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Why do we have to exhale (or inhale) in order to speak?
Every time we speak, sing, or make any other kind of advanced noise with our throats, we exhale, or to put it that way, blow air through our throats. Why is this required? After all, speakers do not need any air blowing through them, they simply vibrate the air and create the vibrations (sounds) they're supposed to.
Why can't humans create (intelligible) sound just by having an organ that vibrates the air around us? Also, are there any animals that can? (None that I can think of at least). Would it be an evolutionary gain, or just rather pointless?
PS:
Obvoiusly we can clap out hands and the like, but that's not what I'm talking about.
Edit: The question is not about exhaling/inhaling, but rather why we need airflow in the first place; why we cannot use a mechanism similar to that of speakers.

Very similar to this but not quite a duplicate because I think this is asking about why the human voice box needs airflow to make sound, and why it isn't like a speaker.

Exactly. I know we can speak while inhaling (and sometimes I do it myself), but as you said: Why do we need airflow in the first place, why cannot we use a mechanism similar to that of speakers?

My guess is that is that our voice box is similar to a resonator. Our vocal chords provide vibrations at multiple frequencies and by adjusting our throat and mouth we change the resonant frequency and select the frequencies that are used to make voice. A simple speaker must be driven at whatever frequency you want, and while this is simple for electronics, it's probably harder for an evolved biological system. It was relatively simple to adapt the existing trachea for sound than to develop a biological speaker.

You can speak inhaling. It just sounds different.

As part of your question, you ask if other animals can create sound without continuous airflow. Many insects (e.g. cicadas and moths) do exactly this by using tymbals. A tymbal/timbal is an external membrane organ that is controlled by muscles or wing movements, that cause the membrane to flip back and forth, creating clicks or other sounds. So in many ways it produces sound in a similar way as loudspeakers, by creating sounds using a vibrating membrane.
One example can be found in this clip, which nicely shows how the organ functions:
Moth Making Sonar Jamming Sounds (youtube)
On this page (in Swedish) you can also listen to slowed-down butterfly sounds from four species.

Here is a list of woodwind instruments. Do you know of any (non-open) reed instrument that produces a note without anyone blowing air through them? Imagine a clarinet being played on someone's lap pouring out a melody. That would be very, very remarkable indeed.
Our ability to produce sound from our throats is in theory like a reed instrument  in music. Let's take the flute.
The flutist blows a rapid jet of air across the embouchure hole. In the flute, the air jet produces an oscillating (vibrating) component to the air flow. Once the air is vibrating, the energy is radiated as sound out of the end and any open holes. The column of air in the flute vibrates much more easily at some frequencies than at others (i.e. it resonates at certain frequencies). These resonances largely determine the playing frequency and thus the pitch, and the player in effect chooses the desired set of resonances by choosing a suitable combination of keys. (More on that here.)
Our vocal chords don't vibrate without the movement of air through them. They just tense and relax to different degrees. There is no sound made if you go through all the motions of saying yes but don't move any air. The moment you move even a small amount of air, you'll get a sound. Furthermore, vibration of the vocal chords is not enough for speech. The noise must go through a chamber where a particular noise will be made to change to resemble speech. Say ahhhhhh and touch the tip of your tongue to the roof of your mouth. The sound is changed significantly. Now, add your cheeks, lips, teeth, and pharynx all changing shapes and you have language.
Our voices are a wind instrument (not like an electronic speaker. For that, look to the electrolarynx). The air column moving across the vocal chords is the air jet. The vocal chords are what sets the air to vibrate. Our "mouth" (all of those I mentioned above" affect the vibrations to produce the desired sound. That's speech.

Would it be possible, and what would be the downsides/upsides of having a sound box functioning like a speaker, not a clarinette? Do we see any examples in the animal kingdom?

@Ludwik - that, to me, is a separate question. I did my best to answer it as written. ')

While appreciating your efforts, it seems to me the that I must have written badly. Re-reading my question, you're right, it does come across as a question about how our speech system works and why we need the airflow, but my intention was rather to ask why we didn't develop "speaker-like" speech boxes, and the upsides and downsides of that. On the other hand, I might ask that in a new question, if other people interpret my text the same way you did.

@Ludwik it is often hard to explain why something evolved one way and not another. But consider that when our far ancestors developed lungs for breathing air, they also got a windpipe with regular airflow. Transforming it into a wind instrument must have required minor changes, compared to evolving a new "speaker system" from scratch. So, we got our vocal chords because they were easy to get.


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Bee identification
Can anyone help identify this UK bee? The picture was taken in June 2016.
Doesn't have to be exact, really just want to know if it's a honey bee or a solitary bee.

Thanks.

When was the photo taken (time of year)?

@fileunderwater This week

It's useful info since species and/or sexes (males) can sometimes be eliminated based on flight time. Either way, its not a honey bee but a solitary bee. They have an orange band across the abdomen and they have a pollen basket on their hind tibia (scopa).

And I'm in the North East, if that helps.

BTW, if you'd use facebook the UK Bees, Wasps and Ants group by BWARS(  bees wasps and ants recording society) is focussed on questions like this and holds many experts.

I am sure it’s not a honey bee – the eyes are different. It could be a solitary bee of the genus Colletes. According to Wikipedia, their nests
... are lined with a cellophane-like plastic secretion, a true polyester, earning them the nickname polyester bees.

+1 for introducing me to 'polyester bees' - how have I never heard of these before?

Thanks.  There seems to be a few of them going into my walls.  Any idea if it's something I should be worried about?

You are right this is not a honey bee, but I doubt it to be a Colletes. It lacks the stripes at the abdomen and the abdomen is hairy. I think is is Osmia rufa, see my answer for details.

It is indeed not a honey bee, but I don't think it belonges to the genus Colletes. They have a striped, not hairy body. The bee shown seems to have stripes but these are hair bands. I think this is a Mason bee, Osmia rufa (=bicornis). Osmia rufa is one of the most common bees in Northwestern Europe.
Osmia rufa uses holes to lay eggs with some pollen and then closes the hole, usually with clay or loam, hence the name Mason bee. It is probably looking for nesting space. But they live solitary so every nest will give only a handfull of bees next year. They are completely harmless, will not defend their nest. I have them in my garden a lot. Don't worry but enjoy them!

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Why do Sorghum Bicolor leaves roll up?
In A level Bio today we talked about abcesic acid as a stress hormone, and its ability to reduce osmotic potential around guard cells to close stomata.
My question is, is abscesic acid in sorghum bicolor leaves responsible for its ability to roll up in lack of water?

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Choosing appropriate statistical test for ordinal data
Ordinal response variables show up often in biology, but I'm not sure how they are best analysed. Some examples are qualitative assessments (little, many, a lot) or risk assessments (low risk, medium risk, high risk).
My study is about correlation between pain and depression levels. We are measuring pain on an ordinal Likert scale. This is a number scale running from 10 (severe pain) to 0 (no pain).
We will also measure depression on a similar scale (scale: 4 - 0).
What statistical test should I use?

This is perhaps better suited to math SE.

@canadianer This isn't suited to Math.SE, but Cross Validated (http://stats.stackexchange.com/)

This is suited I think, as Likert scales are (ab)used often in biomedical research.

@ChrisStronks the question is not about biology but the application of a statistical method. Your answer is excellent and would make a great addition to Cross Validated but I believe it is off-topic here.

@Luigi No wonder I couldn't find a statistics SE…

Mann-Whitney U test. (?)

I think this question could be useful to have on the site, since this issue can come up in many biological fields. It is clearly on-topic at stats.stackexchange.com as well, but this does not necessarily mean that it's off-topic here. The choice of methods/assumptions can also interact with the biological process you are trying to model, which is why I think it's on-topic here as well. If questions such as this one is closed, I think we need to close many of the other questions using the statistics tag for fairness.

Could do with information about the experimental design, whether it is a balanced design, sample sizes, and normality of the distributions, and hypotheses.

You can use ordinal multinomial regression (also known as ordered logit) if the response is ordered. These methods are basically extensions of logistic regressions, but using e.g. a cumulative logit instead of the logit. However, there are a number of different assumptions you need to consider. For instance, are you going to use a proportional-odds assumption (which is commonly used), which means that there is an equal probability of going from e.g. class 1 -> 2 and class 5 -> 6? You can also evaluate the proportional odds assumption using plots or a score test. If the response cannot be ordered, there are multinomial nominal methods that you can use, and you can also evaluate the results from an ordered analysis by comparing the predictions with ones from a multinomial nominal analysis. I have used these kinds of methods for the analysis is Red list classifications, which are clearly ordered but cannot simply be transformed into a numerical response (similar to your situation).
The book Analysis of Ordinal Categorical Data (Agresti. 2010) is a really good starting point.
In R you can look at the packages polr and vgam for ways to perform different types of analyses on ordinal data. The author of the book above has also published some examples for categorical data analysis in R, using the packages I mentioned: Examples of Using R for Modeling Ordinal Data. In SAS similar analyses can be done using Proc Genmod and Proc Logistic.

The testing of an ordinal scale requires non-parametric statistical tests. Mean and standard deviation are invalid parameters for descriptive statistics whenever data are on ordinal scales, as are any parametric analyses based on the normal distribution.
The report of Allen & Seaman, 2007 describes a number of possible tests:
Nonparametric procedures—based on the rank, median or range—are appropriate for analyzing these data, as are chi-squared statistics.
Notably, Kruskall-Wallis models can be used to replace a standard parametric analysis of variance, as it is based on the ranks and not the means of the responses. Given these scales are representative of an underlying continuous measure, one recommendation is to analyze them as interval data as a pilot prior to gathering the continuous measure.
However, non-parametric tests are notoriously low in statistical power. There is a way of making an ordinal Likert scale like the ones you use continuous by using a ruler or slider, see the following figure (taken from Allen & Seaman, 2007):

This trick makes it continuous and normal parametric tests can be used, ramping up statistical power substantially. It is a lot more work though to analyze the data. Especially when the subjects indicate their perceived pain/depression by physically putting a mark on a paper ruler, as you have to manually measure the responses. A digital slider can make your life easier. If you are planning to do hundreds of subjects you should carefully think about the possible options.
Good luck!

There are parametric tests for ordinal response variables, which are basically extentions of logistic regressions.


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What species is this black, blue and white bird?
I think this species is native to Edmonton, Alberta, Canada, as I see it regularly, especially around the urban locality (Downtown Edmonton).
Season: Early Spring
Date: May 18, 2017
Basic Description: Medium sized bird, and I was not able to observe a characteristic chirp from the bird while I was taking a photograph. Most distinctive feature is the bright royal bluish gradient on the tail and tips of the wings.

If you were in the UK, you'd now have to say "Good morning Mr Magpie. How is your lady wife today?". It's practically a law.

I once took some pictures of this bird while in Africa (in Zaire, as it  was called then.) The onlookers laughed at me (quietly and affebly). It was so common in Zaire it would be like someone marveling at a pigeon in NYC. Good memory, thanks.

That bird is commonly called a magpie. The only species found in Alberta is Pica hudsonia. You can see a reference image on the left and their distribution throughout Canada on the right:

[source]
Interestingly, it is one of the only non-mammals studied that is able to recognize itself in a mirror. In fact, these and other corvids are thought to be some of the most intelligent species on Earth.
You mentioned that you didn't hear them chirp. These birds are actually quite loud and about fifty of them used to wake me up every morning. Have a listen (not my video).

Your attached video makes me realize how lucky I am to not have heard the bird chirp.

@ImtiazRaqib Ha! Just imagine 50 of them on your roof at 6 am ;)

A species-id question with no research effort again. :)

It's clearly a magpie, a member of the crow family (Corvidae). There are many magpie species throughout the world, but since you say it's native to Canada, it must be the black-billed magpie (Pica hudsonia). There are only two magpie species native to Northern America, the other being the yellow-billed magpie (Pica nuttalli), occuring in California.

Image source:
http://www.audubon.org/field-guide/bird/black-billed-magpie

Finally one of these silly questions I could answer and you beat me to it!


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What do you call clearly different sub-groups within a species?
If you look at species of bees and ants, you can clearly see there are drastically different specialized ants, like queen ants and workers. They're both part of the same species, yet are still obviously different. What is the proper name for that phenomena?

Just to clarify; you are asking specifically about non-taxonomic groupings right, e.g. functional or behavioural groups/phenotypes within species?

Right, specifically the physical/behavioral differences within one species.

also allotype

In eusocial insects, especially ants and bees, these groups are called "castes" (see e.g. Hölldobler & Wilson, 1990. This is the same term that is used for social stratifications in some human societies e.g. in India.
One definition of caste is:

...the physical or the behavioural/physiological phenotype of a eusocial individual, or both.

(from Hölldobler & Wilson, see also antwiki.org)
Some division of labour as well as collective rearing of young can occur in prosocial animals as well, but there the term caste is not used.

Is it really just as simple as alleles which accounts for castes like honeypot ants?

@JohnJoe In ants, the traditional view is that the worker-queen determination is largely due to nutrition/environment, but some studies also show a clear genetic component. Males/drones are determined by being haploid, so that is a separate issue.

@JohnJoe Just to clarify, there is infinitely many possible ways to define sub-groups within species. The term "castes" is not a general term, it is a term that applies to the specific subgroups you describe in eusocial insects. For other types of subgroups different words may exist such as subspecies, subpopulation, family. One could decide to make any kind of arbitrary grouping such as considering the set of all individuals that went to the woodstock festival for example. There is of course no general term to refer to any kind of subgroup, other than just subgroup.

The difference here is that these individual castes have the capacity to reproduce as part of the same species, whereas this can't happen between other generalized groups.

Or not. Typically there are only two castes which are fertile.

Which still result from the reproduction of castes within the same species.


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Development threshold of a blowfly species differ depending on situation?
Within a species, does the lower development temperature threshold remain the same in all situations (also known as the development zero temperature)? For example, would the temperature threshold be the same for larvae grown on small carcasses compared to large carcasses? e.g. mouse carcass compared to human/pig carcass.

Are you talking about minimum developmental time when you write "lower development threshold"? To me, it is unclear what the threshold is referring to.

@fileunderwater I am referring to the lower development threshold, t, expressed in the equation D(T-t) = k, and also known as the development zero temperature.


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Help me identify this insect found in fishtank

This bug appeared in my fish tank,transparent 6 legged with 3 tail insect. Anyone able to identfy this, please help. Many thanks

Please add some more images, including a better close-up, some morphological details, your location, etc.

This is a Damselfly, suborder Zygoptera. Together with the Anisoptera (true dragonflies) they belong to the order Odonata, usually also named dragonflies.
Damselflies are smaller and more slender then Dragonflies, both as larva and as adult, although there are exceptions (mostly tropical species).
It can be distinguished from mayflies by it's broad head and the broad, flat lamellae; the 3 'tails' as you call them.
Some beautiful pictures can be found here


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Help identifying an insect (I think it was an insect)
While I realize this may be difficult without a photo, I'm hoping someone can say "This is a list of possible species given your location and description" and I can attempt to find a photo that matches from there.
I'm in NE Indiana. I think it was an insect. The species in question looked a bit like a leech, black and shiny but wasn't segmented and it was a bit flattened out (but not entirely), maybe an inch long. It wasn't tapered. Also I don't believe it made any attempt to bite me (or just wasn't around long enough to). Unfortunately it startled me so I smashed it pretty quickly so I didn't get a picture, but I got a good look and couldn't identify any legs, eyes, antennae. It moved fairly quickly, almost in a pulsating motion.
When I smashed it, there was only a bit of white, mealy paste left behind, the body almost seemed to liquefy.
If it hadn't moved so quickly and wasn't so small I'd have thought it was a baby slug. It's possible it could have been some sort of larvae.
I also don't think it was a leech because I found it on my body but I was in my home and can't think where I could have been that would have exposed me to one. I noticed it when after removing my shirt and lying in bed. So it was either inside my shirt for several hours without me noticing, fell out from the covers when I got in bed, or fell from somewhere after I got in bed.

This is not easy to answer without a picture. However, if it was unsegmented, it was definitely not an insect (which have a segmented body plan, both as larvae/nymph and adult). Your description also sounds nothing like an insect. However, the overall description fits fairly well with a flatworm (Phyluym: Plathelminthes), see e.g. Geoplanidae. They can resemble slugs or leeches, but both lack segmentation and antenna. Finding one inside your house sounds a bit strange though, as they generally prefer moist habitats.
Terrestial flatworms are relatively mobile and most are predators or scavengers
Example pictures:

Okay that makes sense. Looking at images, it looked similar to Microplana terrestris or Rhynchodemus sylvaticus But I'm not sure on the range/size of these species or the probability of encountering them in the home.

It was raining outside, is it at all possible it fell onto my clothing from some surface while outside and I just didn't notice until later, or are these likely to be low to the ground?

The terrestial species in Geoplanidae are quite mobile, so you might well have picked it up outside. Most species in Plathelminthes are however marine or parasites.

I would say the bottom picture you provided look almost exactly as I remember it, with the exception of the sliminess. Could it have just been drying out?

@PatrickSchomburg That is definitely possible. I'm not familiar with US flatworms personally though.


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Isn't sexy son hypothesis circular?
Sexy son hypothesis.
It states that females are attracted to certain traits in males, because these traits will be attractive in her sons either. But isn't this circular?
Like "I'm attracted to that male because he is the son of an [formerly] attractive male". And you can repeat the process infinitely, going through granddad, great-granddad and so on. Doesn't this hypothesis presuppose some sexy traits that are sexy with no cause?

It's never only one single factor that influences reproduction. "Sexiness" can play a big role in some species, but other factors have a role as well. Also, it is perfectly possible that a factor that has a big role in the present, could have had a very minor role in the past.

@alec_djinn I believe in good genes hypothesis and that attractive traits signalize an individual who has greater chances of reproduction taken his attraction per se out. But it's not what sexy son hypothesis is about.

@rus9384 I think this is clear from the other answers, but "attractive traits signalize an individual who has greater chances of reproduction" could mean traits that mostly improve survival or fecundity (the 'good genes' hypothesis) but it could also mean traits that mostly improve reproduction success (i.e., chance, especially for a male, to successfully mate: 'sexy son'). It's important to remember that fitness is not just about survival, it's about reproduction.

@BryanKrause But sexy son hypothesis is then an addendum to the good genes one?

@rus9384 I think you could view it as that, or look at it the other way around and consider good genes to be an addendum to sexy sons. It's likely that specific case examples will be better described by the particulars of one or the other but I don't see any way that they are incompatible.

@BryanKrause But the point is that, certain features are seen as attractive because they signified greater fitness. And that fitness was not solely to being attractive, because then it again reduces to "these features are attractive because they were attractive". But we know some features could not always be attractive since they were non-existent some time before.

The process is self-reinforcing but the argument is not circular (no tautology implied).
As soon as some male traits are considered more sexy than others, then there is selection for females to like those traits even more, which causes those traits to raise in frequency, which increases the selection for liking these traits. In other words, in this model, the state where there are no sexy traits in males is an unstable equilibrium.

"As soon as some male traits are considered more sexy than others" And they are in the first place because they signalize (maybe formerly) good genes? But I agree mostly there is a double selection for traits in species with sexual reproduction. Sexual selection is just a layer above non-sexual selection.

@rus9384 they don't have to signal good genes they jut need to draw the females attention, A problem bird researches have is it turns out many female birds prefer males with sexy colorful plastic bands around their legs. Something that just happens to draw a females attention is beneficial in and of itself.

@John Well, female birds prefer those male birds who are more noticeable, because even before that preference has developed in them more noticeable male birds had more offsprings. Why? Whom does the female bird notice first? That one male she chooses. Of course then those females who had a preference towards such males actually had an advantage: their male offsprings could have more offsprings. I already though about that about a year ago.

@rus9384 Could you please to a reference for the claim that female birds like "more noticeable" male birds? I have already heard something along these lines but I would love to see a reference.

@Remi.b I'd wish to provide a reference but this one idea is the one I came up by myself. Sure, I'm not the first.

Taken by itself I can agree that it might seem circular. However, in practice, all traits act and occur in a pre-existing background, i.e. in organisms with their genetic background and their living environment. All that is needed is a preexisting difference in fitness (for instance connected to the related good-genes hypothesis), that a new gene for female preference of sexy traits can act on. Then the process can become self-reinforcing. The major difference between the sexy sons hypothesis and the good genes hypothesis lies in whether the traits signal increased chance of mating for future sons or if they signal higher quality/viability of offspring (see e.g. Huk & Winkel 2008). My point is that traits that first signaled the latter (quality) can later signal the former (sexiness/mating chance).

Well, good genes hypothesis is an intuitive one. With one amendment though: those traits which displayed greater fitness in the past (a few tens or hundred generations ago) appear attractive now. But sexy son hypothesis does not add anything to it. Also "higher quality/viability of offspring" contains "increased chance of mating".

@rus9384 Yes, that is my point, that past viability effects of offspring is probably often the original trait that might later get caught up in runaway sexual selection due to sexy son. I agree that higher viability of offspring usually leads to increased chance for mating (unless there is a negative tradeoff between viability and "attractiveness"/display traits), but the opposite doesn't have to hold. You can have "increased chance of mating" without "higher quality/viability of offspring".

Consider the difference between "vanilla" natural selection and sexual selection.
On paper sexual selection sounds strange; while straightforward selection says that a trait spreads because it makes an individual better at life meaning they'll have more descendants, sexual selection says that a trait spreads because it makes an individual attractive to potential mates, resulting in more descendants sure but it suggests that "being better at life" isn't required. And indeed sexual selection is often used to explain traits that make an individual worse at life, like the peacock's tail.
What's going on is that there is a first-order and a second-order process of causality, that are related but distinct. Say for instance you have a trait that makes your offspring 10% fitter. Awesome, they'll be 10% fitter. Except that this means the offspring of your mate will also be 10% fitter... which means other individuals have an incentive to be your mate, meaning you can get a better mate who will also give fitter offspring, so actually you might end up with offspring that are 50% fitter. The latter process is sexual selection, and while it's dependent on the first process to happen in the scenario I described, the causality, mechanics and results are different. You can have one without the other; for example if a trait makes you 10% fitter but this is completely undetectable to anybody else, they won't be able to select you as a mate on the basis of it so you won't have sexual selection. On the other hand sexual selection can indeed in theory function with something that doesn't improve fitness on the first order.
You can see the sexy son hypothesis as a third-order distinct process. It's not just that you have an incentive to mate with a person because your offspring will be fitter; there is an additional incentive involved in the fact your offspring will also be more attractive. This isn't a tautology because it isn't a foreordained conclusion; for example if you have a "love red hair" gene but nobody else does then you'll pick a redheaded mate on the basis of their sexiness, but your sons won't be sexier for it. On the other hand if everyone except you has the "love red hair" gene, you have an incentive to get a redheaded mate even though you yourself don't find them sexy (or not for the same reason everyone else does at least).
This process certainly allows for sexiness to have no fitness-based cause but it doesn't presuppose it; indeed one would expect for there to have been a fitness-based cause at the beginning of the chain if not at the end.

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What species of spider is this, living in India?

Found in India during summers in not humid, just very hot weather.
Please tell me what species it is, what it eats and how to care for it?

Please [edit] to include location, size, and other useful info.

We can deduce from the abdomen pattern that it is a Housefly Catcher of the genus Plexippus
The location further aids in narrowing down the exact species as their is only one spider in the area that is of the genus Plexippus. And that is the Pantropical Jumping Spider (Plexippus paykulli).

Plexippus paykulli is a species of jumping spider. It is native to south east Asia but has spread to other parts of the world and globe. In the United States it is called the pantropical jumping spider. It is usually associated with buildings and may be found near light sources catching insects attracted by the light. It is named in honor of Gustaf von Paykull. Source: https://wikipedia.org

Image reference: https://www.inaturalist.org/photos/294156075, Photo 294156075, (c) John Sim, some rights reserved (CC BY-NC), uploaded by John Sim


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Is the golden ratio of anatomic measurements universally beneficial for sexual reproduction?
It is often claimed, in popular media, that the golden ratio (Fibonacci series) in for example some face measurements is aesthetically (and hence reproductively) attractive with respect to the humans. I wonder if this is particular for today's (maybe since 10,000's of years or so) human anatomy and aesthetics. As in an after-the-fact acquired taste which was culturally psychologically emerged from the actual human ratios of anatomy as it has happened to evolve for whatever practical reasons, way out of intuitive comprehension for human consciousness. Or if it is deeply biological and evolutionary across all lifeforms.
Is the golden ratio as verifiable (if at all) also for the primates who came before us? Some examples are easy to find, but how statistically significant is the golden ratio as an advantage for sexual evolution for non-humans?

Interesting question. However, I'd consider removing the subjective sections in your second paragraph, as the question is not really about what you individually find attractive but what the pool of reproductively capable peers find desirable in a mate.

This question seems fairly opinion-based

Perhaps Cognitive Sciences is more receptive to this kind of flavor of questions.

@AliceD I'm actually interested in the anatomy of animals here. If anatomies in general somehow follow the golden ratio, it would indicate that animal minds do too.

I have some insight into this from an engineering perspective. Years ago, I worked on some computational and search algorithms which used a growth factor to determine how far to widen a search space, or how much more memory to allocate. For some of these algorithms, I ran a series of random trials to search for an optimal growth factor and found that for some, that optimal factor approached 1.618. Completely outside the realm of biology, this golden mean popped up as the most efficient growth factor for some of my algorithms.
Over the years since then, I have recognized that this is an optimal factor for various engineering problems (although in practice I often find it more trouble than it's worth to explain to colleagues why they want to use it). So, I have gradually come to believe that this is why we see this ratio all over nature, in the way seashells grow, the proportions of various body parts, the arrangement of seed structures, etc. It appears that natural processes have ultimately led various lifeforms all over our world to tend toward this ratio to optimize their own functions.
The fact that we find this ratio "beautiful" is a far more fascinating study of what appears to be a meta-adaptation. Consider all of the various ways that the recognition of this ratio is important beyond just sexual reproduction. When we select our food, choosing vegetable or meat specimens which exhibit this ratio most perfectly is more likely to lead us to the healthiest food. Choosing to take shelter under the more "beautiful" tree may also be a good bet that it is the more stable, healthy tree. Making tools, clothing, or structures with this ratio may serendipitously lead us to better formed products. We don't have to find this ratio more beautiful to look at, but because we do, it leads us to better choices in a variety of odd ways. So, those of us whose brains appreciate these things thrive a little more.
Your question was not about underlying causes, but about statistical prevalence. I don't know the answer to that. And I think it would be very difficult to obtain those numbers accurately for another loosely related reason. The human brain is very attuned to finding patterns, and the human brain likes to find this ratio. Taken together, this presents a huge bias for any researcher trying to objectively measure the frequency of this ratio in nature.
However, once we understand that this ratio is the solution to a variety of engineering problems, it becomes clear that it is an indicator of optimization, or proximity to perfection. And even if we cannot say how many species are able to recognize, appreciate, and seek after this ratio, we can say that those who do will most likely find it a beneficial adaptation.

Are those who don't "find this pattern" really less successful?  Our brains do like to find this particular ratio pattern (imagination maybe). Me, I do care. But I wonder if my dog cares about it. If my dog's loved one, which it has only sniffed and never seen, has a Fibonacci nose length to leg length or something. Maybe I'll subject my best friend to some experiments... However I know that it would cheat, just like I would. Could the Golden Ratio be a human cultural construction without relevance to common natural structures?

@LocalFluff Relevance to common natural structures is precisely what I'm trying to demonstrate here. If this number turns up as an optimal growth factor in a context in which the ratio itself is not the target at all, per se, then it certainly carries meaning independent of the observer. The algorithms preferred it. In most contexts, our own preferences muddy the observation, but in this case, I would consider it an objective finding. And if it is objectively useful, then the ability to recognize it must be beneficial (provided said ability does not cost the organism more than it's worth).


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What has caused life to choose this unfathomably tiny subset of all possible proteins?
I wonder why life uses the particular proteins that it does, about 10^6 different proteins, I think? Evolution cannot explain it because the number of possible proteins is far far too large to ever come into existence anywhere in the visible universe, let alone on Earth. And evolutionary selection only works on stuff that exists.
Is there some chemical or other explanation, or is this an unresolved paradox in biology?
The median number of amino acids in a human protein is 375. Most are longer than 200 and maybe all are longer than 100. The 20 different kinds of amino acids can be combined to 20^375 = 10^487 different proteins which have the length 375.
If the entire crust of the Earth consisted of proteins which all were 375 long and each protein mutated once every nanosecond during 5 billion years and each mutation resulted in a protein which is unique in time and space, and there exists 100 such "protein Earths" around every star and 1000 billion stars in each of 1000 billion galaxies in the visible universe, it still only adds up to something like 10^100 proteins. Adding 10^37 years until the last star remnant has cooled down to less than 1 Kelvin, doesn't change this picture, almost all of the possible proteins will literally never exist anywhere. Even if I'm off by a factor a million on each of those numbers, only one in 10^300 of all possible median length proteins could ever exist.
Since our mind-bendingly small subset of possible proteins supports life, shouldn't we expect that many many (as in 10^300) other potential subsets of different proteins would do so too? And can we conclude that if DNA/protein based life has originated somewhere else, it will not have even one single protein in common with us or with any other independent origin of life? Or is this focus on proteins somehow invalid?

Sentences "...evolutionary selection only works on stuff that exists." and
"What has caused life to choose this..." Look like "Life suddenly started to use arbitrary set of proteins, like guy who buys some tools in nigh-infinite shop" and it's not true - it has everything to do with evolution.

@Mithoron If mutations are random, then the median protein can mutate to 10^487 different new proteins. Less than one in 10^300 will ever happen anywhere, and still that works fine for life! Maybe 10^200 other mutations would have worked fine too? Or are we that lucky? Evolution has nothing to do with selecting proteins which never exist. Evolution only kicks in given this ridiculously small subset. I wonder if any known mechanism can explain this selection of protein varieties.

This question is a bit like shuffling a deck of cards and asking why they ended up in that particular order. They just are by chance.

@CactusWoman And having to conclude either that you got a one-in-a-10^100 straight flush, or that almost any hand given would have been as good. Doesn't matter much how proteins mutate, they will cause life anyway.

@LocalFluff Proteins don't mutate. Genes mutate. Individuals are selected. Species evolve. Even when genes mutate they could not do so every nanosecond. The phenomenally large amount of radiation that could cause every gene on earth to mutate every nanosecond--I've got that correct? That is akin to your gedanken experiment?--would obliterate life on earth in less than a second. No life, no endless pool of 375 amino acid long proteins. When we say that there are 10^6 different protein sequences on the planet--is that your assertion(?)--that is misleading, they don't have 10^6 functions.

"Maybe 10^200 other mutations would have worked fine too?" Yes they would have. Luisi (I strongly suggest you to ree his work if you are really interested in this topic) made a good point on that. There are plenty of studies showing that purely random proteins have high probability of having function, it turned out, for example, that for a given environment (buffer condition), a consistent percentage of random protein will collapse into a folded structure and have some biochemical reactivity.

The answer is chance or, even better, contingency.
About your calculations, it is true that the theoretical sequences are almost unlimited, but the basic scaffolds are not. Very different sequences can fold into the same basic scaffold and have a similar reactivity/function. So, even if not all the sequences have been explored on this planet, most of the scaffolds and functionalities have been. It is true that protein-based life could be evolved somewhere else, and it is true that the overall sequence space evolved somewhere else would be different from the one evolved on this planet. However, I would expect to find almost the same palette of biochemical reactions that we have discovered on our proteins.
I would suggest reading the work of P.L. Luisi here. He makes really good points on this issue.

+1 for the sequence - scaffold comparison. Good insight,

That is not a logical answer. Evolution has no relation to which "scaffolding" would be optimal, since evolution never ever can test and select any protein which is better than 10^100 or so times worse the actual theoretical optimum, for a protein which exactly consists of a medium number of amino acids. "Chance" is not the answer. "Chance" is precisely what is utterly defeated by these grotesque monster numbers!

Evolution doesn't know indeed which scaffold will be optimal and it will never try all the possibilities, but this is not the point. My point is, that given an infinite number of sequences you do not end up with an infinite number of functions nor domains. Most of the infinite sequences will fold in few main scaffolds, with more or less the same shape and will end up having very similar biological functions.

Let's consider a very easy protein to make an example, the GFP. The only function it has is to be fluorescent. Many variants of this fluorescent protein are known, all with a different sequence. The sequence may vary a lot, however all the proteins ends up having the same main structure and function. Now, all the variants differ for absorption/emission spectrum and for stability under different conditions. These factors will be selected by evolution but it will depend from case to case whether  a red fluorescent protein will be more advantageous of a green one for example.

Will all the fluorescent protein variants be tested by evolution on our planet? Nope! Does exist a better, more stable and more efficient GFP in the universe? Probably. So the "optimal" you refer to is always a local optimal, local in time and in space, i.e. that particular protein have an advantage now, in that environment and for that organism and it will not be the best solution ever anyway. That is the contingency! and it is mostly governed by chance... That is what evolution is about.

I'm not sure I understand the question. You've elegantly demonstrated that only a tiny fraction of all protein sequences could possibly exist, but then asked why only a tiny fraction of all protein sequences do exist. Your conclusions about independent origins of life having no proteins in common are accurate, but also consider that you as a human being have not even a single protein in common with the bacteria in your yogurt (I mean you do, but they have slightly different sequences).
As far as which protein subsets make life, there are demonstrably thousands of sets of proteins that support life. Each genetically distinct individual has a slightly different set of proteins, most of which support life.
As far as how many of these subsets exist, that's unknown. Maybe aliens use only ribozymes based on RNA molecules. Maybe they have a different set of amino acids, or a silicon backbone to their proteins, or what have you. Until we find alien life(or perfect abiogenesis in the lab) the total diversity of life-like things is unknowable.

I thought all life on Earth shared some genes, even me and the bacterial yogurt I eat at breakfast. But maybe none of that is expressed as proteins? And is it really "demonstrable" that thousands of sets of proteins support life? And what has "thousands" got to do with the orders of magnitude involved here? This is not about thousands, it's about one in a trillion of a trillion of a trillion of a trillion of a trillion of a trillion of a trillion of a trillion of a trillion. At the very least. For the median length protein which keeps you and me alive and happy.

again, it is not the sequence that matter in this case but the "protein domain". To make an easy analogy, think about a car, has 4 wheels and an engine and have one main function. Now you can think of trillion trillion trillion different cars, each of a different colour, a different shape, a different size, different setups... do the math and you will find that the numbers are huge. However the function will be always more or less the same. So in other planets, with other combinations of pieces, always the same kind of machines will arise. Proteins are molecular machines.

You and a yogurt share many genes, but the sequences are not identical. Metaphorically you both have a steering wheel but it is a different steering wheel. Maybe slightly smaller or with a leather inset or whatever. Does the same thing but isn't identical.

@alec_djinn Are you sure that all 'life' has precisely the same set of molecular functions? 'RNA world' life would be similar to life that we recognize, but the vast majority of the proteins would have completely different functions, or not be proteins at all. 'RNA world' life is also the most similar to familiar life we can conceive of, and there's a statistical certainty alien life would be more alien than we can conceive of. 'The same kind of machines' needn't necessarily arise.

@ Resonating Well, if we talk about "chemistry based life" then yes. Whatever set of molecules you choose, there will be common problems to solve to have life, like how to store information, get energy flow running etc... In a molecular scenario these problems are solved by coupling chemical reactions (oxidations, reductions, bonds formation etc...) in larger pathways. If those pathways are catalyzed by proteins, nucleic acids or other molecules it doesn't matter and may vary from life form to life form. Don't you think?

You ask why living things use the proteins they use, and not something different.
It's mainly because they must do something that works, and they have found something that works OK.
Each protein serves one or more functions for its cell. If it changes at random, probably it will change into something which does those functions less well. Because it has been selected for thousands of generations to get something that works well, and so most of the alternatives are worse.
Many mutations have no effect. But if you have 300 proteins and you have a change in each of them, chances are you will not live so well. And if your son has another change in each protein, he will probably do worse than you. It won't take many generations before your descendants can't compete and die out.
So each change is a gamble. If you don't make any changes, then eventually something which does change will do better and will drive you extinct. But if you make too many changes your descendants will do worse because of them. Ideally you would make just the right number, to balance the weighted odds of  damage from bad changes versus benefit from good changes.
For many organisms, the rate of change is down somewhere around 1% -- 99% of the time they get no change when they reproduce.

Since our mind-bendingly small subset of possible proteins supports life, shouldn't we expect that many many (as in 10^300) other potential subsets of different proteins would do so too?

Sure. And we have tended to find some that we could get to from where we were before. Point mutations tend to happen in small steps. You change an amino acid to a similar one. The genetic code is a Gray Code, often mutations have no effect, or hydrophobic amino acids are replaced by other hydrophobic ones, amino acids are replaced by others of similar size, etc.
Some of the best enzymes might be things that have nothing else good similar to them, so that they are very hard to evolve to.
Science fiction writers have sometimes written about life that has evolved for different times, and they usually suppose that the more-evolved one will simply and easily outcompete the ones that have not had so long to discover better ways. That isn't necessarily so. Human beings transported back to the Silurian Period might eat well (once they figured out which seafood is poisonous) and might not be eaten by anything (but they might get mobbed by centipedes if they sleep, and be unable to make hammocks out of cooksonia, and have no trees to hang the hammocks from either). They still may not thrive. Half a billion years evolving to fit into a different ecosystem might not be that useful after all.


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Are there any animals that gradually approaches the predator to search for food?
I was wondering if there is an animal (or insect, bird, etc.) that eventually comes close to its predator to search for food, but only does so if it couldn't find food in the environment it is in. So it first searches part of the environment farthest away from the predator, but gradually comes closer and closer to the predator as it searches for new food. That is, over time it dares more to come closer to a, lets say ambushing predator, since it has ran out of food (or perhaps for other reasons). Similar behavior is ok, but note that the key behavior that I want in the animal is that it "gradually" comes closer and closer to the predator.
Thank you.

Also see: Turkeys Circle Dead Cat :p

The behaviour that you describe is common in most animal species, as part of the natural trade-off between access to food, minimizing risk, habituation and hunger. Animals usually choose to forage in high-quality habitats that has a low risk of predation, but if food sources are depleted (or competition and/or territoriality is high) they will move to other areas with lower food quality or higher risk (since they are desperate for food).
In general, the effect of predators are both direct (killing of prey) and indirect (changes in prey behavior to avoid predation). The indirect effects means that prey will often choose to feed in habitats that are suboptimal from the perspective of forage quality, which will have negative effects on their foraging efficiency. These types of indirect effects of predators are often labelled as 'The landscape of fear' or the 'ecology of fear' (see e.g. Brown et al, 1999). However, as food resources run out this will trade-off against the fear of predators (along with possible habituation effects), which will lead to the behaviour you are asking for. You might also be interested in Gamelius et al (2014), as an example of how prey behaviour can be influenced by the presence of predators (here, roe deer and lynx), but there is a large number of studies looking into these issues. The review "Fear in animals: a meta-analysis and review of risk assessment" by Stankowich & Blumstein (2005) will also give you a good background and many examples.
The use of scarecrows is a simple way to understand the 'landscape of fear'. By placing a scarecrow in a field you strengthen the "landscape of fear" (by adding an artificial 'predator'), which will modify the behaviour of perceived pest species (prey), so that they avoid the areas around the scarecrow. However, if the animals you want to scare away ("pests") run out of food they will take larger risks and venture closer to the scarecrow to forage. Over time, they will also become habituated to the scarecrow, and will discover that it doesn't seem to pose a big threat, which will decrease the effectiveness of the scarecrow.
References

Brown et al. 1999. The Ecology of Fear: Optimal Foraging, Game Theory, and Trophic Interactions. Journal of Mammalogy
Gamelius et al. 2014. Habitat Selection and Risk of Predation: Re-colonization by Lynx had Limited Impact on Habitat Selection by Roe Deer. Plos One
Stankowich & Blumstein. 2005. Fear in animals: a meta-analysis and review of risk assessment. Proceedings B


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Why is there no symmetry in pigmentation when comparing people north and south of the equator?
If you are at the equator and start moving north, the further you travel, the lighter the skin of the indigenous peoples. Considering that we live on a ball, why do we not find the same traveling south from the equator? This relationship does not hold for individuals as you move south from the equator.  At the very least, one could say there are no blond hair blue eyed peoples south of the equator.

Welcome to BiologySE...interesting question... if you could cite some examples online to back up your statements in the question it would make the question much better

Because there are no significant land masses that far south of the equator that have been occupied by humans long enough for selection to have had an effect?  Africa doesn't extend that far south (and the southern tip is relatively small), and has plenty of opportunity for admixing/invasion by peoples to the north (see e.g. Zulu history), Australia doesn't extend far south, South America was only settled ~10K years ago, and like Africa, the southerly portion is small.

I rather would say that the lack of North/South Symmetry in pigmentation is that we forget how quickly human beings have spread. In prehistory, people have come to populate every continent over perhaps the last 60,000 years.
While in that time its clear that several mutations have popped up to influence skin color, they are pretty rare compared to the speed with which we migrated over the globe.  The dark color of our earliest ancestors has been lost and regained more than once, but not so often that the selection pressure of latitude have made indigenous in the tropics of south america or south east asia uniformly as dark as africans. Or for that matter have lightened the skin of pre-colonial South Africans.
One might guess that clothing and shelter have reduced the selection pressure on pigmentation further over the past few thousand years.
Individual cases should be studied - this is just a sketch - but the general thought here is that the pigmentation of human beings have more to do with where they have been and how quickly they have recently come from in their migrations.
Summarizing the comments below: There is a correlation between pigmentation and latitude.  The answer is really a combination of latitude, how long a people has been there, and the speed at which pigmentation mutants show up. It doesn't change so quickly that all people are equally dark at the same latitude or so slowly that you find completely pale people at the equator.

The dark color of our earliest ancestors has been lost and regained more than once That looks interesting, can you please add some references?

Just remembering some of the south pacific and australian aborigines being so dark sometimes.... no strong reference. I did find this reference that pigmentation is correlated to latitude. To the extent that it is symmetric or not depends on how perfect you expect the symmetry to be... sciencedirect.com/science/article/pii/S0047248400904032

If the dark color of our earliest ancestors has been lost and regained more than once and pigmentation is correlated to latitude, does it mean that our ancestors traveled several times between the equator and poles?

It means that the answer is really a combination of latitude, how long a people has been there, and the speed at which pigmentation mutants show up.  It doesn't change so quickly that all people are equally dark at the same latitude or so slowly that you find completely pale people at the equator.

@shigeta: But as I noted above, the mass of Australia isn't that far south.  Excluding Tasmania, the southernmost point is only 39°08' S latitude, and the mass of the continent is quite a bit closer to the equator.  It's also a mostly desert climate with lots of sun, unlike most of Europe north of 40° or so.

Its true but remember I'm not really trying to justify that latitude is the perfect correlation with skin pigment, just noting that the skin tone for some first nations people is darker than other neighboring peoples.


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What animal has the longest juvenile period?
I just heard the following complaint from a comedienne.

Humans are the only animal that is completely useless for the first twenty five years of life.

Obviously this is just a joke but it is true that primates and especially humans do have profoundly long juvenile periods compared with most animals. It's got me wondering whether humans really do spend the most time in sexual immaturity.
Unfortunately I have found this question hard to search because Google thinks I'm asking about the longest gestation period (which seems to be a much more popular question). To be clear, I am not asking about the longest gestation period.

As you indicate in your question, the average age of sexual maturity is probably the best way to approach this, since immaturity is usually how juveniles are defined. Age of puberty is also different in boys and girls (the same goes for many animals), and has also decreased in the 21 century. However, as an historical average for humans 15 years is probably fair, even though there is a lot of variance. That is high compared to most animals, but there are some that have similar or higher ages of maturation, e.g.:

Cicadas in the genus Magcicada, which can have a 17 year life cycle
Elephants reach sexual maturity at about an age of 8-15 years, but usually dont start to breed until they are at least 18-20 years (see e.g. elephantsforever.co.za and Association of Zoos and Aquariums). Males mature and start reproducing later than females, and in practice it is mostly older bulls that reproduce.
The Nile crocodile, which reach sexual maturity at at an age of 12-16 years (largely dependent of body size though).
Some species of Tortoise reach maturity at ages 13-16 years (e.g. Gopherus
sp, see Germano, 1994), and, again, which is largely due to body size and growth rate. Captive bred individuals can mature more quickly.

As you can see, there is a difference between sexual maturity and reproductive age. To actually be able to reproduce, especially in some male mammals, you often need experience and size, which means that reproduction is delayed in practice. Whether this period from sexual maturity (with respect to producing mature eggs/sperm) to reproductive age should be defined as least partially as "adolescence" will affect how humans compare to other animals. In my examples, I have focused on sexual maturity (which usually has less variation between individuals).
For other examples, you might want to look at insects other than Cicadas that have delayed larval stages. This does for many woodliving beetles, where development times can be very variable, and under poor conditions take up to 20-30 years. This is usually not the norm though.
When searching for other examples, use the terms "age of maturation, "reproductive age", "sexual maturity" etc, to focus on sexual maturation and not gestation.

The Greenland shark (Somniosus microcephalus) has been reported to need at least 156 ± 22 years reach to sexual maturity1. This is also thought to be the vertebrate with the longest lifespan.
Reference
1: Nielsen, J., Hedeholm, R. B., Heinemeier, J., Bushnell, P. G., Christiansen, J. S., Olsen, J., ... & Steffensen, J. F. (2016). Eye lens radiocarbon reveals centuries of longevity in the Greenland shark (Somniosus microcephalus). Science, 353(6300), 702-704.

This should be the answer

This article provides general facts about Tuataras, one of which is:

Tuataras reproduce slowly. They take 10-20 years to reach sexual maturity. Males can mate every year, but females breed every two to
five years. It takes the female between one and three years to provide
eggs with yolk, and up to seven months to form the shell. Then it
takes an additional 12 to 15 months from copulation to hatching,
possibly the longest incubation rate of any reptile.
A male tuatara named Henry, living at the Southland Museum and Art
Gallery, became a first-time father at the age of 111. He fathered 11
babies with a female named Mildred, believed to be in her seventies.

Those creatures are therefore one of the many that can be added to the list of the above answer.

Welcome to Bio.SE. Please [edit] your post to include a citation to a reputable source that supports your claim. Without it, your post will likely be downvoted or deleted. The goal here is to compile accurate and supported information about biology, as the internet already has too much misinformation. Please take out [tour] and visit our [help] for more information about how we work. Thanks.


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How much weight/volume do microbes occupy within the human body?
Microorganisms constitute the bulk of all the biomass on Earth. I weighed myself yesterday, and wondered how much less I would weigh if I were completely free of bacteria and microbes, inside and out.
Approximately how much weight and volume do microbes occupy within the average human body? How were these values obtained?

@AlanBoyd's calculations are reasonable, I think the estimate is off though.  The human microbome includes other bacteria which are not necessarily E.coli equivalent.
The human microbome projects give estimates that microbes are 1-3% total body mass.  i.e. several pounds of bacteria.
The GI tract alone has most of the microbome mass - faeces is ~60% intestinal flora/fauna by dry weight, which for many adults alone must be hundreds of grams at any given moment.

The bacterial flora weighs approximately 90 g and, assuming bacterial cell density is approximately 1 g ml-1, occupies a volume of 90 ml.
The human body has 1013 human cells and hosts 9x1013 bacterial cells.
One E. coli cell has a mass of 0.95×10−15 kg (wet weight).
Assuming that E. coli is typical with respect to mass of human microbial flora:
mass of bacterial cells in one human body = (0.95×10−15 * 9x1013) kg
 = 0.0855 kg = 86 g

Just human intestines have over a kilogram of bacteria! A good enema will leave you 2kg lighter and that's mostly bacteria.

The number I read where more like 1-2 orders of magnitude more bacterial cells than cells in our body.

According to this source, it's about 2 kg:

Our gut microbiota contains tens of trillions of microorganisms,
  including at least 1000 different species of known bacteria with more
  than 3 million genes (150 times more than human genes). Microbiota
  can, in total, weigh up to 2 kg. One third of our gut microbiota is
  common to most people, while two thirds are specific to each one of
  us. In other words, the microbiota in your intestine is like an
  individual identity card.

Other source, confirm it:

Le chiffre a de quoi surprendre. Il s’explique par le fait que les
  bactéries sont en général beaucoup plus petites que les cellules de
  notre propre organisme. Il y en a donc une quantité énorme dans un
  volume restreint; enfin sachez quand même que nous portons en moyenne
  1 à 2 kilos de bactéries, pour la plupart localisées dans notre colon.
  Il semblerait d’ailleurs que le colon humain soit l’un des écosystèmes
  les plus denses que l’on connaisse.


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Pasteurization and Bioavailability of Antioxidants in Beet Juice
What are the effects of pasteurization on the antioxidants found in beet juice ? Does the process render most of the beneficial nutrients (betaine) useless and make them unable for the body to process as efficiently as it would with raw beet juice? Also, does the pasteurization process do this to most fruit and vegetable juices ? I appreciate any insight, I've seen a lot of conflicting reports and am curious of anyones thoughts. Thank you

So, when they subjected "ready to drink" beetroot juice to thermal pasteurization, they found the betacyanin and betaxanthin (our major antioxidants, and pigment molecules) content to be 39.9 and 42.28% degraded, respectively (1). Their conclusion was as follows:

Standardization of process condition and
  quality degradation of beetroot juice due to thermal
  pasteurization was studied. The standardized T2
   batch
  with total heating time (fh) of 720 s thermal in-pack
  pasteurization leads to the minimal degradation of
  color, betalain content (Betacyanin and Betaxanthin),
  antioxidant activity and complete inactivation of
  micro flora of beetroot juice. The color, betalain
  content (Betacyanin and Betaxanthin) antioxidant
  activity and sensory of the beetroot juice was
  significantly (p < 0.05) reduced during 180 days
  ambient (27-30°C) storage, but still the quality of the
  juice was adequate upto 180 days. We concluded that
  thermal pasteurization of 96 °C for a total heating time
  (fh) of 720 seconds with P-values of 11.16 would be
  a good method to produce microbiologically stable
  beetroot juice with the retention of quality attributes.

So our goal is to get a juice that retains as many "good" attributes as possible, while producing a product that isn't going to get anyone a foodborne illness. As for the net effect of pasteurization on fruit juice in general, im still coming to a conclusion there. The process shouldn't render too much of the fruit/vegetable ineffective, though I'd still expect some degradation either in storage or processing.

If we read the previous statement, we can note two things. Firstly the percentage they mention are not in the quoted material at all. And secondly that the quoted material does not suggest degradation of the health boosting effects from the process of pasteurisation, but rather from long term room temperature (Very warm room) storage for 180 days. "The standardized T2 batch with total heating time (fh) of 720 s thermal in-pack pasteurization leads to the minimal degradation of color, betalain content (Betacyanin and Betaxanthin), antioxidant activity and complete inactivation of micro flora of beetroot juice."


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Is there an 'anti-virus'?
A virus spreads around and usually attaches itself to the host, multiplies & causes diseases. But is there something like an anti-virus? A single celled entity that does the opposite: spreads around 'kills' other viruses and/or cures diseases. Has anybody discovered something like it or is there any research group working on synthesizing one? If so any links to their publications?
Forgive me if I got my facts wrong, I am physical sciences person and know nothing about biology. :)

The immune system is something that is fixed to the host organism and does not spread around in the atmosphere or water like a normal virus.

you could think of antibodies as "anti-viruses" (although they don't grow exponentially...

There is a "anti-virus," although many call it a virophage.In 2008, a paper in Nature was published about the observations of a new strain of a virus known as Acanthamoeba polyphaga mimivirus. This virus mainly attacks amoeba. It was discovered in 1992. It was one of the biggest viruses ever found.Later, a related virus called the mamavirus was discovered. But, after observing this specimen under an electron microscope, scientist found tiny viral particles attacking the mamavirus. It was called Sputnik. The Sputnik virus hijacks the mamvirus's machinery and depends on the mamavirus to survive. It made scientists wonder if the mamavirus is a living thing.
Here is a picture of it attacking the mamavirus:

You can see small subviral particles attacking the bigger virus. That is Sputnik.
Note that it is a virus that coinfects other organisms but needs a virus infecting an organism to survive. According to Wikipedia:

Sputnik virophage is a subviral agent that reproduces in amoeba cells that are already infected by a certain helper virus; Sputnik uses the helper virus's machinery for reproduction and inhibits replication of the helper virus.

It seems that there are more species of virophages, including one that infects the marine phagotropic flagellate Cafeteria roenbergensis in the presence of a second virus — Cafeteria roenbergensis virus and another one known as the Organic Lake virophage but not much detail is known about this virus.
Here is the link to the Nature article on the Sputnik virophage, published in 2008:
http://www.nature.com/nature/journal/v455/n7209/full/nature07218.html
It may be possible to synthesize one in the future. However using this to kill viruses would not make sense because the virophage technically still attacks the host of the virus it is hijacking, plus, from what I understand, it only uses the virus's machinery.
Hopefully this was helpful. If you have questions, you can comment on this answer...

+1 Thank you Abraham for sharing this! Have you found anywhere how many viruses the Sputnik can attack? I think it is unspecific, but some characteristics, it must have.

@Masi I didn't understand..

Can Sputnik virus attack only some viruses? Which receptors does it have?

@Masi Sputnik only co-infects with one species.. About receptors, i don't know..it's probably in the nature article..

Here one publication with good references to possible receptors http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0094923 We do not have currently enough tools to specify all the receptors of Sputnik virophage, I think. Only the tail protein has been used there.

@Masi yes you are correct.. Thanks for the article BTW...

There is no anti-virus to all viruses and there is no such anti-virus against a single virus yet, but there is immune response to virus.
How efficient the immune response is then depends on many things.
There is no perfect immune response.
To develop such an antivirus that decreases viral load requires cooperation with the immune response.
To develop such an antivirus is still in very very early stages, since we do not understand the fine regulation of many processes going on in the viral pathogenesis and how to stop them.
There exists in the nature some viruses that attack other viruses.
However, we do not understand if they attack just one or two viruses.
See Abraham's good answer here for the latest publications in Nature.
The immune response tries to eliminate the virus through antigen presentation and cell-mediated immune response.
The humoral immune response works in the local sides where the cell mediated immune response does not reach.
However, the immune response is sometimes (and often) insufficient to kill the virus.
To develop such a general anti-virus is difficult because of a variety of different viruses: (RNA vs DNA; positive sense vs negative sense; single strained vs double stranded; intracellular replication vs extracellular).
Here is an example of antigen presentation for HIV virus deduced from this answer:

where HIV infects the antigen presentation cells (APC) (dendritic cell and macrophages) and monocytes.
It replicates actively in the lymphatic circulation.
Since APCs are out, it is difficult to kill the virus.
To develop such a general anti-virus against HIV would require very specific understanding of many things: probably, iPS cells and development of antigen presentation cells.
My conjecture is to develop an APC cell that has receptor to HIV virus and so can reach it.
However, only theory.
Gamma interferon should be included in the intersection between innate and adaptive immune systems.
Interferons may play a central role in the future in the development of such anti-viral drugs, because they are specific.
For instance, the activation of IFN-gamma stimulates the phagocytosis of macrophages against the mycobacteria tuberculosis which is facultatively intracellular (can be intracellular when necessary).
Innate and adaptive immune systems are visualised on the plane in the figure.
You have then humoral immunity working around that plane as circles.
I emphasize with that the local nature of humoral immune system and how it extends the cell-mediated immune system. Any attack on the heart of this system i.e. antigen presentation will also risk the humoral immunity and thus cause fast progression of the disease.
In summary, all measures that are used to decrease the viral load aim to target the immune system to express efficient way of decreasing the viral load (killing is just one of them!).
This can be done through many ways - most of which we do not know much yet.
iPS stem cell research and interferon research can be some good ways in the development of good anti-virals.
However, this will take still many years (probably at least 40-50 years) to have enough control of the specific viral pathways.

Excellent, always like the use of a Venn diagram!

But is there something like an anti-virus? A single celled entity that
  does the opposite: spreads around 'kills' other viruses and/or cures
  diseases. Has anybody discovered something like it or is there any
  research group working on synthesizing one?

Actually there is, it is called immune system. :-)
Most of the cells in your body have proteasomes, which can degrade proteins from the inside of the cell. The cells randomly choose sample proteins (possibly viral or cancer proteins) which are degraded by a proteasome into small 8-10 amino-acid length peptides. After that the cell chooses some of these peptides and send them to the endoplasmatic reticulum in where each of them meet with an MHC1 molecule (major histocompability complex) and binds to it. After that the cell sends the MHC1-sample complex to its surface. So every cell with nucleus has a lot of MHC1-randomProteinSample on its surface. These samples are checked an immune cell type called cytotoxic T-cells. These immune cells attach to the MHC1 of other cells using their TCR (T-cell receptor) and their CD8 coreceptor. The TCR has a part which consist of a random amino-acid sequence. Thanks to this random part it can recognize a very specific pattern of the small peptides which are bound to MHC1. So every cytotoxic T-cell is different and each of them can recognize a very specific pattern with its T-cell receptors. When a T-cell has a pattern match for the first time it waits for verification signal. It gets that signal on its CD28 receptor. The signal B7-protein is provided by a professional APC (antigen-presenting cell) which is infected by the virus or which phagocytized the virus, processed it, and now expresses it on MHC1 and MHC2 (MHC2 is similar to MHC1, but it can be found only on professional APCs). By virus infected APC the MHC1 can be enough to activate the cytotoxic T-cell. By not-infected APC the cytotoxic T-cell requires further help for activation. This help can be provided by a helper T-cell, which attaches to the MHC2 receptor and after the verification it sends the necessary cytokines to activate the cytotoxic T-cell. After the activation the cytotoxic T-cell can destroy every cell on which it finds an MHC1 with matching protein sample, and it can proliferate, so make many copies of itself. This whole process (activating the adaptive immune system) takes appr. 3-4 days. Until that the innate immune system holds the infection. The innate immune system is not so specific as the adaptive immune system, but it contains most of the APCs, so these two systems work together in order to defeat the infection. By the next infection there will be already active memory T-cells available, so the whole process will be much faster... This is shortly how a human immune response works by viral infections. Note that I left out the B-cell response against viral surface polysaccharides to stay short and simple. ;-)))
Synthetic drugs usually have a single active ingredient or just a few of them, so you cannot do an universal cure for viral infections because every virus is different. There are a few treatments already available (viral interference, receptor antagonists, viral enzyme inhibitors, RNA interference, etc...), but the most important thing is prevention due to vaccination (create memory T-cells by an infection with attenuated virus strains or by fooling the immune system with viral proteins, polysaccharides and some chemicals which kill a few cells). Probably in the distant future there will be nanobots which will be programmed to cure any type of viral infections and cancer, but with current technology that seems like a miracle...

Since most answers have already covered multicellular immune systems, I will try to explore the concept of unicellular immune systems.
The now famous CRISPR-CAS system originally evolved as a bacterial immune system to protect itself against phages.

Much like computer-based antivirus solutions, CRISPR CAS relies on a "signature" system.
Known targets for the CRISPR CAS system are encoded on bacterial DNA, and these known signatures are then transcribed and processed into short guide RNAs known as crRNAs.
These crRNAs are then used by the CAS protein complex to target and cut up (therefore inactivating) these DNA strands that match. This therefore allows the cells to possess a native antivirus system that can "receive live updates" just like a commercial software antivirus program by simply modifying their "signature list" of possible pre-crRNAs.

+1 for new idea. Can you please explore this topic a little more in relation to anti-virus. Now, your answer seems to be like from Wikipedia mainly.

Well, there are antiviral drugs that inhibit virus development. However, they are drugs, not cells but they can be quite effective in controlling diseases.
They are also quite available to the public and perhaps you (or someone close) have used them. For instance, Zovirax (acyclovir) is used in lip herpes.
Also, HIV therapy is used effectively to increase the life expectancy of AIDS patients.


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Does a presence of ants on a plant mean that the plant has been infested by aphids?
Ants protect aphids from their predators (such as ladybirds):

Aphids and other hemipteran insects secrete a sweet liquid called honeydew, when they feed on plant sap. The sugars in honeydew are a high-energy food source, which many ant species collect. In some cases, the aphids secrete the honeydew in response to ants tapping them with their antennae. The ants in turn keep predators away from the aphids and will move them from one feeding location to another. (source: wiki: Ant)

Does a presence of a large amount of ants on a plant in my garden (especially fruit trees, willow trees, flowers, vegetables) mean that the plant has been infested by aphids?
It's easier to spot the ants rather than the relatively smaller aphids so I am wondering if I may use this as a trigger for using an anti-aphid pesticide before the aphids start causing visible damage to the plants.

On the last paragraph, never treat for pests unless you know they are there. Ie, wait until you see aphids or actual damage. Ants do not necessarily mean aphids.

When I see the actual damage it's already too late. And also for early fruits I must not apply the pesticides too close to the harvest time. So any early clue gets useful.

@J.Musser perhaps you should post that as an answer. presence of ants does not mean presence of aphids.

Simple answer is no:
$Ants \neq Aphids$
However, they could be used as evidence that aphids are there depending on the reliability of the coexistence. Ants and aphids are independent entities and do not rely on each other so can exist in non-overlapping populations. Applying this idea to the correct species of ant and aphid is, of course, important for it to work as an indicator - it will only be true in those combinations where this "aphid protection" occurs.
I can't find any information on the reliability of the relationship, especially not knowing which species you are looking at. If there was a high positive correlation of ant density and aphid density then one would expect the presence of ants to be a good indicator to the presence of aphids. If the correlation is low there is a higher chance of a false positive (where a false positive = when you see ants, conclude there must be aphids, and there are no aphids).

What are the other possible reasons why you may observe a lot of ants on a plant/twigs?

@HonzaZidek Probably means some resource (food, water source, etc.) the ants "want" is on, or accessed by moving along, the plant you are observing - can't say more without knowing very specific details about the ants, plants, and aphids you are seeing, maybe watch some of the ants (follow individuals and see where they go).


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The biology behind tree pruning and hedge trimming
I read two contradictory arguments which both seem logical to me, related to the tree pruning and hedge trimming:

You should prune/cut trees only outside the growing season, when the tree is "sleeping". In some countries there is even a law forbidding to cut/prune trees within the growing season!
You should trim the hedges only within the growing seasons, when the tree is not sleeping and thus able to heal the cuts.

Which of these two arguments is true and how are they supported by the plant biology?

The difference has to do with the concept of "thinning and heading" and how plants respond to abiotic damage. Thinning refers to the removal of a branch or shoot all the way back to the node which it originated from. This is the primary type of pruning used on trees - either to limit growth or to increase the amount of light permeating to lower branches. Late winter is generally the best time to do this, just before the tree breaks dormancy, since plant pathogens are generally less abundant. By pruning in late winter, this also reduces the amount of time that the wound is exposed before the tree begins active growth.
In contrast, "heading" refers to the partial removal of a branch, usually 1/2 to 1/3 back to the node.  The purpose of heading is to stimulate shoot growth on the remaining branch - hedges being a primary example. Because new shoots and leaves are desired, heading is usually performed at the height of stem growth (in most climates late spring to early summer).
The biologic processes behind this are complex (botanists are just beginning to understand how plant behavior adapts to predation) but in very general terms, plants respond to damage in two ways: by compartmentalizing the wound; and by stimulating growth on the remaining tissue. Many types of woody plants produce latent (or adventitious) buds, which lie dormant within the cambium tissue. Normally these buds are suppressed by auxin hormones produced in the meristem by active shoots. When the meristem is removed (such as through heading the branch), these buds rapidly develop to produce new shoots and leaves. Most species used for hedges are selected because of this ability.
So long story short: thinning is best performed in late winter, when the plant will quickly be able to seal off the damage while limiting the production of unwanted water sprouts and suckers. In contrast, heading is usually done in early summer, when the hedge can vigorously produce new growth and fill out any gaps.
Some resources:
http://extension.wsu.edu/maritimefruit/Pages/PruningBasics.aspx
http://puyallup.wsu.edu/~linda%20chalker-scott/horticultural%20myths_files/Myths/Wound%20sealer.pdf


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How do sharks and other fish conserve and gain water in marine environments?
With the osmolarity of the average vertebrate being around 300mOsml, and salt water having an osmolarity of 1000mOsml, why does the water from the shark not leave to the salt water around it?
I presume the scales must act as a barrier to stop water form leaving, but with the blood vessels being exposed to the saline water in the gills, why does water not leave the body?

The mechanisms of osmoregulation is different for sharks (and other elasmobranch fishes) and teleost fishes.
In Elasmobranchs the body osmolarity is maintained equal to the seawater by Na⁺ Cl⁻ and urea. Toxicity because of high concentrations of urea (strong chaotrope) is counteracted by high levels of trimethylamine oxide (TMAO). So, the elasmobranchs do not need to drink water to prevent dehydration. But sometimes they do drink water for adapting to different salinity levels [1].
Teleost fishes, however, need to drink water in order to prevent dehydration. Initially Na⁺ and Cl⁻ are absorbed in the esophagus via cotransporters (Na-Cl/Na-K-Cl), thereby reducing the osmolarity of water. The cells that absorb Na⁺ maintain its low concentration by pumping extra Na⁺ in the Extracellular fluid, using Na⁺/K⁺-ATPase. Cl⁻ is also exchanged with Bicarbonate (HCO3⁻) via anion exchangers [2].
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How does blue white screening work in selecting E coli that have taken up a plasmid vector?
The plasmid vector I am referring to is pCR 2.1 - TOPO. I added the vector to the E coli and plated them up onto LB+amp+X-gal plate, then incubated. After incubation the plates had two types of bacterial culture on them, one white and one blue.
I think that the blue cultures have accepted the plasmid as they are able to grow on ampicillin, so have the ampicillin resistance gene, and are able to convert the X-gal substrate to blue via the lac Z gene. What i'm confused about is the white colonies. If the colonies are able to grow on ampicillin, surely they have accepted the gene because they have the resistance, and surely they should to be able to convert the X-gal?
So why are these not expressing the lac Z gene? Is it that the lac Z gene and ampicillin resistance aren't on the same plasmid, or is it that the lac z gene didn't make it into the plasmid?

What was the strain of E. coli that you used? Was this a TA cloning kit? Did you also add insert DNA of any kind?

I believe it was the k12 strain, yes it was a TA cloning kit, and I added DNA from Aequoria victoria to the vector that caused the bacteria to fluores


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Is there any evidence telling us what the oxidation state of early earth's atmosphere was?
I ask this question in relation to the origin of life. I realise it would probably be better suited to a geology stack exchange, but it does not yet exist.
The Miller-Urey experiment gives a lab based demonstration of how organic compounds may have been produced. It recreates that conditions that are thought to have existed in the early atmosphere (Hadean period).

What this experiment relies on however is an assumption that the atmosphere lacked oxygen (reducing). The Miller-Urey experiment does not produce proteins if it is conducted in a oxidizing environment. I've seen that there is some debate over the oxidation state of the atmosphere, and the main evidence for a reducing atmosphere is that life wouldn't have been able to begin without it. Is there evidence supporting an oxidized early atmosphere, and if so, how did life come about?

There are wikipedia pages on Geological history of oxygenation and on Great Oxygenation Event
I don't know much about geology and someone else might be able to give an exhaustive list of evidence (and method of measuring) concerning the oxygen concentration on earth but that would be a very long answer I guess! Rather than a full answer, I give you a list of wikipedia pages below that will interest you and should help answering your own question.

Banded Iron Formation
Evolution_of_dietary antioxidants
Huronian Glaciation
Ice core


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Does anybody know what this shark is eating?
Looking for a species identification on the orange fish that the shark is eating. The shark is a goblin shark filmed as part of the BBC's 'Legends of the Deep: Deep Sea Sharks'.

It might be Helicolenus dactylopterus, but it is difficult to say for sure without being able to see the dorsal fin.

That's great, thank you. Just had a quick Google image search and I think you're right. Answer the question rather than a comment and I shall accept it!

The fish in this image is Helicolenus dactylopterus. Shown below;

This fish, is more formally known as a Blackbelly Rose-Fish. This fish, is one of the Goblin Sharks' many prey in the deep sea.
In the photo you posted it looks as if the Goblin shark effortlessly and oddly so caught the fish - it did. This is due to how it consumes most of its prey:

When they approach it their jaw goes out similar to how a human can stick out its tongue. Then with a sucking motion they draw they prey into their mouth where very powerful teeth are waiting to consume it.

Goblin sharks are quite terrifying...


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What kind of ants are these? Are these venomous?
I found these ants on a small mango tree in front of my home. Could someone identify them for me.
Length: 2-3 cm
Location : North India(Chandigarh)
Temperature: 21-24 degree celsius
More info: They built a home out of leaves of the tree.

Found it from google images. Its weaver ants. Its not venomous but they can inflict painful bites along with formic acid spray.

These ants are called weaver ants, they are in the genus Oecophylla.
'Helcium is attached relatively high on abdominal segment III only in Oecophylla'
http://www.antwiki.org/wiki/Formicinae
They use the silk produced by their larvae to bind leaves together to make chambers for their brood. As any ants in the Formicinae subfamily, they do not have a stinger. They can however bite and drop formic acid on your skin, which can cause irritation. They are used in orchard as biological control agents against pests.

You seem to be answering a lot of questions about ants recently. That's fine, but please try to add a reference or citation to your answers if possible,

This is a very broad question about ants, there won't be any useful citation for this because the question is too broad. With the name of the genus, Sumeet will be able to find all the information needed.

I think there is a real issue on this forum, wrong answers get accepted with no reference while I get in trouble for rightful identification. Forcing me to add references is irrelevant because none of them provide support for identifications based on the habitus.


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What species is this bug that appears in my bathroom?
I'm trying to identify the attached. A few of them appear every day in my bathroom, never more than that, but new ones are there every day. Length is 2-3 mm, and location is the United Kingdom.

Based on my knowledge of species found in Sweden, I think this is a species of Ptinus (Spider beetles), for instance Ptinus sexpunctatus. The general appearance, along with long antenna and long legs fits well. Species in this genus are often also found indoors. Some of the other species in the same genus can also have white/light markings on the elytra, so I'm not absolutely sure about the species. Typical of P. sexpunctatus is that is has six white marking on the wings, but the two hind ones on each wing can sometimes merge into one.

(picture of Ptinus sexpunctatus, from http://www.coleoptera.org.uk/)

(side view, from Wikipedia)


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What is this weird spider?
Today while we're cleaning our storage room I saw this strange looking spider and I'm not even sure if this is a spider, it has two claws folding inward to its mouth and two long weird limbs, it is about 2 inch long and rarely move on its place. Is it poisonous or dangerous to us? What should I do with it?

Could you give a size estimate for one of the features, and tell us what continent you live on?

It is about 2 - 2 1/2 inches, it is hiding in our storage room which is so dark and full of mosquitoes here in Leyte, Philippines.

It looks like a species from the Arachnid order Amblypygi (Tail-less whip scorpions), which are closely related to Thelyphonida (Whip Scorpions). As part of Arachnids, both of these taxa are related to spiders and scorpions, but belong to a separate order.
Even if they look scary, they are harmless to humans, even if they can sometimes bite.
According to this checklist/site only three species are listed from the Philippines, so if you want to determine it more closely, it might be useful to start from this list. The list includes: Sarax brachydactylus, Phrynus grayi and Charon grayi.
Here is an example picture (from wikipedia):

Charon grayi (giant whip-spider) from biotagua.org:


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How fast can a human run?
I'm a runner (cross country) and I'm always amazed at how fast Olympic sprinters are. There's a lot of hype about those in the 100-meter dash being the fastest in the world, and we're constantly seeing the 100-meter time dropping. But is there a limit? How fast can human being, propelled only by its own energy (i.e. without any external assistance) run?

Me about 13km/h average, or by sprint about 18km/h :D I guess far from olympic ranges...

An older answer that referred to the physiological feats of ancient humans, and why modern humans are wimps made me look up a couple of papers on running speeds a while ago. One of the examples used to support the statement that modern humans are "wimps" is a study of ancient fossilized footprints from Australia, which claim that the individuals making the footprints were running close to Olympic record times. The footprint studies (Webb, 2007) basically attempts to describe the humans that have created the footprint paths, and also tries to calculate the speeds they were running at. For one of the individuals (T8), the estimated running speed is 37 km/h (i.e. 10.3 m/s). The interpretation by Peter McAllister in his book Manthropology seems to be (I haven't read the book) that these barefoot individuals running on mud could easily have outrun current day sprinters, especially with training and on a rubber track (also see this huffintonpost article on the book). If the estimates in Webb (2007) are close to accurate, it would seem that modern top-trained athletes might not have reached the edge of what is humanly possible when it comes to top speeds.
There is also a biomechanical study on potential human running speeds (Weyand et al., 2010) that you will probably find interesting. This paper looks at factors such as gait, stance, force application etc, and includes empirically estimated values from 10 subjects to discuss the limits to human speed. They conclude that (natural) human speeds are likely to be limited to ~50 km/h (as reference: Bolt's top speed during his 9.58 WR was ~44 km/h).

Consequently, human running speeds in excess of 50 km/h are likely to be limited to the
  realms of science fiction and, not inconceivably, gene doping.

They also look at different scenarios and e.g. point out how important limb length is for top speed:

Second, limbs lengthened through evolution or perhaps prosthetically could
  substantially increase the top running speed attained at the minimum period of foot-ground force application. For example, a relatively small increase in leg length of 10 cm would
  increase contact lengths by 9 cm and the top speeds of the subjects tested here from 9.1 to 9.8 m/s.

In general, important factors for maximum speed in animals are ground  reaction force and ground contact time. An earlier study by Weyand et al. (2002) also show how faster human runners in general have shorter ground contact times compared to slower runners. As a sidenote, this seems to be in contrast to cheetahs, which have longer ground contact times than greyhounds, while still being much faster (Hudson et al. 2012 and popular summary).
View these as a couple of interesting examples and a starting point. This is not my area, and I do not know the literature well.

This is a superb answer! On reading the question, I actually felt that it was hard/impossible to answer.

Fantastic answer. Very comprehensive.

Recent article from New york times, on the same subject: https://www.nytimes.com/2020/01/21/science/human-running-speed-quadruped.html

Also Kinugasa & Usami. 2016. How Fast Can a Human Run? − Bipedal vs. Quadrupedal Running. Front. Bioeng. Biotechnol.

It is interesting to look at the pre-motorized past when it was very common for people to travel on foot great distances since horses were expensive. I have read that some suspect mile records may have been beaten much earlier in history. On the other hand, older olympic marathon times are significantly worse than modern which may imply better training, nutrition and technique play a big role.


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what is this ant-sized black insect?
I have found these tiny ant-sized black bugs on the floor that are a little hard to kill; I have to hit them with so much force otherwise they stick to the back of my sandals alive! or i have o squeeze them hard between the Kleenex.
Can anyone identify these please so i know how to get rid of them.
I live in Asia, Iran by the way, thanks.

In the edit box there is an icon for inserting pictures to your posts. Please Click that and then drag and drop the photo there so that it will be displayed on the site and not require people to click through to the image.

I don't think you can get a proper species-id based on that picture. It looks like a beetle though.

Can you try taking a higher quality image?