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Why Lungs can't work in water and gills can't work in air?
Animals with lungs (such as most terrestrial mammals) cannot breathe if submerged in water, and soon suffocate.
Whereas, fish can variously breathe air (at least for few-hours, as some fish frequently need to get air periodically), including those that are bigger than a human (say sharks).
But why? Do fish require less oxygen than lunged terrestrial-animals, despite being active and variously engaging in activities like predation? (so that uptaking only dissolved oxygen, and probably less surface area of gill than lung-alveoli is enough for them?)

at least for few-hours in case of some fishes those have frequent need to come to air for a while... They are not fishes; they are mammals (cetaceans).

@WYSIWYG Maybe the confusions are due to I don't know any terminology for the phenomenon where fishes comes-out towards upper-surface of the pond-water at a certain interval of time (hours). This is why I had used the phrase 'at-least few hours'. In my place (West bengal, India), a very hot place,  fresh-water-ponds it happens. Probably it is not due to predation, because aquarium-fishes sometime do that.

@WYSIWYG ...contd...  There was an experiment in class 5 and 6 textbook (though I never performed it)... "take a fish that has additional respiratory system, Such as Heteropneustes fossilis/ Clarias batrachus/ Anabas testudineus and lock them in water inside a wire grid and within several hours the fish will die due to lack of oxygen".

Perhaps you can add a picture (of the fish in West Bengal that you are referring to) and the explanations that you gave in the comments (along with relevant references) to the question. It may clarify the question a bit. Don't use comments for additional explanation. Nobody will go through your comments. Moreover, comments are not indexed and are therefore not searchable.

You probably know the colloquial name of the fish. Do some search and try to find some images online. Also, you can search the fishes described in your book and see if they indeed show such behaviour.

Please add these details in the question for the reasons already mentioned. Plus comments are not for extended discussion; this conversation has been moved to chat.

Go to this one

Gills usually require constant movement and need the support of water to work well. Lungs are usually inflated and deflated by muscles, which doesn't work in water due to the density of water. Also the amount of oxygen in water is much lower and insufficient in particular for warm-blooded animals.

Misleading sentences in your question

fishes can breathe in water (at least for few-hours)

Fishes can breathe for much longer than a few hours under water as they spend their whole life underwater.

Animals-with-lungs (such as most terrestrial mammals)

All mammals, whether terrestrial (like a cow) or not (like a dolphin) have lungs. While all mammals have lungs, most fish (but not all) have gills.
Lungs vs Gills
To understand the answer, you need to understand two key organs involved in gathering oxygen from the environment: gills and lungs.
Lungs are organs that allow the transfer of oxygen into the blood when inhaling air, while gills are organs that allow the transfer of oxygen into blood when inhaling water. Lungs don't do their job properly in water and gills don't do their job properly in the air. You should have a look at the following wikipedia entries to further your understanding of these organs:

Lung
Gill

Energy consumption
You say

does fishes require much-much less-amount of oxygen than lunged terrestrial-animals, though they stay in physical activities including predation?

I am not sure I understand the meaning of this sentence but anyway.
Making generalization about fish metabolic rate can only be misleading as there are an immense diversity of fishes. For example some fishes are endotherm (see here to understand the definition of this term) while some are not and this will vastly affect the metabolic rate.
Although eventually too advanced for the OP, Chabot et al. (2016) is an interesting reading to get an general overview of the Metabolic rate in fishes.

Small addition: some salamanders have gills. Also, another important point is that deep diving cetaceans have high concentration of myoglobin (or perhaps high oxygen affinity; don't remember that now. There was an article about that perhaps a year or a two, back) so that their muscles can store oxygen for a long time. I am not sure if all huge aquatic animals have this adaptation.

Cetaceans means dolphins and allied groups, google says. They are mammals. So their lungs doesn't take oxygen from water. They breathe in air and hold their breathe when they're under water.

A fish maintains a baseline of respiration through-out body mass, plus do respiration to obtain energy for task like predation, fly-away etc. that probably needs a lot of energy (so a lot of respiration  so lot of oxygen), and in case of a massive shark probably greater than human.

The only fruitful part of this answer (yet) is  "Lungs don't do their job probably in water and gills don't do their job properly in the air" . However it is here not explained why gill would not work in air and lung would not work in water.

@AlwaysConfused read the linked Wikipedia articles, as suggested by this post's author. Lungs evolved to move oxygen from gaseous air to the blood, while gills evolved to move dissolved oxygen from water to the blood. Lungs don't work in water, because they didn't evolve to work in water, and vice versa for gills. There's nothing else to explain. It's like asking why fins on a fish don't work for flying through the air - they didn't evolve to do that.

@AlwaysConfused (1) as MattDMo said, please just read the wikipedia articles on gills and lungs to have a better understanding of their physiology. (2) if then you have any question that are specific to the physiology of gills and lungs (your current question is not), then please open a new post, explain what you understand about this physiology and what you don't. Good luck!

@ Remi.b "Lungs don't do their job properly in water and gills don't do their job properly in the air." . But why? also I didn't found yet in wikipedia articles. Wikipedia tells how lungs work on air ... but not why it fail work in water (or opposite for gills).

@AlwaysConfused The question was edited. The original question was not so focus how on the physiology of lungs and gills. A question should not be modified after an answer has been posted. My opinion is that it would be better to roll back your edit and ask your specific question about the physiology of lungs and gills on another post.

@Remi.b thanks very much  for your response I'm trying to improve it.

Anything other suggestions are welcome

Some crabs breathe air using gills. The linked wikipedia articles don't explain well how these organs work (and I'm quite sure this is the expected response).
Also, "read wikipedia" is not an answer, but avoiding to give one. "because they evolved so" is not an explanation, but a mere statement that natural selection is a fact.

@Remi.b Terribly worded and confusing questions should absolutely be edited. It seems like it is for this precise reason there exists the option to edit them. Answers should similarly be updated. StackExchange should not exist to archive questioners and answerers talking past each other. Pointing out that fish can survive more than a few hours breathing in water is funny but not altogether productive.

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When a muscle contracts, but not all the muscle fibers are activated, what happens to the remaining muscle fibers?
I understand how motor neurons work, but I would like clarification on what exactly is going on when a muscle contracts. For the sake of simplicity, let's just use the bicep as an example. If I do a bicep curl with a weight that is the maximum weight my bicep can lift, all the muscle fibers in my bicep will be activated and contract(more or less). If I remove the weight and do the same bicep curl, now only a small percentage of the muscle fibers in my bicep will be activated and contract, because that extra force isn't needed. But, the whole bicep muscle is still contracting! It must be, otherwise wouldn't the other muscle fibers staying at regular length prevent the bicep from contracting?
So the only thing I could think of is that the unactivated muscle fibers are pliant and DO contract, they just don't initiate the contraction, but instead go along for the ride. So if you looked at the level of sarcomeres, in the activated muscle fibers, the myosin heads pull on the actin, causing contraction. In the unactivated muscle fibers, myosin heads are NOT pulling on the actin, but the sarcomeres are still contracting, due to the forces from the activated muscle fibers. Is this a correct interpretation of what's going on or am I wrong?

I don't think the unused sacromeres will contract though because every time you contract, it requires ATP and so it will be really expensive if you contract when you don't need to. I believe the unused muscle fibre will just be compressed or bent, since cells have a certain degree of compliance. I am guessing that is also why you won't feel your muscle as hard if you are not doing MVC

If you define contraction, as the myosin heads pulling on the actin and engaging in the cross-bridge cycle, that requires ATP, so yes, that can't be happening. I agree with you and that's not what I was saying. Rather, I was talking about contraction as simply the shortening of the muscle fiber. I was describing would be what you said, compression. So if you were able to see the sarcomeres during contraction, the actin relative to the center of the sarcomeres would be in the same position in both the activated and unactivated muscle fibers.  But...

It would be due to the cross-bridge cycle in the activated fibers, and due to compressive forces in the unactivated fibers. Still, this is speculation on both our parts. I would like a reference that can verify this.

References please! To support your answer

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Can a protein falling below a threshold trigger another response?
Is it possible that the falling of the concentration of a protein below a threshold triggers the release or production of another protein?

Welcome to SE Biology. Your question is very broad. You need to provide some context — is this a homework question or do you have a specific system in mind? Why are you asking this question and what attempts have you made to solve it yourself. See "How do I ask a good question". Oh, and please spell-check your titles at least. I'll correct this one.

A: Yes. There are too many examples to list.

Of course, that is possible. I'll give a simple example. If your protein (X) is an inhibitor of the other protein (Y), then when X falls, Y will rise. This would not really be "thresholded".
There are many mechanisms that can lead to thresholding which include co-operativity (in the action of X) and positive feedbacks. How these mechanisms work would be a different question altogether. (A quick read would be this wikipedia article).

Thank you very much. I'm a physicist and I'm interested in how axons can regulate its length. In a model I'm dealing with, the concrentration of a protein falls below a threshold when the axon reaches a distinct length. The question is if this falling below the threshold can stop the axon from growing.

@Peter123 As I mentioned above, it is possible. If you are asking an example of what those proteins X and Y may be in case of axon growth then I think you should do that literature mining yourself. There may be several examples. Check out a review on this topic.

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Ways to distinguish between purifying selection and selective sweep
When looking a population genomic data, regions of low diversity (lower than expected; such as in a region of high recombination) can indicate either purifying selection of deleterious mutations or a selective sweep of an adaptive mutation. What are some ways one can tell which one occurred?
One way I've heard of is to use an outgroup that did not live through the same events as the main group. If the outgroup also has low diversity, it means nonsynonymous mutations in that region are deleterious regardless of events, and so those homogeneous regions likely underwent purifying selection. If the outgroup has high diversity in those regions, the main group likely went through a selective sweep.
What are other ways to distinguish between the two?

Welcome to Biology.SE!
I actually recently went through the literature on this and similar subject, so I'll be happy to answer.
The answer will not be easy to formulate as a number of authors are working and arguing on the question. I will try to give a quick overview of methods.
Definitions: Background selection and selective sweep
First off, let's use the correct terms. As you described, both positive and purifying selection is reducing genetic diversity at nearby loci. When the reduction in genetic diversity is caused by positive selection, we call the process selective sweep . When the reduction in genetic diversity is caused by purifying selection, we call the process background selection.
What affect background selection?

Recombination rate
Strength of selection.
For a given neutral locus at distance $r$ centimorgans from a locus under purifying selection, the selective coefficient $s$ that is causing the highest decrease in genetic diversity is $s=r$ (Nordborg 1997).
Mutation rate
population structure

What affect a selective sweep?

Strength of selection
population structure
Number of loci involved under adaptation
Whether adaptation comes from de novo mutation or standing genetic variation

By the way, you might want to have a look at the terms 'soft sweep' vs 'hard sweep' in relationship to the two last elements of the above list and in relation to local adaptation.
How to disentangle Background selection from selective sweep?
There are a number of technics but again all of that is a work-in-progress. I would like to classify these methods into four themes.

Environmental covariate

This first element talks about disentangling local selection from background selection. It is maybe not exactly what you asked for but this discussion often comes to center stage in the literature talking about both.
If we assume to know the environmental variable causing the adaptation, then you can compare divergence between population present in different environments and those present in the same environment. If loss of genetic diversity is caused by local selection, then divergence should be higher between population occurring in difference environments. If loss of genetic diversity is caused by background selection, then all populations will show similar divergence. Bayesian Technics such as BayEnv2 (Gunther and Coop 2013) take advantage of this technic.

Among lineages comparisons

By comparing related species, it is possible to find out regions of low genetic diversity. If all related lineage show similar loss of genetic diversity irrespective to the existence of an adaptive event, then the loss of genetic diversity is likely caused by background selection.
From such methods (but I might not totally understand them, I should read the paper again), some authors (such as McVicker 2009) have build B-map and recently implemented in BayeScan (Huber et al. 2016; BayeScan is an Fst outlier method to detect local adaptation), that is map of the genome of the intensity of background selection measured by the B-value introduced by Charlesworth (history of the term reviewed in Charlesworth 2012)

Allele-Frequency-Spectrum

Both background selection and a selective sweep affect the Allele-Frequency-Spectrum as to cause an excess of rare alleles (Tajima's D < 0). However, the strength of the effect and the detailed effect on the Allele-Frequency-Spectrum is not quite the same and some authors have suggested to use such differences to disentangle the two.

Machine learning (thank you @ atongsa)

Recently, there has been much interest in using machine learning techniques to develop methods to detect selection. For example, many people are performing numerical simulations of evolving populations and are training a machine learning algorithm to detect loci under selection. Hejase 2020 apply a SVM method and find a rapid avian radiation have been driven by recent selective sweeps. Hejase 2022 developed a Recurrent Neural Network (RNN) by using the Ancestral recombination graph to infer how selective sweeps shape genomic diversity.
Reading suggestions
There is a lot to read on the subject. I would recommend the recent special issue in Molecular Ecology DETECTING SELECTION IN NATURAL POPULATIONS including the review Haasl and Payseur 2016.

@user25375 Do you think I answered your question?

thank you, you give a great review of this question.  i am newbie, and i think 4. machine learning maybe good at distinguish such two selection process just by input huge data and build a good model for selection sweep and background selection.

@atongsa Good point! I suppose, that was not much of a thing back in 2016 when I wrote this answer but it has become quite a popular topic of research nowadays. I don't know much about it but I quickly added a fourth point above. Please feel free to edit if you can add more information and/or cite a few papers.

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Hardy weinberg equilibrium and Wright Fisher model
Is the hardy weinberg equilibrium derived by using a model similar to the Wright Fisher model, just without assuming genetic drift and finite pop size? Both seem to use the same assumptions except Wright Fisher takes into account finite pop size and genetic drift. What is the model used to derive Hardy-Weinberg equilibrium called?

Welcome to Biology.SE
When you talk about the 'Wright-Fisher model' I suppose you are referring to the 'Wright-Fisher model of genetic drift (WF)'  involving the use of a binomial distribution.
You are correct that the two models make very similar assumptions. However those assumptions are generally speaking found in a large set of different models just because they often simplify the math. I think it is quite wise to consider these two models as very much independent.
Shared assumptions
Both the WF and the Hardy-Weinberg model (HW) assume

non-overlapping generation
panmictic population
absence of selection, migration and mutation
random mating
no sex-ratio bias

Of course, violation of some of these assumptions are relatively easy to model but such complication is often not taught in intro classes to population genetics.
Wright-Fisher model derivation
Let $2N$ be the total number of haplotypes, where $N$ is the population size. I here just assumed a diploid population but derivation for a haploid population is just as easy. Let $k$ be the number of occurrences of allele A, so that the frequency of the allele A is $p=\frac{k}{2N}$. Assuming sexual reproduction only, the number of occurrences of the allele A in the next generation is
$$k' = {2N \choose k} p^k (1-p)^{2N-k}$$
Quick side note: Effective population size
The variance of this distribution is $var(k') = 2N p (1-p)$. The variance of the allele frequency in the next generation is therefore $var(p') = var(\frac{k'}{2N}) = \frac{1}{4N^2} var(k') = \frac{2N p (1-p)}{4N^2} = \frac{p(1-p)}{2N}$.
Replacing $N$ by $N_e$ and solving for $N_e$ yields
$$N_e = \frac{p(1-p)}{2 var(p')},$$
which is the definition of the effective population size $N_e$.
Wright-Fisher model assumptions
The WF does not per say assume a finite population size, it is just that when the population size is infinite, the model loses all of its appeal!
Hardy-Weinberg model derivation
See here for a more complete discussion
The derivation of Hardy-Weinberg genotype frequencies is simple enough to not rely on any pre-existing model. Let's consider the simple version of the HW model, the one with a bi-allelic locus. The two alleles A and B exist at frequency $p$ and $1-p$ respectively. Imagine you have to draw an allele from this population. The probability to draw a given allele is equal to its frequency. Now draw a second allele. Assuming the population is large enough or assuming that selfing is allowed, the probability of drawing a given allele is still the same at the second draw than at the first draw.
As such the probability of drawing the allele A twice is simply $p p = p^2$. Similarly the probability of drawing the allele B twice is simply $(1-p)(1-p)=(1-p)^2$. The probability of first drawing the A allele and then the B allele is $p(1-p)$ and the probability of first drawing the B allele and then the A allele is $(1-p)p$. If we don't make the discrimination between AB and BA genotypes and just call them all AB, then the frequency of the AB genotypes is $2p(1-p)$. Of course $p^2 + 2p(1-p) + (1-p)^2 = 1$.
Hardy-Weinberg model assumptions
It is common to say that HW assume infinite population size. This is correct if you make from HW the interpretation that the genotype frequencies are exactly at $p^2$, $2p(1-p)$ and $(1-p)^2$ and that no evolutionary change will occur. But if you interpret HW as indicating the expected genotype frequencies from which deviation exist, then you do no make the assumption of infinite population size. Under this second interpretation, one can test deviation from HW expectations with a binomial test (or most often, when the population size is large enough with a $\chi^2$ goodness-of-fit test).
Related post

Solving Hardy Weinberg problems is very related and offers a good tutorial.


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Is there a link between digestion and nightmares?
A common belief is that eating too much before going to sleep can cause to have nightmares. In fact, I often experience it: I systematically have nightmares after eating too much in the evening.
Then I was wondering: is there really a link between digestive system's activity and unconscious brain's activity?
If it actually exists,
- is the influence linked to the neurons we have in out gut?
- or is it linked to the augmentation of the concentration of a nutrient in our bloodstream (which can then reach our brain and)?
- or is the neuronal activity which control digestion that interferes with the process of dreaming?
If the influence is linked to the augmentation of the concentration of a nutrient in our bloodstream, does this mean what we eat actually controls our mood or level of anxiety, or any subconscious process? (regardless of compounds known for having a particular effect, like theobromine, etc...)

Although I haven't experienced this specific thing, it's reasonable to say that if someone is uncomfortable somehow when they're sleeping, that that would translate to bad things happening in dreams, as the brain tries to figure out a scenario that would account for the body's sensations. So my thought would be, maybe some stomach sensations are somehow uncomfortable, or maybe similar to how your stomach feels when you're scared. Or maybe this would be something totally different.

According to http://www.medicaldaily.com/bad-dream-more-just-dream-science-nightmares-327586 the extra energy from late night eating can increase brain activity and may contribute to nightmares.

Speaking from experience, I slept really well yesterday after my weekend lunch when I ate so much that I had trouble moving around. So, on a very light note I don't think overeating leads to nightmares. Rather, for me they would lead to a no dream sleep.

Thanks for you answers. I'll try to follow the lead of extra energy to figure out more precise processes.

I just wanted to note that I never felt any feeling of discomfort due to over eating in those situations, and I think this aspect of discomfort adds more complexity to the activity of the organism in its entirety, because it is a "violent" state compared to a normal digestion. Though, it could be interesting to study too.

A nightmare is basically an alarm; typically your subconcious mind trying to wake you. Nightmares often occur when you are experiencing pain or discomfort (like needing to use the bathroom).
Dreams are a way of sorting through questions in a "what if" sort of way. When it comes to a nightmare, you are in a panic-situation, often without a solution, or where a "logical" solution is unsuccessful.

Could you cite some sources for your claims regarding dreams and nightmares? While not implausible, the claims raise more questions than they answer without any supporting evidence.


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Earth overshoot day: is it a sound concept?
Today, August 8th, is Earth Overshoot Day (EOD) for 2016, the day when humanity supposedly has consumed the natural resources available from the planet for the year 2016; we're now running a deficit, somehow. At least if your believe the calculations of the Global Footprint Network (GFN), the think tank behind this concept. EOD is well reported by media every year, and perhaps it does some good as an ecology awareness thing. But is the idea scientifically sound?
EOD is based on the ecological footprint concept. The ecological footprint of a person (measured in hectares) is the area of the earth required to extract the natural resources needed to sustain that person: to grow crops, keep farm animals, obtain natural resources for consumables, etc. It's a very complex thing to calculate, and of course people argue about what the correct formula should be. One article by Willis Eschenbach (2010) goes into some depth and argues that the formula used by GFN vastly overestimates the footprint. I don't know who is right, but it does seem like the footprint is very difficult to estimate, so we should probably be careful with drawing strong conclusions.
But I have a more fundamental problem with EOD. Regardless of how it's calculated, the claim that we have today "overshot" our yearly earth-budget, at 8 months out of 12, means that we are consuming about 1.5 of the available food and natural resources available; or that the footprint of humanity is 1.5 Earths. This is not some kind of parable: GFN really claims that we have exhausted our natural resources, by a wide margin, and that this has been going on since the 1970's.
My question is, what are we all living on then?
As of today there should be no more food around, or any other natural-derived product for that matter. If GFNs estimate is correct, shouldn't humanity be long dead? Shouldn't we expect 1/3 of the earth's "surplus" population to die off pretty quickly? Doesn't the fact that we're not dead prove that EOD is wrong? Isn't it physically impossible for our total footprint to exceed 1 Earth?

EDIT: Nice to see that this question stirred a lot of debate! :) I think several answers bring up one key point that resolves the problem: GFN defines the footprint not as the actual area required for production at present (which must be < 1 Earth), but the area required for sustainable production (which is larger). Exactly how the sustainable area is defined is still mysterious to me, but I guess it is at least theoretically possible.

Why do you think humanity would be dead? I guess the point of the EOD is, that humanity now starts killing other species off, not itself. If we used up our resources, we now would be taking them from others. Taking more than earth can sustainably recover.

The point of EOD as I understand it is to present a bleak picture to the general public, so that they buckle up. Anyone who is a scholar or in one of the sciences or has pursued some sort of advanced education knows that calculating a foot print is very hard. Example, I am from India, where people routinely go hungry and die of hunger. Is it because India wants for food? No, we have been in surplus production for a long time, but the logistics is lagging behind.

@skymningen  I don't see how that's related to the ecological footprint of humans. If we kill/outcompete all other species in order to grab our require hectares, that's one thing. But as I understand it, EOD claims the footprint of humanity exceeds 1 earth, which seems logically impossible.  Are you saying that EOD includes the footprint of non-humans?

@KoustavPal   Yes, I understand that EOD can be a good move for ecological awareness, and might be motivated because of that. That's not my question, I'm wondering if the scientific underpinning is sound.

Scientifically, it isn't a sound concept. If I may bring a similar concept here. Consider Newtonian gravity versus Einstein's general relativity. Newtonian gravity describes gravity as best as possible for the average man's understanding, but it isn't the most scientifically accurate concept. General relativity though is scientifically accurate, but it is very hard to wrap your head around.

You've grossly misinterpreted it. Imagine a company that has a turnover of £1M per year. This would be the equivalent of the natural resources produced each year. Now the company spends £1.5M in a year. This would be the equivalent of using the natural resources produced for the year, the turnover, by August. However, the company has been around for 4.5 billion years and has some money in the bank becuase it was only recently that a stupid new CEO (humans) came in and started spending more money than they were making. The company's best hope is that the CEO dies before he destroys the company.

I also think your question is more philosophical. I say so because, to me you are asking when do we draw a line and say that the results are accurate. Accuracy for me is sufficient when the gain in accuracy would be 0.001 for another step in complexity. But I guess an astrophysics major would say, accuracy for them is sufficient when the gain is 0.00001 for another step up in complexity. So maybe this question belongs in philosophy

@rg255  Sure, that's one way to explain it --- that the Earth somehow has "reserves" that we can live off, but they are finite and will be used up. If so, then the footprint can be > 1 Earth for some limited time, until reserves run out. But what would those reserves be? I'm not an ecologist, so I'd really like to know. Perhaps you can write up an answer to explain?

@KoustavPal  No, this is not a question of accuracy. I'm wondering how the total footprint can exceed 1 Earth. That's a fundamental, conceptual problem, not related to accuracy of any estimate.

"EOD is well reported by the media each year" Really? This is the first I've ever heard of it.

Forests take many years to fully recover. If we use up the right fraction of forest land every year, we can continually utilize a different forest area without reducing total forest area. If we use a larger fraction, the world's forested area will get smaller every year, eventually effectively being wiped out. Using "1.5" as the excessive fraction, it means we use up half again as much forest as can naturally replenish itself "forever". It doesn't mean it's completely gone after 8 months; it means we use as much in 8 months as should only be used in 12.

@TylerH  Well, it is where I live (Sweden).  Perhaps not everywhere.

TL;DR: it's a simplified measure of sustainability, but accurate enough to be useful for public engagement
EOD is hosted and calculated by Global Footprint Network (GFN), an international think tank. The GFN estimates national and global net supply and demand for renewable resources, specifically:

food and fiber products,
livestock and fish products,
timber and other forest products,
space for urban infrastructure, and
carbon sequestration.

From the website:

Global Footprint Network measures a population’s demand for and
  ecosystems’ supply of resources and services. These calculations then
  serve as the foundation for calculating Earth Overshoot Day.
On the supply side, a city, state, or nation’s biocapacity represents
  its biologically productive land and sea area, including forest lands,
  grazing lands, cropland, fishing grounds, and built-up land.
On the demand side, the Ecological Footprint measures a population’s
  demand for plant-based food and fiber products, livestock and fish
  products, timber and other forest products, space for urban
  infrastructure, and forest to absorb its carbon dioxide emissions from
  fossil fuels.

The results are reported in 'global hectares', the area which would be required using global average productivity, to aid intercomparability.
The methodology was published in 2013 (Borucke &al 2013).
So, to answer the question in your title ("Earth overshoot day: is it a sound concept?"), data quality may be an issue (I haven't pored over the paper in detail) but the basic methodology is arguably appropriate for the question they're asking. The only issue I might have is that they effectively consider land and sea use to be interchangeable, but I'm not sure the alternative would be an improvement.
To answer the second part of your question ("what are we all living on then?"), it is possible to harvest more from a system than it can sustainably produce. Exceeding this harms the future productivity of the system. To take the specific examples named for EOD:

Overharvesting plant-based food and fibre products can result in soil acidification, soil erosion, and/or soil salinification;
Overharvesting livestock and fish products can result in overgrazing and/or overfishing;
Overharvesting timber and other forest products results in deforestation;
Using more space for urban infrastructure reduces the availability of land for the other examples on this list;
Producing more carbon emissions than can be absorbed by its forest leads to an increase in atmospheric carbon, resulting in climate change.

Ultimately, while 'Earth Overshoot Day' is a public engagement activity, there is a reasonably robust and transparent methodology behind it which is good enough for the job. Remember: all models are wrong, some models are useful.

Thanks, this is very helpful. I will look at the Borucke et al paper. I take it that the key number is the amount of resources that can be sustainably produced. But I think that fits poorly with the "footprint" concept, unless you define it as the hectares required for sustainable production, not as the hectares required for actual production.

@Roland I'd say sustainability is implied in most similar questions. For example, consider "how much do you need to earn to rent a flat in London?" - most people would infer that the asker is interested in sustainable renting (i.e. a salary that would allow you to rent indefinitely), and wouldn't consider an answer that says 'you can rent a flat in London with zero income, assuming you're willing to eat into savings or go into debt" very helpful.

Yes, I understand you point, but I don't think that's so obvious in the case of the "footprint" idea, because "sustainable" is hard to define here.

Upvote for correct use of "pored over"

@Roland Why is it harder to define here? We have a source (the earth's resources) and a sink (our consumption of those resources). If the two are in long-term balance, we have sustainability.

@AkselA  I agree with that, I meant that it's hard to determine in practise what the conditions for long-term balance is.  At least I would think so.

@Roland - it certainly can be; model predictions can be based on incorrect assumptions (https://en.wikipedia.org/wiki/Maximum_sustainable_yield#Orange_roughy) and there can be hidden environmental impacts in supposedly sustainable systems (http://www.heraldscotland.com/news/11962874.Islanders_polluted_Utopian_idyll_for_centuries_Discarded_seabird_remains_responsible_for_heavy_metal_toxins_which_contaminated_the_soil_of_St_Kilda/). But in the case of arable production and commercial forestry I'd say it's quite well understood, and carbon sequestration rate estimation is getting better fast.

@Roland Ah, ok. arbivoral is pretty much on point in that case, but I might add that a certain amount of forecasting is also added to the models in some cases. The IPCC, for instance, when they propose what they consider to be a sustainable level of growth, the assumption that we become more energy efficient in the future is added in. There is naturally a lot of uncertainty associated with predictions like these.

I think that your question comes from a misunderstanding in the definition of the overshoot day, here is the definition in your question:

Regardless of how it's calculated, the claim that we have today "overshot" our yearly earth-budget, at 8 months out of 12, means that we are consuming about 1.5 of the available food and natural resources available; or that the footprint of humanity is 1.5 Earths.

And here is the definition from the website:

Earth Overshoot Day, falling on 8 August this year, marks the date when humanity’s annual demand on nature exceeds what Earth can regenerate in that year

(emphasize mine)
The difference is that you define resources as available while the website defines availability on a yearly basis.
Like you wrote, it's impossible to consume 1.5 Earths, that would mean that we harvested more fish than are in the ocean, for example.
But if we take it on a yearly basis (as the website do), it's easier to tackle that we harvest more fish each year than fish can reproduce and grow during the same time. So we are harvesting in the fish stocks that developed during the previous years.

Technically, an overshoot means the amount by which a certain dynamic variable shoots above its final steady state value. So, to know overshoot, you need to know the steady state. In this case, as you said, the steady state is just predicted and not really known.
Regarding your question:

what are we all living on then?

Assuming that the overshoot concept holds in this case then we are actually living on the available resources. However, if we are using more than a certain limit then we would deplete the resources in future. This will lead to decline in our population because we need resources to survive. Because of declined population, the resources would accumulate (because of the feedback) and we may finally reach the steady state via a damped oscillatory dynamics (compare with the fox-rabbit situation in the simple Lotka-Volterra models). There are other possible solutions too (sustained oscillations, extinction, etc).
Note that overshoot happens because of a delay and it would not happen (at least using deterministic models), if there is no feedback i.e. a fixed amount of resource is present and we just consume it.
Now, the main issues are:

How accurately do we know the rate and mechanisms of resource production?
How accurately can we calculate the steady state, or in other words, how accurate is our model of resource-population dynamics?

"Assuming that the overshoot concept is true, we are living on the available resources." how can we deplete food resources? Food production has a nonfinite limit (I mean a cap value which cannot be determined atm). How is it possible that we will exhaust natural finite resources such as iron? wouldn't we find newer sources with the advances of technology? We are already in the early stages of transitioning to renewable source. How is it that we will deplete available resources?

@KoustavPal As I said, there are many complexities. I am not commenting on whether whatever model is used, is correct. I am just explaining the concept of overshoot. However, food production is an easy concept that can be nicely explained using Lotka-Volterra. Renewable resources are resources that are formed constantly in nature. If the energy consumption rate is more than production, then the population will be affected again. In a timespan of million years even oil is renewable :P

That's a nice connection to dynamic systems. But this particular overshoot has been going on since at least the 1970's according to GFN ...

"Food production has a nonfinite limit" How can you say this? Food is not just agricultural. There are already the beginnings of protein wars (fighting over food from the sea.) Cod is a good example: cod populations are at record lows despite once being so plentiful that Explorers wrote that one could walk on the surface of the water (off Maine/Newfoundland) by stepping on the backs of cod. We are hunting many species to the brink of extinction. That's not non-finite.

@anongoodnurse when did I say "food production has a nonfinite limit". I didn't say anything like that. Extinction is one of the outcomes. I just said that to say something is an overshoot, you need to have an estimate of the steady state, given by some dynamical model. However, to account for extinction, you would need stochastic models. Deterministic continuous approximations work when the numbers are large.

@Roland I am not quite aware of how GFN estimate is calculated but technically an overshoot usually happens in feedback systems when one variable has faster rates than the other. So we could have overshot an estimate in 1970. However, the estimate should be based on a complex model that would account for all kinds of relationships otherwise you would not really know whether you have actually overshot or not. It is, however, always better to be cautious.

@WYSIWYG Koustav said it in the first comment, not you.

@WYSIWYG - Good grief, I forgot to use the @-user. That comment was not directed at you. Sorry!

Consider an investment earning interest x.
If I spend x dollars a month I cover the interest and will have spending money forever.
If I spend less then x the interest adds to the principal and the investment grows giving me potentially more interest to spend.
If I spend more than x I decrease the principal and so reduce the interest I get the next month. Even if I switch to only spending x I will still eventually run out of principal . To be stable I have to switch to spending x' a smaller limit.
They have modeled the whole earth as a group of investments and expenses using hectares as currency.
Note: in a mortgage when you are paying about 1/3 into principal you are about 2/3 through repayment. Counting  about 40 years to get here might mean maybe another 20 till we are "paid off" if a string of assumptions are true.

While it's not as direct an answer as some of the others, I find this metaphor to be extremely helpful in understanding the concept in clear mathematical terms.


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Identify hematophagous insect
There's a small insect that seems to enjoy residing near trees and takes blood meals. The pain is sharp, comparable to being stung by a wasp.
I'm located in Serbia, Eastern Europe, bordering Hungary and Romania. It's currently August, warm and very moist from the grass being regularly sprinkled.

This is an "aphid lion", a larva of a lacewing (family Chrysopidae). They eat aphids and other small animals, not blood, but are capable of biting humans. Here is a text about that (seems reasonable even with the silly title). It also says that "When a lacewing larva bites a human, it’s likely that any persistent itch or redness is due to the saliva injected at the site of the bite" so that would explain your pain.

Great! Apparently, they seem so beneficial you can't simply swat them off your person.

yes, just keep them off your skin!


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How did Extracellular electron Transport evolve?
According to an on-line article at Smithosonian.com “Some microbes can eat and breath electricity”. This refers partly to the fact that Shewanella use extracellular electron transfer. Does such a different metabolic process imply a separate origin for this type of life, or, if not, how could it have evolved?

can you provide the link to the article you are referring to?

I find the down-votes of this question very negative. The poster is quoting an article in a publication of The Smithsonian Institute, which I had thought was a prestigious publication. The particular bacteria it describes a unusual, and few of the readers of these pages will be familiar with their mode of respiration. This at least makes it question with the potential to invoke educative answers. No prizes for guessing whose answer I am talking about, but I learned something I didn't know in researching it.

Prestigious publication in the above was unintended. What I meant was establishment. I have edited the question to make the provenance of the report and its specific claims clearer.

Very interesting how journalists can make something catchy out of scientific evidence. Kudos to that!

supposedly "eat" electricity

Bacteria don't eat electricity. Electricity in it's most basic form is the flow of charge (in this case ions) from a higher gradient (concentration) to a lower gradient (concentration).
So these bacteria, they utilise this flow of charge within their biological processes allowing them to survive and propagate.

if these exotic bacteria really originate from a separate genesis or just an example of how diverse life on Earth can get if given the chance?

These bacteria are not the only ones utilising electrochemical gradients to power their biological processes. Eukaryotic cells contain an organelle called mitochondria. I will not go into details, you can read that here, but eukaryotic life arose as a result of an endosymbiosis event where two organisms developed a symbiotic relationship, and the mitochondria was born, when organism A engulfed organism B. Mitochondria, also called the powerhouse of the cell, contains it's own DNA, which is very dissimilar from the nuclear DNA, which leads many people to believe that originally they came from an integration event between two different organisms. Mitochondria functions, by ways of the ETC to provide energy to the cell.
That is the dominant role for mitochondria, and it also processes an electrochemical gradient. So no, the answer is no these exotic bacteria did not originate from a separate genesis, but rather an example of how diverse life on earth can get. Believe me there are more weirder things nature has come up with, that bacteria processing heavy metal ions in their biological processes.
As stated by David, I may have created a correlation where there was none. My apologies for that. To point you the right way though,
Shewanella belongs to a class of bacteria called Dissimilatory metal-reducing bacteria, which are characterized by their ability to couple metal reduction with metabolism, if you take a look at the link you will find that Shewanella also contain a very high concentration of sigma-factors; factors which are associated with providing transcriptional robustness under environmental stress.
Coming to their origin, which is the topic of discussion here. I would point you towards MRSA here, the analogous question here is was Methicillin resistant staphylococcus aureus born out of nowhere? The answer to this question is no, this relates to the overuse of antibiotics. Here is a link from the NIH which will give you a brief history of the origin of MRSA.
Principally, this same concept can be generalized here, if you put a population (in this case Shewanella) under stress (heavy metal ions), a large number of the population will die off, but a smaller subset will develop a resistance towards the stress.
Please note, that this line of thought contains two possibilities, the first being that individuals developed the resistance with the aid of mutations in their DNA allowing them a survival advantage over the population, a popular example is the presence of the Delta32 mutation in the CCR5 gene which makes a subset of humans resistant to HIV(AIDS) infection. Did this happen in response to the HIV outbreak the world faced in the late 20th century? No, this most probably happened much earlier (In humans a mutation must move to the germline to propagate across generations) and only came to light after a significant amount of resources had been invested into HIV research. Meaning, that the mutant was already present during the diagnosis, but the selective advantages came to light after the stress response had been faced.
Therefore MRSA could have developed from an existing subset of Staph since antibiotic treatments began in the 1940s (please take into consideration that bacterial replication is faster than human, therefore time flows faster and there is no concept of germline and somatic mutations in bacterial fission). But also, it is entirely possible that MRSA existed beforehand, and that continued treatment with antibiotics resulted in the emergence of the same subset.
So no, the answer is no these exotic bacteria did not originate from a separate genesis, but rather an example of how diverse life on earth can get. Believe me there are more weirder things nature has come up with, that bacteria processing heavy metal ions in their biological processes.
The presence of the sigma factor already tells you that they share the same genesis as all other existing microorganisms on earth, and as to how they developed to gain a survival advantage in environments containing high concentration of heavy metal ions, that relates to the stress response of a population outlined above.

I find your statement that "Bacteria and for that matter all life on earth are gene machines…" as contentious and completely irrelevant to the question. I suggest that you remove it. Likewise superfluous are statements about mitochondria, as this is a question on bacteria, and even more so that they have their own DNA. You would have done better to explain what precisely the electron transfer to the metal oxides achieves in relation to metabolism. As it is, you seem to be confusing electrochemical gradient and terminal electron acceptor.

Addendum: The shoddy article that provoked this question concerns two completely different bacteria (although you would be forgiven for not knowing)
The article concerns mainly Shewanella, which is one of a number of well-known bacteria that can use metal ions as terminal electron acceptors for the electron transport chain: i.e. they donate electrons to the metal.
However the authors have also done work on completely different — and also well-known — bacteria called chemlithotrophs that obtain electrons, which they can use as a source of reducing power (analogous to electrons from light energy).
Shewanella
The question of whether Shewanella has a separate origin is easily settled by the phylogenetic similarity to other bacteria based on its DNA and its repertoire of proteins, including those involved in energy generation and electron transfer.
So, No, Shewanella oneidensis MR1 is just one of several bacteria that use final electron-acceptors other than oxygen in their respiration.
However, there seems to be a misunderstanding about the role of the extracellular electron transport in the provision of energy for the organism — people seem rather shocked by the electric current — so let me clarify the situation.
The initial source of ‘energy’ is reduction of carbon metabolites
The metabolism of Shewanella has been reviewed by Fredrickson et al. Like other bacteria it can be grown on carbon compounds which give rise to intermediates that are oxidized by NAD+ — e.g. in the tricarboxylic acid cycle — resulting in NADH. (I’m ignoring FAD/FADH2 for simplicity.) This involves the transfer of two electrons (the second is to H+) — as we remember from chemistry, oxidation is the removal of electrons. It is the NADH that can be thought to embody the ‘energy’, in so far as the reaction of its reoxidation by an appropriate electron acceptor can result in a large decrease in Gibbs free energy (see, e.g. Berg et al. 18.2).
The electron transport chain allows the free energy changes to produce ATP
Just as with aerobic bacteria such as Escherichia coli, all the potential free energy of oxidation of NADH is not liberated in one step, but in a series of steps, with smaller free energy changes. Some of these result in the extrusion of hydrogen ions into the intermembrane space, producing an electrochemical gradient which drives the production of ATP via the trans-membrane ATP synthase in oxidative phosphorylation. (It’s still oxidative phosphorylation even though oxygen is not involved.) The components of the electron transport chain differ partially from the standard one presented in text books for bacteria with a different final electron acceptor (see e.g. review by Haddock and Jones). However it is important to realize that this is where the ATP is generated in Shewanella, before the electrons get to the cell surface and have any involvement with the extracellular space.
The role of the extracellular metal oxide is as final electron acceptor
For the sequence events from the reoxidation of NADH to be completed, the two electrons have finally to be transferred to some external oxidizing agent. For E.coli it is molecular oxygen with cytochrome oxidase catalysing its conversion to water. Other bacteria use different electron acceptors, some use sulphate (which becomes reduced to sulphite) for example, although the free energy changes of these reactions will not be the same as with oxygen. In the case of Shewanella the final electron acceptor is usually Mn(IV), which is reduced to Mn(III), or Fe(III), which is reduced to Fe(II), although other metal electron-acceptors are known (see e.g. Hartshorn et al. 2009).
What about the electricity?
What’s clearly different about Shewanella is that the solid metal oxide electron acceptor is extracellular, and therefore not in contact with the multi-cytochrome electron donors in the bacterial outer membrane, unlike the diffusable oxygen or sulphate ions. Furthermore, no enzyme is involved. Hence, rather than the electrons being transfered in a reaction at the active site of an enzyme, they flow through the extracellular milleu as an electric current. The electrochemistry of this may be intriguing, but what is clear is that this is not providing any energy to the bacterium, which is certainly not ‘eating’ — or in any other way utilizing — electricity.
And evolution?
Shewanella is certainly different, and had to evolve new electron-transport components and transporters to take these components to the outer membrane (see diagram, below). But bacteria with other electron acceptors had to evolve similarly new redox components (Alberts et al. discuss this in The Molecular Biology of the Cell). Whenever bacteria have taken over a new (and often unpromising) niche, new enzymes or protein have evolved to allow them to do so. And electricity certainly isn’t foreign to Nature, nor is the interaction of bacteria with their external environment.

Multi-haem cytochromes in the outer membrane of Shewanella and reduction of extracellular Fe(III): from Fredrickson et al. 2008.
Chemlithotrophs: something completely different
The original article actually refers to two types of bacteria. The first is Shewanella, which is well studied and for which the quotation below is entirely in concord with my answer, above

Shewanella consumes electrons from carbohydrates, but it sheds them in
  an unusual way: “It swims up to the metal oxide and respires it.”
  Nealson says.

However, the title of the article is based on the following teaser:

One of Nealson’s graduate students, Annette Rowe, has found six new
  bacterial strains dredged from the ocean floor that don’t need a
  source of carbon at all, reports Powell. They can live off of
  electricity alone.

Now it is clear nonsense that anything can live — in the sense of grow — without a source of carbon (and other elements) to supply the structural components that make up the organism, but it turns out that it has been known for a long time that certain micro-organisms can oxidize metals — i.e. in contrast to Shewanella obtain electrons from metals, rather than donate them to metal ions. These are known as chemlithotrophs and often obtain their carbon from carbon dioxide, and usually use molecular oxygen as the final electron acceptor. The enzymic details of this process obviously differ between chemlithotrophs, and the down-voting of this question makes me reluctant to invest the time into researching and then presenting details of the metabolism.
The latest paper that I can find from Rowe and Nealson, published in Frontiers in Microbiology 2015, makes it clear that they are studying lithotrophs, and what is new is that they are replacing the metals by electrodes as electron donors, partly in order to find new lithotrophs which can utilize different redox potentials. Very different from the smoke and mirrors of the Smithsonian article!

Updated my answer, having finally realized that the articled quoted is about two different types of bacteria, the metabolism of which is well-known (although not previously by me). The answer is rather unbalanced, but, I hope, clarifies the situation.


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Are myosatellite cells myoblasts or do they differentiate into myoblasts?
Can satellite cells immediately fuse to a myotube/myofiber (meaning it is a myoblast already) or do they differentiate into a myoblast first and then fuse to myotubes/myofibers?

Where and how have you looked for an answer to this question already?

Why? I have looked at the (many, slightly different) definitions for what a myoblast is, which leads me to conclude (without certainty) that a myosatellite is a myoblast. I have searched this specific question but of course nothing has come up. I am doing a research project on cultured meat, and all the sources I am using do not mention specifically or imply what a myoblast is. Wikipedia says that myosatellite cells differentiate into myoblasts, from what the definition of a myoblast is it doesn't really add up.

Why -- so that potential answerers know how much you already know about the topic. It gives them a place to start with their answer. See http://biology.stackexchange.com/help/how-to-ask

I see, thanks. I am not at university yet, so I am a beginner when it comes to research. I don't know much about muscle fibres at all, or stem cells.


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How does a bacterium age without cell division?
If somehow a bacterium, let's say E. coli, is engineered in such a way that it loses the formation of ftsZ ring (or other ways that inhibit cell division), and if other conditions are optimal for bacterial growth, then will the bacterium grow without cell division? If so, how long will it live? And how will it age?

what do you mean by bacterial growth without cell division? I didn't know that was even possible.

You need to be more specific about your definition of "growth". Many mycelial Actinobacteria   develop and replicate without undergoing cytokinesis for long periods of time, but they evetually break into separate cells. The strict classic definition of bacterial growth implies cell division.

Your question is a bit open-ended (of the kind "given an imaginary situation X, what will happen?") . Such questions attract answers that would be based on guesses and opinions rather than actual facts. If you add some more details then the question may become answerable.

If you post about bacteria, please be aware that the singular is bacterium and the plural bacteria. I appreciate this is not self-evident as it is Latin, not standard English, but it's not that hard. I've corrected it in your posting.

First of all, the growth of a bacterium is associated with an increase in cell biomass.So if a bacterium is restricted from replicating it does not grow. Coming to your later parts of the questions about how long will it live and will it age;
Yes, a bacterium would age irrespective of its ability to replicate.According to The Free radical hypothesis, all organisms age due to random deleterious events, oxidative damage by ROS produced during normal metabolism. It has also been found that cells undergo irreparable damage which can also lead to cell death eventually.
A complete review on bacterial ageing:
http://www.ias.ac.in/article/fulltext/reso/017/04/0347-0364


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PCR limits of detection calculate method
Is any standard method for use to gain PCR sensivity or limit of detection? my mean is not for RT-PCR or Real-Time or any other kind and just simple PCR. After making PCR product free of dNTP and Primers I have a microtube that contain 40ng/micro Liter dsDNA. My product size is 200bp. If I  should diluted it or any other standard acceptable method expain to me please.


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Do swarm of the same species attack each other?
What happens when two swarms find each other?
For example: When a swarm of bats, of the same species, go through another bat swarm. Do the bats attack one another or they simply merge into a bigger swarm?

Welcome to BiologySE - thanks for your question... you are actually asking several questions that may all be difficult to answer in one posting. You may want to try and narrow the focus at bit.

Look for the keywords agonistic behavior, ethology, swarm, group, flock, herd... https://sciencebasedlife.wordpress.com/2011/09/26/what-do-you-call-a-group-of/ Not sure how accurate it is, but seems interesting.

@VanceLAlbaugh I don't think the OP is asking several questions. It's one interesting question with different answers depending on the taxon. That's the kind of question that makes biology so interesting.

I'm sorry if I was unclear. My question was about swarms in general and how they interact with their same species swarms. And if one single animal of its kind joins the swarm if he is accepted or not.

It will depend on the species and group you're talking about. If the species is territorial, one swarm will tend to chase the other away. If it's a locust, they'll merge until they get to trillions of tons...
A study on wasps (Vespidae) I've read years ago showed an interesting experience. One individual wasp was tied by the waist and put close to different nests. The violence demonstrated by the nest was greater in a different species, median in the same species with a greater genetic distance, and none to her own or related nests.
Some "solitary" bees are very interesting in this respect, because they show many different kinds of sociality in related or even the same species, like many Halictidae and Euglossina (Apidae).


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What's the best sign language to teach a dolphin?
I know some scientists and trainers used hand signals to communicate with dolphins. The problem is: the dolphins have no hand to express themselves. With chimpanzees, we see how creative they are, not only in creating new words, but also in teaching their offspring without being told to do so (not sure if it was Jane Goodall who told that story in Through a Window).
So, what additional techniques could be used with cetaceans to really communicate with them?

I’m voting to close this question because it is vague and open-ended (encouraging opinions rather than fact-based answers). It also doesn't demonstrate the expected prior research.

In terms of training dolphins, it doesn't matter that they can't replicate a hand signal - just that they can learn to associate that visual stimuli with a behaviour.
For communicating with dolphins, one of the most common modalities is sound, either through playbacks of their own/conspecific sounds, or through synthetic sounds that aren't thought to be in their repertoire. Here is a review from Denise Herzing who has done a lot of this work on a wild dolphin population, with some reference to bird and primate work: https://www.animalbehaviorandcognition.org/uploads/journals/13/04.Nov2016-Herzing_HH(6)-final.pdf

That's a very interesting paper. Thank you!


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Plaque rupture flow chart reading
I am having a bit of trouble interpreting flow charts given in my biology question sets.
Given the following stimulus

The Question is :
In which of the following options does each substance play two different roles in the series of events from plaque ruprture to MI?

ADP and collagen
Collagen and Fibrinogen
Antithrombin III and collagen
Fibrinogen and antithrombin III

The answer is:
"Fibrinogen binds to the glycoprotein (GO) IIb/IIIa leading to the cross-linking of platelets. It is also converted into fibrin which stabilises these cross-links and leads to aggregation. Antithrombin III inhibits the activation of the coagulation cascade and also inhibits the production of thrombin. The answer is D.
My issue is:
This answer doesn't make sense to me.
The fibrinogen square connects to the "Cross links-platelets via GPIIb/III receptor" square, which THEN connects to the "Platelet cross-links stablised" square (i.e. "Fibrinogen" doesn't directly connected to "Platelet cross-links stablised").
Why does this count as "two different roles" yet e.g. "Exposure of collagen" connecting to "platelets adhere to collagen" which connects to "Platelet activation release of TXA2 and ADP" not count as "two different roles".

The given correct says fibrinogen has two roles. It links to itself, and it links to other proteins. These are two separate functions. The drawing makes it harder, but it still shows fibrinogen in two distinct places. You seem to have missed it under "thrombin".

I see. The arrow coming out of "converts fibrinogen to fibrin" is a bit faint and I missed it. Thanks for pointing that out, spent hours trying to figure it out.


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Creating a Phylogenetic tree using DNA sequences
I was wondering given DNA samples, how can we create a phylogenetic tree? I mean I don't even want to have actual DNA sequence. Can I generate small samples, like reads of a length 100 or 1000 of nucleotide chains and figure out how they are related.
Suppose we have two reads of DNA samples, for brevity let's have them really small like: AAAGGTCTTGA and ATAAAGTGTA. I can run the sequence alignment algorithm on the strings and I will get {"A", {"", "T"}, "AA", {"G", "A"}, "GT", {"C", "G"}, "T", {"TG",""}, "A"} So basically what alighns then where you have indels or substitutions. I can easily now write up a function that calculates how close are these two strings by giving positive weights for matches strong negative weights for indels, etc. Now I want to know if these two guys with really short DNA are related or no. What is the mathematical measure of relatedness? And after I do Multiple Sequence Alignments and get similar results how do I build a tree from it.

There's a lot of information about creating phylogenetic trees readily available online; e.g. http://evolution.berkeley.edu/evolibrary/article/phylogenetics_07 - can you add more specifically what you're having problems with?

I am looking for rigorous mathematical explanation of how to use multiple sequence alignment of DNA sequences to build a phylogenetic tree. I can find the algorithm anywhere, but exactly how you build a Dendrogram after receiving output from sequencing?

I'd recommend editing any additional details or clarification into the question. I still don't think this answers my question ("what you're having problems with") though - if you have the algorithm (and I'd include this in your question, or a source to it; you may be using the wrong one) then what specifically are you having problems with? If you apply your algorithm to some sample data, what happens?

Sorry, just noticed you're a new user - welcome to Biology.SE. I'd recommend taking the tour (http://biology.stackexchange.com/tour). Questions have to be specific and show what research you've already done, otherwise they won't get answered and may be closed.

Well, that doesn't answer your question of "what I am having trouble with",  because I'm not having trouble with anything except actually finding good sources on how one builds a tree. The link you initially sent was not rigorous enough. Anyway thanks for the welcome. I'll edit the question a bit to give some more info.

@arboviral Done.

This is where it started: http://link.springer.com/article/10.1007%2FBF01734359 presuming you have an aligned sequence to begin with.

There is no single mathematical measure of relatedness.
In the context of phylogeny, you need a model of evolution in order to be able to evaluate some relatedness between your strings of nucleotides. Then you would have various option for how to build a tree so that it reflects this relatedness. See for instance the wikipedia page about computational phylogenetics: https://en.wikipedia.org/wiki/Computational_phylogenetics.
Through what kind of historical process were your sequences generated ?
If there is no historical process underlying the generation of your sequences, then it is not meaningful to build a phylogeny with them. You can still define distances between them and use clustering techniques to build a tree, but that tree will not be a phylogeny.

Now I want to know if these two guys with really short DNA are related or no. What is the mathematical measure of relatedness

First of all this line of thought is dangerous, and creates a lot of room for misrepresentation, which have far reaching consequences when dealing with real DNA samples. Failed marriages are just one example.
Never infer phylogeny from short DNA sequences. You can read up on DNA fingerprinting here, which is used to infer ancestry and used in criminal prosecutions. But I think you already know about this.
Coming to inferring phylogeny on DNA samples where you have real DNA samples. For short sequences (upto 10kb, after that it becomes very time intensive), what you want is a Multiple sequence alignment such as Clustal Omega.
But the other procedure is to align entire genomes. Towards this end, you can check out this article from the UCSC team  on the creation of their phylogenetics track, with the multiz package, the how to is described here. This procedure is based on an existing evolutionary model as stated by @bli. Finally, these alignments were used to generate conservation scores for the template genome (hg18,hg19 etc. etc.) using phastcons. If you go here, you will find the various multiz alignments between different phylogenetic trees, with the pattern multiz*way. Similarly, the inferred conservation from the respective multiz alignments with the use of phastcons and phylop is provided with phastcons*way or phylop*way. The help page for phastcons is here and for Phylop is here


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Do RuBisCo and Haemoglobin have any similarity?
In RuBisCo and haemoglobin both can bind to CO2 as well as O2. Do these proteins have any structural similarity?

Why is this tagged "human-biology"? 2. Did you just wiki these proteins up?

No I was reading photosynthesis in NCERT where I found that RuBisCo also accepts CO2 and O2 and so the question came in my mind..!

I deleted "In plants" at the start of your question as there is no haemoglobin in plants. (There is leghaemoglobin, but, although structurally related, it’s not the same.)

Try reading about these proteins. Apart from wikipedia, you can check out pfam which classifies proteins into families. Globins and RuBisCO are very different protein families. Perhaps the only similarity is that both these are made up of amino acids!

Isn't Pfam classification a bit too advanced for someone reading grade 10 textbooks? :P

@KoustavPal No, I don't think it is that difficult (the summary page at least). Plus, RuBisCO is probably not introduced in 10th grade. I remember it was 11th. The question is a closure candidate on the grounds of "homework" without an effort. I didn't VTC because the OP is probably a highschooler.


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Identification of a small to mid-sized, yellow moth species found in India at monsoon season

I am from India and it's monsoon here. What is the name of this insect?
Description:

Length: ~4cm
Width: ~2.5cm
Color: yellow, almost uniform across the wings. Slightly darker, dandelion yellow across the body.
Small black dot in the middle of each large wing.
White, speckled iridescence on wings.
Short antennae.
Longer than average hair for moths.

I am confused between Porthesia Atereta and Yellow Tussock Moth

This is likely a member of the Nygmiini moths. The Nygmiini are a tribe of tussock moths of the subfamily Lymantriinae (formerly called the Lymantriidae) of the Erebidae family

This is likely a member of the Nygmiini moths. The Nygmiini are a tribe of tussock moths of the subfamily Lymantriinae (formerly called the Lymantriidae) of the Erebidae family
A specimen that closely resembles yours can be seen here, and copied below:

I have not found a definitive species for you, but will keep looking. I'd advise you try to do the same given this information.


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How to edit/insert new gene after cutting with CRISPR/cas9
I'm a student started who has started learning about CRISPR/Cas9. As I understand it, CRISPR/Cas9 is an enzyme that is used to cut a gene at a specific sequence.  I would like to know how scientist do the next step to insert/edit a genome.
For example, say I have an original sequence ...AAATTT... Is it possible for me to insert a new sequence into the middle so it becomes like this: ...AAAGCGCGCTTT... ? Or is it possible for me to edit a single nucleotide of the sequence like this : ...AACTTT... ?
How is a new sequence inserted at the cut region? Is there any enzyme required to make them join each other?  How is it ensured that the sequence is not inserted or joined at the wrong position ?

https://youtu.be/2pp17E4E-O8?t=1m50s

@Dale thank you for this video, i looked at the video but don't clearly understand, does it mean that the cut make a sticky end instead of blunt end and we need to design a sticky oligo so they can join each other?  And as i see on the video, no enzyme is required for joining them together. Can you explain more a bit?

@Dale As i known, to join 2 sticky end dna together, it seems that we need to use an enzyme called 'dna ligase', isn't it ?

Cas9 is used to create a double-stranded break (DSB) in genomic DNA. The cell can then use homology directed repair (HDR) to repair the break. The cell can also use non-homologous end joining (NHEJ) to repair DSBs, but this isn't useful for inserting specific sequences. In HDR, a sequence homologous to either side of the break site is used as a template so that the break can repaired error free. Naturally, the homologous template could be a homologous chromosome or replicated copy of the broken chromosome.
However, consider a situation where you introduce DNA into the cell with regions of homology to the break site and whatever other sequence(s) you wish to insert/delete/change. In this case, the break can be repaired using this exogenous DNA as a template and your changes will then be incorporated into the genome.
There are other methods of introducing site-specific DSBs to the genome, such as TALENs. The big advantage of CRISPR/Cas9 is that site recognition is performed by RNA rather than protein (it is much easier to synthesize small RNAs than to engineer large proteins).

While this answers covers all of the OP's points, it might be worth to point out a few more specifics. (i.e. which proteins are needed for HDR or the probability of successful target integration)

@Nicolai More detail is always good but, given the lack of interest in this question and answer, I'm not sure it's warranted. I encourage you to post your own answer or edit this one if you have more information to add.

There are multiple Cas9 proteins so much of the information is specific to a particular protein for the specifics.
Inserting genes in the point cleaved by CRISPR is definitely possible--of course this requires other proteins. Cells often contain those proteins, so complementary sequences on the ends of the insertion sequence is technically all that should be needed for insertion inside cells. There are many details to all this, but that is not what your question is asking about.
A single point mutation has recently been edited: however it was not inside a cell:
https://www.statnews.com/2016/04/20/clever-crispr-advance-unveiled/


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Olympic's epidemiological impact on Zika?
I've seen a lot of fear mongering, misinformation and overall general panic concerning the zika virus surrounding the Rio Olympics. However, little has been said about the actual epidemiological impact of these Olympics concerning zika.
I would assume that sending hundreds of thousands of people into this 'zika hotspot' and then having them return to their home countries will likely only accelerate the spread of this virus. I understand that Zika has been present in other tropical parts of the world for 50+ years, but the South American strain has had a higher incidence of more dire effects.
My question:
Has anyone actually modeled how these 2016 Olympics will impact (likely accelerate) the spread of this dangerous viral strain throughout the world?
I know the CDC and WHO have people working on this, but I haven't seen any direct reports or evidence of such work. I know it's difficult to create too accurate of a model due to the lack of knowledge about other mosquito species' abilities to become carriers, so I would assume that if a model does exist, it's likely just using Aedes species as the main vector.
Regardless, if anyone knows about epidemiological modeling being done about the Olympic's impact on the spread of zika, please provide some resources.

Though I have not found direct access to a model (which is what I'm really looking for), I have found evidence of such modeling efforts.
The CDC apparently put out a risk-assessment report in mid July discussing the results of such epidemiological modeling (reported by FivethirtyEight, ABC and others).
The report (available here), suggests that the risk of accelerated zika spread due to the 2016 Olympics is low.
They cite two major reasons:

Low mosquito activity due to colder winter weather

and more importantly....

The number of increased visits to the Olympics will make up only a fraction of the number of people that travel to/from zika-affected countries on a regular basis.

The estimated 350,000 to 500,000 international visitors and athletes
  from 207 countries who are expected to travel to Rio de Janeiro for
  the 2016 Olympic and Paralympic Games represent a tiny fraction --
  0.25 percent -- of total travel to and from Zika-affected countries,   according to the CDC report.

According to CDC director Tom Frieden:

"Compared with all travel to Zika-endemic areas, the Olympics account
  for about one-tenth of 1 percent of travel from the U.S. and globally
  about one-quarter of 1 percent, so even if Olympics didn’t exist,
  99.75 percent would be the same risk."

I will contact the CDC directly and ask for additional information regarding the model they used for this report. I will update this answer with any additional information I can gather. However, I'm sure others are producing similar models using different criteria, so please feel free to add additional examples or provide direct links to any available models.


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Figuring out if populations from two regions share the same Neanderthal haplotypes
I am going to preface this post in that I am not sure if it belongs here, but considering it has been ignored everywhere else I have tried I thought it is worth a shot. I am a graduate student who is still relatively new to bioinformatics and is currently utterly and completely lost.
I am studying Neanderthal ancestry in modern populations from two different regions of the world. These two regions have relatively similar levels of Neanderthal ancestry, and they aren't that far from each other. I have SNP data from an Affymetrix genotyping array (the data are in Plink format) for these populations as well as for the corresponding sites from Neanderthal and Denisovan genomes.
Using the SNP data, I need to try to find out if they have Neanderthal haplotypes in the same parts of their genome. I've found a map of putative Neanderthal introgressed haplotypes from 1000 Genomes Project's European and East Asian genomes (http://akeylab.gs.washington.edu/Vernot_2014/all_haplotypes_populations.bed.files.tgz).
I am trying to figure out where the individuals from each regions have Neanderthal haplotypes and how they differ between regions. Does anyone have guidance on how I could proceed?

What I am saying here is the way I would approach the problem. And as such this post is meant to give you some direction. Please do not hold me responsible if you do not get the expected results.
First off, I don't know how the Plink format works, you would do well if possible to convert that to a BED/GFF/GTF file somehow.
I looked up the file format, and most of your columns are significance scores. For a start I would use the BH FDR & p-value as a preliminary filter and later use the Bonferroni corrected p-value.
Wiki link to FDR
The wiki link should also give you an idea why I say later on move onto bonferroni.
Interesting questions asked on cross validated for FDR

Provides a vague idea on FDR
Provides a relation between p-value and FDR: Re-read the answer a few times and you'll get it.
Check out the books if you want some understanding of Statistics

Using the SNP data, I need to try to find out if they have Neanderthal haplotypes in the same parts of their genome. I've found a map of putative Neanderthal introgressed haplotypes from 1000 Genomes Project's European and East Asian genomes

I looked up the file, these are regions with an average span of 73.4kb across the entire genome. So what you want to do is map the "statistically significant" SNPs from your plink file to these regions.
If you don't know how, check out the UCSC genome browser. A detailed step by step would be too big an answer, but the overview goes something like this;

Choose your reference genome from assembly
Create two custom tracks, here you can upload your SNP data in bed format, which is the easiest to make. Link to format And add the existing haplotype population.bed file.
Go to intersection, to create an intersection between these two tracks.

This will give you an idea as to which of your haplotype regions are present in the population.
Ofcourse, it isn't that easy, because you have to make a consideration here. Do you choose to say the population is carrying that haplotype if a single SNP is present in a region which spans 73kb? That is more than the average size of a gene in Humans.
As far as the Neanderthal and Denisovan genomes are concerned. I would again point you to the UCSC genome browser where they have the Neanderthal and Denisovan assemblies and their corresponding variants mapped to the Human genome (assembly hg19). You can again get these files and see where the neanderthal/denisovan variants lie in the haplotype file using the same approach. Finally you can then use these two overlaps to find where your variants had mapped and if any ancient variants had mapped in the same region. You must also make consideration for Insertions and deletions within the genome, so the variants may not map at the same location but it will map nearby.
UPDATE

You can check out this link for retrieving allele frequencies from 1K genomes, for the overlapping variants. I never meant that you would use the bed files for finding allele frequencies. What I outlined is;

Use the haplotype population regions as a template and overlap your significant affy SNP variants on it.
Next, because the Neanderthal and Denisovan variants are mapped on the hg19 or hg18 assembly, you map back those variants to the same regions
Find the regions where an affy SNP and an ancient SNP exactly overlap

What I understand from your comment is, you have already done step one. And you want to know the allele frequencies for a particular ancient variant. You need to do step 2 and 3 before coming to allele frequencies.
Then you can look up the allele frequency of the variants which mapped exactly at a position which had an ancient variant in the 1K genome vcf files.

you can do it with awk....there's a lot of stackoverflow tutorials on awk processing...and you can google up awk as well

Check the Updates


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Help to identify this large, slow-growing mushroom?
Here in my backyard in Southern California, there appears to be this relatively smooth, mottled-colored dome-like structure a little larger than a chicken egg in the dirt. Can anyone identify it? Is it some sort of insect nest or a multicellular fungus?

Edit: After a couple weeks, I've observed some changes. It appears as though this is definitely a fungus and it has been growing taller out of the base. I also see a few feet away something that looks a little different, but not that different, which appeared even at first to be more mushroom-like. Right now the closest thing I could find online is something like a Shaggy Mane. Here are the new photos:

Edit #2: It's been about three more weeks, and the fungus has continued growing larger. Also I am pretty confident that the second one is also the same species. Both have been growing longer and have started to crack at the top.

It looks like a fungus to me. It might be some sort of stinkhorn, and in that case you should see it taking form (and smell) soon!

@picapica How are you concluding what it is? Can you give more information?

Hmm, I'm obviously not confident enough to post a proper answer. Just that it looks similar to mushrooms I've seen. Search for "stinkhorn egg" to see pictures of the early stage of the fruiting body. Unfortunately I don't see anything that looks just right. Have you tried poking it to see what texture it has?

@picapica I haven't, a little afraid to poke it.

understandable! but, nest or fungus, if you have it in your back yard you can keep an eye on it and see how it develops! i'm really curious, you must promise to keep us updated. another mushroom thought: perhaps some sort of puffball?

@picapica I'll see if it changes appearance. My brother told me that it is possible he remembers seeing it a few months ago, but I don't know for sure.

@picapica it still looks the same.

weird! hope you find out eventually...

@picapica OK it is clearly a fungus. The base has been growing longer.

Cool! Maybe you'll be able to answer your own question soon then. Or post pictures to make it easier for someone else to answer...

@picapica I'll probably add a picture. I think it looks a little like a shaggy mane mushroom, something like Coprinus comatus or Coprinus narcoticus.

This fungus is known as a puffball, although that is no longer a taxanomic order. Some of these fungi don't have small openings through which the spores disperse, but they burst open when the spores are ripe. This proces can be clearly seen in your last pictures. The brown stuff below the cracks are the spores. I think when you press it, the brown stuff will come out
Looking at the appearance, I think this is a Calvatia, but as I am unfamilair with the American fungi I can't name a species.

Is there anything else I should know about it? Should they be removed, are they edible? Does it vary?

It varies. Some are edible when young, but yours isn't any more. I see no reason to remove it.

OK thanks. But wouldn't leaving them cause more to grow?


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Is scalable growth the main reason why Darwinian systems select Fibonacci sequences?
The other day I was thinking about evolution of multi-cellular organisms, and why from the earliest onset of the development of communal cellular structure building, life may have selected a simplest possible strategy for building scale-able structures.
We humans employ relatively complex mathematics and measuring tapes to engineer structures, and we build them to full size, or modular so they assemble. We like proportionality, and there are strength and weight considerations associated with it, but we are not entirely ruled by these considerations. But it maybe that life is far more dependent on proportionality considerations. Life grows sequentially from a single cell, and each cell possesses both the building machinery, and what must be a relatively simple genetic program to govern growth. Because the generic programming operates on the basis of individual cells, there is conceivably a limit to the complexity of program you can expect life to be employing. And even if genetic coding is capable of tremendous complexity, life’s still going to select the simplest most effective approach. So how does lifes growth system achieve such consistently proportional results?
The answer may reveal itself, when you try to conceive of a building method that achieves the same outcome life does. That is to say, building a small scale structure, that will later scale up to full size through a growth cycle, and maintain a proportionality. If for example you build a small scale brick building, whereby the bricks can replicate and divide like living cells. Then so long as each brick does so at an overall synchronous rate, starts with select proportions and follows a very simple program governing growth that abides a proportionality which stays constant at all scales. Like the Fibonacci series rectangle does. Then the building can be scaled up through a smooth growth cycle while remaining structurally proportional. What you start with will determine your end result. And most importantly, having used a minimalistic coding system.
So what’s interesting, is that this is potentially a sound reasoning for why Fibonacci series emerges from such a fundamental level within Darwinian life. Life in the oceans subsisted as single celled organisms, but as soon as it started experimenting with multi-cellular structures, it needed to solve these issues of scale-able growth.
If this is correct, then it opens a fascinating window on a process of early life. Who knows what types of biological evolutionary insights might be derived from it.
Does this scenario sound plausible to more people than just me?

I didn't know there was something called theoretical biology! highly thought inducing!...I need to find some references for the answer in my head.

@KoustavPal I didnt know there was either. Here's a documentary which played a part in my realizing https://www.youtube.com/watch?v=h1qVloZKmdM

In any science there is theoretical side of this science. Theoreticians build hypotheses that can be tested. Theoretician also often build the necessary statistical tools. Btw, I am a theoretician

The question is very long and lack any kind of formatting. I am too lazy to read it. If you want people to make effort to read your questions, try to make them as appealing as possible. Also, by experience, long wordy question are often bad questions (but I can't tell for yours as I haven't read it but seeing expression like "Darwinian life" is not encouraging :)).

I have now read the question :) I still think it should be reduced in length. I know little to nothing in this field but it sounds worthwhile to me that you keep thinking about it! The fields of interest to you are system-biology and developmental-biology. You might want to have a look at plant mathematics: Fibonacci's flower.

TL;DR. There are some Markov processes that generate Fibonacci sequences. Perhaps that could be the reason why they are so common. I don't remember what exactly it was as I read this a while back in a relatively obscure (but good) book on Markov processes. And I lost that book unfortunately. I do remember that rabbit breeding was used as an example.

Okay. This is the book and it is not that obscure. I read an old edition which was in my university library.

I really wanted to put my thoughts into words as to why biological systems conform to Fibonacci's series.
What you say is entirely plausible and it does make sense. But what I wanted to address was why do these systems conform to it.
It is because of the interactions with the environment
Explaining this concept on multicellular organism first requires answering the same question in bacteria. Towards this end, I would like to point you towards this wiki page
It comes down to parameters such as medium concentration and hardness, parameters which we can influence. If we can extrapolate from this that cells, any cells will always follow a chemokine/nutrition gradient then we can start to understand why the system conforms to a fibonacci sequence.
Next, check out this video on a wound healing assay, what i would like to bring to your notice is that you'll find the cells replicate and move at the same rate.
If you follow a chemokine gradient, and move at approximately the same rate as your 2 billionth cousin, wouldn't you end up inevitably creating a symmetric structure?
Finally, I would, point you towards this article, where they explain a phenomenon called cell migration. This is particularly responsible for creating the symmetry which you see. And this is a similar article as the top one but it should be open access. Both support an idea which has been observed, I tried searching for the video but couldn't find it. The idea being that cells migrate collective, but there are some cells which are leaders and some followers. The leaders lead the collective migration (creating some sort of chemokine gradient) while the followers follow this gradient.
I attended a seminar last year by D Gilmour from EMBL. He showed us this particular video on collective cell migration and deposition of small clusters of cells which go on to establish the lateral line in zebrafish. You will find that a periodicity exists in this migration pattern. He relates it to a ligand activation. The related article to the video should be this one (I thought so after reading the abstract)

Thank you Koustav for your detailed answer. There's quite a bit here to think about, and follow up on. I'll go through everything you presented


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Formulation of Biomass reaction for metabolic model
What are some good review articles that could help me develop basic knowledge regarding biomass equation formulation?
I read this paper titled biomass objective function, but it only gives a general idea, and I'd like to learn more about the specifics of the process.

Please have a look at the tag wiki for reference-request. Your question should have all the details outlined in there. There is a book called Metabolic Engineering by Stephanopaulos et al.. That should give you some basic knowledge.

What precisely do you want to know? Are you interested in biomass composition for a particular cell type / experiment, or in the math involved? The paper you cite provides a good starting point for biotechnology applications I think. But for most organisms, there is little experimental data available on biomass composition.


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How did we get self-aware?
Imagine being under a lot of stone age people and you are the only one who thinks something like "Hey I am a human being, and now I am thinking about this and that and maybe I change myself to become a better person". You would see the world in a totally different way. No one would understand your behaviour because nobody thinks about himself (self-aware) or sees the world as you do.
So my question is: How did we get self-aware? how did we develop this "feature"? And why did we develop this, how could the nature think that this would be an advantage?
There has to be a small "jump".
I mean, somebody has to be the first who thought about himself. Either you know (or think about) that you are a being or you don't. So you can't just be a little self-aware right?

There is no scientific consensus on this. The very nature of consciousness / sentience / self-awareness has been debated for centuries but is still not well understood. Some people argue like you do that self-awareness is a "jump", while others think that it is gradual. See https://en.wikipedia.org/wiki/Consciousness  for some more information.

Agree with Roland. I just want to add that you assume a first, remarkable jump toward self-awarness but there is eventually a gradient of self-awarness (as you suggested in  the last line of your question) and the position in any individual on this gradient also depends on social experience. Note also that there is no reason to think that such feature had been under direct effect of selection but may have evolved as a correlated side effect of some other trait.

The use of the term "feature" instead of "trait" and "develop" instead of "evolve" made me thing that you might eventually want to follow an very short introductory course to evolutionary biology such as Understanding Evolution by UC Berkeley for example.

When talking about the evolution of self-awarness or other psychologic trait (evolutionary psychology), we often fall into a field where (1) empirical test of predictions are difficult to perform and (2) terms for which we have vague intuition need formal definition to be properly tackled and (2a) not everybody end up agreeing on a definition and (2b) there might not exist a natural category which corresponds closely enough to our vague intuitive understanding of a concept.

I think that through hunting all the time the ability of communication was more and more important. A failure of understanding could have ended in a disaster. Through communication they organised themselves and looked for the best way to hunt in group. Because of this they could have been thinking how to hunt better and, to work in a group the best way, how to be better in order to provide better understanding (social intelligence). Couldn't that be a possible way how this has evolved?