text:
Why does yawning impair hearing?
When I yawn I can't hear anything happening around me. I also feel some kind of muscles inside my head contract and hear a faint hum, but it is not loud enough to explain not hearing other sounds. I can force those muscles to contract even without yawning and it produces the same effect of humming and no other sound, so I suppose they cause this effect, but how?
What really happens? What muscles do I feel?

There may be some clues here. it sounds as if you may have some voluntary control over the opening of your Eustachian tubes as described in the article.

It is related to Eustachian tube. It links the back of throat and the middle ear and allows air pressure to equalize in the middle ear. When you yawn air pressure goes up in this and it bends the ear drum and causes impair hearing (notice, just impair and not stop).
Yawning also helps to open Eustachian tube.

This answer contradicts itself. You are correct in saying that yawning opens the Eustachian tube, and it does this precisely to keep the pressures equalised - so why would yawning 'bend' the ear drum when the tube is open? (This is the same effect that you experience in an aeroplane during landing - anything that you can do to open the tube, including yawning, will restore impaired hearing caused by pressure changes.

Function of Eustachian tube is equalization of pressure. But yawning create pressure in Eustachian tube and cause bend.

Yawning increases pressure in eustachian tube because it takes place during inspiratory phase of respiration, so pushes Ear drum on the outer side

Welcome to Biology SE! I think this is a great answer, but could you elaborate a bit more? For example, why would a (more or less) static pressure difference affect frequency analysis in the kilo-Hertz domain? Also, a reference would be nice, or a picture, a website...

Plus, it may not add anything to the existing answers in its current form. Please elaborate.


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Would oxygen levels be stable without photosynthesis?
I learned how the CO$_2$ cycle works in several biology classes, high school, elementary school, geology, and physics. Then today there was an article published in the NY Times claiming:

...it is a myth that photosynthesis controls the amount of oxygen in the atmosphere. Even if all photosynthesis on the planet were shut down, the atmosphere's oxygen content would change by less than 1 percent.

I'm really confused. If the earth naturally has 20% oxygen in the absence of photosynthisis, why did it spike durring Great Oxygenation Event? I reread that several times. There's no citation; no further context that can explain this. If this were coming from the climate change denier camp, I'd just shrug it off, but the credentials would say otherwise. It's in the NY Times and Nadine Unger is an atmospheric chemist at Yale.
My guess is that this is simply a misleading paragraph with a grain of truth. The question is, where is that grain? How long would the atmospheric oxygen content remain at within 1% of the current level if we turned off photosynthesis?

The answer to your question is in the first graph of the Wikipedia article you linked to: Great Oxygenation Event. In that graph, where time is measures in billions of years, you see that O2, as it was produced, was absorbed in oceans, seabed rock, land surfaces, and finally, about .85 billion years ago, O2 sinks filled and the gas accumulated in the atmosphere.[1] The spike you speak of was probably due to

the evolution of the large vascular land plants that brought about increased O2 production and increased O2 levels due to the enhanced global burial of microbially resistant, lignin-rich organic matter during the Permo–Carboniferous (Berner 2004).

More simply put, there hadn't been equilibrium established yet between the amount of oxygen being produced, the stabilization of the ocean layers and the 'burial of excess carbon' in the deepest ocean layers. Most of the O2 on earth was produced many millions of years ago; it is a myth that the O2 we breathe today is the same O2 made by, say, ocean phytoplankton yesterday.
Nadene Unger states in the NYT article that

[I]t is a myth that photosynthesis controls the amount of oxygen in the atmosphere. Even if all photosynthesis on the planet were shut down, the atmosphere’s oxygen content would change by less than 1 percent.

This is because there are tremendous oxygen sinks that store oxygen gas, such as the surface layers of the ocean. As O2 is used, the ocean would give up free O2. Because of these sinks, some estimate that

if photosynthesis were to cease, atmospheric oxygen would be depleted in 5000 years due to respiration, weathering, and combustion.[2]

while others state that

If photosynthesis were for some reason to stop, oxidation of the entire organic carbon reservoir would consume less than 1% of O2 presently in the atmosphere and there would be no further O2 loss (since there would be no organic carbon left to be oxidized). Conversely, if respiration and decay were to stop, conversion of all atmospheric CO2 to O2 by photosynthesis would increase O2 levels by only 0.2%.[3]

It is very hard to get a comprehensive answer of what would happen exactly. Do we assume all vegetation/phytoplankton suddenly disappears, or does it die (thus increasing to the carbon drain on O2)? Do we assume quick quick death of animals based on lack of vegetation/plankton, etc. as food, or would it be slower? As I said, a comprehensive answer is difficult to find. In any case, the atmospheric O2 would not fluctuate wildly in any immediate fashion.
[1] The oxygenation of the atmosphere and oceans Heinrich D Holland, Phil. Trans. R. Soc., 29 June 2006
[2] The Global Oxygen Cycle
[3] Introduction to Atmospheric Chemistry

So basically Unger's claim is based around the ideas in third reference (The last link is worth a read): carbon is the limiting reagent in the C + O2 -> CO2 reaction? My gut reaction is that in the absence of photosynthesis we don't live in a bistable system: we'd eventually return to the state from billions of years ago. But I can believe that initially there would be very little change.

Also, maybe worth clarifying what "the entire organic carbon reservoir" is referring to. I'm assuming it means all life on earth, plus all fossil fuels we could conceivably dig up.

@Shep, yes, I believe you're right. In other times, other things also needed O2, like iron, etc. but now, it's mostly carbon.

source: Stack Exchange

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

sort: votes


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Organs lifespan out of the body
What organ can be conserved outside of the body for the longest time and still function when reimplanted?

you may want to be more explicit... this is hard to understand...  Do you mean when transported for transplantation for instance?

Yes it can be. I mean in the any best conditions.

this is really too vague to answer. I might say cervix since there is an immortal cervical cancer cell line.  It has never died.  really the question is not precise enough for you to get a satisfactory answer.  the cells may live but the organ can lose all its function..

Sure there are many immortal cancer cell lines. I read in somewhere in the internet mentions that before transplantation, organs lives 4 to 24 hours. I just couldnt find most durable one  on the internet. :)

It sounds like what you are really asking is "What organ can be conserved outside of the body for the longest time and still function when reimplanted?" - Is that correct? If so, please edit your question to reflect that and provide more detail!

Depends what you consider an organ. Typically though it's the cells which require the most metabolic activity which have the shortest life span. The kidney is the most of the major internal organs with up to 36 hours with liver coming second at up to 16 hours.

... on ice i think?

Yes in optimal preserving conditions.

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


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Why do some internal organs regenerate?
I have been reading about the human liver and zebra fish heart muscle having the ability to regenerate. It seems to me that these organs have very little chance to become damaged or worn out. At the very least their chances of being damaged are comparable to other internal organs. So why those particular organs have the regenerative capability?

It makes perfect sense for the liver as this is the organ which carries the biggest load in terms of metabolism. The liver is also very important to metabolize a lot of substances that we take up (think of the Cytochrome P450 system). So it is a good idea for this organ to be able to regenerate.

I am unsure of what exactly you are asking. Is your question "Why does the liver regenerate but not other organs?" or "What important organs have the capacity to regenerate?"

@Chris - it doesn't make perfect sense to me on that basis. That argument can be made for any organ: "it's function is vital, therefore it makes sense that it has regenerative capability."

see @Chris, liver perform many vital tasks but those tasks wont cause it to physically worn out. Or do they? I am not sure.

@anongoodnurse why not what.

@anongoodnurse The liver plays a central role in removing toxins. So it can get exposed to a too high dose and suffer damage. See alcoholism for example. You can treat your liver very bad for years and it will still work somehow.

The liver's position in the circulatory system means that it's the first organ hit by toxins absorbed by the intestines (except maybe the intestines themselves). Detoxification of these compounds can involve generation of reactive oxygen species that damage DNA or protein. It doesn't even need to be chronic damage, excessive acetominophen with a little alcohol can destroy a liver pretty quickly. carbon tetrachloride or galactosamine are used to induce liver failure in lab animals.

Chris and user137 makes sense :) similar things should be true for other animals too I guess. Great guys :) thanks

@Chris and user137: could you make an answer out of your comments? It is all based on obvious knowledge so don't bother with too much cites. Just to prevent deletion - I like the question as it has crossed my mind often!

@PankajPhartiyal I made some edits to the question to try and make the grammar and wording more easily understood. Please check the edits to make sure I haven't accidentally changed the meaning.

I think it is fairly obvious what is being asked here. The main question is, are there other organs - besides those listed - that can repair/regenerate? If there are why do those repair/regenerate while others do not.

Edited the question again. Thanks for the help Chris Stronks. I was not aware of the damage a liver undergoes and I wanted to ask why internal organs have regenerating capacity at all if they don't wear out. Seems Liver do wear out constantly.

It is not really essential that all vital organs should have regenerative potential (for example brain).
The cellular composition of a tissue is a big factor in deciding if the organ/tissue will regenerate or not. Some cells divide while others do not; highly specialized and polarized cells like neurons do not divide perhaps because the act of division itself will compromise their function. That doesn't mean these tissues cannot regenerate; they would need stem cells that can differentiate into the type of cells that died.
So regeneration can happen via:

Division of the tissue cells (skin healing, liver regeneration)
Differentiation of stem cells (erythropoesis, muscle regeneration)

Organs that do not have non-dividing cells can regenerate by simply proliferating whereas others would need to maintain a stem cell niche- which is not possible in all tissues. Maintenance of stem cells also adds up to the cost of metabolism; so there is some tradeoff.

authors: Александра Гридина


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Consumption of NAD+ in glycolysis
Out of 10 steps in glycolysis, only one reaction- Glyceraldehyde 3-phosphate (G3P) to 1,3-bisphosphoglycerate (PGP), uses NAD+ and thereby producing NADH. Furthermore, this very step is solely responsible for net gain of 2ATP in glycolysis since here phosphorylation occurs without the expenditure of ATP.
Why is NAD+ used only in this step? Is it possible to predict by other information that this is the only step to require NAD+? Is it possible to make this reaction happen without the involvement of NAD(P)+? Is it possible to skip this step and directly produce 3-phosphoglycerate (Lets not worry even if we cannot produce ATP in this process). I am interested in this because, this step necessitates the ferementation for regeneration of NAD+ in anaerobic condition. E. coli produced acetate as a side effect, as expected during anaerobic situations, but also rather unexpectedly during aerobic and high-growth rate situation (acetate-swtich, overflow problem). Production of acetate is unwanted in many industrial applications.

NAD+ is important in this step, since it is co-factor for the glyceraldehyde-3-phosphate dehydrogenase (G3PDH), which acts as a acceptor for the hydrogen atom from the C1 (see below).

If you look at the reaction, the aldehyde from the C1 is oxidized to a carboxylic acid which in a second step is turned into a phosphoester. To do so, a cysteine from the active center of the G3PDH attacks the G3P and forms a hemiacetal. This is oxidized into a thioester, the hydride which is split off in this step is transfered to the NAD+ bound by the G3PDH. In the second step the thioester formed between the enzyme and the G3P is attacked by a molecule of inorganic phosphate to form 1,3-BPG. This step is only made possible by splitting the very energy rich thioester bond. So for this reaction to happen you need both steps, as the formation of an energy rich phosphate ester bond would otherwise not happen. See here for more details.
To go directly from G3P to 3-PG you would need an enzyme which oxidizes the aldehyde group in the G3P. And then you need again an acceptor for the hydrogen which is split off here.


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Does scratched Teflon coated frying pans contain carcinogens which can cause cancer?
Is it true that using scratched Teflon-coated pans contain carcinogens, and if so, can they be consumed through the food cooked in them?
E.g.

The deadly toxins from non-stick frying pans

I think the moderators didn't like the way you worded your question, but I think its answerable.  I tried to edit it, but it was hard to edit and not lose the intent of the question so I will try to answer it...

Thank you, eventually you can post your re-phrased question, I'll update.

i know what you mean, but the moderators would appreciate it. lmk what you think of my answer :)

You should ask your question on Skeptics.SE.

Very close to: http://biology.stackexchange.com/questions/9343/are-there-dangers-to-teflon-and-aluminium-cookware

Improved the question, please check.

Teflon is a polymer of perfluorooctanoic acid (PFOA) and related compounds.  PFOA is thought to be a carcinogen.
I think there's an urban legend that if you really heat teflon up or burn it (it doesn't burn as flouroxides are not stable in air) that you might get some of the constituent chemicals out into the air.
Once the flourocarbons are polymerized into fibers and surface coated a metal pan, they are chemically inert and aren't carcinogenic.  Teflon can be made to burn and some noxious fumes produced, but they are not especially carcinogenic.
Even after all this, this paper reviewed PFOA exposure and points out that most people in industrialized countries have some PFOA in their blood and this does not seem to be related to a strong incidence of cancer as the level of exposure is so low.
Flouro-carbon compounds are terribly inert - thats why teflon is so tough.  If PFOA is dangerous, then Teflon is > 10 million times less dangerous.  If PFOA is dangerous, crossing the street is many more times dangerous.
Even PFOA will be eliminated from Teflon production, supposedly next year (2015).

The question and link imply that if cooking with Teflon generates carcinogens that carcinogens then always lead to cancer. This is not always true. In some cases exposure to carcinogens may signal protective pathways. Oncogenesis and exposure to both genotoxic and non-genotoxic carcinogens are not always positively correlated. Cooking with Teflon influences how you cook, and it's how you cook that has the greatest effect on the levels of carcinogens in food.
Cooked food contains carcinogens in the form of reactive oxygen species. This is related more to the heat its cooked at than the type of cookware used. Carcinogen exposure in the heating of biological material is an interesting subject.
Carcinogens can be classified in 2 categories (1):

Genotoxic carcinogens (Reactive Oxygen Species/ROS)
Non-genotoxic carcinogens (PFOA is thought to be here)

Genotoxic carcinogens facilitate the formation of cancer through alterations in a cell's DNA.
Non-genotoxic '...carcinogens have no direct interaction with DNA; they are believed to cause tumors by disrupting cellular structures and by changing the rate of either cell proliferation or of processes that increase the risk of genetic error. (1)'
The molecular mechanism most often thought of for cancer formation is genotoxic oncogenesis, damage to DNA. Here, genotoxic oncogenesis often involves a reactive oxygen species (ROS). ROS may generate free radicals which, when reacting with other molecules, generate more free radicals. Another example of a reaction involving free radicals is a fire. Human cells contain genes for antioxidant enzymes, like glutathione and superoxide dismutase, which catalytically converts the free radical superoxide into hydrogen peroxide.
The abundance of ROS in our cells has 2 components:

Production of ROS
Depletion of ROS by upregulation of antioxidant enzymes

Intracellular levels of ROS positively regulate levels of antioxidant enzymes like glutathione and superoxide dismutase (2). This means that more oxidative stress leades to more protection from ROS by antioxidant enzymes. This is why exercise, while increasing ROS levels, actually protects against them.
ROS are also produced during the cooking of food, especially meat (3). This applies to any type of cookware, any method of heating of any food: protein, carbohydrates, fats.

'For example, it only takes a few hours at 70C to have the same extent of autoxidation which at room temperature requires months (4)'

Intracellular ROS are unavoidable. They are produced by normal metabolism, exercise, cosmic radiation, during the consumption of food. Balancing this are endogenous antioxidant enzymes. The antioxidant power of glutatione exceeds any known nutritional supplement (5).
Exercise is an extremely effective upregulator of antioxidant enzymes, eclipsing any antioxidant supplement or change in cookware. Regular physical activity will most likely be the best prevention one can take against ROS induced genotoxic oncogenesis.

This does not answer the question.

Carcinogens in cooked food come mainly from the cooking process not the cookware.

Right. The question is whether the pans themselves contain carcinogens, not whether it's possible to generate carcinogens by cooking foods in the pans.

There is mixed data suggesting PFOA may or may not be genotoxic. If it functions as a ROS, it's important to know that total levels of ROS in the body is not a good indicator of risk for developing cancer. The question implied that carcinogens - > cancer. This is not always true. In some cases a raise in the levels of ROS or other carcinogens may signal protective pathways. Oncogenesis and exposure to both genotoxic and non-genotoxic carcinogens are not always positively correlated.


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Is 5-HTP a SSRI?
Can 5-Hydroxytryptophan (oxitriptan) be categorized as selective serotonin reuptake inhibitor (SSRI)? Since they both act on the serotonin pathway and are used to treat depression and other mood disorders?
For example on this page, they're treated under the same category.
If they're not, how 5-HTP is different from SSRI?

That page you linked doesn't consider 5-HTP an SSRI: "Since 5 HTP (increase serotonin synthesis) and SSRIs (prolongs serotonin action) affects the serotonergic system in different ways,"

I know, it says: 5 HTP and SSRI in the title, but later on describes what are SSRIs, so like it's describing them both together. I'm sure some time ago I've seen some info that 5-HTP is same as SSRI, could be invalid, that's why I'm trying to double check that. Theoretically 5-HTP should work the same as SSRI, so I'm looking for some reliable sources how they're different.

No, it isn't considered an SSRI. SSRI stands for selective serotonin re-uptake inhibitor or serotonin-specific reuptake inhibitor, which designates the mechanism by which this category of drug (supposedly) works: on the serotonin transporters in the brain. It's a term only used for a limited range of drugs, like sertraline and citalopram.
5-HTP (Oxitriptan being a trade name) is a chemical precursor to serotonin. The way it affects the serotonergic system is by increasing the rate at which it is generated. The category to which it belongs is the "serotonin precursor" category, similarly to e.g. L-tryptophan (which is actually itself a precursor of 5-HTP).
If it is prescribed to treat depression, it might be called an anti-depressant, but SSRI is a term for a  mechanism of action moreso than an effect. Tetracyclic and tricyclic antidepressants, for example, also affect neurotransmitter uptake in the brain, but aren't called SSRIs.
Further reading: How Different Antidepressants Work

Thanks, so to which category 5-HTP/Oxitriptan goes then?

@kenorb I'm not sure what you mean. I can't find any reliable source that calls it an antidepressant right now. Until then, I'd just call it an amino acid...


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How closely related are two parasites Giardia intestinalis and Trichomonas vaginalis?
How closely related (from the evolutional point of view) are parasites Giardia intestinalis and Trichomonas vaginalis? Giardia genome is about 12 Mb and its major cellular proceses are rather simple. The genome of Trichomonas is approximately 160 Mb. What about its cellular processes, is it also a 'minimalist'?

Basically, Giarda is a an Excavates while Trichomonas is a Cercozoa meaning a Rhizaria (Chromealveolates in the broad sense as noticed by @har-wradim in the comments (now deleted) because Cercozoa are neither Chromista nor alveolata). Because the very basis of the tree of eukaryotes is still unresolved (eukaryotes), the most recent common ancestor of these two species is just an old eukaryote! In other words, these two species are not more closely related than are related a cat and a chestnut tree!
The links yield to Tolweb.org which shows you the phylogenetic tree and allows you to explore the relationships between organisms. Have a look to eukaryote tree especially to see the positions of the Rhizaria and Cercozoa.

One more point: While Giardia and Trichomonas both lack mitochondria, the former has mitosomes and the latter has hydrogenosomes. Mitosome has the most reduced functionality

Be careful though that Tolweb is not always very up-to-date.


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Why do dogs try to cover their poop?
It may seem obvious to us humans to hide our excreta, but this is not quite normal behavior for animals.
Interestingly, dogs have the habit to pee all over the place. It's know that they do so to mark their territory. So when they want to mark their territory, why do they cover up their poop?
I found an old web article where someone asks the same question, without getting a credible answer. He quotes a Yahoo Answers answer making the following claim:

This behavior is natural in dogs. They cover up their "waste" so that
  an enemy does not find them, from the scent of the poop or pee. It is
  an instinct handed down from wolves, who hid their scent by covering
  up their feces in leaves, sticks, soil, or other nearby natural
  materials. They also rolled in animal carcasses to hide the scent of
  them. Your dog is just using her natural instinct to protect herself
  from predators.
Another things that dogs do, called marking, is when the dog pees in a
  certain area. They do not cover it up, as it is marking a territory as
  their own. Male dogs usually do this on trees, wooden posts,
  furniture, and other things. Female dogs do this in heat. Dogs do not
  poop to mark something, only pee. When you dog pees or poops and then
  covers it up, this does not mean she is marking her territory. Just
  wanted to add it so you don't get confused. :)

I find it hard to believe these two opposite claims. One time dogs want to mark their territory and the other time it's scared from predators. I know many dogs that do not cover their pee, but do cover their poop, sometimes even within the same walk (and so the same territory).
If this is true, why do dogs do both in the same walk?
On Wiki Answers I found this answer:

The animals are not actually covering up the pee or pooh but spreading
  their scent. This often happens with animals that are dominant (for
  instance show dogs).

It's so that dogs never actually cover their poop anymore, they only perform some random scratches, throwing a little sand on the turd, sometimes even nothing. That fact makes this answer quite more likely than the previous one.
Another take that's similar to the previous one is this one from Dogster:

So, why do dogs scratch with their hind legs after defecating? You
  might think the dog is trying to cover up his poop like a cat does,
  but it’s actually a way to mark territory, with the scratch marks in
  the ground pointing to the scent the dog has left.

I also found an eHow article on this subject. It seems to agree with the previous two explanations, but is more detailed.

It is normal for dogs of both sexes to vigorously kick the ground with
  their hind legs after defecating. This is called scraping or peeling
  out. Some dogs will also do it after urinating. Dogs are descended
  from wolves, which also perform this behavior. It is not a bad habit,
  but a vital part of a dog leaving a visual message and scent message
  to any other dogs that happen to pass by.

They also say that the specific reason why they spread scent with their paws is because paws just contain a lot of scent.

Dog paws contain scent glands. There are also glands in between the
  toes. The action of scraping the paws against the ground helps release
  the scent inside of the glands. Dogs scrape the ground in order to
  increase their scent on the area near the feces pile, according to
  veterinarian Dr. Justine Lee. Before domestication, dogs wandered in
  large territories. One vital way to communicate with other wandering
  dogs is through scent marking. This instinct has not been bred out of
  the domestic dog.

So, which theory is the most valid? I tent to go for the scent one. Any additions?

...maybe because dogs that didn't do that were more likely to get sick (or get members of their pack sick) and die, giving an evolutive edge to the ones that randomly started to do that. Or maybe it is so the smell doesn't cover another more important smells. Or maybe we humans selected the ones who did, because...well, obviously we prefer the ones who bury their feces without even training them to do it. Or maybe, the ones who buried them just happened to survive in greater numbers, but it may not be a relevant trait in said survival (correlation doesn't imply causation)

I cannot find any definite articles on why there would be a reason for this behaviour other than the same ones that you have mentioned in your article. It could be because it wants to mark its territory or the dog wants to hide its scent.
One point that I would also like to add is force of habit. As Charles Darwin (the father of evolutionary biology) had said in his book titled "The expression of emotion in man and animals"

‘Certain complex actions are of direct or indirect service under
  certain states of the mind, in order to relieve or gratify certain
  sensations, desires, etc.; and whenever the same state of mind is
  induced, however feebly, there is a tendency through the force of
  habit and association for the same movements to be performed, though
  they may not then be of the least use’ (reference 1 and reference 2).

It is more of a guess that we make when we see them hide their faeces but in the end, there may not be a reason at all but a habit that do not serve much purpose passed on through evolution. It is left upto our own liberty as to guess what the exact reason is.


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Do cockroaches have less health issues than humans?
Cockroaches are known to live in very dirty places like sewers. Does this cause them to evolve to be stronger against parasites and bacteria? Recently I read online that cockroaches can sustain radioactive harm 6-15 more than humans, so does that mean that cockroaches are less likely to get cancer?
refernece for the radioactive exposure:
http://www.abc.net.au/science/articles/2006/02/23/1567313.htm?site=science/greatmomentsinscience

It would be nice if you could add where you read that about radioactive harm.

@Armatus - Is that good enough?

According to Wikipedia, the most common types of cockroaches live between 6 months to two years.  Humans, on the other hand, live about 70 years.  Humans simply have a much longer time to develop cancer than cockroaches do.

@AndrewSalmon - But compare with short-lived cockroach and short-lived human, the human brain stroke rate seems to be higher since never heard of cockroach brain-stroke

Two ways that you can improve your question: 1) "Dirty" doesn't necessarily imply "filled with parasites and bacteria", or imply an increase in radioactivity. What is it that you're really asking for here? 2) Cockroaches and humans have very different physiologies (cockroach cells divide much less quickly that human cells), cell types and of course, size (amount of cells) is definitely an issue. A comparison of generic cancer rates between both would be meaningless.

Note that humans in general get more cancer than other "wild" organisms since they live  much longer then what they would live in the wild. I am guessing this is also why pets have a relatively high rate of cancer.

I have heard that cockroaches are usually infested with parasites.

AndroidPenguin, where did you read that our immune systems are far better than those of 'a cockroach'? This seems pretty strange to me, but I'd be interested in reading a study that compared human and cockroach immune systems if you can provide a reference.
Victor, with respect to cockroaches, there are numerous species of cockroaches. Here's a page about cockroaches with a link to publications on cockroaches and a phylogenetic tree of the families and subfamilies.
http://www.bio.umass.edu/biology/kunkel/cockroach.html
All those species tend to occupy distinct niches with distinct traits. With respect to cockroach evolution, sewers are too new a phenomenon to have had an influence on cockroaches. Rather cockroaches have been successful in adapting to this novel 'habitat'. The same holds for rats and other denizens of sewers. Sewers are a very nutrient rich environment, and as in many nutrient rich environments, a few species tend to possess the right traits (whatever those may be) to survive and out-compete other species. To take an example from coral reefs, when coral reefs suffer from eutrophication, this leads to a growth in phytoplankton and a reduction of the euphotic zone that can lead to the death of all but the most resistant corals. Likewise in the terrestrial environment, only the most tolerant or opportunistic species tend to survive in highly perturbed and nutrient rich environments like sewers. With respect to cockroaches getting cancer, I've never read anything about insect cancer, but I imagine in theory that they could get cancer. I'm not sure, however, of the impact given the much shorter life spans of insects. It's an interesting question though.

Our immune systems are more advanced. Whether that means ours is better is disputable, but specifically older organisms don't have an as well-established adaptive immune system. However of all the insects, cockroaches have one of the most robust adaptive immune systems. They produce primitive antibodies like IgM-like Ig but other immunoglobulins are much more specific to humans and allow us to fight a large range of pathogens more efficiently. Furthermore you can add advances in some of the novel immune cells we possess.

I'm not sure you can call a given cockroach species an 'older' organism. I would need to see a phylogenetic tree of cockroaches, but there may be species, which are younger, that is, evolved later than humans. I don't know enough at present about the immune systems of cockroaches to compare them to those of humans, but you raise some interesting points that I'd like to look into. Any suggestions on relevant publications?

Different pathogens affect different organisms. We live longer because we have an advanced immune system far better than that of a cockroach and because of a hundred other reasons. A cockroach that were to keep itself well fed and clean would live longer, but they can't manage that as well as they could if they had a brain as powerful as ours. Furthermore they're evolutionary suited to live in the environment they do with less consequences than we would. But look at the opposite. A cockroach and a human are in identical locked rooms with a key on the floor. The rooms have no food or water. WHo dies first? The cockroach, because the human simply walks out. For those that will be brutal, the cockroach cannot get out unless it unlocks the door because it's a cockroach escape-proof room :P
Now for your cancer question. Cancer was much rarer in the human population hundreds of years ago than it is now. That's because it's a disease you get due to damage by radiation and other mutagens over time. Cockroaches don't live long enough. But radiation isn't the only mutagen, we could feed them something if we really wanted to give them cancer. As long as cells are dividing, cells can get cancer.


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How can I keep pond water "alive"?
I've been preparing wet slides for my kids to look at from pond water. I have a mason jar of pond water. What can I do to keep the microbes in the jar alive going forward so that we can look at it any time we want without having to go back to get more pond water.
I remember we did something like this in 7th grade biology, it seems like we put in sugar, or oatmeal, or something. I can't quite remember that though, it's been over 30 years. Thanks!

Thanks for the comments. The pond water I get keeps for a couple of days easily. I can always get more at the pond.
If I want amoebas, I go near dark and get them at the bottom of the pond. If I just want paramecia and other critters, I grab some scum and fill the rest of the jar up with water.
The paramecia water I give moderate sunlight. The amoeba sample I keep in the dark. And I just pitch it after a few days. No Legionella for my family, please and thank you.

How long do you want to keep it. I think the water will have a sustainable microecosystem if it is kept open.

Is there anything in particular in the pond water you want to look at specifically? Do you want to look at microbes, or more tardigrades and daphnia, etc? You could always fix the slides. Sunshine should keep it going on a microscale, but stuff like brine shrimp or around that size require snacks.

I'd like to keep it alive indefinitely. As far as tardigrades/daphnia/microbes, yes, yes, and yes!

And how open would it need to be? I have the mason lid sealed on it, but with a bunch of holes in the lid.

You want to keep live water indefinitely? I don't know if you'll be able to tell if it gets colonized by Legionella.

Yikes. Maybe I'll just go back to the well then. Or the pond, in this case.

The answer will be to replicate the conditions as best possible, given the biotic and abiotic variables it could be very difficult to answer this.

"No Legionella for my family, please and thank you.".

"No Legionella for my family, please and thank you.". Legionella pneumophila ocurs in oxygen rich, fresh, standing water, maintained at temperatures between 30 and 50°C (86 - 122°F). Infection occurs trough the air, by inhaling water droplets from aerosols (drinking Legionella containing water is harmless). Unlikely to become infected by a jar of pond water, I would say... There's nothing wrong with being cautious, but there's no need to exaggerate...


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Selective Androgen Receptor Agonist
I'm looking for an inducer that strongly activates the androgen receptor, but not the glucocorticoid receptor that is not DEA regulated. I know that SARMS (Selective Androgen Receptor Modulators) are something of a hot topic in some corners of some fields, but I'm having some trouble in my laboratory finding one. My research necessitates the independent induction of AR (Androgen Receptor). Does anyone know how to go about this search or know of some chemical?

Are you looking for literature? If so this is a recent review: Zhang et al. (2013) Deciphering the selective androgen receptor modulators paradigm. EXPERT OPINION ON DRUG DISCOVERY 8: 191-218   DOI: 10.1517/17460441.2013.741582

Take a look at the paper by Ojasoo et al. [1] It reports the relative binding affinity for a wide variety of steroids for the AR, PR and GR.
Nandrolone (19-nor testosterone) does not have any affinity for the GR, but is a potent activator of the AR. However, it does have some affinity for the progesterone receptor (does this matter for your research?). Additionally, nandrolone bound to the AR also binds estrogen response elements (does this matter for your research?).
5a-DHT also is a potent AR activator with no affinity for the GR. Do note that a metabolite of 5a-DHT has significant affinity for the estrogen receptor, might that matter for your research.
You might also use a strong GR antagonist in conjunction with an androgen which also has some affinity for the GR. Then you can simply use methyltrienolone, as commonly used as AR ligand.
On a sidenote: do note that androgens usually only lead to significant dissociation of a GR ligand for the GR at very high concentrations. Therefore, androgens most likely act as GR antagonist by heterodimer formation of the AR with GR [2], as well as through squelching [3].
References

Ojasoo, T., et al. "Towards the mapping of the progesterone and androgen receptors." Journal of steroid biochemistry 27.1 (1987): 255-269.
Chen, Sei-yu, et al. "Androgen and glucocorticoid receptor heterodimer formation A possible mechanism for mutual inhibition of transcriptional activity." Journal of Biological Chemistry 272.22 (1997): 14087-14092.
Zhao, Jingbo, et al. "Oxandrolone blocks glucocorticoid signaling in an androgen receptor-dependent manner." Steroids 69.5 (2004): 357-366.


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What risk to DNA does long-term exposure to low-dose radiation pose?
A new study from MIT scientists suggests that long-term exposure to low-radiation poses no risk of DNA damage for mice (it is also important to note that mice are unusually susceptible to cancer). So apparently there may be a threshold for radiation damage to DNA.
But is this study conclusive? What are some other studies that show the biological effects of long-term low-dose radiation on DNA?
There are some studies that do show increased rates of cancer in frequent flyers. So are are we going to reconcile this finding with the finding above?

Can you say that anything in science is conclusive?

@Kevin Yes of course. Why not? “conclusive” doesn’t mean 100% sure – otherwise nothing would be conclusive, thanks to Gödel’s incompleteness theorem. It just means “reasonably sure” given some fitting threshold.

I agree with @Kevin - there are no ultimate statements in science. The answer is 'its all relative'.
With radiation and risk, more radiation means more risk of cancer or any number of other types of damage that can result.  The question is is this significant?  And this is a somewhat subjective question.
When someone says:
'there is no health risk from XYZ'
what they mean is..
"to the extent that we can determine, we can't see any more chance of adverse health if you are exposed to XYZ conditions than if you weren't"
DNA damage happens all the time.  The frequent flier study you cite is trying to see if the additional exposure to cosmic radiation while flying, which is largely blocked by the atmosphere, causes a change in the rate of some cancers.
Radiation and cancer is like a lottery.  If you buy just one ticket you might win.  If you step outside, the thousands of extra gamma rays you get outside might start a cancer that will eventually take your life.  If you buy 20 million tickets you will very likely win.  If you hang out next to high levels of radiation, even for a short while, you will get so much damage you will not live long.
Its difficult to study the effect of low levels of radiation. The lower the levels of radiation we are asking about, the longer you will have to wait to see if there is an effect.  If 10% more people get cancer, you have a very real concern that some of these folks might have done something else, like sunbathe or live in a poorly ventilated basement for too long.
The real question is, what is significant?  I once saw a 60 minutes segment where a dermatologist said that she simply never directly exposes her skin to direct sunlight.  I'm betting she never got a melanoma.  She carried a parasol and wore light gloves outdoors.  (sorry I can't find the link)  She was at least in her 50s and she had the skin of a teenager.  I still go out in the sun.  I assume my risk of melanoma is 5-10 times more than hers was (this was a pretty old broadcast).  (mine is 0.03% in the next 5 years btw).  Its just not worth it to me.

See my answer to Kevin’s comment. This is a red herring, “conclusive” isn’t the same as “ultimate statement”.


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How does the eukaryotic cell synthesize all of the proteins of a protein complex (like ETC complex I) at stoichiometric ratios/numbers?
(eg synthesize all proteasome proteins at the appropriate ratios to which they are used)
How often are proteins of the same complex (eg all the proteins of the 20S/19S parts of the proteasome or complex I of ETC) controlled by the same enhancers/promoters? Is it often the case that you just have non-stoichiometric synthesis and then the cell degrades the excess protein if it can't put them both together?

You seem to have reputation here, so you should know that you are expected to demonstrate that you have done some research before asking questions here. This is a complex question, the answer to which differs between eukaryotes and prokaryotes (e.g. for ribosomal proteins) and probably between organisms and protein complexes. Tell us what you find when you search for something like “coordinate regulation of ribosomal protein synthesis” or whatever.

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


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How do trees manage to grow equally in all directions?
I was walking down a road with these beautifully huge trees when this question occurred to me.
Large trees with many thick branches have to grow equally in all directions, or they would tip over. Is there some sort of mechanism to ensure this uniform growth? Or is it just a happy coincidence arising from uniform availability of sunlight on all sides? If one branch of a tree becomes too heavy due to many sub-branches, does this somehow trigger growth on the opposite side of the tree?
I have seen that potted plants in houses tend to grow towards sunlight. My mum often turns pots around by 180 degrees to ensure that plants don't bend in any one direction. I assume that this is because sunlight increases the rate of photosynthesis, leading to rapid growth of the meristem.
For trees growing in open spaces, this wouldn't be a problem. But there are many large trees that grow in the shadow of buildings without bending away from the buildings, even though this is the only direction from which they would receive any sunlight. Is there any explanation for this?

Lots of questions are nested here - tree growth and its regulation, reaction wood, heliotropism - might be good to focus it

I was asking the same question when I had observed my tropical plant to balance on the very margin of the shelter as it was becoming more and more tilted against the wall. No magic, one day it just fell over.

Growth in plants is tightly controlled by auxins – plant hormones. Auxin itself usually has an inhibitory effect on growth [EDIT: see comments and Richard’s answer for correction]. As far as I know there is no active control to restore plant symmetry once it has gone awry (but I could be wrong!) but the inhibitory effect of auxin synthesised at the meristem and diffusing in all directions causes a symmetrical pattern of inhibition and activation, forming shoots at symmetrical distances around the shoot apical meristem – this is very visible in the symmetry of the romanesco broccoli:

Furthermore, there are several mechanisms involving auxin which shape the general growth of the plant. The most important ones are:

Apical dominance which causes the apex (the stem) of the plant to grow more strongly than other parts of the plant, ensuring a general centring of the growth.
Phototropism causes the plant to grow towards sunlight. Unlike you hypothesised, this isn’t simply due to more photosynthesis and hence faster growth at the front of the plant facing the light, it’s actively controlled.
Gravitropism is a very interesting effect which causes the plant to grow generally upwards. It’s interesting because the mechanism is actually using gravity: the auxin synthesised at the meristem diffuses downwards in the plant due to gravity, inhibiting the growth in lower regions (but note that in the root apical meristem the effect is somehow reversed).
Hydrotropism causes the plant to grow towards water.

All these effects combined cause the plant to grow in a generally upwards, laterally distributed fashion.

This makes sense. The gravity thing is really interesting! Isn't there also a hormone which induces growth? I can't remember what it's called. Maybe that's more dominant in the root. Again, just hypothesizing.

Giberellic acid is another plant hormone that can induces plant cell growth or elongation, among many other functions.

@Amu There are, yes. I’ve forgotten the exact names though. If I remember correctly different types of auxins have different influence anyway.

Konrad you have the role of auxin backwards - it promotes growth rather than preventing it. I'll try to answer with the stuff you've missed about restoring plant symmetry.

@Richard I’m pretty sure there are auxins for both, and their effect differs depending on other factors (which is why I wrote “usually”). Now, I’m sure you know much more about plants than I do (admittedly, that’s not hard). But the specific function I was thinking of is indeed inhibitory. I can’t remember the name of the particular auxin I’m thinking of, I have it somewhere on my other computer. By the way, just saw that you’re about to start a PhD in Cambridge, congratulations & welcome!

@KonradRudolph Thanks, I was actually going to email you as I saw you were at the EBI. With auxin perhaps you are thinking of the fact that high auxin conc. can stimulate ethylene production, which in turn stimulate abscisic acid, which is inhibitory to growth? This helps maintain apical dominance by preventing lateral meristem formation. IAA is by far the most important auxin and is the one which generally coordinates growth, and its specific action is to promote cell elongation.

I'd be interested to see if there is an auxin which inhibits though.

the direction of sunlight changes as earth rotates so the direction of sunlight is varying...then i think the tree bends where the intensity is more. in the whole day.

There are some other good answers which provide part of the picture, but I think there is a fundamental organising principle which has been missed. Konrad has touched on it in his answer.
The reason trees, and most plants, tend to grow equally in all directions is that they have iteratively generated branching and radial symmetry which is controlled in a feedback loop of the growth promoting hormone auxin and auxin-sensitive auxin transporters. This is an elegant biological algorithm which explains all branching growth.
The things Konrad identifies (phototropism, gravitropism, etc.) serve as orientation cues which help the plant determine which axes to grow along, but fundamentally the process is about auxin gradients. There are exceptions, as others have pointed out in their answers, and they usually result from severe imbalances in the orientation cues.
I'll try to explain the growth process clearly (and it gives me an opportunity to try my hand at diagramming again ^_^)...

Auxin is a plant hormone (actually a class of hormones, but mostly when people say auxin, they mean indole-3-acetic acid) which promotes cell elongation and division. The basic principle which allows auxin to act in the organising way it does is that auxin is produced inside cells, and proteins which export auxin from a cell develop on the side of the cell which has the highest auxin concentration (see figure below).

So auxin gets transported up the concentration gradient of auxin! Thus if you get an area of high auxin concentration developing somehow, more auxin is then transported towards that area. An area of high auxin concentration relative to the surrounding tissue is called an auxin maximum (plural 'maxima').
For most of the life of the plant, auxin is produced pretty much equally in most cells. However, at the very early stages of embryo development, it gets produced preferentially along the embryonic axis (see figure below, part 1). That creates a meristem - a group of cells where cell division is taking place - at the auxin maximum at each end of the embryo. Since this particular meristem is at the apex of the plant, it is called the apical meristem, and it is usually the strongest one in the plant.

So by having a meristem at each end, the embryo then elongates as cell division is only taking place at those points. This leads to part 2 of the image above, where the two meristems get so far apart that the auxin gradient is so weak as to no longer have its organising effect (area in the red square). When that happens, the auxin produced in cells in that area concentrates in a chaotic way for a short time until another center of transport is created. This happens, as the first one did, when a particular area of the tissue has a slightly higher concentration of auxin, and so auxin in the surrounding tissue is transported towards it. This leads to part 3 of the figure, in which two new meristems are created on the sides of the plant (called lateral meristems).
Lateral meristems are where branches occur on plants. If you then imagine this process continuing to iterate over and over, you will see that the branches, as they elongate, will develop meristems at the tips and along the sides. The main stem will also continue elongating, and develop more lateral stems. The root will begin to branch, and those branches will branch, etc. If you can understand how this elegant system works, you understand how plants grow, and why they grow in repeating units as opposed to in a body plan like animals.
It also explains why, if you cut off the tip of a stem, it promotes branching. By removing the apical meristem, you get rid of the auxin gradient and enable the creating of multiple smaller meristems which each develop into branches.
So far I've explained regular branching, but the same system causes the radial symmetry which makes trees (usually) grow in all directions equally...

Imagine taking a cross section through a stem and looking down all the way through it (as depicted crudely above). Just as auxin gradients act to coordinate growth along the length of the plant, they also coordinate it radially, as the maxima will tend to space themselves out as far from one another as possible. That leads to branches growing in all directions equally (on average).
I welcome comments on this answer, as I think its so important to understanding plant growth that I'd like to hone my answer to make it as good as possible.

They don't always.  For example, this apple tree grows just outside my window:

So far, it hasn't fallen over yet.  The reason it grows that way is because all the light is coming from the right side of the picture: the tree leans roughly to southeast, while the building is to southwest of it and casts a shadow on the center of the yard for much of the day.  Also, to the left you can see the branches of other, taller trees that block pretty much all scattered skylight from that direction.

I like the tree. :)

that also happens in areas with strong wind

+1 for the tree! :) I guess the roots would also spread towards the southeast, so that the center of mass of the tree remains above the roots.

As shown in the answer by @IlmariKaronen, that is not always the case. most trees grown next to the shady sides of buildings tend to lean away from the building. Some trees can stand more shade than others, and these will send branches into the shade of buildings. They never grow as dense or robust in the shade. The reason for the plants growing toward the light is Phototropism. When light hits the plant stem, the auxins that determine the length of the stem are destroyed, decreasing the amount of growth on that side of the stem. When this happens, the stems bend toward the light source from the imbalance of auxins in the stem. The reason that the shady side is weaker is that all trees rely on photosynthesis for their energy. Of course, the side without direct sunlight will not perform as much photosynthesis, and so has that much less energy to grow with. Also, many large trees are imbalanced, sometimes all of the weight on one side. The roots hold them up.


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Do all plants photosynthesize with equal efficiency?
Just what the title states.
Given identical, necessary and favourable conditions (Probably nutrients, humidity, and light but what I mean is all necessary requirements are fulfilled) - Is photosynthesis equally efficient in terms of the amount of sugar/carbohydrates generated by all plants/trees, or are some plants/trees more adept at it?
My background in biology/botany is high-school, so my list of necessary requirements may be lacking for which I crave your indulgence

I think you would have to define the conditions. Even a single plant will vary in photosynthetic output over the course of a single day. Would maximal photosynthetic output be sufficient?

Define efficiency: carbon fixed per unit of what [h2o, nitrogen, light, CO2]? Any way you look at it, the answer will be "no".

@Kevin: Yes, assuming that maximal photosynthetic output refers to the quantity of food available after the process completes

Zhu et al, 2008 provide a review titled "What is the maximum efﬁciency with which photosynthesis can
convert solar energy into biomass?" in the Journal Current Opinion in Biotechnology.

@David that's an excellent paper.

If you mean the efficiency at which plants convert light energy to chemical energy (in sugar or other reduced C compounds) then there is definitely variability between plants, both at the species and individual level. The photosynthetic efficiency WP page gives ranges of between 0.1 and 8% of total solar radiation converted to "biomass", but these values are not cited. In their review, (Zhu et al, 2008) state that the maximum maximum efﬁciency with which photosynthesis can convert solar energy into biomass is 3.5% and 4.3% for C3 and C4 plants (both observed for crops), respectively. Biomass is not a measure of energy, but perhaps they mean potential chemical energy in that biomass.
Its a pretty complicated question though. Photosynthesis is a complex process involving many interdependent chemical reactions and physical processes. All species (or even individuals) of plants have different morphology, physiology, and biochemistry that influences overall photosynthetic efficiency. In addition, they each inhabit different ecological niches and climate space. Therefore, all species or individuals would have a slightly unique maximum potential efficiency. Here are a couple other efficiency related concepts to consider:
There are 2 systems in photosynthesis that work in tandem, the light reaction and the dark reaction.  The light reaction uses light energy, pigments like chlorophyll, and a bunch of electron transport chain proteins to generate ATP and NADPH. These 2 molecules then provide the reducing power for use in the dark reaction (the Calvin Cycle). In the dark reaction, the enzyme RuBisCO joins CO2 and RuBP, creating simple reduced carbon chains which are then used to assemble sugars. This is an over-simplification, as both reactions are very complex systems with lots of biochemical machinery, but this is the basic process used to convert light energy to chemical energy. To operate at peak efficiency, the entire process must not be limited by incoming energy (light), substrate supply (CO2, RuBP), or nutrients used to construct all the needed cellular and molecular machinery (N, P, K, and many others). In reality, there are limits that vary from plant to plant, species to species. For example, a species or individual with a very reflective leaf surface converts less of the light reaching the leaf surface to chemical energy, thus lowering the output of ATP and NADPH. This reduces the chemical energy supplied to the dark reaction and limits the amount of carbon fixed by RuBisCO. So the reflective surface of the leaf, which might be advantageous to the plant in other ways, has a large impact on overall photosynthetic efficiency (compared to a less reflective leaf or leaves).
If you want to search for more information, there are a number of terms that plant physiologists and ecologists use when describing a plant's (or communities of plants) photosynthetic efficiency. Each of these is used in different ways and can have many variations in units.

Light use efficiency: The amount of carbon fixed per unit of light incident.
Water use efficiency: The amount of carbon fixed per unit of water transpired
Nutrient use efficiency: The amount of carbon fixed per unit of nutrient concentration (usually in leaves).

reference:
Zhu, Ort, and Long 2008 "What is the maximum efﬁciency with which photosynthesis can
convert solar energy into biomass?" Current Opinion in Biotechnology.

According to Zhu et al,, 2008 the maximum observed conversion of photosynthetic energy to biomass is 6% at 30C. I am not sure why there is a discrepancy, but Wikipedia has no citation nor reference temperature and Zhu et al do not consider CAM plants or algae.

Great reference that I wish I had seen before posting. If I'm reading it right, the 4.6 and 6% figures are theoretical. They give the highest observed efficiencies as 3.4 and 4.3% (C3 and C4 respectively), so values in the WP article are very high.

Yep, you are correct, I read a good bit of the article, but when it came to writing down the numbers I just grabbed them from the Abstract where they are called "maximum
conversion efficiency of solar energy to biomass", in the text they explain that this is the theoretical max. The numbers you give are short term max reported values (for the record, the C3 value is 3.5%, second line of p 157). I changed your answer.


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Conjugate secondary antibody
Why is the secondary antibody conjugated to the enzyme in ELISA, instead of the primary antibody? Wouldn't it be easier to conjugate the enzyme to the primary antibody?

Making an antibody-enzyme conjugate isn't trivial. By using a primary/secondary set-up you can use the same well-characterised conjugate in combination with many different primary antibodies (as long as these primaries are all raised in the same species). There is also the possibility of some amplification: for example, if the secondary is an anti-Fab then two secondary Igs will bind to each primary.
Response to OP comment
Most primary antibodies in common use are derived from rabbit or mouse, and most are IgG. So, for example, the secondary antibodies goat anti-rabbit IgG and goat anti-mouse IgG will cover most experiments.

In other words; otherwise you would have to make a conjugate for every primary antibody?

Yes, that's right.

@ZafarS: in fact, that is what you do for most immunological techniques, like Western blotting, immunohistochemistry etc.: use an unconjugated primary and a conjugated secondary.

@AlanBoyd Sorry, I still have some doubt whether I grasp secundary antibodies. Every species has (or better: can have) a secondary antibody per animal right? So for example; we can have secondary antibodies for primary antibodies of rabbits, chimps, mice, etc. So that would still be a lot of possible secondary antibodies, but anyway less than primary antibodies.

This answer could be improved with an explanation that many times primary antibodies are monoclonal, providing a high degree of specificity to the interrogation of the protein in questions and reducing off-target binding, while the secondary ABs are polyclonal and will bind to multiple sites on the primary AB, thus increasing the signal, say of a fluorescent marker, HRP, or radioactive probe. Though alluded to, cost and time of preparation are important considerations. You can have a stock of goat-antirabbit secondary ABs that will work with every assay you use a rabbit primary AB.

Another reason that secondary antibodies are used is to look for the production of antibodies by a test animal. Follow me for a second with an example that I think will make it clear.
Our Purpose:
We have identified a protein (call it 'V_Entry') that is vital for Ebola to infect human cells.
We wonder if antibodies against V_Entry will block Ebola infection.
We then use this V_Entry protein as a vaccine in a clinical trial.
Our Question:
Do patients have generate their own anti-V_Entry antibodies as a response to the vaccine. (note: at this point we are not addressing whether these antibodies will be protective or not- that's a separate question)
Our basic protocol:

Day 0: Take blood sample
       Vaccinate patients
Day 14 Take Blood Sample
       Booster Patients
Day 30 Take Blood Sample

To test the ability of the vaccine to generate an antibodies specific to V_Entry, we will assay serum from our cohort via ELISA.
Our Test:
(I'm ignoring controls and other details here to be clear)
Coat ELISA plates with V_Entry protein
Add aliquots of serum from each of out patients at each timepoint.
Wash
Add a secondary antibody conjugated with a detection enzyme
Wash
Add substrate for Enzyme
Allow Enzyme to develop the substrate (usually colorimetric)
Read on a plate reader
Some expected results:

Nothing happens - a control well works, but none of our patients
show antibody generation

Patients have pre-existing antibody that binds V_Entry (maybe these people were already exposed to Ebola?)
Patients have no pre-existing antibody, but they generate antibody in response to the vaccine (control patients not given
vaccine show no new antibody)

Why Secondary Antibody was Necessary:
We can't practically label every antibody made by the patient, but we can use a secondary antibody (perhaps Goat Anti-Human IgG) to detect any human IgG that has stuck to the V-Entry on our plate.
Was this a long run for a short slide?
I considered making a slide for each step of the protocol, but I started wondering if I'm avoiding something...


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In a human, what non-germline cells have the highest/lowest mass?
I'm just curious which cells are largest/smallest in the human body other than sperm/ova.

Definitely by mass or by length?

Am I missing a clue or is this as straightforward as: biggest cell - ovum, smallest cell - sperm? Or are you only concerned about non-germline cells?

Sorry to move the ball @Armatus, but yes, I was thinking non-germline (I give you a comment upvote anyway for the "real" right answer).

Definitely by mass @Rory M♦

Large cells: adipocytes, the cells that store fat are possible the largest in humans, because after puberty they rarely divide and just enlarge if a person gains weight. A typical adipocyte is about 0.1mm in diameter, but may be a lot larger. Another good candidate is a megakaryocyte, which is a gigantic (up to 0.1mm), cell with multiple copies of its genome producing blood platelets. Depending on your definition of a single cell, also myocytes may be considered large cells, because during development several cells fuse to form one muscular fibre. Additionally, myocytes gain weight if a person excersises and strengthens muscles.
Small cells are more common, and it is difficult to point to some consistently smallest cells. The smallest kind-of-cells are definately platelets and erythrocytes (red blood cells - they are anucleated, thus may not be considered "real" cells). Generally, the part that determines the minimum size of the cell is the nucleus, so any cells, that are more-or-less metabolically inactive may be just a tiny bit larger than the size of their nucleuses. These may be for example polar cells, the tiny cells, that carry the excess of genome during meiosis in women and die soon afterwards.
If you are interested in all kinds of strange cells inside yourself, you might start by browsing this beautiful, though longish list.

If multiply nucleated cells count, the syncitiotrophoblast of the placenta is a big candidate :)

Right, I forgot about that one. I think I just focused on adult cells.

Are nerve cells not larger (1 meter or more)?

Quote: Definitely by mass @Rory M♦ – joseph_morris 2 days ago

If tissue density is constant, then volume is proportional to mass. I would posit that a very long axon has more volume than an adipocyte.

Long human axons are up to 20um in diameter, their bodies are very small, so I think we can assume, that such a very long human axon is a long, thin tube of 20umx1m. This means it's volume is about 31,400,000um^3. If a large adipocyte is 0.2mm (200um, same source as previously) in diameter and a sphere, it is 4,190,000um^3. So yes, an extremely long axon is larger than a large adipocyte, but I could go on searching for a largest adipocyte known to science and I'm almost certain, that I could find something larger ;)


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Action Potential Distribution On Synapses
This is a biology+physics question. Since there is no biology section, I am asking here.
In brain, when a neuron reaches to threshold value, it fires an action potential. In most graphics, that is shown as 40 mV. An example is

Neuron's this potential reaches to all synapses where this neuron is connected to, and chemically transferred to other neuron and transformed into electric charge again.
My question is, because in artificial models not shown, if that whole 40 mV is distributed to those synapses according to synapse strengths, or do all synapses take a total 40 mV which is like creating a potential while it is not there?
Another small question is if the collected potential is stored in neuron if it cannot reach to threshold value like a capacitor in circuit?

I'm migrating this because you probably would've posted on [biology.se] first if you'd known about it, and it doesn't look like you're going to get the answer you're looking for here.

Can you revise your question? I am not sure what you mean when you say the "whole 40 mV is distributed" versus "a total 40 mV" which is "not there."

Well, it is about electron movements actually. That's the reason I have written it is biology+physics question. Normally, in an electric circuit, if you have 40 mV in circuit, this voltage is divided according to resistance in parallel wires. I mean electrons are divided, but with resistance it can be defined as voltage. Anyway, neurons send their signals to other neurons by both electric charge on axon and chemical at synapses. My question was if that electric charge is shared when the active potential reaches to where axon starts making branches to axon terminals.

I think you are really wondering how axonal morphology affects the voltage along the axon. The short answer to your question is that each synaptic terminal sees the same voltage because that voltage is generated "fresh" at each site. This has nothing to do with synaptic strength, which determines the amount of voltage deflection in the postsynaptic terminal but not in the presynaptic terminal.
The axon has two major properties that allow for this even activation across its branches. First, as @Armatus said, the axon is an active structure, meaning that the action potential (AP) regenerates as it travels along the axon. This means that there is essentially no decay of the voltage as the AP propagates.
Second, the axonal geometry appears to be carefully regulated. As you seem to have guessed, there has to be sufficient current flow to activate an action potential in the neighbouring patches of membrane or else there is a propagation failure and the AP stops. This is a problem at axonal branch points (see Box 1 in Debanne, 2004), where the diameters of daughter branches have to be correctly sized so that there is little or no extra electrical load. (For instance, if one branch stays the same size as the mother, the other branch is an extra load that will "steal" current and leave less current travelling down the mother branch). Recent work using voltage-sensitive dyes have shown that in mammalian neurons, in practice, propagation failures are rare (Foust et al, 2010). This suggests that there is fine regulation to ensure that the geometry is "just right." (Those "just right" rules are basically governed by cable theory, which I've previously described here.)
To your last question, yes, there is time-dependent decay of subthreshold potentials because the membrane is a capacitor (~1 uF / cm^2). I wouldn't call this "storage" exactly, but it does work just like a capacitor in a circuit. Many people think of the membrane as a capacitor and a resistor in parallel.

Debanne, D., 2004. Information processing in the axon. Nature Reviews Neuroscience 5, 304–316.
Foust, A., Popovic, M., Zecevic, D., McCormick, D.A., 2010. Action Potentials Initiate in the Axon Initial Segment and Propagate through Axon Collaterals Reliably in Cerebellar Purkinje Neurons. J. Neurosci. 30, 6891–6902.

Action potentials are governed by the ion concentrations on different sides of the membranes. When an AP is triggered locally, it spreads because the ions which travel across the membrane during the AP spike diffuse to neighbouring regions and trigger the same response in the ion channels there.
Hence, it is irrelevant where an AP is, it is always the same voltage. The 40mV are not "distributed" at all - they diffuse and cause new depolarisations around them, triggering new 40mV potentials until they reach the neuron terminals. So in a way, yes, the AP propagates by "creating a potential while it is not there". All terminals will have the same 40mV potential (the exact voltage of course may be different between cell types).
Potentials which do not reach the threshold value are stored to some extent. This is in the sense that potentials around neurons are always established by ion gradients - a potential in your sense means a change in concentrations from the resting state. Until the concentrations are normalised again by the various transport mechanisms for ions across the membrane, the potential across the membrane will remain changed and it may be closer or further away from the AP threshold.

I need to get my essay in by thursday so I can't spare much more time right now, but if someone bumps this on thursday night I can gather some further reading :)

I liked your answer. As far as I understand, there is no connection between strengths of different synapses of same axon also. This has collapsed all the theory I was telling myself. Anyway, I want to ask one last question. Is it discovered that what kind of events change the value of threshold, or maybe is it fixed for all neurons?

I would make the guess that the voltages (resting potential, AP, threshold) are characteristic for each neuron type, but can be changed for individual cells according to circumstances, like most things about neurons.

Threshold is not fixed, even within a single neuron over short periods of time. Fundamentally, threshold is reached when enough voltage-gated sodium channels open so that a rapid depolarization occurs--that is, when inward current is much greater than outward current. When this occurs is a complicated function of membrane resistance, leak currents, the recent history of the membrane, other inward currents present, the kinetics and voltage-dependence of outward currents, etc., etc.

@Armatus, the ions that flow in through ion channels during the action potential are almost certainly not the same ions that carry current axially to depolarize adjacent sites. The charge travels (that's what current is) but the ion fluxes are local.

Both of you guys have given quite good information. I appreciate it. I have one little question. This is the last one I think about this topic. Is it possible that when 40 mV reaches to axon terminal, it is raised let's say 45 mV? Technically speaking, can I say min and max transferred potential everytime between -40mV and +40mV according to excitatory or inhibitory effect?


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Preferred Aspect Ratio for Human Eyes
Our eyes are spherical, our retina is circular, but still our eyes can see more in the horizontal direction than in vertical direction. Why is it so, why is the preferred aspect ratio not square?

This is just a hypothesis: but there is probably not one "preferred" aspect ratio, even for one individual. It probably has to do with the following points: 1. the eyes are positioned on a horizontal line; 2. the width between the irises; 3. how far you are looking.
And let's not call it a "preferred" aspect ratio. It's more like an "effective" aspect ratio. My hypothesis is that the closer you look, the wider the effective aspect ratio is, and the further you look, the more circular it is. And if you cover one of your eyes, you'll probably get a circular FoV regardless of distance.

I have to agree with Kal, but mainly about #1. Essentially, the eyes are next to each other, and this allows for stereoscopic vision. If you cover one eye, your field of view is more or less circular (due to the retina and macula), but you'll lose depth perception. Plus, your eyelids slightly limit the amount you can see in the up-down directions.

@jello Surely the eyelids can't be having an effect as you describe because they don't normally cover any part of the pupils.

@AlanBoyd I think you're right. For some reason, I was probably thinking about ptosis, when a drooping eyelid does limit your visual field.

I will add that in other animals, having a wide horizontal angle helps in hunting and also in defending against hunters. The vertical angle is also important, for example for hunting birds, but not so much for terrestrial animals.

I found the explanation given below here (my emphasis). It may not be authoritative, but it makes sense to me.

You can determine the approximate shape of your visual field by looking straight ahead, and holding a hand out to each side and noticing where you can no longer see them. Do the same for above and below, and you'll see that your peripheral vision probably extends to about 180 degrees (or a little less) left and right, and about 100 degrees up and down. Your brow, nose, and cheeks narrow the vertical angle.
So your visual field has a ratio of about 1 to 1.8.
Interestingly, and not entirely coincidentally, ordinary films and wide-screen TVs have a ratio of 1.78 (16:9).

Another way to see this effect is to look at someone's head in profile and from directly above. In the former  case you have a clear view of their eyes, in the latter you don't. (Tested on a small sample - one 3 year old male, playing with an iPad).

The reasons your field of view is not circular are:

Even when looking directly forward your nose, brows, and cheeks obstruct your view.
You have two eyes which are aligned horizontally.

The field of view is measured by a method called perimetry, and looks approximately as depicted in this graphic. The guide here provides further comments on the graphic.
As you can see in the image I linked to, the field of view (were it to be approximated with a rectangle) spans 180° horizontally and 130° vertically. Yielding a width-to-height ratio of 0.72. Which is better approximated by the traditional 4:3 screen size and NOT by modern 16:9 displays. Having said that, 16:9 may not necessarily be a worse format, as researchers found that horizontal saccades are faster than vertical ones.


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(Web)app to search metabolic/signalling pathways
I'm looking for an application where you can find pathways by selecting a chemical occurring in it.
So, for example,
selecting 6-phosphogluconolactone brings up the pentose phosphate pathway or any other where it occurs as an intermediate or product.
Same could be possible for endocrine or any other signalling. The target organism is human.
Is there anything like this in existence?

KEGG  http://www.genome.jp/kegg/kegg2.html
GLAMM http://glamm.lbl.gov/
I had to truncate to gluconolactone to make the search work in both cases.

Thanks, the first seems better though less fancy.

Many would agree with you; KEGG may be the best established pathway database of all.

KEGG has also a very nice API, if you plan some automatable tasks.


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How is transport of glucose into prokaryotic cells different from transport into eukaryotic cells?
I was reading page 92 of Fundamentals of Microbiology, 4th edition, which states

In facilitated diffusion, the substance (glucose, for example) to be transported combines with a plasma membrane protein called a transporter.

The section of text that says this is in a section describing prokaryotic cell anatomy. As far as I understand human biology, (just to use one example) that facilitated diffusion is regulated by insulin, which, to use less than perfect language simply to streamline my question, uses insulin to "unlock" the plasma membrane proteins.
What's the difference when prokaryotic cells aren't dependent upon insulin to get glucose in?

In prokaryotes the glucose transporter is always present in the cell membrane; in cells whose glucose uptake is insulin-regulated the transporter is only present in the plama membrane when hormone levels are high.
GLUT4 is the isulin-regulated glucose transporter found in muscle and adipose tissue. When insulin levels are low the GLUT4 protein is in the membrane of small vesicles inside the cell. The appearance of insulin signals the fusion of these vesicles with the plasma membrane. In this way the number of GLUT4 molecules in the plasma membrane is increased, raising the capacity of the cell for glucose transport. GLUT4 transports glucose into the cell by facilitated diffusion.
More information about the GLUT family of glucose transporters can be found here.

Interestingly, bacterial and eukaryotic glucose transporters are similar in structure, though bacteria do not have insulin. http://www.ncbi.nlm.nih.gov/pubmed/23075985


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Where does all the carbon go?
I found it hard to get numbers on global primary production, but apparently it's somewhere around 50-60 $Gt / year$ for carbon content in the terrestrial production, and a similar figure for the oceans. Global oil and coal extraction together are around 10 $Gt/year$, only a part of which is pure carbon (iirc, around 80%). Since carbon in the air actually increases, does that mean that most or all of the carbon fixed in Net Primary Productivity go back into the atmosphere through consumption and destruction of the biomass?
I was assuming that the biosphere in total was fixing more carbon that it emitted, and that the surplus was what turned into oil and coal. But with these figures it looks a lot more like a full circle that nets to zero input / output. Which is true, or is that unknown?

NPP? Gt/a? it's good practice to expand abbreviations

@GriffinEvo probably $Gt/a$=gigatons/acre and $NPP$ is Net primary productivity.I am not sure enough to edit the question to include this.

@satwik pasani I am sure about the second one, edited in the question.

I believe most of it goes into the oceans

... where it causes acidification H2O + CO2 <-> CO3H2 carbonic acid.

Good question! The way that the carbon budget stays balanced was a bit of a mystery until recently. The amount of carbon in the atmosphere (and the rate at which it was increasing) was lower than models suggested that it should be, given rates of photosynthesis, respiration, and other carbon releasing processes. Somewhere, there was a "missing carbon sink" that wasn't being accounted for. After many years of debating whether the sink was terrestrial or aquatic, it turned out to be a little of both (which is the conclusion to just about every debate in ecology), although somewhat skewed towards the terrestrial (I think). Forests were sequestering more carbon than had been thought, and so were oceans to some extent (although ocean sequestration relied on a chemical reaction that is in danger of reversing if the water warms up too much). For a thorough account, see this article.
But it sounded like you weren't wondering what the missing sink was so much as how there continues to be enough carbon in the air for plants to photosynthesize (if I'm interpreting your question correctly). Carbon gets back into the air for the most part because of cellular respiration, which all organisms, including plants, do. Net primary productivity takes plant cellular respiration into account, but there are still tons of living things on earth eating plants (and thus taking in their carbon) and then breathing it back out after they break down the carbon-containing molecules for energy. There is also natural combustion and volcanoes and such putting carbon back into the air.
EDIT (to address the new part of your question): Oil and coal were produced when large quantities of carbon were buried deep under ground (and thus subjected to lots of pressure) for thousands of years. This is suspected to have happened during the aptly name Carboniferous era, which featured giant plants and, scientists hypothesize, no decomposers to break them down. Since we have much decomposers now, and much smaller plants, oil and carbon are not currently being produced. This is why we call them non-renewable resources. By extracting them from the ground and burning them, we are taken carbon that had effectively been removed from the pool of actively cycling carbon and adding it back in.
The carbon cycle doesn't really have input or output (except the occasional carbon exchange with outer space), because it is defined as already including standing sinks like oil and coal. When we take carbon out of a sink, like oil or coal, it needs to go somewhere else. Terrestrial and aquatic sinks can store some of the additional carbon that we're adding to the not-underground part of the cycle. However, they can't store all of it, so some is staying in the atmosphere instead.

So is the biosphere overall a carbon sink, or is it exactly balanced without anthropogenic emissions?

There are sinks and sources within the biosphere. Overall, the sinks are not enough to balance anthropogenic emissions, hence the rising CO2 content of the atmosphere. The mystery was just over why CO2 content was not rising more quickly than it already is, and the answer was that the biosphere contains more sinks than we had initially realized.


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Are there known minimal marine ecosystems that are stable?
A more entertaining phrasing of the question would be "what would a marine ecologist put into a perfect aquarium?"
I was reading about Prochlorococcus, among other photoautotrophs, and found that they seem to get their nitrogen from ammonia, which must be produced by some other organism. This set me off wondering what different species I would need in a hypothetical aquarium (how big that would have to be is another question, I guess), such that a sustainable ecological equilibrium occurs (one different from everybody dead, I guess), only requiring sunlight and air from the outside.
I realize that I'll have to put other components like iron etc in the water, but let's say I only put some fixed amount in during setup. What exactly that would have to be is probably another can of worms, so let's keep that out of this question as much as possible.
Has there been research towards such model ecosystems, and are there known minimum configurations?
It's hard to give an authorative "no" to this answer. But maybe there's research that looked for such a system and failed, or maybe marine ecologists use model cultures in their labs that show instabilities (meaning the culture dies, you have to replace the water, or keep adding fertilizer, or keep removing some waste) which allow some generalizations.

This is the one I've heard of - Its a sealed acrylic globe that contains algae and brine shrimp.  There are quite a few references in the bibliography here to previous systems.
Of course, it needs sunlight, but all the elements are recycled.  Its really closed and has reasonable endurance.

The basic commercial version of his closed world -- sold under the label of "Ecosphere" -- is a glass globe about the size of a large grapefruit. My world #58262 was one of these. Completely sealed inside the transparent ball were four tiny brine shrimp, a feathery mass of meadowgreen algae draped on a twig of coral, and microbes in the invisible millions. A bit of sand sat on the bottom. No air, water, or any other material entered or exited the globe. The thing ate only sunlight.
The oldest living Hanson-world so far is ten years old; that's as long as they have been manufactured. That's surprising since the average life-span of the shrimp swimming inside was thought to be about five years. Getting them to reproduce in their closed world has been problematic, although researchers know of no reason why they could not go on replicating forever. Individual shrimp and algae cells die, of course. What "lives forever" is the collective life, the aggregate life of a community.

All of this is a real subject of research for those interested in creating entirely useful ecosystems.

It turns out that ecospheres scale up well. A huge commercial Ecosphere can weigh in at 200 liters. That's about the volume of a large garbage can -- so big you can't reach your arms around it. Inside a stunning 30-inch-diameter glass globe, shrimp paddle between fronds of algae. But instead of the usual three or four spore-eating shrimp, the giant Ecosphere holds 3,000. It's a tiny moon with its own inhabitants. Here, the law of large numbers takes hold; more is different. More individual lives make the ecosystem more resilient. The larger an Ecosphere is, the longer it takes to stabilize, and the harder it is to kill it. But once in gear, the collective give and take of a vivisystem takes root and persists.

Unfortunately larger systems that can support people have not been made yet.

Algae and man lasted a whole day. For about 24 hours, man breathed into algae and algae breathed into man. Then the staleness of the air drove Shepelev out. The oxygen content initially produced by the algae plummeted rapidly by the close of the first day. In the final hour when Shepelev cracked open the sealed door to clamber out, his colleagues were bowled over by the revolting stench in his cabin. Carbon dioxide and oxygen had traded harmoniously, but other gases, such as methane, hydrogen sulfide, and ammonia, given off by algae and Shepelev himself, had gradually fouled the air. Like the mythological happy frog in slowly boiling water, Shepelev had not noticed the stink.

Here is an academic reference you can use to start looking around if you like...

Very nice answer. And very interesting.


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Do SSRIs downregulate or upregulate the 5-HT3 receptor?
What effect do SSRIs have on the expression of the ligand-gated ion channel, the 5-HT3 receptor?

SSRI's theoretically increase Serotonin levels.  Serotonin is an agonist to the 5HT-3 receptors. The 5HT-3a primarily associated with the upper gut and the 5HT-3b with the lower gut.  I would guess that theoretically again, SSRI's would tend to increase nausea, emesis, and diarrhea.  There may be other effects, but these are the ones I have researched.
The anti-emetics Dolasetron, Ondansetron, Granisetron, and Tropisetron are 5HT-3 antagonists.

You didn't answer the question. I asked what effect SSRIs have on the expression of the 5-HT3 receptor, not its signalling. I already knew that SSRIs would serve as an indirect agonist of the 5-HT3 receptors, but my question was would it affect the expression (think gene expression) of the 5-HT3 receptors!


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Which Enzymes Catalyse the Deacetylation of Drugs in the Human Body?
If you would like more specifics seeing how I realise that this question is very broad and may be difficult to answer in general then hopefully the following will help you out:

I am particularly interested in acetyl groups bound by carbon single bonds
Drug metabolism in the liver particularly interests me
The drug paracetamol's (acetaminophen) deacetylation to p-aminophenol is of particular interest to me.

Acetyl esters can be deacetylated by carboxylesterases.
In case of an acyl/aryl group attached to acetate group (e.g., benzoate), I guess it will first undergo ring opening and then beta oxidation (as in case of tyrosine).
Paracetamol -> p-aminophenol is a deamidation (I am not sure, but enzymes like ornithine decarboxylase can do that job... just a guess).


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Does the NMDA antagonist, Memantine that's used to prevent Excitotoxicity cause brain damage?
Does the NMDA antagonist, Memantine that's used to prevent excitotoxicity in Alzheimer's disease (AD) and Dementia with Lewy Bodies (DLB) cause brain damage? I know that in rodents NMDA antagonists like ketamine and phencyclidine (PCP) cause a form of brain damage known as Olney's lesions. Despite Olney's lesions never being directly observed in primates like humans, permanent brain damage from chronic ketamine exposure has been observed in adolescent cynomolgus monkeys.1
Reference List

Sun, Lin; Qi Li, Qing Li, Yuzhe Zhang, Dexiang Liu, Hong Jiang, Fang Pan, David T. Yew (2012). "Chronic ketamine exposure induces permanent impairment of brain functions in adolescent cynomolgus monkeys". Addiction Biology. doi:10.1111/adb.12004. PMID 23145560.

Yes, it does cause lesions in rats, although I don't think it's been observed to do so in humans.
See: http://www.druglib.com/druginfo/namenda/description_pharmacology/

Thanks, mate. That's helpful for me, of course in human studies would be more helpful but c'mon there's no such studies on the most widely-used NMDA antagonists like ketamine and PCP so I can hardly expect it for memantine -- a drug I had trouble finding evidence even in rodents.

@BrentonHorne Apparently, memantine might cause hallucinations in humans (N=3): http://jnnp.bmj.com/content/78/5/546.1.short

What do you mean by N=3?

N is commonly used to refer to sample size (at least among the biologists that I've spoken with).  The article I linked is a case study of 3 individuals.  My point is that this is an extremely small number of individuals with documented adverse affects to memantine. If you want to read the article, you can read the 1 page preview (as an image)...the whole article happens to be 1 page.

Ah, thanks, I assume you're talking about hallucinations because it makes the link between its NMDA antagonist activity and potential brain damage more clear by demonstrating that it has one of the effects characateristic of NMDA antagonists, i.e. hallucinations.

Yes, I did mean the hallucinations.


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What effect do oligosaccharides, like those found in legumes, have on the composition of intestinal flora in humans and if so how so?
I know that intestinal flora metabolising oligosaccharides, like those found in legumes, is the cause for the well known fact that legumes cause flatulence, but does an oligosaccharide-rich intestine change the composition (i.e. which specific bacteria make it up) of intestinal flora in humans?

The answer to this is fairly complex, and it depends on whether you are talking about short-term or long-term changes to the microbiota.
When talking about short-term changes, the answer is almost certainly a resounding yes. Any ingested nutrient will lead to an increase in the growth rates of bacteria capable of metabolising that nutrient, and will therefore lead to a change in the composition of the intestinal microbiota.
This is, unfortunately, difficult to observe, as most studies of the intestinal microbiota use fecal samples to look at intestinal microbial composition. Since stool represents an average of what happens between two bowel movements, it is difficult to draw inferences about short-term changes in the microbial composition of the bowel. However, there is evidence from Pythons that suggests extensive remodelling of the microbial composition does indeed occur, at least in animals with less regular feeding schedules.
In the case of long-term changes, there is strong evidence that specific oligosaccharides contained in human milk specifically select for certain strains of Bifidobacterium and Lactobacillus. Apart from this very specific set of oligosaccharides however, there is a paucity of studies dealing with the effects of diet on the gut microbiota, and even fewer looking at specific nutrients.
The premise that long-term changes to the gut microbiota can be made with diets is the foundation on which the entire prebiotics industry is built. The most popular prebiotics are fructo-oligosaccharide, inulin, galacto-oligosaccharide and lactulose. These are said to encourage the growth of beneficial strains of Bifidobacterium and Lactobacillus. However, there is currently no consensus on the long-term effects of these oligosaccharides on the microbiota.


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Is it harmful for someone to consume things full of bacteria if they don't get physically sick from the bacteria at all?
Or as another example - what if you touch a surface that's contaminated with potentially pathogenic bacteria (like the ones at http://arstechnica.com/hardware/news/2008/05/study-keyboards-make-excellent-homes-for-nasty-bacteria.ars) and introduce those bacteria into your body and don't get sick. Then could there be some other damage that the bacteria could do your body? Like, at the very least, maybe promote a not-particularly-noticeable increase in inflammation in the regions where the immune system decides to fight the bacteria? Inflammation only starts to get noticeable when some really high threshold gets crossed.
By "sick", I mean, that the symptoms of the infection become noticeable enough to cross the threshold of being unpleasant to the person carrying the infection. I'm sure that there may be some sub-threshold effects that come in first.
And why is this important? We have to establish some sort of balance between using too much soap/other cleaning agents and not using enough of it. If we use too much, the bacteria could develop antibiotic resistance. And if we use too little, there could be an increase in the types of bacteria that cause chronic infections that don't get noticed, even though some of us might not even get physically sick more.

There is some confusion: bacteria develop antibiotic resistance if we use too much antibiotics. If you use too much soap, what is likely is that your immune system will not find any bacteria and will develop some exagerated response against 'safe' exogeneous material (allergies) or endogeneous material (autoimmune diseases).

Some bacteria produce toxins when alive. The infamous Clostridium botulinum produces botulinum, a very powerful toxin that can cause total body paralysis in very small amounts.
C. botulinum cannot survive the acids in the stomach, but the toxin and the spores can pass through and still affect (kill) you. This is an example of a bacteria that you cannot get physically sick from just eating, but from its by-products.