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Are small CO₂ concentrations devastating to certain cognitive tasks?
A new study shows strong effects of what should be a negligible CO2 concentration.
The paper "Is CO2 an Indoor Pollutant? Direct Effects of Low-to-Moderate CO2 Concentrations on Human Decision-Making Performance" exposed people to three levels of CO2: 600, 1000, and 2500 ppm while keeping constant other factors such as ventilation, humidity, temperature, and indoor pollutant concentration. Of course, the participants didn't know how much CO2 was in the air.
At the 2500 ppm level, most cognitive performance measures were temporally reduced (they used the SMS management test). Some changes were drastic.
Since normal air is 400 ppm, 2500 ppm sounds like a lot. However, it is dwarfed by internal production. Humans exhale 50,000 ppm CO2 in the lungs, meaning that the lung air averages 25,000 ppm (as a rough approximation). The extra 2500 ppm is only a 10% increase in the average "atmosphere" that the blood is exposed to. Furthermore, people partially compensate increased P(CO2) with deeper ventilation (the effect takes much larger concentrations to be noticeable). Why would this extra 10% have such a strong effect?
Personally I am skeptical. This study has such high impact (millions of people's performance) that it needs replication. Maybe the hissing sound of the injector got people worried (more hissing at a higher concentration!). Maybe an experimenter (who knew the concentration) was watching the people and that subconsciously affected them.

Interesting question. I will take a look at the original paper, but this can take a day or two.

@Chris: Thanks. I am not the best at including links and other formatting. Can editors be rewarded 5 rep when the asker likes it?

You only get rewards for accepted) edits when you are below 1000 reputation points (and only 2). Good that you like it. :-)

I have read it now but I am not decided yet. The first and biggest problem I see is the relatively small number of participants (only 24). This is pretty small to do real statistics (it can be done, but needs extra care and is not as conclusive as larger groups). And I am not sure, if the differences are really so big. If you look on the single results in figure 1, than these results vary quite a lot. So personal factors seem to play an important role here, too. I am not too convinced by this study.

I think that the diffusion of carbon-di-oxide in the alveolar surface depends on the residual P(CO2) in the inhaled air. If the partial pressure of CO2 is high in the inhaled air then the amount of CO2 that diffuses out of the blood decreases

That and the carbon-di-oxide dissociation curve is not linear. This means even a small increase in the partial pressure of CO2 in the inhaled air can cause dramatic shift in the CO2 exhaled. See this:http://www.umc.edu/Education/Schools/Medicine/Basic_Science/Physiology_and_Biophysics/Core_Facilities(Physiology)/Physical_Exercise_-_Bicarbonate.aspx


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Ribosomal Turing Machines, DNA/RNA computation
I'm a computer science guy, recently crossing over to do some research in computational biology on RNA secondary structure prediction. While looking through the materials I got a crazy idea, what if you could design a synthetic ribosome that acts as a Turing Machine on strings of RNA? (you could do similar things with DNA enzymes)
The immediate applications could be stuff like correcting mutations in RNA to cure genetic diseases, which is a relatively simple computation:

Check if a string is bad.
If so, fix bad letter.

Another could be "shredding" DNA/RNA of viruses:

Check if a string is a virus.
If so, shred it.

I'm not sure the status of the literature on this is, or synthetic biology's ability to create something like that. Do you think it is a good idea to pursue this idea or not?
I realize this is a soft question. Perhaps a better one would be, is this possible?

There are some papers on simple computations using nucleic acids, if nobody answers I'll look them up later. As for your examples, nature already does some of them (see RNA interference). And for correcting genetic diseases, the hard part is actually correcting the sequence in all cells in your body, not the detection itself.

Where would the 'table' of the machine be? In other words how would the 'bad string' be recognised?

@AlanBoyd An immediate thought would be to keep a copy of the bad string, say a mutated RNA strand, in the machine. Combine it with an enzyme bound to it with 2 functions, check if the letter it's currently bound to matches the current input letter, and slide right. That could do the check step. For the replace step you could do the same backwards and then splice the correct protein in. For a general Turing Machine, you could keep a string of the current state in RNA, keep the rules in another string, and slide along it to find the rule and execute it.

I'm no expert at this but I don't think you need a Turing machine to achieve this, at least for DNA, since in conventional sense (not including carcinogenic factors such as UV) the most probable stage in which a DNA mutation can happen is during DNA replication so DNA polymerase (http://en.wikipedia.org/wiki/DNA_polymerase) engages in proofread to ensure accurate DNA replication, and then the DNA can get back into being heterochromatic (eventually). This will be more difficult for RNA as they are single stranded although they do fold onto themselves.

Also there many many strands of RNA that are produced through alternative splicing, VDJ recombination and RAG imprecise rearrangements for antibody production, which can give rise to infinite possible RNA productions. So how would you know what is "good" and what is "bad" in terms of RNA and its production. Half the time we don't even know what they do and what their roles are and the only reason we call something as a "bad" or "faulty" RNA is because it is having a negative effect not because we understand the precise role of the sequence, which means a theoretical table would be useless.

So in short, a turing style protein machinery is neither possible (due to almost infinite potential number of RNA produced) not feasible (since the number of proteins that would have to check each RNA sequence would in turn have to be almost infinite). And none of these takes into account SNPs i.e. individual variations, which ban produce proteins with different sequence but identical structure/function, since obviously any lethal variations would be selected against but thats a whole different argument.

In answer to first part, isn't this exactly what mismatch repair genes do? They scan for errors, I'm not fully confident with my understanding of Turing machines to give you a definitive answer, but I'm fairly sure this is the case.

@Bez could you change your comments into an answer? It's a decent answer worth saving before this question gets closed

@ChrisStronks done! :)

I'm no expert at this but I don't think you need a Turing machine to achieve this, at least for DNA, since in conventional sense (not including carcinogenic factors such as UV) the most probable stage in which a DNA mutation can happen is during DNA replication so DNA polymerase engages in proofread to ensure accurate DNA replication, and then the DNA can get back into being heterochromatic (eventually). This will be more difficult for RNA as they are single stranded although they do fold onto themselves.
Also there many many strands of RNA that are produced through alternative splicing, VDJ recombination and RAG imprecise rearrangements for antibody production, which can give rise to infinite possible RNA productions. So how would you know what is "good" and what is "bad" in terms of RNA and its production. Half the time we don't even know what they do and what their roles are and the only reason we call something as a "bad" or "faulty" RNA is because it is having a negative effect not because we understand the precise role of the sequence, which means a theoretical table would be useless.
So in short, a turing style protein machinery is neither possible (due to almost infinite potential number of RNA produced) nor feasible (since the number of proteins that would have to check each RNA sequence would in turn have to be almost infinite). And none of these takes into account SNPs i.e. individual variations, which can produce proteins with different sequence but identical structure/function, since obviously any lethal variations would be selected against but thats a whole different argument.

It should be possible to create Wang tiles using DNA or RNA. Different colored edges could be represented by different sequences selected to bind to each other selectively (DNA and RNA are very good at this!). Wang tiles can be used to implement a 1D cellular automaton, which can implement a Turing machine -- it will keep a record of its complete history as a big wobbly mat. Wang tiles are collections of square tiles in which each edge has a certain color, adjacent edges having matching colors. They can produce infinitely extendable patterns that can't be periodic (similar to Penrose tiles).

@PaulHarrison - Welcome to SE Biology. I really feel, like the original post over four years ago, you are on the wrong list. One reason there was only one answer to the original question is that few biologists know what a Turing machine is, and most of those who do feel it has no relevance with biology. I have even less idea what Wang tiles are. However if you feel that you have a useful point to make you can post your own question on SE and then answer it. I would suggest that you do that on SE Bioinformatics, though, as you are more likely to get a response there.

@PaulHarrison - I don't see how your post targets the question in any way. It's more of a comment to the other answer I think. As David says, I indeed know what a Turing machine is but the tiles are over the top of my head too. I'm converting the answer to a comment of the other answer for now. Feel free to modify it to make it a more specific answer to this site in a biological context. Don't forget to include sources to your material.

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What are good sources of free-to-use images and diagrams
I am looking for good image repositories for biology teaching. Photos and textbook-like diagrams.
I am interested  in images that can be used commercially without payment, or, at least, that require a small one-time payment. They would be used in videos, not only on lectures, hence the worry about copyright.

i take it you mean on biology?

I'm guessing the videos are for a flipped/online course and posted on YouTube or Coursera?  I've done this. Biology is hard -- perhaps because I am picky and really want good images.
I used Wikimedia.com to search for many free images. I also contacted the publishers of the free online version of Molecular Biology of the Cell and asked if I could use up to 20 for my free online course, and they agreed.
My university was also able to work out an agreement with the textbook publisher to use 200 of the textbook images for the Coursera course as long as they were credited, and a link to purchasing the textbook was available on the site. They want to keep my university happy as our students buy a truckload of books every year.
I've also gotten somewhat decent at using a drawing tablet and powerpoint image (boxes, circles) manipulation to make some of my own cell processes and chromosomes and such.
Lastly, OpenStaxCollege.org has a wonderful collection of free textbooks for students, and they make their images available to faculty as free powerpoints. They aren't usually "good" enough to satisfy me, but definitely check them out.

You could use CC Search. It allows you to find Creative Commons licensed content that you can use commercially.

Another interesting source is somersault18:24.

An excellent source for images is the wellcome collections image library http://wellcomeimages.org/. You can negotiate commercial use with them, they are very reasonable, especially if it's for teaching purposes.

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Are there critical points in ecosystems?
Some days ago, I was thinking (partially) about the complex balance that is needed for an ecosystem to exist. I got curious about the existence of some sort of critical point, something - that when taken out of the system - makes life vanish.
Is there a single species that when took out of one ecosystem destroys the life in it? Perhaps there's not a single species, perhaps there could be a minimal set of species in which this could happen.
Excuse me for the poorly formulated question. I'm not a biology student, I just get random curiosities from time to time.

You will definitely be interested in reading on the concept of ecosystem resilience

Another (overlapping) interesting place to look: the concept of keystone species.


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How to find a PDB structure of a protease with a peptide like inhibitor
I wonder how, for purposes of just illustrating some concepts like substrate alignment in the catalytic triad active site, I can quickly and efficiently find a protease structure (irrelevant of what organism exactly) that has a peptide like inhibitor on the PDB database.
Hints appreciated.

I'm not a Google search expert but "pdb structure protease peptide inhibitor -non-peptide" seems to provide some useful hits

Here's one: http://www.rcsb.org/pdb/explore/explore.do?structureId=2IPH. It was crystallized with the inhibitor bound to the protein.

How did you find it?

I searched within the pdb for protease inhibitor. Since the inhibitors themselves are not proteins, most of the search results are proteases with inhibitors.

go to http://www.uniprot.org and enter the protease accession number you are interested in and look at the 3D structure databases section to see if its PDB file is deciphered or not. I came across this database (http://www.cf.ac.uk/biosi/staffinfo/ehrmann/tools/proteases/allproteases.html) just by typing into google "protease PDB databases"


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How can cells produce antibodies despite error-checking mechanisms in their genomes?
How can immune cells produce so many different kinds of antibodies with different variable regions if there are so many mechanisms inside the cells that try to keep the DNA sequence as constant as possible (i.e. prevent mutations, which are actually necessary to create the different kinds of antibodies)?

This process is called somatic hypermutation. I just looked it up in my Alberts and it seems the exact mechanism is not known (though the book is a bit older now, this might have changed).

B- and T- cell receptors are the only place where the DNA sequence is edited, changed, mutated and altered in the body on purpose. Have a look at somatic hypermutation in the Wikipedia.


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What is the smallest known organism with a skeleton?
See question title. After doing some looking around on my own I haven't found much so I figured I'd ask some experts.

What kind of skeleton?

what he's asking is if you are talking about bones or including chitin (insects and things like crabs and shrimps) or other exoskeletal structures?

Shall we include the cytoskeleton?

further information http://en.wikipedia.org/wiki/Smallest_organisms

The smallest vertebrate is the male Photocorynus spiniceps anglerfish at 6.2-7.3 mm, females are over 50 mm. Schindleria brevipinguis is 6.5-10 mm, and Paedophryne amauensis is 7.7 mm. Paedocypris progenetica is 7.9-10.3 mm.

The smallest vertebrate (if that's what you mean; there are many invertebrates with endoskeletons that are not made of bone) is Paedophryne amanuensis, a Papua New Guinea frog that's about 7 mm long.

do you have a reference for this?

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0029797


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How do some plants grow in salt water, while others die?
My question is basically out of curiosity and comes from observing how certain plants (such as mangroves or salt cedar) can grow in seawater. If this gives the plant an advantage, why haven't all plants that grow in coastal areas developed a salt tolerance? How can the plants keep from intaking salt, while absorbing other soluble nutrients through the roots?

It wouldn't be an advantage if there was no salt water near by.

A few things you have to realize when you ask 'why hasn't species x evolved trait y':

What is the cost of evolving this trait? If you gain one trait, you lose another (or others). Everything in evolution is a tradeoff: that's why you're not nine feet tall, you'd be able to beat up all your enemies great, but it would take so much food to sustain you, it wouldn't be worth it.
Not every trait can be easily evolved. When you're starting as a freshwater plant, there are many, many, many, many mutations that have to occur for you to become salt-tolerant. Every one of those mutations would have to give a fitness advantage to be positively selected. The chances of this happening are low, which means if it happens at all, it would take a long time.
Who knows, perhaps these plants are, slowly, becoming more and more salt-tolerant and you're seeing them at an intermediate point in their evolution. Everything is evolving all the time, if these plants were not in a salty environment until recently, mutation and selection haven't had time to work their magic.

Update from comment:

Can you flesh out a little on "How can the plants keep from intaking salt, while absorbing other soluble nutrients through the roots?"

Sure! I'll give you the simple answer first: there are different mechanisms for absorbing salt and for absorbing nutrients, so they can function largely independently.
Now the longer explanation: Salt and nutrients don't just diffuse (much) through cell walls, they have to be transported across by what are called transmembrane proteins. Think of the cell membrane (a layer inside the cell wall) as basically something like a layer of oil (it's called a lipid bilayer) -- you know oil and water don't mut, and for the different ions in salt (sodium ion and chloride), neither do oil and salt or oil and many nutrients so they get sort of escorted across that barrier by big proteins that form sort of a tunnel through it.
There's a different transport protein for different substances; the salt ones will only let salt through, and in fact there are different ones for letting salts in and letting salts out, and for the different ions (sodium and chloride) in salt.
Update from comment:

This makes me wonder how salt harms most plants, if it can't get in except by 'invitation'

Quite a bit of salt can diffuse in, the molecules are small enough (unlike most nutrients) to pass through the membrane via the channels that let water in. Every living creature has a quite sophisticated setup of "ion channels" to pump salt out. If suddenly its cells are in a very salty environment, these pumps can't keep up.
Update from comment:

So if salt can diffuse in, what do salt-tolerant plants have that other plants don't?

Mostly, if I recall correctly, three things: They will have enzymes that have evolved to work in higher salt concentrations, they will have cellular functions to "sequestrate" salt, i.e. store it in organelles called vacuoles instead of leaving it where it can harm other organelles, and of course they will expend more resources on ion pumps to get the salt concentration in the cell to an acceptable level.

Can you flesh out a little on "How can the plants keep from intaking salt, while absorbing other soluble nutrients through the roots?"

@proofreader Nice. Thanks for the info. This makes me wonder how salt harms most plants, if it can't get in except by 'invitation'.

@proofreader So if salt can diffuse in, what do salt-tolerant plants have that other plants don't?


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What's the smallest organism that can produce voice?
What's the smallest organism (animal, insect, or any living creature) that can produce voice. And not just make sound, but has an organ to specifically to create sound, like how us mamals have vocal chords.

How do you differentiate between an animal that makes sound and one that has a sound-producing organ? If a beetle makes a sound by rubbing its wings together, it has a sound-producing structure, does it not, even if that structure is not dedicated to only making sound?

@MattDMo Does it know it's producing the sound, i.e. is there a purpose for it do make sound, or is it a by-product of rubbing its wings?

would you consider ultrasonics as voice too?

@WYSIWYG Sure, sound is sound. Although, if it doesn't become "too broad" of a question, the best would be an animal from each of both categories.. (or all three if infrasonic is also considered)

I rolled back the question to the original, which is not a duplicate.

I will go with lesser water boatman(Micronecta scholtzi).
The loudest of everything as well as small.
Size: 0.07-inch (2-millimeter)

Produces the highest sound by size ratio.
It's sound is almost equivalent to pounding jackhammer at two feet distance.

http://www.plosone.org/article/fetchObject.action?uri=info:doi/10.1371/journal.pone.0021089.g001&representation=PNG_L
Source and Image Courtesy:
So Small, So Loud: Extremely High Sound Pressure Level from a Pygmy Aquatic Insect (Corixidae, Micronectinae)
Youtube: https://www.youtube.com/watch?v=i7-hREXmMFM
Update:
If we consider voice, I will go with Paedophryne amauensis

Smallest frog an known vertebrate
size: 7.7 mm (0.30 in)

I'm putting my bets on the Pistol Shrimp (Alpheus heterochaelis)
They can be grow 3cm to 5cm Long which is incredibly small for the amount of db it can create.
Their sound is a by-product of their large claw snapping shut and creating a cavitation bubble that creates a lot of pressure and then produces up to a recorded 218 Decibels.
This "click" or "pop" of the bubble only lasts less than 1 millisecond. It also produces around 5000k in heat from the popping of the bubble.
(According to the Daily Mail which I honestly may say is probably not the most trustworthy source of accurate information http://www.dailymail.co.uk/sciencetech/article-1085398/Deadly-pistol-shrimp-stuns-prey-sound-loud-Concorde-UK-waters.html
Wikipedia Article : http://en.wikipedia.org/wiki/Alpheidae )

Wow! Watch them in action.

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

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

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

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

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

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

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

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

@Masi I didn't understand..

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

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

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

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

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

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

Excellent, always like the use of a Venn diagram!

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

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

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

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

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

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


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Can the psychology of a person alter their immune system and health?
Can the psychology of a middle-aged person alter their immune health? I have read about the different types of linkage between nervous system and immune system.
Can someone outline the general facts about what is understood about this?

Can you provide some references for this?

I think you are referring to psychoneuroimmunology (http://en.wikipedia.org/wiki/Psychoneuroimmunology), which is an expanding field.

This paper should be helpful, effects of the placebo on immune response https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3504052/

I'm not sure what you mean by psychology exactly, but assuming you are referring to a persons mental state there is a known link between stress and immunity. This link occurs through neuro-endocrine pathways. The central nervous system and endocrine (hormonal) systems are linked through the hypothalamus, a key controller of hormone release in the central nervous system. In a state of stress our central nervous system reacts by increasing the release of hormones such as the steroid cortisol and catacholamines such as adrenaline (a.k.a epinephrine in USA).
We know that steroids have an effect of dampening down the immune system (in fact steroids are often used for this intentionally in the case of autoimmune conditions for example). Thus based on this we have a scenario where stress can lead to increase in cortisol (and other hormones) which in turn can have an effect on your immunity. The effect to which this impacts on your life is then further dependent on your psychology and social support.
More generally, the links between illness and psychology are integrated together in what is called the biopsychosocial model of illness. I suggest you look this up to gain a more in depth understanding of this complicated issue.

As a reference for stress causing inhibition of the immune system, here is a quote from Life: The Science of Biology (10th edition): "Within minutes of a stressful stimulus (one provoking fear or anger, for example), blood cortisol levels begin to rise. [...] Cortisol also inhibits the immune system (because dealing with the immediate stressor is more important than feeling sick, having allergic reactions, or healing wounds)."

Yes. It's called Psychoneuroimmunology Ziemssen & Kern 2007:

There is evidence for rich neural connections with
lymphoid tissue Steinman et al.(2004). Receptors for various neurotrans
mitters beyond acetylcholine and norepinephrine are
also present on lymphocytes. Whereas the parasympa
thetic neurotransmitter acetylcholine potently modu
lates several classical immune reactions via the vagus
nerve, the sympathetic nervous system can alter the
TH1/TH2 balance through stimulation of the beta-
adrenergic receptor for example Elenkov et al. 2000

In general: Personal well being (PWB) makes you healthier, Psychological Ill-Being (PIB) makes you unhealthier, here are some snippets of a review (Abdurachman & Herawati 2018):
Coping mechanisms improved the outcome of AIDS patients

Religious coping and social support as an effort towards PWB showed to boost the immune responses in people living with HIV/AIDS (Dalmida et al, 2013). They used CD4 + cell count to prove their findings. Then, the effort to PWB via religious coping was definitely associated with reduced psychological distress, increased health-related quality of life (HRQoL), and better medication adherence (8-item Morisky Medication Adherence). Dalmida et al, 2013

Weeks of Playing music shifts your immune system from inflammatory to anti-inflammatory

Researchers found an increased immune response through various indicators obtained through saliva samples such as: cortisol, cytokines and interleukin (IL) -4, IL-6, IL-17, tumor necrosis factor-alpha (TNF-α), and monocyte protein chemoattractant (MCP) -1 (Fancourt et al., 2016b). This study shows the psychological benefits of group drumming and shows the underlying biological effects, supporting the therapeutic potential for mental health.

One might think that this all comes down to happy = no stress. Since there is tons of research out there proving that
STRESS makes you unhealthy
Spinorial already mentioned the stress hormone cortisol and its effect on dampening the immune system. Here I wanna provide some more facts that I took from this review (Yaribeygi et al. 2017 doi: 10.17179/excli2017-480):
Stress makes your immune system to attack your guts
Stress can re-activate previous inflammation of your gastrointestinal system. It can get worse:

As a result, there is an increase in the permeability of cells and recruitment of T lymphocytes. Lymphocyte aggregation leads to the production of inflammatory markers, activates key pathways in the hypothalamus, and results in negative feedback due to CRH secretion, which ultimately results in the appearance of [gastrointestinal system] inflammatory diseases. [...] It has been suggested that even childhood stress can lead to these diseases in adulthood (Schwartz and Schwartz, 1983, found in Yaribeygi et al. 2017).

Stress stops the immune system from killing cancer

stress can decrease the activity of cytotoxic T lymphocytes and natural killer cells and lead to growth of malignant cells, genetic instability, and tumor expansion (Reiche et al. 2004 found in Yaribeygi et al. 2017)

Stress slowly kills you by damaging your blood vessels and heart
Most human deaths can be related to accumulated damages to the cardiovascular system (So stop worrying about immune system). The mechanism behind stress killing you seems to be fairly simple:

Stress can stimulate the autonomic sympathetic nervous system to increase vasoconstriction, which can mediate an increase in blood pressure, an increase in blood lipids, disorders in blood clotting, vascular changes, atherogenesis; all, of which, can cause cardiac arrhythmias and subsequent myocardial infarction

Stress Shortens Telomeres
I came across a paper when I was answering a question about telomeres. Mental stress shortens telomeres (Epel et al 2004). To understand how short telomeres affect the immune system, aging and health see Does Telomere length shortening cause our cells to stop functioning properly?

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
On evolution statistics
This basic evolution theory question has been haunting me since childhood and I'm kind of embarrassed that I can't explain it yet:
Consider a butterfly. It's wings have evolved to look like the eyes of an owl, so to prevent it's predators who are themselves preys of the owl to attack it.
From what I've learned (and feel free to indulge me in the very basics if I get this wrong), natural selection suggests that the butterflies that didn't have the owl's eyes in their wings would be eaten, leaving the ones with the eyes to survive, right?
But that implies that this useful trait appeared in the butterfly's wings by chance. Now, I know trillions of butterflies have been born before this, but trying to figure out the possibility of this to happen by chance doesn't look like it's plausible. Let's go through the things that have to work right before this trait is passed over:

For a butterfly to be born in a different wing colour, it should be a genetic mutation which doesn't happen this often, for what I know.
The wings are composed of micro-scales. For every scale to compose an image so similar that confuses even us, the margin of error is very slim. It could be anything. It could be a picture of Tom Selleck for all we know. The scales must be in the correct spectrum of colour by a small margin of error. So that is already a very unlikely thing to happen.
Then, this butterfly cannot be eaten out of bad luck (mind you, the wings don't guarantee it will not be eaten, just enlarge her chances).
It has to mate, which also is not a guarantee to happen, since nature deals with competition. If this butterfly we are considering is a male, the female must find the wings hot, instead of being afraid of those creepy eyes.
The genes of this mutations must also be dominant, so when it mates and generates offspring, at least part of the new butterflies inherit this trait.

And this is a simple example. There are animals that evolved so smartly I can't even start to think of the possibilities.
My question is, more precisely, how likely is it for a species to evolve into complex solutions?

And still: Mutations happen by chance. Having a relationship where one of the participants is eaten when his mimicry isn't good enough puts a strong selection pressure on the related genes. So you will gradually collect mutations which are responsible for this pattern.

As link only answer are discouraged here is a link only comment; See On the Origin of Species (1859)

This is the OP's only post and basically is asking an ID sort of question that has been answered elsewhere at great length.

have you stopped to imagine that it is us that associate random patterns on butterly wings with different identifiable features like eyes .. It could be anything that scares off predators.. It supposedly looks like eyes doesn't mean that this is the only pattern that came with mutation.. There would have been many others among which this particular pattern was probably more effective at its job..

Thanks @Chris! You started to enlighten what Remi.b and prooffreader tackled in larger detail.

@daniel I am sorry, I tried to build a lightheaded question, otherwise people well above this knowledge level would feel like they wasted their time reading (since it ended up longer than I expected). But now I see that I exaggerated the beginning. I am not that guilty of not looking for an answer though. I searched around, but my vocabulary on the matter is not as vast, as you can notice. I thought on making an effort to change the question, but since you already pointed it out and both answers were more than satisfactory, the change would be frivolous. Promise to be careful next time.

@TheLastWord Yeah, as the others pointed out, it makes more sense that more detailed images come up in time.

what exactly is your question? Is it "How many years would it theoretically take to achieve this?" ?

@daniel.. Actually I am sympathetic towards the OP. The wikipedia article on evolution or any other online discourses and even most books on evolution do not emphasize on the timescales associated with the process of evolution. The OP is not hinting at ID. I think they are just flabbergasted about the fact that such a complex process is generally explained in one line without a substantial explanation. A good book on phylogenetics is what I can suggest to OP (such as Molecular Evolution & Phylogenetics by Masatoshi Nei).

I am closing this question as too broad.. I still think this is not off topic.

Ok, @WYSIWYG I think I found a way to ask what I was curious about simply. Let me know if it's satisfactory.

@WSIWYG: Yes--OP responded reasonably and I deleted my longer comment. 'Too broad' works fine. I left the original comment because that reason for closure also applies. There is a history of such questions here, which is not the OP's fault.

@Digger. this is still very broad. There are two aspects to this. A general mutation rate giving rise to a phenotype and fixation of some mutations due to predation. In a question which encompasses all aspects, it is difficult to answer (one can write a review article rather:P). You can check this article out; it is about evolution of predator-prey interactions. Remi might know better about the best mathematical models for this.

@WYSIWYG Oh, both answers below were exactly what I was looking for and beyond. I'm also reading new articles about the subject (together with The Selfish Gene, although it doesn't seem to go over this broad question). So what I'm trying to do is find a question that the answers below correspond, otherwise it would seem as if they didn't answer me correctly. Since I'm already satisfied, the idea is to make this post searchable, right?

This question is only off topic if evolution has nothing to do with biology.

Remi.b's answer is great, but here's something less technical if that's what you're looking for:

Genetic mutations happen ALL THE TIME. Every time a cell divides, there is an error rate of about one per billion. That's a very low error rate per division, but when you multiply it by the number of divisions, times the number of cells, times the number of individuals, times the number of years the species has existed... well, that's a lot of mutations. Mind you, way fewer mutations will get passed along to offspring, because the vast majority of mutations are non-advantageous (because there a lot more ways to make a bad butterfly than a good one). But that's the job of selection, not mutation.
Evolution is a step-by-step process. There doesn't just have to be mutation and advantage, there has to be an advantage every step of the way. If big circles were selected for, that means intermediate forms (smaller circles, perhaps?) were selected for too. A blob that sort of looks like Tom Selleck will not confer as many fitness advantages as a blob that looks a lot like Tom Selleck (assuming the butterflies' predators hate Magnum P.I., which as far as I'm concerned is a perfectly reasonable assumption ;-)
Lots of butterflies get eaten by bad luck. But it's unlikely any trait was the result of one mutation in one individual (although it does happen sometimes). There are lots of mutations happening, and if one individual doesn't pass it along, another will. Think of this: maybe 100,000,000 years ago some butterfly developed a mutation that would be ten times more effective at discouraging predators than the owl-eye circles ... but then it got stepped on by a dinosaur. You'd never know it happened, and you're left eons later wondering how a way less impressive mutation happened.
There's natural selection, and there's sexual selection. Maybe the females don't like the owl-eye wings so those butterflies mate half as often as their more attractive brethren. But if the resulting offspring is four times more likely to survive, that ugly butterfly just won the gene pool lottery.
That's a common misconception, traits don't have to be dominant in order to be selected for. Think of this: lactose intolerance is dominant, but in many populations lactose intolerant people are in the minority, because after the domestication of the cow being lactose intolerant was enough of a disadvantage to make those people less likely to have offspring.

One of the concepts people most often lack when dealing with evolution is of scale. You're looking at a tiny, tiny, tiny fraction of all the mutations that could have possibly happened and thinking, "What are the odds that that happened, it seems so improbable!" But that's because you're not seeing the trillions and trillions and trillions of mutations that could have happened if random chance had taken things in an ever so slightly different direction. SOMETHING had to happen, it's the laws of physics. You're only able to see and be amazed by what did happen... well, because it's the thing that ended up happening. The more you think about it, the easier it is to wrap your mind around.

Incredible! Thank you! Putting it that way made me realize what I've been missing easily. It's wondrous to think that so many incredible mutations could happen that didn't move forward out of bad luck...

In your 5 points you basically cover several concepts of evolutionary biology.
1) The number of mutations depend on mutation rate. The mutation rate varies along genome sequences, species and individuals. According to the recent DECODE study (Kong et al., 2012) a human mother transmit on average 15 mutations to her offspring and a human father transmit on average $25 + 2(g-20)$ mutations to his offsprings, where $g$ is the age of the father and where the formula stands only for father older than 20 years old.
2) Mutations happen by chance and are not directed toward creating some specific feature. But it is much more likely to create a round of color on the wings of a butterfly than creating the picture of Tom Sellek. The reason has to do with the developmental and biochemical pathways linking the given mutation to its phenotypic effect. Looking at a given mutation, you can understand how it yield to the modification of some phenotypic trait by looking at the biochemical and devlopmental pathways.
3,4) The third point that you raise is called "genetic drift". Shortly speaking the concept of genetic drift may be called the good luck/bad luck effects. Stating differently genetic drift is the random sampling of alleles (gene variant) from a population. If some alleles are favored over some others at a given locus, then sampling is not 100% random but is not either 100% deterministic. The only case where genetic drift is absent is in infinite population (which is obviously an unrealistic case). Genetic drift is inversely propotional to population size and you'll understand it better by reading this post.
5) When the mutation is at very low frequency, the mutation needs to be dominant in order to be expressed, this is true. But an allele may increase in frequency due to genetic drift up to the point that some individuals are homozygous for this allele and therefore express the trait. Dominance and recessivity are just extreme case of a continuum and most often alleles have intermediate level of dominance. Pleiotropy is also something to consider. Note also thaat the frequency of the three possible genotypes $AA$, $AB$ and $BB$ are given by Hardy-Weinberg law (under some assumptions) $x^2$, $2x(1-x)$ and $(1-x)^2$ respectively, where $x$ is the frequency of the allele $A$.
Hope that helps!

@Digger There is no such think as a question in your post so please let me know if I missed your point or if I answered your question.

Thank you so much! Your answer not only enlightened my question but also gave me new vocabulary for me to know more about it. I will be reading more about the matter, specially your answer on my 2nd topic. @prooffreader's answer only got my vote because a few thing on your answer went over my head (not your fault, obviously). I wish I could vote on both your answers.


text:
Is it possible to get infected with HIV from old blood?
Let's say that someone uses a needle which has some old blood infected with HIV. In this case, is it possible for them to get infected with HIV?

Doesn't the oxygen of air eliminate the virus?

It's important to define how old is "old", here, I think.  I rephrased the question a bit so that it focuses more on the science than an individual diagnosis.

Thanks. Let's not define old in order to have a complete answer. I suppose the answer is based on that.

Yes, you can transmit HIV with infected needles/syringes. This is a quite common mechanism of transmission when drug addicts share and re-use needles and syringes and also in third world hospitals with poor hygiene standards.
A drop of blood is considered infectious at least until it has completely dried up (some research showed that it might be contagious for up to 5 days longer when the conditions are right, see reference 1 below). Mostly HIV is senstive against high temperatures (over 60°C), while it is stable at low temperatures. It is very sensitive against shifts in pH (below 7 or above 8) and also against desinfectants like bleach. Have a look at the references below, a lot of research has been done by Abdala et al. in this field. You can find his whole reference list here (it contains more articles in this field).

References:

Survival of HIV-1 activity after disinfection, temperature and pH
changes, or drying.
Survival of HIV-1 in syringes.
Survival of HIV-1 in syringes: effects of temperature during
storage.
Viability of HIV-1 in syringes: implications for interventions among
injection drug users.


text:
What Aquatic Mammal has no Tail?
Found in a waterway in Butte County, CA. First thought it was a beaver kit, but it has no
tail.
What aquatic mammal has no tail?

Are you sure there is no tail? Muskrat?

Muskrats have a rat tail. This critter may have had a small knob of a tail, but the hair at the hindquarters was too wet to reveal much of anything.

Your individual might have had an accident in the past!

What size is it? I'd agree with kmm and Remi.b that it's a muskrat which lost its tail.

What a great picture!

Looks like a mountain beaver (Aplodontia rufa) to me. Location, appearance, and minimal tail all match.

A bit more detail:
Where I'm from on Washington's Olympic Peninsula, they're not uncommon, but Butte County is near the southern end of their distribution (eol map page) and they may be less common there, and limited to cooler higher elevations (Beier 1989), and to wet habitats (their inability to concentrate urine (!) means they need to drink enormous quantities of water).
This white paper from USDA (Arjo 2007) is a great source, and more comprehensive than the  the wikipedia page, which is also good.

Arjo, Wendy M. (2007). "Mountain Beaver: A Primitive Fossorial Rodent". USDA National Wildlife Research Center - Staff Publications. Paper 675.
Beir, Paul (1989). Journal of Wildlife Management 53(3) 649-654

Hey, Oreotrephes, thanks for taking the time to respond with the correct answer.
This is a video I shot of this animal, and it reveals that it definitely is the mountain beaver:
http://youtu.be/8Ljp1NiLvLU

Aw, what a cute little guy. Great footage!


text:
Which organs do cats not eat on their prey?
My female cat is a very active hunter and brings me her prey daily. Except for shrews and birds, she always eats them entirely.
This afternoon she brought me this:

It was quite large (maybe between half and two thirds of the length of a mole), and I couldn't identify it (I'm in Europe if that matters).
The prey was already dead when my cat brought it to me, and she quickly started eating it. I noticed that she didn't eat this part:

I'm not a biologist, but I guess this is the stomach of an herbivorous animal?  What's inside looked like wasabi.
Why didn't she eat it? She is not so picky with smaller animals. Is it because of the size of this one?
Are there some organs or parts of the prey that cats usually don't eat ?

Yes probably. They're surely better at identifying the inside of animals.

When I first looks at that I thought it was a fetus of some kind!!!

This isn't exactly an answer but my 2 male cats always eat only the head of all the mice they catch. It seems very strange.

That looks like some sort of rodent.  The rodent stomach, while not as acidic as the human one, is still strongly acidic:

The mouse stomach pH was 3.0 (fed) and 4.0 (fasted), and the corresponding values in the rat were 3.2 (fed) and 3.9 (fasted).

From this article
Since it's clear from the picture that the organism had just eaten (the stomach had not yet emptied), the pH would be on the lower end of that spectrum.
In humans, acidic foods often taste sour, so it may be that the cat ran into a terrible taste at the base of the esophagus that caused her to stop there, but I don't know whether the taste buds on the cat are comparable to those in a human.

I think it depends on hunger, preferences....
Domestic cats can pretty much eat it all.  They might discard items they can't digest like fur, relatively large bones... other than that what they leave behind is rather individual.
I'm guessing this cat doesn't like salads.
Typically I haven't seen hunting cats discard digestive organs.  Aside from fur and big bones sometimes they might discard a head (probably because they don't feel like dealing with the skull).

We had a hunting cat years back that seemed to leave the kidneys alone when eating rabbits.

It is known that Grizzly bears catching salmon during times of plenty only eat the head (the fish brain, as any brain, is rich in fats, easy to digest and basically luxury food). However, in times of shortage they consume pretty much the whole fish, as every scrap of food, even untasty and non-nutricious tail fins and the likes are better than nothing.
Your cat will chase, hunt and catch prey following its hunting instincts. When its well-fed, however, your cat is not really hungry and will eat only the tastiest and easiest parts (say liver etc), but will definitely skip smelly intestines with undigested plant material.
I can try to find a reference to the Grizzly study (pretty interesting study :-)

My cat brings us those too. So I guess it is very common to cats to not eat that part of a animal. My cat brings us one almost every morning so it is very common. This item they leave behind is called a gizzard. A gizzard is a part of the stomach that has strong acid in it so they know not to eat it.


text:
Which of the following demonstrates the pattern of development in Greylag Geese?

Which of the following demonstrates the pattern of development in Greylag Geese? {Please give specific answers, which among the following gives the best available demonstration?, If needed, have a look at the Paragraph (Image Embedded)}
(A) Geese reared by humans cannot be taught to respond to its own species.
(B) The hatching at an advanced stage is critical for imprinting.
(C) The capacity to recognize an adult of its own species is necessarily inherited.
(D) Rearing by humans does not alter the object of the behavioral routine.
Option A: “Geese reared by humans cannot be taught to respond to its own species” is correct.
This is inferred from the 4th paragraph 2nd line: “When young geese are reared wholly by human beings it is towards humans that the young geese direct their behavioural routines”. This line clearly states that geese wholly reared by humans respond only towards humans. Also from the 2nd Paragraph 3rd line It is clear.
Option B: “The hatching at an advanced stage is critical for imprinting” is false.
Hatching at an advanced Stage is not shown by Greylag Geese, it is shown by Godwits. (3rd Paragraph, 1st & 2nd Line: The young of Godwits hatch at an advanced stage of development and soon after hatching can recognize the adult bird.) (So the fact is not conclusive from Behavioural Pattern of Greylag Geese) Imprinting can be shown by Greylag Geese, which do not have a prolonged period of hatching, and imprinting totally depends on whatever creature happens to be present at the right moment in their development.
Options C: “The capacity to recognise an adult of its own species is necessarily inherited” is false. According to the 2nd Paragraph, 2nd line: The capacities to recognise the right stimulus are not always inherited.
Option D: “Rearing by Humans does not alter the object of the behavioural routine.” is false, as shown in 4th Paragraph 2nd & 3rd line: When young geese are reared wholly by human beings it is towards humans that the young geese direct their behavioural routines.
Hence, answer should be A.
So Am I correct?

Homework questions are off-topic unless you show some effort solving them.

Mr Chris, This isn't a Home-work Question! It is an exam question, I have already answered it in the Paper, I want to know from Experts what should be correct! & Please If you are unable to answer don't comment the things you don't know!
I hope you Understand.
DWITI

Still: How about adding your answer? And I comment on everything I want.

Ok I am adding my logic, (Option wise)
Option A: “Geese reared by humans cannot be taught to respond to its own species” is correct.
This is inferred from the 4th paragraph 2nd line: “When young geese are reared wholly by human beings it is towards humans that the young geese direct their behavioural routines”. This line clearly states that geese wholly reared by humans respond only towards humans. Also from the 2nd Paragraph 3rd line It is clear.

Option B: “The hatching at an advanced stage is critical for imprinting” is false.
Hatching at an advanced Stage is not shown by Greylag Geese, it is shown by Godwits. (3rd Paragraph, 1st & 2nd Line: The young of Godwits hatch at an advanced stage of development and soon after hatching can recognize the adult bird.) [So the fact is not conclusive from Behavioural Pattern of Greylag Geese]
Imprinting can be shown by Greylag Geese, which do not have a prolonged period of hatching, and imprinting totally depends on whatever creature happens to be present at the right moment in their development.

Options C: “The capacity to recognise an adult of its own species is necessarily inherited” is false.
According to the 2nd Paragraph, 2nd line: The capacities to recognise the right stimulus are not always inherited.
Option D: “Rearing by Humans does not alter the object of the behavioural routine.” is false, as shown in 4th Paragraph 2nd & 3rd line: When young geese are reared wholly by human beings it is towards humans that the young geese direct their behavioural routines.
Hence, answer should be A. (Therefore, It is not B) {Actually the examiners say that It is B SO I need expert's help}

Your logic seems fine to me..
Option B: The hatching at an advanced stage is critical for imprinting.
This is wrong because Konrad Lorenz (who rediscovered imprinting)

demonstrated how incubator-hatched geese would imprint on the first
  suitable moving stimulus they saw within what he called a "critical
  period" between 13–16 hours shortly after hatching (reference).

So saying that the hatchling should be at an advanced stage is incorrect.
Option C: The capacity to recognize an adult of its own species is necessarily inherited.
Again this is incorrect because Lorenz has also stated that

The human-imprinted gosling will unequivocally refuse to follow a
  goose instead of a human, but it will not differentiate between a
  petite, slender young girl and a big old man with a beard (Lorenz,
  1965) (reference).

Also in this article it is implied that starlings that are imprinted to humans do not relate to its own kind.
Option D: Rearing by humans does not alter the object of the behavioral routine.
From the earlier findings, this is obviously false. Moreover a duck keeper has explained imprinting thus:

An imprinted duck--a duck that was raised from the moment of hatching
  by a human and so views the human caretaker as a parent or equal--may
  become accustomed to riding in the car. Imprinted ducks might go
  camping with you (although you must keep them beside you at all times
  or in a crate) or go on play dates to a friend's house (you will not
  want to take them to a farm or a public pond where they may contract
  diseases). If your duck is in a diaper, you will need to change the
  diaper every hour or so (reference).

This shows clear behaviour changes.
Option A:  Geese reared by humans cannot be taught to respond to its own species.
It is mostly accepted that it is not with Lorenz himself stating that

imprinting is irreversible. It is essential in learning that what has
  been learned can be either forgotten or modified (reference).

However there are claims to the contrary nowadays with it now firmly established that filial and sexual preferences are reversible (reference). Another interesting article by the American Psychological Association with a few links you might want to check out.
In conclusion, Option A could also have its problems with some response to its species possible, but overall it is the most and best plausible answer.

Dr Lorenz with his imprinted geese. Also a very interesting read (reference)

See I need to claim for this, because The answer given by the question setter is B (Which according to you & me is wrong), So I am using your answer as Reference for my claim apart from my explanation!
So Permission Needed!

Help urself to it. if ur claim works toh bata dena

Ya Ya, I will tell you (How can I contact you, any e-mail or Fb account?)

This is pretty much an open forum. My answers are not copyrighted and it is very much open to change or dispute. I personally have no problems with my answers being used for any educational purpose

Buddy, according to you, B is never possible, Isn't it?

From references, lorenz used to imprint between the time period I mentioned. There are also articles that peg the best time for imprinting between 24 and 48 hours. I wouldn't call that an advanced stage. I would be very interested in his references and proof if he decided to refute what I have pointed out in the article.

Let us continue this discussion in chat.


text:
Why does max heart rate decrease with age?
I have heard that max heart rate declines steadily with age, and can be approximated by the equation Max Rate = 220 - Age.
What is the physiological reason for this decline, and how is it consistent with the fact that most endurance athletes reach their peak cardiovascular performance at around age 30?

There are many reasons why the maximal heart rate decreases with age.
The most prevalent is the heterogenous thickening of the walls of the heart.
Cardiac output is stroke volume times heart rate.
When the wall thickens, the heart needs more energy to achieve the same pumping (bigger stroke volume) or it needs to increase heart rate at rest.
Because of physical limitation, the stroke volume cannot be increased.
Heart needs to also rest which it does before the action potential reaches the AV conduction system.
Note the long time just after the action potential reaches AV node.
However, the heart cannot increase its maximal heart rate if the elasticity of the walls have decreased in ageing.
Ageing often leads to heterogenous thickening of walls of the heart.
If this is the case, then T wave gets high fast; which causes the risk of bleeding when exercising.
Doing sport or just feeling tired can cause a long-standing pain in the heart area in the chest.
Sport then again leads to dynamic hypertrophy of the heart tissue, which increases the maximal heart rate.
Ageing then again does not have such a dynamic changes.
There are secondary reasons caused by ageing

hormonal changes
decreased metabolism
decreased physical activity
...

which are associated with decreased maximal heart rate.
Why most endurance athletes reach their peak cardiovascular performance at around age 30?
Human's best age is at about 25 years old physiologically.
Muscles grow in rest.
When practicing at that age, recovery time of muscles is short.
It takes long time to improve cardiovascular performance (1-5 years), since heart muscle improves slowly.
I think the slow hypertrophy of heart musculature and the best physiological age of human are the reasons why the most successful endurance athletes are about 28-30 years old.


text:
what is the margarine metabolism in our body?
margarine is commonly used food ingredients that contribute to both inflammation and
obesity , but actually I want to know the margarine metabolism in the human body
I can find some resources talk about its impact on health but I can't get the idea of its metabolism.

You probably need to look at the components of the margarine, then research the metabolism of each component.

What are its components  ?

Mostly plant oils. Have a look into Wikipedia about it.

As pointed to by @Chris the Wikipedia link for margarine explains that these are formulated upon vegetable oil-based fats. Their melting points and other properties are adjusted by industrial hydrogenation of the unsaturated fatty acids in the vegetable oil.
Most unsaturated fatty acids present in nature are in the cis conformation at the double bonds. The hydrogenation process, if it is not carried to completion, produces the trans isomers of fatty acids. These so-called trans-fats are blamed for the undesirable side effects of consuming margarine, or other foods containing hydrogenated oils.
Most of the fatty acids present in margarine (i.e. cis unsaturated and saturated fatty acids) are metabolised by the normal route (β oxidation).


text:
How can Taenia solium (tapeworm) lay 35,000 eggs per proglottid?
As far as I know TAENIA SOLIUM is an acoelomate which basically means that the space between the alimentary canal and the gut is completely filled [or] occupied by the mesoderm and they do not have primary body cavity as well as secondary body cavity then from where does the space comes in taenia to store that huge amount of eggs

The eggs are very small compared to the proglottid.
According to this site:

T. saginata can be up to 4 to 6 meters long and 12 mm broad; it has a pear-shaped head (scolex) with four suckers but no hooks or neck. It has a long flat body with several hundred segments (proglottids). Each segment is about 18 x 6 mm with a branched uterus (15-30 branches). The egg is 35 x 45 micrometers, roundish and yellow-brown. It has peripheral radial striations and contains an embryo with 3 hooklets.
T. solium is slightly smaller than T. saginata. It has a globular scolex with four suckers and a circular row of hooks (rostellum) that gives it a solar appearance. There is a neck and it has a long flat body (0.1 meter in length). The proglottids are 5 x 10 mm with a 7-12 branch uterus. The eggs of T. solium and T.  saginata are indistinguishable.

I assume that the measurements given for the T. solium proglottid relate to the dimensions of your diagram, and since this is a tapeworm it is thinner than either of these values, so let's assume 2 mm to make the arithmetic easy.
volume of proglottid = 5 * 10 * 2 * 10-9 = 100 * 10-9 = 10-7 m3.
The egg approximates to a 40 µm sphere = 33,500 * 10-18 m3
So, volume of 35,000 eggs = 1.2 * 10-9 m3
So, volume occupied by eggs = (1.2 * 1010-9 * 100)/1010-7 % of proglottid = 1.2 %
So, not much of an accommodation is required for the volume of the eggs, even allowing for errors in this approximation (e.g. I neglected spherical packing which would add somewhat to the volume occupied by the packed eggs).


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What causes headaches (biologically)? What does it mean directly?
Even though your brain can't feel pain, thingies in your head are installed to compensate for that.
Once I thought your head starts to hurt when your brain is tired. I can't believe this any more. Several times I happened to skip sleep completely - while intellectually working (not just watching TV or something like that). The next day I didn't go to sleep to prevent breaking the day/night biorhythm. Yet I don't remember any headaches from not sleeping enough - and working instead.
However, when I was worrying about something deeply I often got a headache to the top. Also, you get headache when you're ill. You get them after drinking too much alcohol (or getting poisoned by some other things too as I've heard).
As non-biologist I believe that pain receptors are triggered when whatever they're guarding is damaged. Also I thought that they're installed so that you can do something about the cause of the pain - that doesn't seem possible in case of headaches.
But I do hope that headache doesn't mean that my brain is sustaining damage.
So what's triggering pain sensors? Is it a chemical/hormone that is released when the organism feels endangered (by illness or something else)?


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Senescence, immortality and evolution?
Many have heard about the fabled "immortal" jellyfish, Turritopsis dohrnii, which doesn't die from aging (senescence) and can revert the aging process indefinitely. It is rather remarkable that only one, or very few species show this type of behavior.
I wonder if at some earlier point in evolution, when life was predominantly simpler and sea based, there were more species with this feature, but this "immortality" caused overpopulation and/or didn't allow for proper action of natural selection, meaning that "immortal" species didn't evolve much and got wiped out almost entirely by whatever phenomenon.
In this scenario, aging and dying from old age would be an important evolutionary trait which would allow for populations to maintain reasonable sizes and would allow for natural selection to impart changes.
I was wondering how plausible all of this is, since I'm not an expert in the area and know little about the appropriate technical concepts behind these things.

Are you asking what the drawbacks of cellular immortality are to the individual or the species? They're slightly different. Try http://biology.stackexchange.com/questions/17077/why-does-evolution-not-make-our-life-longer?rq=1 for more information on aging and evolution.

You will find here a very good overview of the main hypotheses that explain senescence.
I am not sure I will answer your question but here are some reactions to your post..
What you say has to do with species selection. Selection selects between various objects/units that differ. These objects may be genes, individuals, populations, species, etc… In other words, there are various level of selection or different units on which selection acts. Wiki
Generally speaking, it is often assumed better to think in terms of selection acting on alleles (gene variants) or on individuals. Therefore, we tend to think that selection acting on genes or on individuals is more effective than selection acting on species. However, selection acts on species and we should not necessarily discard explanation using the concept of species selection.
What you say, if I am not mistaken, if we consider a set of species that are either mortal or immortal, we would predict that selection would benefit the mortal ones. Stating differently, mortal species have some advantage over immortal species that allow them to not get extinct or eventually to speciate more.
However, I don't quite understand the reasons why immortality would be deleterious to species. You say that it leads to overpopulation. So would you expect that a population is lead to overpopulation due to immortality and suddenly disappear because it is overcrowded. It doesn't sound like a well formulated argument to me. You could however argue that mortal species have a much greater individual turnover allowing them to adapt faster to environmental change than would immortal species.


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Simple experimental design of a chemostat without pumps
A chemostat is a device to maintain a cell culture in equilibrium, by continually pumping nutrients in and pumping excess cells and nutrients out.
What's the simplest design of a chemostat one can make? Has anyone tried to mount one without pumps?
A particularly sensitive issue here is sample taking, because you risk contamination of the culture.

Here is a link to a design in which electrolysis is used to generate gas which displaces liquid from the reservoir into the culture chamber, which in turn displaces culture into an outflow (where samples could be collected). The design does however require a pump for aeration, and I can't think of a way in which this could be avoided, although there is a reference cited in this article which apparently describes the use of gravity flow (I haven't checked it out).
Just for interest, this link is to a design which does require a peristaltic pump and a vacuum line but it looks to be achievable.


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Biosphere that simulates sun and moon shifts
Is there an enclosed biosphere that artificially simulates the movement of the sun and moon at increased intervals?
It is known that the sun and moon alter plant movements therefore I was wondering how far experimentation has gone.  Ideally I am wondering if they have experimented with different speeds of the moon and sun rotation and how it effects plant(and possibly other animal behavior ideas) growth.

You think about research with different day/night length and the effects on plant/animals?

@Chris Yes.  Should I give a further explanation?  The moon effects fish migration through the altering of water currents and tides.  In addition the moon alters wolf pack hunting and feeding schedules.  The sun is fairly more obvious and straightforward altering temperatures and altering bird feeding schedules and flight patterns.  There have been a couple studies down on this, but nothing I have seen that demonstrates if the abilities are instinct or learned.

Sun and moon-faking devices exist. Not sure about 'biosphere'. I have personally observed one for honeybees, but that one was fairly crude(bees are dumb). It was just a big room with a hive stand in the middle and a series of fluorescent lights on the ceiling that turned on one after the other. The goal was to mess with bee circadian rhythms and see which genes became more or less expressed in their brains.
There's a slightly more sophisticated thing called a 'grow cabinet'. It has expensive lights to produce sun-spectrum light at direct sunlight intensity and humidity and temperature controls. Scientists use them for crop research when the weather is too random and unpredictable and absolute control is required.
I believe advanced versions simulate moonlight and angle of insolation, but that sort of thing is expensive.
I don't know of any full-sized biodomes with fake celestial objects. The cost of such a biodome would be prohibitive, and the experiments it enabled might be easier(certainly cheaper) to do in a smaller container.


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What are some useful physical information of a protein?
Beside energy and heat, I don't know any useful physical information of a protein. Can you help me list some of it. Somethings like Fourier-transform infrared spectroscopy to provide protein structure aren't what I'm looking for.

What about the sequence and the 3D-structure? This is important information...

Please clarify what kind of information you are looking for.

Somethings like energy, heat, entropy, which are physical measurable things. The structure is a good point, I don't know what the sequence information are.

sounds like you mean 'typical means of monitoring the folding of a protein' or something like that?  such a question would work...

Something like that. I need some new conceptions to research deeper.

I'll make a list, by wavelength then 'others'.  This is only the most common techniques list.  i'd be here all week if I tried to get all the applications.  Scientists are crafty and are always coming up with stuff.
Electro magnetic protein derived measurements:

NMR spectroscopy (radio) - can detect the structural variations in
the individual amino acids allowing a protein structure with the
dynamics of the peptide chain to be modeled.
IR spectroscopy - can
look at bond-bond vibrations.  Mostly used to observe for non-peptide
moities and cofactors of the protein like heme in hemoglobin for
instance.
RAMAN spectroscopy - also an IR spectroscopy, but which
can look for dynamic qualities of the interatomic vibrations.  Like
IR this is used with cofactors usually and not the protein, which
looks very much the same over most of a peptide.
UV/visible spectroscopy - on the low end, examine the behavior or concentration of chromophores associated with the protein.  used for kinetics - study of enzymes in the act of catalysis.  On the high end can also be used for things like watching photon-energy transduction in photosynthetic systems and things like this. The peptide itself has no Visible absorption, but the colored molecules are often used as a probe to watch the peptide in action - like folding.
FRET is a technique that can measure how far apart two colored labels are - two separate points of a protein are labelled and a distance measurement obtained.
UV circular dichroism.  the aromatic side chains of Phe, Trp, Tyr, His etc absorb in the UV and are directly observed to follow folding some times.  Circular dichroism looks for differences in the absorption of right and left circularly polarized light and can show secondary structure.
X-ray.  Scattering of proteins in solution can measure the so called 'radius of gyration' which profiles the overall shape of the protein.  X-ray scattering off of 2D and 3D crystals can reveal the molecular protein structure.

Others:

Calorimetry.  By tracking the heat capacity/heat given off/taken in by a protein, its folding state, binding and other structural characteristics of a protein sample can be measured.
Mass Spectroscopy - generally this just measures whether a protein is present, by fragmenting it and measuring the mass of the fragments.  useful for mixtures of many proteins (like a living cell).
Peptide sequencing - like Mass Spec, but often used when there is just one protein in a pure sample.

There's lots more - just depends on where you want to cut off the list.  Hopefully this is a good start.

All the information about a protein, biochemical or functional is encoded in its structure, which are primary (Amino Acid (AA) sequence), secondary (alpha helix or beta pleated sheet), tertiary (overall 3D structure of a single peptide) and quaternary (overall 3D-structure of a protein composed of multiple peptides which are attached together through various different bonds) structures (http://en.wikipedia.org/wiki/Protein_structure).
Obviously, the key determinants for all these structures is the AA sequence of a protein, since that determines the biochemical property of a protein as well as its function (e.g. enzymatic residues and active sites, functional domains, motifs, whether it is post-translationally modified or not by phosphorylation and whether that causes its activation or inactivation through conformational changes or its interaction with other proteins etc).


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Can human change its morphology or anatomy due to ecological changes?
According to Charles Darwin, as the surrounding environment changes, so changes the anatomy or morphology of a specific organism.
But nowadays, humans have become very advanced in the technology and when the surrounding temperature changes, humans in turn change the surrounding temperature (e.g. the use of ACs), and maintain the surrounding as they like.
What I want to emphasize is can human being evolve with these scopes in mind?

related question: http://biology.stackexchange.com/questions/8401/has-medical-progress-stopped-human-evolution Incidentally, Darwin was not awarded a knighthood.

I went ahead and changed it, as other people are going to come in trying to correct it as well.

i think we have bigger bellies now :P

It's important to note that populations evolve; individual organisms do not.

@p.s.w.g very good concept to be focused so can the population evolve now

@agharehanabbas Yes, human populates can and do evolve now

@ p.s.w.g That's Berkeley opinion. Which is wrong :)


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What does irregular heartbeat mean in simple language?
I bought a blood pressure monitor (A&D UA-851) which has the option to measure irregular heartbeat.  I do understand what 'irregular' means, but why do irregular heartbeats happen and what are it's implications short and long term?

I wouldn't put too much trust in the option to measure irregular heartbeats. Its specificity shouldn't be too high, especially when you consider that some more advanced digital monitors used in hospitals give a lot of false positives.

I understand the OP wants to understand how his blood pressure monitor works. Some of you are thinking that it works by just interpreting cardiac rhythm. This is false! It is done by interpreting the frequency space of regular/irregular heartbeats. Please, note the difference between irregular cardiac rhythm and irregular heartbeat.

Masi - I understand something completely different from the question. He is not asking how his blood pressure monitor works, he is asking in layman's terms why an irregular heartbeat happens. I haven't voted your post down, but I think if you answered the question and were less confrontational and aggressive in comments you may get more upvotes.

I think you should re-think the accepted answer for one of the other answers.

@dustin are you telling me what to do? I understand Masi's answer and see that he's passionate about answering it right.

Is that rethink means to you?

The normal cardiac cycle is comprised of two distinct phases: the systolic phase in which the heart contracts, ejecting the blood, followed by the the diastolic phase when the cardiac muscle relaxes, refilling the heart with blood.
This cycle is assured by specialised cardiomyocytes (Cardiac muscle cells) that conduct electrical impulses through the heart. When there's interference in this electric activity, the cycle becomes irregular or arrhythmic.
Arrhythmias can be divided by their place of origin:

Atrial (atria are the upper chambers of the heart)
Ventricular (ventricles are lower chambers of the heart)
Junctional (the junction between the two)
Heart blocks (caused by a blockade in the conductivity of the electrical specialised cardiomyocytes)

Some arrhythmias are physiological, such as the Respiratory sinus arrhythmia, a naturally occurring variation in heart rate that occurs during a breathing cycle. Also, in healthy individuals, some extra sistoles might occur without being the translation of a subjacent heart condition and have benign prognosis in individuals without other conditions.
However, some arrhythmias can have a wide range of health implications, from asymptomatic, to a mild intolerance to exercise, to Cerebrovascular Accident (CVA or stroke) or even sudden death due to cardiac arrest.
Therapeutic varies with the underlying cause but can be medical (with drugs such as Na+, K+ and Ca+ channel blockers, beta-blockers and Digoxin) or surgical (ie: Artificial pacemaker).

Great answer but it would be fantastic if you added some references.

-1 This answer is about the origin of the cardiac rhythm with major simplifications in the cardiac cycle. Irregular heart beat is not the same thing as arrythmias, also dangerous overloading of tachycardia with arrythmia. Focus on the explicit classification of heartbeat based on origin, not how those machines work.

I think it's a very good answer - although references would be ideal all the content is factual as far as I can see.

@RoryM I recommend you to study little more Physics and Mathematics if you want to understand the big flaws in this answer. He does not answer to the main question explicitly what is irregular heartbeat. He does not try to explain how those machines work. This answer is biased and not useful to understand how the electronic device can do the analysis of the heartbeat, particularly of irregular heartbeat. You make extremely big simplifications if you do the analysis of the blood pressure based on these implicit facts, just ignoring the frequency space completely.

@Masi well, this is a Biology Q&A site so answers should really focus on the biological aspects of the question.  The original question "why do irregular heartbeats happen and what are it's implications short and long term" is succinctly answered in the above without over complication.

@RoryM This is Biology Q&A also for researchers! Not just for high-school students and for repeating pieces of information found in books.

@Masi What on earth does "dangerous overloading of tachycardia" mean? (I don't even mention tachycardia anywhere!)

@Tivie Yes, you are right. Arrythmias are rarely benign. I get an interpretation that there is a risk of going into tachycardia in your answer: "Some arrythmia are physiological" and then you describe situation tachycardic processes as arrythmic which is not necessary. This I call overloading which can confuse.

Very simply putting, irregular heat beat means that the pulse is not regular. It can be diagnosed by checking your pulse clinically.
Irregularities are further classified as:

Regularly Irregular: this occurs in heart blocks where every second or third beat is skipped regularly causing a pattern. Usually as time progresses the degree of block worsens and result in the final form which is complete block (fourth degree heart block)
Irregularly Irregular: this occurs in arrhythmia where there is total dissociation between atria and ventricles and the ventricles beat very irregularly with no pattern. The ventricles don't follow intrinsic rhythm because every SA nodal impulse that occurs at the end of latency of AV node will get conducted. Thus the heart rate is very high without any pattern. (Here heart rate means ventricular rate)

-1 because it is not correct answer to the functioning of the blood pressure monitoring. This answer emphasizes the melodies that are events in time interval of the heartbeat. There are also irregularities in the amplitudes of the heartbeat. There can be many amplitudes or energy levels in one heartbeat. Those machines do not only consider cardiac rhythm in making the diagnosis. They consider the energy levels and cardiac rhythm together. Without energy, you cannot even get pressure!

@Masi, you cannot measure irregular heart beat using blood pressure. Even a BP monitoring machine can measure irregular heart beat using pulse only. The only other way is using an ECG or echo cardiography. Irregular heart beat is a defined medical term. And my answer is the correct one.

Think a moment what you say, please. You have no references. You only assert. You cannot distinguish between subjective and objective measuring systems in your answer and comment, it seems. You exaggerate by using word only many times, which gives me a signal that you do not know this field well.  ECHO is the golden standard for the dynamics of the heart, but please remain in the topic and do not go sideways. We consider here personal blood pressure monitoring systems like pointed by the OP.

http://www.m.webmd.com/heart-disease/guide/heart-disease-abnormal-heart-rhythm what I said is correct. No one measures irregular heart rate using bp. Bp measuring in a patient with irregular heat rhythm is only done to prevent shock. Echo cardiogram can visualize heart beats thus irregularities can be seen and diagnosed. Please check thoroughly before telling someone is wrong.

Please, stick to the topic here. The topic is about what is irregular heartbeat and how the blood pressure monitoring devices work. Not about deducing irregular heartbeat from blood pressure. You confuse in your comment now also heart rate and heartbeat too. Please, read carefully before asserting again. Also, please use trustworthy sources like Harrison, Merck's manual and some publications. Your webpage is not a good source.

@masi you are incorrect. Read the OP again. It states that OP bought a BP cup, it has a setting, and then ask what are the implications of an irregular heart beat. That is, the fact they own a BP cup is irrelevant.

@dustin Last sentence is arrogant in your comment. The question has many parts. Some answers have focused here on explicit implications. This thread should be split in many parts to answer it completely. Heartbeat, how the device detects it and what the irregularity of the heartbeat mean.

@Masi read the sentence how you deem fit. The question is clear cut. From your profile, it says you are in medical school. Then you should know from case studies that there is information put in them that is irrelevant. When you do your differential diagnoses, I hope you don't include the useless information. The same is occurring here. The question is: why do irregular heartbeats happen and what are it's implications short and long term? The question came about due to a setting on a BP. The question doesn't say anything about relating the two.

@dustin This forum is not for medical advice! I do not even write such answers here. This is for understanding in Biology which means real world and living organism. This requires understanding. Yes, I understand how the question comes. To explain how the measurement result comes is one point here - it is just an approximation from the machine which can have many designs. To explain the main question in the title is another thing too. Third thing is about indications. 4th thing is about implications from subjective results which should not be made, since this is not for medical advice!

@Masi no one is saying give medical advice. Read my comment one more time. Again, I am telling you to re read something.


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Software to calculate Fst from sequence data
I'm looking for a software to calculate Fst from 3 loci DNA data of individuals from a metapopulation. I don't have any prior on the population structure (have no idea of the number of subpopulations for example)
I've been looking at FSTAT but it doesn't run on MAC.
Do you have any easy alternative?

it should be pretty easily implementable in perl or python.

If You are familiar with R, try package adegenet. It contains very nice tutorials explaining its usage, including the very R basics. If You require graphical interface, install RStudio - very nice front-end for R. There are more possibilities how to calculate Fst in R, but adegenet is one of the most powerful genetic packages there.


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Weinman AIF and High temporal resolution AIF difference
I'm dealing with MRI DCE maps. Actually I need to find such parameters as the transfer constant $K^{trans}$ and rate constant $k^{ep}$ according to the two-compartment model.
Mathematically, this dynamic system can be described by the following equation:
$$C_t(t)=DK^{trans} \sum\limits_{i=1}^2 a_i [exp(-k^{ep}t) - exp(-m_it)]/[m_i-k_{ep}]$$
Now if I have contrast agent concentration $C_t(t)$ time series from experiment I can extract transfer constant $K^{trans}$, and rate constant $k^{ep}$ by least square fitting. The only problem is that I need to know $a_i$ and $m_i$ constants. For this purpose I use the next formula for blood plasma concentration: $$c_p(t)=D \sum\limits_{i=1}^2 a_i exp(-m_it)$$
However I can't find the relation between the blood plasma concentration: $c_p(t)$ and $c_t(t)$. In the next article:
 Geoff J.M. Parker et. al. "Experimentally-Derived Functional Form for a Population-Averaged High-Temporal-Resolution Arterial Input Function for Dynamic Contrast-Enhanced MRI"
I have found that biexponential function $c_p(t)$ is used to describe AIF (arterial input function). It's presented on plot as Weinmann AIF.

QUESTIONS:
1) How Weinman AIF and High temporal resolution AIF can describe the same processes, actually from mathematical point of view it's two completely different functions?
2) Do I really can find $a_i$ and $m_i$ parameters by fitting AIF curve with $C_p(t)$ function?
P.S. I'm just a programmer so I completely unaware in the field of biology and any help is appreciated.