in question are that of FM.
Example
I weigh 175 lbs and my body fat percentage is 10%. That means I have 17.5 lbs of FM. My theoretical limit of energy transfer from FM to FFM is anywhere from 17.5 * 28 = 490 calories per day to 17.5 * 34 = 595 calories per day.
That's:

Min: 490 cals * 7 days = 3,430 cals per week
Max: 595 cals * 7 days = 4,165 cals per week

So if we take 1 fat lb at 3,500 calories it's 0.98 lbs to 1.19 lbs maximum fat loss per week.
Dr. Alpert Later Remarks
Here's the thing though, the late Dr. Alpert went on to later state he miscalculated the numbers in the paper and it was more like 20 cal/lbs d to 25 cal/lbs d. Unfortunately he didn't republish the paper though.
Personal Experiments
I highly recommend performing your own experiments as the paper was done for a somewhat esoteric sample which was very small. A friend and I ran two personal experiments that might be of interest using DEXA scans to see how our results add up to those in the paper.
I followed a progressively restrictive deficit until I started experiencing muscle loss. I collected 7 intervals of scans. For me the maximum amount of fat loss was in fact 21 cal/lbs.
Interestingly enough once I experienced muscle loss my body started upregulating how much muscle it utilized and preserved fat which caused my fat utilization to drop all the way to 9 cal/lbs. I theorize this is some sort of evolutionary switch as I am very muscular. The body probably senses an "emergency" and starts preserving fat while utilizing muscle. Given muscle consumes more energy to maintain than fat, this seems like it would kill two birds with one stone for increasing the chances of survival.
My friend did a more extreme test where he fasted for 7 days and measured the FM change. He was able to hit 23 cal/lbs d of fat loss so it matched the paper very closely as well. His FFM was all over the place during the experiment but it's tough to tell what was water, carbohydrate, glycogen, etc. loss so we only looked at how much fat he lost.


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Is there any disease that is proven to originate from malfunction of alternative splicing or post translation changes in the genome?
The most common diseases with genetic origin like muscular dystrophy seem to originate from issues with the primary structure of the DNA itself. Also it seems to be somewhat controversial as to whether alternate splicing of a single gene is actually a functional process, rather than biomolecular noise. In that context, do we know of any disease where the primary structure of a certain gene is normal, but the end products are not.

Misconceptions etc. in the Question
There are several misconceptions and erroneous or unclear statements in this question, which first need to be dealt with.

Whether or not muscular dystrophy is a common genetic disease, depends on whether you think 1 in 3500–6000 male births is common. I would term it ‘well-known’.
It is not controversial whether alternative splicing of a single gene is a ‘functional process’ (whatever that may mean). One well studied and unequivocal example is in sex determination in Drosophila melanogaster — see the Wikipedia entry for Alternative splicing and my own answer to a question on this list.
Alternative splicing of a gene involves splicing sites that may or may not be part of the spliced transcript (the mature mRNA). The title of the question asks for diseases of malfunction of alternative splicing, whereas the body of the question refers to a normal “primary structure” for the gene. I shall assume that examples in which there are mutations in splice sites that are in introns — and hence not in the mRNA or the protein — satisfy the criterion. However enhancer mutations will also be considered.
The reference to “post-translational changes in the genome” in the title does not relate to the rest of the question or make much sense to me. I shall ignore it.

Examples
There are several reviews on this topic, but I shall confine myself to the first that I found from an internet search — one entitled Splicing mutations in human genetic disorders: examples, detection, and confirmation by Abramowicz and Gos in J Appl Genet. 2018; 59(3): 253–268. Table 1 of that paper list examples of genetic diseases extending to three pages (perhaps easier to read online horizontally here) which include the following:

congenital cataract
Neurofibromatosis type 1
Ehlers-Danlos syndrome
Succinyl-CoA:3-ketoacid CoA transferase deficiency
Becker muscular dystrophy
Familial dysautonomia
Cystic fibrosis
Androgen insensitivity syndrome
Fabry disease

The mutations causing the aberrant splicing include mutations in the donor or acceptor splice site, intron variants, and exonic and intronic splicing enhancers. The results of these mutations include exon skipping, cryptic exon inclusion, and alteration of the relative frequency of occurrence of different spliced transcripts.

+1. Maybe you could also find examples of diseases caused by splicing regulators, so that primary sequences of targets may be completely normal including splicing sites.

@KaPy3141 — I agree, that would be good. Now finding the time...


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Could metastasis be driven by a healthy organ?
Could the cancer cell be called to itself by the organ to which it will metastasize? Maybe when the cancer cell enters the bloodstream, it is not according to the seed-soil hypothesis, but by releasing the messenger molecules into the bloodstream by the healthy organ, it allows the cancer cell to perform chemotaxis on itself?

I don't really understand your question. Do you want to know if metastasis happens by release of messenger molecules by the cancer cell which are taken up by the cells of the organ where the metastasis happens instead of cancer cells invading the organ?

@chris, I don't understand you either

Ok, easier: What do you want to know? You can either edit the question or we help you with it, no problem.

@chris, Since healthy cells have less glucose, I thought maybe by changing some gene expressions and synthesizing biomolecules, they could form a signaling network with tumor tissue.

@chris, Yes, attracting cancer will ultimately be to his detriment, but on the other hand he will be deprived of glucose. I thought it was like he might be stuck in a dilemma and going down such a path.

What's your goal here?

@krause, what do you want to say??

Why do you put "@krause"? There is no user "@krause", so what's the purpose of that? You seem to be attributing intention to someone or something that you refer to as "he". It is very unclear what you are saying in your comments and unclear what the question means to ask. Might you perhaps consider enlisting the aid of a translation program?

Google çeviri oldukça iyi çalışıyor. Belki bunu dene. Because clarity would help us help you.

Do you mean to ask why different cancers metastasize to specific locations? https://www.sciencedirect.com/science/article/pii/S1535610805002345

No. Maybe because a healthy cell cannot get enough glucose from the blood, it expresses a protein and this activates a signaling pathway (like hormones) in the cancer cell. This cancer cell then migrates to the healthy cell. Yes my english is not good but it is not that hard to understand!!!

Well,  the absence of such a reason in a review about specific localization of metastases lowers its probability though.

@Furkan I want to know what the goal/objective is of what you're asking; I think that would help the rest of us figure out what it is you're trying to ask.

I love science and I'm curious. I have no other purpose

Although not by glucose as you mentioned. https://pubmed.ncbi.nlm.nih.gov/30423299/ Ca seems to have the ability

@user237650 Finally, someone understood what I meant. thanks

If I understand your question correctly, you are wondering whether a cancerous cell might be 'recruited' to a healthy organ because that organ is releasing some sort of molecule that the cancerous cell recognizes in some sense and that results in the cancer cell moving toward the higher gradient, until eventually it is at the organ.
With respect to flowing towards a gradient in blood: A cancerous cell that has found its way into the bloodstream will be at the mercy of the flow of the blood and not much else. If you've ever seen a video of how aggressively red blood cells get moved through the blood, a cancer cell will similarly move in the direction of the flow, regardless of any molecular gradient that is or isn't present. This flow will carry the cancerous cell through the body and it seems implausible that any molecular gradient will have any impact on this.
With respect to chemotaxis in an area that has no pressure gradient (i.e., a cell 'crawling' over organ A to get to organ B because of some signalling molecules being released by organ B) there is simply no evidence that I'm aware of that this occurs.


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Intelligence without natural selection?
Natural selection is not the only driving force of evolution. There are other mechanisms such as genetic drift, mutations, gene flow, etc... To what extent can these different mechanisms (which don't influence adaptation to new environments as much as natural selection) evolve a more 'complex' species than when there is no natural selection?
Using a very utopian example... imagine that the first living beings that appeared in the world had access to an infinite amount of resources and space. Thus, the mechanism of natural selection would not make sense because it wouldn't be necessary. However, there could be other mechanisms that allow evolution such as genetic drift.
In a world like that, would it be possible (even if it took a long time) to emerge certain 'complex' species with, for example, traits like intelligence (like human beings)? Or in this case, as there is no natural selection, species would evolve with just 'simple' variations like, for example, bacteria that reproduce faster than others?

"imagine that the first living beings that appeared in the world had access to an infinite amount of resources and space. Thus, the mechanism of natural selection would not make sense because it wouldn't be necessary" - That's not how natural selection works. Even with infinite resources and space, selection would increase the frequency of genes that improved reproductive success.

@BryanKrause Yes, you're right. I was imagining a scenario where species have the same reproductive success. I mean... I know it is not really possible with the laws of physics in our universe, but... if there was no selection/selective pressures... Could a species become intelligente given enough time? Or is it something impossible?

I mean, if you want to go for a thought experiment then you can make almost anything possible, that doesn't mean it's interesting or useful to state for understanding the actual universe we live in or understanding how evolution actually works.

@BryanKrause I've already heard about that thought experiment. With this post I was trying to understand how important is natural selection. In other words...  when complex traits (like intelligence) occur in a species, it means that they were always the result of natural selection? Maybe, given enough time, intelligence could arise in a species randomly, without selective pressures. I don't know... I appreciate your help!

Welcome to SE Biology. Please read the Help on What types of questions should I avoid asking? You will see that "You should only ask practical, answerable questions based on actual problems that you face", and that you are asked to avoid asking subjective questions where "you are asking an open-ended, hypothetical question: “What if ______ happened?”". That is why I do not think your question is on-topic here and have voted to close it.

a lively conversation - its a good question!

The answer is yes, but really no.
It’s probably true that things were kind of laid back at first for life. But selection was still going on. A strong wave might break the membrane, a strong wind or storm. A long cold winter. These were all selective. Selection comes with any sort of challenge, not just from other living things.
Natural Selection sounds like Big Science but it has many simpler humbler forms. A good way of defining it here is that any different traits between two living things can be passed down to their progeny. If a trait conveys even a very small advantage to producing progeny that survive to reproduce themselves then it is selected.
What you are saying is that if a fantastical being appeared that were infinitely superior then it would not be part of natural selection. In fact 'genetic drift' 'mutations' and are the source of nearly all these advantages. An infinitely superior being as you describe would disappear without progeny that maintained the advantage you are right - no natural selection. If that being had progeny and they produced the same advantage it would be preserved by natural selection and part of natural selection as we all know it.
That being said it’s very hard for a large advantage to show up. Even let’s say naturally green hair hasn't shown up on many millennia of human selection. If such a mutation or 'genetic drift' showed up I’d bet that gene would be pretty popular and there would be a good number of green haired people around in about 100 years. But none have shown up. Why? Because it requires too many very unlikely events to happen at once.
It’s difficult to overturn a theory like Natural Selection. It’s really very simple at its base. "If you can print copies of a book, more people will read it." is a similar theory. It’s possible all the books would just show up on peoples' doorsteps sure. It could happen but in all human history it has not become a common experience. People do give books away but they almost always print them. People could give away books that were written at random or by throwing a die. It’s possible to even write a best seller that way. But it’s so improbable that you might wait until the end of the universe before you see it happen. Look at Borges' 'The Library of Babel' which dramatizes the odds you are talking about.

Thanks for your answer. It is a very detailed answer. Our universe wouldn't be like it is if there wasn't natural selection. I was trying to understand that if genetic drift alone could give rise to a human being even with infinite time. I was thinking that, in some way, due to some biological or physical laws, if there are any selective pressures, complex traits can't occur in a species. Maybe they can, but we have to wait a very long long time. Althought, in a universe where species have infinite resources...

every species could reproduce without stop (infinite food and water, for instance)... there would be infinite species, infinite traits, so... given some time... the odds of something identical to humans appear become greater and greater. So it might be possible in a universe like that. I really appreciate your answer. And I'm going to read that short story. Thanks!

its another level up to explain that without eating and drinking that there would be no advantages for competition.  mutation and variation are going to make come offspring more or less advantageous Id think.. anyway its becoming very fantastic a scenario at this point... i dont think were done yet either. Kudos for asking this question!

No
Large multicellular animals only have an advantage in resource conservation monopolization.
So with infinite resources and infinite space you won't have anything that could even have a brain.
In your situation reproductive speed is the only competition, which means a race to the simplest. You can't even get significant predators because prey is a limited resource.
When you throw around words like "infinite" most common sense starts to break down. Of course infinite can't exist in this context in a universe like ours, so it is just a thought experiment anyway.


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Are these microscopic star-like structures on a dead leaf some sort of organism? If so, which one?
I’m wondering what these star-shaped organisms are on a dead leaf I found in my backyard (Texas, USA). This was taken under my microscope at 40x magnification. They seem to be clear organisms with multiple outgoing “rays” that somehow benefit with being on the leaf. What’s the identification? Are they even organisms? They appeared stationary. Response to comment asker: The leaf did not feel hairy.

These are stellate ("star-shaped") [and possibly peltate ("borne on a stalk")] hairs ("trichomes") of the leaf itself.

From Harris & Harris's (2001) ""Plant Identification Terminology: An Illustrated Glossary":

Peltate. a flat structure borne on a stalk attached to the lower surface

Stellate. Star-shaped, as in hairs with several to many branches radiating from the base. Figure 1686.

Trichome. A hair or hair-like outgrowth of the epidermis.

You can see a magnified image of stellate peltate trichomes on a leaf of a Texan native, Croton monanthogynus below:

 Leaf surface (abaxial) showing stellate, peltate trichomes. SOURCE: Nickrent, D.L., Costea, M., Barcelona, J.F., Pelser, P.B. & Nixon, K. (2006 onwards) PhytoImages. Available from: http://www.phytoimages.siu.edu

this looks like a cactus

@Féileacán I don't believe common species of cacti have stellate hairs. See https://www.nature.com/articles/ncomms2253 for an example. (Also, note: that cactus "hairs" you're used to observing are actually spines not trichomes -- specifically, spines that tend to be more delicate are called glochids. Trichomes on cacti typically associate with clusters of glochids for water capture, but such clusters of trichomes would appear clumped and apeltate unlike the imaged stellate trichomes.


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Why is iodine added to salt? As opposed to fluor or fats/oils like iron and vitamin A?
Is there a particular reason why certain foods are enriched or fortified with certain nutrients?  Such as salt with iodine?  Or did we just get used to doing things a certain way since we started enriching foods about a century ago?

Where I live, supermarkets offer cooking salt enriched with iodates and fluorides. "Food grade salt shall be used when salt is used as a carrier for food additives or nutrients for technological or public health reasons. Examples of such preparations are mixtures of salt with nitrate and/or nitrite (curing salt) and salt mixed with small
amounts of fluoride, iodide or iodate, iron, vitamins, etc., and additives used to carry or stabilize such additions." (FAO, 1985)

Please demonstrate the research you have put into this question (which is to do with health policy, rather than biology) yourself. Did you look at the Wikipedia article on this topic, for example?


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TMPRSS2 Primer Design
I am trying to design a primer for TMPRSS2 PCR reaction. However, this gene is in reverse position like in the picture I'll show.
From the nucleotide sequence I got from NCBI, should I reverse the sequence and start designing the primer, or do you have any other solution? Thank you!

Welcome to the site. Please take a [tour] and visit the [help] for more information about the site and what we do here, as well as about good questions and answers. Can you please specify if you aim to amplify genomic DNA or coding sequence only (e.g. off RNA/cDNA).

If your goal is simply PCR amplification than it makes no difference whether you flip the sequence or not: By convention the 'forward' primer refers to the primer that is designed against the anti-sense strand and your 'reverse' primer is designed so it is complementary to the sense strand. In practice however the PCR reaction obviously doesn't care what we call the primers, it will amplify the region that is encompassed by them, producing double-stranded DNA fragments that are indistinguishable regardless if the sequence/design was flipped or not.

Thanks for your answer. I am considering to use the original sequence (unflipped) retrieved from NCBI RefSeq to cover the whole region I'd like to amplify.


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When is the sex of a human not determined by their chromosomes?
This might sound like a silly question, but what chromosomes determine whether a human is born a boy or a girl? I ask this because I got https://embryo.asu.edu/pages/sex-determination-humans when googling the subject and it contains the word "typically" in places I did not expect. For example:

Humans typically develop as either male or female

Humans who inherit two X chromosomes typically develop as females, while humans with one X and one Y chromosome typically develop as males.

Because females tend to only have X chromosomes, the egg cells that they produce typically carry an X chromosome

Is this a form of political correctness, or are there legitimate cases that justify the insertion of the word typically? I'm genuinely curious what these exceptional cases might be.

To answer points 1 and 2:
People born karyotypically male (XY) with complete androgen insensitivity syndrome (AIS), can be born without developed male genitals. People with a certain set of sex chromosomes develop in varying different ways.
To answer point three: An egg cell will indeed carry a single X chromosome in most cases, however, there are situations where an egg cell can carry two X chromosomes. If an egg cell containing two X chromosomes is fertilized with a sperm containing a Y chromosome then this could lead to XXY chromosomes — Klinefelter syndrome.
Side notes:
For those interested in the impact of social standards regarding this syndrome, there is a good interview with a Dutch person with AIS. (One can set the translated captions to most languages.)
You can find information on the occurrence rate of intersex here:
Intersex Society of North America

Very interesting! Thank you very much.

There is a a whole mess of inhibitors and activators proteins that need to be triggered for typical sexual development, a mutation or error in any one can lead to atypical results even if they have typical chromosomes. A graphical overview is below. You may note than several factors are common to both sexes. Atypical can range from just malformation of genitals to full on sex reversal. XY female and XX male exist.  Then you have all the atypical chromosome combinations, Xo, XXX, XYY, XXYY, ect. A full breakdown of most the known options (as of 2016) can be found here. And that's just the gross physical manifestations, the brain has largely separate pathways for sex determined development, meaning an alteration of those pathways can lead to what is essentially a male brain in a female body and vice versa.

https://www.semanticscholar.org/paper/Sry-and-SoxE-genes%3A-How-they-participate-in-sex-and-She-Yang/3860ee65052aebecc48a85a79a36221160458b30
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5866176/


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How do DNA methylation canyons/DNA methylation valleys/DMCs differ from CpG islands?
Are these just both regions of the genome that are undermethylated? Is the only difference that for something to be a CpG islands it needs a high level of CpG sites and DMCs don't?
So could a 3.5kb undermethylated region of the genome be considered a DMC even though there are not many methylatable CpG sites there?
Thanks!

The level of methylation does not play a role in defining a CpG island, whereas it is central to defining canyons/valleys.
CpG islands are areas of the genome that are >200bp in length and which contain an observed-to-expected number of CGs > 0.6, and a CG% > 50%.
A methylation canyon or valley is instead an area that is >3.5kb in length and contains < 10% average methlation at any given CpG.

This looks like a helpful answer, but it would be improved by citations or links to supporting materials.

@Risk, Do you have any references to back up those numbers? I found that it sort of matches the definition of CpG island in a paper: "annotates the segment as a CpG island if it satisfies the following criteria: (1) G + C content >50%, (2) length >200, and (3) the ratio of observed to expected number of CpG dinucleotides (“CpG O/E”) >0.6". But in a paper the methylation valley is longer "> 5kb" and notes that most contain few CpG islands.

@llrs The CpG definition is taken from UCSC genomics institute here: link The definition for valley/canyon came from here: [link[(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4719427/#B1).

@Risk many thanks! I'm not sure about the second link: In the paper "Epigenomic Analysis of Multilineage Differentiation of Human Embryonic Stem Cells", (first reference from the second link) under the section "Identification of DNA Methylation Valleys" it says "These DMVs range in size from 5 kb to 68 kb and are much larger than the CGIs in these regions ". Did you meant to link a different paper?

@IIrs - Sorry I must've messed up the link. If you look in the introduction of that paper, 4th paragraph: "identified around 1,000 larger (>3.5-kb) genomic domains with low average methylation levels, termed DNA methylation valleys or DNA methylation canyons (1, 15). These elements remained unmethylated during differentiation and were often associated with developmental genes".  One of those papers is the paper you're referring to, the other one is the one I tried to link to.


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Superbugs in eusocial animals
I am not a biologist, and I'm interested in eusocial animals, and the porous habitats in which they live. I know few facts about diseases in these animals: I know some interesting instances of viruses, bugs and about cancer, respectively [1] in Spanish, the hygroscopic property of honey (I don't know the article [2]), and [3].
Question. I would like to know if there are eusocial animals which suffer diseases due to superbugs. In such case add the most relevant facts from your knowledges or cite/refer the most relevant articles from the literature.
I add as general references that Wikipedia have edited the article Eusociality and Antimicrobial resistance redirected from the search Superbug (https://en.wikipedia.org/wiki/Super_Bug). I hope that my question does make sense (for some eusocial species), in other case I can to delete my post. Feel free to add your feedback in comments if my post isn't suitable for your site Biology Stack Exchange.
References:
[1] David Pride, Los virus de nuestro cuerpo, Investigación y Ciencia, Febrero 2021, Nº 533, pages. 76-83.
[2] Manisha Deb Mandal and Shyamapada Mandal, Honey: its medicinal property and antibacterial activity, Asian Pac J Trop Biomed. 2011 Apr; 1(2): pages 154–160.
[3] Elizabeth Pennisi, Why Naked Mole Rats Don't Get Cancer, from the web of Science (19 Jun 2013).

Welcome to the site. Please take a [tour] and visit the [help] for more information on what we do here and what makes a good question and answer. In particular, have a look at the homework section and see how that applies to your question. As it stands there is little linking your statement in para 1 to the question and the references to cancer and honey don't seem appropriate given that these have nothing to do with superbugs.

If I understand right, you are considering the antibacterial properties of honey to be similar to antibiotics, considering other eusocial animals may produce anti-pathogen substances, and asking if pathogens that resist these substances cause disease in the eusocial animals. Is that correct?

No, I don't assert it, and I'm sorry @timeskull if I've introduced a misunderstanding with my references. The references cited [1], [2] are to illustrate that I know that some eusocial animals suffer infections/ diseases caused (respectively) by viruses and bacteria, and that the case of cancer was studied in the mammals in [3]. I would like to know if there is some eusocial animals that suffer disesas causes by superbugs. Many thanks and I hope don't bother you or your colleagues (professors of the site).

Well, a "superbug" is a pathogen that is resistant to antibiotics or antifungals. No eusocial animals produce those so resistance wouldn't affect them.

Not an answer because I can't give a definitive yes/no to eusocial animals. Well, human to dog transfer of MRSA has been recorded in 2004, and although dogs/wolves are not technically eusocial, it would indicate a first step in the transmission to non-human animals. Superbugs in livestock are a matter of great concern too.

Many thanks for the comments @JiminyCricket. and for your colleagues


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does retrovirus need to manipulate cell cycle by neutralizing Rb and/or p53?
Early studies of transforming retroviruses led to discovery of oncogenes, while studies of DNA viruses (like AV40) led to discovery of p53 and Rb and tumor suppressor genes. Frank McCormick says in https://www.youtube.com/watch?v=wag9ISMeLDg&t=347s at 4:33 time: "DNA viruses have very different lifestyle than retroviruses, they need to inactivate Rb to get into S phase to replicate DNA...and then neutralize p53".
Why would retroviruses have "very different lifestyle" than DNA viruses? I assume they need to hijack same cell machinery to replicate (since its RNA is reverse transcribed to DNA firstly) as DNA viruses do. Can someone explain, please?

Welcome to SE Biology. Why do  you "assume" retroviruses need to use the machinery for DNA-dependent DNA polymerization that DNA viruses use? They have their own RNA-dependent DNA polymerase (aka as reverse transcriptase) to generate dsDNA copies which are not replicated further but integrated into the host genome. Have you researched the host cell components the two types (very much a simplification as DNA viruses differ) use?

@David thanks for your explanation, my bad I haven't realized reverse transcriptase is used for amplification as well, not only to create single DNA copy of virus' RNA to be integrated into host's genome.


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Does the most known image of Long-finned pilot whale depict one with the melon inflated or not inflated?
The most common image of the Long-finned pilot whale shows a bulbous head. Some may think this is merely an inflated melon:

https://upload.wikimedia.org/wikipedia/commons/thumb/7/76/Pilot_whale_spyhop.jpg/330px-Pilot_whale_spyhop.jpg
...but images of an inflated melon in Long-finned pilot whales show what seems a lateral position:

https://s3-eu-west-1.amazonaws.com/wwhandbook/sidebar-images/_sidebarPromo/PIFSC_20170901_S104_G-0384_PAO.jpg
...so does anyone knowledgeable in LFPWs know if it's an inflated melon or a big brain in top picture?
After all, they have the highest neocortical count:
https://www.frontiersin.org/articles/10.3389/fnana.2014.00132/full


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Why do you have to submerge your gel in buffer before adding DNA
When you run a gel electrophoresis, you add your gel and then submerge it in TAE or TBE buffer before you pipette your ladder, DNA, loading dye, etc. Why must the gel be submerged in buffer before you add anything? If anything, doesn't this make it harder to pipette into the well due to the diffraction of the buffer?

This has a very simple reason: Adding the buffer later poses the risk to wash out your sample from the well as well as mixing samples.
There is another reason: It makes loading easier. The sample is mixed with loading dye which contains glycerol. This mixture is denser than the buffer and makes the sample sink to the bottom of the well. So you only need to get your pipette tip into the well (and not all the way down the bottom to deposit a very small drop of sample) and then you can release the sample from the tip. It will sink down due to gravity to the bottom of the well.


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Why can't other electron acceptors produce as much ATP as oxygen?
I have been wondering about life using a different "Final" electron acceptor(replacing oxygen), but every thing I can find in my research say that oxygen produces more ATP because of its higher affinity for electrons.
But as far as I know, in the electron transport chain, the ATP produced is because of protons going through the ATP synthase because of an imbalance in protons(the protons being generated by the electrons moving through the ETC). But since all the protons are generated by the time the electrons have made it through and are ready to be accepted by oxygen, then shouldn't the number of protons generated be the same regardless of that final electron acceptor? And if the number of protons produced is the same, then shouldn't the same amount of ATP be produced?
Why, despite the same number of protons being generated by electrons in the ETC, do other "Final" electron acceptors (such as Fe3+) besides oxygen produce less ATP?

Welcome to Biology StackExchange! Can you please include some references for your statements, that is: which sources did you use in research that has these claims?

Short answer: The "worse" final electron acceptor will just not accept the electron, and electrons will just get back up in the electron transport chain, shutting down oxidative phosphorylation.
Long answer: This is related to a deceptively dissimilar question: "Why do cells throw away perfectly good organics in fermentation?"
To really explain this, you'll have to know some quantum mechanics.

Every nucleus, atom, molecule and ion has orbitals (MO theory) , little "slots" for electrons to exist in (shown as horizontal lines). Orbitals have distinct "energy levels", thanks to the electromagnetic interaction between the electron, the nucleus (nuclei) and other electrons. Typically, electrons will exist in the lowest energy level not occupied by another pair of electrons. Electrons release energy when they move down and absorb energy when they move up. A free electron ($n= \infty $) will release more energy moving to the lowest energy level ($n=1$) when that lowest energy level is more negative, and will have to absorb more energy to become free again. This is what is meant when we say an electron acceptor has "higher affinity for electrons".

The ENTIRE gimmick of the electron transport chain is that the electron moves to progressively higher affinity acceptors, releasing energy in the process. By the time the electron reaches the penultimate of the electron transport chain, its energy level is so low/the acceptor affinity is so high (equivalent) that it takes another acceptor with even higher affinity to attract that electron.
But what if the cell just... throw the electron away? Well, that would completely defeat the point. For the electron to become free it needs to be provided with energy. More energy than what the electron transport chain has extracted for sure, because the electron in the food molecule isn't even free to begin with.
Ok, but WHAT IF the cell use the electron to build organics instead? Every cell requires an energy source, a carbon source and an electron source. Unfortunately, that won't work in this case. Organics in biology usually requires electrons with energy equivalent to that of NADH. Since that is the very beginning of the electron transport chain here, it won't work.
The ONLY productive way to throw an electron away is to give it an acceptor and then throw that away too.
So that's why Fe3+ etc cannot accept an electron from the penultimate of the aerobic electron transport chain. Because you'd need to provide energy to the electron to do so.
Back to the question I proposed in the beginning. "Why do cells throw away perfectly good organics in fermentation?". By definition, fermentation means using an organic terminal electron acceptor. What usually happens is that cells do this clever maneuver where they rip the electron from an high energy position in the molecule and puts it in another position with lower energy.

Notice the cycling of the electron carrier NADH.

The items of information assembled in your answer may be individually correct, but imho they miss the wood for trees, and they do not address the actual question. The wood is that the potential to obtain energy from oxidation depends on the negative magnitude of ΔG, and the question is not why no energy is produced if Fe(III) replaces O2 — dissimilatory oxidation of NADH by Fe(III) exists (https://ecampusontario.pressbooks.pub/bioc2580/chapter/redox-reactions-review/) — but why it is less than with O2 This is not obvious as the ΔG is not significantly different, despite the assertion in the Q.

I highly doubt that the ΔG°' is "not significantly different". ΔE˚' is. However, oxygen accepts 2 electron per water, while ferric iron accepts 1 per iron. Using ΔG°' = -nFΔE°', where n is the number of electrons transfered... Yeah you can see where this is going.

Ok. Point taken. But nevertheless, the fact remains that the overall ΔG is sufficient to reduce Fe(III) in dissimilatory oxidation, and your answer does not acknowledge this fact or address the energetics of this process. I have not answered myself because I have not yet tracked down sources for the details of the components of the ETC in dissimilatory iron-reducing bacteria. If you wish to apply your chemical knowledge to the actual situation it will  save me the effort.


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evolution of a preference for cooked meat
When I got a meat thermometer a few years ago, I was startled at how low optimal cooking temperatures are for beef, less that 140 degrees Fahrenheit. Also, as a kid, I remember reading that the desert floor in Arizona gets up to 180 degrees Fahrenheit, which is much higher. I haven't been able to confirm that, and frankly find it a bit doubtful, but if it's even close, it does imply that an an animal carcass lying on the African plains for a couple of days may be legitimately cooked.
Now, I'm not a biologist, and this is pure speculation, but I'm imagining that if proto-humans picked up a diet consisting largely of medium-rare carrion (probably killed by other predators), this might explain why humans prefer cooked meat and why they lost jaw size (because cooked meat is a lot easier to chew).
Has there been any research along these lines?
Addendum: published temperatures in Arizona seldom get above 120 degrees Fahrenheit, but those measurements are taken in the shade at about 5 feet above the ground. What I'm talking about is measurement of the temperature of sun-warmed rocks on the desert floor. I still think 180 is a little high, but 140 wouldn't surprise me at all.

Almost all predatory animals prefer cooked meat when offered it, cooked meat is way easier to digest and your senses can pick up on that. Animals carcasses lying out for a couple of day are eaten by scavengers and insects very quickly. also 140 internal temperature, which means sustained heating, if you a steak on a rock it cools the rock as the steak warms you need a really hot rock or a way to keep heating the rock, which humans did with fire. we were using fire long before our jaws and teeth shrank


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Can Iron(III) accept electrons from NADH without the other enzymes?
During the electron transfer chain in cellular respiration, the NADH turns into NAD+ while donating an electron. Those electrons pass through many enzymes and chemical reactions. One such chemical reaction is when it passes through iron II or iron III. Is it possible for NADH to react with iron II or III without any other reactions with enzymes and chemicals? I am asking this because I am interested to know if the reaction between NADH and iron can give oxidize NADH and reduce iron.

Please clarify. 1. When you refer to iron II and iron III, please indicate whether you are talking about free iron or iron in cytochromes etc. 2. Are you talking about what actually happens in the electron transport chain (ETC) in cells or what would happen if iron were mixed with NADH in a test tube? 3. Or are you asking why the many redox pairs are need in the ETC? Your language ("turns into", "chemicals and enzymes") suggests you might benefit from reading about the ETC and redox couples in a biochemical text (best) or on line. Are you aware that oxygen is the ultimate electron acceptor?

Thank you for your response and for clarification: 1. I am referring to free iron atoms and 2. I am asking what would happen if iron were mixed with NADH in test tubes. I realize oxygen is the ultimate acceptor but my main question is: if iron(II) or iron(II) and NADH were mixed, could NADH transfer electrons to iron? and lastly, could NADH donate electrons to regular iron?

Preamble
Although the question relates to a non-biological test-tube reaction, I feel it worth posting an answer because the principle involved is relevant to biological redox reactions.
Qualified Answer
For a chemical reaction to proceed requires two things:

That ΔG, the overall change in Gibbs Free Energy, is negative.
That the activation energy for the reaction can be overcome.

As regards 1: For reactions consisting of two redox half reactions, one needs to first calculate the reduction potential and then, from this, ΔG. (A positive ΔE gives a negative ΔG.) A table of standard reduction potentials taken from this on-line source is shown below.

Without actually doing the calculation (I’ll add it later as an appendix, if requested) it can be seen that ferric iron is almost as good an oxidizing agent as molecular oxygen, and thus has the potential to oxidize NADH.
As regards 2: I know nothing about the activation energy for the reaction of ferric iron with NADH in a test tube, so cannot say whether it would occur spontaneously.
Fe(II) as oxidant
Whether or not a reaction is energetically feasible in which ferrous iron (Fe(II)) oxidizes NADH depends on the redox potential of the half reaction for the reduction of ferrous iron. I cannot find anything for Fe(II)/Fe(I), so perhaps only Fe(II)/Fe(0) is possible, values for which can be found on this Wikipedia page. I leave it as an exercise for the reader to do the calculation.

Thank you for your answer, this was very helpful!