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Why do plants have green leaves and not red?
I know plants are green due to chlorophyll.
Surely it would be more beneficial for plants to be red than green as by being green they reflect green light and do not absorb it even though green light has more energy than red light.
Is there no alternative to chlorophyll? Or is it something else?

I find it even more puzzling why plants don't absorb all of the visible spectrum altogether (resulting in the leaves being black).

@CrazyJugglerDrummer - I thought about it but didn't want to get the chlorophyll response without people reading =P

It is even more strange becouse green algae evolved in water. And red light is absorbed by water. Rhodophyta (red algae) are red due to phycoerythrin but it seems that red color is advantageous for them only in sea depths.

@AdamZalcman: There's probably no organic substance with this absorption spectrum, and adding further pigments to cover the entire VIS spectrum might not pay off.

@MartaCz-C: I think that's because of the solar spectrum, and as you said water absorbs red light stronger so at deep sea levels red light becomes more and more unusable and can the red-absorbing pigments can then be dropped in favour of green absorbers

Surely it would be more beneficial: not if the red pigment is less efficient in converting light to energy...

I would like to point to a dissuasion that took place at John Baez's google+ on the subject https://plus.google.com/117663015413546257905/posts/emyoML3CrvY It contains relevant links along with references to actual  articles devoted to the question. This is a nice point to begin further investigation.

If anybody is interested in a short video on the topic (~6.5 min), watch Physics Girl's video: Why aren't plants black? disclaimer: This is not my video, but I think it is very well researched and informative.

I know it's been a couple of years, but I just added a new answer to this question that focuses on the early evolution of plants. Hope this helps!!

The real answer is that they do not. The majority of plants have green leaves, not all of them. It's just they don't need to evolve towards having leaves of other colors, the same way as human don't need to evolve to get rid of nails, hair and coccyx. There are even black plants.

According to a new model of photosynthesis plants are green to reduce noise: https://www.quantamagazine.org/why-are-plants-green-to-reduce-the-noise-in-photosynthesis-20200730/

Surely it would be even more beneficial for plants to be black instead of red or green, from an energy absorption point of view. And Solar cells are indeed pretty dark.
But, as Rory indicated, higher energy photons will only produce heat. This is because the chemical reactions powered by photosynthesis require only a certain amount of energy, and any excessive amount delivered by higher-energy photons cannot be simply used for another reaction1 but will yield heat. I don't know how much trouble that actually causes, but there is another point:
As explained, what determines the efficiency of solar energy conversion is not the energy per photon, but the amount of photons available. So you should take a look at the sunlight spectrum:

The Irradiance is an energy density, however we are interested in photon density, so you have to divide this curve by the energy per photon, which means multiply it by λ/(hc) (that is higher wavelengths need more photons to achieve the same Irradiance). If you compare that curve integrated over the high energy photons (say, λ < 580 nm) to the integration over the the low energy ones, you'll notice that despite the atmospheric losses (the red curve is what is left of the sunlight at sea level) there are a lot more "red" photons than "green" ones, so making leaves red would waste a lot of potentially converted energy2.
Of course, this is still no explanation why leaves are not simply black — absorbing all light is surely even more effective, no? I don't know enough about organic chemistry, but my guess would be that there are no organic substances with such a broad absorption spectrum and adding another kind of pigment might not pay off.3
1) Theoretically that is possible, but it's a highly non-linear process and thus too unlikely to be of real use (in plant medium at least)
2) Since water absorbs red light stronger than green and blue light deep sea plants are indeed better off being red, as Marta Cz-C mentioned.
3  And other alternatives, like the semiconductors used in Solar cells, are rather unlikely to be encountered in plants...
Additional reading, proposed by Dave Jarvis:

http://pcp.oxfordjournals.org/content/50/4/684.full
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3691134/
http://www.life.illinois.edu/govindjee/photosynBook/Chapter11.pdf
https://www.heliospectra.com/sites/default/files/general/What%20light%20do%20plants%20need_5.pdf

I would also add the fact that blue light reaches earth surface greately scattered due to Rayleigh scattering, so the absolute amount of energy carried blue light is comparable (or even less) than that of other parts of the visible spectrum.

@AlexanderGalkin: True, but that should already be included in the red curve (together with atmospheric absorption): for blue you can see a stronger deviation from sunlight (yellow curve) than for red/IR (Unfortunately I don't have the dataset but it would be better visible for the photon density)

If leaves were black, they would get too hot.

@David only if the absorbed energy weren't used efficiently, which would, as you suggest, be a reason for leaves to be not black. You could also have green but inefficient and therefore hot leaves, but evolution would have gotten rid of these already

@TobiasKienzler green leaves stay cool via transpiration, not because they efficiently use solar radiation.

Also don't forget - evolution only produces something which is good enough - not optimal. If green turned out to be good enough, then there would be impetus to develop black leaves.

I'd note as well that there are other photosynthesizers that utilise the energies that plants do not - so-called purple bacteria - and these may predate green photosynthesizers. It's plausible that the "green gap" originally evolved as a means to exploit light not exploited by competing organisms.

I think it is as S.Albano says: In normal conditions, plants collect more photons than they can process by the photosynthetic chemistry. Excess energy creates singlet oxygen, which is highly toxic. Plants are getting rid of the excess energy with help of carotenoids in xanthophyll cycle. I think that chlorophyll is preferred because it also has largely structural role. (Special pair in the reaction center, photosynthetic antennae, etc.)

Worth noting that leaves are white in infrared. Only we can't see this with a naked eye.

@sanmai That's a rather confusing statement, what do you mean by "white in infrared"? Reflective?

@TobiasKienzler yes, they don't absorb infrared because there isn't enough energy in it to start photosynthesis, and moreover you don't want to overheat; hence reflection

This still does not explain why they are green and not say yellow or purple.

You say that "deep sea plants are indeed better off being red", however according to Wikipedia there are no deep sea plants.
"Natural light does not penetrate the deep ocean, with the exception of the upper parts of the mesopelagic. Since photosynthesis is not possible, plants cannot live in this zone. Although some light penetrates the mesopelagic zone, it is insufficient for photosynthesis". - Wikipedia

The high energy photon thing is a RESULT of them being green, not the cause. With a different pigment instead of chlorophyll they could absorb it just fine.

I believe it is because of a trade off between absorbing a wide range of photons and not absorbing too much heat.  Certainly this is a reason why leaves are not black - the enzymes in photosynthesis as it stands would be denatured by the excess heat that would be gained.
This may go some of the way towards explaining why green is reflected rather than red as you suggested - reflecting away a higher energy colour reduces the amount of thermal energy gained by the leaves.

I think the solar spectrum is also quite relevant.

It is more to do with the specific photon energy level (see Tobias) than the thermal heat  supplied per se. Heat is probably not a concern for temperate/arctic plants which are also green.

Heat is the least of a plant's problems. That is why we can breed black tulips without self-cooking petals. ;)

There is quite a fun article here which discusses the colours of hypothetical plants on planets around other stars.
Stars are classified by their spectral type which is dictated by their surface temperatures. The Sun's is relatively hot, and it's spectral energy distribution peaks in the green region of the spectrum. However the majority of stars in the Galaxy are K and M type stars which emit mainly in the red and infrared.
This is relevant to this discussion since any photosynthesis on these worlds would have to adapt to these wavelengths of light in order to proceed. On planets around cool stars plant life (or its equivalent) might well be black!
OK, this is not entirely pie in the sky astrobiologist rubbish. It is actually quite relevant to the search for biosignatures and life on other planets. In order to model the reflectance spectrum of planets we observe (i.e. the light reflected from the primary star) we need to try and take into account any potential vegetation.
For example, if we take a reflectance spectrum of the Earth, we see a characteristic peak in the red "the red edge" which is due to surface plant life.
NASA also has a short page on this here.

nice links, though I doubt black plants are likely to happen anywhere since that would most likely need too many different pigments

OK, maybe not completely black but very dark. There are various terrestrial plants which have very dark leaves (e.g. Oxalis triangularis). Admittedly, many are cultivars but this does demonstrate that there are some dark pigments available (I suppose anthocyanins?)

good point. Maybe in most cases absorbing green was just the first thing that happened (by evolution) and it was sufficient, but I'm just speculating...

I know this question was asked and answered a number of years ago (with many great answers), but I couldn't help but notice that no one had approached this from an evolutionary perspective (like the answer to this question)...
 Short Answer
Pigments appear as whatever color is not absorbed (i.e., they appear as whichever wavelength(s) of light they reflect).
Blue light was the most available wavelength of light for early plants growing underwater, which likely led to the initial development/evolution of chlorophyll-mediated photosytems still seen in modern plants. Blue light is the most available, most high-energy light that continues to reach plants, and therefore plants have no reason not to continue taking advantage of this abundant high energy light for photosynthesis.
Different pigments absorb different wavelengths of light, so plants would ideally incorporate pigments that can absorb the most available light. This is the case as both chlorophyll a and b absorb primarily blue light. Absorption of red light likely evolved once plants moved on land due to its increased abundance (as compared to under water) and its higher efficiency in photosynthesis.

 Long Answer
 Early Plants Develop Modern Photo-system
It turns out, just like the variability in transmittance of different wavelengths of light through the atmosphere, certain wavelengths of light are more capable of penetrating deeper depths of water. Blue light typically travels to deeper depths than all other visible wavelengths of light. Therefore, the earliest plants would have evolved to concentrate on absorbing this part of the EM spectrum.

However, you'll notice that green light penetrates relatively deeply as well.  The current understanding is that the earliest photosynthetic organisms were aquatic archaea, and (based on modern examples of these ancient organisms) these archaea used bacteriorhopsin to absorb most of the green light.

Early plants grew below these purple bacteriorhopsin-producing bacteria and had to use whatever light they could get. As a result, the chlorophyll system developed in plants to use the light available to them. In other words, based on the deeper penetrative ability of blue/green light and the loss of the availability of green light to pelagic bacteria above, plants evolved a photosystem to absorb primarily in the blue spectrum because that was the light most available to them.

Different pigments absorb different wavelengths of light, so plants would ideally incorporate pigments that can absorb the most available light. This is the case as both chlorophyll a and b absorb primarily blue light.

Here's two example graphs (from here and here) showing the absorption spectrum of typical plant pigments:

 So Why Are Plants Green?
As you can guess from the above paragraphs, since early under water plants received so little green light, they evolved with a chlorophyll-mediated photo-system that did not have the physical properties to absorb green light. As a result, plants reflect light at these wavelengths and appear green.
 But Why Are Plants Not Red?...
Reason to ask this question:
This would seem to be equally plausible given the above information. Since red light penetrates water incredibly poorly and is largely unavailable at lower depths, it would seem that early plants would not develop a means for absorbing it and therefore would also reflect red light.

In fact, [relatively] closely related red algae did evolve a red-reflecting pigment. These algae evolved a photo-system that also includes the pigment phycoerythrin to help absorb available blue light. This pigment did not evolve to absorb the low levels of available red light, and so therefore this pigment reflects it and makes these organisms appear red.

Interestingly, according to here, cyanobacteria that also contain this pigment can readily change it's influence on the organism's observed color:

The ratio of phycocyanin and phycoerythrin can be environmentally altered. Cyanobacteria which are raised in green light typically develop more phycoerythrin and become red. The same Cyanobacteria grown in red light become bluish-green. This reciprocal color change has been named 'chromatic adaptation’.

Further, (although it's still under debate) according to work by Moreira et al (2000) (and corroborated by numerous other researchers) plants and red algae likely have a shared photosynthetic phylogeny:

three groups of organisms originated from the primary photosynthetic endosymbiosis between a cyanobacterium and a eukaryotic host: green plants (green algae + land plants), red algae and glaucophytes (for example, Cyanophora).

So what gives?
Answer:
The simple answer of why plants aren't red is because chlorophyll absorbs red light.
This leads us to ask: Did chlorophyll in plants always absorb red light (preventing plants from appearing red) or did this characteristic appear later?

If the former was true, then plants don't appear red simply because of the physical characteristics that the chlorophyll pigments evolved to have.

As far as I know, we don't have a clear answer to that question.

(others please comment if you know of any resources discussing this).

However, regardless of when red light absorption evolved, plants nevertheless evolved to absorb red light very efficiently.

A number of sources (e.g., Mae et al. 2000, Brins et al. 2000, and here) as well as numerous other answers to this question,  suggest that the most efficient photosynthesis occurs under red light. In other words, red light results in the highest "photosynthetic efficiency."

This NIH page suggests the reason behind this:

Chlorophyll a also absorbs light at discrete wavelengths shorter than 680 nm (see Figure 16-37b). Such absorption raises the molecule into one of several higher excited states, which decay within 10−12 seconds (1 picosecond, ps) to the first excited state P*, with loss of the extra energy as heat. Photochemical charge separation occurs only from the first excited state of the reaction-center chlorophyll a, P*. This means that the quantum yield — the amount of photosynthesis per absorbed photon — is the same for all wavelengths of visible light shorter than 680 nm.

Note, however, that other sources suggest blue light is better than red. For example, see Muneer et al, (2014).

Biomass and photosynthetic parameters increased with an increasing light intensity under blue LED illumination and decreased when illuminated with red and green LEDs with decreased light intensity

 Why Did Plants Remain Green?
So why have plants not evolved to use green light after moving/evolving on land? As discussed here, plants are terribly inefficient and can't use all of the light available to them. As a result, there is likely no competitive advantage to evolve a drastically different photosystem (i.e., involving green-absorbing pigments).
So earth's plants continue to absorb blue and red light and reflect the green. Because green light so abundantly reaches the Earth, green light remains the most strongly reflected pigment on plants, and plants continue to appear green.

(However, note that other organisms such as birds and insects likely see plants very differently because their eyes can distinguish colors differently and they see more of the strongly reflected UV light that ours cannot).

Citations
 Moreira, D., Le Guyader, H. and Philippe, H., 2000. The origin of red algae and the evolution of chloroplasts. Nature, 405(6782), pp.69-72.
 Muneer, S., Kim, E.J., Park, J.S. and Lee, J.H., 2014. Influence of green, red and blue light emitting diodes on multiprotein complex proteins and photosynthetic activity under different light intensities in lettuce leaves (Lactuca sativa L.). International journal of molecular sciences, 15(3), pp.4657-4670.

This answer needs more love, it is the only one that actually explains why plants are green and not say yellow or pink.

There are two factors at play here. First is the balance between how much energy a plant can collect and how much it can use. It is not a problem of too much heat, but too many electrons. If it were a question of heat, a number of flowers selected for their black pigmentation would have their petals cooked off. ;)
If a plant does not have enough water, is too cold, is too hot, collects too much light, or has some other condition that prevents the electron transport chain from functioning properly, the electrons pile up in a process called photoinhibition.
These electrons are then transferred to molecules that they should not be transferred to, creating free radicals, wreaking havok within the plant's cells. Fortunately, plants produce other compounds that prevent some of the damage by absorbing and passing around the electrons like hot potatos. These antioxidants are also beneficial to us when we eat them.
This explains why plants collect the amount of light energy they do, but does not explain why they are green, and not grey or dark red. Surely there are other pigments that would be able to generate electrons for the electron transport chain.
The answer to that is the same as why ATP is used as the main energy transport molecule in organisms rather than GTP or something else.
Chlorophyll a and b were just the first things that came about that fulfilled the requirement. Certainly some other pigment could have collected the energy, but that region of parameter space never needed to be explored.

I think you are right, that the bottleneck is not in collecting the photons, but in processing them without creating too much singlet oxygen. One of important factors might be that chlorophyll plays also a big structural role: It is not only a collector of light, but also allows separation of charge in the special pair of the reaction center and constitutes many pigment-protein complexes structurally.

The biologist John Berman has offered the opinion that evolution is not an engineering process, and so it is often subject to various limitations that an engineer or other designer is not. Even if black leaves were better, evolution's limitations can prevent species from climbing to the absolute highest peak on the fitness landscape. Berman wrote that achieving pigments that work better than chlorophyll could be very difficult. In fact, all higher plants (embryophytes) are thought to have evolved from a common ancestor that is a sort of green alga – with the idea being that chlorophyll has evolved only once. (reference)
Plants and other photosynthetic organisms are largely filled with pigment-protein complexes that they produce to absorb sunlight. The part of the photosynthesis yield that they invest in this, therefore, has to be in proportion. The pigment in the lowest layer has to receive enough light to recoup its energy costs, which cannot happen if a black upper layer absorbs all the light. A black system can therefore only be optimal if it does not cost anything (reference).
Red and yellow light is longer wavelength, lower energy light, while the blue light is higher energy. It seems strange that plants would harvest the lower energy red light instead of the higher energy green light, unless you consider that, like all life, plants first evolved in the ocean. Seawater quickly absorbs the high-energy blue and green light, so that only the lower energy, longer wavelength red light can penetrate into the ocean. Since early plants and still most plant-life today, lived in the ocean, optimizing their pigments to absorb the reds and yellows that were present in ocean water was most effective. While the ability to capture the highest energy blue light was retained, the inability to harvest green light appears to be a consequence of the need to be able to absorb the lower energy of red light (reference).
Some more speculations on the subject: (reference)

Water absorbs red light far more than blue light! That's why everything looks blueish below a certain depth. This explains why phytoplankton always hovers on the top layers of the ocean. And it's perhaps an explanation why chlorophyll has a second absorption peak in the blue region.

There are several parts to my answer.
First, evolution has selected the current system(s) over countless generations through natural selection.  Natural selection depends on differences (major or minor) in the efficiency of various solutions (fitness) in the light (ho ho!) of the current environment.  Here's where the solar energy spectrum is important as well as local environmental variables such as light absorption by water etc. as pointed out by another responder. After all that, what you have is what you have and that turns out to be (in the case of typical green plants), chlorophylls A and B and the "light" and "dark" reactions.
Second, how does this lead to green plants that appear green?  Absorption of light is something that occurs at the atomic and molecular level and usually involves the energy state of particular electrons.  The electrons in certain molecules are capable of moving from one energy level to another without leaving the atom or molecule.  When energy of a certain level strikes the molecule, that energy is absorbed and one or more electrons move to a higher energy level in the molecule (conservation of energy).  Those electrons with higher energy usually return to the "ground state" by emitting or transferring that energy.  One way the energy can be emitted is as light in a process called fluorescence.  The second law of thermodynamics (which makes it impossible to have perpetual motion machines) leads to the emission of light of lower energy and longer wavelength.  (n.b. wavelength (lambda) is inversely proportional to energy; long wavelength red light has less energy per photon than does short wavelength violet (ROYGBIV as seen in your ordinary rainbow)).
Anyway, chlorophylls A and B are complex organic molecules (C, H, O, N with a splash of Mg++) with a ring structure.  You will find that a lot of organic molecules that absorb light (and fluoresce as well) have a ring structure in which electrons "resonate" by moving around the ring with ease.  It is the resonance of the electrons that determine the absorption spectrum of a given molecule (among other things).  Consult Wikipedia article on chlorophyll for the absorption spectrum of the two chlorophylls.  You will note that they absorb best at short wavelengths (blue, indigo, violet) as well as at the long wavelengths (red, orange, yellow) but not in the green.  Since they don't absorb the green wavelengths, this is what is left over and this is what your eye perceives as the color of the leaf.
Finally, what happens to the energy from the solar spectrum that has been temporarily absorbed by the electrons of chlorophyll?  Since its not part of the original question, I'll keep this short (apologies to plant physiologists out there).  In the "light dependent reaction", the energetic electrons get transferred through a number of intermediate molecules to eventually "split" water into Oxygen and Hydrogen and generate energy-rich molecules of ATP and NADPH. The ATP and NADPH then are used to power the "light independent reaction" which takes CO2 and combines it with other molecules to create glucose.  Note that this is how you get glucose (at least eventually in some form, vegan or not) to eat and oxygen to breath.
Take a look at what happens when you artificially uncouple the chlorophylls from the transfer system that leads to glucose synthesis.  http://en.wikipedia.org/wiki/Chlorophyll_fluorescence  Notice the color of the fluorescence under UV light!
Alternatives?  Look at photosynthetic bacteria.

Small addition to the conversation: plants reflect green yes, but chlorophyll (a and b) does not (it is mostly transparent to it).
The organic material (walls of cells, etc.) around the chlorophyll behave as reflectors and scatterers of the non-absorbed green light, and that's what we see.
https://www.tandfonline.com/doi/full/10.1080/00219266.2020.1858930
In general there are 3 types of interactions of a photon with matter:

reflection (and scattering elastic or not)
absorption (inelastic process)
transmission (no energetically-lossy-interaction)

(My reply targets better the OP formulation of this duplicate question)

Tobias Keinzler does a good job of explaining why black plants would not work, this is an explanation of why plants are green and not some other color.
Color of foliage is based on whatever the color is of bacteria (or archaea) that get incorporated to become chloroplasts. Or more specifically the color of their light absorbing pigments. there is a huge range in nature for color in photosynthetic organisms, plants are green becasue chlorophyll is green, it could have just as easily been red or purple. http://www.ucmp.berkeley.edu/glossary/gloss3/pigments.html
There is decent evidence that chloroplast ancestors absorb the  margins of the visible spectrum becasue halobacterium absorb the major constituents, becasue the chlorophyll users did not compete with them directly instead absorbing the leftover light.  It was only later when they got incorporated into larger cells that they came to dominate and eventually giving rise to plants.
Plants are not green becasue green is better, plants are green becasue that is the first efficient photosynthetic pigment to evolve that did not compete with the dominate photosynthesizer.


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What does the human body use oxygen for besides the final electron acceptor in the electron transport chain?
My biology teachers never explained why animals need to breathe oxygen, just that we organisms die if we don't get oxygen for too long. Maybe one of them happened to mention that its used to make ATP. Now in my AP Biology class we finally learned the specifics of how oxygen is used in the electron transport chain due to its high electronegativity. But I assume this probably isn't the only reason we need oxygen.
What other purposes does the oxygen we take in through respiration serve? Does oxygen deprivation result in death just due to the halting of ATP production, or is there some other reason as well? What percentage of the oxygen we take in through respiration is expelled later through the breath as carbon dioxide?

Doesn't the body use sunlight and oxygen to create Peroxide in the skin for immune reasons? I heard this once from somewhere

Oxygen is actually highly toxic to cells and organisms – reactive oxygen species cause oxidative stress, essentially cell damage and contributing to cell ageing. A lot of anaerobic organisms have never learned to cope with this and die almost immediately when exposed to oxygen. One classical example of this is C. botulinum.
Oxygen is incorporated in several molecules in the cell (for instance riboses and certain amino acids) but as far as I know, all of this comes into the cell as metabolic products, not in the form of pure oxygen.
The oxygen ($\ce{O2}$) we breathe is completely used up during aerobic respiration. The stoichiometry of this is given by the following simplified equation:
$$\ce{C_6H12O6 + 6 O2 -> 6 CO2 + 6 H2O + heat}$$
WYSIWYG’s answer goes into more detail.

Oxygen is not converted to carbon dioxide!  It's converted to water.

Superoxide, O2− is created by the immune system in phagocytes (including neutrophils, monocytes, macrophages, dendritic cells, and mast cells) which use NADPH oxidase to produce it from O2 for use against invading microorganisms. However, under normal conditions, the mitochondrial electron transport chain is a major source of O2−, converting up to perhaps 5% of O2 to superoxide. [1]
As a side note, there are two sides to this coin.  While this is a useful tool against microorganisms, the formation of the reactive oxygen species has been incriminated in autoimmune reactions and diabetes (type 1). [2]

[1] Packer L, Ed. Methods in Enzymology, Volume 349. San Diego, Calif: Academic Press; 2002
[2] Thayer TC, Delano M, et al. (2011) Superoxide production by macrophages and T cells is critical for the induction of autoreactivity and type 1 diabetes,60(8), 2144-51.

You probably know by now that cytochrome c oxidase, the last complex of the electron transport chain, belongs to a class of enzymes called oxidoreductases, that use oxygen atoms as electron acceptors. One type of oxidoreductases are oxidases, enzymes that (at least in theory [1]) use molecular oxygen--O2, like in air--as their electron acceptor. From what I know, however, sometimes that isn't the case: xanthine oxidase, that converts xanthine to uric acid, gets its oxygen atoms from water [2]. Examples of the "true" oxidases include L-amino-acid oxidase and cytochrome P450 (aka. CYP family).
Despite cytochrome P450 being a numerous and important enzyme family, responsible for most of known drugs metabolism and some essential lipids transformations, it probably consumes only a fraction of oxygen that animals breathe in. I wasn't able to find any estimations, but would be surprised if it was more than perhaps 0,1%.

[1] Introduction to EC1 class
[2] Metz, S. & Thiel, W. A Combined QM/MM Study on the Reductive Half-Reaction of
Xanthine Oxidase: Substrate Orientation and Mechanism. J. Am. Chem. Soc. 2009, 131, 14885–14902, PMID: 20050623.

The overwhelming use of oxygen is to provide us (in combination with food) with energy.  We have a great need for energy in our cells, which is why we have these lungs, diaphragms, red blood cells, etc.; they assure we get the oxygen to obtain the energy (via the electron transport chain).
The overall metabolism of glucose (C6H12O6) is a representative reaction:
 C6H12O6 + 6 O2 --> 6 CO2 + 6 H2O + energy
You can see that just as much oxygen goes out as gaseous CO2 as came in as gaseous oxygen (O2).
The energy is temporarily kept in the form of the phosphate bond in ATP molecules so that it can be shuttled around the cell to the multitude of cellular processes that need energy.
Energy is so essential to the cellular processes that maintain animal cells that lack of that energy, which results quickly when there is oxygen deprivation, soon causes irreversible damage and death.

Why is not fermentation a possible solution? We need numbers (about the amount of energy) and references.

This representative reaction is not really correct and you know that. The OP has already indicated that they know about the role of oxygen as the terminal electron acceptor.

Another small addition

There is class of oxidoreductases called oxygenases which incorporate molecular oxygen into the substrates and not just use it as an electron acceptor like in oxidases (note that the terminal enzyme in ETC is an oxidase and there are other such oxidases). In other words, oxygen is not a cofactor but a co-substrate. Oxygenases are further classified into dioxygenases and monooxygenases which incorporate two oxygen atoms and one oxygen atom respectively. Examples:

Cytochrome P450 family (monooxygenease): involved in detoxification of xenobiotics
Cyclooxygenase (dioxygenase): involved in production of prostaglandins which are involved in pain and inflammation. Many NSAID painkillers like aspirin, paracetamol and ibuprofen target cyclooxygenase-2 (COX2)
Lipoxygenase (dioxygenase): Involved in production of leukotrienes which are involved in inflammation.
Monoamine oxidase (monooxygenase): Involved in catabolism of neurotransmitters such as epinephrine, norepinephrine and dopamine.

Does oxygen deprivation result in death just due to the halting of ATP
  production, or is there some other reason as well?

Death predominantly occurs because of halt in ATP production. Some cells such as neurons (and also perhaps cardiac muscles) are highly sensitive to loss of oxygen (for energy requirements) and clinical death because of hypoxia usually occurs because of loss basic brain function.

What percentage of the oxygen we take in through respiration is
  expelled later through the breath as carbon dioxide?

As already mentioned, it is said that there is a rough 1:1 ratio of CO2 production and O2 consumption. However, as indicated in a comment by CurtF, O2 does not form CO2; it forms water in the last reaction of ETC. CO2 is produced in other reactions of Krebs cycle.
Glycolysis produces 32 molecules of ATP for 1 molecule of glucose via ETC (see here). There are three complexes in ETC and the third is dependent on oxygen; so you can assume that 1/2 a molecule of O2 consumed for production of 3 ATP molecules. Therefore 32 molecules of ATP would consume 4 molecules of O2. Seems like there is a 1:1 ratio of CO2 production and O2 consumption.
We can see it like this:
FADH2 enters ETC at the second complex whereas NADH enters at the first. We can say that as long as NADH is present FADH2 would not require an extra oxygen.
An NADH or a FADH2 molecule would require 1/2 molecule of O2. There are 8 molecules of NADH and 2 molecules of FADH2 produced during glycolysis+krebs cycle which would require 10/2 = 5 molecules of O2. Glycolysis produces 4 molecules of CO2 during krebs cycle.
However, 2 cytosolic NADH molecules require 2 ATPs (in other words another NADH molecule) to be transported to mitochondria. So the net effect may be actually close to 1:1 O2:CO2.
Another factor to keep in consideration is that the three complexes do not actually produce ATP; they just pump proton to create a chemical potential. The F0F1-ATP synthase would probably work only after a threshold of H+ potential is established. The 1 ATP molecule per complex is most likely the mean value and not exactly what really happens per reaction.

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Height and natural selection in humans?
I watched the documentary "Evolve" recently and in the segment on "size" Scott V. Edwards, Harvard evolutionary biologist mentioned the idea that humans might evolve to be 7' tall in 'hundreds of years'. (I think this may have been taken out of context... I have emailed him to find out, but do not expect a response from someone so busy)
The reasoning goes that the trend in the past 100 years has been greater height, and women show a strong preference for men who are taller than they are. (Though a large share perhaps all of this difference has been due to diets higher in protein at an early age)
I wonder, though, if this is only part of the story. The preference women have is not just for tall men, but for a man who is taller than she is. Likewise, men seem to prefer woman who are shorter than they are. There is even cultural pressure: the classic western image of a couple on wedding cake always shows a man who is about 4" (to scale) taller than the bride.
Thus, women who are short have an advantage as they have a greater pool of men to choose from. (Colloquially, simply ask any 6' tall woman if she feels her height helps her find dates.)
Let's say that men seek women who are shorter than they are, but no more than 8" shorter. Women seek men who are taller than they are but no more than 8" taller. Given that the current average height for men is 5'8" and for women it is 5'4" (and distributed normally SD 2.8") will we have selective pressure that leads to greater or lesser height? (This is, obviously, oversimplified, but it is a starting point.)

It is oversimplification to say that height is the only parameter that defines female preference. There are plenty of other characteristics in males that female will take into account.

I'm somewhat skeptical of the assumption that attractiveness is correlated with number of offspring (to the extent that any substantive selection will take place).

@kate has what is probably the more correct answer for the observed pattern.
But as an experiment, I set up a basic simulation to approximate the conditions that you lay out:

Starting mean heights of 5'8" (172.72 cm) and 5'4" (162.56 cm) with standard deviations of 2.8" (7.112 cm). I used cm, because it's easier than dealing with inches.
Males will not mate with females that are taller than themselves.
Females will not mate with males more than 8" taller.
Males will not mate with females more then 8" shorter (follows from #3 above).

The problem that I quickly ran into was that, by truncating part of the normal distribution, the variance in height at each generation gradually decreased. After about 20 generations, the means weren't evolving because there was so little variation in height.
Human height is one of the most studied quantitative traits, going back over 100 years to some of the very first statisticians (Fisher, Galton). Height is a polygenic trait with very high heritability (h2 = 0.8)1. Genome-wide association studies have reported 54 genes involved in determination of human height2.
Imagine that each of these 54 genes has just two alleles: a and b. a gives a +1 to height. b gives a -1 to height. So aa would be +2, ab or ba 0, and bb -2. The sum of all those alleles is correlated to height. So if all 54 were aa, then the height would be +108.
The problem comes in when people only mate with taller people. Over time, the proportion of b's will decrease, and the proportion of a's will increase, but only to a point. Once all the alleles are fixed at a, there won't be any room left. The genetic variation will be exhausted. Without the input of new alleles, height will cease to evolve.
1 Lettre, G. 2011. Recent progress in the study of the genetics of height. Hum Genet 129:465–472.
2 Visscher, PM. 2008. Sizing up human height variation. Nat Genet 40(5):489-90.

Directional selection nearly always reduces level of variation, but in case of 54 genes and population over 7*10^9 - mutations are not negligible.

Excellent answer (you did a simulation!). Marta is right: mutation generates variation, but also human mate selection is not driven by height.

(This should have been a comment, but I don't have enough reputation yet. Sorry!)
You asked an interesting question, but I'm not sure about your reasoning.
Firstly, the "trend" you describe, that in the past century humans grew taller that ever before, is a phenomenon known to most European countries, one of the so called "secular trends": a uni-directional change in height (or growth rate) over a period of time. It was established that adult hight increased by 1 to 3 centimeters for each decade until 1980 (except for the times of World War 2, which had an opposite effect in some places). Such changes, however, happened much too quickly to be of genetic origin; and are much better explained by an increase in quality of life. In line with this explanation is the increase in height and growth tempo we see now in Third World countries, clearly the effect of improving life conditions.
Secondly, in my opinion, womens' preference for higher men can be another manifestation of their wanting simply the best male. I don't see any particular advantage for a woman to want a man higher that she is, but, as you pointed out, anecdotal evidence suggests otherwise.

Based on:

Cole, T.J. Secular trends in growth. Proc Nutr Soc 59, 317–324 (2000), PMID: 10946801.

See more on secular trends in:

Cole, T.J. The secular trend in human physical growth: a biological view. Economics & Human Biology 1, 161–168 (2003), PMID: 15463971.
Sargent, M. Biomedicine and the human condition: challenges, risks, and rewards. (2005).

To answer the question with a complicating question, suppose the anecdotal preference for "tall" men and "short" women is really just an urge toward the norm? Suppose that women seek taller men in proportion to their self-perception as "shorter than average"--the closer a woman is to average (female) height, the less likely she is to seek a mate who is markedly taller?
In my unscientific experience, height matters less to people whose height is more or less normal.
Then, with some assumptions about the heights of offspring of couples whose heights are different, the tendency might be toward a stable average. As noted in other answers, nutrition is probably a big factor in recent gains in Europe, Asia, and Africa.
This would be hard to model mathematically and I am not convinced the result would shed much light on the question, especially (as noted above) in light of the polygenetic nature of the trait.

The tendency for mean height to be pushed upward is natural when you consider two facts
(that so far have been left out here):

With the higher costs to females in general for reproducing, they are the "choosier" gender, so when it comes to mate selection, females' preferences matter more.  Therefore, a tendency for males to prefer shorter females (if that is even true) would not have an equal and opposite effect.
There is not a 1:1 ratio between males and females who pass on their genes.  The standard deviation on number of children is higher for males, and a higher proportion of males than females produce 0 offspring, thus "truncating part of the normal distribution", every generation, more for males than for females.  Again, even if there were just as much preference for short females by males as there is preference for tall males by females, there would still be a trend upward in mean height.  This fact has more to do with the speed of the change rather than whether or not the change will happen, though.

Two facts that have been discussed already but not widely acknowledged here should be explicitly mentioned again:

Male and female height each influence height in both male and female offspring.  This matters because even if there were preference not for the male to be too much taller than the female, this would not stop the trend upward in height because females would be constantly be trending upward in height.  Thus, females would not serve as any kind of "anchor" for height.
Height changes are due to more than just genes (whose effects could "top out" in the absence of mutation, as kmm mentioned), but in any case mutation is not negligible for human height (as Marta Cz-C mentioned), so a lack of possible genotypes for the extreme height we are talking about is not an issue.  Actually, this is obvious from the fact that there already are (fertile) people taller than the threshold mentioned in this question.
(The only real reasons for an upper limit on human height, which have not be brought up here, are nicely presented in this video: How big can a person get?, and those lead to a maximum height somewhere above the 213 cm (7 feet) we are talking about.)

Some things that have been mentioned here, though true or possibly true, are not really relevant to the question:

A limit on how much taller the father is than the mother for the typical child (imposed by female or male preference) does not change the answer to the main question (direction of mean height change, if any), only the speed ("in 'hundreds of years'").  (This follows from the "anchor" comment above.)
The fact that there are many other factors than height for mate selection, and even that many of these factors are more important than height, also does not change the answer to the main question.  (That is unless the other factors which correlate with lower height put downward pressure on it.  I don't think anyone would argue this, but I will provide an example because I think it is interesting:  If shorter males were, on average, more intelligent than taller males, then even if females preferred taller males (intelligence being equal), if they also preferred more intelligent males then human height could go down (while mean human intelligence goes up).)

Of course, generalizing all of this to humans in the present and in the future (switching language from "males" and "females" to "men" and "women") is predicated on some assumptions:

that women, particularly the ones who have children, do prefer and get taller men.  This could fail to be the case in the face of competition from women who also prefer taller men but do not have children.  This could also change due to reversal of the preference for height or due to increased preference for other factors that correlate with lower height combined with a reduction in the lustre of male height for females.  As one example, the ever-decreasing importance of physical competition between males and the ever-increasing level of safety from unarmed attack in the modern world means that height (and other measures of strength) matters less and less.  As another example, the reduction in face-to-face workplace settings, which are no doubt at least partially responsible for taller men being paid more than shorter men, should lead to wealth (which is a factor on its own) being less of a correlate with height and therefore reduce selection for height.
that the preferences of women will continue to matter more than the preferences of men, for mate selection.  If women and men were completely rational actors, this one could already have changed due to recent decreases in reproduction costs for females (mostly due to medical changes, such as lower death rate associated with pregnancy) and increases in reproduction costs for males (mostly due to legal changes, possibly to the point where the costs for males are higher than for females).  The way women and men think and feel with regard to mate selection is very strongly biased toward the normal conditions in our evolutionary history, though (higher female investment), and are hard to act against.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Which human cell lines do not express the GLP-1 receptor?
I need a human cell line that does not express the GLP-1 (glucagon like peptide-1) receptor.
I'm working with HeLa cells, do those express the GLP-1 receptor? Which other cell lines exist that don't express this specific receptor?
Are there any general resources where I could find this kind of information?

AbCam suggests HeLa cells as positive controls for their antibody to GLP1R. They provide the following pictures of HeLa cells labeled with their antibody:

(The image of the right is treated with synthesized peptide.)
According to Wikipedia, GLP1R is also expressed in pancreatic beta cells and the brain.


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What is the functional and structural distinction between core (H2A, H2B, H3,H4) and linker(H1/H5) histones?
Many explanations of histone biochemistry isn't quite elucidating for the undergraduate student. How does histone structure (dimers, octomers) relate to their specific functions as core or linker histones? Also, how do both linker and core histones interact within nucleosomes to ultimately regulate gene expression?

The core histones are H2A, H2B, H3, and H4, and the linker histones are H1 and H5. The structure of the nucleosome is well explained in wikipedia:

Two of each of the core histones assemble to form one octameric nucleosome core particle, and 147 base pairs of DNA wrap around this core particle 1.65 times in a left-handed super-helical turn. The linker histone H1 binds the nucleosome and the entry and exit sites of the DNA, thus locking the DNA into place and allowing the formation of higher order structure. The most basic such formation is the 10 nm fiber or beads on a string conformation. This involves the wrapping of DNA around nucleosomes with approximately 50 base pairs of DNA separating each pair of nucleosomes (also referred to as linker DNA). The assembled histones and DNA is called chromatin. Higher-order structures include the 30 nm fiber (forming an irregular zigzag) and 100 nm fiber, these being the structures found in normal cells. During mitosis and meiosis, the condensed chromosomes are assembled through interactions between nucleosomes and other regulatory proteins.

The core histones have a positive net charge, which facilitates the interaction with the negatively charged phosphate groups of DNA.
Apart from defining the nucleosome structure, the function of the core histones is regulatory: it can switch on/off gene expression by histone modifications like acetylation or methylation.
The gene expression is ON when there is:
• DNA demethylation
• histones acetylation
• H3K4 methylation
• H3K36 methylation
• H3K9 demethylation
• H3K27 demethylation
The gene expression is OFF when there is:
• DNA methylation
• histones deacetylation
• H3K4 demethylation
• H3K36 demethylation
• H3K9 methylation
• H3K27 methylation
// H3K4 demethylation is abbreviation for: Lysine 4 of H3 is demethylated.
Berger SL. 2002. Histone modifications in transcriptional regulation. Current Opinion in Genetics & Development 12: 142–148 is also a nice review.


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Why does regular exercise increase brain volume?
It has been shown in several studies that regular aerobic exercise increases brain volume in aging humans. The changes were observed in hippocampus and were correlated with dramatic reduction of age-related dementia. Interestingly, the intensity of training had little influence on the results: walking, climbing stairs, gardening were just as effective at reducing dementia as more strenuous exercise.
What is the biological mechanism behind this phenomena?

Fig. The aerobic exercise group showed an increase in the anterior hippocampus and no change in the posterior hippocampus.[1]

Erickson et al. Exercise training increases size of hippocampus and improves memory. PNAS. 2011.
Colcombe et al. Aerobic exercise training increases brain volume in aging humans. J Gerontology. 2006
Ravaglia, et al. Physical activity and dementia risk in the elderly. Neurology. 2008

Well, Erickson et al (2011) attribute the increase in brain volume in the aerobic exercise group to brain-derived neurotrophic factor (BDNF).
Specifically (p. 3020):

In fact, we found here that changes in serum BDNF levels were
  associated with changes in anterior hippocampal volume; an important
  link because the hippocampus is rich in BDNF, and BDNF levels increase
  with exercise treatments in both rodents and humans. BDNF is a
  putative mediator of neurogenesis and contributes to dendritic
  expansion and is also critical in memory formation. Our results suggest that
  cell proliferation or increased dendritic branching might explain increased
  hippocampal volume and improvements in memory after exercise

with the caveat:

however, increased vascularization (15, 16, 33) and dendritic
  complexity (34) may also be contributing to increased volume


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How does the Golgi Apparatus perform its function?
The Golgi Apparatus is an organelle with a great number of functions, I am particularly intrigued in the role it plays in packaging macromolecules and sending them to their target organelle or to leave the cell in exocytosis.  I would love to know more about how this process works.  How does the Golgi Apparatus recognise which molecules are which and how does the vesicle it places the molecule into navigate to where it is needed?

This is actually is an awesome story: both how it happens and how it was discovered. This is one of those stories people get Nobel Prize, and this was Günter Blobel who was awarded this highest possible prize for his discovery, which is according to his Nobel prize certificate:

"for the discovery that proteins have intrinsic signals that govern
  their transport and localization in the cell"

If you watch or read his Nobel prize lecture you will find answers to your question formulated much better than I can do it here. His Nobel lecture was opened with the following words which might already answer you question:

Imagine a large factory that manufactures thousands of different items
  in millions of copies every hour, that promptly packages and ships
  each of them to waiting customers. Naturally, to avoid chaos, each
  product requires a clearly labeled address tag. Günter Blobel is being
  awarded this year's Nobel Prize in Physiology or Medicine for having
  shown that newly synthesized proteins, analogous to the products
  manufactured in the factory, contain built-in signals, or address
  tags, that direct them to their proper cellular destination.

Still, I recommend you to read (or watch) to the end, there are some interesting points on how it was discovered and what experiments were done to do it.

07:55-10:06 is the relevant section of the video for anyone wishing to jump to it.  I read the lecture you linked to which was very interesting, however is there anywhere which goes into more detail? =)

The most complete reference for cell biology is The Cell by G. Cooper, here is the article about Golgi apparatus available online. Does this answer your question or you want even deeper overview?


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Why is DNA replication  performed in the 5' to 3' direction?
DNA replication goes in the 5' to 3' direction because DNA polymerase acts on the 3'-OH of the existing strand for adding free nucleotides. Is there any biochemical reason why all organisms evolved to go from 5' to 3'?
Are there any energetic/resource advantages to using 5' to 3'? Is using the 3'-OH of the existing strand to attach the phosphate of the free nucleotide more energetically favorable than using the 3'-OH of the free nucleotide to attach the phosphate of the existing strand? Does it take more resources to create a 3' to 5' polymerase?

Prof. Allen Gathman has a great 10-minutes video on Youtube, explaining the reaction of adding nucleotide in the 5' to 3' direction, and why it doesn't work the other way.
Briefly, the energy for the formation of the phosphodiester bond comes from the dNTP, which has to be added. dNTP is a nucleotide which has two additional phosphates attached to its 5' end. In order to join the 3'OH group with the phosphate of the next nucleotide, one oxygen has to be removed from this phosphate group. This oxygen is also attached to two extra phosphates, which are also attached to a Mg++. Mg++ pulls up the electrons of the oxygen, which weakens this bond and the so called nucleophilic attack of the oxygen from the 3'OH succeeds, thus forming the phospodiester bond.
If you try to join the dNTP's 3'OH group to the 5' phosphate of the next nucleotide, there won't be enough energy to weaken the bond between the oxygen connected to the 5' phosphorous (the other two phosphates of the dNTP are on the 5' end, not on the 3' end), which makes the nucleophilic attack harder.
Watch the video, it is better explained there.

While the video explains the basics nicely, it ignores the possibility of adding a triphosphate to the primer (through another enzyme or a secondary polymerase functionality). The spontaneous hydrolysis of the triphosphate puts the 3'-5' variant at a disadvantage, but the idea is not as impossible as Prof. Gathman claims in the video.

DNA replications needs a source of energy to proceed, this energy is gained by cleaving the 5'-triphosphate of the nucleotide that is added to the existing DNA chain. Any alternative polymerase mechanism needs to account for the source of the energy required for adding a nucleotide.
The simplest way one can imagine to perform reverse 3'-5' polymerization would be to use nucleotide-3'-triphosphate instead of the nucleotide-5'-triphosphate every existing polymerase uses. This would allow for a practically identical mechanism as existing polymerases, just with different nucleotides as substrates. The problem with this model is that ribonucleotide-3'-triphosphates are less stable under acidic conditions due to the neighbouring 2'-OH (though this obviously only applies for RNA, not for DNA).
So any 3'-5' polymerase would likely need to use the same nucleotide-5'-triphosphates as the 5'-3' polymerase. This would mean that the triphosphate providing the energy for addition of a new nucleotide would be on the DNA strand that is extended, and not on the newly added nucleotide.
One disadvantage of this approach is that nucleotide triphosphates spontaneously hydrolyze under aqeuous conditions. This is no significant problem for the 5'-3' polymerase, as the triphosphate is on the new nucleotide and the polymerase just has to find a new nucleotide. For the 3'-5' polymerase spontaneous hydrolysis is a problem because the triphosphate is on the growing chain. If that one gets hydrolyzed, the whole polymerization needs to be either aborted or the triphosphate need to be readded by some mechanism.
You can take a look at the article "A Model for the Evolution of Nucleotide Polymerase Directionality" by Joshua Ballanco and, Marc L. Mansfield for more information about this. They created a model on early polymerase evolution, though they don't reach any final conclusion.

In my opinion, Prof. Allen Gathman's "great 10-minutes video on Youtube" is a pretty waste of time if you already know how hydrolysis happens. In fact, he has not considered the 3'->5' route in an unbiased manner; he doesn't seem to look at the possibility of a triphosphate appearing at the growing 5' tip of the strand in the 3'->5' case.
Actually, the only difference between the two routes (5'->3' and 3'->5') is that the reacting triphosphate appears in different places. In the usual case, the triphosphate which is hydrolysed belongs to the added nucleotide, while in the latter case, the triphosphate which is hydrolysed belongs to the nucleotide on the growing strand. Both are feasible.
In fact, it is known that RNA polymerase has dual activity, but you see, RNA polymerase doesn't have proofreading activity!.  Proofreading requires removal of the mismatched base, but in the 3'->5 direction the base's attachment had consumed the triphosphate at the 5' tip of the strand, so it is no longer available to add the replacement base. 3'->5' activity readily destroys  proofreading capability of a polymerase  So, basically, it is the need for proofreading that restricts the synthesis of DNA strands to 5'->3'. Why it is so, would need a lot more explanation (if in words) but I think a picture has far better explanatory power than a thousand words. I've added a picture from Essential Cell Biology that shows the answer to the 'WHY' question:
The other important consideration is repair. If one or more nucleotide is missing in one strand, repair of the missing nucleotide would be impossible for 3' to 5' synthesis, because no 5'-triphosphate is present. On the other hand, 5' to 3' synthesis does not require a 3'-triphosphate present at the repair site. This is important. That is 3' to 5' synthesis does not allow nucleotide repair.

This should be the accepted answer.

Actually there is a polymerase that catalyzes 3' - 5' elongation.  See for example the Thg1 superfamily.  "Doing it in reverse: 3'-to-5' polymerization by the Thg1 superfamily." Jackman, et al.

No reference, no use.


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Why is the  microbial ecosystem of the gut so susceptible to disruption by pathogens?
From all accounts, it seems as if the Escherichia, Enterobacter, etc. that live and thrive in the human gut are pretty well entrenched.  I know that these microbial populations are often analyzed as an ecosystem.
What surprises me is that it seems like minor food poisoning can throw the whole ecosystem off.  I know superficially that Clostridium are contenders in the fight because they remain viable after traveling through the acid of the stomach, but why are these populations so sensitive to other invading bacteria?

Hi! Could you please give some references to the fact that minor food poisoning can throw the whole ecosystem off? This is very interesting to me, as a personal health matter.

@dignor.sign I was more making an observation, but see http://en.wikipedia.org/wiki/Gut_flora#Alterations_in_flora_balance, A reduction in levels of native bacterial species also disrupts their ability to inhibit the growth of harmful species. They cite 3 references, including a Lancet article, but say that this may in fact not be the cause of symptoms such as diarrhea (apologies for the graphic description).

I was just curious about how weak this ecosystem can be; these papers will do it. Thanks!

Keep in mind one of the most common harmful species is a native species in many people: Clostridium difficile.

@EpiGrad Excellent point.  If your up for it, elaborate it a bit as an answer.  I don't know much about how it achieves balance with E. coli.

I would actually disagree with the whole idea that the bacterial community in the gut are very susceptible to disruptions. Imagine how many different potential pathogens we ingest every day, and how often do we actually show symptoms?

@Zewz Overall, I would certainly agree, but I've seen otherwise healthy people reduced to nothing over what started as a minor Clostridium sp infection.  Certainly, if you want to elaborate on this point, I'd always welcome another answer on the question.

There are two types of food poisoning:
Alimentary intoxication
This is the case when you consume food which is contaminated with some toxins, and those are responsible for development of the poisoning symptoms. The source organisms of these toxins might not be present anymore (killed by heating during cooking, for example). In this case there is no massive invasion of any foreign organisms into the gut.
Alimentary toxico-infection
This happens if you eat the food contaminated with microorganisms, and these start to massively proliferate in your alimentary system causing the symptoms of poisoning. The massive intake of the bacteria (even 2-3 spoons of contaminated food might contain millions of bacteria, like Staphilococcus in contaminated diary products). In this case the balance of gut microflora is dramatically changed due to introduction of a considerable amount of foreign microorganisms.
So, even the poisoning seems to be "minor" (e.g., its symptoms are not so dramatic), there could be different amounts of bacteria invading the guts.
The second important point here is the increased emptying of the gut due to diarrhea that leads to the washing out some of the "good" bacteria from the guts, especially in case of profuse diarrhea. The newly coming bacteria are not necessarily those that are present in normal microflora, and it takes days or even weeks until the microflora reaches homeostasis again.
One last point: even without poisoning, microflora varies, and the amount of different bacterial fractions can fluctuate over time. This is normal and depends upon your eating habits, your environment, immune status, and many other factors.

As requested, elaborating this into a full answer.
Three things to consider:

"Alterations to gut microflora" need not only be the invasion of a different, aggressive species of bacteria. One of the most common, and most dramatic forms of alteration to our gut flora is something we do to ourselves: antibiotics. Most ecosystems, micro or macro, are pretty vulnerable to the equivalent of a sustained firebombing.
Some of the "harmful bacteria" that benefit from a disruption of the gut microflora are constituent components of said flora. Clostridium difficile is part of the normal flora of many people - and acquired by many more transiently without incident - yet when the environment is sufficiently disrupted by antibiotics, peptic acid suppressors or some other factors, it proliferates and causes illness.
While it may feel awful to you, many GI illnesses are really just a transient invasion before the body clears the infection, and are only marginally disruptive, or not disruptive at all. This can include the intake of toxins without the actual organism, or things like norovirus, which has a low enough infectious dose that even small amounts will make you ill.


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How does the stem-loop cause intrinsic transcription termination?
In this animation, towards the end (about three quarters) the process of transcription termination is shown. It states that the transcribed RNA forms a hairpin loop (or stem-loop), which halts the transcription process.
My question is, why does it halt the transcription process, considering that the RNA polymerase moves in the opposite direction of where the stem loop is created? Does it somehow change the RNA conformation such that no further bases can be added? Interpreting it as a physical obstacle doesn't seem to make any sense here.

There are two mechanisms of transcriptional termination in prokaryotes.  The one shown here is "rho-dependent" because it involves rho, a DNA-RNA helicase that loads on and unwinds the RNA from the DNA, terminating the elongation by the polymerase.  Check out [1] which shows a model for how rho multimers move through the RNA.
The other mechanism involves just a hairpin. The paper [2], especially Page 23, part C, shows how "rho-independent" or "intrinsic" termination works.  Basically, the hairpin slows down the polymerase and destabilizes the transcription bubble, allowing the intrinsically-weaker A:U bonds to fall apart.
There is no requirement for a hairpin in rho-dependent termination, and I think the movie is mixing them up.

 Geiselmann J, Wang Y, Seifried SE, von Hippel PH. 1993. A physical model for the translocation and helicase activities of Escherichia coli transcription termination protein Rho. Proceedings of the National Academy of Sciences of the United States of America 90: 7754–8. [pdf]
 Datta K, von Hippel PH. 2008. Direct spectroscopic study of reconstituted transcription complexes reveals that intrinsic termination is driven primarily by thermodynamic destabilization of the nucleic acid framework. The Journal of biological chemistry 283: 3537–49. [pdf]


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What is the modern state of the theory of evolution?
When I studied biology at my medical school, we used to learn topics around a century old: the famous Darwin's voyage on "Beagle" to the Galapagos Islands, the classical triad of his Theory of Evolution, etc.
At the same time we were told that there is no evidence found in nature for many of these statements of his evolutional theory. For example, people studied wildlife around Chernobyl and found that no new species emerged due to much higher mutation rate as a consequence of radiation. On the contrary, there were no significant differences between the species living under elevated radiation level and those living in "normal" conditions.
Do these facts somehow influence our understanding of the theory of evolution? Are there any breakthrough findings which happened in the last 20 years that prove or disprove it?

Similar to http://skeptics.stackexchange.com/questions/2057/demonstrable-and-repeatable-examples-of-evolution, and probably a better match for that site.

Some books may be written on this topic.
Evolution is not only speciation and boundaries of species are more or less arbitrary. About Chernobyl - read also this paper.

Wow, you were told complete BS. :-(

I think that BS is a mild word for that sort of total deceit (ie. LIES).

These sound like the sort of things you'd learn at Oral Roberts University (being a total caricature of what the theory of evolution actually says...).

I think the question as it stands currently is too broad. The "fact" about animals around Chernobyl is also pretty much a giant straw-man, radiation certainly increases the mutation rate for exposed animals, but you still wouldn't expect that to cause new species to develop in those extremely short timespans. Evolution takes a lot of time, it doesn't happen over night.

I wanted to have it a little bit broader than usual to get a nice answer and to have a good search entry for Google :)

My friend Brightblades is right in one thing.  It seems your teacher was working off a caricature of what the theory of evolution actually says.  First of all, you should read Sklivvz's excellent answer at this question.  Now to address the elephant in the room, the accident at Chernobyl only happened in 1986.  That was only 26 years ago.  In that timeframe, noticeable effects in an animal population really would not be at all noticeable.  Furthermore, the paper cited by Marta Cz-C actually shows that there have been some changes (in fungi though, not animals).

fungi seem to interact with the ionizing radiation differently from other Earth’s inhabitants. Recent data show that melanized fungal species like those from Chernobyl’s reactor respond to ionizing radiation with enhanced growth. Fungi colonize space stations and adapt morphologically to extreme conditions. Radiation exposure causes upregulation of many key genes, and an inducible microhomology-mediated recombination pathway could be a potential mechanism of adaptive evolution in eukaryotes.

Read the rest of the paper for more information on how there have been some other slight changes to fungi at Chernobyl as well as other locations throughout the world.
Now I am going to repeat a bunch of stuff from one of my web pages that talks about evolution.  This web page is set up mostly to deal with creationist arguments, however, the caricature is so severe as to warrant this.  As I said earlier, evolution is a population phenomenon.
Evolution acts upon heritable variation of characteristics, and you can only have variation of this sort within a population. A single individual organism, at least if its a multicellular eukaryote, has a fixed genome. It can't change what it has inherited. But a large number of organisms can all have different genomes, and can disseminate variation via inheritance to the next generation. It is upon the population as a whole that evolution acts, with various mechanisms coming into play to remove some variations from the population, and propel other variations to numerical dominance within the population. The organisms in question remain part of that population, and within a generation, those organisms don't change. But the moment a new generation is produced, dissemination of variation can result in the appearance of a new feature in one or more members of that population. If that new feature leads to greater reproductive success for the organism possessing it, that feature spreads through the population, as more and more future offspring inherit it. Over time, the population changes, and more and more organisms with new features appear within that population.
Understanding inheritance basics and mechanisms for changes (genes), we have all that is needed for the appearance of cladogenesis events. Split a decent sized population of living organisms into two, and let's call these new, separate populations A and B. Now let a barrier be erected between population A and population B, so that individuals from one cannot reproduce with individuals from the other. This barrier can be an insurmountable physical obstacle, for example, but this need not be the only form such a barrier can take. Now, first of all, there is no reason whatsoever to think that population A and population B will start off in identical states to begin with. After all, those two populations were derived from an original population comprising lots of organisms with different genomes, and the likelihood of population A and population B being identical at the start of this process is vanishingly small. Then, once our barrier is erected, and our populations are allowed to reproduce separately from that point on, there is no reason to think that those populations will move in the same direction in the long term. Indeed, it is far more likely that they will be subject to different environmental and ecosystem influences, and those different environmental and ecosystem influences will shape the long term heredity of those populations. Indeed, that's all that natural selection IS - it's a single, concise term used to encapsulate all of those environmental and ecosystem influences succinctly, and additionally to encapsulate the fact that those influences affect the inheritance of characteristics within a population over the long term.
As a consequence, any two separated populations of living organisms, that originated from a single population, will diverge from each other. If the extant influences on those two populations are sufficiently different, that divergence will take place more rapidly. Eventually, we will arrive at a point where those two populations become sufficiently diverged from each other that individuals from population A can no longer produce viable offspring with individuals from population B, and vice versa. When this happens, we have a speciation event. Indeed, this has been observed taking place in the wild AND in the laboratory, and has been documented in the relevant scientific papers. So, if anyone wishes to assert that there are 'magic barriers' to speciation or other cladogenesis events, then reality doesn't agree.
You will not have any animals giving birth to any radically different animals as a result of radiation.  Most changed sue to radiation will not provide any particular advantage to an animal anyway.  Also, a change may also be dependent on a previous change and require many generations to fully manifest.  All this was demonstrated by the long term evolution experiment led by Richard Lenski at Michigan State University.
So in essence, your teacher was just plain wrong.  As for the findings of the past 20 years, we are always learning more and more.  For instance, there has been an explosive capability in DNA analysis and sequencing, which has only provided more support for the theory of evolution.  A mechanism that Charles Darwin could not have had any idea about in his day and age, yet it perfectly supports his conclusions.  Again, read the answer provided at Skeptics.

+1 Great answer, but a minor technical note on the barriers part of your speciation example. These are not necessary, and sympatric speciation is a pretty active field of research right now. So the answer might mislead people into thinking that a physical barrier is necessary for speciation when it is not.

Perhaps the biggest advance since you studied evolution has been the sequencing of DNA and it's exhaustive analysis and decoding by computers and mathematicians.
Previously the proofs of evolution were geographical, anatomical, genetic, fossil, and a variety of other proofs.
Today there is also a vast library of genetic information.
You, judges. police, doctors and families all trust genetic tests for parentage, they provide incontrovertible proof of family relationships.
Here are 33000 sequenced species. https://www.ncbi.nlm.nih.gov/genome/browse/#!/overview/
If a single one of them showed that it had appeared spontaneously and was not related in an evolutionary tree, people would be amazed, evolution would have been disproved, 2+2 would make 7, people would be confused.
Fortunately all the 33000+ species sequenced recently since 2000 have proven an inherited relationship between all species in a very orderly and hyerarchical evolutionary tree. They find where many genes arise, how humans diversify and new genes appeared, what genes we share with mammals and lizards and fish.
It's a bit like having 33000 forensic pathology tests all in agreement that evolution is very real, it's like the block chain of bit torrent, DNA code is a very powerful method of understanding evolutionary relationships with massive precision and statistical depth.
Big surprises in evolution have happened too since 20 years, such as neanderthal DNA in humans, discovery of feathered dinosaurs and many flying dinosaurs species, 4,6 billion year old stromatolite fossils, and many others.

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


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Is there a reason why human eyesight and plants make use of the same wavelength of light?
The accepted range for the wavelengths of light that the human eye can detect is roughly between 400nm and 700nm.  Is it a co-incidence that these wavelengths are identical to those in the  Photosynthetically Active Radiation (PAR) range (the wavelength of light used for normal photosynthesis)?
Alternatively is there something special about photons with those energy levels that is leading to stabilising selection in multiple species as diverse as humans and plants?

The human species (and presumptive many of our close ancestors) have an extraordinary ability to detect shades of green and red. there is a theory behind this saying that we evolved this ability to better distinguish ripe fruits and thus optimizing the foraging. Most other mammals do not in fact have the ability to detect color. P.S. I have no direct reference to this theory, but I have most likely read about it in Campbell & Reece's biology textbook. D.S.

Good question.
If you look at the spectral energy distribution in the accepted answer here, we see that photons with wavelengths less than ~300 nm are absorbed by species such as ozone. Much beyond 750 infrared radiation is largely absorbed by species such as water and carbon dioxide. Therefore the vast majority of solar photons reaching the surface have wavelengths that lie between these two extremes.
Therefore, I would suggest that surface organisms will have adapted to use these wavelengths of light whether it be used in photoreceptors or in photosynthesis since these are the wavelengths available; i.e., organisms have adapted to use these wavelengths of light, rather than these wavelengths being special per se (although in the specific case of photosynthesis there is a photon energy sweet spot).
For example this study suggests that some fungi might actually be able to utilize ionizing radiation in metabolism. This suggests that hypothetical organisms on a world bathed in ionizing radiation may evolve mechanisms to utilize this energy.

For further reading, this review by Dartnell in 2011 discusses multiple roles cosmic and planetary ionizing radiation may have played in the origin of life.  http://online.liebertpub.com/doi/abs/10.1089/ast.2010.0528

Plants and our eyes are evolved to use attainable wavelength to have more Efficiency.The evolved intermediate eyes and plants must have used high wavelength when there was not ozone.If there is a plant which use high wavelength ,Can you give me an example?

The selection you refer in multiple species could be due to a mutual advantage.
If fruits absorb visible wavelengths, they can be spotted by other animals and eaten together with the seeds. Seeds can then mature inside the host and, once eliminated with the feces, grow up a new plant in a different place.
This is not only valid for light absorption, but for light emission also: for some fruits, the ripening causes a blue-UV luminescence that can be spotted by some insects.

If they absorb visible light, they don't reflect it, which would make them harder to see.

They preferentially absorb one or more colors, rendering the others easy to see. For instance, chlorophyl absorb more blue and red light, so you see leaves as green.

A rule of thumb in optics is that light interacts with materials that have features with  dimensions similar to the wavelength of light. For example, radio waves with large wavelengths interact with large objects like airplanes ,as in the case of radars, and really small wavelengths (x-rays & gamma rays) interact with really small objects like nuclei of atoms. If you take the visible spectrum, light interacts with materials with similar dimensions and/or energies like the C-C, C=O etc that constitute most of the organic compounds. Heck, light with the appropriate wavelength may even interact (or get diffracted in this case) with an organic material that possess many C=O-OH groups spaced with distances similar to the wavelength of light that is shone on it (provided they are regularly spaced and there are lots of them to produce an observable result). Since all organisms are carbon-based the C-C, C=O, C-O, C=_N etc dominate the constituents of the living matter from retina of the human eye to the photosensitive compounds in plants. Hence from the light-matter-interaction perspective all living beings are made up of more or less same materials and this is the reason why plants use the similar wavelength the human eye can detect for photosynthetic processes.
Source: just my intuition

This makes a lot of sense, and in combination with the "adaption based on wavelengths availability" answer provides the complete answer.

This question is related to the question: Why are some things transparent and others opaque?
Being able to see something requires that it is opaque and that sufficient light illuminates it.
UV and shorter wavelengths are not as prevalent as visible light on earth. The world would appear too dark to see if we used UV and shorter wavelengths. This is because our atmosphere absorbs most high energy light.
Infrared and longer wavelengths of light pass through many objects which would make vision difficult. There's less light here reaching the earth and even less being refracted.
Think about how much our vision relies on indirect light. The frequencies at which most objects are opaque makes those frequencies useful for vision due to the accumulation of refracted light.
Why are many objects opaque in the visible spectrum of light? Longer wavelengths of light have less energy than the valence electrons on most matter. Shorter wavelengths have too much energy, they cause chemical reactions, in addition to not being very prevalent on the surface of the earth.
Electrons are what absorb then remit light and have thresholds based on their chemistry for what they can absorb. No absorption = transparent. Too much energy and chemical reactions start to happen, which may be undesirable, or desirable in the synthesis of vitamin D by UV light.
Plants extract energy for chemical reactions from wavelengths shorter than infrared, which is too weak to drive photosynthesis, and not as abundant as visible light. But also absorb wavelengths longer than ionizing frequencies, which are not very prevalent, and usually cause damage.
Visible light is the spectrum of light which is prevalent enough on earth to see, but is not so energetic it would harm biological systems. The qualities for optimal light frequencies in sight and photosynthesis overlap because they have similar mechanisms for interacting with light. What is this mechanism? The chemistry of carbon based life.


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Are there viruses that affect cells across different species?
I'm not a professional in biology nor a student, but I'm curious about this. To be more specific: why doesn't a plant virus affect animal cells?
I suspect that different kinds of cells have different ways to replicate DNA and that this is the reason for the specialization of viruses.
I wonder if someone in the field can explain this to me. Thanks.

Firstly, it's important to recognize that "plant viruses" do not exist. There are only "viruses that affect particular plant cells", or "viruses that affect a particular cell type". You'll see why in a moment.
One of the structural components of many virus is its protein coat. Different types of biological molecules protrude from the surface of this protein coat, deemed signalling molecules. The structure of these molecules are specific to a certain type of virus.
Analogously, specific cell types have specific biological molecules that protrude from their plasma membrane, deemed receptor molecules. For a virus to affect a particular type of cell, their signalling and receptor molecules must "fit within each other", like lock and key. Once they do so, a virus may interact with this molecule, in whichever way it does.
Although your hypothesis wasn't entirely correct, as viral contact with a cell must first be established, viruses do interact with DNA replication in different ways, as in the lytic or lysogenic cycle.

Let me know if I understand. The specialization of the viruses relies in the initial contact with some specific cell.

@leo: in great part. The virus first needs to enter the cell and to do that it needs to recognize some specific protein on the outside of the cell. Then, of course, once inside the cell it needs a specific set of enzymes/protein/conditions that will allow it to replicate.

Further to LanceLafontaine's answer I'd just like to mention that, although as he mentioned viruses interact with DNA replication in different ways, DNA replication in itself is the same process in both plant and animal cells.  For example, a human cheek cell and a potato root cell replicate their DNA  in the same way (as both are eukaryotic cells - cells with internal membrane bound organelle): see Eukaryotic DNA replication for more information.

Thanks for your answer and your edit. The thing with the plant virus that attack an animal cell was just an example. Originally, I was thinking: why a virus that attack a bacteria do not attack an animal cell. Anyway, the answers here really enlighten me.


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Acknowledging differentiation of species, in historical times
This is at least partly an historical question, and I am not even remotely a biologist of any sort, so apologies beforehand if it's a little obscure.
I often wonder how many distinctions were made in pre-Renaissance times, between species of animals.
For example, though I'm sure there have always been those with enough of an interest in nature to tell subtle differences, how were lemmings or voles, for example, told apart from rats or mice? Or did this recognition of speciation only come later, once more detailed (intrusive) forms of analysis became common?
I've looked up the etymologies for vole, lemming and hamster and all are dated post-Renaissance, so at least in these instances it may be safe to assume that people might simply not have noticed the differences before closer study took place. But I guess there are other animals where the same question applies (particularly smaller, harder-to-scrutinise animals where there are a large number of species similar at a glance).
EDIT: Vole means field (same root as wold), giving rise to the 19th c. term volemouse, meaning that originally, mouse and vole were indeed seen as one and the same -- proof of point.
P.S. Of course, this question need not apply solely to animal species.

The branch of science you are looking for is taxonomy, that is the science of identifying and naming species, and arranging them into a classification.
Modern taxonomy was born from the studies of the Swedish zoologist Carl Linnæus (1707-1778), who first introduced, in his books Systema Naturae (Systems of Nature) and Species Plantarum (Plants Species) the now common binomial nomenclature where each different species is given a Latin name composed by two parts: one identifying the genus and one identifying the species.
For instance, various species of mice are in the genus Mus: the common house mouse is Mus musculus, but in the West Mediterranean you have another type of mouse, called Mus spretus.
Although this rigorous type of classification is quite recent, taxonomy existed much earlier.
Shennong, Emperor of China somewhere around 4000BC apparently tasted hundred of plants to test their curative properties. He wrote his observations in a book called the Shennong Ben Cao Jing.
On a similar note the Ebers Papyrus, dating ~1550 BC contains description of the properties of many plants.
To more "recent" times, around 300BC Aristotle was the first who actually classified animals (e.g. vertebrates and invertebrates) and his student Theophrastus wrote a classification of plants in his Historia Plantarum (Hystory of the Plants).
Some 400 years later Plinius in the Naturalis Historia (Natural History) enumerated many plants and animals and gave some of the first binomial names to certain species.
As to the point of how did they distinguish species: well, with their eyes and ears, of course!
You can distinguish a mouse from a vole because it is skinnier and has a longer tail.
Even more similar species can be easily distinguished without needing special equipment.
A good birdwatcher can distinguish a chiffchaff from a willow warbler by listening to their songs, looking at how they behave how they fly, the subtly different tones of their feathers etc.
We can do that now, without any special equipment, so they could before the Renaissance!

@Nick Wiggill: I am not aware of any ancient book that makes such comparison (this does not mean it does not exist, just that I don't know it!). Modern field guides usually do this type of comparisons. I don't think you will get a throughly comprehensive one though, you will need to get specific books for specific genera.

@Nick Wiggill: also, for sure certain species were just considered the same one until recently. Some species have been defined as different just recently since DNA analysis has become commonly available and cheap.

What you are looking for happens all the time when taxonomic groups are "revised." For example, a researcher in that area will review all of the species in a particular genus, and merge or split based on morphological, genetic, or other criteria. E.g., see the comments section of http://www.vertebrates.si.edu/msw/mswcfapp/msw/taxon_browser.cfm?msw_id=961 where the elevation of Loxodonta cyclotis is mentioned. You can find recent revisions pretty easily using google scholar: http://scholar.google.com/scholar?q=vole+phylogeny

I had completely forgotten about this question till I was reminded today by a badge received for it. Thank you for your attention to detail, accepted at last.

If I understand John S. Wilkins' magnificent book on the history of the "species" concept correctly, the basis of biological taxonomy can be traced back to the Aristotelian idea of per genus et differentiam: you can define something as consisting of a general type ("a plant") with a difference ("made of wood") to define an entity ("a tree"), which could then itself become the general type for a more specific category ("an oak tree"). So the idea of an infimae species (an entity that cannot be split any further) has been around since antiquity.
Whether or not a specific group of people would have split similar-looking species is a bigger unknown. I can't find a good online reference for Aristotle's classification of living things; you can read a summary on Wikipedia. Sorry I can't be more helpful!


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How does the microbial environment in your gut initiate?
Clearly, a zygote does not harbor any microbes. As it develops, and the alimentary canal tissue is differentiated, I logically assume that there is still no microbial activity in the fetus's gut. I'm thus also assuming that the commencement of microbial activity in the intestines occurs after birth, but when, and how?
Do newborn babies just happen to ingest only certain e.g., E.coli strains? Is the gut a selective environment in which only certain E.coli strains develop?
Are there any mechanisms to ensure that harmful bacteria do not initially reside in the gut? Is a newborn's digestive tract particularly unstable and ineffective until the proper microbes are established?

The gastrointestinal tract of a normal fetus is sterile. During birth and rapidly thereafter, bacteria from the mother and the surrounding environment colonize the infant's gut. Immediately after vaginal delivery, babies may have bacterial strains derived from the mothers' feces in the upper gastrointestinal tract.[15] Infants born by caesarean section may also be exposed to their mothers' microflora, but the initial exposure is most likely to be from the surrounding environment such as the air, other infants, and the nursing staff, which serve as vectors for transfer.[16] The primary gut flora in infants born by caesarean delivery may be disturbed for up to six months after birth, whereas vaginally born infants take up to one month for their intestinal microflora to be well established.[citation needed] After birth, environmental, oral and cutaneous bacteria are readily transferred from the mother to the infant through suckling, kissing, and caressing. All infants are initially colonized by large numbers of E. coli and streptococci. Within a few days, bacterial numbers reach 108 to 1010 per gram of feces.[16][17] During the first week of life, these bacteria create a reducing environment favorable for the subsequent bacterial succession of strict anaerobic species mainly belonging to the genera Bifidobacterium, Bacteroides, Clostridium, and Ruminococcus.[18] Breast-fed babies become dominated by bifidobacteria, possibly due to the contents of bifidobacterial growth factors in breast milk.[19][20] In contrast, the microbiota of formula-fed infants is more diverse, with high numbers of Enterobacteriaceae, enterococci, bifidobacteria, Bacteroides, and clostridia.[21][22] By the second year of life, the fecal microflora resemble that of adults (wiki source).

The initiation of gut flora come from maternal cervical and vaginal flora (Bezirtzoglou, 1997)1. These predominantly include facultative anaerobes (e.g., Staphylococcus, Enterobacteriaceae and Streptococcus). Birth by caesarean section can cause problems because these bacteria are not passed on in the  usual manner.
Vael et al. (2011)2 found an association between early gut flora and obesity later in life

High intestinal Bacteroides fragilis and low Staphylococcus
  concentrations in infants between the age of 3 weeks and 1 year were
  associated with a higher risk of obesity later in life.

suggesting that monitoring or alterations of gut flora might be effective in reducing rates of obesity.
Bezirtzoglou E. 1997. The intestinal microflora during the first weeks of life. Anaerobe 3:173-177.
Vael, C., Verhulst, S.L., Nelen, V., Goossens, H., Desager, K.N. 2011. Intestinal microflora and body mass index during the first three years of life: an observational study. Gut Pathog 3: 8.


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Do antigens protrude through the capsule/slime layer in prokaryotic organisms where these features are present?
In prokaryotic organisms that have a slime layer or capsule, do intrinsic/extrinsic proteins and other molecules that could be used as antigens protrude through the capsule?

I assume that they must in order to maintain their function for the cell, yet am struggling to suggest another way in which the presence of a capsule/slime layer could serve as a defence against phagocytosis?  Unless the slime layer directly resists lysosomal activity after the pathogen has been recognised and engulfed?
On a related note, could the flagella of an organism (which must protrude through the capsule as above) trigger an immune response on its own?

Well, to use one example, Salmonella has surface, somatic, and flagellar antigens...

Well that answers the question about flagella at least

They don't have to -- there are times in life of a bacteria (cell division, hunger, mutations, attacks of lysozyme and other enzymes, cell lysis) when any possible antigen gets less or more exposed.
About escaping phagocitosis, there are numerous strategies to achieve it -- from forming a large slime-covered colony, through killing or disabling phagocytes up to stopping digestion, escaping the phagocyte back to the environment or even living inside it (Listeria monocytogenes is a prime example -- it can even directly move from one cell to another).
EDIT: Here is a nice overview.

Thanks for the link to the article, it's really interesting!  It seems that the mechanisms I was imagining do actually exist and are quite fascinating. +1