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Does animal blood, esp. human, really have similar salinity as ocean water, and does that prove anything about evolution?
It is an often-repeated claim that human, and in fact all animal blood is salty because we evolved from aquatic organisms, and that blood has a similar concentration of salts as ocean water, or at least as primordial ocean water.
Is any of that true? Does science know what the salinity of the oceans was billions of years ago, and was it indeed similar to the blood of today's organisms? Does that knowledge prove anything about evolution and the origin of life?
I am wondering, because I tried to Google for the answers, and unfortunately all I could find were creationists referencing each other how it couldn't possibly be true because evolution is a lie in the first place etc., and they claim that there is no empirical research that would compare salinity levels of organims' cells and ocean water.

Related: https://biology.stackexchange.com/q/74748/3340

'blood is salty because oceans are salty, and life began in oceans' is a weird way of putting it. Can you cite non-creationist sources that put it this way?

Do you have any citation for this claim being "often-repeated"? I've spent quite a bit of time studying literature on both sides of the evolution and creationism debate, and I can't remember ever seeing this argument having been made. I'm quite curious where you ran across it and who is promoting it. It is quite absurd, so I'm especially curious if it's some kind of disinformation propaganda by anti-evolution activists.

I agree that it's most likely a creationist talking point, since several creationist websites showed up on a google search, which are mostly quoting other creationists. But there are also more reputable sources making the claim. AliceD provided one, though I can't verify it because paywall. Here is another.

Also note that freshwater fish actively retain salt, and ocean fish actively try to excrete salt. This means that animals are quite able to maintain a desirable salinity even if that's different from our surroundings. This basically means that even if the levels had been the same, it'd have proven nothing at all.

@Hackworth That's a very weird link. There's a claim that ocean salinity is similar to blood salinity, but a few paragraphs later he says the (modern) ocean salinity is four times larger. The follows the claim that early oceans were this "quarter the salinity of modern oceans", but without any reference. Indeed, there's no references in the article at all, which should already be suspicious, and I couldn't find any references to a related paper or much about the author either. And as already noted, I never saw anyone claiming this is a proof life came from oceans, except from creationists.

@Hackworth Don't forget that just because a claim was (maybe) made by a scientist isn't enough to have it be worthwhile. Scientists don't receive truths from a god of science - we've designed processes that help us separate truth from falsehoods. If the process isn't followed, you really shouldn't trust the results at all. As the article stands, it's just a bunch of unsubstantiated claims, that also happen to conflict with many things we expect about the early Earth's environment. It's may be just a retelling of the actual subject of study - e.g. how saltwater fish adapt to fresh water etc.

@Gloweye And saltwater crocodiles excrete salt on their tongue, and bull sharks can switch between salt and brackish water, regulating osmosis I think via urea.

After you maybe confusing blood with cytoplasm? Like others, Iʼve never heard this claim being made about blood, but a similar claim regarding the salinity of cytoplasm is somewhat common, and makes a lot more sense biologically.

FWIW, I recall hearing the same claim in my high school health class nearly 20 years ago (in a classroom video that seemed old back then). Not that necessarily qualifies as "often-repeated", but anecdotal evidence of the claim dating back a while. (Though I'm not sure how that fits into the creationist/evolution "debate", I'd think evidence that life began in oceans would run counter to the standard creationist viewpoint, no?)

Short answer
Early sea water had a very different osmolality than blood plasma.
Background
The reference range of serum osmolality is 275–295 mosm/kg (mmol/kg) (MedScape). The osmolarity of sea water is about 1000 mOsm/l (Wikipedia), but it can vary substantially between different seas, namely between 642 and 1,480 mOsm/kg (Ninawe & Banik, 1998). Nonetheless, the range of osmolalities are substantially higher than that of serum. That's why we cannot consume sea water, without losing more water than gaining it (NOAA). According to Astro Biology Magazine, the salinity of early oceans 3.5 billion years ago, when life first developed, was even higher. So popular accounts that they are the same and that this has important evolutionary consequences are likely far-fetched.
Reference
- Ninawe & Banik, J. Mar. Biol. Ass. India (1998); 53(2): 230-36

Do you have any idea why the oceans were MORE salty in the past? I thought they are salty because water brings salt to them from surface and then evaporates, so I naturally expected them to be less salty in the past. This really surprised me.

I'd think that the salinity or osmolality of the oceans when tetrapods' ancestors first started venturing on to land (around 400 million years ago) would be a lot more important to the argument than what it was when life first developed.

I think the two pieces this answer is missing are a) Some reference to the first animals, which were likely osmoconformers (since modern sponges and cnidarians are), and b) Relative ion concentrations and the consistency of high extracellular sodium/high intracellular potassium, which user1136's answer touches on: this is the way that blood and ocean are "similar" even if total osmolarity is not.

Just a caution for anyone who is tempted to directly compare the numbers provided, you will have to first change units. The blood concentration is given in mOsm/kg, and the ocean concentration in mOsm/L. Since these are salty solutions more concentrated than pure water, it would not be appropriate to use the density of water and say 1 L = 1 kg. The density of the actual solution would have to be used. However, the orders of magnitude of these concentrations are probably still appropriate for direct comparison and lead to the same conclusion.

@electronpusher - good point. I should've converted those numbers. Can attempt to correct them in the future.

It is said that nearly all terrestrial reproduction and sperm/egg fertilization takes place in fluids just like it does for ocean fish. Mammals, insects, spiders, all have sperm and eggs that are designed like their ocean cousins. It's a stronger evidence for evolution than blood chemistry, all terrestrial animals have kept a sea-like environment in their reproductive regions.

The argument that blood plasma resembles sea-water, in essence, relies on the notable similarity in concentration of two ions in plasma and sea-water, compared with their intracellular concentration: sodium and potassium.

The concentration of sodium-ion in sea-water is about 450 mM, whereas the concentration of potassium-ion is only about 10 mM (ref)
The plasma concentration of sodium-ion is about 140 mM and the concentration of potassium-ion is about 3-5 mM (ref, but many clinical biochemistry sources will confirm)

That is, both plasma and sea-water are 'high-sodium, low-potassium' and the concentrations are remarkably similar.  If we contrast this with the intracellular concentration of these ions:

The intracellular concentration of potassium-ion is about 150 mM, whereas the concentration of sodium-ion is about 10-20 mM (ref)

That is, the 'intracellular milieu' is 'high-potassium, low-sodium'. Blood plasma, of course, is considered an extracellular fluid.
We can generalize further and say (Skou, Nobel lecture):

The intracellular concentration of potassium-ion is about 150 mM whereas extracellular concentration is about 4 mM.
The intracellular sodium-ion concentration is 10-20 mM whereas the extracellular concentration about 140 mM

Thus sea-water, in terms of sodium-ion and potassium-ion concentrations, resembles the extracellular milieu, leading to the somewhat hyperbolic view that "blood can also be thought of as a private ocean...".
But the similarities are striking.
At one time it was thought that this concentration difference was due to cells being impermeable to sodium-ion, a hypothesis first put forward by E.J. Conway.
It is it now known, of course, that concentration imbalance is maintained by the sodium-potassium pump, which is present in animal cells but not in plant cells (W.D. Stein). The presence of this pump allows animal cells to be in osmotic equilibrium (no change in osmotic pressure) with their surroundings. (Plant cells, in contrast, have developed a cell wall that allows high internal osmotic pressures and which may (to again quote Stein) "have condemned [them] to a largely sessile life")
The history of its discovery (and much more) is given in The Identification of the Sodium Potassium Pump, the Nobel lecture by J.C. Skou
Addendum 1: Historical Origins
According to a review by Mulkidjanian and colleagues, it was Macallum in 1926 that first drew attention to the similarities in inorganic composition of sea-water and plasma and its significance as evidence that the first animals emerged from the sea.
I think R.L. Berg (see Addendum 3), at a famous conference in 1957, also drew attention to this, but I do not have access to the reference.
But just because animals emerged from the sea does not necessarily mean that life began in the sea. Mulkidjanian and colleagues point to the fact that "inorganic composition of the cell cytosol dramatically differs from that of modern sea water" (which was also first pointed out by Macallum in 1926) may indicate that life began in a high-potassium, low-sodium environment and that life in the sea only became possible after the evolution of the sodium-potassium pump allowed organisms to maintain their 'fundamental biochemical architecture' (the chemical conservation principle).
These authors suggest condensed geothermal vapours as a likely environment for life's origin but not everone agrees.
I notice from the comments that the similarity and blood plasma and sea-water is considered somewhat heretical and perhaps not sufficiently backed up by evidence. This viewpoint has a long history in 'mainstream' science.
Pearse in The migrations of animals from sea to land (1936), for example, has this to say:

The general similarity of the bloods of animals to seawater has been interpreted as indicating that all animals originated in the sea.
...
While there are many discrepancies to be explained, it is a common belief that "blood is modified seawater" (quoting Pantin,1931).

Another good source with some great references is The Oceans, Their Physics, Chemistry, and General Biology (1942) by Sverdrup, Johnson and Fleming, which is available as an e-book, especially the section in Chapter VIII on Sea Water and the Body Fluids.
Finally, there is nothing 'creationist' about the above arguments, but creationists, in the main, don't like them.  See Is the Sodium Chloride Level in the Oceans Evidence for Abiogenesis? by Bergmann, for example.
Although I do not agree with any of the views expressed in this article (especially the view that the Flood "likely carried to the earth’s surface  many  tons  of  pulverized  crustal  material containing large amount of salts and other minerals"), it contains many good references to the 'mainstream' point of view (which the author attempts to debunk).
Addendum 2: Serum and Plasma
Plasma is liquid component of blood that is clinically obtained as the supernatant (upper 'layer') generated by centrifuging blood collected in the presence of an anti-coagulant such as heparin or EDTA.
Serum is plasma without clotting factors and is clinically obtained by first letting blood clot, centrifuging, and then collecting the supernatant.
Both serum and plasma are considered extracellular fluids, in contrast to cytoplasm, which is the intracellular fluid that 'holds' the organelles and other cellular components.
There is no clinical difference in serum and plasma sodium levels, but serum concentrations of potassium are somewhat lower (about half-millmolar or thereabouts) than those of plasma (ref)
Addendum 3
It appears that the  R.L. Berg quoted above is Raisa L Berg, the eminent Russian Darwinist and geneticist who, among many other achievements, wrote In Defense of Timoféeff-Ressovsky.
As I stated above, I do not have access to the original reference but R.L Berg is quoted in Bergman's article (also quoted above) as follows:

Berg  (1959,  pp. 169–170)  notes,  “The  most important arguments in favor of the hypothesis that life originated exclusively in the ocean” are, first, “the similarity between the salt composition of the body fluids of land animals and that of the waters of the ocean.”
He [sic] then adds that the “similarity in the salt composition of the waters of the ocean and that of the body fluids of land animals could be accounted for” only by evolution (Berg 1959, p. 170).

It would be very nice to have her views recorded 'first hand' here (the OP question has generated a lot of interest).
Perhaps someone with access to the article could post a separate answer?
Addendum 4
Adrian (in a comment) has drawn attention to the following quote,
from the best-selling book The Sea Around Us by Rachel Carson, first published in 1951:

"Fish, amphibian, and reptile, warm-blooded bird and mammal - each of us carries in our veins a salty stream in which the elements sodium, potassium, and calcium are combined in almost the same proportions as in sea water."

Congratulations on an excellent answer. I am travelling at the moment, but will see if my University library has access to the article on my return, although if it is in Russian I won’t be able to translate it myself.

I am having trouble in tracking down the the paper of R.L Berg in First International Symposium of The Origin of Life on the Earth, Moscow, August 19-24, 1957. My University Library does not have a copy or online access, and they won't process my Inter-Library Loan request (The British Library will have a copy) because I don't know the title and page numbers for them to photocopy. Apologies.

I found this answer after reading a passage in The Book of Eels, by Patrik Svensson, which references a passage in Rachel Carson's The Sea Around Us (see https://www.goodreads.com/work/quotes/2423508-the-sea-around-us, "each of us carries in our veins a salty stream..."), so this idea has been mentioned in popular science books for several decades now.

@Adrian Thanks!  I have included the quote as an addendum to the answer (comments can get deleted... )

This is the link to the report by Berg in the symposium on "The Origin of Life on the Earth": https://doi.org/10.1016/B978-1-4831-9737-1.50023-0 (paywalled). Interestingly, just this chapter costs 22 Euros on Elsevier but I found the first volume of the proceedings for 14 Euros (the actual citation by the Bergman article; on this site: https://www.booklooker.de/).

Great answer, very thorough. The quality we should all strive for.

Even shorter answer: This can be easily (well, not that easily since you need to convert mols to milligrams) answered by looking at your last lab result.
Say you had Na: 135 mmol/ml on there which would be a plausible value. That's 135*22.88/1000 mg/ml or 3.1 g/l. Sea water has around 19 g/l, so that's a clear, definite "no".
It wouldn't be quite such a strikingly obvious "No!" if you had asked about osmolarity instead of salinity. Because unlike blood, oceans usally don't have significant amounts of plasma protein. The answer would still be a clear "No" (for non-fish animals, anyway), but not nearly as strikingly.


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Is there any evolutionary reason for why some organisms (wrasse) change their sex in adult stage?
In San Francisco, I saw this fish:

and quoting the aquarium's page:

Part of the wrasse family, the California sheephead is a protogynous hermaphrodite. Simply put, all sheepheads are born as females, but eventually transform into males. Due to hormonal changes triggered by environmental and social cues, this fish can go from a reproductively-functional female to a fully-functional male.

I have never heard of something like this for any organism. Is this behavior unique?
But the real biology question is why they do that and not simply retain one gender throughout their life? In other words, what's the evolutionary advantage of such a weird approach?

This is not the only organism that does that. See https://en.wikipedia.org/wiki/Sequential_hermaphroditism. The wikipedia page also mentions some reasons for why such a phenomenon happens.

What you see is what you get (aka @WYSIWYG), would you like to post an answer? :)

I get what you say (:P) but I'll be merely repeating what is written in wikipedia. You can actually wait for a better answer. There are people here who would know about this topic better than me.

@WYSIWYG I only know because I had worked on such an editor when I was in Switzerland! :) Anyway, nobody seems to be able to answer, thus I would tell you to think twice for whether you should be posting an answer or not! If a better answer arrives later, trust me, I will check it up! ;)

@WYSIWYG You're probably better for judging this than me (you're a mod), but I'd say your WP link with a brief summary would be sufficient for now, and if a better answer does come along, we'll respect it as well.

Related Bio-SE question: Why are not all species hermaphrodites?

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What are the on-rate and off-rate constants for 5-HT1 receptors binding 5-HT?
The class of 5-HT1 receptors binds serotonin (5-HT) reversibly (Wikipedia). I'm interested in the on-rate and off-rate constants $k_{\text{on}}$ and $k_{\text{off}}$ of this process.
So my question is: Have these constants already been determined experimentally for any member of the 5-HT1 receptor family, and, if so, what where the values observed?

Edit: Since this question didn't get much attention yet: Instead of the on-rate and off-rate, maybe the dissociaton constant/binding constant of the binding process is known?

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Why do SRIs help in serotonergic neurotransmission?
Serotonin reuptake inhibitors (SRIs) block the action of the serotonin transporter (SERT) which, according to Wikipedia, leads to an increase in serotonergic neurotransmission.
Now this book summarizes serotonergic neurotransmission as follows:

[The neurotransmitter] binds to specific receptors on the postsynaptic cell, thereby
  generating a postsynaptic electrical signal [...]. The transmitter must then be removed rapidly to
  enable the postsynaptic cell to engage in another cycle of
  neurotransmitter release, binding, and signal generation. [Neurotransmitters are removed by] reuptake into nerve terminals [...].

So my question is the following: If, as stated in the quote, the transmitter must be removed rapidly, shouldn't an increased amount / binding potential of SERT actually be a good thing because if there are more transporters, the process of removing the neurotransmitter is much faster? And consequently, why would blocking the SERTs help in serotonergic neurotransmission? Is it because the neurotransmitter must remain in the synaptic cleft for a certain amount of time? Is it because the reuptake takes place before the neurotransmitter could bind to the receptors of the postsynaptic cell? Or ist there yet another reason?

Excellent question.
Different neurotransmitters operate at different temporal scales (and even the same transmitter can operate at different temporal scales). Examples of the fastest-acting neurotransmitters are glutamate, GABA, and acetylcholine (with the caveat that they can also act more slowly). These neurotransmitters (usually) open ion channels in the postsynaptic cell, and are cleared rapidly after release, which allows for a temporally precise code, with each release event individually important.
Other neurotransmitters are also considered neuromodulators, such as dopamine, serotonin, epinephrine/norepinephrine, and others. While the basic machinery for release is the same, these neuromodulators aren't cleared as fast, bind to g-protein coupled receptors, and their concentrations can build in the synaptic space between neurons when the presynaptic cell fires multiple action potentials in sequence. For these neurotransmitters/neuromodulators, the amount of neurotransmitter sitting around outside the cell acts as a time average of release in the recent past.
SRIs/SSRIs/similar drugs slow down the reuptake process, such that the concentration of serotonin reaches higher levels with the same presynaptic activity.
Although reuptake can also be important to "restock" the presynaptic cell with neurotransmitter for release, there is typically enough precursor around that reuptake is not the only limiting step.
Your suggested reasoning that is closest to the truth is both: "...because the neurotransmitter must remain in the synaptic cleft for a certain amount of time? Is it because the reuptake takes place before the neurotransmitter could bind to the receptors of the postsynaptic cell?" but it isn't that the transmitter "must remain" longer or that reuptake takes place "before" it can bind: it is that if the neurotransmitter remains longer it has a larger integrated effect on the postsynaptic cell.
Lastly, "good thing" is relative - of course increasing SERT activity would help with faster transmission, but faster transmission might not be important/necessary/fit the function of the circuit where serotonergic signalling is involved.


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Derivation of Michaelis-Menten kinetics for discrete stochastic simulations
According to this article,

[...] the propensity function for the conversion reaction S → P in the
  well-mixed discrete stochastic case can be written $a(S) = \frac{V_{max}\cdot S}{K_m + S/\Omega}$ where $\Omega$ is the system volume.

I don't quite understand how this formula is derived from the non-discrete Michaelis-Menten kinetics $v = \frac{V_{max} \cdot [S]}{K_M + [S]}$ (see Wikipedia). According to my understanding, $[S] = S/\Omega$. If we apply this to the formula from Wikipedia we get
$$
\frac{V_{max} \cdot[S]}{K_M + [S]} = \frac{V_{max} \cdot S/\Omega}{K_M + S/\Omega} = \frac{V_{max} \cdot S}{\Omega \cdot K_M + S}
$$
which is not the same as $\frac{V_{max}\cdot S}{K_m + S/\Omega}$. So, how can one derive the formula from the quoted article (if it is correct)? If not, how can we correctly get to a discrete propensity function from the Michaelis-Menten kinetics?

I guess the article is incorrect. I checked different possibilities but none of them seem to give this relation. The papers cited by this article also do not have this formula. Their supplementary data also does not explain anything. If $K_M$ is defined differently then this formula may possibly be right but since the article does not mention anything like that, we should not assume so.

I think I figured it out myself. Since $a(S)$ is in $\frac{mol}{s}$ and $v$ is in $\frac{\frac{mol}{l}}{s}$, we have that $a(S)= v * \Omega$.
Therefore
$$
a(S) = \frac{V_{max}\cdot [S]}{K_M + [S]} \cdot \Omega = \frac{V_{max}\cdot S / \Omega \cdot \Omega}{K_M + S / \Omega} = \frac{V_{max}\cdot S}{K_M + S/\Omega}.
$$


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Possible calculations with temperature, humidity, images and VIS spectrum of a plant in an Integrating sphere
I am currently working on a project which involves growing some plants in a integrating sphere made of foam. I have added temperature, humidity and soil moisture sensors as well as a Spectrometer (350 - 800nm) and a webcam which takes images of the plant every 30 minutes.
I thought of calculating the LAI (Leaf area index) from the webcam images.
Does anyone have any other suggestions/ideas on what I could calculate with the given data from these sensors?

Are you designing an analysis around the data or have you gathered data to do an analysis? In other words, do you have a goal with this experimental set up?

Both. I have already gathered some data from a previous set up, but only with the spectrometer and webcam. The main goal is to observe water stress in different plants.  I curious what else i could calculate and predict once i have the data from the new set up.

Thanks for elaborating. Perhaps you could add this background to the question proper. Regardless, +1, thanks and welcome to Biology!

With the images you could, perhaps, assess growth rate of the plant which can be plotted against spectral content of light to investigate effects of light quality on growth. Using moist and water and temperature the same can be done. Multivariate analysis can help to implement all the values, while ANCOVA may may help to correct for covariance.
A detailed experimental set up may help to answer this question. Not specifically the hardware, but how the effect of water stress is measured. E.g., are multiple plants tested under different watering conditions? In that case all the other measures (temperature, light) are probably used to check whether everything is constant across all specimens except water availability. This may limit the usefulness of analysis of these additional measures. I think the other parameters (light, water, temperature) may be not so interesting other than covariates for water stress as they are either not controlled or deliberately kept constant. Moreover, probably their effects on plants are pretty obvious too.


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Can neurotransmitter concentrations in the synaptic cleft add up if there are several impulses in quick succession?
When an electric signal reaches a chemical synapse, the signal is transmitted using neurotransmitters. Afterwards, the neurotransmitters are removed from the synaptic cleft. My question is whether it happens in a normally functioning brain that neurotransmitter concentrations in the synaptic cleft add up if there are several impulses in quick succession? If so, does this serve any purpose? Or is the time between two impulses always long enough for all of the neurotransmitter to be removed from the synaptic cleft?
Edit: To further clarify (as the currently only answer does not really adress my issue), I am aware of the principle of summation, however I do not know whether this is actually caused by multiple neurotransmitter emissions "adding up" in the synaptic cleft or whether the postsynaptic membrane can just somehow remember if there was an increased amount of neurotransmitter recently.
To describe it graphically: According to this article, the concentration of serotonin in the synaptic cleft during a single impulse looks somewhat like that. Now when there is a quick series of impulses, does the neurotransmitter always get removed before the next impulse as on the right side of the following image, or can it add up as on the left side? And if it does add up, does this actually serve the purpose of temporal summation or some other purpose?

I think as bpedit said the temporal summation also occurs at the body of the neuron as well as at the synapse, although I do expect that your left hand image will represent the concentrations if the APs follow each other close enough by overloading the transport mechanisms.

The answer by bpedit is a good explanation of temporal/spatial summation, which can be partly a postsynaptic phenomenon (due to membrane time constants or second messenger sytems, for example).
Your specific question is about whether extracellular neurotransmitter levels sum over time. This definitely occurs regularly with "neuromodulatory" neurotransmitters like serotonin (others that behave similarly include dopamine and norepinephrine/epinephrine). "Faster" neurotransmitters like glutamate and GABA are cleared more quickly, though there are complicating factors there as well that are outside the scope of this question.
Although the summation has been shown many times, I looked quickly for an example and found the paper by Bunin and Wightman, 1998. Figures 2-6 all show extracellular serotonin concentrations that are elevated for seconds after release (let me know in the comments if you can't access this paper at your institution), and they show the changes in extracellular concentrations with multiple stimulus pulses (see in particular Figure 3).

Thanks, something like the figures in the quoted paper was just what I was looking for!

The addition of multiple impulses is termed summation and is instrumental in whether an action potential will be induced in the post-synaptic neuron. If the neurotranstitter released by one action potential in the pre-synaptic neuron was enough to cause an action potential in the post-synaptic neuron, the whole idea of neruotransmitters would be a waste of energy and resources. In these circumstances an electrical synapse would suffice, the chemical synapse being "overkill".
Temporal summation happens when several action potentials arrive in quick succession from a particular neuron. Spacial summation occurs when action potentials arrive from multiple neurons, at roughly the same time, to act on a localized area of a post-synaptic neuron. In either case, the effect of a single action potential is not enough to cause a large enough influx of ions to initiate a new action potential, whereas the combined effect of several action potentials is enough to reach the threshhold value necessary.
There can also be inhibitory contributions to this process as well. These typically increase the resting membrane potential making it harder to reach the threshold needed to initiate an action potential. All-in-all it's rather like a voting process that occurs at the synapse (or small region of multiple synapses). This "voting" allows for complex integration of all the inputs neurons receive.
Here's what appears to be a good reference on summation:
https://www.ncbi.nlm.nih.gov/books/NBK11104/
Here's the Wiki link as well:
https://en.wikipedia.org/wiki/Summation_(neurophysiology)#Temporal_summation
Here's an instructive video, I've only watched a couple minutes but it appears a reasonable visual treatment:
http://www.interactive-biology.com/1660/what-is-summation-2-types-episode-19/

Some of the information contained in this post requires additional references. Please [edit] to add citations to reliable sources that support the assertions made here. Unsourced material may be disputed or deleted.

This is all right out of any introductory Biology textbook, stuff I've taught for over 20 years. All easily verifible online, hundreds of thousands of hits. With what particularily do you have an issue?

You may be familiar with the material, but that doesn't mean everyone else is. I'm an immunologist, and I know the difference between T and B cells, but I always include links to Wikipedia when I mention them here because others may not know, or may simply be interested in learning more. I could not cite them with the excuse that "it's all easily verifiable online", but you could say the same about every citation in a primary research paper. I highly recommend reading completely through this Meta discussion regarding citations.

Just to be sure: the summation is not only caused by the fact that the postsynaptic membrane somehow remembers that there was an increased amount of neurotransmitters shortly before the second impulse, but that there actually still is neurotransmitter left from the first impulse in the synaptic cleft?

@vauge I don't know for sure. There is another mechanism at play as well. Gates in the post-synaptic membrane have opened to allow the influx of ions which depolarizes the membrane. It takes a finite time for these gates to close, independently of how they were opened, which contributes to summation. There is also variation in the nature of these gates and the particular neurotransmitter involved in different synapses. So it's possible a slower degradation of neurotransmitter allows summation in some cases but not others.

@vauge - Both, in a way; there can be residual neurotransmitter in the synaptic cleft, and there can be neurotransmitter that remains bound to receptors (you could possibly think of this as 'memory'). Finally, to add to bpedit's comment, your question referred to serotonin, and most serotonin receptors are g-protein coupled receptors; g-protein receptors subsequently affect second messenger systems like cAMP and IP3/DAG whose effects remain over long time scales, seconds and longer.


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Does the dissociation of serotonin receptors and their ligands really take hours?
If I understand the principle of neurotransmission correctly, then after binding to a receptor on the postsynaptic side, neurotransmitter molecules must be dissociated from the receptor and removed quickly from the synaptic cleft (see this book).
This article states that the off-rate $k_{\text{off}}$ for the 5HT3 receptor and some ligand is approximately $43 * 10^{-6} s^{-1}$. If we ignore the binding process for now and denote by $C$ the complex formed by 5HT3 and the ligand, we can describe the dissociation process by the following simple differential equation:
$$
\frac{dC}{dt} = -k_{\text{off}} * C
$$
(see Wikipedia).
Using the $k_{\text{off}}$ from above, we get that the half time of this dissociation process is $\frac{\ln{2}}{k_{\text{off}}} \approx 16116s \approx 4,5h $. A similar $k_{\text{off}}$ rate for all other kinds of 5HT receptors binding serotonin can be derived from the dissociation constants found in the Ki Database.
But wouldn't that mean that, when serotonin is released from the presynaptic axon terminal and the 5HT3 receptor binds it, not even half of the neurotransmitter molecules are dissociated from the receptor after more than 4 hours? That seems to clearly contradict the statement from the beginning of this post - so is something wrong with my calculations or does it really take that long? Or have I understood something completely wrong about the principle of neurotransmission?

You're comparing5-hydroxytryptamine to 1,2,3,9-tetrahydro-3-[(5-methyl-1H-imidazol-4-yl)methyl]-9-(3-amino-(N-fluorescien-thiocarbamoyl)-propyl)-4H-carbazol-4-one (in other words, apples to oranges.)

That paper is describing the binding between the 5HT3 receptor and some high-affinity ligand, not serotonin.
Numbers of serotonin probably vary according to the precise receptor (species, subunits, etc), but for a ballpark figure this source says 1.7/s, giving half time of ~400 ms. That estimate is based on solution changes, so I'd say it's an upper bound.
Remember from the other questions you have asked and I have answered, serotonin is a slower-acting neurotransmitter, and clearance of serotonin is not as fast as for other, faster-acting neurotransmitters. However you are correct that your initial calculation of a ~4-hour dissociation time is unreasonable.


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Why is the brain white?
I have read many articles about how the brain is the most power-hungry organ in any living complex organism, requiring about 70% of it's oxygen supplies in the resting state.
Since the usual medium of oxygen delivery is through respiration, this should mean that a lot of blood is supplied to (and hence present in) the brain.
Why then is the color of the brain almost always white? There is usually a little red tainting on the exterior and that's it, you can see the interior is still white. Should it not be red? Presuming that for a higher surface area to volume ratio, most of the brain cells are in direct contact with the bloodstream.

If I recall correctly, most of the brain cells are not in direct contact with the bloodstream, there is a famous blood-brain barrier that aims to shield most of the brain from the blood. The barrier is that thin, that fat cannot pass through it. Therefore brains can only work on sugar supply.

@CommuSoft - The blood-brain barrier shields of constituents in the blood from the brain. It is formed by tight junctions between the epithelial cells lining the blood vessels in the brain. The only difference with the brain is that these tight junctions are absent elsewhere. Hence, less molecules pass into the brain from the bloodstream than elsewhere. Sugar is imported in every cell with dedicated transporter proteins  - i.e., sugar cannot pass the bloodstream passively anywhere, not in the brain, not in the rest of the body.

The brain is indeed stacked with blood vessels, as shown in a 3D model in Fig. 1.

Fig. 1. 3D-printed model of blood vaculature. Source: Biobots.
The blood supply on the surface of a live brain is readily seen during a craniotomy (Fig. 2.)

Fig. 2. Surface of the brain. Source: The Sterile Eye.
When freshly prepared, the interior of the brain appears pink, indicative of the presence of blood (Fig. 3):

Fig. 3. Coronal sections of a non-fixated brain. Source: Documenting Reality.
Mostly, images of the brain are taken after fixation of the brain. The fixation process includes removal of the blood in the brain and the fixative pales the color of the tissue markedly. Fixation results in the more familiar pale-appearing pictures of the brain as shown in Fig. 4.

Fig. 4. Coronal section through a fixated brain. Source: Wikimedia.
Also note that the blood supply mainly targets the areas where the cell bodies are located, i.e., the gray matter. The white matter is pretty much devoid of blood supply and mainly consists of heavily myelinated, fatty tissue supporting axonal fiber tracts (Fig. 5).

Fig. 5. Arterial innervation of the brain. Source: Human Physiology Academy.

Nicely illustrated answer :) +1

Nice answer. Can you also add a note on blood-brain barrier and the role of CSF as a medium of metabolite exchange?

@WYSIWYG - the blood-brain-barrier is not really of relevance for oxygen exchange. And since the question is on oxygen, and not on metabolites, I deliberately left CSF out of the answer.

@AliceD Fine enough. I have seen some sources say that CSF "stores" oxygen.

@WYSIWYG - I didn't know that, but I'd rather not overcomplicate the answer. Thanks for the appreciation and the comments!

A person can be alive and awake with his skull open and brain exposed like that? o.O

@Abdul Not only can be, it's necessary for them to be, for most forms of brain surgery. Feedback from speaking with the patient is vital to allow the surgeon to find and identify the right bits to cut/prod/etc.

@MatthewNajmon that's gotta be worrisome as the patient as you feel pressure to give very accurate feedback, and try to be as least subjective as possible. It's like during an eye exam, it's not too big of a deal when you choose the wrong lense, when the optometrist asks you which lense allows you to see clearer, and you can't really tell


text:
Is Batesian mimicry more important for females?
Myrmarachne plataleoides  is a jumping spider that mimics the Kerengga or weaver ant (Oecophylla smaragdina) in both morphology and behaviour. However, the two sexes appear different:

Myrmarachne plataleoides (Female)

Myrmarachne plataleoides (Male)
Some links suggest that in dimorphic arthropods the females more exactly mimic the model. Is this true? If so, why would this sex difference exist?
Reference
Phyologenetics of mimicry

I slightly edited your question. However, the reference link is empty. I like this question a lot. +1

@AliceD:Sorry I just put insects there, LOL.....thank you for ur answer and edition. You did well

All good! Thanks for the interesting question.

In sexually dimorphic ant-mimicking spiders, it depends on the specific species which sex resembles the ant most (Cushing, 2012).
In many cases of sexually dimorphic spider myrmecomorphs, the male is more mimetic than the female, such as in Corinnidae species and the genus Castianeira, Oonopidae and Antoonops.
Such sexual dimorphism may be adaptive if the sexes are exposed to different predation pressures. The spider's mimicry of noxious ant species yields protective benefit from predators who would avoid the ants. However, the mimicry often results in being more conspicuous in their color markings than related spider species that are more camouflaged. Hence, conspicuousness can be considered a cost of Batesian mimicry. A palatable species may be evolutionary maximizing its level of protection for the smallest cost (in terms of conspicuousness). Sexual dimorphism, in which the more active sex (which, in spiders, is typically the males) evolves mimetic resemblance to noxious ants, whereas the other sex remains relatively more concealed and camouflaged behaviorally and morphologically.
Reference
Cushing, psyche (2012); 151989: 1-24

Great reference - wonderful review of a very interesting association!

"whereas the other sex remains relatively more concealed and camouflaged behaviorally and morphologically." this points towards the female, but the female is the more closest resemblance. Then how could it be called as concealed and camouflaged. Do you mean the resemblance itself is camouflage ?

@Jay, The author says that it is often the males that mimic the ants more closely, see the bolded-out text

The male (Myrmarachne plataleoides) pictured have a pair of fangs, which make it differ from the female counter part. So here the female is the closest mimic and without these fangs the males would be too. I think these fangs are for display.

agreed, totally. it depends on the species.

the article you referred seems awesome.

One more think. male spiders(most males) needs some extra decorations and attachments in order to attract females and catch a fight for sex. The males are considered to be more mimetic but they do have an overhead of putting up these male display, in this case they may vary from the model. Isnt ?

@Jay  - I am not an enthomologist, but from what I understand your theory is correct and mimicry and sexual dimporphism is species dependent. I however don't know if spider males fight, for one thing.


text:
What proportion of salt in water would make it not dehydrate nor hydrate someone?
Drinking sea water can be deadly as it contains too much salt, basically de-hydrating the body. Normal tap water contains little salt and is good for re-hydration. My question: How much salt needs to be dissolved in water such that it does not hydrate nor de-hydrate? For instance, would a physiologic saline solution (9 grams of salt per liter of water) meet this criterion?

You are looking for physiological saline which is isotonic to most tissues. It is about 0.9% w/v, which equates to ~9g NaCl per liter water.

@kmm I thought isotonic solutions were often used in sports for rehydration?

There is no saline solution which will not either hydrate or dehydrate someone. Pure water hydrates, sea water dehydrates, and everything in between does one ot the other. You need to clarify your thinking on what constitutes "hydration".

@anongoodnurse Why do you say that? There are solutions that can be isosmotic with the cytoplasm. I agree that the cytoplasm can have small variations in osmolarity and you may not find a mathematically exact universal isotonic solution. Why do you think 0.9% saline won't be grossly isosmotic?

@AliceD The sports drinks are mostly for restoring electrolytes.

@anongoodnurse I disagree with your comment. Why would there be only two extremes and no middle ground?

@Nit - "everything in between does one ot the other." That's the middle ground. If you're not dehydrated, you cannot "hydrate" with a perfect imaginary solution. The body will remove the unnecessary salts of anything added. There is no magic solution.

@WYSIWYG - see above. The body doesn't keep solutes it doesn't need. There are isotonic solutions, but if a person is normally hydrated, the solutes of the solution will be removed, in effect reducing it to something close to water. There is no one answer for this question. It depends entirely on the state of "hydration".

@anongoodnurse That still makes no sense. What about solutions that are perfectly balanced between the body-needs-solutes and body-doesn't-need-solutes?

@anongoodnurse I still did not get it. I am talking in the sense of cells and tissues, not a human body. Isosmotic is not enough for excitable cells like neurons, for which the ions also have to be balanced; so lets assume PBS instead of normal saline.

@WYSIWYG - I didn't realize you were speaking about a cell; of course there are isotonic solutions. But the OP is asking about a human body (I presume), and my answer is unchanged for that question.

@anongoodnurse Perhaps you would want to write your point up as an answer (with references etc) on the other post. The comments do not explain the situation properly and are also confusing.

@Nit Oh sorry.. there was a confusion. I thought you asked anongoodnurse to read about loops of henle etc. Sorry. However you have to work on your other question- on terminologies and w.r.t addition of your own analysis on the issue.

I am closing this question as a dupe of this post since the latter has an answer.


text:
How do electrons destroy DNA bonds in radiation?
Malignant tumors can be treated by radiation therapy. Most commonly it's radiotherapy with photons, or protons and so on. The common denominator for both types is that the radiation creates electrons inside the body via different effects.
What I haven't quite understood is how these electrons destroy the DNA bonds in the tumor and how this aids in killing off the cancer cells? Is it due to the generation of heat, or otherwise?

(1) Molecules are held together by bonds. Jamming energy (not necessarily heat) into the bonds causes them to become unstable and behave differently (electrons jump to different energy shells). (2) Cancers propagate through modified cellular pathways. To do this, the DNA needs to be functioning. Not properly, just functioning. (3) DNA functions by producing RNA. It's all about the sequence! Damaged sequence = damaged tumor pathways = death. Relevant mechanistic paper on direct damage by ionizing radiation.

I think you have a fundamental misunderstanding of the chemical reactions involved in radiation therapy. Neither photon based or proton based therapies "create electrons", but they do cause ionization by adding enough energy to existing electrons around atoms so that the electron is ejected from the atom, creating an ion or free radical, which can then undergo chemical reaction.
Photons, typically gamma rays, X-rays, and high energy UV, typically interact with water molecules and produce free radicals, including the dangerous hydroxyl radical. The hydroxyl radical can interact with proteins and DNA and damage those molecules, but has a very short half-life. Molecular oxygen can help increase the damage by reacting with the hydroxyl radical to produce Reactive Oxygen Species, ROS, which can also damage DNA or protein. However, many tumors have low oxygen concentration that reduces the effectiveness of photon based radiation therapy.
To overcome this, many patients receive proton based radiation therapy. Protons are much heavier than photons (I guess infinitely heavier than a photon, since photons have no mass) and therefore scatter to a much smaller extent. They just sort of plow through tissue and knock electrons out of orbitals as they collide with molecules such as DNA or protein. They don't rely so much on free radical generation or ROS, so low oxygen levels don't reduce their effectiveness.
The goal is damage the DNA to induce double strand breaks which are hard to repair in fast growing cancer cells. Because they grow so quickly, they are already stressed and their DNA repair machinery is less effective than in healthy cells. If their DNA can be sufficiently damaged, the cell will die.
For more information about these processes, please see these wikipedia articles on Radiation Therapy, Radiolysis, Linear Energy Transfer, and Free Radical Damage to DNA.


text:
Would a vial of anticoagulated, warm blood attract mosquitoes?
Would mosquitoes feed on free blood as an easy source of nutrients? They home in on veins by means of infrared light (heat detection). Also, blood needs to be in liquid form. So would they feed on anticoagulant-treated blood kept at 37oC? Or is there some physiological phenomenon that mosquitoes necessarily need to pierce something to draw in blood?
I am asking this, because just keeping a vial of blood at the end of a room might save us from mosquito bites.

Here's a link to the answer - https://redd.it/4h2j0g

Feel free to answer your own question if you found an answer elsewhere. Other option is to delete the post (not advised).

According to wikipedia they locate "prey" by detecting CO2 and some other compounds, so I don't think mosquitoes will actually find the blood unless they're accidentally right on top of it.
And for your reason: if you have the equipment to regularly draw some blood, keep it at 37 C and have some anticoagulants on hand, you might be better off using some tried and true anti-mosquito tech (nets, insecticides, preventing them to breed in the local area).
Or maybe this: https://en.wikipedia.org/wiki/Mosquito_laser


text:
Do oral vaccines exist?
Do edible vaccines exist, and if yes, what is their mode of action? Are there any edible vaccines commercially available now?

In short, yes.
A good example of an orally-administered vaccine is this Polio vaccine.

Other than polio..?? Have anyone heard about that vaccine that are incorporated into food items like potato or banana?

Rabies, typhoid and many others are available as oral formulations. @Ashwin.N You are asking about a GM Food with vaccine properties?

Yes sir!! You are right!! I was asking about that only!! Can you tell me more about GM food with vaccine properties with real life examples!! Plz

Ah. My mistake. Yes, those exist. I am not aware of any large-scale deployments, but there have certainly been trials.
Examples: Hepatitis B vaccine trial in transgenic potatoes: http://www.pnas.org/content/102/9/3378.short
E. coli vaccine, also in potatoes (mouse trial): http://www.sciencedirect.com/science/article/pii/S0264410X98800200

@Ashwin.N In that case can you edit your question to add this information?


text:
Is there an absolute minimum intensity level to the stimuli we can perceive?
By stimuli that we can perceive, I mean what our five senses can perceive.
Is there an absolute minimum for humans, or can we "train" ourselves to perceive stimuli at lower intensity?
And if there is an absolute minimum intensity, do we know what its value is?

Why the downvote? Downvoting without commenting is useless.

downvoting without comment is the best.

i think absolute lower limit is defined by chemical bonds energy and activation energy of enzymes. For eye, for example, lowest energy of photons that produce visual response is somewhere around 750nm

@aandreev - The title mentions 'perception' and Matt asks about training as well. Chemical bonds are far away from perception, and cannot be changed with training. This question is about the perceptual level I guess.

You should specify what kind of perception you are interested in. Though the voltage threshold for action potential may be more or less same for all neurons, the different neuromodulators and other modulatory neurons (interneurons) would affect different neural paths differently.

@AliceD I think any discussion about votes should go on meta. Also, perception has very defined (in some known cases) chemical&physical basis. Leaving it out and talking only about what people measure/observe is tangential to the question IMHO. Physics of transduction is the ultimate barrier for perception.

@aandreev - we might continue this on chat, but just shortly - eventually the way to measure perception thresholds is by asking subjects if they perceive a certain threshold stimulus yes/no. Going to the test tube isn't perception and more importantly, the ultimate bottleneck determining the threshold isn't the question I think?

@AliceD chat is fine. My line of thought is following: between cognitive perception (or any other observable manifestation of excitation by stimulus) there are several layers of amplification and inhibition. Each of which might be optimized (in principle). The only true limit to my taste is around energy of chemical interactions. Or maybe I am off the course of OP's thoughts

@aandreev,  I would consider answering the question then, it sounds plausible. Bio.SE Often answers questions, but often lacks multiple answers. Mine hasn't been accepted.

There are limits to what a sensory system can detect, which is called the detection threshold. To determine the detection threshold psychophysical methods can be used. A straightforward way to determine the detection threshold is with a yes/no task, where the subject receives stimuli with various intensities. An arbitrary point, mostly the 50% correct-rate, is then defined as the detection threshold. At this point, the subject correctly detects the stimulus 50% of the times. The response curve in a psychophysical task typically takes the shape of a cumulative function such as the one shown in Fig. 1.
Hence, the detection threshold is an arbitrary point, because people are not machines and show variability in their decisions. The detection limit of, e.g., electronic devices is much more precisely defined. The exact values of the detection limits depend on the exact stimulus (visual, tactile etc.) and depend highly on the exact stimulus. For example, in the visual domain the detection limit of light depends on the color, the location in the retina tested, dark adaptation etc etc, and in the tactile domain static pressure stimuli have a different threshold than vibratory, different body parts have different thresholds etc. etc.

Fig. 1. Psychometric curve showing 50% threshold of a visual stimulus. source: Webvision
Training to lower the detection threshold (i.e. improve detection limits) is indeed possible (Sterr et al., 1998).
Reference
Sterr et al., J Neurosci (1998), 18: 4417-23


text:
How does the structure of the pancreatic acinar cell relates to its function?
So the pancreatic acinar cell synthesizes, stores and secretes digestive enzyme precursors called zymogens e.g. pepsinogen.
The structure of the acinar cell shows that there is an apical and basal side. The basal half of the cell is almost entirely filled with rough endoplasmic reticulum which can be shown with pyronin stain showing up pink due to the rRNA of ribosomes. The nucleus is also on the basal side which explains why rER is there too, since the nuclear envelop is connected with the ER membrane. Zymogen granules are on the apical region. Any thoughts as to why there is this polarity in cell?

The secretion pushes the cell organelles to the basal part.
(although the fat cells have no polarity, their organelles have been pushed to one side of the cell:

Comparing to adipose cells, the acinar cells secrete their specific proteins on one specific end of the cell, this is why in contrast with fat cells they have well defined polarity.


text:
Is the sun's damage to skin sufficient to warrant protection anytime the average person goes outside or just for extended periods?
According to the American Academy of Dermatology website,

Everyone needs sunscreen
Sunscreen should be used every day if you will be outside. The sun emits harmful ultraviolet (UV) rays year round.
Even on cloudy days, up to 80% of the sun’s harmful UV rays can penetrate your skin.

I also saw this video a while ago.
The two of these make it sound like we should be wearing sunscreen even if I step outside to get my mail.
Is the sun's damage to skin sufficient to warrant protection anytime I go outside or just for extended periods? What is the general criteria this kind of organization uses to determine what is "sufficiently" damaging to warrant sunscreen protection?

There are dermatologists who advocate for never exposing the skin to direct sunlight.  The interview I saw had terrific looking skin. The increase of UV content of sunlight over the past few decades makes this seem like a better idea now than previously.  Clothing, hats, gloves and parasols may be recommended in these cases because of the chemicals in sunblock.

Interesting. As an aside though, specific opinions are part of the problem. I don't know what the criteria are by which they are making these recommendations. Doctors are not infallible. I need to know the metric they are making these recommendations based on so I can decide for myself who is being rational and who is just saying stuff.

It is very much dependent on skin type.

@WYSIWYG What specific properties do you have in mind?

@StanShunpike A simple parameter is melanin content. Dark skin contains higher concentration of melanin which helps protecting the skin against UV. I have seen many people who are constantly exposed to sunlight but do not suffer from skin cancer or even sunburns.

Probably as important, the incidence of skin cancer is up over the past 30 years because of 1) the idea that getting a tan is healthy 2) the intensity of sunlight hitting the earth's surface is going up. An increase in melanoma has been documented.  http://www.who.int/uv/faq/skincancer/en/index1.html  http://www.skincancer.org/skin-cancer-information/skin-cancer-facts

@shigeta thanks for that comment. Very interesting. I never thought of it like that

related: Radiation and “Safe Dose”

Since your questions seems to be motivated by personal health protection, consider an alternate view, which is that not only is the sun's damage to the skin not "sufficient to warrant protection anytime I go outside or just for extended periods", but that lack of sufficient unblocked exposure to the sun may be, overall, even more harmful--not only for the risk of various cancers, but for a large number of serious diseases.
Dr. Michael Holick is a Professor of Medicine, Physiology and Biophysics at Boston University School of Medicine, and has researched vitamin D--which is produced by our skin when exposed to the sun's UVB radiation--and its critical role in health for over 30 years. In addition to his book, The Vitamin D Solution and an entertaining and informative (and at times, zany) lecture, he recently (Jul 24, 2015) wrote about this in The Washington Post. For example:

the risks associated with sensible sun exposure have been exaggerated
  by well-meaning health authorities, and the measures to guard against
  them often have nothing to do with the sun’s occasionally malignant
  effects. Contrary to the paranoia generated by years of messaging, the
  sun is not our enemy. It’s safe to step back outside — and, please, go
  easy on the sunscreen.

The book and lecture provide much more detail, but the main points are that 1) vitamin D, a hormone, is critical to many bodily functions, 2) that lack of it in a majority of people in many countries is a "pandemic" related to many important diseases, 3) that the current United States 400 IU/day guidelines are too low, 4) that it is easily produced by sufficient exposure to unblocked mid-day summer sun, and, importantly, 5) that there may be additional "photoproducts" (other molecules our skin manufactures in response to UVB rays) that we may find are similarly important to cellular processes and so he prefers sun exposure to taking supplements. In regards to diseases that are related to vitamin D deficiency, he writes:

A lack of vitamin D is associated with increased risk for Type 1 and 2
  diabetes, multiple sclerosis, rheumatoid arthritis, Crohn’s disease,
  cardiovascular disease, stroke, depression, Alzheimer’s disease,
  schizophrenia, colon and breast cancer, influenza and tuberculosis....Of the 30 leading causes of deaths in the
  United States in 2010, 19 were linked to low vitamin D status.

He does not deny that one needs to limit exposure to the sun reasonably, and recommends sun block for the face and basically exposing arms and legs something like 10-20 minutes at a time, several times a week, from 10am--3pm (when UV-B is sufficiently strong, else one only gets UV-A, which does nothing for vitamin D but is linked to skin damage), though exact "dosing" will be dependent on latitude, skin color, time of year, and perhaps other factors (which he covers in the book).

Because the website you link speaks of cancer, they probably go by the rule that a single exposure and even a single photon of UV may be sufficient to cause that one mutation in that one skin cell that will eventually lead to cancer.
In the end, they are right, because mutagens (UV, cigarettes, radiation) do not follow typical toxicological rules. There is no threshold dose of UV that does not cause cancer, as even a single short exposure may do the trick. Obviously, multiple exposures and longer exposures increase the chance. This, as opposed to toxic substances that generally feature a threshold dose. Below this threshold dose they are considered harmless.

Let's suppose a person gets cancer from a small does of radiation. This person could just be an outlier, in which case we simple must accept that that person just has bad luck. But is there a general trend --- a statistical threshold --- of radiation exposure? For example, I walk to class which takes about 5 minutes. Am I supposed to put sunscreen on for that walk? Do I need to put it on if I take a bus downtown? Knowing the statistical threshold of sufficiently "safe" sun exposure to determine if it warrants all those precautions is what I am asking about.

'sufficiently safe' is opinion-based. Obviously, the linked website adheres zero-tolerance policy. As I say above, there is no safe threshold. It's a gradual thing.

There should be objective measures I would think. Rates of skin deterioration. Risk of cancer. These are objective measures. What one considers safe is subjective. Am I thinking about this question the wrong way? Just asking. I haven't really asked a question like this before.

@StanShunpike - And I normally don't answer these kind of questions :) +1 for the question btw. It's a good one.

AFAIK, other than acute radiation sickness (where someone gets a massive dose of radiation within a short period of time) there is no way to tell. When we talk about radiation damage, usually we end up using metrics equivalent to "x dose will increase your chances of cancer within y years."

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


text:
Do rare earth metals actually repel sharks?
Stroud claims that sharks are effectively repelled by the use of rare earth metals in the water. There has even been a patent issued by the same author for rare earth-wrapped fish hooks to reduce the shark by-catch.
Apparently these metals work by generating an electric current that repels sharks via the shark's electric sensing organ.
Is the repellent action of rare earth metals scientifically confirmed? And if so would it be effective even on the largest and aggressive white sharks?
Also if effective why haven't dive equipment manufacturers developed shark repellent devices for sport divers?

@AliceD from Canberra - thanks for the edit and go at it. So looks like good science hasn't sifted all the facts through the sieve quite yet. There are demonstrations of the effect on YouTube & the NOVA episode with David Pogue that are impressive. But looks like no one is investing in the design of rare earth diving gear quite yet ; )

@AliceD A small correction. Elements cannot degrade (unless it is a nuclear reaction). You should say that lanthanides react with water.

I'm voting to close this question as off-topic because this question does not ask about the biology of this phenomenon and is therefore much more suited to skeptics SE

I really hate it when science blogs do not cite the original articles and in such cases the authenticity of the information is not only questionable but also unverifiable. However there seems to be a wikipedia and a natgeo article on this. Even these do not cite any scientific research. Overall the claim seems unverifiable.

As pointed out earlier by AliceD, lanthanides react with water to form hydroxides with a concomitant release of hydrogen. A single electrode like that  cannot generate EMF.

@rg255 - this is definitely not for skeptics (way too specific) and I got disciplined by a mod of late for referring people there :)

personally I think it is absolutely perfect for skeptics, and not well suited to here. From skeptics help pages: "Skeptics is about applying skepticism — it is for researching the evidence behind claims you encounter." Specificity cannot be a valid reason for not being suitable to skeptics because the very nature of the posts on their site is the search for specific and solid detail.

@rg255 - OP is asking for scientific evidence; If that is Skeptics and not Bio, then that way every question asking for evidence (Is-This-True? questions) should be deterred to skeptics

@WYSIWYG regarding "one electrode" not necessarily so. You can consider the shark's body serving as the other electrode with seawater as the electrolyte, but also as current paths. Current grows larger as the shark gets closer to the metal. Like biting down on aluminum foil with amalgam fillings. Just a few milliamps - very uncomfortable.

Please don't kill the question. Give it some time and perhaps someone working in this area will come up with an answer. If you throw it over to physics, chemistry or skeptics it certainly won't receive the same attention some ichthyologist may give it. It is a multidisciplinary question but belongs with biology. Also I'm not asking for experimental 'proof' - that doesn't exist. And I'm not asking for help from the mythbusters. Just looking for strong experimental inference and further detail of what's going on.

@docscience Have a look at this article. It suggests that permanent magnets (both iron and rare earth based) affect shark's electroception. But I don't know what they mean by electropositive metals (all metals are electropositive).

@WYSIWYG I believe that's common knowledge - that electromagnetic fields in general affect sharks. More so of what I'm interested in is if any of the lanthanides (cerium, neodymium, samarium, etc.) by themselves - not necessarily in the form of an alloyed magnet accomplish similar reactions.

@docscience See this too. They actually say that nothing of that sort happens.

Can't believe the moderators closed this question. If it doesn't 'fit' in biology, not sure where else would be a more appropriate spot that would receive that many views. It's received over 1000 views, and a good answer.

Short answer
Electropositive metals such as the Lanthanides generate electrical currents when they come in contact with (sea) water. This electrical activity may repel sharks by over-stimulating their lateral line organ. However, the effectiveness of lanthanides as shark repellent depends on many factors. For example, hungry sharks, or sharks engaged in a feeding frenzy may simply ignore the stimulus altogether.
Background
Rare earth metals are Lanthanides - metals with a low electronegativity. Metals with low electronegativity are called electropositive. Electropositive metals (EPMs) react vigorously with water when immersed and generate electrical potentials that are thought to overstimulate the sharks’ highly sensitive electroreceptors, the ampullae of Lorenzini.
Many electropositive metals fall in groups I and II of the periodic table and explosively react with water. Examples include sodium and lithium. The Lanthanides, on the other hand, contain some less reactive elements.
There is in fact a considerable body of primary literature on the use of EPMs to deter sharks, because the by-catch of sharks is a recognized problem of modern fishery. However, much of this literature shows very mixed results of EPMs, and therefore I have based my (second :-) answer attempt on a recent review article by Hart and Collin (2015), which is available on-line and cites some fifteen primary research articles on the topic:
EPMs are primarily intended as a mechanism to reduce shark bycatch and catch depredation in longline fisheries, without affecting the catch of non-electrosensitive target teleost fishes. As you indicate in the question, EPMs can be formed into shapes that are easily attached to a fishing line or hook.
Early tests in the laboratory with captive sharks showed that several EPMs (including magnesium and rare-earth lanthanide elements such as cerium, lanthanum, neodymium and praseodymium) were effective in repelling various shark species. However, more recently, several studies showed no such repellent effects other species of shark, and it was shown that aversive behavior was highly dependent on various factors such as duration of food deprivation prior to testing. Specifically, hungry sharks ignored the EPM, especially when feeding in groups (feeding frenzies).
The results of field trials with EPMs were also mixed, with some studies showing a reduction in the catch rate of various shark species, while other studies showed no such effect. The authors of the review article summarize a range of factors that may influence the efficacy of EPMs in repelling sharks, including the type of EPM used, the relative sensitivity of the electrosensory system, shark density and competition, hunger level, and differences in feeding ecology. Other impediments to large-scale adoption of EPM technology by commercial fisheries include the relatively high cost of the rare-earth metals (although magnesium may represent a cheaper alternative), potential toxicity to other marine animals, and the fact that they dissolve rapidly in seawater and, therefore, must be replaced frequently. The use of EPMs for personal shark deterrent devices is also hampered by the limited effective range (<85 cm) of the electrical field they generate.
Instead, for use in scuba dive gear a rechargeable battery-powered capacitor-discharge unit connected to two or four electrodes is sufficient as shark repellent. Also, electro-magnetic induction using permanent magnets may be a more suitable alternative (Hart and Collin, 2015).
Regarding the great white: this shark has a lateral line featuring ampullae of Lorenzini, so EPMs may repel it, theoretically.
Reference
- Hart & Collin. Integrative Zoology; 10(1): 38–64

"Lanthanides are very rare elements, and that is the reason your article speaks of rare earth elements" - actually 'rare' is a misnomer. The lanthanides are highly abundant in the earth's crust. Reference to rare rather comes from the difficulty in separating them from one another since the chemical properties are very similar.

"However, when a magnet is combined with a rare earth element the repellent action is more vigorous" So then why? Is it something chemical plus the magnetic field of the ferro magnet or just because you can make stronger magnetic fields with rare earth materials?

@docscience - The Lanthanide definition is updated in my secnd attempt, and it's about current, not magnetism for EPM, so your second comment is also answered as such.

Nitpicking: Magnesium does not react explosively with water. From the second group calcium metal would react strongly.

@Chris - I  have deletet the Mg example, thanks! Nit pick away!


text:
How did the introduction of artificial light changed the life cycle of a plant?
Plants in urbanized areas are constantly exposed to artificial light after sunset. In their natural habitat there is a more distinct day and night cycle.
Since light is an important factor in a plant life cycle, I wonder if the introduction of the artificial light forces any changes in the life cycle of plants in urbanized areas?

According to this study, artificial lighting similar to that provided by streetlights in the UK can reduce flowering in at least one plant, which also affects the aphids that feed on it.
This article discusses it in more general terms - night lighting doesn't affect photosynthesis, but can affect the length of day/night perceived by plants and alter growth accordingly. There are two examples given of how it is harmful:

Young trees grow longer and don't enter dormancy, making them increasingly susceptible to cold temperatures.
The stomatal pores of leaves remain open longer, making some trees more susceptible to pollution and water stress.


text:
How to conceptualize the action potential?
In my AP Biology class, we were taught that action potentials are not electrical impulses in the same way current travels through a wire. Rather, we were taught that action potentials are changing concentration gradients of sodium and potassium ions.
However, when I looked into modeling action potentials I saw capacitances, inductances, and currents--properties associated with electrical circuits.
My question: action potentials--are they electrical currents in the classical sense? If so, what is the charge that is flowing (is sodium and potassium ions?), and how is the overall charge neutrality of the body maintained?

A changing concentration gradient of Na+ and K+ means that these ions are flowing and thus there is a flow of charge, which is the definition of electric current. However, as opposed to a wire, this current is largely travelling perpendicularly to the direction of the impulse.

@canadianer good point about signal direction and currents. But signal -- membrane depolarization -- goes along axon/whatever

@aandreev What?

@canadianer current flows normal to membrane surface, but signal travels parallel. that is due to nature of ion channels (e.g. inactive phase of Na-channels)

@aaaaaa Yes, I said that.

First of all, electric current is defined as movement of charges, $I=\frac{dQ}{dt}$. In electronics that you see around that is not very useful definition, because electrons move much slower than signals, that is changing electric field. Speed of electric field propagation reaches speed of light, whereas electrons move at 1%-30% or $c$.
In biology, especially regarding action potential, only movement of charges is important, not propagation of electric field, probably because conductance is much smaller than in copper wires. that is signal propagates not through interaction between charges, but via intermediate agent/amplifier -- ion channels.
Charge in body is more or less constant, because action potentials are cyclic: after depolarization membrane comes back to -70mV or something. There is no flow of charge out of the body.

Short answer
Action potentials are mediated by electric currents and can be modeled by electronic circuits.
Background
An electric current is the flow of charge. Therefore, action potentials are mediated by current flow. However, action potentials are mediated by the flow of ions across the membrane (Fig. 1), whereas current flow in electric circuits is typically mediated by the flow of electrons (Fig. 2).

Fig. 1. Action potential propagation. Source: Chen, Carnegie Mellon.
The action potential propagates in the direction of the dendrite. However, the underlying current flow is perpendicular to the axonal membrane and is mediated by ion channels. These ion channels are activated through the sensing of the electrical field. For example, voltage-operated Na+ channels are activated by a small depolarizing potential, while voltage-gated potassium channels open during the later phase of the action potential by a large depolarization.
Whatever the differences, an axon can be well modeled by a parallel resistor-capacitor circuit powered by the membrane potential. The electrochemical properties of the cell membrane makes it equivalent to a circuit with a set of resistors (which are voltage-dependent), batteries (whose voltage depends on ion concentration differences), and a capacitor all connected in parallel (see Fig. 2).

Fig. 2. Electronic circuit representation of the axon. Source: Yale University.
As to your question on charge balance; neutrality is maintained, because Na+ and K+ flow are going in opposite directions and neutralize the net flux of charge.


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Where does the exudate comes from during inflammation?
During inflammation transudate and exudate is formed by vessels. I would like to make sure if it comes from arterioles, venules, or both, and the reason why.

exsudates almost exclusively come from the capillary compartment. If you think about the structure of the vessels, this appears logical.
The capillary compartment :

has vessels only several microns thick
has only the endothelial and basal lamina layers
spans an enormous surface, far greater than arterioles or venules

So when the fenestrations and tight junctions of the capillaries are impaired, serum directly passes into the extracellular medium.
A good example of that would be advanced anaphylactic shock. In this situation, the general inflammatory state causes a loss of endothelial integrity. Adrenaline given in such a state will have an inotropic and chronotropic effect on the heart, will cause vasoconstriction, but will also act to restore endothelial integrity. This last element is the main reason why allergic people carry an epinephrine syringe at all times.


text:
Why does the membrane of a neuron not stay at its depolarized state?
When an action potential is transmitted along the axon, the membrane reaches its depolarized state by opening Na+ channels. Both K+ (potassium) and Na+ (sodium) are now on both sides with close to equal concentration-ratios. It is the next step that confuses me: the K+ rushing out of the cell, thus repolarizing the membrane.
Wouldn't the two substances balance themselves out according to the Electric-/Substance-Concentration-Gradient once the Na+/K+ channels are open? I don't understand where that energy comes from, the energy that not only mediates polarization, but also the subsequent re-polarization.

I edited the question to improve clarity. If the current question does not reflect your original question anymore feel free to roll back

As a short answer: K+ is high in the cell, so it rushes out along its concentration gradient

Three facts:

The K+ ions are heavily concentrated on the inside while the Na+ ions are heavily concentrated on the outside

The Na+/K+ ion pump is unidirectional. It can only pump K+ ions inside the cell while expelling the Na+ ions.

Finally only the Na+/K+ ion pumps can restore the ionic equilibrium.

The full scene:

Once the threshold is reached the Na+ voltage gated channels open up. So Na+ ions rush in, causing depolarisation.

Then the Na+ channels close while the K+ channels open. This causes rushing of K+ ions outside, thus slowly reducing the potential difference starting the process of repolarisation

Now the Na+/K+ ion pumps are geared up as the extracellular concentration of K+ and intracellular concentration of Na+ ions are high (which is the ideal environment for the pump to work.

PS:
Without the high extracellular concentration of the K+ ions the pump can't function any faster than the basal rate even though the intracellular concentration of Na+ ions exceed the normal value by many times. High concentration of K+ ions in the extracellular environment is essential for restoration of the ionic equilibrium.

Edit:
I meant unidirectional in the sense that when actively pumping sodium is always pushed out while potassium is always pushed in.
Thanks to AliceD for pointing out that when the gradient is reversed, the pump synthesizes ATP due to forced movement of ions in the opposite direction.

Correction - Na,K-ATPase is not unidirectional - it is an enzyme, which per definition means it establishes a certain equilibrium. In effect, Na,K-ATPase is an ATP synthase under the correct conditions, such as reversed Na/K gradient: http://link.springer.com/article/10.1007%2FBF00592639

@AliceD I meant unidirectional in its pumping action. Though synthesizing ATP when gradient is reversed is new to me! Thanks for that!

@OneFace Reverse behavior takes many interesting forms. ATP synthase in mitochondria can become proton pumps, for example.


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What is the difference between a graded potential and an action potential?
I was under the impression the only signals neurons send using changes in membrane potential are action potentials. But my biology professor showed us diagrams of graded potentials and action potentials and to me they looked very similar.
What is the difference between a graded potential and an action potential?

Short answer
An action potential is a binary all-or-nothing event, while a graded potential is an analog signal.
Background
Action potentials, once initiated, are basically all-or-nothing events. Amplitudes may admittedly be variable, but basically it is the spike rate that is relevant to the neural code (Gerstner et al., 1997).
In contrast, graded potentials code information mainly by amplitude. A notable example of the significance of graded potentials is the function of the inner hair cells in the cochlea (the inner ear). The mechanoreceptors on the hair cells open when deflected in one direction, while they close in the other. This is important, as that property depolarizes the cell on one phase of an input sinusoid, while it hyperpolarizes the cell in the subsequent phase. Also, stronger (louder) input increases the response, while softer stimulu generate less response (Fig. 1). In the auditory nerve this graded potential is translated into spike rates (Fig. 2). Basically the hair-cell and auditory nerve system is an analogue-to-digital converter.

Fig. 1. Cochlear microphonic: a graded potential that increases amplitude with increasing loudness. Source: Juaristi & Martínez-Conde, 2014

Fig. 2. In the auditory nerve amplitude is coded as action potential (spike) rates, low frequencies as burst-repetition rate. Source: NY University
References
- Gerstner et al., PNAS (1997); 94(24): 12740–1
- Juaristi & Martínez-Conde, Acta Otorrinolaringol Española (2014); 65(04)

This is a really nice answer. I have never understood this concept this well. It goes beyond a surface description and actually identifies the specific mathematical/code property that makes the two distinct. Really cool.

@StanShunpike - thanks for your nice feedback. I had to ponder on this one for a few days before answering :) I'm glad the answer was helpful. Thanks for accepting too. Late answers often don't get a lot of upvotes  :)

Graded potentials are initiated by a stimulus that vary in magnitude depending on the strength of the stimulus. (The stronger the stimulus the more gated channels open causing larger depolarisation). Graded potentials occur in dendrites, cell bodies and sensory receptors. Graded potentials dissipate with distance from stimulus.

On the other hand, action potentials occur when graded potentials reach the axon hillock at a certain level of depolarisation (around -55mV). This opens the activation gate letting sodium flood into the membrane. This is an "all or nothing" event, once the threshold triggers the membrane depolarises quickly to around +30mV.
I could just save you time and show you this table:


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Is the immune system suppressed during sleep?
Of course we have heard that during stress our immune system is suppressed. This leads me to wonder, does the immune system get suppressed when we are sleeping and why? During both these conditions the body might need to save energy for other biochemical processes, so I wouldn't be surprised that the immune system is suppressed while a person is asleep.

@AliceD is this better?

Nope. 'I' and 'my' should be removed. Importantly, questions should be generalizable and interesting to the community at large. No one can possibly know why your immune system is, or is not suppressed. Again, it is an interesting question, but it needs re-wording.

@AliceD what about this question?: http://biology.stackexchange.com/questions/24555/what-causes-feeling-of-feet-falling-asleep-to-be-delayed/25875#25875

It is a gray area, but that linked question is not a medical issue, it is an observation of a physiological process that is generalizable to something everyone has experienced in their life. Your question is not readily generalizable as you start of with an unsupported personal anecdote that likely not many folks agree upon.

@AliceD I have significantly edited it, now what do you think?

I don't have the time for a full answer, so I may come back, but generally 'no'. There is a difference between hibernation (a reduction in metabolic rate to survive prolonged periods of fasting) and sleeping. Humans do not hibernate, and when we are asleep the body doesn't try to save energy. Our brains go through REM sleep, which is just as active as waking hours, our organs -- especially dermal and muscle tissues -- amp-up their repair mechanisms while sleeping. Given that prolonged poor and/or lack of sleep significantly lengthens illnesses, the immune system should be very active.

During stress glucocorticoids, which are steroid hormones produced by adrenal glands (such as cortisol and corticosterone), are released into the blood-stream. These hormones have anti-inflammatory effects. You may say that they suppress the immune system.
The circadian rhythm, which controls the sleep-wake cycle, also controls glucocorticoid secretion, thereby reinforcing the sleep-wake responses [1]. Sleep deprivation is a form of stress and it causes an elevation in the levels of glucocorticoids. The effect of sleep deprivation could be replicated by adrenectomy (surgical removal of adrenal glands); there is a transcriptional downregulation of several neuroprotective genes [2]. Via glucocorticoid mediated signalling, sleep deprivation also results in inhibition of adult neurogenesis in the hippocampus [3].
Another study says that cytokine (TNFα and IL6) secretion by immune-system cells, are inherently affected by circadian rhythm via a glucocorticoid independent mechanism [4].
Overall, sleep is inversely correlated with reduced inflammation because both the processes are under the control of the circadian clock. Sleep deprivation, as a form of stress, is also correlated with glucocorticoid secretion. It should be understood that sleep doesn't necessarily inhibit glucocorticoid secretion and it would be incorrect to say that reduced inflammatory effects are because of sleep.

So this means that sleep does NOT cause immunosupression?

@TanMath Yes it is the opposite actually- immune system may be activated during sleep. But I wanted to refrain from saying that. Because such a strong statement cannot be made.


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C1q attachment to antibodies
After reading about complement pathway and the complement components, I was wondering, does the C1q component attach to the Fab fragment or to the Fc fragment? The pictures in Janeway's Immunobiology are confusing and the text don't mention about this.

You said Fab fragment twice.

Can you please edit your question for clarity?  Right now it is unclear what you're asking.

I think voting for question closure based on a typo is a bit harsh. If journal referees would start rejecting manuscripts on that basis even Nature would have trouble filling its pages  =)

@ChrisStronks While I agree about the closing - an article in a bad grammatical style or with too much typos will never reach the reviewers. It will be sorted out by the editors when they do an initial review.

Complement factor c1q binds to the constant Fc portion of an antibody (Duncan & Winter, 1988). Indeed, the constant (Fc) tail of the antibody is where other proteins involved in immune responses typically bind, most notably the Fc receptors (e.g., Clynes et al., 2000) found on immune cells such as B lymphocytes. Fc receptors mediate the recruitment of immune cells to a site of infection. The primary role of the Fab region is antigen binding as it contains the highly variable antigen binding domain. See the following figure (from the site of Invivogen) for the Fab and Fc region showing the constant and variable regions of antibodies:

Figure legend from Invivogen): The Fc region mediates effector functions, such as antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC). In ADCC, the Fc region of an antibody binds to Fc receptors (FcγRs) on the surface of immune effector cells such as natural killers and macrophages, leading to the phagocytosis or lysis of the targeted cells. In CDC, the antibodies kill the targeted cells by triggering the complement cascade at the cell surface. I

The constant regions of antibodies are located on the heavy chain (CH1,2,3) and the light chain (CL). These constant regions are potential binding sites for other immune molecules as they are constant between antibodies, irrespective of the variable region in Fab. Most of the constant regions are found on the Fc region explaining its major role in binding other molecules involved in the immune response, including complement factor c1q. However, the constant regions in Fab (CL) may also provide binding sites for other proteins and indeed some bacterial compounds are known to bind to this region (Bouvet, 1994). However, I have not found evidence of c1q binding the Fab region.

So Fab fragments can't activate the complement?

No, not as far as I am aware.


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What causes the bright flash of light when poking my eye?
Recently, I poked myself in between my eye and eye socket, right below my eyebrow, and sometimes I would get this flash of light. Others have tried this too, and they also had a flash of light. I am wondering why is this the case. Does it have to do with the nerves in the eye?

Yes. You somehow stimulated your optic nerve.

Im probly stating the obvious here but i reckon you should probly go to the doctor for this one:)

@MattDMo so really, I am really asking which optic nerve I stimulated?

I would like to point out to you that that is exactly what Isaac Newton did and set off his interest in light. I hope you become like him! ;) (you might find this interesting: http://www.psmag.com/health-and-behavior/newtons-needle-scientific-self-experimentation-86583 or even watch http://www.ensemblestudiotheatre.org/isaacs-eye-lucas-hnath)

@TanMath - there's only one "optic nerve" per eye. That's the name for the bundle of nerves, made up of (?hundreds of thousands?) of nerve cells receiving signals from various nerve endings in the eye.

Short answer
Pressure phosphenes are believed to be induced by stretch-induced activation of retinal ganglion cells.
Background
Flashes of light (phosphenes) due to pressure on the eye ball are referred to as pressure phosphenes. Based on an electrophysiological study (Grüsser et al., 1989), eyeball indentation presumably tangentially stretches the retina locally, which variably depolarizes horizontal cells. This in turn depolarizes ON-bipolar ganglion cells, while hyperpolarizing OFF-bipolars. Some ON-center neurons also seem to respond to the removal of the deformation. Bipolar cells connect to the retinal ganglion cells. These ganglion cells carry visual information from the retina via their axons in the optic nerve to the brain. Hence, to answer your question: yes, pressure phosphenes are related to activity in the optic nerve.
Reference
- Grüsser et al., Vis Res (1989); 29(2): 181–94


text:
What's a mouth ulcer/canker sore "made of", and why do they develop?
Mouth ulcers are red/white rings with a crater. They are sore and last for 7-10 days.
What I want to know is what they are 'made of' - i.e., what is the ring filled with, and why is the centre crater so sore? And why do these relatively benign and short-lasting ulcers have to hurt so much when they simply heal in a couple of days

I'm especially interested in the latter half of this question, specifically in the case of minor oral injuries. What is the mechanism by which a small wound (e.g. from accidentally biting the inside of your lip) can develop into a wide open sore that's many times the size of the original injury?

The redden area around the grayish-white indentation of the canker sore isn't filled with anything. This circular area is simply inflamed. The grayish-white area in the center is not filled with puss or anything else as well. This is an area of dead cells but underneath this layer of dead cells the tissue red [1],[2],[3].
Canker sores, Aphthous stomatitis, is an ulcer. An ulcer is a break in the membrane. That is, you have an open sore in your mouth. As with any open wound, pain and discomfort will occur but the mouth is how we consume our food. Since we intake our daily bread in this manner, what we consume can cause the pain to increase; for instance,

acidic foods
spicy foods
abrasive foods

The cause of canker sores is not entirely known, but according to the Mayo clinic [2], possible triggers are

A minor injury to your mouth from dental work, overzealous brushing, sports mishaps or an accidental cheek bite
Toothpastes and mouth rinses containing sodium lauryl sulfate
Food sensitivities, particularly to chocolate, coffee, strawberries, eggs, nuts, cheese, and spicy or acidic foods
A diet lacking in vitamin B-12, zinc, folate (folic acid) or iron
An allergic response to certain bacteria in your mouth
Helicobacter pylori, the same bacteria that cause peptic ulcers
Hormonal shifts during menstruation
Emotional stress

Canker sores may also be caused by the following diseases as well [2]

Celiac disease, a serious intestinal disorder caused by a sensitivity to gluten, a protein found in most grains
Inflammatory bowel diseases, such as Crohn's disease and ulcerative colitis
Behcet's disease, a rare disorder that causes inflammation throughout the body, including the mouth
A faulty immune system that attacks healthy cells in your mouth instead of pathogens, such as viruses and bacteria
HIV/AIDS, which suppresses the immune system


text:
Introducing novel genes to an adult multicellular organism?
Is it possible to introduce a novel gene into the genome of every cell (or at least most cells) of an adult multicellular organism? How would this be done?
Thanks,
CDB

How multicellular? Are you referring to sponges or mammals? What is "most"? Does the gene need to be expressed as well? You need to give more detail.

Short answer, in theory yes, in reality, at the current state of the art, no.
I guess you are speaking about higher organisms (such as mice or humans), if you are referring to small non-complex multicellular organisms then the answer is yes as far as you can transfect every cells with the system described hereafter.
The most promising technique is using the CRISPR/Cas9 system which has already been used to create all types of modified organisms but starting from the embryo. Here a good Nature reference http://www.nature.com/nbt/journal/v32/n4/full/nbt.2842.html.
There are no ways, at the moment, to transfect an entire organism with the full system. The most recent attempts I heard off is to target specific cells using an encapsulation techniques that only merges with the membrane of specific cells therefore delivering the CRISPR/Cas9 system in a targeted manner. This was in an attempt to knock-out a defined genomic regions in those specific cells, not to introduce a new gene.
I believe in the near future that this will be possible. Not necessarily every cells of an organism but at least some specific cell types.


text:
Stable and strong promoter?
I need a mammalian promoter that will maintain stable expression through differentiation.
I was originally planning to employ UbC for this specific project, however new information from a different experiment has come to light and now I need a promoter that has both extreme stability and high strength (as you know, UbC is renowned for it's very low expression rates).
Do any of you have suggestions? Perhaps I should look into a hybrid promoter of sorts...
Thank you,
CDB

I know the CMV promoter is pretty strong, not sure about its stability.

How about SV40?

is there any specificity for cell type or do you need a ubiquitous promoter?

@MattDMo In my experience, the SV40 promoter is at least 10 fold weaker than the CMV and only expresses for 4 - 5 days. I haven't seen how long CMV expresses for.

@user137 Yes, I have looked into CMV a little, it has low stability in quite a few cell types though.

@MattDMo I will look into that.

@RoverEye It must be ubiquitous (might I add that this requirement has been quite a pain?)

beta-actin promoter?

While looking into your suggestions I came across two promising candidates. Does anyone have experience with PGK-1 or EF1a? How stable are they and what is their expression rate?

HSV-TK promoter is also quite good. Never used PGK-1 and EF1a

There seems to be quite an amount of resources to help OP.
Addgene has a page on topic with list and description of common promoters usable in variety of organisms: Plasmids 101: The Promoter Region
Experimental biophysics textbook mentions some useful promoters as well, or this review.
Surprisingly, there has been some quantitative analysis of promoter strength: Systematic Comparison of Constitutive Promoters and the Doxycycline-Inducible Promoter, as well as effort toward stronger synthetic (version of CMV) Synthetic design of strong promoters
My conclusion is that either viral, or CAG (based on chicken actin) promoters might be useful candidates. But one cannot expect ubiquitous and even expression in various tissues/cells types without fine-tuning expression cassette.