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Why are humans only so tall/large?
In biology I've learned that cells rapidly divide and can grow and split undefintely, and that certain parts of the body have to grow and evolve before growing, but I am tied up on the fact that the body produces hormones to have only grow up to a few feet tall and stops growing at a certain age.
Why does it stop in terms of height or physical mass when it can still keep on growing? Why do the hormones tell the body to stop growing when it can continue?

Welcome to Biology.SE. Can you please clarify certain parts of the body have to grow and evolve before growing

Is there any reason you phrased your question as being specific to humans? You seem to assume "bigger is better" for humans. Would you assume the same for other species as well?

“Can grow and split [indefinitely]”, this is incorrect for normal cells due to something called the Hayflick limit. This statement isn’t essential to your question, but I felt like it needed to be clarified.

The question is a bit vague but I will take it to mean the following

Why does it (the body) stop in terms of height or physical mass when it can still keep on growing?

The answer is physics, specifically the ability for a body of a specific shape and structure to support itself and move itself, followed by the energy requirement to feed all those cells.
Strength of a bone scales with its cross sectional area, similar to muscle. Mean while mass scales with its volume. As a result, mass increases faster than bone strength. So the bigger your are, the weaker your bones become if all proportions are maintained. As a result for a certain design of animal there is an upper limit of how big it can become before it unable to support its own weight or able to move.
Next comes energy requirement. In general the more living bio mass you have, the more energy you require to keep it alive. The scaling isn't proportional but there is a general trend. And the more energy required the more food is needed, and given the habitat an animal lives in, there is only so much food around. And this places a limit on how big an animal can grow. An animal living in its niche has an energy budget.
Associated with energy budget, we meet biology and natural selection. Energy placed into growing, isn't energy placed into reproducing. All animals eventually die, either by predator or bad climate (winter, drought, even bad luck) . So it becomes a balance, given the amount of energy available, how much energy should be put into growth to give a more robust structure to survive vs how much energy should be put into reproduction so that the organism can multiply.
Put too much energy into growing bigger, your probability of dying before reproducing increases as you take too much time growing before becoming sexually mature. Put too much energy into reproducing, upon sexual maturity your body is small and weak and your die before you spend much time reproducing.
The ultimate right answer is dependent on the animal's niche, the physical environment around it, its biology, and the predators around it.

Your third reason seems to me more relevant. Arguably we should look for the first clue in reproductive success. After all we grow until... maturity. Bones could grow stronger, larger bodies can gather more food.
Contra, we could carry on growing stronger to protect our progeny. Socially though, we reach maximum power when we have to pay for the tuition fees.

I'm not sure this answers what the OP is asking.  Granted that the question is far from clear, but I took it to be asking what mechanism the body uses to control size. For instance, in Africa we can find ethnic groups with an average (male) height of 1.45 m ("pygmys"), other groups, other groups that average 1.9 m.  And of course we can breed dogs from chihuahua to Irish wolfhound, horses from minis to drafts, & likewise for most domesticated animals (and plants, e.g. miniature roses).  So what are the biological pathways that regulate size?

Thank you for the answer, it's answered and clarified my question; but, going along the thought of limited resources/energy, say that someone lives in some sort of "utopia" where resources are abundant, there are no environmental threats, no need for sexual reproduction, and some sort of evolutionary design that can support the body regardless of how large it is. Although this thought may be very abstract and impossible to happen, if such could, should a person be able to grow "indefinitely" (or very large)?

I would expect that organism to become very large and very old. I have listed two real world examples. These is a honey fungus colony that spanning 8.9 square km with an estimated weight of 605 tons, and about 2400 years old. There is also Pando a clonal colony of an individual male quaking aspen, about 6600 tons in mass and 10,000 year old, although some sections may be 1 million years old.  https://en.wikipedia.org/wiki/Largest_organisms>


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Where does weight go when you lose it?
When one loses weight, where does the lost poundage (I assume comprised mainly of fat) go?
Is it urinated out? Defecated out? If a combination of both, does the percentage of each differ depending on how much of what your are losing was pure fat?

You breath it out, for the most part. Fat is "burned" to convert the carbons to CO2, which is breathed out. There's not very much fat-derived carbon in each breath, but you breath a lot, all day long.

At rest, an average 70 kg person consuming a mixed diet (respiratory quotient 0.8) exhales about 200 ml of CO2 in 12 breaths per minute. Each of those breaths therefore excretes 33 mg of CO2, of which 8.9 mg is carbon. In a day spent asleep, at rest, and performing light activities that double the resting metabolic rate, each for 8 hours, this person exhales 0.74 kg of CO2 so that 203 g of carbon are lost from the body. ... Replacing one hour of rest with exercise that raises the metabolic rate to seven times that of resting by, for example, jogging, removes an additional 39 g of carbon from the body, raising the total by about 20% to 240 g. ...
Our calculations show that the lungs are the primary excretory organ for fat.

--When somebody loses weight, where does the fat go? Ruben Meerman and Andrew Brown, BMJ 2014; 349

Hello! This question was deemed worth of an answer, so why not upvote it? Vote early, vote often to encourage new users and keep the community alive!

This answer is very interesting. I think it is a good example of order estimation in biology.

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What options exist to quantitatively detect enzyme activity in non-model insect tissue?
Evolution/genomics person here: what are the options to measure the activity or presence of broad categories of enzymes--like peroxidases or catalases--active in a specific tissue (in a non-model insect)?
I understand that antibodies, e.g. ELISA, may be one approach but am unsure if it's the best option or what the alternatives would be. Are any sequence based-approaches available, if I know the peptide sequence (or at least a specific function domain, ie Pfam ID)?

"I understand…". I don't think so. Antibodies are specific to one protein (you hope). They cannot be raised against a "broad category of enzymes". I think your question requires a little more thought.

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Minimum age to reproduce
How old does one (male and female human) have to be in order to reproduce
Im thinking that it's 13 for a boy and 3 for a girl, is that right?

What is your definition of reproduction?  Does it just involve a female getting pregnant, or does it involve carrying it to term.  It seems highly unlikely that a 3 year old could carry a fetus to term.

Cross-posted at Health and underresearched.- please delete one post and refine the other, most of all add some prior research and correct the 3 years for a girl's reproductive age. That's just plain nonsense.

The youngest fathers recorded were 11 years old (see wikipedia >
List of youngest birth fathers).
The youngest mother recorded is L. Medina was 5 years, 7 months and 21 days old when giving birth, which is rather astonishing! Of course, she gave birth by a caesarean section. She had an extremely early puberty; she appears to have had her period when she was 3 years old only. You might want to have a look at wikipedia > List of youngest birth mothers. According to this article, a mother (L. Gryshchenko) became a mother at 6 years old and gave birth "naturally" (not by cesarian section).

Not propably but definitly :). But  it is nice answer.

@L.Diago Not probably, not definitely, but definitely not - in its current shape the question is unfit for any site in the SE network. Whoever upvoted the question should re-think their motivations to do so -1. The answer is fine but removed my upvote as it's an answer on a question that should've been improved first, or put on hold altogether.

Dear ALiceD i was on your side. I didnt mean it on that way. :D Btw thank you, because i have never noticed that mistake.


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What is the dependent variable of a relative fluorescence graph?
So it was asked what was the dependent variable of this experiment. I know that as students, we're wired to think that the y-axis is the dependent variable while the x-axis is the independent variable (probably good that way, I dunno).
However, I thought that the dependent variable in this kinetics would be time. Since this has relative fluorescence from 100 to 0, isn't the change in fluorescence for all four conditions the same, while the only affected variable being rate (which in this experiment is more dependent on change in time)?
Sorry I can't give more information about the conditions of the experiment, it's a test question that I wouldn't be allowed to post, which is why I whited-out the conditions of each line. Any help would be greatly appreciated.

When a variable is independent, it's not affected by any other variable. Relative fluorescence obviously depends on the time parameter in this case. If you stopped at 30 minutes and took readings ever 3 minutes, your data would look very different.
Without more information about the experiment, however, it's hard to tell if there are additional variables.


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Fixing plant leaf tissue for tensile tests
I'm a new master's student in mechanical engineering, and I'm researching crop biomechanics. We need to do some tensile tests on samples of corn stalk sheath, which involves securely and evenly gripping a sample at two ends in a machine and pulling slowly until the sample experiences mechanical failure.
My advisor thought we might simply be able to use an adhesive such as super glue to fix the sheath samples to the tensile test machine, but he found that super glue doesn't adhere well to the sheath because of a waxy layer on the surface.
As someone who doesn't have a botany or biology background, I'm wondering if there are adhesives out there already that would serve such a purpose? Or perhaps another way of fixing the sheath to the machine? Normally tensile machines are used to grip metal or polymer samples, and have simple claw-like grips at either end.

Just as a thought: if it is epicuticular waxes that are causing the problem (or the cuticle itself), you might be able to get better traction by dipping the ends you want to grip in 70% ethanol or nail polish remover


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Why are treatment periods with antibiotics longer than 1-2 days?
Antibiotics are given prophylactically for several indications (e.g. prior to dental surgery).

Why are the treatment periods for prophylactic antibiotics much shorter than when treating an infection?

Example: Prophylactic antibiotics may be the day before surgery, but in the case of infection, they are often given for 10-14 days.

Is there something different about pre-infection bacteria (or the body) compared with after the infection has set in?
Looking for general concepts here, as I recognize there are many different types of bacteria and antibiotics.

Generally when you have an infection, pathogenic bacteria have colonized a tissue, and you need to keep antibiotics circulating in that tissue long enough to kill all/the great majority of them. To prevent infection, you only need to kill the few that might be able to settle in and multiply (which would lead to infection down the line.) If the antibiotic level is already acceptably high in the target tissue before a procedure, the bacteria will die, not colonize and infect. Is this an adequate explanation?

@anongoodnurse I think your comment answers the question nicely. Why not post it as an answer?

@anongoodnurse In the case of a septic surgery, most infections are localised sepsis, hence I do not think that the main concern is to just prevent bacterial seeding, as they might not need to undergo a hematogenous spread before infection ensues. Not sure though.

@SatwikPasani - It doesn't matter where the bacteria might end up (though some places are more likely than others.) Oral antibiotics generally cover the entire body with obvious limitations. Dental procedures are covered in susceptible patients to prevent hematogenous seeding of a heart valve. Does that answer your question or have I misunderstood your comment?

@anongoodnurse That is a good explanation thanks!

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What kind of drain fly is this?
Habitat:  Men's room at a rest stop in Syracuse, New York.
Size: ~1 cm
Based on my limited searching ability, I think it's a type of "drain fly" (Psychodomorpha): https://en.wikipedia.org/wiki/Psychodomorpha
Hard to get a better picture without a macro lens, but is anyone able to speciate this fuzzy urinal-fly?

This is the same species as is featured in the question "What's the name of this bug from Toronto, Canada?" (see: https://biology.stackexchange.com/questions/38665/whats-the-name-of-this-bug-from-toronto-canada); there the question has two answers.  As further support of the answer I gave there, see the diptera.info thread https://diptera.info/forum/viewthread.php?forum_id=5&thread_id=69927, where a European specimen is identified to species by an expert (the species is VERY widely distributed!)

Interesting to hear about it's expanding range.  When I first saw it I wasn't sure if I should call it a moth or a fly, that "moth fly" description fits well. I feel sorry for its sad little life around the urinals :(

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Photosynthesis production of oxygen
If you are to increase the intensity of light indefinitely, would you expect the production of oxygen to continue to increase?

Welcome to Biology.SE! We encourage you to do some research on your own and then ask questions informed by what you have learned (ideally with references to reliable sources). Your question as currently written is easily answered by thinking about a moderately extreme case — what would happen to leaf if you directed an industrial laser at it? ——— Please also take the time to go through the [tour] and the help pages starting with [Ask] questions effectively on this site. Thanks!

No. But a simple google search for a graph that shows the relationship between photosynthesis and sunlight (or temperature) would demonstrate this quickly.

No — there are both theoretical limitations and experimentally proven ones.
Chemistry in cells is subject to the same laws as chemistry in general. For photosynthesis to take place, certain molecules (e.g. ADP and NADP+) have to be present to transport the energy harvested to the place where carbohydrates are synthesized from this energy. The transport rate of molecules is limited by the rate of diffusion (see Brownian motion) within a fluid at roughly room temperature (where photosynthesis takes place). This limits the amount of energy that can be processed within a defined volume of plant tissue.
There are further limiting issues. Above certain light intensities, some parts of the plant cell suffer heating and destructive effects, which also limit photosynthesis.
See an abstract on this topic
There are also measured limits. Most plants with leaves exhibit stagnant photosynthesis rates at light with $$600 \frac{μmol}{m^2 \cdot s} $$
or higher.

I made some suggestions that I think improve the wording, but overall a nice answer.  However, I think it would also be good to add references for: 1) the limiting light intensity, and 2) that photosynthesis is limited by the diffusion rate of molecules like ADP/ATP and NADP⁺/NADPH.

I'm going to update that, I'm currently dissatisfied with my answer because it leaves too much unclear about my reasoning and its sources.

Light is one of the factors affecting the light-dependent reactions of photosynthesis. The very low intensity of light will not let the Photosynthesis reaction to occur at its maximum rate and also too much intensity of the light will lead to the bleaching of the chlorophyll. S0, neither very low nor very high intensity is needed for the photosynthesis to occur at its maximum rate.
You can read about this in the article given in the link below:-
http://www.rsc.org/learn-chemistry/content/filerepository/CMP/00/001/068/Rate%20of%20photosynthesis%20limiting%20factors.pdf


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What forms this pad on the side of the face?
I've been trying to figure out this for the best portion of this morning, but what structures are responsible for the pad highlighted in red? (sorry for low quality of picture, was just watching the show at the time)

It's from my understanding that the zygomatic (in green) runs to the edge of the ear in a relative straight line and most muscles have their origins or insertions bellow it. I know there are some fat pads (such as the nasolabial fold in purple) on top of everything on the face, but are these all fat pads that just allign? I've seen this pad on both man and women often, although it seems more proeminent in women.

That padding is apparently from a prominent zygomatic arch also known as high chickbones (pictures).
The bones between the eye, nose and ear are: the zygomatic bone below and behind the eye, the zygomatic process of the frontal bone above/behind the eye and the zygomatic process of the temporal bone, which extends toward the ear canal. It makes sense that when the zygomatic bone is more prominent, the zygomatic processes of the connecting bones will be also more prominent and appear as high cheeks.

Image source: Wikimedia, CC license
Here's the photo of Abraham Lincoln from the Wikipedia's article about zygomatic bones:

A Youtube video The Zygomatic Bones and Ogee Curve

I can see the presence of the zygomatic bone on the front of the face, and consequentially on its profile and shape under the eyes. What I am refering to is the continuation of the form on the side of the face, behind and above the lateral eye line and where the zygomatic and zygomatic process end, all the way to above the ear.

@omiyage, I changed the answer and the pictures. I believe, the padding is due to prominent zygomatic arch, so due to the bones.


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The First Polymerase
Knowing that polymerase protein is needed for the transcription of genes, which polymerase is used in the transcription of polymerase protein itself?

Please clarify whether you are enquiring about the evolution of RNA polymerase, or about the different RNA polymerases (I, II and III) in contemporary higher organisms.

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Possible duplicate of What came first? The DNA or the DNA polymerases?

In eukaryotes its RNA polymerase II. In bacteria it is the normal RNA polymerase. Although it is true that polymerases are now needed transcription of more polymerases, this mechanism may not have always been present. In the RNA world hypothesis, RNA coded for proteins and not DNA, so with the emergence of DNA, RNA polymerases may have formed as well. To produce proteins from RNA, organisms use complexes called ribosomes, which are ribozymes (RNA enzymes), which have undergone many rounds of evolution from original ribosomes, so there wasn't an issue with the production of proteins from RNA and throughout the course of evolution, polymerases were then developed, but they were only necessary with the rise of DNA.

I think you misunderstand the question. I suspect it's the old chestnut of the chicken and the egg. And even in an RNA world, polymerase (RNA-dependent RNA polymerase) must have developed very early — certainly before ribosomes, as these were only needed to make protein. The answer would seem to be that there was non-enzymic methods of RNA replication, followed by a ribozyme-like enzyme. Whether protein RNA replicases developed before DNA came on the scene is a moot point.

I dont know if we have a solution as to how functional RNAs were first formed. I have found a polymerase that was rationally developed for RNA polymerisation, although the paper is unsure as to whether this was feasible DOI: 10.1126/science.1060786. if you know of any research that has gotten any further please let me know!

I prefer a link I can tap on, especially on the phone. I’ll check it out tomorrow.

Thank you. I checked out the RNA World Hypothesis, it is very interesting, though it is a shame that some scientists were criticizing it.

Oh the cell has premade RNA polymerase from the mother's egg cells


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Can germs spread by tissues out of box?
Firstly, I don't know if this is the best site to ask this question. Please guide if its not.
Now my question:
If we take out a tissue out of its box, a new tissue comes out partially so we can easily take it next time. Now that tissue can easily collect germs from sneezes and coughing of other people around us.
Can that cause problems/infections? Why doesn't tissue box have a better design?

I think the current design of tissue boxes is more about ease of use than cleanliness.  Though you do bring up a good point, considering that many human pathogens can persist on surfaces

This definitely possible. Due to the microscopic scale of bacteria and viruses, even very light forces(like those from pulling a tissue out of the box) will lead to those bacteria and/or viruses being tossed to the rest of the box.
However, a large portion of the infectious viruses in humans will struggle to survive on the dry, low nutrient substrate of the tissues and box for extended periods of time(especially given high absorbance), albeit the above comment show many that can(depending on the surface).
To answer why there is no better design, I think the simplest explanation is monetary incentive. There is little incentive to create something better both due to R&D cost and inevitable increase in product price, as well as a steep consumer education cost to let customers know, why this is better. However, if you have a good solution in mind that does not raise product cost beyond a few cents per unit, you should a decent shot(if you patent) to license it to the big players.

Maybe it's not better in the long run? Let's say you have a hermetically sealed tissue dispenser under a UV lamp. How will that help when you grab the door knob or touch your clothes that came into contact with who knows what or walk down wind of a group of people breathing? It will probably be very difficult to prove it reduces infection in everyday life.

^ Yes this is correct. The research costs associated with an alteration of this nature will be extremely prohibitive.


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How much Oxygen can the Human body carry?
Basically - the title: How much Oxygen does a human body carry at a single point?

What have I tried: A friend of mine has done some calculations and came up with the following numbers. Neither of us are biologists or have higher degrees in biology. His calculation went something like:

Our body absorbs about 0.033g of Oxygen when we inhale (source).

That's about 0.00103 moles of oxygen.
Through ATP reaction that's about 0.00515 moles of ATP

We have 270 millions of hemoglobin per red blood cell, and roughly 25 trillions of blood cells in our body (wiki), and each Hemoglobin molecule "carries" up to 4 oxygen molecules.
Thus, in total, our body's hemoglobin can carry about (2.5 * 10^13) * (270 * 10^6) * 4 = 1.437 grams of oxygen

How far is the 1.437g number have?
Related (but not the same question) question I found here: How much energy we get from oxygen?.
Note: this is specifically about oxygen we use in our respiratory system - and not the oxygen in the water :]

What do you mean by "carry"?  My first thought is a strong person carrying a large Dewar vessel full of liquid oxygen :-)

@jamesqf as in - "our blood carries oxygen through our body - how much oxygen does it carry at a given point?"

Don't forget that all of the water and many of the organic compounds in our bodies also contain oxygen...

Presumably you have your own reasons for asking this question, but you should not be surprised if nobody else is interested unless you explain why it is of interest.

@David I am interested in this because it is interesting and because we are trying to practice doing these calculations as non-biologists :]

Fair enough. This sort of thing is a minority interest, but you may find a physiologist on the list who does these types of calculations.

@David that is fair, this site and community does not owe me an answer and I am not entitled to anyone's help. I am just hoping that someone who also finds this interesting but has more technical competence than me takes a look and does the calculations better than me.


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Can human brain memory be removed by EMP?
The human brain is the most complicated human organ so it is hard to examine it completely but based on what we know do you think (or do you know from some source) if a human memory can be removed by emp(electromagnetic pulse) ? (If so do you think it would be pernament or temporary?)

Given the large number of people who were exposed to atomic bombs in Hiroshima and Nagasaki and subsequent atomic testing in the 50s and 60s and did not lose memory, I doubt EMP could erase memory ( unless you count total brain obliteration ). However, I am not aware of actual studies exposing brains to high EM fields to test memory.

This is perhaps best suited for http://skeptics.stackexchange.com

http://www.reddit.com/r/askscience/comments/z3lkd/if_you_were_hit_by_an_emp_pulse_would_you_notice/ it won't have any effect on neurons

I think humans are a less interesting case than electric fish, platypuses, and other such animals. To them, the EMP is probably like a flashbang. I believe there have also been reports of birds being confused by strong electromagnetic fields.

This isn't a ridiculous idea; Transcranial Magnetic Stimulation is used in research and even has some use as treatment for depression (http://www.mayoclinic.org/tests-procedures/transcranial-magnetic-stimulation/basics/definition/prc-20020555)

http://en.wikipedia.org/wiki/Electromagnetic_pulse mentions the following natural sources of EMP, which I have ordered by frequency / period, from the shortest to the longest:

Electrostatic discharge from objects coming into contact (normally too small to be of any concern)
Lightning (milliseconds)
Solar flares (hours.) Such flares cause geomagnetic storms (more on this later.)

Several artificial sources of EMP are mentioned, of which the only ones of interest are military:

Non-nuclear weapons. The page links to a general article on directed-energy weapons, which mentions microwave devices for causing pain and for targeted damaging of electronic equipment.
Nuclear weapons. http://fas.org/nuke/intro/nuke/emp.htm gives more information on this, listing three phases.

The EMP produced by the Compton electrons typically lasts for about 1 microsecond, and this signal is called HEMP. In addition to the prompt EMP, scattered gammas and inelastic gammas produced by weapon neutrons produce an “intermediate time” signal from about 1 microsecond to 1 second. The energetic debris entering the ionosphere produces ionization and heating of the E-region. In turn, this causes the geomagnetic field to “heave,” producing a “late-time” magnetohydrodynamic (MHD) EMP generally called a heave signal.

The same reference also indicates:

...the region where the greatest damage can be produced is from about 3 to 8 km from ground zero. In this same region structures housing electrical equipment are also likely to be severely damaged by blast and shock.

As far as I am aware, memory loss was not a major recorded symptom among the survivors of Hiroshima and Nagasaki. The only recent data for sufferers of EMP would be from victims of lightning stikes. While the frequency spectrum is admittedly different from nuclear weapons, victims of lightning strikes are surely subjected to greater magnitudes of EMP than those who managed to survive nuclear bombings (who suffered many other traumas, such as blast waves and radiation.) Those who survive the immediate physical (burns) and neurological (cardiac arrest) effects of lightning strikes must surely be knocked unconscious and be disorientated when they regain consciousness. But again, I am not aware of medium or long term memory loss being a particular symptom.
It is worth comparing the structure of the brain (a fairly homogenous mass of tissue of high water content, relatively conductive) with the structure of electronic equipment (components of ever smaller size and greater resistance in order to save power, surrounded by a nonconductive medium such as air, and interconnected by wires, which serve to channel voltage.) It is unsurprising that the brain is less subsceptible to electrostatic damage than electronic components (electronics workers have to take precautions in order to avoid damaging sensitive components with static discharges from their bodies and clothing.)
The most widespread damage to equipment caused by EMP is from the long-period pulses, which are channeled by electric cables. These act over distances much larger than the size of the human body.
From the last reference:

...distortion of the geomagnetic field was observed worldwide in the case of the STARFISH test. ... the signal from this process is not large, but systems connected to long lines (e.g., power lines, telephone wires, and tracking wire antennas) are at risk

and

The first recorded EMP incident ... nuclear test over the South Pacific ... resulted in power system failures as far away as Hawaii.

http://en.wikipedia.org/wiki/Geomagnetic_storm mentions cases of damage caused by long period EMP, including electric shocks suffered by telegraph operators during solar flare events.
So in conclusion, any amnesia caused by EMP is likely to be caused by normal biological shock mechanisms to individuals unfortunate enough to be electrocuted, and not by any direct electrical effect on the brain itself.

Perhaps it is worth mentioning also people who work on high-voltage electrical transmission lines - they also experience dramatic EM changes (though perhaps less rapidly). While they have many involved procedures to avoid electrocution, I haven't heard of anything beyond some anecdotes of slight headaches or dizziness in terms of impairing brain function.

@Superbest I think long term exposure to mains and higher frequencies is a separate question. There are a lot of people who campaign against mobile phone masts while hypocritically carrying a mobile phone around in their pocket. I would be cautious about concluding mobile phone masts have ZERO health effects, but the phone you are carrying right next to your body will affect you more than the mast. Years ago I used to get a slight headache after talking for half an hour (my phone was a big brick and it got hot) but I phones have improved since then.

@steverrill Agreed, but I was referring to alleged headaches experienced by electrical workers when they come near (as in, within a meter or so) high voltage lines.

The brain is not an electronic device.
An EMP is basically a large amount of electrons flying by all at once. They are negatively charged, and as they pass by they distort your local EM-field (hence the name). This distortion induces current in the wires (a phenomenon known since Faraday) - since most wires aren't made with a large tolerance, the sudden current spike overheats the wire and burns components. In the brain, there are no wires to induce current on.
It is true that electromagnetism plays a role in neuron function, and action potentials can be measured or manipulated with electrodes. However, this is just a consequence of the ion concentration being used for signaling - there is not a flow of electrons across a conducting wire that is driving the process.
Memory is not stored electrically. The two major mechanisms of memory are strengthening of the synapses and the chemical state of the neurons (metabolites and proteins such as cAMP or CaMK, RNA levels, DNA methylation). These aren't very sensitive to electrons moving past - you're essentially trying to catalyze a chemical reaction by applying a strong EM field outside of the beaker.
Also, I suspect the skull and tissue surrounding it may act as a Faraday cage to shield the brain itself from the EM field.
I'm sure it is possible to create an electron flux so heavy that it manages to induce enough current in cells to kill them (or current in your bloodstream to cause cardiac arrest). However, the nuclear explosion that produces this would probably be much deadlier due to other effects, like blast shockwave or gamma rays. So to answer your question, a nuclear EMP would either kill you or not affect your memories, although if you had some exotic, very powerful, very precise pure EMP generator perhaps you could get some sort of stunning effect or give people a headache. I don't think it could erase memories without killing large parts of the brain.

This isn't a ridiculous idea; Transcranial Magnetic Stimulation is used in research and even has some use as treatment for depression (http://www.mayoclinic.org/tests-procedures/transcranial-magnetic-stimulation/basics/definition/prc-20020555)
In TMS a strong, localized magnetic field can disrupt normal functioning of regions of the brain. For instance it can be used on the visual cortex to cause temporary blindness (actually, can cause a condition called blindsight: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2234142/)
As for memory though, TMS does not seem to be able to cause permanent memory loss (in fact, there is research indicating that it may be able to boost memory). Plus, the magnetic pulse would have to be either extremely strong, or very close, for it to have an appreciable effect.


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What species of viper is this?
I think that the snake in the pictures here below is a viper. I found it on a hiking trail on a mountain in Bulgaria. Height was about 2000 meters and the weather wasn't warm as you might expect in a late Spring days, but it seemed quite active.
If it really is a viper what species of viper? Otherwise what could it be?

This is most likely the common European adder (Vipera beris). A list of the reptiles of Bulgaria lists it as occurring in the mountains of Bulgaria up to 2700 metres.
There are a couple of other contenders in the list of vipers, but two of them are incredibly rare (not found since the 1930's) and the last is the horned viper (Vipera ammodytes), which has distinctive horns on the tip of its nose.

Thank you. The description of the common adder is a good match and it had no horns, although it was quite young I think the second option can be discarded.


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Why do dozens of preys run away from a clearly outnumbered predator? (e.g. zebras and lion)
We are all familiar with scenes where dozens (if not hundreds) of zebras, sheep, or other preys are chased by one lion, one wolf or other predator. Examples are all over youtube, but here is one of lion versus zebras. In that video you can count at least 30 zebras. Even more, zebras (particularly adult ones) are bigger than lions. There is also evidence of prey defending itself against predators, but this seems to be not the norm.
So my question is, why do high numbers of preys always run away from a clearly outnumbered predator?
Surely evolution would have already taught these animals that numbers can make a difference, so that coordinated defense strategies would be part of their natural repertoire, or of their social learning. Why nature seem to be so oddly incapable of making use of relative numbers as defense strategies?

This definitely doesn't always happen. I've seen videos of groups of larger prey standing their ground against predators, e.g. walruses against polar bears, elephants against lions.

Why run?
To some extent, selfishness. Remember that natural selection acts within species.
Combat is dangerous. Very dangerous. Even if you are not immediately killed and successfully fend off a predator, wounds can weaken you, damage your senses, and/or kill over time with infection.
If you are a zebra, or a sheep, and you are in a group of other conspecifics, the safest action for you may be to not be the individual that is attacked. Sometimes, you might achieve this by simply advertising being a tough target. Other times, your best bet is to run away. This concept is sometimes humorously discussed in the context of humans and bears: you don't have to be faster than the bear, you have to be faster than the slowest person with you. This is called selfish herd behavior.
Fleeing predation is likely to be the default behavior
If you imagine an allele that changes an animal's behavior to combat an attacking predator (when other conspecifics predominantly run from predators), it is difficult for this allele to grow in the population. Individuals with the allele will get in fights, and although they may reduce predation of the herd as a whole, they will individually be selected against.
Similarly, imagine an allele that changes an animal's behavior to run from an attacking predator (when other conspecifics predominantly attack predators). Individuals with this allele will avoid fights, stay healthier, and breed better than their conspecifics that are getting beaten up, and eventually the herd will be mostly escapers.
Exceptions to the default
However, as pointed out in a comment by gardenhead, not all prey try to escape.
To avoid the 'default' escape behavior, there must be some other motivation: fighting back has to be special some how. In the context of group selection, fighting back may be selected for if it means improved survival of related conspecifics. This behavior is often seen in defense of offspring, but can expand to larger related groups. However, even defense of offspring can be risky, and it is not uncommon in nature for mothers to abandon offspring they cannot defend. It may be safer and more productive in the long run to survive and produce new offspring next year.
Another alternative would be some sort of social/sexual selection, where strong individuals who defend the group (likely males) have increased likelihood to mate.

References
Fischhoff, I. R., Dushoff, J., Sundaresan, S. R., Cordingley, J. E., & Rubenstein, D. I. (2009). Reproductive status influences group size and persistence of bonds in male plains zebra (Equus burchelli). Behavioral Ecology and Sociobiology, 63(7), 1035-1043.
Hamilton, W. D. (1971). Geometry for the selfish herd. Journal of theoretical Biology, 31(2), 295-311.
King, A. J., Wilson, A. M., Wilshin, S. D., Lowe, J., Haddadi, H., Hailes, S., & Morton, A. J. (2012). Selfish-herd behaviour of sheep under threat. Current Biology, 22(14), R561-R562.
Sjare, B., & Stirling, I. (1996). The breeding behavior of Atlantic walruses, Odobenus rosmarus rosmarus, in the Canadian High Arctic. Canadian Journal of Zoology, 74(5), 897-911.
Smith, W. P. (1987). Maternal defense in Columbian white-tailed deer: when is it worth it?. The American Naturalist, 130(2), 310-316.
Wood, A. J., & Ackland, G. J. (2007). Evolving the selfish herd: emergence of distinct aggregating strategies in an individual-based model. Proceedings of the Royal Society of London B: Biological Sciences, 274(1618), 1637-1642.

Thanks! A lot to digest. Just to start, I don't see how the phrase "Remember that natural selection acts within species." fits into the picture. Do you mean that individuals only care about the survival of their own genes and have no regard for those of their fellows? So, in this sense, there is no probability of species survival function to maximise, which could help understand why such strategies might gain little traction in selection processes?

@luchonacho "Do you mean that individuals only care about the survival of their own genes" - to a primary extent, yes. When you talk about natural selection of alleles, you are talking about variation of allele frequency within a population, which means individuals that can interbreed. Interspecific competition is separate. On some macro scale you might think some of the ideas of natural selection apply across species that compete for the same ecological niche, but really only by analogy.

@luchonacho You should also be aware of the idea of the "selfish gene" which takes the individual-centered approach to selection even further and says that individual genes are 'selfishly' self-promoting. There are criticisms of that approach, but if you apply it to this particular case like the 'default behavior' paragraph in my answer you will find it works.

why do some animals like elephants team up and fight the predators?


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Do we know how animals refer to us, humans?
In human languages, we have "sounds" (or words) to refer to animals. For example, in English, we denominate a dog using the vocal sound dɒɡ. So, from the perspective of dogs, if they knew that the sound dɒɡ refers to them, then they "could deduce" that a human emitting the following collection of sounds is referring to them:

lʊk, ðæt ɪz ə kjuːt dɒg. aɪ ˈwʌndə ˈwɛðər ɪt ɪz lɒst?

Now, what about the reverse? Do scientists know of a particular sound (or maybe a sign, a movement, or related form of communication) used by any animal which signifies "human"? In case the current answer is no, is this ever possible to know? Maybe for animals where studies are more advances, like primates?

Downvoter(s), please comment.

The question assumes that animals (as a weirdly inclusive group) have a "word" to refer to humans. The vast majority of animals species do not use any specific signal to refer to humans. Very few species has the social intelligence needed to communicate about the the presence of individuals of a difference species and among them few have important enough direct relationship with humans to have do so. Some species make sound to indicate the presence of a flying vs terrestrial predators. If a human shows up, then the sound should be the one associated to terrestrial predator but ...

... that would not qualify as a sound to refer to humans. Outside of eventually, a very small zoo population of some vertebrate species, I doubt there is any species that would have a term for "human". If you have any reason to think the opposite, can you please try to focus on this specific species for which you think individuals might vocalize (or signal in any way) to convey the concept of "human" to its congeners. Likely the only species that has a "word" for "humans" are humans!

The only other species that actually has what we would consider words are velvet monkeys who do not have much contact with humans. Some birds appear to have a  nascent language, with something similar to words and sentences , the japanese great tit for instance but I have not seen a list of known words. https://www.nature.com/articles/ncomms10986

@Remi.b "In case the current answer is no, is this ever possible to know?" Maybe you missed that bit. Why not translate your comment as an answer?

@luchonacho Comments made into an answer as you asked! Cheers

The question seem to assume that animals (as a weirdly inclusive group) have a "word" to refer to humans. The vast majority of animals species do not use any specific signal to refer to humans. Very few species has the social intelligence needed to communicate about the the presence of individuals of a difference species and among them few have important enough direct relationship with humans to have do so.
Consider vervet monkeys as an example. Vervet monkeys make sounds to indicate the presence of a flying vs terrestrial predators. If a human shows up, then the sound should be the one associated to terrestrial predator but that would not qualify as a sound to refer to humans. See Seyfarth, R.M.; D.L Cheney; Peter Marler (1980). "Vervet Monkey Alarm Calls: Semantic communication in a Free-Ranging Primate". Animal Behaviour. 28 (4): 1070–1094. doi:10.1016/S0003-3472(80)80097-2
Outside of a very small zoo population of some vertebrate species, I doubt (but might be proven wrong, who knows?!) there is any species that would have a term for "human". If you have any reason to think the opposite, can you please try to focus on this specific species for which you think individuals might vocalize (or signal in any way) to convey the concept of "human" to its congeners. Likely the only species that has a "word" for "humans" are humans!

Do scientists know of a particular sound (or maybe a sign, a movement, or related form of communication) used by any animal which signifies "human"?

It is not a matter of knowing what sound they use. Excluding humans, animals likely don't use any sound to refer to the concept of "human".

In case the current answer is no, is this ever possible to know?

The answer is not "no, we don't know" but rather "there is nothing to be known here as animals just don't do that."

based on the work on japanese great tits some song birds use something similar to words, with combinations of sounds in specific orders, with different sequences having different meaning but we are pretty far form having a tit dictionary.

If we look at how human infants develop language skills (this is anecdotal evidence, N = 3), the first “words” spoken are nouns. For example (in English), sounds that represent mama, cookie, or ball. Verbs seem to appear later on; in the beginning we want to describe the world around us.
For me, the idea of a non-human language, does not have a clear sense.  In other words, we have no definitive evidence that any other species attempts to somehow “describe” the world they inhabit.  That is not to say that other animal species are unable to communicate among themselves with scents, pheromones, sounds, calls, vocalizations, or tail slaps (I was thinking of the North American Beaver for that last reference), just that we currently have no way of telling, or determining, if they have nouns (in the human language linguistic sense of nouns).
Consider the North American Prairie Dog communities on the Great Plains, where one, or more, individuals appear to be posted as lookouts, ever vigilant, and whom send out an alarm call when a perceived danger approaches.  It probably doesn’t really matter if the predator is a hawk, a fox, a wolf, a snake, or a human with a gun; the alert means something like “Run and hide unless you want to die, and bye-bye, it’s been nice knowing you, because I am drawing them away by making this sound.”


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How do predators avoid "food poisoning"?
How do predators avoid becoming ill in cholera, diarrhoea, dysentery and similar diseases?
They aren't exactly careful when eating a kill, especially pack animals where there can be quite a fight over a catch and, I assume, should regularly get pieces of the large intestine in their mouth - which should be very unhealthy, shouldn't it?
Even house cats, when they eat mice and rats, seems to swallow them more or less whole and then cast up the skeleton = all contents of their prey's intestine remains in their stomach.

They’ve evolved and adapted to be able to eat what they do without getting ill (although they probably do get ill from eating bad food on occasions) because of natural selection. Remember, humans are quite different to other animals and what makes us ill doesn’t make most other animals ill.

Pet owners might disagree with you that their fluffy predators do indeed avoid food poisoning.

@BryanKrause - I immediately thought about my dogs when I read the title of this question. Luckily, the three I have right now have GI systems of steel, but some of my previous dogs... did not.

Not only "should [they] regularly get pieces of the large intestine in their mouth", but when I lived on my farm(ette) in the woods, where individuals were allowed to hunt, the dogs would go looking for guts to eat. We took to requiring every hunter to bury the deer's innards. The dogs would come back covered in dirt with guts to eat. We then took to requiring burial of innards with rocks stacked on the site. The end results of enjoying the contents of small and large intestines were unpleasant, to say the least.

Eating the meat freshly killed helps rather than letting it fester in the fridge for a week before eating it.

@user438383 So have humans. We clearly aren't that different from chimps, and they eat meat whenever they get the chance (gorillas and orangutans are more vegan). But what is the difference between humans and dogs? We mostly eat the same stuff. In what respect do you mean humans are quite different from dogs when it comes to infections and diseases?

@d-b - I would say that dogs are about as close to humans as a non-primate can get, with 50,000 years of co-evolution with us, eating our food, living with us, etc. They share hundreds of diseases with us, even rare ones. Dogs are the reason we have a treatment for narcolepsy. Their contribution to our knowledge is profound.

If you live in a country where things like cholera and dysentery  are endemic, how many healthy dogs do you see roaming around. How many are emaciated? When they die, who does autopsies on them to determine cause of death? My point is, you're making assumptions.


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Is there a name for the natural law that any population of a species will increase until it utilizes all available resources in the area it inhabits?
A squirrel population in a forest will only be as big as the available food source allows, and probably a little smaller after you account for predators, disease, etc. What is the name of the tendency of a species to multiply until it reaches terminal population?
Sort of like how when you drop a tennis ball from a building, gravity will only accelerate its fall so much until wind resistance counteracts it. This results in the ball reaching a constant velocity, known as “terminal velocity” in physics.
Similar to the phrase “evolutionary niche”, but not really involved with evolution.

Malthus is the fellow usually credited with the idea of exponential population growth: that a population unchecked by resource limitations will grow proportional to its own size. He was particularly concerned by the catastrophe that would occur when this growth would lead a population to exceed the ability to support itself.
Later, Verhulst came up with the idea of logistic growth. The logistic function approximates exponential growth when populations are small, but eventually growth slows as it gets closer to some capacity. If you think just in terms of food, this would represent members of a population having more and more trouble finding the limited food supplies as it gets closer to the limits.
I would simply call the scenario you describe "logistic growth". It's a fairly common "null hypothesis" on which other models can be built.
Accounting for predators is a bit more complicated, but you could see the Lotka-Volterra equations as a starting point.

the term closest to "terminal population" is probably "carrying capacity" ( https://en.wikipedia.org/wiki/Carrying_capacity ) though that's a property of a particular environment rather than a species within it.


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Strength of Female Chimpanzees vs. Male Chimpanzees?
Where can I find studies done on the strength dimorphism between male chimps and female chimps?
For example, "one-arm pull strength is 300 pounds for male chimps and 200 pounds for female chimps"

try google scholar or pub med.  Nothing obvious here: https://scholar.google.ca/scholar?hl=en&as_sdt=0%2C5&q=chimpanzee++sexual+dimorphism+%22strength+differences%22&btnG= ... maybe useful references here? https://www.pnas.org/content/114/28/7343.long

Note this is likely do to the difference in size between male and female chimps more than anything else.

not necessarily entirely; the (very small!) sample I show in my answer does show 2 males that both have higher weight-specific strength than 3 females ... (p-value=0.1 ...)

I searched for "chimpanzee strength" on PubMed and followed links from

O'Neill et al. PNAS 2017 "Chimpanzee Super Strength and Human Skeletal Muscle Evolution"

to

Bozek et al. PloS Biology 2014 "Exceptional evolutionary divergence of human muscle and brain metabolomes parallels human cognitive and physical uniqueness" where I found this figure:

which shows pulling strength normalized by individual body weight, with circles for females and diamonds for males.  In fact, the Excel spreadsheet given in supplementary materials shows there were two males and three females, tested in three sessions; in each session weight and pull strength were listed. The ratios of max pull to weight for males were 3.44 and 3.49, for females were 2.9, 3.14, and 3.25 (one of the males was quite small ...)
O'Neill et al. give a few other references, you could follow those as well and see what you come up with.  (I found that "chimpanzee strength" gave better results as a search term than terms including "sexual dimorphism", which tended to be swamped by more general discussions of the evolution of dimorphism in apes.)
@jackaidley notes in a comment that

extreme caution is needed in interpreting these results for Chimp sexual dimorphism, quite apart from the very low number of individuals, there is a significant problem with these measurements - as the paper itself notes "The inability to control nonhuman primates' motivation hinders the exact quantification of the muscular strength difference between humans and nonhuman primates, even in a highly controlled experimental setup." This problem equally applies to male/female differences.

In other words, male chimpanzees might pull harder at least in part because they are more motivated than females in this particular setting, rather than because of intrinsic differences in strength. (That may or may not matter for what you are trying to do with this information.)

Good find, and I suspect this is about as good as it gets. But I think extreme caution is needed in interpreting these results for Chimp sexual dimorphism, quite apart from the very low number of individuals, there is a significant problem with these measurements - as the paper itself notes "The inability to control nonhuman primates' motivation hinders the exact quantification of the muscular strength difference between humans and nonhuman primates, even in a highly controlled experimental setup." This problem equally applies to male/female differences.

Is the x-axis individuals? It seems to not be equally-spaced for some reason.

What is the x-axis even? Some human-chimp-macaque function?

I believe the x-axis just represents individuals (individuals are measured in 1-4 sessions). Don't know about uneven spacing.  The data are there if you want to draw your own version ...


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Why isn't life expectancy normally distributed?
Lots of phenomenon in nature can be plotted onto some sort of normal distribution, and that makes intuitive sense to me (such as human height). Why then, does global human life expectancy drop off so suddenly after ~85 years old? Is there some factor which suddenly increases mortality significantly? How come so few people (statistically speaking) age above 85 years old?

Inspried by this question

There's no particular reason everything in nature needs to fit a normal distribution; normal distributions are just one of many different types of naturally-occurring distributions. In some cases, the other types can be transformed (e.g. by logarithms) into a normal distribution (e.g. a log-normal distribution), in other cases not so much.
As to why it doesn't match a normal distribution? Normal distributions tend to occur when they're the sum of many independent processes. Mortality factors aren't independent. Many factors that affect mortality are age-dependent (cancer, heart disease, etc), so they depend on the same factor (age) and accumulate at the same time, not independently. Therefore longevity doesn't meet the basic expectation for a normal distribution.
If you look at specific mortality factors, you might well find some that are relatively independent of age, and these might be closer to normally distributed. But age is extremely important for most forms of mortality, even those that don't accumulate with age (automobile mortality is higher in younger drivers; infectious diseases disproportionately target the very young and very old; maternal deaths are more common in younger to middle-aged women).
Instead, longevity is a negatively skewed distribution. It may crudely be considered as a log-normal distribution, though not perfectly. There are also more sophisticated approaches to model mortality distribution, such as the Gompertz–Makeham model (simplistically, an exponential increase in death rates with age), or the Weibull distribution.
Various publications compare models, or come up with new and shinier models, for longevity:

Comparison of the Gompertz and Weibull functions as descriptors for human mortality distributions and their intersections
A Novel Generalized Normal Distribution for Human Longevity and other Negatively Skewed Data
Predicting Human Mortality: Quantitative Evaluation of Four Stochastic Models

The histogram you show isn't a distribution of age-at-death for individuals, it's a distribution of life expectancies for different countries.  The post you link takes data from a table on the Wikipedia page List of countries by life expectancy.  Interpreting the histogram you posted, we see average life expectancy seems to hit a wall around 85.  This does not mean that individual human life span is not normally distributed.
Excluding deaths at infancy, the peak of the death rate curve appears to be at about 88 years for women in the United States in 2014, as seen in a blog post by the The Max Planck Institute for Demographic Research:

Lifespans are increasing and becoming more similar: While life expectancy of US women rose by almost 19 years between 1933 and 2014 (from 62.8 to 81.3 years), the variance in the distribution of deaths over age shrank by ten years. Data: Human Mortality Database © MPIDR


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Which fishes produce alarm signals to warn other group members about in coming predators
Atlantic Goliath Groupers are fishes which produce unique low frequency sounds to mate and when approached by predatory fish . The sounds produced when approached by a predator (or even a scuba diver) are different from those produced whilst mating.
The problem is this fish is found only in the Atlantic.  I'm specifically looking for fishes in the Indian ocean . Thank you for ur time :)

Here are some fishes produce alarm signals as sounds.
members of family Pamadasyidae-the grunts.
the family scaridae e.g.—Parrot fish.
sea catfish Galeichthyes felis
gafftopsail catfish
Indian loach
Trigger fish
Epinephelus striatus
For mor information see the link. http://www.fishfarmingtechniques.com/fish-structure/specialized-organs/sound-producing-organs/sound-producing-organs-in-fishes-specialized-organs-fisheries/13563


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Genetic analysis of one sibling relevant to other
My sister, my only sibling and I have literally no physical traits in common. Whatever trait I inherited from one parent she inherited from the other. We're thinking of using one of those genome analysis services to learn information about our mysterious geographical ancestral origins.
We're wondering if, despite our differences in appearance, if only one of us submitted our genome for analysis, the geographic origin results would still be accurate for the other. Because our parents may both have diverse lineages, the answer might not be so cut and dried.
Understand, please, that we are not so much looking to find out the general "where" of our origins as we are to have each of us know what our individual genetic heritage is.

You should be aware that DNA tests can't give highly localized "geographic origin" information.  Genes spread around, so exact locations can't really be pinned down.  Many gene variants can be confidently assigned to continental areas (Africa, Asia, Europe), but it begins to get hazier as smaller areas are considered.  For example, many British Isles variants can be distinguished from other European variants, but French versus German genes really can't reliably be separated for the most part.  You might care to see what other people think of their results, for example by looking at Reddit posts about 23andMe results.
Most siblings will get pretty similar origins results.  If each of the parents individually has several very distinct origins, then siblings can have somewhat more divergent origin results depending on the randomness of inheritance.  The only way to know what you two each have is for both of you to get tests.  You should consider that if, in actuality, you two are half-siblings, or are not closely related (as e.g., one or both of you were adopted), the results will show that.

If you are siblings, then, outside the Y chromosome (if you are a man, otherwise, you both only have X chromosomes), the results should be very similar. There might be some slight variations of course but it is unlikely to come out as important.
If you are not siblings (e.g. you might be half-sibling if your mother is hiding an affair; sorry for suggesting this possibility but that's no so unusual), then the results might well be quite different.

Hello! This question was deemed worth of an answer, so why not upvote it? Vote early, vote often to encourage new users and keep the community alive!

@LinuxBlanket I was not 100% sure that the question would be considered worth of an answer. It has happen to me a few times in the past to be criticized of answering questions that aren't worth it. But thanks for pointing this link to me and everyone else!

@LinuxBlanket Btw, why haven't you upvote then?

Even if it's not considered worth of an answer by the community, your opinion still counts and can be expressed not only by answering, but also by voting. With that upvote, you gave the OP the chance and maybe the will to participate more. Thanks, and remember to vote early and vote often! :)

I admit that I didn't do it in order to see what was the effect of my comment - I didn't want to have answerers think "the question has an upvote anyway". Now I'll do it!

Ok! I'll make sure to apply this logic. Let's vote early and let's vote often! Thanks


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How long could a shark breathe pepsi?
Sharks breathe seawater. Seawater isn't 100% pure water, but mostly water. Pepsi (other colas are available) isn't 100% pure water, but mostly water.
How long would a shark be able to breathe if submerged in Pepsi (other colas are available) and what, precisely, would kill them?

I don't think the dissolved $\ce{CO2}$ would do them any favours. And I doubt the chemicals from the cola would be very good for the shark (caffeine is toxic to many animals).


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Where can I find datasets containing large phylogenetic networks?
There are many datasets out there for phylogenetic trees, one can example can be found here.
However, I couldn't find something for phylogenetic networks. According to Wikipedia:

A phylogenetic network or reticulation is any graph used to visualize
  evolutionary relationships (either abstractly or explicitly)2
  between nucleotide sequences, genes, chromosomes, genomes, or
  species.2 They are employed when reticulation events such as
  hybridization, horizontal gene transfer, recombination, or gene
  duplication and loss are believed to be involved.

Of course a phylogenetic tree is a phylogenetic network, but phylogenetic networks can be thought of as rooted directed acyclic graphs, meaning that more complicated evolutionary structures can be captured.

For what purpose?

I have an implementation of an algorithm that I would like to run on a phylogenetic network.

I handled your flag. This question was, however, not asked as a guest, as you have a user name and rep. So you cannot login under Jonathan?


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Cichlid fish in Africa
Are the cichlid fish in Africa an example of divergent or convergent evolution? On the one hand they have evolved similar features to each other indicating convergent evolution, but on the other, they formed as a result of an adaptive radiation which indicates divergent evolution.

The level of lake malawi has dropped by 200 meters at least 20 times in the previous 1.3 million years, forcing them into small lakes, and there are lots of theories about "cichlid evolution" on google, including a 54 minute talk video. Fish have a lot of convergent evolution too, there are kinds of holotype fish forms which appear again and again in different continents and different seas, the same as an australian and european magpie. Cichlids are similar to many species like snappers, even dolphins are said to be convergent with sharks.

Writing "convergent evolution" in google images is one of the most fascinating pages out there: https://www.google.fr/search?biw=1572&bih=857&tbm=isch&sa=1&ei=-9bBW5fILoi6ac7ltrAC&q=%22convergent+evolution%22&oq=%22convergent+evolution%22&gs_l=img.3..35i39k1l2j0l8.72634.74183.0.74652.2.2.0.0.0.0.90.168.2.2.0....0...1c.1.64.img..0.2.166....0.iTe5In6n1qg#imgrc=7pBcz3R6hTpCHM: ........ and ..... https://www.google.fr/search?q=convergent+evolution+in+fishes&num=100&source=lnms&tbm=isch&sa=X&ved=0ahUKEwjk0OLMp4PeAhUIz4UKHXnRDOgQ_AUIDigB&biw=1572&bih=857#imgrc=u293tbb5Xe8mzM:

They have diversified to fit into many different niches.

You might want to read about adaptive radiation

Both.

Recent theoretical models, however, predict that convergence should be common within species-rich communities, such as species assemblages resulting from adaptive radiations. Here, we present the most extensive quantitative analysis to date of an adaptive radiation of cichlid fishes, discovering multiple instances of convergence in body and trophic morphology. ...

Independent adaptive radiations often produce convergent phenotypes
In Lake Tanganyika, convergent phenotypes evolved within a single adaptive radiation
These convergent morphologies are associated with adaptations to the same niche
Distantly related yet morphologically similar species coexist in the same habitat

--Convergent Evolution within an Adaptive Radiation of Cichlid Fishes


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Have traditional categories such as phylum, class, genus, been dispensed with in modern taxonomy?
Looking through the one zoom and EOL projects I see no reference to such categories.

We still use these concepts because they help communication but they are mainly arbitrary. Some of the discussion in this answer might be of interest to you.

Thanks Remi, is there scope for a listing of species in terms of supersets and subsets - most likely from an evolutionary perspective.  If this has been done do you know where I could see some examples.    I don't have the required knowledge to give a detailed example but something along the lines of lion<feline<carnivore<mammal<vetebrate<chordate<etc might be one.

I am afraid any categorization of lineages of this kind will necessarily end up being somewhat arbitrary. I could picture categorizing into a <enter taxonomic level; e.g. family> everything that share a common ancestor less than  years ago. It would still lead to issues with horizontal gene transfer but that might be feasible.

But presumably some worthwhile subsets / supersets can be shown particularly from a structural point of view.   Again I lack knowledge here but I am guessing that a term like feline is arbitrary but mammal and invertebrate are demonstrable and also that all mammals are invertebrates.  Am I on solid ground with that?

Oh yes of course. What I meant is whether we choose to call mammals a class or an order is somewhat arbitrary. But we can clearly define monophyletic taxa and investigate their relationship to other monophyletic taxa. This post that offers an intro to phylogeny might be of interest to you


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Is it tautological that all living humans descended from a single male and single female human ancestor?
Many popular science articles cite high sequence conservation of mitochondrial DNA and the Y chromosome among living people as evidence that all humans are descended from a single male and single female human ancestor.
Is sequence evidence necessary to make this assertion, or does it follow tautologically from the definition of speciation? What would a speciation pedigree look like for a species that does not pass through a single-individual bottleneck?

Can you give an example of an article making this claim? The way you are describing it is not an accurate representation of what mitochrondrial Eve or Y chromosome Adam means.

@J-- Why are you talking about speciation while dealing with a single species?

@J-- It will be true for any non-recombining sequence (which is the case of mtDNA and most of the Y chromosome) that all individual living at some point in time will coalesce into a single individual, yes. This is predicted by coalescent theory and is a rather intuitive consequence of any pedigree. Evidence is still good to confirm our theory though and evidence is mainly about dating the common ancestor rather than anything else.

Possible duplicate of Do all living humans literally descend from one ape?

The assertion is not tautological because the definition of speciation does not involve single individuals.1
From Wikipedia:

Speciation is the evolutionary process by which populations evolve to become distinct species. [emphasis added]

Speciation is a process of populations, and it is not necessary for only a single pair of sexually reproducing organisms to be the sole ancestors of a species.
There did exist one female ancestor, dubbed mitochondrial Eve, who is the most recent matrilineal ancestor of all living humans. Because mitochondria are passed from mother to offspring, and do not recombine, that individual's mitochondrial DNA is the ancestor of all human mitochondria.
Similarly, there existed one male ancestor, Y-chromosomal Adam, who is the most recent patrilineal ancestor of all living humans. The Y-chromosome is passed through the father, and most of it does not recombine, so that individual's Y-chromosome is the ancestor of all current human Y-chromosomes.
Note that mitochondrial Eve and Y-chromosome Adam do not have to and almost certainly did not live at the same time.2
The age estimate for mitochondrial Eve is about 150,000 years ago.
The age estimate for Y-chromosomal Adam is about 200,000-300,000 years ago.
These time frames are around or after the origin of anatomically modern humans, so it is correct to call these ancestors humans. (This is didn't necessarily have to be true, it's possible these individuals could have predated the separation of humans from other species.)
Finally, is sequence evidence necessary to make these assertions? For knowing the existence of mitochondrial Eve or Y-chromosomal Adam, no; their existence is a logical consequence of constructing a pedigree (see coalescent theory). However, for dating these ancestors and being able to claim they were human, some examination of the DNA is necessary, and DNA sequencing provides the most precise estimates.

1 We'll ignore asexual organisms, where the definition of species becomes especially difficult.
2 I will add these additional cautions from the mitochondrial Eve page, that equally apply to Y-chromosomal Adam.

Caution: This does not make Mitochondrial Eve the first woman, or the first human, or the first member of a new species. Further Caution: This does not mean that other women alive when Eve was do not have descendants today; they simply do not have living descendants who are descended only through female links. Yet Further Caution: If a person were to be discovered whose mtDNA showed a pattern of mutations of greater time depth, then the status of Mitochondrial Eve would be reassigned to the most recent female ancestor shared by both that person and the person we now call Mitochondrial Eve.


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Two state exponential growth model
I want to write an expression to model exponential growth of a microbe that scholastically and irreversibly acquires a mutation at a fixed rate that slows growth.
I can do it iteratively, but am curious whether a simple expression can be written.
I started with:
$P_{total} = P_{wt}e^{r_{wt}t} + P_{mutant}e^{r_{mutant}t} $
How do I factor in the mutation rate that converts $P_{wt}$ to $P_{mutant}$?

Can you please explain what your variables stand for?

What is the variable you are interested in tracking? Growth rate? Population size? Do you want to model drift and selection in your model to figure out the probability of a given deleterious mutation to fix?

I want to track the number of wild-type and mutant cells over time, given the growth rate of each and the mutation rate.
P_total = total # of cells,
P_wt = # of wild-type cells,
P_mutant = # of mutant cells,
r_wt = growth rate of wild-type cells,
r_mutant = growth rate of mutant cells,  r_mutation = mutation rate
t = time,  .

$P_{total} = P_{wt}e^{(r_{wt}-r_{mutation})t} + P_{mutant}e^{(r_{mutant}+r_{mutation})t}$ ?

What do you mean by scholastically in this context?

In general
Analytic solutions only exist for special cases. Therefore a good way of approaching these problems is to first act like they don’t and be happy if you can see how to derive one. It’s also more straightforward than wild guessing.
Your problem
Notation:

$P_\text{w}$ denotes the original population and $g_\text{w}$ its growth rate.
$P_\text{m}$ denotes the mutant population and $g_\text{m}$ its growth rate.
$r$ denotes the mutation rate.

The differential equations that describe your problem are:
$$
\dot{P}_\text{w} = g_\text{w} P_\text{w} - rP_\text{w},\\
\dot{P}_\text{m} = g_\text{w} P_\text{m} + rP_\text{w}.
$$
This system of differential equations is linear as it can be written in the form $\dot{\vec{P}} = A·\vec{P}$ with $\vec{P} = (P_\text{w},P_\text{m})$ and:
$$A = \pmatrix{g_\text{w}-r & 0 \\ r & g_\text{m}}.$$
Linear systems in turn can be solved by finding the eigenvalues and eigenvectors of the matrix $A$, which are:

$\vec{v}_1 = (0,\frac{r}{g_\text{w}-g_\text{m}-r})$ for the eigenvalue $λ_1 = g_\text{m}$.
$\vec{v}_2 = \left( 1, \frac{r}{g_\text{w}-g_\text{m}-r} \right)$ for the eigenvalue $λ_2 = g_\text{w}-r$.

This means that the solution can be written as:
$$\vec{P} = c_1 e^{λ_1 t} \vec{v}_1 + c_2 e^{λ_2 t} \vec{v}_2,$$
where $c_1$ and $c_2$ are constants determined by the initial condition:
$\vec{P}(0) = c_1 \vec{v}_1 + c_2 \vec{v}_2.$
If you assume that you have no mutants at the beginning and you initial wild-type population is $1$, you have $c_1=-1$ and $c_2=1$.
With this you get:
$$
P_\text{w} = e^{ (g_\text{w}-r) t},\\
P_\text{m} = \frac{r}{g_\text{w}-g_\text{m}-r} \Big(e^{(g_\text{w}-r) t} -e^{g_\text{m} t} \Big).
$$


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Is any animal born adult-size?
Size growth after birth seems to be the norm in the animal kingdom (as well as among plants). This makes sense. It's evidently physically challenging for an animal to produce an offspring of its equal size, both if born through gestation or eggs.
But, is this always the case? Are there exceptions, i.e. animals that are born at their "normal", adult size? I don't seem to find any (nor that I am a biologist or expert on the topic).

You may perhaps want to more specifically ask whether, for instance, there are any animals (e.g. placental mammals) that do not grow in size after birth. There are terms for this, such as altricial babies (babies that are less developed in some ways, or require additional care) or precocial babies (those that develop less post-birth). You could ask for extreme examples of precociality! It may also help to read up on neoteny which is related but not directly linked; you may get some good ideas there.

Also, birth is something that we can interpret fairly easily for many vertebrates. However, what counts as birth for a moth or butterfly? The embryonic egg is certainly very small. The larvae grow. Then they pupate, and undergo eclosion (finishing metamorphosis) and come out of their pupa usually completely adult sized. It is not unusual for flies to eclose as very large imagos (adults) and then slightly shrink during the rest of their lifetime.


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Is there any biological basis for the commonplace "eyes popping out" cartoon?
We might all be familiar with images like these below:

I see this clearly "works" in a cartoon context. It makes a point. That "eyeballs" hanging outside belong to the individual and can be shown next to him and not in the floor or so. But, is there any biological basis for this? Is something like this ever possible? Probably the answer is no, as the (optic) nerve connecting the brain with the "eyeball" surely cannot be extended like that. Would the eyeball actually hold its shape?
PS: for the sensitive among the crowd (including myself), please do not post gore-like pictures to show what actually happens. If want to provide some visuals, diagrams might suffice.

I once saw a guy in "Ripley's believe it or not" who could pop his eyes out to some extent (not till the optic nerve is visible).

Also, see this guy. What extent of eye popping are you asking about? Usually, in cartoons eye popping is associated with an extremely delightful visual stimulus. Are you asking if such a thing happens in real life?

@WYSIWYG "What extent of eye popping are you asking about?" Well, that's probably an important part of the answer. If this is ever possible to any extent, or if actually it doesn't work that way at all. E.g. optic nerve cannot be extended and so can ever be visible.


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Exactly what biochemical factors control the intensity of an allergic reaction?
I think have a functional understanding of how an allergic reaction (Type I Hyper Sensitivity) occurs: basically the allergen causes production of antibodies that attach to mast cells and basophils. Later, if the same allergen binds to those antibodies, the cells release histamine and other unpleasant chemicals.
However, it's clear that the degree of allergic reaction varies a lot from person to person. For example, if my wife goes outside all day during peek grass pollen season, she'll end up with a sinus reaction, and not much else. If I go outside for a few minutes, I'll develop that, and if I stay longer, I'll get hives, weepy eyes, and so on.
Clearly I'm more sensitive to grass than my wife, but what exactly causes this? I can imagine a lot of possible factors!

Maybe I have many more antibodies (but why?)
Maybe I absorb more of the allergen per unit time (but why?)
Maybe my mast cells require less allergen to react (but why?)
Maybe my mast cells contain more histamine per cell (but why?)
...

So I guess my question is: What drives the variation in allergic hyper sensitivity responses?

Network of possible factors that contribute to the variability of the immune reaction between individuals is still not well investigated.
Type I hypersensitivity is mediated by IgE antibodies, which means that lymphocytes B after initial contact with antigen undergo oligoclonal selection. Only these with the highest affinity towards the antigen will survive. During this process (see: germinal centre reaction) genomic regions responsible for antigen binding change their sequence in non-deterministic manner. So, each individual has slightly different set of antibodies targeting the same antigen.
Moreover, within the same antigen (allergen), different regions (epitopes) can trigger the immune reaction in different individuals.
Other, more general factors also contribute to the symptoms associated with hypersensitivity reaction. For example: hormones, infections, medications, microflora condition, genetics (eg. major histocompatibility complex) or even psychological status.
Also see:
Article 1
Article 2
Article 3


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About Frameshift Mutation
I am coding a DNA translater, based on the homosapiens genome, & i knowing that the data provided from NCBI is surely not 100% precise (there may be some base changes / removes etc...)
, & i want to prevent/bypass those mistakes to get a 'close' list of the REAL chain of proteins produced, so i was wondering how the frameshift do not change an entire species, taking into consideration that if 1 or 2 bases are removed , => then all the dna/rna translation will be modified therefore => ALL proteins will change & even the start/stop codons will change its location
(am not a biologist, am asking why the frameshift doesnt do that & create a new species from 1 or 2 base changes??)

It does change the location of start/stop codons, but they still remain the start/stop codons

Genes (here defined as protein coding sequences) are not perfectly aligned the ones after the others in the genome. In fact, in humans (like in most eukaryotes), only a small fraction (of the order of the percent) of the genome directly code for proteins.
Each gene translation unit starts with specific markers. Not even talking about what will be or won't be transcribed, a translation unit starts with the start codon (AUG). Hence, a frameshift mutation will only affect the gene in which (or even, only the exon) in which the mutation happened.
For writing a software that finds coding sequences (and translate them), you will need to learn much more about genetics. You might want to have a look at an intro course on molecular genetics / central dogma / translation, transcription such as a number of the biology classes on Khan Academy for examples.


text:
What kind of longhorn beetle is this?
I live in Europe and found this interesting longhorn beetle I think and I was curious what species it is or what's it's name!
Thanks to anyone who identifies it!

Rosalia alpina (common name: Rosalia longicorn)
See here: Rosalia longicorn
The link I added shows a picture of an identical Alpine Longhorn Beetle. This longhorn beetle occurs mainly in the European Alps and the neighboring countries (e.g. Germany, Hungary, and France). Minimum height is around 700m above sea level. The adults are active from June to September. The color varies between blue and grey, the head is characterized by one spine on each side of the head. The number of black dots on the elytra varies.

Welcome and thanks for your answer. For species ID answers we expect users to post an identifying picture and additional evidence that it is indeed the beetle in question, for example by mentioning geographical distribution and check whether that matches OP's location.

Thank you for your comment. The link I added shows a picture of an identical Alpine Longhorn Beetle. This longhorn beetle occurs mainly in the European Alps and the neighboring countries (e.g. Germany, Hungary, and France). Minimum height is around 700m above sea level. The adults are active from June to September. The color varies between blue and grey, the head is characterized by one spine on each side of the head. The number of black dots on the elytra varies.

Also see https://commons.m.wikimedia.org/wiki/Rosalia alpina for further pictures

You can edit the question to add this information to your answer. I think the downvotes are harsh when you appear to have the correct ID but those leaving them may reverse them following an edit.


text:
Glucose Carrier Proteins in Cell Membranes
I'm using Campbell's Biology textbook, and it states that certain carrier proteins transport glucose across the cell membrane much faster than would occur normally. It states that the "glucose transporter" is an extremely selective protein, which doesn't accept even fructose, which is an isomer of glucose. However, another hexose, galactose, appears to me to be even more similar to glucose- it's just that one of the H-OH pairs is flipped. In comparison, though fructose is indeed an isomer, it's a ketose, but glucose and galactose are both aldoses. Given this, I'm pretty sure galactose is more similar to fructose.
My question is: is the carrier protein specific enough to carry only glucose and not even galactose? If it isn't and it's able to carry galactose, what would happen if galactose was transported into the cell in greater quantities?
Note: I'm a bio beginner, so please have some patience if my questions are nonsensical or my facts are incorrect, any corrections would be welcome.

First thing's first: there are many different kinds of glucose transporters (genes), even within the same organism. These genes share partial sequence identity in mammals, and are part of the SLC2A, or "GLUT" gene family. In yeast, there exist glucose- and galactose-specific transporters.
Often, not always, a glucose transporter type may be tissue specific. GLUT3 is expressed in neurons, in the placenta, and elsewhere. Compare this to the expression of GLUT1, found in red blood cells, and GLUT4, found in adipose and skeletal muscle tissue.
Each kind of transporter has various affinities for glucose (or other sugars for that matter), and various levels of permeability for similar molecules. This is what is called the specificity of the transporter. The rate at which sugars can pass through the pore of the transporter is called the frequency. Together, these properties define the function of a hexose transporter, and hence why there are different kinds with site-specific expression across the body.
In terms of regulation: GLUT1 is dynamically regulated based on available glucose (up-regulated during shortage and down-regulated during excess). This is not the case with GLUT4; instead, GLUT4 is insulin-regulated, so that muscles and fat tissues can uptake glucose for storage, which is a hormone-controlled process.
Here is a great webpage to help you understand the characteristics of hexose transporters, especially with regard to galactose, fructose and glucose.


text:
Could the Immune Gene HLA-B27 be gentically altered, snipped, switched off, replaced, edited within the body
Could the Immune Gene HLA-B27 be genetically altered, snipped, switched off, replaced, edited within the body.?
Thousands upon thousands suffer immune disease as do I from this highly implicated gene.
Is their a gene manipulation mechanism that 'could' work for this gene from within the body ?


text:
What animal is this bone from?
10.5 ounces, found laying on ground, central California coast.

This is the cannon bone of an adult artiodactyle.. The size points towards sheep or goat.


text:
Is the mutation rate in pseudogenes higher than in coding regions?
Coding genes are subject selective pressure that are not present for pseudogenes, that would suggest that pseudogenes have a higher mutation rate than coding regions. If so, how much higher?

It is important to distinguish between the rate of mutation, which is a biochemical process, and the rate of fixation, which is a population process whereby an allele with a particular mutation becomes fixed (present in all individuals) in the population. Relaxed purifying selection, such as that experienced by genes undergoing pseudogenisation, affects the fixation rate of mutations because new variants are not being filtered from the population by purifying selection. The mutation rate itself is probably constant, unless some other factor is at play.
In response to comments, I will say this: if functional constraints on the gene are relaxed to the point where all mutations are selectively neutral, then the process of mutation and substitution can be modelled by neutral theory and the expected rate of substitution (or fixation) is the same as the rate of mutation. This rate is dependent on several factors - lineage, life history, etc., and the difference between this rate and the fixation rate for a given coding region is dependent on the severity of functional constraint on that region.

OK, but the poster obviously means the fixation rate of mutations. The answer is obviously yes, but if one is going to answer here shouldn't one provide experimental justification?

Actually @David I have found that the distinction between those two in relation to questions around functional constraint is a pretty common misconception, especially as the question specifically states "mutation rate". As the poster is new, I have no way of gauging their prior knowledge.


text:
Does homology of a trait necessarily imply that the most recent common ancestor had the trait?
If two different species have a trait that is homologous, does this mean that the most recent common ancestor necessarily had the same trait?

Yes, assuming you treat the term strictly.
The term homologous implies that the most recent common ancestor had the trait, although it would be possible for the term to be used in error, when something thought to be a homology is actually not.
If the trait is shared but the trait evolved separately twice, instead you would refer to it as an analogous trait rather than homologous; analogous traits are often the result of convergent evolution.
I can imagine some edge cases, however, where one could argue about homology, although I don't have a specific example in mind (maybe someone can help me out if they can think of one). Imagine you have a trait that is present in an ancestral population, becomes minimized in a common ancestor, and then multiple species descending from that ancestor start to exhibit the trait again. This is called atavism. In some ways, atavism could be seen as convergent evolution and an analogous trait: each has separately evolved that trait from the last common ancestor. However, one would expect a lot more genetic similarity than other examples of convergent evolution and therefore outside of cladistics it might be more appropriate to think of it as a homologous trait in that you can find some ancestor that shared the trait, it just doesn't happen to be the most recent one.


text:
Flow diversion for cerebral aneurysms or stabilizing the hemodynamics?
I'm doing research of flow diverter for cerebral aneurysms applications and I'm wondering the reason behind stent placement underneath of cerebral aneurysms is to divert the flow or stabilize the hemodynamics (e.g. reduce wall shear stress or blood flow velocity in the aneurysmal region)? Let's say people do it to divert the flow and prevent blood to enter the aneurysmal region. That looks fine for side wall aneurysms when there is no smaller arterioles or branches connected to the aneurysm, but for terminal aneurysm where the flow diverter may block the blood flow into smaller arterioles, is it a appropriate case to deploy stent? I mean if we prevent the blood to enter some part of smaller arterioles how brain could maintain its functionality due to its need for oxygen. I appreciate if someone could explain the logic behind the flow diverter placement in the cerebral aneurysms.

I don't quite understand the dichotomy you present between diverting flow and stabilizing hemodynamics. The former is a direct outcome and the latter is a secondary outcome: both are goals.
The overall goal is to isolate the blood in the aneurysm and allow it to clot and heal over time. Embolic coils are also used to assist the process, in which case the flow diverter helps to keep the coil in place and the resulting embolism out of the primary circulation.
One would not typically deploy a flow diverter over branches that one wishes to remain patent, although patency can be maintained in smaller vessels. In many neurovascular situations, collateral circulation can make it acceptable to occlude a branch, however.
You may be confusing plain stents with flow diverters; a plain stent has as few struts as possible while maintaining structural support (though high flow through the struts can cause turbulence and is something you want to avoid if possible), and creative stent placement techniques including deployment of multiple stents and use of balloons to break open strut configurations can be used. These do not block flow per se, but can help keep coils in place and maintain the desired structure of the vessels involved.
I've included several references that I quickly gathered; these may not be the most ideal references but should give you a look at some of the approaches used. I would strongly suggest you look through the rest of the literature using search terms from your question to get an idea of how interventionalists approach different situations.
I'll add that I am not a physician and am not up-to-date with the latest guidelines or standard of care, but in my experience with the literature a lot of these decisions are up to the experience of the physicians involved and based on a lot of case study; randomized trials aren't really possible to cover all the anatomical variety that is experienced.

Burkhardt, J. K., Riina, H. A., Tanweer, O., Shirani, P., Raz, E., Shapiro, M., & Nelson, P. K. (2018). Flow diversion and microvascular plug occlusion for the treatment of a complex unruptured basilar/superior cerebellar artery aneurysm: case report. Journal of neurosurgery, 1-6.
Chow, M. M., Woo, H. H., Masaryk, T. J., & Rasmussen, P. A. (2004). A novel endovascular treatment of a wide-necked basilar apex aneurysm by using a Y-configuration, double-stent technique. American Journal of Neuroradiology, 25(3), 509-512.
Miyachi, S., Matsubara, N., Izumi, T., Asai, T., Yamanouchi, T., Ota, K., ... & Wakabayashi, T. (2013). Stent/balloon combination assist technique for wide-necked basilar terminal aneurysms. Interventional Neuroradiology, 19(3), 299-305.
Puffer, R. C., Kallmes, D. F., Cloft, H. J., & Lanzino, G. (2012). Patency of the ophthalmic artery after flow diversion treatment of paraclinoid aneurysms. Journal of neurosurgery, 116(4), 892-896.
Siddiqui, M. A., Bhattacharya, J. J., Lindsay, K. W., & Jenkins, S. (2009). Horizontal stent-assisted coil embolisation of wide-necked intracranial aneurysms with the Enterprise stent—a case series with early angiographic follow-up. Neuroradiology, 51(6), 411-418.
Wong, G. K., Kwan, M. C., Ng, R. Y., Simon, C. H., & Poon, W. S. (2011). Flow diverters for treatment of intracranial aneurysms: current status and ongoing clinical trials. Journal of Clinical Neuroscience, 18(6), 737-740.

The flow diverter and plain stents are used interchangeably by authors, whom do not have any medical experience and are engineers like me, in the literature. At least is there any way to find out in which case we need to put plain stent or flow diverter?! Also, is it possible to explain a little bit more about plain stents and its application and what does it do to change hemodynamics? I appreciate your help.

A plain stent has no covering on it, it's just metal mesh. It provides structural support and keeps an embolic coil inside the aneurysm. If you are engineers and have no medical experience, you should really find an interventional radiologist/neurosurgeon/whoever does intracranial embolism at your institution to discuss with. I'm neither an engineer nor a physician but I did have a job bridging exactly that gap for engineers in the area of intravascular devices; the engineers often didn't even know what they didn't know when they came to us and talked a lot about how much they benefited.

Ok you made the question more interesting to me! What is that cover you are talking about in the flow diverters? it's a coating? If yes, do you know what's the material of that coating and its purpose perhaps? I mean I really apologize to ask a lot of question from you. But I believe you are the only person here which knows these kind of things. I really appreciate your help!

Yes this is a small community, I doubt you will find another person here who did R&D with stents. I think I am partly mistaken about the flow diverters, as I was thinking these are covered stents but it seems they are just high-metal density stents. They just have more struts for a given area and are meant to occlude to some extent, whereas normal stents are meant to avoid occulsion as much as possible (i.e., to provide as much support as possible with minimal contact to tissue). I'll make sure to update my answer.

One interesting question about occlusion is that: a lot of researches in the literature claim that low wall shear stress is responsible for cerebral aneurysms' rupture but when we put flow diverter (FD) it will reduce the wall shear stress in the aneurysmal region because it prevents the blood to enter the aneurysm. So, does it increase the rupture risk or decrease it? I mean in the literature people are saying FDs reduce the wall shear stress and that will help to occlude the aneurysm but if the low wall shear stress is responsible for rupture, it looks counter intuitive to me.

I'm not an expert in aneurysm biology but my suspicion is it isn't low wall shear stress per se, but rather that the vascular wall in the area of the aneurysm thins where wall shear stress is low, leading to rupture risk. In the case of aneurysm treatment, the goal is to clot up the aneurysm space and have it heal, and that this should happen faster than the wall integrity would decay. That said, I also would expect that intervention would create a brief period of higher risk for rupture; that risk must be accepted to prevent longer term risk.

I really appreciate your help! Do you have any reference or keywords for these low wall shear stress things and maybe higher risk of rupture after intervention for a brief period of time? Thank you so much! You cleared a lot of things to me!

Search google scholar for "low wall shear stress aneurysm": first result I get is Boussel, L., Rayz, V., McCulloch, C., Martin, A., Acevedo-Bolton, G., Lawton, M., ... & Saloner, D. (2008). Aneurysm growth occurs at region of low wall shear stress: patient-specific correlation of hemodynamics and growth in a longitudinal study. Stroke, 39(11), 2997-3002. and seems very relevant. For the latter, I would just search for "complications" after embolic coil/neurovascular stent/etc etc.